Out-of Hospital Ventilation: An Interdisciplinary Perspective on Landscape and Health 366264195X, 9783662641958

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Hartmut Lang  Editor

Out-of Hospital Ventilation An Interdisciplinary Perspective on Landscape and Health

Out-of Hospital Ventilation

Hartmut Lang Editor

Out-of Hospital Ventilation An Interdisciplinary Perspective on Landscape and Health

Editor

Hartmut Lang Hamburg, Germany

ISBN 978-3-662-64195-8    ISBN 978-3-662-64196-5 (eBook) https://doi.org/10.1007/978-3-662-64196-5 © Springer-Verlag GmbH Germany, part of Springer Nature 2023 This book is a translation of the original German edition “Außerklinische Beatmung” by Lang, Hartmut, published by Springer-Verlag GmbH, DE in 2017. The translation was done with the help of artificial intelligence (machine translation by the service DeepL.com). A subsequent human revision was done primarily in terms of content, so that the book will read stylistically differently from a conventional translation. Springer Nature works continuously to further the development of tools for the production of books and on the related technologies to support the authors. This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors, and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, expressed or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. This Springer imprint is published by the registered company Springer-Verlag GmbH, DE, part of Springer Nature. The registered company address is: Heidelberger Platz 3, 14197 Berlin, Germany

V

Preface Nonclinical ventilation claims to be a companion book for colleagues who attend the training course “Basic qualification in nonclinical ventilation” DIGAB-accredited providers. Since 2011 (2012), the German Interdisciplinary Society for Out-of-­ Hospital Ventilation (Deutsche Interdisziplinäre Gesellschaft für Außerklinische Beatmung e. V.) has been developing a curriculum in which the contents of the training course are developed. Participants in this training course are to acquire extensive knowledge for the care of ventilator-dependent people. The book is therefore aimed at all professional nursing colleagues who attend this advanced training course and also at those who feel insecure in the care of these people, patients, and residents. The aim of my co-authors and myself is to provide a comprehensible orientation on the topic of artificial respiration in the context of out-of-hospital care. Out-of-hospital ventilation is didactically divided into six parts and is based on the requirements of the DIGAB curriculum: 55 Part I: Basics of breathing and respiratory failure 55 Part II: Ventilation options 55 Part III: Ventilation modes and patterns 55 Part IV: Further treatment measures 55 Part V: Monitoring and nursing care of the patient and ventilation 55 Part VI: Legal bases for out-of-hospital ventilation Part I deals with the anatomical and physiological basics of respiration, explains respiratory failure, and describes diseases that can lead to the need to ventilate. Part II gives an overview of the different ventilation options, either noninvasive ventilation or invasive ventilation with tracheal cannula. Part III explains the different ventilation modes, their nomenclature, settings, and functions of the individual settings. The purpose of the different ventilation modes is illustrated using case studies. Part IV gives an overview of other treatment measures that are additionally given to people who are ventilated outside the hospital, including various drugs and often oxygen therapy. The people affected suffer from swallowing disorders, have to be artificially fed, and require psychosocial care, which must also include their relatives. Part V represents the comprehensive care and supervision of people. It gives an overview of terms used in ventilation and describes the alarm and measurement values of ventilation. In addition, there are respiratory therapeutic measures that are of great importance in the ongoing care, such as respiratory gas conditioning, secretion management, and weaning. Part VI summarizes the legal basis of out-of-hospital ventilation. An orderly discharge management ensures the transition to domestic care. Liability and the Medical Devices Act are immediate issues for professional caregivers. Important for all people are topics concerning care or the patient’s will. Out-of-hospital ventilated patients pose high challenges for all professional caregivers. Understanding the reasons for ventilation, understanding the types of airway access, differentiating between the different ventilation modes, and providing comprehensive patient care are very extensive and complex aspects. This is the aim of our book, and we would like to be measured by your, the readers’, experience.

VI

Preface

I wish all readers an exciting read in an area that is not always easy to understand and that all those who work on and with respiratory patients find a common working basis and working language in which the technical and factual uncertainties are removed. Hartmut Lang

Hamburg January 2017

VII

Acknowledgments Without the help of many people and companies, this book would not have been written the way it is now before you. First of all, I would like to thank all my co-­ authors who helped to create “out-of-hospital ventilation.” Thanks to their participation, it was possible to bring in a competent and specialized knowledge in their respective fields: Dr. Huhn (Hospital Friedrichstadt Dresden, Senior Physician of the Department of Pneumology, Dresden), Dr. Schröter (Klinik Hoher Meißner, Head Physician of the Department of Neurology, Bad Sooden-Allendorf), Mr. Malte Voth (Teaching Rescue Assistant, Bad Bramstedt (safety-in-emergency)), Mrs. Britta Behrens (Pharmacist, Dorfplatz Pharmacy, Hamburg), Mrs. Monika van den Boom (Speech and Language Therapist, Viapallia Wedel/Holstein), Mr. Peter Otte (Certified Pedagogue, Detmold), Mr. Michael Thoms (Specialist Nurse, MediClin Lingen), Mrs. Elke Strelow (Nursing Pedagogue, Bad Segeberg), and Mr. Andreas Böhme (Nursing Pedagogue, Hamburg). I would like to thank my colleagues Martin Effenhauser, Franziska Hummel, and Claudia Hajabatsch for their untiring proofreading and technical correction. Special thanks go to our friend Mrs. Brigitte Poggemeier, who was constantly on the lookout for superfluous filler words, sentence order, orthography, and expression. A huge thank-you goes to my colleague and illustrator Mrs. Isabel Guckes, who has created many illustrations and edited all my drawings. I would like to thank Prof. Dr. Stefan Kluge, chief physician of the intensive care clinic at the UKE-Hamburg, for his permission to use illustrations and pictures of the University Hospital Hamburg-Eppendorf. Many companies and institutions were also willing to provide graphical material and tables for the book: 55 Idiag AG, Mülistrasse 18, CH-8320 Fehraltorf 55 IFP—International Foundation for Research in Paraplegia, Rämistrasse 5, 8001 Zurich 55 Prof. Martin Schwab, Institute for Brain Research, University of Zurich 55 Prof. Dr. med. T.O.F. Wagner, Department of Pneumology/Allergology, University Hospital Frankfurt 55 R. Cegla GmbH & CO. KG, Horresser Berg 1, 56410 Montabaur 55 Federal Association “Craniocerebral Patients in Need,” Deutsche Wachkoma Society 55 HEIMOMED Heinze GmbH & Co KG, HELPING INNOVATION®, Kerpen 55 GHP Pflegedienst—Society for Home Care in Hamburg and Surroundings 55 Covidien Deutschland GmbH, Neustadt/Danube 55 ResMed GmbH & Co KG, Martinsried 55 Philips GmbH Respironics, Herrsching 55 Center of the health services Dresden, nursing service Dresden 55 Radiometer GmbH, Willich 55 Medtronic GmbH, Meerbusch 55 Seilnacht Verlag & Atelier, Thomas Seilnacht, Bern 55 Gründler, ResMed Martinsried 55 Intersurgical, Sankt Augustin

VIII

Acknowledgments

55 Medisize Germany, Siegburg 55 Trudell Medical, Ontario, Canada 55 P.J. Dahlhausen & Co. GmbH, Cologne 55 INSPIRATION Medical GmbH, Bochum 55 National Association of Statutory Health Insurance Physicians, Berlin To all of you a very warm thank-you for your support! Last but not least, I would like to thank Mrs. Sarah Busch from Springer-Verlag for her trust in my work. Mrs. Busch has always accompanied my work in a stimulating way. She has contributed significantly to the didactic structure. I would also like to thank my editor, Ms. Ute Villwock, for her corrections and the structure. Hartmut Lang

IX

Contents I

Basics of Breathing and Respiratory Failure

1

Anatomy and Physiology of Respiration........................................................................ 3 Hartmut Lang

2

Indications and Goals of Ventilation................................................................................. 35 Hartmut Lang

3

Diseaseology..................................................................................................................................... 43 Matthias Huhn

II

Ventilation Options

4

Tracheotomy..................................................................................................................................... 75 Hartmut Lang

5

NIV (Non-invasive Ventilation).............................................................................................. 95 Hartmut Lang

III

Ventilation Modes and Patterns

6

Respirator Models......................................................................................................................... 107 Hartmut Lang

7

Spontaneous and Positive Pressure Ventilation....................................................... 115 Hartmut Lang

8

Ventilation Modes......................................................................................................................... 119 Hartmut Lang

9

Pressure-Controlled Ventilation (PCV/A-PCV)............................................................ 125 Hartmut Lang

10

Volume Controlled Ventilation (VCV)............................................................................... 139 Hartmut Lang

X

Contents

11

Pressure-Regulated-Volume-­Controlled Ventilation............................................. 149 Hartmut Lang

12

Pressure Support Ventilation (PSV)................................................................................... 155 Hartmut Lang

13

SIMV (Synchronized Intermittent Mechanical Ventilation)............................... 167 Hartmut Lang

14

AVAPS (Average Volume Assured Pressure Support)............................................. 173 Hartmut Lang

15

Emergency Management.......................................................................................................... 177 Malte Voth

IV

Further Treatment Measures

16

Pharmacology.................................................................................................................................. 195 Britta Behrens

17

Oxygen Therapy.............................................................................................................................. 225 Hartmut Lang

18

Dysphagia........................................................................................................................................... 239 Monika van den Boom

19

Communication in Care Relationships............................................................................. 253 Peter Otte

V

Monitoring and Nursing Care of the Patient and Ventilation

20

Hygiene................................................................................................................................................. 275 Michael Thoms

21

Resistance and Compliance..................................................................................................... 289 Hartmut Lang

22

Control Mechanisms and Types of Control................................................................... 299 Hartmut Lang

XI Contents

23

Flow and Flow Curves.................................................................................................................. 303 Hartmut Lang

24

Alarms and Alarm Settings...................................................................................................... 315 Hartmut Lang

25

Ventilation Measured Values................................................................................................. 321 Hartmut Lang

26

Monitoring......................................................................................................................................... 329 Malte Voth

27

Blood Gas Analysis (BGA)......................................................................................................... 333 Hartmut Lang

28

Breathing Gas Conditioning................................................................................................... 361 Hartmut Lang

29

Secretary Management............................................................................................................. 371 Hartmut Lang

30

Weaning............................................................................................................................................... 389 Hartmut Lang

VI

Legal Bases for Out-of-­Hospital Ventilation

31

Discharge Management in Nursing................................................................................... 403 Elke Strelow

32

Criminal and Liability Aspects.............................................................................................. 415 Andreas Böhme

33

Implementation of MPG/Operator Regulation.......................................................... 421 Andreas Böhme

34

Care, Power of Attorney and Living Will......................................................................... 425 Andreas Böhme

Supplementary Information Appendix................................................................................................................................................. 430

XIII

Contributors Britta Behrens  Stapelfeld, Germany Andreas Böhme  Hamburg, Germany Monika van den Boom  Viapalla Reha GmbH, Wedel, Germany Anita Büchli  University of Zurich, Institute for Brain Research, Zurich, Switzerland Matthias Huhn  Fachkrankenhaus Coswig GmbH, Zentrum für Pneumologie und Thoraxchirurgie, Intensivstation, Coswig, Germany Hartmut Lang  Hamburg, Germany Peter Otte  Detmold, Germany Arne Raupers  Krummesse, Germany Carsten Schröter  Klinik Hoher Meißner W. und M. Wicker GmbH, Neurologishe Abteilung, Bad Sooden-Allendorf, Germany Martin Schwab  University of Zurich, Institute for Brain Research, Zurich, Switzerland Elke Strelow  Bad Segeberg, Germany Michael Thoms  Haselüne, Germany Malte Voth  Notfallmedizinische Fortbildunge, Bad Oldesloe, Germany

1

Basics of Breathing and Respiratory Failure Contents Chapter 1

 natomy and Physiology of Respiration – 3 A Hartmut Lang

Chapter 2

I ndications and Goals of Ventilation – 35 Hartmut Lang

Chapter 3

Diseaseology – 43 Matthias Huhn

I

3

Anatomy and Physiology of Respiration Hartmut Lang Contents 1.1

Upper Airways – 5

1.1.1 1.1.2 1.1.3 1.1.4

T asks of the Upper Airways – 5 Reference to Artificial Respiration – 6 Nose – 6 Larynx and Vocal Cords – 6

1.2

Lower Airways – 8

1.2.1 1.2.2 1.2.3 1.2.4 1.2.5 1.2.6 1.2.7 1.2.8

T rachea (Windpipe) – 8 Carina – 8 Bronchial tree (Bronchial System) – 8 Mucociliary Clearance – 10 The Position of the Lungs in the Body – 11 The Lobes, Lobes and Segments of the Lungs – 13 Alveoli and Surfactant – 15 Pulmonary Vessels – 16

1.3

Respiratory Support Musculature – 17

1.3.1 1.3.2

I nspiration – 17 Expiration – 18

1.4

Physiology – 19

1.4.1 1.4.2 1.4.3

 reathing Air – 19 B Diffusion Time: Diffusion Distance – 20 Breathing Regulation – 20

© Springer-Verlag GmbH Germany, part of Springer Nature 2023 H. Lang (ed.), Out-of Hospital Ventilation, https://doi.org/10.1007/978-3-662-64196-5_1

1

1.4.4 1.4.5

 hysiological Shunt Volume – 20 P Breathing Mechanics – 20

1.5

Central and Peripheral Nervous System – 22

1.5.1 1.5.2 1.5.3 1.5.4 1.5.5

 natomy of the Brain – 23 A Brain Structure – 23 The Lobes and Regions of the Brain – 25 Pyramidal and Extrapyramidal System – 26 Blood Supply to the Brain – 27

1.6

Spinal Cord – 28

1.6.1 1.6.2 1.6.3

S tructure of the Spinal Cord – 28 The Internal Structure of the Spinal Cord – 28 Structure of a Nerve Cell – 31

1.7

Phrenic Nerve – 31

1.8

Interconnection of the Nerve Tracts – 32 References – 33

1

5 Anatomy and Physiology of Respiration

1.1 

Upper Airways

Components of the Upper Respiratory Tract (. Fig. 1.1)  

55 55 55 55

Nose and nasal cavity Mouth Throat (pharynx) Larynx

1.1.1 

Tasks of the Upper Airways

During normal breathing, the upper respiratory tract has four functions (. Table 1.1): heating, humidification, filtration and turbulence of the respiratory gas.  

..      Fig. 1.1  Upper airways (courtesy of Isabel Schlütter)

.       Table 1.1  Tasks of the upper airways Heating

Inhaled air is heated and can therefore absorb more water vapour

Humidification

With aqueous secretion from the glands of the upper respiratory tract, self-cleaning mechanism is maintained

Filtering

Interception of larger particles through nasal hairs and through the mucus coating of the nasal and tracheobronchial mucosa

Turbulence

Causes the greatest possible contact between air and mucous membrane

6

1

1.1.2 

H. Lang

Reference to Artificial Respiration

The upper airways can no longer perform these tasks if they are bypassed by means of a tracheal cannula. In this case, artificial respiration must provide technical aids to perform the above-mentioned tasks. Active or passive humidification systems are used. 1.1.3 

Nose

On the side wall of each nasal cavity there are three nasal conchae lying one above the other (. Fig.  1.2). The nasal mucosa consists of a ciliated epithelium with many mucous glands. The ciliated epithelium beats the mucus film backwards towards the throat. In the upper space of the nasal cavity is the olfactory mucosa. Beneath the mucosa runs a dense capillary network,  

partly as a voluminous venous plexus (septal plexus). Nosebleeds mostly occur in the front part of the nasal mucosa. 1.1.4 

Larynx and Vocal Cords

The larynx separates the pharynx from the windpipe (. Fig. 1.3). It lies palpably at the front of the neck. The larynx has three functions: 1. Protection against Aspiration during Swallowing When swallowing, the larynx is pulled forward and upwards. The epiglottis closes the trachea. Food and drinks are thereby directed into the oesophagus. This protects the lower airways from aspiration. Aspiration describes the penetration of foreign bodies into the lower airways. Unlike babies, adults do not have the ability to swallow and breathe at the same time, which can lead to aspiration. 2. Transition from Upper and Lower Airways The glottis is the narrowest part of the airways in adults. The inhaled and exhaled air flows through the glottis each time. However, the diameter is large enough to allow breathing without effort and respiratory exhaustion. 3. Voice and Speech Training The vocal folds regulate the flow of the breathing air. The vocal folds are thus set into vibration and thus voice and speech are formed (. Fig. 1.4).  

 

..      Fig. 1.2  Nasal cavity: nasal conchae (courtesy of Isabel Schlütter)

The vocal folds are visualized by means of a laryngoscopy of the larynx. When breathing calmly, the vocal folds are at a sufficient distance from each other. The opening between the vocal folds is called the glottis. The vocal folds lie close together during voice and speech formation. Thus the glottis narrows. Voice and speech are produced with the exhaled air stream, not during inhalation. The exhaled air flow is regulated, sometimes

7 Anatomy and Physiology of Respiration

1

..      Fig. 1.3  Larynx (from Spornitz 2010, Anatomy and Physiology, Textbook and Atlas for Nursing and Health Professions, 6th ed. Springer, Heidelberg Berlin)

..      Fig. 1.4  Glottis when speaking (left) and breathing (right) (courtesy of: Isabel Schlütter)

the air flows faster, sometimes slower and makes the vocal folds vibrate. Depending on the tone and voice, the glottis narrows so that a very varied tone and voice formation is possible. At the same time, the exhaled air flow is delayed; this enables the person to form very long sentences or sing long song verses. The exhalation with voice and speech formation can thus be as long as 10–20  s. This also extends the I:E ratio from 1:2 to 1:10 or 1:20.

z Reference to Artificial Respiration with Tracheal Cannula

A tracheal cannula is inserted into the trachea below the larynx (7 Chap. 4). A speech formation is possible with the cannula unblocked. In cases of swallowing disorders, the secretion of the upper respiratory tract also collects below the larynx (subglottic) and above the tracheal cannula and can lead to microaspirations.  

8

1

H. Lang

1.2 

Lower Airways

1.2.2 

Components of the Lower Airways 55 55 55 55

Trachea (windpipe) Bronchia Bronchioles Alveoli (only they are used for gas exchange)

The first branch from the trachea to the two main bronchi is called “carina”. It is traversed by a dense nervous network. If the carina is irritated by aspirated foreign bodies, a coughing sensation develops. This can also be triggered by endobronchial suction. 1.2.3 

1.2.1 

Trachea (Windpipe)

The trachea stretches as a tube between the larynx and the trunk bronchi. It is approx. 10–12  cm long, elastic, and has 12–20 horseshoe-­shaped cartilage clips towards the front, which can be palpated from the outside. They prevent collapse of the trachea. The back wall is elastic and consists of connective tissue and muscles. Adjacent to this is the esophagus. Due to the elasticity of the back wall, the inner diameter of the trachea can be narrowed to approximately ¼. This has its significance in coughing and sneezing, where air is forced out at high pressure (. Fig. 1.5 right).  

Carina

 ronchial tree (Bronchial B System)

The right, somewhat stronger main bronchus is 1–2.5  cm long. It runs somewhat straighter than the left main bronchus and has a kink of only about 20% compared to the trachea. The left, weaker main bronchus is 4.5–5  cm long. Its angulation is at least 35% in relation to the trachea (caused by the aortic arch). Aspirated foreign bodies enter the right main bronchus more often than the left main bronchus due to the angle between the trachea and the bronchi. Trachea and bronchial tubes dilate slightly during inhalation. This causes the inner diameter of the airways to increase and inhalation is effortless. During exhalation, the trachea and bronchi narrow slightly.

..      Fig. 1.5  Cross-section trachea (courtesy of Isabel Schlütter)

1

9 Anatomy and Physiology of Respiration

This causes the inner diameter of the airways to decrease. The exhalation lasts a little longer than the inhalation when at rest. This results in a resting respiratory time ratio of I:E = 1:2. The airways remain securely open due to the cartilage braces and plates. The walls of the bronchi are made up of three layers (. Table 1.2). The bronchial tree serves to transport the inhaled air. It branches out further and further, a total of 23 times. Each branching is called generation. Up to the 16th generation, the bronchial tree serves exclusively to transport air. From the 17th generation on, the area where gas exchange is possible begins. This is where the alveolar region begins (. Fig. 1.6). The total volume of the bronchial system is quite small, only 100  ml. Therefore, the entry of fluids and foreign bodies is dangerous for humans, as the volume can be filled quickly.  

Anatomical Classification of Bronchial System (. Fig. 1.7)

the

 

55 55 55 55 55 55 55

55 55

Main bronchus Flap bronchi (right 3, left 2) Segmental bronchi (right 10, left 9) Medium and small bronchi Bronchioli (all cartilage elements are missing) Bronchioli terminales Bronchioli respiratorii (beginning of the respiratory part of the bronchial tree) Alveolar duct Acini (1 acinus comprises 1500–4000 alveoli, diameter 2.5–5 mm)

 

.       Table 1.2  Structure of the bronchial walls Inside

Cylinder epithelium and cilia

Middle

Glands for moisture and slime formation

Outside

Cartilage (cartilage braces) for keeping open and for external splinting

z Dead Space

The air from the nose or mouth to the bronchioles of the 16th generation is called dead space. It is the part of the respiratory system that is ventilated but not involved in gas exchange. The dead space can be further subdivided. kAnatomical Dead Space

These include the upper airways of the nasopharynx, larynx, trachea, bronchia up to the 16th generation. They serve to transport, clean, humidify and warm the air we breathe. The anatomical dead space is about 2 ml/kg

..      Fig. 1.6  Bronchial system, left 1st-16th generation and right 17th-23rd generation (courtesy of Isabel Schlütter)

10

H. Lang

1

..      Fig. 1.7  Bronchial system, middle bronchi up to alveoli (courtesy of Isabel Schlütter)

body weight. For an adult person with a weight of 75 kg, the dead space is therefore approx. 150 ml air. The air of the anatomical dead space is the last amount of air that is breathed in. It is also the first to be exhaled again. kAlveolar Dead Space

Part of the alveoli is insufficiently supplied with blood. In lung-healthy people, this is about 2% of the respiratory volume (tidal volume). Breathing air that enters the alveoli therefore does not participate in the gas exchange. z Functional Dead Space

Is the sum of the anatomical and alveolar dead space and is approximately 30% of the tidal volume.

z Alveolar Ventilation

The proportion of the breathing air that enters the alveoli, and can thus participate in the gas exchange, i.e. the difference between respiratory minute volume minus dead space volume. Alveolar ventilation is approx. 4500 ml/min or 60 ml/kg bw/min in adults and approx. 400  ml/min or 100– 150  ml/kg bw/min in neonates, and is thus more than twice as high as in adults. 1.2.4 

Mucociliary Clearance

The ability of the respiratory tract to cleanse itself is called mucociliary clearance. The inner walls of the respiratory tract are lined throughout with ciliated epithelium, the cilia, interspersed with mucus-producing

1

11 Anatomy and Physiology of Respiration

..      Fig. 1.8  Mucociliary transport system (courtesy of Isabel Schlütter)

cells (. Fig.  1.8). The mucus settles as a mucous layer on the cilia and serves to self-­ cleanse the airways. The cilia move back and forth like a whip, about 30 times per second (30 hearts). They thus ensure that the mucus and foreign particles are transported in the direction of the larynx. A continuous secretion of mucus takes place. The mucus layer traps and encloses foreign particles. Finally, they are transported upwards towards the trachea. Most foreign particles that enter the air-­ conducting airways through breathing are thus removed within 24 h. Longer transport times affect foreign particles that have been deposited in the alveolar region. The mobility of the cilia depends on the humidity of the air. If the air humidity is not sufficient and the temperature is too low, the cleaning mechanism is hindered.  

kReference to Artificial Respiration

Without humidification and warming, the respiratory tract cannot perform its clearing tasks. Even reducing the humidity to 90% can severely impair the mobility of the cilia. However, the mobility of the cilia is reversible if the respiratory air is temporarily insufficiently humidified and heated.

1.2.5 

 he Position of the Lungs T in the Body

The lung lies in the thorax (. Fig. 1.9). If you feel above the clavicle, the top of the lung is below it. The diaphragm (diaphragm) limits the lung to the bottom and at the same time separates the thorax from the abdomen. The lung is limited to the front, sides and back by the ribs, the sternum and the spine. At the same time, the ribs provide protection for the lungs and heart. The lung is enclosed by a skin, the pleura and consists of two “leaves”. The inner leaf, the pleura visceralis, lies adjacent to the lung (. Fig.  1.10). The outer leaf, the pleura parietalis, lines the thorax from the inside. Between the two leaves is the pleural gap, which is filled with fluid. Thus the lung is stretched out against the thorax, it cannot collapse. Only through the entry port for blood vessels and the trunk bronchi (hilus) is the lung firmly connected to the thorax. The two sheets can shift against each other. This allows the lungs to move around and breathe. The lung thus passively follows the movement of the rib cage, which is  

 

12

H. Lang

1

..      Fig. 1.9  Hull view (courtesy of Isabel Schlütter)

visceral pleura Pleural space parietal pleura

..      Fig. 1.10  Pleura and pleural gap (courtesy of Isabel Schlütter)

13 Anatomy and Physiology of Respiration

actively moved during breathing. The lung itself has no musculature that can produce active movement. Within the pleural gap there is a negative, subatmospheric pressure. During exhalation it is approx. −5  cm H2O, and during inhalation approx. −8 cm H2O. Due to its elastic fibres, the lung tends to want to contract. During inhalation, however, it follows the movement of the thorax and diaphragm, thus increasing its volume. This reduces the negative intrapleural pressure during inhalation. With more intense inhalation effort (e.g. forced inhalation during physical ­exertion) the intrapleural pressure decreases more strongly. During exhalation the thorax becomes smaller and the diaphragm slackens. The lung also shrinks and the intrapleural pressure rises again. z Measurement of Intrapleural Pressure

The intrapleural pressure can be measured directly in the pleural gap using probes. An indirect but reliable method of measurement is the use of esophageal pressure probes. At the end of the esophagus there is a comparable pressure. The pressure difference between intrapulmonary pressure and intrapleural pressure is called transpulmonary pressure. This is always negative during spontaneous breathing. z Reference to Artificial Respiration

Patients whose lung tissue is diseased have to exert more effort when breathing. This effort can be measured indirectly by means of oesophageal pressure probes. If the inhalation effort is high, it is to be expected that the intrapleural pressure will show a greater difference. The thorax widens, diaphragm contracts during inhalation, but the lung cannot directly follow the movement because it is less elastic and more rigid in lung diseases. The greater the negative pleural or esophageal pressure, the more the patient struggles to breathe. The patient is at risk of respiratory exhaustion.

1

Artificial respiration is intended to help respiratory exhausted patients not to have to exert themselves so hard during the breathing work. Air is forced into the lungs at positive pressure, which relieves the patient’s work of breathing. During artificial respiration, the pressure within the lungs (intrapulmonary) is therefore always in the positive range. The same applies to intrapleural pressure, as the air-filled lung presses on the pleural gap. Thus the transpulmonary pressure is also in the positive range.

 he Lobes, Lobes T and Segments of the Lungs

1.2.6 

The lung consists of a right and a left lung. The right lung has three lobes, the left lung two (. Fig. 1.11). The lobes of the lungs divide into segments again (. Fig.  1.12). The right lung lobe consists of 10 lung segments: 55 3 belong to the upper lobe, 55 Two to the middle lobe, 55 5 the lower lobe.  

 

The left lung is smaller than the right lung and consists of 9 segments. It has no middle lobe. This results in a different division: 55 5 belong to the upper lobe and 55 4 the lower lobe The segments 4 and 5 are called lingua. Segment 7 is not formed on the left. z Reference to Artificial Respiration

During normal inhalation, the air is distributed evenly to all lobes and segments of the lungs. During artificial respiration, this equal distribution of the inspiratory air does not always succeed. The air of artificial respiration is forced into the lungs with overpressure and tends to be distributed unevenly, usually with good ventilation of the upper apical lung segments and insufficient ventilation of the lower basal and dorso-basal lung segments.

14

H. Lang

1

..      Fig. 1.11  Lung and pulmonary lobe (courtesy of Isabel Schlütter)

..      Fig. 1.12  Lung segments (courtesy of Isabel Schlütter)

15 Anatomy and Physiology of Respiration

With some ventilators you will find over ten different ventilation modes. The purpose of this is to achieve even air distribution with the help of the different ventilation modes. 1.2.7 

Alveoli and Surfactant

The alveoli, which total approximately 300– 400 million, are covered by a fine capillary network. The actual gas exchange then takes place between the air-filled alveoli and the capillaries that emerge from the pulmonary artery. >>The gas exchange in the lungs is called external respiration. The gas exchange in the tissue or at the individual body cells is called internal respiration.

A single alveolus has a diameter of 10–25 μm (. Fig.  1.13). The approximately 300–400 million alveoli have a combined surface area of approximately 60–80 m2. The individual alveolus does not have a single bronchioli of its own. Approximately 1500–4000 alveoli form alveolar sacs, an acinus (plural acini). The alveoli of an acinus are connected to each other by openings, the Kohnschen pores. Inhaled air can thus be evenly distributed within this small unit.  

..      Fig. 1.13  Acinus (courtesy of Isabel Schlütter)

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z Reference to Artificial Respiration

With artificial respiration there is again the problem that the air inspired by positive pressure is distributed unevenly. Small alveoli are often not ventilated at all or are less ventilated, and large and larger alveoli are even over-inflated. A potential consequence is the loss of gas exchange surface. The alveoli are lined with lung cells, the pneumocytes type I. They form the inner wall of the alveoli, the alveolar epithelium (. Fig. 1.14). Additionally, there is the pneumocyte type II. This forms the surfactant, which 55 lines the inner surface of the alveoli as a thin film, 55 reduces the surface tension, 55 prevents the collapse of the alveoli.  

If there were no surfactant, a much higher pressure would have to be applied to reopen the alveoli, or a greater force of the respiratory muscles would be required in inspiration. The surfactant forms the boundary between breathing air and tissue. Surfactant is already produced intrauterin by the foetus from the 23rd week of pregnancy. Surfactant consists of approx. 90% lipids (fats), 10% proteins and calcium ions.

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..      Fig. 1.14  Alveolus (courtesy of Isabel Schlütter)

Functions of the Surfactant 55 Reduction of the surface tension of the liquid film on the alveolar epithelium → antiatelectatic function 55 Fluid transport from the alveolar space into the space between the alveoli and capillaries or into the interstitium → anti-oedematous function 55 Fluid and secretion transport towards the trachea → clearance function 55 Interaction with infectious agents → direct defence function 55 Regulation of the intrapulmonary immune response → immunoregulatory function 55 Protection against oxygen radicals that can damage cell membranes and genetic material

z Reference to Artificial Respiration

For the surfactant to fully perform its function, it is necessary that the inhaled air or respiratory air is warm and moist. During normal physiological breathing this is ensured by the upper airways: In artificial respiration, this must be ensured by the active or passive humidification systems.

1.2.8 

Pulmonary Vessels

z Vasa Privata

The lung tissue or lung parenchyma and the bronchial system are themselves supplied with blood, oxygen and nutrients from the bronchial artery. This originates in the thoracic aorta or an intercostal artery. This blood is not involved in gas exchange.

17 Anatomy and Physiology of Respiration

z Vasa Publica

The blood that enters the lungs from the right heart via the pulmonary artery does not supply the lung tissue with blood and nutrients. This blood has to pass through the pulmonary circulation to be enriched with oxygen.

Respiratory Support Musculature

1.3 

1.3.1 

Inspiration

The inspiration is due to: 55 Diaphragm 55 Outer rib muscles 55 Neck muscles and respiratory muscles About 2/3 of the work of breathing is done by contraction of the diaphragm (. Fig. 1.15). When the external rib muscles are working, the thorax is lifted and air flows into the lungs. A certain amount of inspiration (comparable to the plateau in 7 Chap. 12) is held by the neck muscles. Other auxiliary muscles for inspiration, which are able to lift the ribs, are the major  

 

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and minor pectoralis muscles, the scaleni muscle and the sternocleidomastoid muscle. The simultaneous muscular work of the diaphragm and the external intercostal muscles causes the lung to expand and dilate evenly in the thorax. In the non-contracted state, the diaphragm forms crests below the two lungs. The contraction of the diaphragm causes the crests to smooth out. The contracted diaphragm thus forms a flattened trapezium when inhaled. As a result, the abdominal organs are displaced downward and forward. This is how you can recognize “abdominal breathing“. The diaphragm stretches the lungs. There is a uniform vertical stretching. The outer intercostal muscles stretch the thorax almost circularly. The thorax is lifted forward, to the side and backward. The lungs are thereby stretched evenly horizontally. The vertical and horizontal stretching creates a slight negative pressure in the lungs compared to the outside air and breathing air flows into the lungs via the airways. In principle, air is “sucked in” during inhalation. The inhaled air can also be distributed evenly within the lungs to all areas due to the uniform expansion of the lungs. Thus there are almost no areas that are less ventilated.

..      Fig. 1.15  Diaphragmatic caps during inhalation and exhalation (courtesy of Isabel Schlütter)

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z Reference to Artificial Respiration

Artificial respiration does not cause uniform expansion of the lungs. The air administered by positive pressure is often distributed unevenly in the lung areas. As a result, some areas are overstretched and others are poorly ventilated or not ventilated at all. Raising the patient’s upper body to an angle of 30–45°, as well as raising or lowering the arms, supports and enables optimal use of the respiratory muscles. Assisted spontaneous breathing of the patient causes an even distribution of the ventilation air in the lungs.

1.3.2 

Expiration

Muscles involved in expiration (. Fig. 1.16): 55 Inner intercostal muscles 55 Oblique pectoral muscle 55 Straight abdominal muscle  

Exhalation is mainly a passive process. The contracted diaphragm slackens and the lungs are slightly compressed. The outer intercostal muscles slacken and the circular stretching is reduced. This also leads to a compression of the lungs. This causes a

..      Fig. 1.16  Inhalation and exhalation muscles (courtesy of idiag ag)

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19 Anatomy and Physiology of Respiration

slight overpressure inside the lungs. As a result, the air flows easily out of the lungs. Breathing work is an energy-saving process. Only about 2–3% of the daily energy requirement of an adult person is used for the breathing work. If a person needs about 2000 kcal/day, only 40–60 kcal/day are needed for the breathing work. Since breathing work requires little energy, we can breathe without effort 24 h a day without exhaustion. z Reference to Artificial Respiration

The spontaneous own breathing enables an even distribution of air to all parts of the lung during inhalation and an even outflow of air during exhalation. One consequence for artificial ventilation is that the patient’s supportive spontaneous breathing should start as early as possible. Even small respiratory muscle activities result in a better distribution of the ventilation air within the lungs. In severe respiratory insufficiency, much more energy is required for the work of breathing, with a proportion of 20–30%. Artificial respiration is intended to reduce this high energy consumption of breathing and thus also helps recovery in respiratory insufficiency.

1.4 

Physiology

1.4.1 

Breathing Air

The air we breathe consists to a large extent of nitrogen (78%). Oxygen is only present in the inhaled air with a share of 21%. We therefore live in a nitrogen atmosphere. However, the nitrogen is exhaled unchanged. Likewise, the 1% noble gases in our atmosphere are inhaled and exhaled again unchanged. These two components therefore do not take part in the gas exchange.

.       Table 1.3  Components of the breathing air Inhalation

Exhalation

Nitrogen

78%

78%

Oxygen

21%

16%

Carbon dioxide

0,03%

4%

Other/noble gases

1%

1%

Oxygen is needed for metabolic processes in the body and takes part in gas exchange. In the exhaled air the proportion of oxygen has dropped to 16%. As an end product of the metabolism carbon dioxide is produced, which is released in the exhaled air with a proportion of 4%. The components of the exhaled air are listed in . Table 1.3.  

z Relation to Artificial Respiration—Blood Gas Analysis

Oxygen is needed and consumed for the metabolic processes (“aerobic metabolism”). The end product of the aerobic metabolism is carbon dioxide (CO2), which is exhaled with each exhalation. This is why the proportion of CO2 in the exhaled air has increased so much. In “anaerobic metabolism”, metabolic processes for energy production take place even without oxygen. The end product is lactic acid (lactate). Lactate is therefore always formed during metabolic processes without the presence of oxygen. Blood transports oxygen to the cells. If the lactate content increases in the blood gas analysis (BGA), it can be concluded that the O2 consumption is higher than the O2 supply, this can be caused by a disturbance of the blood circulation.

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Diffusion Time: Diffusion Distance

describes the pressure in a blood gas analysis, which can be assigned to the gas CO2 (7 Chap. 27). The commands of the work of breathing to be performed are again transmitted by nervous stimuli to the spinal cord and further to the motor fibres of the intercostal nerves. These are the spinal ganglia of the thoracic vertebrae (BWK) 1–12. Impulses are also transmitted via the phrenic nerve to the diaphragm. Inhalation and exhalation are subject to the so-called Hering-Breuer reflex. Stretching reflexes set a vagus stimulus. When stretching is complete, there is a “switch” to expiration.  

The diffusion time describes the time required for gas exchange in lung healthy people. It amounts to max. 0.75 s. An erythrocyte only stays in the lung capillaries for approx. 0.3 s. However, this contact time is sufficient to saturate the erythrocytes with oxygen. This contact time is also sufficient for the gas exchange of carbon dioxide (CO2). In the lungs, the distances for the diffusion of the gases are very short. Oxygen must travel the diffusion distance from the inside of the alveolus to be bound to haemoglobin, i.e.: 55 the alveolar epithelium, 55 the interstitium between alveolus and capillary, 55 the capillary endothelium, 55 the blood plasma and 55 the erythrocyte membrane. The total distance is about 1 μm (for comparison: the size of an erythrocyte is 7 μm).

1.4.4 

This is the volume of blood circulating in the pulmonary circulation that does not participate in gas exchange and is 3–5%. At a cardiac output of 5  l/min, 150–250  ml of blood is therefore not enriched with oxygen. No carbon dioxide can be released either. 1.4.5 

1.4.3 

Breathing Regulation

The central point of respiratory regulation is the brain stem or the respiratory centre in the extended spinal cord (medulla oblongata). Chemoreceptors on the aorta measure the concentration of oxygen and carbon dioxide dissolved in the blood. This information is transmitted by nervous stimuli via the tenth cranial nerve (N. vagus) and 11th cranial nerve (N. accessorius) to the respiratory centre in the brain stem. In the brain stem itself, there are chemoreceptors that react directly to pH, pCO2 and pO2. The primary drive for the work of breathing is the partial pressure pCO2. If the pCO2 rises, the work of breathing is increased. If the pCO2 drops, the work of breathing is reduced. The partial pressure

Physiological Shunt Volume

Breathing Mechanics

Breathing mechanics describes the connections between how air enters the lungs during breathing. It is made up of the respiratory frequency, the respiratory volume and the respiratory minute volume (. Table 1.4).  

..      Table 1.4  Breathing mechanics adults and children Adults

Newborns

Respiratory rate

15–20/min

40–50/min

Tidal volume

450–600 ml

20 ml

Respiratory minute volume

6–10 l/min

800–1000 ml/min

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21 Anatomy and Physiology of Respiration

z Lung Volumes

The resting position is the normal breathing of a person without effort (. Fig. 1.17). This results in a tidal volume (TV or Vt) of approx. 450–600 ml. This respiratory volume is produced on average during ventilation, although there are variations. The respiratory minute ventilation (RMV) is the product of tidal volume (TV) × breathing rate (f). In the resting position, 500  ml of air is inhaled approximately 15 times per minute. This gives a respiratory minute volume of 7500 ml.  

Physical exertion causes the breathing volume to increase. To achieve this, the lungs have an inspiratory reserve volume (IRV)

and an expiratory reserve volume (ERV). However, maximum inhalation or exhalation is very rarely reached (. Fig. 1.17). For an overview of the individual volumes of spirometry . Table 1.5.  

 

z Reference to Artificial Respiration

Patients on artificial respiration are also subjected to physical exertion through various measures. Physical exertion also causes the respiratory rate per minute and possibly also the respiratory volume to increase. Artificial respiration must be able to allow this. The sum of the respiratory volume at rest and the inspiratory reserve volume is the

..      Fig. 1.17  Breath volumes: spirometry (own representation, edited by Isabel Schlütter)

.       Table 1.5  Breathing volumes Tidal volume (TV)

~450–600 ml

Inspiratory reserve volume (IRV): Maximum amount of air that can be inhaled

~2500–3000 ml

Expiratory reserve volume (ERV): Maximum amount of air that can be exhaled

~1200–1500 ml

Residual volume (RV): Volume of air remaining in the lungs at maximum exhalation

~1000–1200 ml

Inspiratory capacity: TV + IRV

~up to 3500 ml

Vital capacity (VC): TV + IRV + ERV

~4000–4500 ml

Functional residual capacity (FRC): ERV + RV

~2400 ml

Total capacity: IRV + TV + ERV + RV

~5000–6000 ml

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inspiratory capacity. Even at maximum exhalation, a residual amount of air remains in the lungs that cannot be exhaled. This is the residual volume and is approx. 1000– 1200 ml. In the resting position, a lot of air remains in the lungs and airways at the end of normal exhalation. This amount of air is called functional residual capacity (FRC). It is about 2000–2400 ml. The Functional Residual Capacity (FRC) 55 The amount of air that remains in the lungs at the end of our exhalation. 55 Serves the gas exchange also during the exhalation phase. 55 This amount of air that remains in the lungs at the end of our exhalation exerts a small air pressure, about 1–2 mb. 55 This air pressure keeps the alveoli and airways open. 55 It pre-stretches the alveoli and airways so that the coming inhalation is easy. 55 It ensures that the gas exchange in the alveoli is ensured even during the exhalation phase

z Reference to Artificial Respiration

Patients who are ventilated invasively, i.e. who have a tube or tracheal cannula, are at risk of having their FRC reduced. If it is reduced too much, the alveoli and airways may not be sufficiently open for the coming inspiration and collapse. In artificial ventilation, this is counteracted by setting a PEEP or EPAP on the ventilator. The sum of respiratory volume, inspiratory and expiratory reserve volume is the vital capacity. This is approx. 4000–4500 ml. The total capacity is the sum of the respiratory volume, inspiratory and expiratory reserve volume and residual volume. This is approx. 5000–6000 ml.

Conclusion Knowledge of the anatomy and physiology of respiration is a prerequisite for understanding ventilation and its tasks. Ventilation air reaches the lungs via the same routes. It must be warmed and humid, otherwise many of the tasks of the airways cannot be maintained, such as self-cleaning, gas exchange and keeping the airways and alveoli open. Respiratory air must be distributed evenly to all areas of the lungs to prevent loss of gas exchange surface.

1.5 

Central and Peripheral Nervous System

The central nervous system, also known as the CNS, is very closely related to the peripheral nervous system and can therefore only be separated topographically. The brain and the spinal cord belong to the CNS.  The peripheral nervous system includes all the nerve tracts of the body that depart from and arrive at the CNS. Tasks of the central nervous system: 55 Control of motor skills, i.e. posture and movements 55 Controlled interaction of all vital systems—from organ functions, hormone balance and respiration to the sleep-­ wake rhythm 55 Processing of incoming information from the environment and inside the body 55 All cognitive functions  - i.e. consciousness, language, thinking, learning and memory, attention and imagination 55 Feelings and drives The peripheral nervous system can be further subdivided as follows: 55 Somatic nervous system (arbitrary nervous system)

23 Anatomy and Physiology of Respiration

55 Vegetative nervous system (involuntary nervous system) is further divided into: 55 Sympathetic nervous system (sympathetic nervous system) 55 Parasympathetic nervous system (parasympathetic nervous system) 55 Enteric nervous system (ENS)

kSoft Meninges (Pia Mater)

It lies directly on the brain substance and the spinal cord and also follows their many curves and curvatures. The pia mater supplies the brain with nutrients from the cerebrospinal fluid. 1.5.2 

1.5.1 

Anatomy of the Brain

The brain of an adult human weighs about 1400 g, but requires about 20% of the total energy requirement. It consists of about 100 billion individual nerve cells that are connected to each other. Innumerable connections can be created and develop further. The possibility of establishing connections is dynamic and not fixed from the outset, i.e. it is not static. z Meninges (Meninges)

The brain and also the spinal cord in the spinal canal are protectively surrounded by three meninges. kHard Meninges (Dura Mater)

It is the outermost meninges. It consists of an inner and an outer leaf and lies against the skull bone from the inside. The dura mater is not connected to the spinal canal in the spine. There is a space between the spinal canal and the dura mater, the so-called epidural space. This is the site of the peridural or epidural anaesthesia. kCobweb Skin (Arachnoidea)

It’s the middle meninges. It is located at the dura mater but is also separated by a thin gap, the so-called subdural space. The arachnoidea has a spiderweb-like appearance, hence the name. Below the arachnoidea is the so-called subarachnoid space. This is filled with cerebrospinal fluid, the so-called liquor. The cerebrospinal fluid protects the brain from vibrations.

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Brain Structure

. Fig. 1.18  

z Brain Stem

The brain stem includes the following structures: 55 Medulla oblongata (extended spinal cord) 55 Pons (bridge) 55 Mesencephalon (midbrain), e.g. substantia nigra The 12 pairs of brain nerves emerge from the brain stem. In the brain stem is the formatio reticularis, an important system of fibres and nerve cells for motor functions. kTasks of the Brain Stem

The brain stem (brain stem) is the oldest part of the brain in terms of developmental history. It is responsible for essential life functions and controls heart rate, blood pressure and respiration. It is also responsible for some important reflexes such as the eyelid closure, swallowing or cough reflex. The brain stem is the interface between the rest of the brain and the spinal cord. It forwards incoming information crosswise, so the left side of the body is controlled by the right side of the brain and vice versa. z Interbrain (Diencephalon)

The following structures form the diencephalon: 55 Epithalamus 55 Thalamus: bilaterally arranged complex of different nerve core groups; switching point for most sensory pathways; from

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..      Fig. 1.18  Brain structure (courtesy of Isabel Schlütter)

all core areas of the thalamus there are fibre connections to the cerebral cortex (and other structures); important regulatory system 55 Subthalamus: e.g. globus pallidus (pallidum), capsula interna 55 Hypothalamus kTasks Diencephalon

The brain stem is followed by the diencephalon. This is where the thalamus is located, the gateway to consciousness. It acts as a filter and distributor, decides which sensory

impressions should penetrate into consciousness and passes them on to the corresponding processing centres. Another important area of the diencephalon is the hypothalamus. It serves as a mediator between the hormonal and nervous systems. It controls, for example, the sleep-wake rhythm, hunger and thirst, but also the sex drive and processes pain and temperature sensations. z Cerebellum

The cerebellum is connected to the brain stem via the cerebellar legs. It is divided into a central part, the so-called worm (vermis

25 Anatomy and Physiology of Respiration

cerebelli), and two cerebellar hemispheres and is located in the posterior fossa. kTasks of the Cerebellum

The cerebellum performs important functions in the control and coordination of motor activities. It coordinates movements, balance and coordination, ensures a fluid movement sequence and regulates the basic tension of the muscles. Disturbances in this area can lead to people suffering from movement and balance disorders. z Endbrain (Cerebrum, Cerebrum, Telencephalon)

The cerebrum is divided into two hemispheres separated by a furrow along the longitudinal axis (fissura longitudinalis cerebri). The main connection between the hemispheres is the so-called beam (corpus callosum), which consists of densely packed nerve fibres that connect similar parts of the brain on both sides (commissure fibres).

..      Fig. 1.19  Cerebral lobe (courtesy of Isabel Schlütter)

1.5.3 

1

 he Lobes and Regions T of the Brain

The cerebral cortex, whose surface is structured by furrows (sulci) and coils (gyri), is divided into four so-called lobes (. Fig. 1.19): 55 Frontal lobe (lobus frontalis) 55 Parietal lobe (lobus parietalis) 55 Temporal lobe (temporal lobe) 55 Occipital lobe (lobus occipitalis)  

Each hemisphere of the brain is specialized for certain tasks (. Fig. 1.20). On the left is usually language and logic, on the right creativity and the sense of orientation. The multiple-folded cerebral cortex (neocortex) forms the outermost layer of the cerebrum. It is between two and five millimetres thick and houses, among other things, the ability to learn, speak and think, as well as consciousness and memory. Information from the sensory organs enters the cerebral cortex, is processed and finally stored in memory.  

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..      Fig. 1.20  Brain regions (courtesy of Isabel Schlütter)

1.5.4 

Pyramidal and Extrapyramidal System

The pyramidal system refers to the direct connection of the motor cortex with the neurons of the corresponding segment in the spinal cord. It consists of approximately one million axons, which run without interruption into the spinal cord and are sometimes over 1 m long, and controls conscious movement. The pathways run through the capsula interna and the pons to the medulla oblongata, where most of them cross over to the opposite side and run down the spinal column as a lateral strand. Some of the axons of the pyramidal tract end directly at the so-called alpha moto-

neurons, which are connected to the corresponding muscle fibers without any further intermediate station. In most cases, however, the connection is made via so-called intermediate neurons, which are located in the spinal column segments adjacent to the alpha motoneurons. The extrapyramidal system is an indirect system; the mediation between the cerebrum and alpha-motoneurons takes place via many intermediate stations, i.e. synaptic connections between neurons in different nuclei of the brain. It controls involuntary movement, but can also intervene in voluntary motor functions. The pyramidal and extrapyramidal systems are thus connected in parallel.

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27 Anatomy and Physiology of Respiration

Blood Supply to the Brain

1.5.5 

The blood supply to the brain is provided by four large vessels that run from the trunk to the

head. At the front of the neck are the right and left internal carotid arteries (arteria carotis interna), at the back are the right and left vertebral arteries (arteria vertebralis) (. Fig. 1.21).  

a

b

Apac

Afip

Aprcu Apo

Afim

Apo

Acam Afia

Acal

Achp

Apca

Aca

Acoa Aci

Afp

Afbm Aca

Aci

Acp Acop

Atia

Asc

Asprc

Aol Aom

Acha Acop Acp

N. lll

Atip

N. IV

Aces

N. V

Ap Fro

N. VIII N. VII

Aspc Asm

m

N. VI

Aceia

N. IX

Aprf Aga

N. XII N. X

Aceip

N. XI

Av Aspa

Ato

Afbl Atpo Acm

Atim

Atp

Ata

..      Fig. 1.21  Cerebral blood flow, (a) Circulus arteriosus Willisi and its influxes, (b) Cerebral arteries in basal view. (from Zilles et al., Anatomy—Springer Textbook, 2010, Fig. 17. 46 (p. 658) and Fig. 17.47c (p. 660))

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Spinal Cord

requires a large number of motor nerve cells (motoneurons) and circuits. In adults, the spinal cord ends at the level Anita Büchli and Martin Schwab. of the first lumbar vertebra, but before birth it reaches the sacrum and in infants it reaches the lower lumbar vertebrae. This is 1.6.1  Structure of the Spinal Cord because the spine grows faster than the spiThe spinal cord consists of five areas: neck nal cord during development. As a result of marrow, breast marrow, lumbar marrow, this phenomenon, the spinal nerves—those sacral marrow and tail marrow. The spinal nerves that exit the spinal canal and lead to nerves leave the spinal cord through the the periphery of the body—travel an increasintervertebral spaces and conduct nerve ingly longer path within the spinal canal in impulses to certain organs of the body, so-­ the lower area before they can leave it. At called conduction pathways. Ascending the end of the spinal cord—i.e. from the first pathways conduct nerve impulses from the lumbar vertebra—only the spinal nerves run within the spinal canal. They form the cauda organs to the CNS. The anatomical division of the spinal equina, which means “horse’s tail”. Motoneurons are nerve cells that are cord into five sections is carried out accordlocated in the spinal cord and whose nerve ing to the exit points of the spinal nerves extension leads to the muscles. (. Fig. 1.22): 55 Neck or cervical marrow with spinal nerves C1-C8 55 Chest or thoracic medulla with spinal 1.6.2  The Internal Structure nerves T1-T12 of the Spinal Cord 55 Lumbar or lumbar marrow with spinal nerves L1-L5 The cell bodies of the nerves of the descend55 Cross or sacral marrow with spinal ing motor pathways are located in the brain. nerves S1-S5 Their axon connects them to a specific 55 Tail mark motor neuron or circuit of a particular spinal cord segment. The signal thus travels Each spinal nerve supplies a specific part of from the brain via the motor neuron to the the body or a specific organ: periphery, where it triggers a contraction in 55 The cervical spinal nerves the neck, arms the muscle. The ascending sensory pathways and respiratory organs conduct sensory signals from the periphery 55 The thoracic spinal nerves the posture via the spinal cord to the brain. and many of the internal organs . Figure  1.23 shows a cross-section of 55 The lumbar spinal nerves of the legs and the spinal cord. There are ventral and dorsal feet areas. 55 The sacral spinal nerves the bladder, the 55 Ventral  =  towards the abdomen or intestines and the sexual organs towards the front towards the belly 55 Dorsal  =  backwards or backwards Interestingly, the spinal cord is clearly thicktowards the back ened at the points where the spinal nerves running into the arms and legs leave the spi- The butterfly-shaped region in the middle is nal cord. This indicates that the control of called grey matter. It contains nerve cell arm and leg movement is complex and bodies. The anterior ventral part of the grey 1.6 

 

 

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..      Fig. 1.22  Brain and spinal cord (courtesy of: IFP—International Foundation for Research in Paraplegia and Prof. Martin E. Schwab)

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..      Fig. 1.23  Cross-section of the spinal cord (courtesy of IFP—International Foundation for Research in Paraplegia and Prof. Martin E. Schwab)

matter is called anterior horn, the posterior dorsal part posterior horn. The posterior horn receives sensitive information from the body and skin via the dorsal (backward pointing) root of the spinal nerve, such as tactile, pressure, heat or pain sensations. The cell bodies of these axons (. Fig. 1.23) are located in the spinal ganglion, i.e. outside the spinal cord but inside the spinal canal. The ascending dorsal pathways leading to the brain transmit sensory signals from the skin and organs to the nerve cells of specific segments of the spinal cord, and from there to the brain. The sensory stimuli originate from various specialized receptors, e.g. in the skin, where they perceive differences in pressure or temperature, or from cells that register, for example, a full stomach and thus monitor the condition of the internal organs. In the anterior horn are the cell bodies of the motoneurons, whose fibres transmit the commands for movements to the muscles. The descending motor pathways coming from the brain run ventrally (on the abdominal side) and control the movements of the  

smooth muscles of the internal organs and the striated muscles belonging to the ­musculoskeletal system. They also support the autonomic nervous system in regulating blood pressure, temperature and the reaction to stress. The cell bodies of these motor nerves are located in the brain and send electrical signals along their axons to certain segments of the spinal cord, where the signal is transmitted to a motor neuron. This motoneuron transmits the signal to the periphery of the body, where it triggers a muscle contraction. In contrast, the nerve fiber pathways of many thousands of fibers (axons) run through the outer white matter of the spinal cord, more precisely the ascending sensory fibers and the descending motor fibers. The lighter colour of the white substance is due to the myelin layer. This layer is formed by oligodendrocytes that coat up to 40 different nerve fibres simultaneously. Myelin is essential for the rapid transmission of nerve signals (. Fig.  1.24). Both the white and grey matter contain other types of cells, such as blood vessel  

31 Anatomy and Physiology of Respiration

1.6.3 

1

Structure of a Nerve Cell

The cell body of the nerve cell has different extensions: Several dendrites receive nerve signals from other cells, the axon is surrounded by a myelin layer and transmits the signal to the next cell (. Fig.  1.24). The synapse is the site of excitation transmission from one cell to another.  

1.7 

Phrenic Nerve

The phrenic nerve (diaphragm nerve) is a spinal nerve that originates in the neck and innervates the diaphragm. In humans, the nerve originates (together with other nerve fibres as a bundle) from C1 to C4 (. Fig. 1.25).  

..      Fig. 1.24  Nerve cell—neuron (courtesy of: IFP— International Foundation for Research in Paraplegia and Prof. Martin E. Schwab)

cells or various types of glial cells, which nourish and maintain the nerve cells. Oligodendrocytes, for example, belong to the glial cells. The spinal cord also contains neural networks that can be activated independently of the brain by sensory signals from the periphery. These include the reflexes. Another example is the walking movement, which is already pronounced in newborns: If you hold a newborn child under your arms and let its feet touch the ground, it starts to make walking movements. At this stage of development, the nerve connections that connect the brain with the spinal cord are not yet fully developed. The neural networks in the spinal cord, on the other hand, are already functional.

..      Fig. 1.25  Phrenic nerve (courtesy of Isabel Schlütter)

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In humans, the phrenic nerve descends in front of the anterior scalenal muscle and behind the deep neck fascia and the sternocleidomastoid muscle, and then enters the upper thoracic aperture, accompanied by the artery and subclavian vein. There it is first located in front of the pleural dome and then reaches the diaphragm between the mediastinal pleura and the pericardium.

..      Fig. 1.26  CNS and PNS interconnection (courtesy of Carsten Schröter, MD)

1.8 

Interconnection of the Nerve Tracts

A schematic overview of the interconnection of CNS and PNS is shown in . Fig.  1.26. The circles with the triangles represent a nerve cell. Representing many nerve cells and fibres, the first motoneuron is shown in the area of the so-called motor  

33 Anatomy and Physiology of Respiration

cortex of the brain and the second motoneuron in the area of the spinal cord. The lines emerging from the triangles represent the nerve fibres, the axons. The arrows indicate the structures affected by the disease. The diagram shows the structures involved in motor function: 55 the brain, 55 the spinal cord, 55 the nerve fibres and 55 the muscles. The offshoot of the nerve cell in the brain (first or central motor neuron) moves into the brainstem or spinal cord, where it is linked to a second nerve cell. From this nerve cell (second or peripheral motor neuron or alpha-motoneuron), an extension (nerve fibre = axon) again extends to a muscle. These are the nerve fibres that run as a bundle for example on arms and legs (e.g. median nerve). The connection point of the nerve fibre to the muscle is called the motor end plate. However, one nerve fibre supplies (innervated) several muscle fibres of a muscle.

1

At all points of the interconnection of CNS and PNS, disorders and diseases can occur, which are explained in Sect. 3.2.4.

References Büchli A, Schwab ME (2006) Querschnittlähmung– Problemstellung und wissenschaftliche Ansätze für eine Therapie. Institut für Hirnforschung, Universität Zürich in: BioFokus 73/2006, Hg: Verein fürs Leben, Zürich Klinke R, Pape HC, Kurtz A (2009) Physiologie, 6. vollständig überarb. Aufl. Thieme Verlag Mutschler E, Schaible H-G, Vaupel P (2007) Anatomie, Physiologie, Pathophysiologie des Menschen, 6.völlig neu überarb. und erw. Aufl. Wissenschaftliche Verlagsgesellschaft Schmidt R, Lang F (2011) Physiologie des Menschen: mit Pathophysiologie, 31. Aufl. Springer Verlag Spornitz U (2010) Anatomie und Physiologie: Lehrbuch und Atlas für Pflege-und Gesundheitsfachberufe,; 6. überarb. Und erw. Aufl. Springer Verlag Zilles K, Tillmann B (2010) Anatomie–Springer Lehrbuch, Springer Verlag http://www.­irp-­zh.­ch/index.­php?id=322 http://www.­irp-­zh.­ch/uploads/media/BioFokus73.­pdf

35

Indications and Goals of Ventilation Hartmut Lang Contents 2.1

Respiratory Insufficiency – 36

2.1.1 2.1.2 2.1.3 2.1.4

F ailure of the Respiratory Pump – 36 Failure of Pulmonary Gas Exchange – 39 Disturbance of Pulmonary Gas Exchange – 40 Interaction Between the Lungs and the Respiratory Pump – 41

2.2

Ventilation Goals – 42 References – 42

© Springer-Verlag GmbH Germany, part of Springer Nature 2023 H. Lang (ed.), Out-of Hospital Ventilation, https://doi.org/10.1007/978-3-662-64196-5_2

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2.1 

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Respiratory Insufficiency

The respiratory insufficiency of a patient results in the obligation to ventilate. Respiratory insufficiency is the loss of the ability to breathe independently and reliably, as people do under physiological conditions. The respiratory insufficiency determines the indications for ventilation. A ventilation access via tracheal cannula directly into the lower airways is called invasive ventilation. If ventilation is performed using ventilation masks via the upper airways, a non-invasive ventilation (NIV) is used. Respiratory insufficiency is divided into: 55 Failure of the respiratory pump 55 Failure of pulmonary gas exchange

2.1.1 

Failure of the Respiratory Pump

The entire respiratory musculature serves functionally as a respiratory pump. The breathing work is performed by the respiratory muscles. However, the respiratory mus-

cles form only a part of the respiratory pump. The respiratory pump is the interaction of the respiratory center, nerves, the bony thorax and the respiratory muscles (7 Chap. 1, . Fig. 2.1).  

 

z How the Respiratory Pump Works

The respiratory center autonomously gives the impulses for the breathing work to be done. The breathing work is determined by the current physical or mental stress. If one is in a relaxed and calm state, depth of breath/tidal volume and breathing frequency are low. If one is in a physically or mentally strained situation, tidal volume and breathing frequency increase. This also increases the respiratory minute volume. The impulses of the breathing work to be performed are transmitted to the respiratory muscles via nerve tracts, also called motor neurons. The phrenic nerve stimulates the diaphragm to contract. Corresponding nerve tracts along the costal arches stimulate the intercostal muscles to contract. Contraction of the respiratory muscles (diaphragm and external intercostal muscles, 7 Sect. 1.3) creates a negative pressure  

..      Fig. 2.1  Respiratory pump model (own representation, edited by Isabel Schlütter)

37 Indications and Goals of Ventilation

within the lungs and alveoli, an “alveolar negative pressure.” This then leads to inhalation. The inflow of air during inhalation is also called ventilation. Faults in the respiratory pump system will cause a malfunction of the air supply and thus a failure of the ventilation. A synonymous term for respiratory pump failure is “ventilatory failure” or “ventilatory insufficiency.” The main symptom of ventilatory insufficiency is hypercapnia, the increase in CO2 content, which can be detected in a blood gas analysis (BGA) as pCO2. The impulse for the respiratory work to be performed is the content of carbon dioxide in the blood, the pCO2. The higher the carbon dioxide content, the greater the respiratory drive. The lower the content of CO2, the lower the respiratory drive. If the respiratory muscles are constantly stressed too much, this leads to fatigue of the respiratory muscles. This can cause ventilatory insufficiency. Increased strain on the respiratory pump thus leads to its failure. The necessary breathing work can no longer be performed. In order to escape ventilatory insufficiency, a period of recovery with reduced breathing frequency and depth of breath is particularly important! z Factors Affecting the Respiratory Pump

The function of the respiratory pump can be impaired by various factors or fail completely. kRespiratory Center

The respiratory center can fail due to disturbances of the respiratory drive. These can be caused by trauma, bleeding or insults of the brain or permanent hypoxic brain damage. Various drugs also have an influence on the respiratory centre: opiates, benzodiazepines, narcotics attenuate the respiratory centre. kMotoneurons

The function of the nerve tracts can be impaired by numerous neuromuscular diseases. The normal transmission speed of

2

nerve impulses is about 100–120 m/s. If, for example, the myelin layer (myelin sheath) of the nerve fibres is degenerately diseased, the speed of transmission is reduced. Causes of a degeneration of the myelin sheath can be both inflammatory and autoimmune. The transmission of nerve impulses to the muscles takes place at the synapses (terminal bouton) of the nerve fibres. There, neurotransmitters (messenger substances) are released into the synaptic cleft. These “dock” at receptors of the muscle cells and pass on the excitation. The muscle contracts. Here, too, inflammatory or autoimmune causes can impede the release of the neurotransmitters. The receptors can also be inactivated so that neurotransmitters cannot “dock” (7 Chap. 16). Anaesthetics can impair or even completely prevent the transmission of stimuli.  

kRespiratory Musculature

If there is no excitation of the muscles, the contraction does not occur. No breathing work can take place. If the muscle is only affected, e.g. as muscular dystrophy or myositis, the contraction can be stopped. As described above, contraction will not occur if the transmitters cannot be released or “dock” at receptors. Muscle relaxants act at these sites and prevent the impulses from being transmitted. kAlveolar Negative Pressure

The creation of an alveolar negative pressure by the respiratory muscles causes the air to flow into the lungs. Deformities of the trunk or thorax impair the alveolar negative pressure. The respiratory muscles are not directly involved, but the deformation does not allow sufficient work of breathing. Severe scoliosis, kyphoscoliosis, post-­ traumatic thoracic deformity and ankylosing spondylitis are some examples of thoracic restrictive diseases. Permanent over-inflation of the thorax, which occurs in emphysema, impairs ventilation as well as the generation of the alveolar negative pressure necessary for

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inhalation. A reduced respiratory musculature does not generate sufficient force for breathing in the long term. People with obesity hypoventilation syndrome (OHS) gain body weight until they become obese, but lose muscle mass and thus the power to generate alveolar negative pressure. kVentilation

The aim of the respiratory pump system as a whole is the inflow of air into the lungs, the ventilation. A ventilation disorder can be caused by a functional obstruction of the airways, e.g. by tumours or other narrowing of the airways. Obstructive sleep apnoea syndrome (OSAS) also hinders ventilation. Air supply/ventilation failure is the final consequence if one or more parts of the respiratory pump system are affected or fail completely. It is not possible to generate sufficient depth of breath, sufficient tidal volume on one's own. If an adequate tidal volume (TV) cannot be generated, the exhalation of carbon dioxide (CO2) is impaired. This leads to hypercapnia. The body can tolerate an increased CO2 content to a certain extent, but not permanently. Normally, the body reacts with increased breathing by increasing the depth and frequency of breathing. If the compensatory possibilities of the human being are exhausted, the necessary increased work of breathing cannot be performed. The

increased CO2 content makes you tired, clouds your consciousness, and results in a CO2 coma or CO2 anaesthesia. >>The main symptom of respiratory pump failure is hypercapnia (BGA: pCO2  >  55 mmHg). This leads to ventilatory insufficiency, hypercapnia and, if left untreated, hypoxemia (BGA: pO2 >55 Respiratory partial insufficiency: de­scribes the disorder of oxygenation and leads to a decrease of pO2 → hypoxia.

..      Fig. 2.4  Lung—respiratory pump diagram (own illustration, edited by Isabel Schlütter)

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H. Lang

55 Respiratory global insufficiency: describes the disruption of ventilation and leads to increase in pCO2 and decrease in pO2 → Hypercapnia and hypoxia.

2.2 

Ventilation Goals

The goals of artificial respiration result from the disturbances of ventilation and gas exchange. To be achieved are: 55 Securing the pulmonary gas exchange: –– Sufficient alveolar ventilation, i.e.: –– O2 uptake to be improved –– CO2 elimination is to be improved 55 Increase of lung volume: –– through individually adapted choice of volume and ventilation pressures –– for adequate alveolar ventilation –– to improve compliance (elasticity of the lungs, 7 Chap. 26) –– to prevent or reopen atelectasis –– to minimize further damage to the lungs 55 Reduction of the work of breathing: –– Bridging the patient's states of exhaustion during breathing  

–– Recovery of an exhausted respiratory auxiliary musculature –– Elimination of respiratory distress Further Goals of Home Ventilation: 55 Reduction of the number of bronchopulmonary infections 55 Reduction of the systemic or myocardial oxygen demand 55 Improve sleep duration and sleep quality 55 Maximizing the quality of life 55 Improve the general state of health 55 Extend survival time!

References Crieé CP, Laier-Groeneveld G (1995) Die Atempumpe, Thieme Verlag Larsen R (2012) Anästhesie und Intensivmedizin für die Fachpflege, 8. vollständig überarb. Aufl., Springer Verlag Matthys H, Seeger W (2008) Klinische Pneumologie, 4. Aufl., Springer Verlag Rathgeber J (Hsg.) (2010) Grundlagen der maschinellen Beatmung, Einführung in die Beatmung für Ärzte und Pflegekräfte, Kapitel 1.8 Der alveolo-­ kapilläre Gasaustausch, S.37–48, Thieme Verlag

43

Diseaseology Matthias Huhn Contents 3.1

Basics and Diagnostics of Respiratory Disorders – 44

3.1.1 3.1.2 3.1.3 3.1.4 3.1.5 3.1.6

T ypes and Frequency of Home Ventilation – 44 Central Respiratory Regulation – 44 Airways – 45 Breathing Mechanics – 47 Lungs – 47 Gas Exchange – 48

3.2

Illnesses and Treatment – 49

3.2.1 3.2.2 3.2.3 3.2.4 3.2.5 3.2.6 3.2.7

 ypoxic Brain Damage – 49 H Stroke: Ischemic Insult – 52 Paraplegia – 53 Neuromuscular Diseases (NMD) – 55 COPD – 64 Obesity Hypoventilation Syndrome (OHS) – 70 Thoracic Restrictive Disorders – 70

References – 72

© Springer-Verlag GmbH Germany, part of Springer Nature 2023 H. Lang (ed.), Out-of Hospital Ventilation, https://doi.org/10.1007/978-3-662-64196-5_3

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3.1 

Basics and Diagnostics of Respiratory Disorders

ous parameters, e.g. pH value, partial pressure of oxygen and partial pressure of carbon dioxide (7 Sect. 1.4.3). The involuntary respiration is primarily controlled by the concentration or partial pressure of CO2. The respiratory center reacts fastest to an increase in CO2 content, much slower to a decrease in pH or partial pressure O2 (. Fig. 3.1). The importance of the central involuntary regulation of breathing by CO2 partial pressure is illustrated by the apnea test, which is carried out as part of brain death diagnostics. It can be concluded that central apnea is a secondary symptom if the failure of cerebral blood flow is detected. The apnea test is not part of a normal clinical function test.  

3

Many human diseases can lead to significant chronic effects on the respiratory system. These diseases affect the disturbance of the central respiratory regulation, the respiratory tract, the respiratory mechanics or the pulmonary gas exchange. 3.1.1 

Types and Frequency of Home Ventilation

According to a European survey conducted in 16 countries in 2005 (Lloyd et al. 2005), the following classification was made for home ventilation (. Table 3.1): Diseases that can lead to the need for ventilation concern the disorder: 55 the central respiratory regulation, 55 of the respiratory tract or the respiratory ducts, 55 the breathing mechanics and 55 of pulmonary gas exchange.  

3.1.2 

Central Respiratory Regulation

The centre of respiratory regulation is the brain stem or the respiratory centre in the extended spinal cord (medulla oblongata). Our breathing is regulated by measuring vari-

 

z Testing of Respiratory Arrest

The apnea test is mandatory for the determination of brain death (7 Excursus “brain death”). Due to the physiological effects of hypercapnia, it can only be carried out as the final clinical examination of brain function failure. Central respiratory arrest occurs when previously healthy people do not start to breathe on their own with a pCO2 60 mmHg (8 kPa). Hypercapnia of at least 60 mmHg (8  kPa) can be induced after an O2 gas exchange disorder either by disconnection from the respirator or by hypoventilation. Sufficient oxygenation shall be provided by intratracheal O2 insufflation or ventilation with 100% O2.  

.       Table 3.1  Frequency of home ventilation Europe

Germany

Occurrence of out-of-hospital ventilation

6.6 patients/100,000 inhabitants

6.5 patients/100,000 inhabitants

Patients with lung and respiratory diseases including COPD

35,45%

42%

Patients with neuromuscular diseases

34,5%

25%

Patients with thoracic deformity and OHS

31%

33%

45 Diseaseology

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..      Fig. 3.1  Chemical respiratory drive (from Schmidt et al. (eds.). Human Physiology with Pathophysiology, 31st, revised and updated edition, Springer 2010, 7 Fig. 33.8, p. 736 Respiration)  

Normally, the involuntary breathing reflex in healthy people starts when the pCO2 level rises. If breathing does not start when pCO2 exceeds 60 mmHg (8 kPa), irreversible damage to the respiratory centre is likely. If people are adapted to pCO2 levels higher than 45  mmHg (6  kPa) due to cardio-­ pulmonary disease, the involuntary respiratory reflex may also start when the level rises well above 60 mmHg (8 kPa). Here, too, if the reflex does not start, irreversible damage to the respiratory centre can be assumed. z Brain Death

Especially in the final brain death diagnosis, as the very last check of the involuntary breathing reflex, an increase of the CO2 content is provoked by an apnea test. Brain death is defined as a state of irreversibly extinguished overall function of the cerebrum, cerebellum and brain stem. At the same time, heart and circulatory function can still be maintained artificially by controlled ventilation. All physiological and pathophysiological changes in respiration are not only controlled by the carbon dioxide partial pressure, but can be changed arbitrarily and involuntarily e.g. by emotions, muscle activity, touch, pain, inflammation and temperature.

3.1.3 

Airways

The respiratory tract is a “static”, anatomically predetermined space. Inhalation and exhalation air can flow through them. The airways are divided into upper and lower ones. The upper airways begin at the external body boundaries of nose and mouth. They continue through the throat and larynx to the trachea. This is where the lower airways begin; they have a diameter of approximately 2–2.5 cm. The trunk and lobe bronchi have a diameter of about 8–12 mm. The further the bronchial system branches out (up to 23 times in total), the smaller the diameter of the bronchioles becomes. The terminal bronchioles have a diameter of less than 1 mm, the subsequent bronchioles and alveolar ducts have a diameter of only 0.4– 0.01 mm (7 Sect. 1.2.3). Physiologically, there is a slight expansion of the diameter during inhalation. Thus air flows well into the lungs during inspiration. During exhalation, the airways narrow a little, exhalation at rest takes about twice as long as inhalation. However, they remain securely open. In respiratory diseases, the diameters of the airways can be acutely or chronically narrowed, making both inspiration and expiration difficult (. Table 3.2).  

 

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.       Table 3.2  Causes of a lower airway constriction

3

Acute inflammation of the airways (bronchitis)

With swelling of the mucous membrane and increased secretion production

Acute narrowing of the airways (obstruction in bronchial asthma)

Narrowing of the airways due to cramping of the bronchial muscles with simultaneous swelling of the mucous membrane and increased secretion production.

Chronic narrowing of the airways (expiratory collapse of the airways in COPD)

Narrowing of the airways during expiration. Small and tiny airways collapse at the beginning and during exhalation.

z Diagnostics

55 Medical history: When, why and where does shortness of breath occur? What makes it better? 55 Auscultation: Clear acoustic signs are breathing sounds, so-called inspiratory and/or expiratory stridor. 55 Body plethysmography: With the help of body plethysmography all lung volumes are determined, stationary system (7 Sect. 1.4.5 and 7 Fig. 1.17). 55 Spirometry: With the help of spirometry partial volumes can be determined, transportable system. 55 Lung function test (. Fig. 3.2)  

 

 

. Figure  3.2 shows on the left a normal result of a lung function test. The graph shows the relationship between the respiratory volume (horizontal axis) and the air flow velocity, the flow (vertical axis). A so-­ ­ called flow-volume curve is created. A patient being examined must inhale to the maximum and then exhale quickly at full power. The maximum inhalation results in a typical semicircle, which is shown below the volume axis. At maximum exhalation, a typical curve is displayed above the volume axis. At the beginning of the exhalation with maximum force there is a rapid increase in air flow. At first the flow rises rapidly upwards until a maximum is reached. This curve drops steadily to the right as the exhalation continues. It is decelerating (constantly decreasing).  

In the second illustration from the left a narrowing of the airways is shown, as it can occur in bronchial asthma. Both the inhalation and exhalation curves are smaller than the reference curve. This indicates a permanent airflow disturbance. Both inspiratory and expiratory stridor can be heard. The third illustration from the left shows a typical ventilation disorder that occurs, for example, with pulmonary fibrosis or mechanical breathing difficulties (severe overweight, thoracic trunk disorders). Here the curve is smaller and narrower in relation to the reference. This is characteristic of a restrictive ventilation disorder in which the gas exchange surface is reduced or shrunk. There is no indication of a narrowing/obstruction in the figure. However, this can also occur with restrictive ventilation disturbances. The illustration on the far right also shows a narrowing of the airways, as typically occurs in COPD with emphysema. Both the inhalation and exhalation curves are smaller than the reference curve. The exhalation curve also has a characteristic kink, which is described as an emphysema kink. This is an indication of the rapid collapse of the airways during exhalation. >>Obstruction = narrowing of the airways → Obstructed airflow. Restriction = reduction or decrease of the gas exchange surface due to expansion obstruction of the lungs → limited airflow. Both lead to aeration or ventilation problems.

47 Diseaseology

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..      Fig. 3.2  Pulmonary function test (courtesy of Prof. Dr. med. Wagner)

3.1.4 

Breathing Mechanics

7 Section 1.4.5 describes the breathing mechanism as the interrelationships through whose interaction air is taken up and released into the lungs during breathing. It is composed of the measurable parameters respiratory frequency and respiratory volume. This results in the respiratory minute volume (7 Table 1.4). A healthy “respiratory pump” is a prerequisite for functioning respiration. Disorders of the respiratory pump result from a failure of the nerves that stimulate the respiratory muscles, from a disease of the respiratory muscles themselves, from a deformity of the incubator or a structural disorder of the lungs, so that the work of breathing is difficult or only insufficient or cannot be performed at all.  

 

z Diagnostics

Capnometry/capnography Capnometry refers to the measurement and graphic, numerical display of the CO2 concentration in the exhaled air. In intensive care medicine, this takes place with each expiration. Capnography describes the representation of the CO2 concentration during the entire respiratory cycle. The CO2 concentration in the exhaled air is a measure of the CO2 concentration in the blood. This is directly related to the depth of breath. Hypocapnia is an indication of hyperventilation (unadjusted too fast breathing), hypercapnia is compatible with hypoventilation. Hypoventilation is an indication of impaired respiratory muscle strength of various causes.

Diaphragmatic fluoroscopy/diaphragmatic ultrasound The diaphragms are the most important muscles for lung development during ­inspiration. They are activated by the paired phrenic nerves. Various diseases lead to disturbances on one or both sides, obstructing the contraction of the diaphragm. This can cause respiratory insufficiency. To objectify a diaphragmatic dysfunction, a radiographic examination of the diaphragmatic mobility in inspiration and expiration can be performed. This examination can be performed with ultrasound without exposure to radiation. The results should be evaluated in the context of the body plethysmography examination. 3.1.5 

Lungs

The lung as a whole is involved in the conduction of respiratory gas through the bronchial system, but is particularly and exclusively responsible for gas exchange at the lung parenchyma, the alveolocapillary membrane. The entire lung system can be affected by a wide variety of its own vascular, pleural, abdominal and thoracic migration diseases in such a way that ventilation and gas exchange functions are individually or jointly impaired. The complex overlapping of the malfunctions in places requires experienced pneumological knowledge in order to provide an explanation for chronic respiratory insufficiency and its prognosis.

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z Diagnostics

3

Radiological diagnostics (thoracic X-ray, lung computer tomography) If a lung tissue disease is suspected, visualization is first performed with an X-ray of the thoracic organs. In this, macro effects of the most important lung diseases (pneumonia, emphysema, pleural rind, lung fibrosis) can be detected. The modern standard for assessing specific lung structural and vascular diseases is computed tomography, sectional image diagnostics, with high-resolution formats. Specific patterns of lung structure changes allow conclusions to be drawn about the presence of individual disease entities. Bronchoscopy Mirroring of the pulmonary tract is performed using rigid and flexible techniques. It is essential for the clarification of lung structural diseases (lung fibrosis, benign and malignant masses). For this purpose, a surface irrigation of the small airways and the alveolar space (BAL) is performed. The qualitative and quantitative change of specific cell populations is a characteristic of interstitial lung diseases. Parallel to this, lung biopsies for histological and cytological examinations are performed in the same examination. Secretory analyses for microbiological examinations are also carried out. Thoracoscopy A large number of diseases manifest themselves in changes near or on the lung surface. These can be accessed by mirroring the pleural space for inspection and tissue sampling. 3.1.6 

Gas Exchange

Gas exchange is the opposite diffusion of the gases oxygen and carbon dioxide through the alveolocapillary membranes in the functional lung tissue. The diffusion occurs passively due to the partial pressure differences of the gases at this membrane. In relation to oxygen, the pressure in the alveolus is higher

than in the capillaries, so oxygen migrates (diffuses) from the alveolus to the blood. Oxygen is bound to haemoglobin and transported by the blood to the body cells. Carbon dioxide has a higher pressure in the capillaries than in the alveolus, therefore carbon dioxide diffuses from the blood into the alveolus. In this way, CO2 can be removed from the body with each exhalation. The physiological gas exchange requires a specific lung blood flow. Pulmonary ventilation and pulmonary circulation are in a specific equilibrium (7 Sect. 2.1.2). If this equilibrium is disturbed, changes in one or both gases result.  

z Diagnostics

55 Measuring the oxygen saturation (7 Chap.17) 55 BGA (7 Chap. 27) 55 Measurement of the diffusion capacity (TLCO/VA)  

 

kDiffusion Capacity

This measurement is performed to assess the severity of lung tissue diseases. The socalled transfer factor for carbon monoxide (TLCO) is measured. Oxygen migrates or diffuses through the membranes between the alveoli and the capillaries (alveolocapillary membrane). The molecule carbon monoxide (CO) diffuses similar to oxygen and is therefore used as an alternative because it can be measured. In the test, 0.3% CO and helium are added to the breathing air. Helium is used to determine the alveolar volume (VA). In the test, 10% helium is added to the air. Both values, TLCO and VA can be put into a mathematical relationship, the so-called transfer coefficient (TLCO/ VA) is obtained. Measuring method: A patient is asked to inhale to the maximum and hold his breath for 10  s and only then exhale again. The inhaled gas mixture contains the above mentioned 0.3% CO and 10% helium. The exhaled quantities can also be measured.

49 Diseaseology

Interpretation: The smaller the exhaled amount of CO is, the better CO can diffuse through the alveolocapillary membrane into the pulmonary and body circulation. The larger the exhaled quantity of CO is, the lower the permeability or permeability for oxygen O2. If the TLCO drops, this is referred to as a reduced diffusion capacity. The oxygenation capacity is reduced and leads to oxygen deficiency, to hypoxemia. If the TLCO/VA ratio falls at the same time, this is a real diffusion disorder, as occurs in lung tissue diseases, e.g. pneumonia, pulmonary oedema or pulmonary fibrosis. If only the TLCO decreases, but the TLCO/VA ratio remains the same, a distributional disturbance is assumed in which ventilation or aeration is disturbed. Conclusion The respiratory system is defined as a socalled 2-compartment system. In case of respiratory disorders, the lung is diseased with the consequence of oxygen deficiency (hypoxia). If ventilation disturbances occur, respiratory air movement is not guaranteed (. Table 3.3). Affected structures are the respiratory centre, the nerves that move the respiratory muscles of the thorax. The consequence is hypercapnia.  

.       Table 3.3  Respiratory system Respiration

Ventilation

Function

Gas exchange

Breathing air movement

Organ

Lungs

Respiratory center Nerves Respiratory musculature Chest

Main parameters

Oxygen

Carbon dioxide

3.2 

3

Illnesses and Treatment

Before extra-clinical ventilation is initiated, fundamental questions must be clarified: 55 Is there a chronic clinical picture that affects breathing? 55 Which part of breathing is disturbed, the respiratory regulation, the respiratory tract or respiratory ducts, the respiratory mechanics or the gas exchange? 3.2.1 

Hypoxic Brain Damage

The brain has the highest oxygen demand of all organs. The brain needs about 20% of the daily energy demand. The brain has an average blood circulation of 50  ml blood per 100  g brain tissue. It needs almost exclusively glucose as energy substance, approximately 115  g glucose per day or 5.3  g glucose/100  g brain tissue per minute. The brain has only minimal energy reserves. It is therefore dependent on a constant blood flow. After about 20  s without blood flow, the oxygen supply in the brain runs out and after about 5 min the other energy reserves, glucose and ATP (adenosine triphosphate), are completely used up. After a complete interruption of the blood and consequently the oxygen supply, unconsciousness occurs after only a few seconds and after 3–6 min, irreversible damage and cell death occurs. The most common cerebral circulatory disorders only lead to localized peripheral brain defects with multiple defect syndromes, e.g. of the motor or sensitive conduction system. The resulting clinical picture is referred to as hypoxic brain damage or postanoxic encephalopathy (disease of the brain following oxygen deficiency). As a rule, the respiratory regulatory system of the brain stem is not affected with chronic deficits (except basilaris thrombosis). The cause of the most severe generalized circulatory disturbance of the entire CNS is usually a circulatory arrest caused by vari-

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ous forms of pumping failure of the heart. Despite the implementation of cardiopulmonary resuscitation measures, severe neurological consequences can remain. Similar generalized hypoxic conditions of the CNS occur as a result of sudden airway obstruction in the event of drowning, bolus aspiration, swelling of the larynx in the event of insect bites, or generalized airway obstruction in the event of asthmaticus status. If irreversible CNS damage remains with loss of cerebral function, this is known as “apallic syndrome”. Brain stem centres can still regulate basal life-supporting functions, i.e. the circulation and metabolism, but breathing is not always reliable.

Anoxia or Asphyxia Anoxia and asphyxia cause various types of organ oxygen deficiency situations. Anoxia refers to death by suffocation. There is an insufficient oxygen concentration in the inhaled air. This leads to a secondary cardiovascular arrest with tissue hypoxia. Asphyxia describes a primary circulatory

arrest with secondary respiratory arrest and organ oxygen deficiency. In both situations CO2, carbonic acid and other acidic metabolites are enriched. Statistically, asphyxia is the most common form of oxygen deficiency in the brain. This leads to acidosis (hyperacidity). This acidosis damages the nerves, nerve membranes and the walls of the capillaries. As a result, the blood-brain barrier collapses, water enters the interstitial brain tissue and brain edema develops. The brain swelling in turn reduces brain perfusion, resulting in secondary ischemia.

Persistent Vegetative State: Rehabilitation Phase Model The typical course of treatment for severely skull-brain injury is described in a phase model. It is not absolutely necessary to run through all phases in succession. The treatment depends on the patient’s state of recovery and his or her regained abilities, which phase is used and which is skipped (. Table 3.4).  

.       Table 3.4  Rehabilitation phase model in Germany Phase A

Acute treatment

Neurological neurosurgical, internal medicine clinic (intensive care unit)

Phase B

Early rehabilitation with still mostly severe consciousness disorders

The patient is incontinent, artificially nourished, intensive care treatment options should still be provided. Through extensive rehabilitative measures (treatment care, therapies) an improvement of the state of consciousness and the establishment of the coma patient’s cooperation in the therapies should be achieved. Admission criteria: No longer requiring continuous respiration, stable circulation, injuries treated, fractures stable for exercise. No cerebral pressure

Phase C

Further rehabilitation

The patient can already participate in the therapy, but still has to be cared for with a high level of nursing effort. Partial mobilization is to be achieved through extensive rehabilitation measures

Phase D

Medical rehabilitation

Occurs after completion of early mobilisation and represents medical rehabilitation in the previous sense. In this case, the pension insurance is the competent service provider, or the accident or health insurance (in case of special insurance law requirements)

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.       Table 3.4 (continued) Phase A

Acute treatment

Neurological neurosurgical, internal medicine clinic (intensive care unit)

Phase E

Follow-up rehabilitation and occupational rehabilitation

In particular, the treatment objectives are concerned with ensuring the success of medical treatment, or the prevention or improvement of a disability (or prevention), its aggravation and the avoidance or reduction of the need for care, and with occupational reintegration (first or second labour market) and social and domestic reintegration

Phase F

Activating rehabilitation

Despite all medical and rehabilitative efforts in acute treatment and in the subsequent treatment phases (usually already after phase B), severe damage remains in a number of neurological patients, ranging from apallic syndrome to various degrees of impaired abilities (often with multiple disabilities). This rehabilitation phase is designed for the long term. A patient in a persistent vegetative state must be classified by the nursing care insurance fund as level 3+ (hardship case). The treatment is carried out at home (70%!), in specialist care facilities and also in retirement homes

Source: 7 http://www.schaedel-hirnpatienten.de/unterstuetzen/rehabilitation/das-phasenmodell/phasenmodell.pdf, Research 29.02.2016  

Clinic Since 1994, a working group, the Multi-­ Society Task Force on PVS, has published a more precise differentiation of the clinic of the coma vigil. A distinction is made between: 55 “Persistent vegetative state“, a partially reconstructive brain damage and 55 “Permanent vegetative state,” permanent irreversible brain damage. Within the framework of this distinction, clinical criteria for persistent vegetative state were also defined: 55 Complete loss of awareness of oneself or the environment and of the ability to communicate 55 Loss of the ability to make arbitrary or meaningful changes in behaviour as a result of external stimulation 55 Loss of speech understanding and speech production (aphasia)

55 Bladder or bowel incontinence 55 Disturbed sleep, waking rhythm 55 Largely preserved brainstem, spinal, hypothalamic and autonomic reflexes

 entilation for Hypoxic Brain V Damage If the brain damage is severe, breathing can be acutely impaired. When deciding how to ventilate, it must be clarified which part of the respiration is impaired (respiratory regulation, airway or duct, respiratory mechanics and gas exchange). In this case the respiratory regulation is affected. All other parts are not affected. >>The treatment is carried out by controlled ventilation, in which there is a complete take-over of the breaths, usually without oxygen administration (gas exchange is usually not disturbed).

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3.2.2 

3

Stroke: Ischemic Insult

A stroke is a circulatory disorder of the brain that leads to a lack of blood and oxygen supply. It is an acute event that must be considered an emergency and the affected patients should be treated in specialized stroke units. This can reduce mortality and complete dependence on care in nursing homes or home care.

Causes The most common cause of stroke in 80% of all patients is ischaemic stroke. In this case a cerebral artery is displaced by a thrombus or an embolus. The blood flow in the affected areas of the brain is interrupted. This leads to a loss of function and possibly to the death of brain tissue. In about 15% of patients, cerebral haemorrhage occurs due to ruptured arterial vessels. The blood then penetrates into the surrounding brain tissue. About 5% of strokes are caused by subarachnoid hemorrhage. Here, blood enters the cerebrospinal fluid and displaces the brain, so that it is “squeezed” (. Fig.  3.3, . Table. 3.5).  

 

Circulatory disorder

Clinic and Symptoms Since different areas of the brain can be affected, the clinical appearance is not uniform. Typical initial signs are: 55 Sudden onset of headache 55 Gait insecurity with possible accompanying fall 55 Sudden paralysis in one half of the body (hemiplegia) 55 Sudden dizziness 55 Sudden loss of sensation in one half of the body 55 Speech or language disorders (aphasia, dysarthria) 55 Swallowing disorders If the symptoms last only a few minutes to a maximum of 24 h, it is called a “transitory ischemic attack“—TIA. The symptoms after a stroke depend on which vessels and areas of the brain are affected (7 Sect. 1.5.1).  

Ventilation for Stroke If the stroke is severe, breathing may be impaired. A chronic impairment of respiration only occurs in the case of a severe genBleeding

Thrombus

Injury

Washed up imbolus

Cervical artery

..      Fig. 3.3  Circulatory disorders of the brain (courtesy of Isabel Schlütter)

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.       Table 3.5  Circulatory disorders of the brain Affected vessel

Complaints

Anterior cerebral artery

Hemiparesis or hemiparesis, especially on the opposite side of the leg

Cerebral artery

Hemiparesis or hemiparesis, especially facial and arm paralysis on the opposite side with associated visual field disorders and speech disorders (aphasia)

Posterior cerebral artery

Half-sided visual disturbances with restrictions of the field of vision on the opposite side

Vertebral artery

Disturbance of movement (ataxia), sensory disturbances, dysphagia, dizziness with nausea and vomiting, drooping eyelid with narrowing of the pupil (Horner’s syndrome), disturbance of speech motor function (dysarthria).

Basilar artery

Paralysis of both arms and legs, sensory disturbances in the whole body, swallowing disorders, respiratory disorders, disorders of consciousness Basilar thrombosis is the most severe form of stroke and leads to ischemia of the brain stem, cerebellum and other brain areas, it has a poor prognosis with high mortality of patients

eralised circulatory disorder (circulatory arrest). When deciding how to ventilate, it must be clarified which part of the respiration is disturbed (respiratory regulation, airway or air duct, respiratory mechanics or gas exchange. In this case, the respiratory regulation is disturbed. All other parts are not affected. >>The treatment is carried out by controlled ventilation, in which there is a complete assumption of breathing and respiratory rate, usually without oxygen administration (gas exchange is usually not disturbed).

3.2.3 

Paraplegia

In paraplegia, the spinal cord is damaged. In the process, nerve tracts of the spinal cord are interrupted to varying degrees, so that it is no longer possible to transmit motor impulses from the brain to the successful organs. Sensory nerve tracts can also be interrupted, so that there is no longer any feedback to the brain.

Causes and Frequency The most common cause of spinal cord damage (lesion) is injuries caused by accidents during sports, traffic, work or household activities. Non-traumatic damage caused by tumours or inflammation is much less common. In Germany, there are about 1500 new cases of paraplegia per year. About 2/3 of these are of traumatic origin. Paraplegia (paralysis of the lower body, abdomen, hips, legs, feet) is about 60% more frequent than tetraplegia (40%) (paralysis also of the arms, fingers and breathing).

Clinic and Symptoms The symptoms are highly variable, as either isolated or combined motor, sensitive and autonomic functions are affected. The typical characteristics can be distinguished as: 55 Motor disorders, initially flaccid paralysis, later spastic paralysis as para- or quadriplegia. 55 Sensitive disorders with reduced or absent sensation (hyp- or anaesthesia) and with reduced or absent pain (hyp- or analgesia)

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55 Autonomic dysfunction with dysfunction of bladder and bowel control, sexual dysfunction and disorders of the cardiovascular system.

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Below the spinal cord lesion, therefore, a variety of clinical failure syndromes occur. The severity of the failures depends on the extent, completeness and acuteity of the spinal cord lesion.

Tetra- and Paraplegia Depending on the height of the spinal cord lesion, a distinction is made between paraplegia and tetraplegia. Lesions at the level of the thoracic or lumbar spine lead to paraplegia. This paralysis affects the trunk and leg muscles with the following effects: 55 Loss of sensation of touch, pain and temperature 55 Loss of sense of position, 55 Bladder, rectum and sexual dysfunction 55 Arms and hands are freely movable 55 Depending on the height of the lesion, intercostal nerves may also be affected, which impairs breathing. 55 Below the thoracic medulla respiration is not affected and there is no need for ventilation Tetraplegia is caused by damage at the level of the lower cervical marrow. The severity of the paralysis depends on the level of the spinal cord damage: 55 Damage below C8: breathing is possible because the phrenic nerve is intact, but the intercostal nerves are already affected, making breathing difficult; movements of the shoulders, arms, hands and fingers are possible 55 Injury below C7: Breathing and movement of shoulders, arms and hands is possible, finger mobility is restricted 55 Damage below C6: mobility of the hands is difficult, breathing is possible

55 Damage below C5: shoulder mobility is difficult, breathing is already restricted 55 Damage below C4: usually complete dependence on nursing care, head control is still present, breathing can already be severely restricted 55 Damage below C3: Respiration is impaired because the phrenic nerve fails 55 Damage above C3: usually complete respiratory paralysis, if a complete spinal cord lesion occurs (7 Sect. 1.6.1, 7 Fig. 1.22)  

 

z Classification of the Spinal Cord Lesion According to ASIA

The classification of acquired paraplegia is based on the ASIA scheme of the American Spinal Injury Association. Paralysis is classified into complete and incomplete lesions based on the function of the last segment of the spinal cord (S5) (. Table 3.6). (From American Spinal Injury Association, International Standards for Neurological Classification of Spinal Cord Injury) The degree of muscle strength is ­classified as follows (. Table 3.7).  

 

Ventilation for Severe Paraplegia If respiration is impaired in the case of severe paraplegia (damage from C4), the decision on how to ventilate must clarify which part of respiration is impaired (respiratory regulation, airway or air duct, respiratory mechanics or gas exchange). In this case, the respiratory regulation is present centrally but the breathing mechanics are disturbed peripherally. All other parts are not affected. >>The treatment is carried out by controlled ventilation, in which there is a complete take-over of the breaths, usually without oxygen administration (gas exchange is usually not disturbed).

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.       Table 3.6  Classification of spinal cord lesion according to ASIA A—complete

No sensitive or motor function is preserved in the sacral segments S4 to S5

B—incomplete

Sensitive but no motor function is maintained below the neurological level and extends to the sacral segments S4/S5

C—incomplete

Motor function is maintained below the neurological level and the majority of the characteristic muscles below the neurological level have a muscle strength level of less than 3

D—incomplete

Motor function is maintained below the damage level and the majority of the characteristic muscles below the neurological level have a muscle strength level greater than or equal to 3

E—incomplete

Sensitive and motor functions are normal

.       Table 3.7  Muscle strength level 0

No contraction to feel.

1

A weak contraction is palpable or the tendon becomes clearly visible during muscle tension, but there is no observable movement of the body part

2

Movement is possible with the release of gravity, but not against light resistance

3

Ability to hold a position against gravity or to move and hold in the test position

4

Test position can be held against moderate resistance

5

Test position can be held against gravity and maximum resistance

3.2.4 

Neuromuscular Diseases (NMD)

Carsten Schröter

Definition Muscle diseases or muscular atrophy are often referred to in a simplistic way, but the neuromuscular diseases are meant. Muscular diseases are strictly speaking only the diseases of the muscle itself. These are in particular muscular dystrophies, myotonies, inflammatory muscular diseases (myositides) and metabolic diseases of the muscle, metabolic myopathies. Neuromuscular diseases also include diseases of the nerve fibres that innervate the muscle. These include, for example, neural and spinal muscle atrophies. The diseases of

the contact point between nerve and muscle, myasthenia, are also to be included. In these diseases, the muscle is the organ whose weakness makes the disease noticeable. However, it is only indirectly affected by the disease of the nerves. In the following, an overview of the various neuromuscular diseases is given (. Fig. 3.4). The diagram shows the structures involved in motor function: the brain, the spinal cord, the nerve fibres and the muscles. The arrows indicate the structures involved in the respective diseases. Representing many nerve cells and fibres, one nerve fibre with cell body in the area of the motor cortex of the brain (first motor neuron) and one in the area of the spinal cord (second motor neuron) are shown. The extension of the first motor neuron goes to the brain stem or spinal  

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..      Fig. 3.4  Schematic overview: the muscle diseases (courtesy of Dr. med. Carsten Schröter)

Brain

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Spinal cord Amyotrophic lateral sclerosis

Polyneuropathies, Neural Muscular Atrophy (Charcot, Marie, Tooth) (HMSN) Spinal muscular atrophy, poliomyelitis Nerve Myasthenia gravis Muscle Muscular dystrophy, myotonia, Myositis

cord. There the impulse is passed on to the second motor neuron (anterior horn cell, alpha-­motoneuron). The axon of the second motor neuron extends to a muscle. The connection point between the nerve fibre and the muscle is called the motor endplate. A nerve fibre innervates several muscle fibres of a muscle. A nerve fibre and the associated muscle fibres are together called a motor unit.

Overview The tabular overview does not take into account the new human genetic findings of recent years, but allows a systematic assignment of diseases to the diseased structures (. Table 3.8).  

Occurrence and Frequency Neuromuscular diseases are rare. For example, 4–5 out of 100,000 inhabitants in Germany suffer from Duchenne muscular dystrophy, the most common form of muscular dystrophy. About 3–8 per 100,000 inhabitants suffer from amyotrophic lateral sclerosis, and about 0.3 per 100,000 from spinal muscular atrophy of the Kugelberg-­ Welander type. Due to the rarity of the diseases, muscle centres have been established at universities, especially for diagnostic purposes.

General Symptoms Typical symptoms of most neuromuscular diseases are, to varying degrees, paresis and rapid fatigue, muscle atrophies, and in some

57 Diseaseology

.       Table 3.8  Overview of neuromuscular diseases (modified according to John Walton) 1. Muscle disease (myopathy)

Muscular dystrophies: –  Type Duchenne –  Type Becker-Kiener –  Limbbelt type –  Fazio-scapulo-­humeral muscular dystrophy –  Type Emery-Dreifuss –  Other Myotonic myopathies: –  Myotonic dystrophy type 1 (Curschmann, Steinert) –  Myotonic dystrophy type 2 (PROMM) –  Myotonia congenita (Thomsen) –  Myotonia congenita (Becker) –  Other Hereditary metabolic myopathies (glycogen storage diseases): –  Glycogenosis type 2 (M. Pompe) –  Glycogenosis type 5 (McArdle) –  Lipid storage diseases –  Mitochondrial myopathies Endocrine myopathies: –  For thyroid diseases –  In Cushing’s disease (hyperactivity of the adrenal cortex) –  Other Congenital myopathies Inflammatory myopathies –  Autoimmune diseases (polymyositis, dermatomyositis) –  Inclusion body myositis

2. Neuromuscular transition

Myasthenia gravis Lambert-Eaton Myasthenic syndrome (LEMS)

3. Diseases of the nerve fibres

3.1 spinal muscular atrophies and motoneuron diseases: Poliomyelitis (polio) Spinal muscular atrophies (SMA): –  infantile form (Werdnig, Hoffmann) –  intermediate form –  juvenile or adult form (Kugelberg, Welander) –  other Sporadic spinal muscular atrophies: –  peroneus type –  type Aran-Duchenne –  type Vulpian-­Bernhardt Amyotrophic lateral sclerosis (ALS) 3.2 polyneuropathies: Neural muscle atrophies (Charcot, Marie, tooth): –  HMSN (hereditary sensorimotor neuropathy) type 1 –  HMSN type 2 Other hereditary polyneuropathies Guillain-Barré syndrome Chronic inflammatory demyelinating polyneuropathy (CIDP) Other polyneuropathies (diabetic, alcoholic ...)

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diseases also muscle pain (myalgia) and muscle cramps (crampi). Polyneuropathies can also cause sensory disorders (hypaesthesia, hypalgesia), mainly distal, i.e. on the feet.

3

Description of Different Diseases z Muscular Dystrophies

Muscular dystrophies are genetic diseases that lead to the destruction of muscle fibres. Pareses are in the foreground, often affecting the proximal muscles in particular. In muscular dystrophies of the Becker-Kiener and Duchenne type, both caused by a mutation of the dystrophin gene, the pelvic girdle muscles are affected first. Muscular dystrophies of the limb belt type are referred to as pelvic girdle or shoulder girdle type, depending on whether the hip and pelvic muscles or the shoulder muscles are mainly affected. Depending on the type and course of the respective muscular dystrophy, however, the weaknesses can spread to other muscle groups. Muscular dystrophies of the limb girdle type have many different genetic causes, which are classified as LGMD1 for autosomal dominant and LGMD2 for autosomal recessive inheritance. A further letter, e.g. LGMD2A, then classifies the exact disease, in the example a disorder of calpain. In facioscapulohumeral muscular dystrophy (FSHD), according to its name, the facial, shoulder and upper arm muscles are usually affected. But also the trunk musculature and the foot lifts are often paretic, these pareses can also exist in isolation without pareses in the typical regions. Which muscle groups are primarily affected and the dynamics of the disease depend on the respective disease. However, the course of the disease is often very variable, even in a family. The affected muscles atrophy, but certain muscle groups can even appear very strong externally, if the muscle tissue is replaced by connective and fatty tissue. This is particularly typical of the calves.

Here we also speak of a so-called pseudo hypertrophy, because the strength of the muscle groups is reduced by the remodelling. Especially due to incorrect and excessive strain, the musculoskeletal system often suffers pain. The paretic musculature is increasingly strained in order to cope with the tasks at hand, for example an upright posture of the body. This can lead to muscular tension. In addition, paresis impairs the guidance of the joints and puts particular strain on the ligaments. This results in pain, which in turn can lead to increased tension. It should also be noted that some muscular dystrophies involve the heart muscles. The resulting cardiac insufficiency and possible cardiac dysrhythmia must be taken into account, especially during therapy. The respiratory musculature can also be affected, which can lead to restrictive ventilation disorders. z Myotonia

The myotonic diseases are characterized by a stiffness of the musculature. Movements can sometimes only be performed slowly and tenaciously. This is in the foreground with myotonia congenita, both with the Thomsen type and the Becker type. In myotonic dystrophy type 1 (Curschmann, Steinert), on the other hand, this component is usually only slightly pronounced. If it is present to a relevant extent, it typically affects mainly the hand muscles. In this disease, pareses mainly occur in the muscles far from the trunk, on the hands and foot lifts, but can also be generalized and affect the trunk muscles to a pronounced extent. In this multisystemic disease, other organ systems can also be affected, e.g. the heart (cardiac arrhythmia, heart failure), the eyes (cataracts) and the hormone status. In myotonic dystrophy type 2 (also called proximal myotonic dystrophy, PROMM), on the other hand, the very different, but mostly slightly pronounced weaknesses are located close to the trunk. Here, too, the heart and eyes can be affected. In addition, muscle pain is often described here. Patients

59 Diseaseology

with myotonic dystrophy, both type 1 and especially type 2, have an increased risk of developing diabetes mellitus. z Metabolic Myopathies

They are characterized by a disruption of the energy supply or production. Carbohydrates and fats are absorbed into the muscle fibre and stored there. However, they cannot be broken down and fed into the energy cycle in the case of glycogen storage or lipid storage disorders. Depending on the nature of the various diseases, there are weaknesses in the muscles close to the trunk, reduced endurance performance or stressrelated muscle pain. Here too, the extent of the symptoms of the various diseases varies greatly, from only slight impairments to death in childhood. Among the glycogenoses, type 2 (Pompe’s disease) and type 5 (McArdle’s disease) should be highlighted. M Pompe typically manifests itself at the beginning of adulthood with weakness of the trunk and pelvic muscles and early respiratory muscles. If present at birth, the disease leads to death if left untreated. Treatment is possible in children as well as in adults with enzyme replacement therapy. For this purpose, the missing enzyme is venously infused every 2 weeks. McArdle’s disease is characterised by a low tolerance to stress, muscle pain and contractures under stress. After a few minutes of low stress tolerance, the performance of the muscles increases, the phenomenon is called second wind and can be exercised in a targeted manner. Overexertion can lead to rhabdomyolysis (muscle fibre disintegration) with resulting dialysis-related renal insufficiency. z Muscle inflammation (Myositis)

Muscle inflammation is a heterogeneous group. Polymyositis and dermatomyositis are classic autoimmune diseases. Typically, pareses of the proximal musculature, i.e. in the shoulder and pelvic girdle area, are the most common. The symptoms of these dis-

3

eases develop acutely to subacutely over weeks and months. Occasionally, muscle pain is also reported. An involvement of the heart musculature in the sense of myocarditis also occurs. In dermatomyositis, inflammatory skin changes can occur. If, on the other hand, other symptoms such as joint pain or circulatory disorders occur, another inflammatory connective tissue disease involving the muscles must also be considered, such as scleroderma and lupus erythematosus. As an autoimmune disease, myositides are treated immunosuppressively. Inclusion body myositis also belongs to the group of myositides, although the inflammatory process is accompanied by degenerative changes. The chronically progressing disease, which occurs more frequently in older people and in men than in women, is characterized by paresis of the forearm and hand muscles, especially the finger flexors, as well as atrophy and paresis of the M. quadriceps femoris. The weaknesses can spread to other muscle groups. The respiratory and swallowing muscles can also be affected. Intravenous treatment with immunoglobulins is often carried out probatorily (on a trial basis), corticoids and other immunosuppressive drugs are apparently not effective. z Myasthenia gravis and Lambert-Eaton Syndrome

Both myasthenia gravis and Lambert-Eaton myasthenic syndrome (LEMS) are classic autoimmune diseases and affect the neuromuscular junction. While in myasthenia gravis the antibody structures of the motor endplate on the membrane of the muscle (postsynaptic disorder) are affected, in Lambert-­Eaton syndrome calcium channels in the membrane of the nerve fiber (presynaptic disorder) are targets of the antibodies. In myasthenia gravis, the strength of the muscles typically decreases rapidly during exertion, but after sufficient rest the muscles can be regained depending on the severity of the disease. Typically, the eye muscles and

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the eyelid lifters as well as the facial muscles are particularly affected. The weakness can also extend or generalise to the muscles close to the trunk, especially in the shoulder and neck area. In severe cases, the respiratory muscles may also be affected. In most cases, the disease can be influenced well by immunosuppression with medication. The main symptoms of Lambert-Eaton syndrome are weakness and premature fatigue of the muscles close to the trunk, especially the pelvic and thigh muscles. Weaknesses of the eye, speech and swallowing muscles occur. During the test the force is typically very low at first, then increases for a few seconds before premature exhaustion sets in again. Vegetative disorders such as dry mouth, reduced sweating, bladder emptying disorders and constipation also occur. In about half of the patients, the disease occurs as a result of a tumor disease, as a so-called paraneoplastic syndrome. Lambert-­Eaton syndrome is usually amenable to drug treatment with Amifampridine.

most common neuromuscular disease in adults. It is caused by a disease of the first and second motor neuron. The degeneration of the second motor neuron leads to flaccid and atrophic paresis, and spastic paresis if the first motor neuron is predominantly involved. The annual rate of new cases (incidence) worldwide is 0.6–2.4 persons per 100,000 inhabitants per year. Overall, it is assumed that about 30–80 out of 1,000,000 inhabitants suffer from the disease. Based on these figures, it is assumed that about 6000 people in Germany have the disease. Exact figures are not available, however. The frequency of amyotrophic lateral sclerosis increases with age, the peak being between the ages of 50 and 70. Life expectancy is significantly reduced and is usually stated as 3–5 years, although the variance is large. About 10% of the patients live longer than 10  years. Amyotrophic lateral sclerosis usually begins locally with paresis, most frequently on the forearm and hand area (40–50%), less frez Spinal Muscular Atrophies quently on the legs (25–30%), here often The disorders in spinal muscular atrophies with foot lifter paresis. In most cases, the are very similar to those in muscular dystro- symptoms begin on one side and spread to phies. The cause is a disease of the second the same extremity on the opposite side or motor neuron. When these cells die, the the other extremity on the same side. In the muscles are no longer innervated, thus forms of progression mentioned above, we becoming paretic and atrophic. Again, it is speak of a spinal form. In the bulbar form, mostly the proximal muscle groups that are which occurs in approximately 25% of cases, affected. There are forms of autosomal the disease begins with dysfunction of the recessive inherited disease that are already bulbar muscles with dysarthria and dysphapresent at birth and progress rapidly gia and in the course of respiratory insuffi(Werdnig type, Hoffmann). Other forms of ciency. The sphincter muscles of the bladder the disease do not appear until adolescence and intestine, on the other hand, are not or adulthood with slow progression and usually affected, nor are the eye muscles. normal life expectancy (type Kugelberg-­ The frequently used term motoneuron Welander). A special facet is the bulbospinal diseases includes all diseases of the first and/ muscular atrophy (type Kennedy), which or second motor neuron. As a rule, spinal occurs as an X-linked disease in men and muscular atrophies and amyotrophic lateral also affects the swallowing muscles. sclerosis are summarised under this term. It is often used when there is a suspicion but a z Amyotrophic Lateral sclerosis (ALS) clear assignment to amyotrophic lateral scleAmyotrophic lateral sclerosis is a progres- rosis is not yet possible. Progressive muscle sive degenerative motor system disease, the atrophy, primary lateral sclerosis and bulbar

61 Diseaseology

paralysis are variants of amyotrophic lateral sclerosis. Progressive muscular atrophy is a course of disease in which the second motor neuron is affected with atrophic paresis. In primary lateral sclerosis, the first motor neuron is damaged with resulting spasticity, without signs of damage to the second neuron. Progressive bulbar paralysis is understood to be a disease process that mainly affects the speech and swallowing muscles, but not the arm or leg muscles. The diagnosis of amyotrophic lateral sclerosis is made taking into account the patient’s medical history and a detailed physical-neurological examination as well as additional examinations using the latest equipment. In particular, electroneurography, electromyography and evoked potentials should be mentioned here. Other important examinations may include magnetic resonance imaging (MRI) of the brain and cervical spine to rule out other causes of paresis. More than 90% of patients with amyotrophic lateral sclerosis suffer from the sporadic form, while 5–10% have a familial, i.e. hereditary, form. First indications of a cause of the familial form were found in a study published in 1993, which proved a mutation in the gene of Cu/Zn-SOD (copper-zinc-­ superoxide dismutase) on chromosome 21. In the meantime, however, a number of other genes are known whose mutation can lead to the occurrence of ALS. These forms give the possibility to develop specific therapy concepts in animal models. A several-month extension of the life span is proven by the administration of riluzole. It is also assumed that the maintenance of body weight, if necessary with a high-­ calorie diet, is prognostically favourable. The treatment is, by the way, symptomatic. Depending on the symptoms, physiotherapists, occupational therapists and speech therapists should care for the patient in coordination with each other. The main objectives are to improve the quality of life in every phase of the disease, to avoid complications and to prolong the life span. It is

3

not possible to train strength, but there is a high risk of overstrain and the resulting increase in pareses. Maintaining motor functions and breathing, coughing up and speaking are central therapy contents. Pathological laughing and crying, i.e. laughing or crying that does not correspond to the intensity of a mood, but cannot be suppressed by the patient, can be a problem in contact with other people; in this case, drug treatment is possible. All in all, once the diagnosis has been made, the treatment is palliative therapy right up to the end of life. The German Society for Muscular Diseases (Deutsche Gesellschaft für Muskelkranke) offers a lot of valuable information for therapists (7 www.­dgm.­org).  

z Poliomyelitis and Postpoliomyelitis Syndrome

Poliomyelitis acuta anterior (short: polio, polio in children) is a virus-related disease of the second motor neuron. Today, the disease is still predominantly active in Afghanistan and Pakistan in Asia, and in Nigeria in Africa. In Europe it is considered extinct. There is also great hope that the disease will soon be eradicated in Africa. As there is still a risk of the viruses being introduced from Asia and Africa by tourism, the Standing Commission on Vaccination (Ständigen Impfkommission, STIKO) of the Robert Koch Institute regularly recommends basic immunisation for children and young people and every 10 years for adults travelling to these regions. Even if the disease no longer occurs as a new disease in Europe today, we are still dealing with the consequences of the epidemics at the end of the 1950s and beginning of the 1960s in particular. On the one hand, the pareses, atrophy and changes in the musculoskeletal system (so-called residual polio) that persist after the onset of the disease place a false burden on the musculoskeletal system. This can lead to premature joint degeneration (arthrosis) and disorders with pain in the spinal column.

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The so-called post-poliomyelitis syndrome (or shorter post-polio syndrome or PPS) must be distinguished from this. Decades after polio, paresis can occur and progress slowly. This particularly affects muscle groups that were often primarily severely affected but have recovered well. Patients often initially report a decrease in endurance and resilience. In the course of the disease, increasing pareses are then also observed. In addition, general exhaustion, sleep disorders and other disorders are also described. If the respiratory musculature was primarily affected by polio, it can also lead to a decreasing vital capacity (see 7 Table 1.5) and thus to pulmonary insufficiency. Often, as in the phase after acute polio, patients try to train intensively in the context of PPS when new pareses occur, and experience a further deterioration of muscular functions. Here, only a dosed and moderate exercise programme can be carried out, overloading should be avoided.  

z Neural Muscle atrophies (Hereditary Sensorimotor Neuropathies, HMSN)

Neural muscular atrophies are mainly diseases of the axons and/or the medullary sheaths. The longest nerve fibres have the highest risk of developing the disease. For this reason, the symptoms are found to be distally accentuated. Hereditary sensorimotor neuropathies (HMSN) have also been established for these diseases. The diagnosis is often supplemented by the names of the first describers: Charcot, Marie and Tooth. Mostly the lower legs and feet as well as the hands are especially affected with atrophic pareses. Foot lifter paresis is often the leading symptom. Sensory disturbances of the feet can also occur, but they are usually not very pronounced. Positional sensory disorders lead to insecurity of gait, especially in the dark. Changes of the foot skeleton are also often present, especially hollow feet with hammer toes. The symptoms can vary greatly, even within a family. Phrenicus paresis with unilateral diaphragmatic hyper-

tension is rarely observed. Otherwise, however, breathing is usually not affected.

Therapy Inflammatory diseases are primarily treated immunosuppressively or by immunomodulation. The goals of therapy and especially rehabilitation for patients with degenerative neuromuscular diseases are to improve and maintain independence in mobility and self-­ care as well as participation in social life. The treatment of hereditary neuromuscular diseases is currently symptomatic, the most important are usually physiotherapy, occupational therapy and speech therapy. First causal therapy approaches have been approved for genetically determined diseases. Advances in genetics are expected to lead to further molecular genetic therapies over the next few decades. z Muscular Weakness

Pareses are the main cause of most problems in neuromuscular diseases. There are a number of well-controlled studies that have examined the effects of exercise and training on strength and function. In slowly progressing neuromuscular diseases, an adapted exercise program can be expected to improve function without evidence of weakness due to overloading. In the long term, however, even optimal treatment measures cannot prevent the disease from progressing. There are also indications that the therapeutic ­procedures are differently effective for the various neuromuscular diseases, but here further investigations must be waited until reliable data are available. In the case of rapidly progressing neuromuscular diseases, the risk of a more pronounced progression of pareses due to overloading is high. Carried out with the aim of improving function, the risk of overstrain is lower due to the treatment. Patients with neuromuscular diseases should be encouraged not to exercise to the point of exhaustion. They should be informed about the warning signs of overstrain. These

63 Diseaseology

include an increased feeling of weakness after exercise or muscle pain 24–48  h after exercise. Other warning signs include more pronounced muscle cramps, a feeling of heaviness in the arms and legs and persistent shortness of breath. An adapted exercise program with light to moderate aerobic exercise such as walking, swimming and riding an ergometer, if the severity of the disease allows it, can improve muscular endurance and function as well as the performance of the cardiovascular system in many neuromuscular diseases. In addition to circumscribed pareses, a generalized reduced resilience as well as reduced performance of the heart and lung function have to be considered. The exercise program helps to stabilize and improve the functions, to maintain the ideal body weight and to reduce pain due to incorrect loading. z Contractures and Scoliosis

Contractures and scoliosis are common problems in a number of neuromuscular diseases. The risk is particularly high in cases of wheelchair dependence and increasing trunk muscle weakness, as well as during growth spurts. Careful stretching of the affected or endangered joints reduces the risk of contractures and slows down their progression. Regular physiotherapeutic exercises should aim at a careful symmetrical stabilisation or preservation of the trunk muscles in order to prevent scoliosis or slow down its progression. Forst and Rideau were able to show that the surgical release of contractures in Duchenne muscular dystrophy can extend the time of walking. There is also the possibility of surgical intervention in scoliosis. Possibly, orthoses can counteract the development of scoliosis by extending the duration of walking ability. In this case, however, further examinations are necessary in order to be able to make reliable statements. The orthoses should be as light as possible so that their weight does not additionally impair the ability to walk. Even with optimally per-

3

formed physiotherapy, contractures and scoliosis cannot be prevented in the case of rapidly progressing neuromuscular diseases. The aim can only be to influence the course of the disease in a favourable way. z Disorders of Lung Function

Weaknesses of the diaphragm, intercostal and abdominal muscles can result in disorders of lung function. The various neuromuscular diseases can lead to these impairments to varying degrees. In the case of diseases that regularly affect the respiratory musculature, regular lung function tests are necessary. The first clinical signs of a respiratory function disorder can be nocturnal respiratory disorders: regular headaches in the morning, restlessness or nightmares at night, the feeling of waking up feeling exhausted in the morning, unresting sleep and increased daytime tiredness. Recording the impairments is necessary in order to be able to initiate non-invasive home ventilation in good time. z Complications of Heart Function

Various diseases of the musculature, such as muscular dystrophies of the Duchenne and Becker type or muscular dystrophy of the limb belt type LGMD2I and myotonic dystrophies can cause functional disorders of the heart. These can be cardiac insufficiency or cardiac arrhythmia. The ­ electrocardiogram (ECG), the long-term ECG or the echocardiogram can provide information. Particularly in the case of the above-­ mentioned diseases, the resilience of the heart function must also be checked before starting an exercise programme. In case of cardiac arrhythmia, the timely use of a pacemaker must be observed. z Swallowing Disorders

Swallowing disorders occur particularly in amyotrophic lateral sclerosis, bulbospinal muscular atrophy and also individual muscular dystrophies. Initial indications may be changes in the voice, such as hoarseness, and increased swallowing. More precise assess-

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ments can be made by endoscopic and X-ray examinations. Swallowing disorders are an indication for speech therapy. The thickening of liquids and the preparation of easy-­ to-­ swallow food are important aids. If swallowing is no longer sufficiently possible, a percutaneous endoscopic gastrostomy (PEG) may become necessary. Here, a thin probe is inserted through the abdominal wall into the stomach or small intestine by means of a gastroscopy.

Ventilation If respiration is impaired in the various neuromuscular diseases, the decision on how to ventilate must clarify which part of the respiration is impaired (respiratory regulation, airway or air duct, respiratory mechanics or gas exchange). If breathing is impaired as a result of a neuromuscular disease, respiratory regulation and gas exchange are not usually affected. The impaired respiratory pump or respiratory mechanics is the main focus. The impairment should be objectified by measuring lung function and its severity assessed. >>The treatment consists of controlled ventilation, in which there is a complete assumption of breathing, usually without oxygenation, unless there is additional lung disease (COPD).

3.2.5 

COPD

Chronic obstructive lung disease is a common reason for ventilation in out-of-­hospital care. Two abbreviations are commonly used: 55 COPD: chronic obstructive pulmonary disease 55 COLD (less common): chronic obstructive lung disease The COPD describes an 55 irreversible (not reversible by treatment), 55 progressive (ever increasing) airflow limitation of the airways

55 through chronic (permanently existing), 55 obstructive (narrowed airways), 55 inflammatory bronchiolitis (bronchiolifibrosis) and lung parenchyma destruction (emphysema), 55 caused by long-lasting, inhaled noxae. Group of lung diseases caused by 55 respiratory distress on exertion, 55 coughing and 55 increased sputum 55 The main obstacle is exhalation (expiration).

Indicator of COPD 55 Hypertrophy (abnormal enlargement) and hyperplasia (abnormal proliferation) of the bronchial mucous glands. 55 Production of tough, glassy mucus (so-­ called dyscrine). 55 As a result, a great deal of mucus is produced in the airways, which is not mobilized and is transported away by the mucociliary transport system. The mucus thus remains in the airways (so-called mucostasis). 55 In addition, there is an expansion of the air space distal (i.e. behind) the terminal bronchioles. 55 This ultimately leads to the destruction of the lung parenchyma (intact lung ­tissue).

Pathophysiology of COPD The persistent, chronic inflammation is the typical feature of this disease. It is initiated and maintained by long-term inhalation of noxious substances of various kinds. In the course of the disease, an increase in respiratory resistance, for example, develops: 55 Bronchoconstriction (spasmodic narrowing of the airways and air pipes) 55 Hypertrophy and hyperplasia of the bronchial mucous glands 55 Bronchodilatation

65 Diseaseology

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End expiratory collapse The small and smallest airways, Bronchioli and ductus alveolaris, Collapse during exhalation or expiration.

..      Fig. 3.5  End-expiratory collapse (courtesy of Isabel Schlütter)

The increase in airway resistance is also amplified by: 55 Airway deformations (mechanical displacement of the airways) 55 Over-inflation, i.e. those affected can only partially exhale the inhaled air because the small and smallest airways collapse and residual air remains in the lungs (. Fig. 3.5).  

The collapse of the airways, which occurs mainly during the exhalation phase of expiration, causes the air to remain “trapped” in the alveoli. >>This phenomenon is called airtrapping (trapped air in the alveoli). Although the air can enter during inhalation, it is very difficult to exit during exhalation.

This trapped air leads to an over-inflation of the alveoli and to an intrinsic PEEP (PEEPi  =  intrinsic PEEP). This phenomenon prevents COPD patients, especially under stress conditions, from being able to adjust the respiratory minute volume by increasing the breathing rate. 55 The intrinsic PEEP, the so-called internal permanent overpressure in the alveoli of the lung, leads to a measurable increase in FRC, RV/TLC in body plethysmography (7 Sect. 1.4.5).  

55 The chronic over-inflation of the whole lung gradually limits the inhalation volume. 55 The overbidding can lead to capillary compression. The small blood vessels of the lung are compressed. The result is reduced blood flow to the lungs, thus disturbing perfusion. 55 The reduced blood flow in the lungs then leads to a rarefication of the pulmonary capillaries. These decrease in number. This reduces oxygenation. Oxygen uptake is impaired and vascular resistance increases. 55 The amount of blood that the right ventricle pumps into the lungs must be equal to the amount that the left ventricle pumps into the major circulation of the body. If the resistance in the pulmonary vascular system increases, the right ventricle must apply an increased pumping force. If pulmonary hypertension leads to right heart weakness due to capillary rarefication, the blood volume can no longer be transported and peripheral oedema develops. . Figures  3.6, 3.7 and 3.8 are intended to illustrate the problem of COPD: During inhalation, the air can easily enter the alveoli (symbolised by the arrow going in), but during exhalation it is difficult  

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3

..      Fig. 3.6  Airway collapse: obstruction (= narrowing) (courtesy of Isabel Schlütter)

..      Fig. 3.7  Intrinsic PEEP (= PEEPi) (courtesy of Isabel Schlütter)

to exit because the small airways collapse (arrow stopping at the dotted line). In addition, the narrowed obstructive airways are characterized by the narrow wavy-dashed lines of the airways (. Fig.  3.6). Due to bronchospasm, hypertrophy and hyperplasia of the bronchial mucous glands and mucous membrane oedema, the airways become permanently narrowed (→ Obstruction). The air remains in the alveoli and is trapped there (air trapping). This increases the air pressure within the alveoli (intra-­  

alveolar), which creates “intrinsic PEEP”. The “intrinsic PEEP” leads to over-inflation of the alveoli. This over-inflation of the alveoli leads to emphysema (. Fig. 3.7). In order to avoid collapse of the airway during exhalation, the patient must avoid rapid breathing and prolong the exhalation time. This leads to restricted ventilation (aeration). Inadequate ventilation results in insufficient “old air” being breathed out of the alveoli and insufficient “new air” being absorbed into the alveoli. Insufficient ventilation increases the CO2 level in the alveolus.  

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67 Diseaseology

..      Fig. 3.8  Hypercapnia (courtesy of Isabel Schlütter)

The pCO2 value also increases in the capillary and means “hypercapnia“(. Fig.  3.8). This is also caused by the fact that the alveolar surface is reduced by emphysema and the alveolar capillary membrane is fibrosed.  

Clinical Symptoms of COPD The recognizable symptoms of COPD are: 55 Shortness of breath 55 Cough 55 Ejection of pulmonary secretions If these persist over a longer period of time without subsiding, there is a suspected diagnosis of COPD with an appropriate risk history. In the course of the disease, further consequences of the disease become apparent, so that it is called a systemic disease: 55 Chronic, recurrent infections 55 Chronic shortness of breath 55 Weight loss and muscular exhaustion, if applicable 55 Osteoporosis 55 Anxiety 55 Vascular sclerotherapy

55 Heart failure 55 Depression 55 Metabolic disorders

Staging The classification of the stages depends on the patient’s clinic, the frequency of exacerbation and the results of lung function diagnostics (. Table  3.9). In the new COPD classification, which has been in effect since 2012, the number of exacerbations (acute worsening of COPD disease) and the CAT or MRC score are included. The CAT and MRC scales are assessment tools for the evaluation of shortness of breath (. Fig. 3.9, . Table. 3.9, . Table. 3.10 and Table. 3.11). COPD patients have to do a lot of “isometric work of breathing” to overcome the intrinsic PEEP (“isometric work of breathing” = non-flow-effective effort of the respiratory muscles)  →  an increased effort of breathing, the muscular load is greater than the muscular capacity.  

 

 

 

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..      Table 3.9  Global Initiative for Chronic Obstructive Lung Disease (GOLD) - old classification (courtesy of R. Cegla GmbH & CO.KG, Horresser Berg 1, 56,410 Montabaur 7 http://www.­leichter-­ atmen.­de/copd-­gold-­stadien  

3

COPD stage

FEV1 (reference value = 100%)

FEV1/FVC

I (light)

≥80% target

5  min. Nocturnal pCO2 > 55 mmHg/7.3 kPa 55 pCO2 > 10 mmHg/1.3 kPa at night compared to the waking state 55 Desaturation SpO2 >The treatment is carried out by assisted or controlled ventilation, with increased breathing strokes, if necessary with oxygen administration, if this is permanently disrupted due to the restriction.

Criteria for Ventilation Symptoms of hypoventilation in at least one of the following conditions: 55 Chronic daily hypercapnia with pCO2 ≥ 45 mmHg/6 kPa

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55 Night-time hypercapnia with pCO2  ≥ 50 mmHg/6.6 kPa 55 Rapid relevant decrease of VC

3

Conclusion 55 Non-invasive ventilation is an offer for patients with severe, advanced chronic diseases affecting the respiratory system to first alleviate the subjective experience of breathlessness and thus improve the quality of life. 55 A clarification of the disease entity that led to the respiratory insufficiency is obligatory. Appropriate specialist treatment must be initiated. 55 The objectification of subjective breathing problems must be proven by appropriate functional tests. 55 Knowledge of the disease-specific functional failure determines the ventilation mode. 55 For diseases affecting central respiratory regulation, ventilation is performed as controlled ventilation. 55 In the case of diseases affecting the respiratory tract or respiratory mechanics, ventilation is initially assisted and later controlled. The focus is on the administration of deep breaths. 55 In the case of illnesses in which gas exchange disturbance is the main concern, assisted or controlled ventilation with additional oxygen is performed. Disturbances of the gas exchange indicate a diseased lung. 55 The ventilation therapies performed must be adapted to the individual.

References Artmann F, Hader C, Rühle KH und Rasche K (2009). Die Diffusionskapazität in der täglichen Praxis, Atemw.-Lungenkrkh., Jahrgang 35, Nr. 1/2009, S. 10–17. http://lungenfunktion.­eu/grundlagen/diffusion.­htm, Recherche 28.02.2016

ASIA American Spinal Injury Association. http://www.­ asia-­spinalinjury.­org/elearning/International%20 Stds%20Diagram%20Worksheet%2011.­2015%20 opt.­pdf , http://www.­asia-­­spinalinjury.­org/index.­ php , Recherche 3.3.2016 Brodbeck DK (2010). Die psychosoziale Anpassung an Querschnittslähmung: Eine empirische Untersuchung Inaugural-Dissertation zur Erlangung des Doktorgrades der Medizin an der Medizinischen Fakultät der Eberhard-Karls-­Universität Tübingen. https://publikationen.­uni-­tuebingen.­de/xmlui/bitstream/handle/10900/45773/pdf/doktorarbeit_daniela_druckversion_27.­12.­2010.­2010.­pdf?sequence=1, Recherche 12.03.2016 Forst J, Forst R (2012) Surgical treatment of Duchenne muscular dystrophy patients in Germany: the present situation. Acta Myol 31:21–23 Kabs HP (2009). Das paraplegiologische Gutachten, in: Rompe et al. Begutachtung der Haltungs-und Bewegungsorgane, 5. Aufl., Kap.­ 2 .7S. 361–374, Thieme Verlag 361–374 Kollmann-Fakler V (2011). Prognosekriterien und Outcome der hypoxischen Hirnschädigung nach Herz-Kreislauf-Stillstand, Dissertation zum Erwerb des Doktorgrades der Medizin an der Medizinischen Fakultät der Ludwig-Maximilians-­ Universität zu München Lloyd-Owen SJ, Donaldson GC, Ambrosio N et  al (2005) Patterns of home mechanical ventilation use in Europe: results from the Eurovent survey. Eur Respir J 25:1025–1031 Klinik Hoher Meissner, Bad Sooden-Allendorf. http:// www.­reha-­klinik.­de/index.­html, http://www.­reha-­­ klinik.­de/informationsforum/index.­html, http:// w w w.­r e h a -­k l i n i k .­d e / i n fo r m at i o n s fo r u m / uebersicht-­zu-­muskelkrankheiten.­html Nentwig A (1994) Aktuelle Wachkoma-Studie über Betroffenenzahlen (Deutschland). Medical Aspects of the Persistent Vegetative State, The Multi-Society Task Force on PVS. N Engl J Med 330:1499–1508 Reid Graves J, Herlitz J, Bang A et al (1997) Survivors of out of hospital cardiac arrest: their prognosis, longevity and functional status. Resuscitation 35:117–121 Rideau YM (2012) Requiem. Acta Myol 31:48–60 Schmidt RF, Lang F, Heckmann M (Hrsg.) (2010). Physiologie des Menschen mit Pathophysiologie, 31. Überarb. und aktual. Aufl., Springer Verlag Wissenschaftlicher Beirat der Bundesärztekammer (1998). Richtlinien zur Feststellung des Hirntodes: Deutsches Ärzteblatt 95, Heft 30, 24. Juli 1998 (53) (Hirntod)

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Ventilation Options Contents Chapter 4

Tracheotomy – 75 Hartmut Lang

Chapter 5

NIV (Non-invasive Ventilation) – 95 Hartmut Lang

II

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Tracheotomy Hartmut Lang Contents 4.1

Terminology – 76

4.1.1 4.1.2 4.1.3

I ndication for Tracheotomy – 76 Advantages and Disadvantages of Tracheotomy – 76 Places of Tracheotomy – 77

4.2

Tracheotomy Procedure – 77

4.2.1 4.2.2 4.2.3

I mplementation of PDT (According to Caglia) – 78 Plastic Tracheostoma – 80 Changes Caused by a Tracheostoma – 81

4.3

Various Tracheal Cannulas – 82

4.3.1 4.3.2 4.3.3 4.3.4 4.3.5 4.3.6

T racheal Cannula with Cuff – 83 Construction of a Tracheal Cannula – 83 Speech Valve: Inhalation Valve – 87 Tracheal Cannula Without Cuff – 88 Core or Inner Cannula – 88 Fenestrated Cannulas – 89

4.4

Dressing Changes for Tracheal Cannulas – 90

4.5

Changing the Tracheal Cannula – 91

4.5.1 4.5.2

 reparation – 91 P Implementation – 91

4.6

Closure of the Tracheotoma – 92

4.6.1 4.6.2

 uff Leak Test – 92 C Placeholders – 93

References – 93

© Springer-Verlag GmbH Germany, part of Springer Nature 2023 H. Lang (ed.), Out-of Hospital Ventilation, https://doi.org/10.1007/978-3-662-64196-5_4

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4.1 

4

Terminology

The tracheotomy is an established procedure for obtaining secure airway access in a patient. If a patient is expected to require invasive ventilation for more than 10–14 days, a decision will usually be made in favour of tracheotomy. In intensive care units, patients are usually treated with a dilatation tracheostoma. People who are transferred to out-of-hospital care by tracheostomy should receive a plastic tracheostoma. Terms 55 Tracheotomy/tracheostomy: Tracheotomy is the surgical creation of an opening in the front wall of the trachea. This creates a tracheostoma. In tracheostomy, the trachea is moved outwards and sutured into the skin of the neck. 55 Trachea: Windpipe 55 Tomie: Cut 55 Stoma: Mouth/opening

4.1.1 

Indication for Tracheotomy

The indication depends on the expected duration of invasive ventilation, whereby the decision should be made between the 10th and 20th day after intubation: 55 Expected duration of invasive ventilation shorter than 10 days → translaryngeal intubation 55 Expected duration longer than 10 days → tracheotomy 55 Expected duration longer than 21 days → weighing up an early tracheotomy on the 3rd–5th day of ventilation

If the duration of the invasive ventilation cannot be estimated, a daily decision on the pros and cons of a tracheotomy should be discussed. Further Indications: 55 Airway obstruction due to tumors 55 Respiratory injuries due to trauma, scalding or chemical burns in the pharynx and larynx 55 Laryngeal or tracheal stenosis 55 Long-term ventilation during intensive care therapy 55 Aspiration for swallowing paralysis 55 Inflammatory or oedematous swelling of the larynx, meso- and hypopharynx 55 Surgical interventions in the oro- and hypopharynx and larynx 55 Craniocerebral traumas 55 Paraplegia 4.1.2 

Advantages and Disadvantages of Tracheotomy

The advantages and disadvantages of tracheotomy refer to the comparison with a tube that is not encountered in home care. Advantages: 55 Prevention of laryngeal and tracheal damage depending on the duration of ventilation 55 Dead space reduction with improvement of alveolar ventilation 55 Reduced work of breathing by reducing airway resistance 55 Improved fixation, especially with increasing patient mobility 55 Facilitates and accelerates weaning from the respirator 55 Improvement of oral and pharyngeal care as well as endotracheal suctioning

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55 Reduced need for analgesics and sedatives 55 Increased patient comfort 55 Facilitation of enteral feeding 55 Speech possibility via special cannulas Cons: 55 Tracheostoma infection 55 Displacement of the airways/tracheostoma due to secretions 55 No optimum humidification of the breathing air 55 Formation of necroses 4.1.3 

Places of Tracheotomy

55 The coniotomy, the so-called emergency tracheostomy, is performed between the thyroid cartilage and the cricoid cartilage. 55 The upper tracheotomy is performed above the thyroid gland. Usually between the 1.–2. cartilage of the trachea. 55 The middle tracheotomy is performed through the thyroid gland tissue, usually between the 2nd–4th cartilage clamp. This is the preferred site for tracheotomy. 55 The lower tracheostomy is performed below the thyroid gland, usually between the 4th–5th corpus callosum. The space for a tracheotomy is limited from the lower edge of the cricoid cartilage to the upper edge of the sternum (incisura jugularis). Depending on the neck anatomy, the location of the tracheotomy is determined by the surgeons (. Fig. 4.1).  

..      Fig. 4.1  Tracheotomy sites (courtesy of Isabel Schlütter)

4.2 

Tracheotomy Procedure

A procedure frequently used in intensive care units is the percutaneous dilatation tracheotomy, PDT, also known as puncture tracheotomy. Other procedures include surgical tracheotomy and tracheostomy in laryngectomized patients. PDT is intended for patients in whom it is foreseeable that they will not need the tracheostoma permanently,

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but only temporarily. People who are transferred to out-of-hospital care by tracheostomy usually receive a plastic tracheostoma. Nevertheless, people with PDT are also transferred to long-term out-of-hospital care if: 55 the tracheostoma of PDT remains stably open, 55 the risk for the patient is too high for a surgical intervention of a permanent tracheostoma. Both procedures are presented because knowing which tracheostoma is involved has consequences for nursing risk assessment and care. 4.2.1 

Implementation of PDT (According to Caglia)

A bronchoscope is inserted into the endotracheal tube. The patient is still intubated with a tube and is ventilated through it. The tube is now unblocked and pulled back together with the bronchoscope to a possible puncture site. The light of the bronchoscope shines through by external punctual pressure on the possible puncture site, this is called translumination (. Fig. 4.2). The tracheal puncture is performed with a metal cannula through the skin at the front  

..      Fig. 4.3  Introduced guide wire and pre-dilation (Klemm, Novak (eds.), Kompendium der Tracheotomie, Springer Verlag 2012)

wall of the trachea, exactly in the middle, median. An introducer sheath is then inserted via the metal cannula. The metal cannula is then removed (. Fig. 4.3). A guide wire is inserted into the trachea through the introducer sheath. The guide wire should point towards the bifurcation of the trachea. If the direction is correct (bronchoscopic control), the sheath is removed so that only the guide wire protrudes. A skin incision is made at this point, a transverse (longitudinal) incision 1.5–2  cm long. The puncture channel is pre-stretched with a 14 French dilator. Dilation is then performed with the conically shaped one-step dilator. The dilator is activated by water wetting and advanced via a guiding catheter. The unit of the two is carefully advanced over the guide wire into the trachea until the broad black mark is at skin level (. Fig. 4.4). Once the puncture canal is sufficiently dilated, the one-step dilator is removed and the prepared tracheal cannula is inserted. A suitable activated loading dilator is inserted into the cannula. This has a conical tip that protrudes from the end of the cannula and ensures good insertion of the tracheal cannula. The unit consisting of load dilator and tracheal cannula is advanced into the trachea via the guide wire and catheter and the tracheal cannula is first inserted vertically. Once it appears in the trachea (bronchoscopic con 

 

..      Fig. 4.2  Tracheal puncture (Klemm, Novak (eds.), Kompendium der Tracheotomie, Springer Verlag 2012)

79 Tracheotomy

..      Fig. 4.4  Introduced dilator to skin level (Klemm, Novak (eds.), Kompendium der Tracheotomie, Springer Verlag 2012)

trol), it is turned slightly so that it can be advanced towards the bifurcation until the cuff appears completely in the trachea. Guide wire, guiding catheter and loading dilator are removed. The correct position of the tracheal cannula is checked bronchoscopically. The cuff is then blocked and the ventilator connected. If necessary, the cannula is secured with a skin suture and fixed with a retaining strap. Once the tracheal cannula is securely fixed, the tube is then removed, the O2 concentration reduced and the ventilation parameters adjusted individually. Analgosedation can often be terminated, depending on the underlying disease. If necessary, a control by means of a chest X-ray must be reported. Complications: 55 Bleeding from neck veins or thyroid vessels 55 Perforations of the posterior tracheal wall with or without tracheoesophageal fistula 55 Skin or mediastinal emphysema 55 Fractures of tracheal braces 55 Postoperative via falsa during cannula change/dislocation of the cannula

4

Contraindications: Conversely, the contraindications of PDT usually represent an indication for surgical tracheotomy: 55 Emergency tracheotomy 55 Lack of tracheoscopy or bronchoscopy facilities 55 Difficult anatomical conditions 55 Need for a tracheostoma for more than 8 weeks 55 Planned transfer of the patient within 10 days to a peripheral ward, rehabilitation or care facility 55 Severe coagulation disorders 55 Most severe gas exchange disturbances 55 Difficult or impossible intubation (patient cannot be intubated laryngoscopically) 55 Extreme short neck (distance lower edge of cartilage  - upper edge of sternum < 15 mm) 55 Goiter III 55 Unstable fractures of the cervical spine 55 Pre-surgery on the neck with considerable scarring 55 Manifest infection in the neck area z Problems When Changing Needles

The tracheostoma according to the PDT method is subject to tensile stress. If the tracheal cannula is removed because it has to be changed, the diameter of the tracheostoma will be greatly reduced/reduced. When a new cannula is inserted, it is to be expected that it will be more difficult to insert. This is often associated with pain and discomfort for the patient. A timely administration of painkillers before the change is recommended. The change should always be carried out by 2 persons. This increases safety and a quick change. A specialist should carry out the change of the tracheal cannula with the assistance of a specialist nurse.

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Practical Tip

Keep in standby/prepare at patient's bedside: 55 Speculum for spreading the tracheostoma 55 Replacement needles: one with the same inner diameter (ID) and a second one number smaller 55 Ambu bag or manual resuscitation bag (with O2 connection) 55 Functional suction system with connected suction catheter

4

4.2.2 

Plastic Tracheostoma

In this procedure, too, the patient is intubated and ventilated, because the air supply must be maintained. z Skin Incision

The skin incision is made in the median line between the cricoid cartilage and the jugulum (upper edge of the sternum) and becomes a transverse skin incision about 3 cm long. This is followed by the incision of the subcutis and platysma (skin muscle of the neck) up to the superficial neck fascia (. Fig. 4.5).

..      Fig. 4.5  Median line between the cricoid cartilage and the jugulum (courtesy of Isabel Schlütter)

 

z Access to the Trachea

After cutting through the superficial neck fascia, a median incision (longitudinal cut) of the lamina praetrachealis (a specific area of the soft tissue or connective tissue of the neck) is made, followed by further deep preparation. The ventral tracheal wall in the area of the 3rd and 4th tracheal ring is optimally adjusted with two retractors (. Fig. 4.6).  

z Opening of the Tracheal Window

The trachea is preferably opened between the 2nd and 3rd tracheal cartilage ring. The ligamentum anulare (intercartilage band) is cut through with a scalpel over the entire width of the tracheal anterior wall. Then the

..      Fig. 4.6  Access to the trachea (courtesy of Isabel Schlütter)

3rd and 4th cartilage ring with the ligamentum anulare in between is cut through on both sides of the lateral tracheal wall. This

81 Tracheotomy

4

toma. After blocking the cuff, the cannula is connected to the ventilator. After checking that the patient is properly ventilated, the tracheal cannula is fastened around the patient's neck with a retaining strap. z Change of the Tracheal Cannula

Changing the tracheal cannula in a plastic tracheostoma is usually easier to perform. After removal of the tracheal cannula, the tracheostoma remains open and does not "reduce" its diameter like the puncture tracheostoma. Nevertheless, it is advisable to perform the change with two people and to have the utensils listed below available. Practical Tip ..      Fig. 4.7  Opening the tracheal window (courtesy of Isabel Schlütter)

creates a window wing incision with a caudal base (pointing downwards). Note: When incising the trachea, care must be taken to ensure that the cuff of the translaryngeal tube does not lie in the surgical field. Otherwise the tube should be intubated deeper to avoid damaging the cuff. Only in this way can the procedure be completed under good visibility conditions (. Fig. 4.7).

Keep in standby/prepare at patient's bedside: 55 Speculum for spreading the tracheostoma 55 Replacement cannulas: 55 One with the same inner diameter 55 One number each larger and smaller 55 Ambu bag or manual resuscitation bag (with O2 connection) 55 Functional suction system with connected suction catheter

 

z The Transcutaneous Fixation of the Window Sash

After careful hemostasis, the tracheostoma is epithelialized by adapting the skin to the edge of the tracheal opening. First the "window wing" is sutured to the skin in the caudal (lower) wound area, then the mobilised upper skin edge is fixed to the trachea. z Introduction and Connection of the Cannula

The translaryngeal tube is unblocked and retracted by the anaesthetist. After the tracheal secretion has been aspirated, an appropriately large, usually a 9-gauge tracheal cannula is inserted through the tracheos-

4.2.3 

 hanges Caused by C a Tracheostoma

According to Nancy Roper’s Life Activity Model (LA), the following is a description of what nursing staff and relatives and of course the affected persons themselves must expect when they are provided with a tracheostomy tube. z LA Breathing: Mucus Production

55 The tracheal cannula will keep the airway free. 55 The respiratory air is no longer humidified and purified through the upper airways.

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55 The mucous membranes of the trachea produce increased amounts of mucus as a result of the irritation. 55 The tracheal cannula can become blocked by this mucus. 55 This causes respiratory distress. 55 Suction of the secretion from the cannula and the upper airways opens the airways again. 55 Initially, suction must be performed frequently, but later less frequently. 55 Humidification by inhalation is often necessary. z LA Communication: Finding Meaning

55 Voice training is not possible, communication is limited. 55 Other means of communication must be sought (writing tablet, word board, oral essay, etc.). 55 Loss of voice changes the body image, which can lead to psychological stress. 55 What does it mean to be disturbed in its “body integrity”, what does it mean to have a “hole in the neck”? z LA Breathing: Coughing

55 Coughing and pressing is only possible to a limited extent. 55 Tough mucus is difficult to cough up. 55 Abdominal press during bowel movement is limited. 55 Risk of constipation. 55 “Pulling up” and “blowing” is not possible, therefore increased suctioning of nose and mouth is necessary. z LA Breathing: Airway Humidification

55 Humidification of the airway is necessary, otherwise the bronchial mucus solidifies, forms bark and blocks the cannula. 55 Humidify the airway: 55 Increased fluid supply for the patients 55 Inhalation/nebulisation 55 Use of humidifiers (active/passive)

z LA Food and Drink

55 Tracheostomy tube can cause swallowing difficulties. 55 Swallowing is more difficult and slows down. 55 Aspiration may occur followed by coughing. 55 Smell and taste disturbances, “smelling” is not possible (7 Chap. 18).  

z LA Skin and Body Care: Safety

55 The skin on the tracheostoma can become irritated or inflamed: –– by escaping brochial mucus and secretions of the upper respiratory tract (saliva) or –– by mechanical irritation of the cannula or the cannula shield (holder for fastening band) 55 The skin must therefore be kept dry. 55 At the beginning, therefore, frequent changes of the tracheal dressing and compresses. 55 Supply irritated skin with fatty ointment or stoma oil (apply thinly). 55 Tracheostoma may show a tendency to shrink, which can be painful. 55 Formation of bulging tissue around the tracheostoma (colloquially known as "wild meat"). 55 Appropriate painkillers should be given. 4.3 

Various Tracheal Cannulas

There are trach tubes without a cuff and with a cuff. The former are suitable for keeping a tracheostoma open safely. Patients can also change the cannula themselves. Cannulas with a cuff are indicated during ventilation, as the cuff ensures reliable administration of the ventilation air and provides aspiration protection.

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4.3.1 

Tracheal Cannula with Cuff

4

55 Check the pressure with a cuff pressure gauge 55 Risk of circulatory disorders, pressure necrosis, ulceration, pressure sores on the inner tracheal wall

The block cuff or cuff is a small balloon at the end of the tracheal cannula that is filled with air. Do not fill the cuff with water or other liquids! Otherwise, if the cuff is damaged, the patient will aspirate the fluid (7 Sect. 4.3.2).  

4.3.2  Practical Tip

55 Do not fill the cuff too much with air 55 Pressure on a maximum of 25  cm H2O 55 Pressure as low as possible—as high as necessary 55 No secondary air should escape during artificial respiration

Construction of a Tracheal Cannula

. Figure 4.8 shows a tracheal cannula.  

z Cannula Shaft

The main feature of each tracheal cannula is the tube or cannula shaft through which the respiratory or ventilation air enters and exits. The shaft has a bend (an almost 90° angle). Other cannula shafts have a ¼ circu-

..      Fig. 4.8  Description of a tracheal cannula (courtesy of: ANDREAS FAHL MEDIZINTECHNIKVERTRIEB GmbH)

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lar bend. The part in front of the holding shield protrudes from the neck, the part behind the holding shield is inserted through the tracheostoma into the neck, into the trachea. Depending on the anatomical conditions, the shaft can be short or long. The shaft itself can be flexible or rigid.

4

z Stop Sign

The retaining plate can be flexibly adjusted as shown in . Fig.  4.8, or it is firmly attached to the shaft. If it is flexibly adjustable, this can be done with a clip lock, a click screw or a screw-nut ring. Very often the size of the inner diameter (ID) and even the outer diameter (AD) of the cannula is written on the needle label. The cannula fixation band is attached to the holding plate. Very often the holding plate is elastic, so the fixation band can be threaded more easily. Tracheal cannulas with a flexible holding shield have a scale on the shaft. This allows documentation of the extent to which the holding label should be attached.  

>>The fixation devices must be really tight, otherwise the shaft can slip back and forth in the trachea. The cannula could even slip out of the tracheostoma.

z Universal Attachment

At the dorsal end of the cannula there is usually a universal attachment. The "goose gargling" of the ventilation tube system, the HME filter, a "wet nose" for spontaneously breathing people, a speech valve and the Ambu-bag fit on this. This attachment is standardized and all cannulas of all manufacturers have the same outer diameter. There are also cannulas with a screw thread on the dorsal end. In this way, the respective attachment can be screwed on and off as required. The distal end of the tracheal cannula is located in the trachea, approximately 2–3 cm above the carina. It should not touch the carina, as this causes pain and an unquenchable coughing sensation in those affected.

However, it should not be higher than this, otherwise the respiratory air may not flow evenly into the airways. z Cuff

The cuff is located above the distal end. . Figure. 4.8 shows a cylindrical cuff, a so-­ called low-pressure cuff. However, the cuff is also available in a spherical shape. The low-­ pressure cuff has the advantage that the pressure exerted on the inner wall of the trachea is distributed over a larger area, thus preventing a tracheal decubitus. The bearing pressure of a spherical cuff is concentrated on its equatorial plane and has a greater effect on the tracheal mucosa (7 Sect. 4.3.2).  

 

z Valve

The cuff is filled with air. This is administered through a valve. A cuff tube runs along the shaft of the cannula, is incorporated into it and exits as a separate tube near the dorsal end. This is followed by a test balloon or pilot balloon or control balloon, which is then connected to the valve. Syringes or the cuff pressure gauge fit onto the valve equally, as it is a Luer approach. This allows air to be pumped in or vented. The valve is secured by a spiral spring and a small sealing ring. This prevents air from escaping from the cuff sleeve. However, there is no 100% tightness, some air escapes nevertheless, so that the cuff pressure must be checked several times a day with the cuff pressure gauge. Practical Tip

Check the cuff pressure at the beginning of each shift and additionally: 55 When manipulating the tracheal cannula, e.g. changing bandages 55 After mobilisation or change of position of the person 55 Post-suction 55 After changing the tracheal cannula

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85 Tracheotomy

Practical Tip

The cuff pressure can also be increased on the doctor's orders, if necessary before manipulation, but must then be lowered again and checked.

z Cuff Hose

The cuff hose or air supply hose is very thin. The air is led over it to the cuff sleeve. At the point where the cuff hose emerges from the shaft and runs separately, it can kink. Practical Tip

55 The cuff hose must run straight. 55 It should be freely accessible. 55 It should not be hidden under the tracheal cords. 55 It should not be hidden under the clothing of the person. 55 It should not be wrapped around the tracheal cannula. 55 It should not be under tensile stress.

z Control Balloon or Test Balloon

This follows the valve directly. When the cuff is inflated, air will also enter the control balloon through the cuff tube. Thus, it can be checked with the fingers whether and to what extent the balloon is filled. However, this does not replace measuring and checking the pressure with the cuff pressure gauge. However, if the control balloon is very easy to push in, it can be assumed that there is not enough air inside. It will probably have to be re-blocked. If the control balloon is very bulging, the pressure will probably be too high. >>If the cuff sleeve is bent, the test balloon may still be well filled, but perhaps the cuff sleeve is not sufficiently filled. Therefore, avoid kinking the cuff hose!

z Cuff

The cuff seals the trachea so that no air is drawn in during ventilation or artificial respiration (. Figs. 4.9 and 4.10). The inspiratory airflow is directed through the cannula shaft towards the lungs. During expiration, the air also only passes through the cannula shaft. If the cuff were not filled, air would pass the tracheal cannula and escape upwards towards the larynx. During artificial respiration, one hears a typical exhalation sound, a kind of gargling caused by vibrating the cheeks of the face. The cuff also provides some protection against secretions and microaspirations that form below the larynx and above the cuff. It prevents—but not completely—secretions from entering the lungs immediately and directly through the airways (. Fig. 4.9). If the cuff is unblocked (. Fig.  4.11), this leads to secondary air with the typical exhalation noise. This is used in some patients to intentionally direct the exhaled air flow past the vocal cords. In this way voice formation may be possible. However, it is to be expected that the patients will find it difficult to breathe and will quickly become exhausted.  

 

 

>>Before unblocking, suction is to be performed orally and nasally, thus reducing the amount of secretion. When unblocking, it is always necessary to perform this with endotracheal suction. This manoeuvre should be planned and carried out specifically to remove secretions.

z In a Nutshell

55 The cuff is filled with air, not with water/ liquids. 55 The cuff thus seals the trachea and: –– ensures that the air is directed towards the bronchi and lungs, –– thus also offers protection against aspiration, so that stomach contents, blood or foreign bodies cannot enter the lungs

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4

..      Fig. 4.9  Principle of a cuff (own representation, edited by Isabel Schlütter)

..      Fig. 4.10  Air flow Inspiration and expiration (own representation, edited by Isabel Schlütter)

z Caution

55 Do not fill the cuff with too much air. 55 Pressure to a maximum of 25 cm H2O. 55 Pressure as low as possible. 55 Pressure as high as necessary, no secondary air should escape during artificial respiration.

55 Check the pressure with a cuff pressure gauge. 55 Risk of circulatory disorders, thus risk of pressure necrosis, ulceration or decubitus on the inner tracheal wall.

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..      Fig. 4.11  Air flow and secretion flow with unblocked cuff (own representation, edited by Isabel Schlütter)

Subglottic Suctioning As described above, the cuff provides protection against aspiration, but this protection is incomplete. Along the cuff furrows are formed through which secretions from the nose, mouth and throat can enter the lungs. This effect is increased in people whose ability to swallow is severely restricted and in people who produce a lot of secretions. Tracheal cannulas can therefore be fitted with subglottic suction. Subglottic means below the larynx. The secretions pass through the larynx and the glottis and onto the cuff. Through a small suction tube inserted in the shaft of the cannula, the secretions that lie on the cuff can be specifically suctioned off. The suction can be done with the help of a syringe or a suction device. Suction with a syringe is always intermittent. The extraction with suction device can be intermittent or continuous: 55 The intermittent suction frequency depends on the secretion production: as often as necessary, as rarely as possible. It is not advantageous to set a time interval for suction. 55 During continuous suction with the device, the suction should be limited,

because too strong a suction can cause injury to the tracheal mucosa. Currently, a maximum of −20  cm  H2O is recommended. Since the secretions can often be very viscous, it must be expected that the integrated suction tube or the suction openings will be blocked. Flushing is then indicated. But be careful, this can cause chunks of secretion to be transported back into the trachea, which can also be aspirated if necessary. >>Subglottic suction does not replace endotracheal or endobronchial suctioning. The lungs also continue to produce secretions that must be cancelled.

4.3.3 

Speech Valve: Inhalation Valve

The speaking or inhalation valve allows a spontaneously breathing patient to inhale air through the tracheal cannula (. Fig. 4.12). During exhalation the valve is closed and the exhaled air cannot escape through the cannula shaft. However, it can escape past the shaft when the cuff is unblocked.  

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4 ..      Fig. 4.12  Inspiration: Air flow at speaking valve (own representation, edited by Isabel Schlütter)

Practical Tip

If the cuff is unblocked, this can only be done with simultaneous suction! The exhaled air will run along the vocal cords. This enables the patient to speak. This is a method frequently used in intensive care units to enable the patient to communicate by speaking for the first time. >>If an intensive care patient is supplied with a simple tracheal cannula with cuff, the cuff must be unblocked if a speech valve is used. With a blocked cuff, inhalation would be possible, but not exhalation. The patient would suffocate!!! (. Fig. 4.12 right)  

It has been observed that a large number of patients produce a lot of secretions when a speaking valve is used. Therefore, measures of secretion elimination are very important.

4.3.4 

Tracheal Cannula Without Cuff

Tracheal cannulas without cuff serve to keep the airways open. Secretion management and aspiration are facilitated. In adult patients, ventilation does not usually take place with this supply. The air inflow and outflow also occurs here through the can-

nula shaft. However, during exhalation the air can also pass the cannula and thus cause the vocal chords to vibrate. This makes speech and voice training possible. In laryngectomized patients, the airflow is exclusively through the tracheal cannula or tracheostoma. Tracheal cannulas without a cuff can be used in patients who are in the final stages of a longer weaning period. 4.3.5 

Core or Inner Cannula

Tracheal cannulae are differentiated according to whether they have an inner cannula, a core, or consist only of the cannula shaft (. Fig.  4.13). The inner core allows a ­comfortable removal and insertion of a new replacement core, so that ventilation only has to be interrupted for a short time. The complete change of the tracheal cannula can be extended to longer intervals. The disadvantages of a core are that it reduces the inner diameter of the cannula, making spontaneous breathing more difficult, and solid secretions can easily clog the core, making breathing and ventilation air more difficult to administer. Advantages: 55 Core is easy to take out. 55 Replacement inner cannula can be inserted immediately. 55 Tracheostoma remains open, thus easier cleaning of adhered secretions or crusts. 55 Outer cannula is usually not so dirty.  

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89 Tracheotomy

..      Fig. 4.13  Core, cannula with cuff (own representation, edited by Isabel Schlütter)

55 Respiration/ventilation remains guaranteed. 55 Needles need to be changed less frequently. Cons: 55 Reduction of the inner diameter, making spontaneous breathing more difficult. 55 Not all contamination is deposited on the core, even the outer cannula can be dirty and hinder breathing. 55 Ventilation is only possible with an adapter for the outer cannula. 55 The appropriate core for the outer cannula must be inserted. 4.3.6 

Fenestrated Cannulas

Fenestrated tracheal cannulas have an additional opening in the part of the cannula shaft that lies in the trachea (. Figs.  4.14 and 4.15). This allows the exhaled air to flow through the larynx and past the glottis, allowing voice and speech to be formed. This possibility also exists with tracheal cannulas with core. The use of fenestrated outer cannulas means that:  

..      Fig. 4.14  Fenestrated TC and core with phonation window (own representation, edited by Isabel Schlütter)

55 Respiration/ventilation remains guaranteed, 55 the patient can breathe spontaneously, 55 voice training is possible, 55 the core/inner cannula must be fenestrated, and 55 the possibility of removing the core exists. >>Spontaneous breathing is possible with windowed tracheal cannulas, but sometimes difficult, since the inner diameter increases the airway resistance → Watch out for respiratory signs of exhaustion. To reduce the airway resistance, the cuff can be unblocked.

Signs of respiratory exhaustion: 55 Rapid breathing (tachypnea) 55 Rapid pulse (tachycardia) 55 Drop in oxygen saturation (7 Sect. 17.4.2) 55 Restlessness of the body 55 Possibly paleness, cold sweat, blue face or skin colour (cyanosis) 55 Fluctuations in blood pressure, mostly hypertension  

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4

..      Fig. 4.15  Air flow for a TC without core with phonation window (own representation, edited by Isabel Schlütter)

4.4 

Dressing Changes for Tracheal Cannulas

Nursing Goals: 55 Respiration/ventilation remains guaranteed 55 Prevention of infections, pressure damage to the trachea 55 Maintenance of clean and dry skin conditions 55 Ensuring free breathing 55 Avoid drying out of the mucous membranes. Dressing Change for Newly Created Tracheostoma: 55 Dressing change within the first 24  h after application only if necessary 55 Pay attention to secondary bleeding and skin emphysema 55 Check the position of the tracheostoma—cannula must not be in tension

55 Check and document cuff pressure regularly 55 Close monitoring of vital signs Procedure for Dressing Change: 55 Remove the wound tray and inspect the wound surface 55 Clean the area around the wound edges with skin disinfectant, observe the exposure time! 55 Clean the wound edges of the stoma with NaCl-soaked sterile compresses if necessary 55 Dry wound edges with sterile swabs 55 Use absorbent slit compresses in case of strong mucus production or metalline slit compresses in case of an irritation-­ free stoma 55 Fasten tracheal cannula with fixation band 55 Check the position of the tracheal cannula by auscultation and cuff pressure

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55 Do not forget the documentation 55 Bandage change indicated every 8 h for non-irritant stoma 55 Change fixing bandage every 24 h, or earlier if contaminated

55 In case of accidental decannulation, oral intubation should be performed first as an emergency. 55 Only after this is the dilatation with recanalization carried out again.

Complications with Dressing Changes: 55 Bleeding 55 Danger of secretion congestion 55 Disturbance of the local blood circulation by constriction of the fixation band 55 Displacement of the cannula lumen by blood and secretion 55 Dislocation of the tracheal cannula 55 Skin emphysema 55 Aspiration (silent aspiration with a leaking cuff)

After Conventional Tracheotomy: 55 Optional on the first day after installation 55 Possible insertion of a low-pressure cuff cannula 55 Change as early as possible, since there is a plastically stable access to the trachea

Practical Tip

Safety measures for tracheostoma: continuous nursing supervision and care. On standby, keep ready at the bed place: 55 Speculum for spreading the tracheostoma 55 Two replacement tracheal cannulas, one with the same inner diameter, a second one number smaller 55 Ambu bag/hand resuscitator (with O2 connection) 55 Functional suction system with connected suction catheter

4.5 

Changing the Tracheal Cannula

4.5.1 

Preparation

Material: 55 Tracheal cannula with corresponding accessories 55 Retaining strap 55 Cuff pressure gauge (when using a cannula with balloon) 55 5 compresses 10 × 10 cm, lint-free 55 1 slit compress made of fleece, not woven 55 Cleaning brushes for the cannula 55 Cleaning can 55 Cleaning agent for cleaning the cannula 55 Bark tweezers 55 Tracheal spreader/speculum Further Preparation: 55 Turn on the oxygen saturation pulse tone 55 Have the Ambu-bag ready, with connection for oxygen 55 Preoxygenation 55 Sedation according to AVO

>>Before each use of the cannula: Hand disinfection!

4.5.2 

After PDT: 55 Change of the tracheal cannula on day 10 at the earliest, as the tracheostoma is only dilated and under tension. 55 This makes the introduction of a new cannula more difficult.

Preparing the New Tracheal Cannula: 55 Testing the cuff 55 Cleanliness is the top priority: first disinfect your hands thoroughly 55 Only then insert the inserter into the new cannula

Implementation

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55 Attach the retaining strap to one side of the retaining plate 55 Then pull the slit compress over the cannula 55 Apply lubricant to the cannula shaft with a compress, the smallest amounts are sufficient

4

Remove the Old Cannula: 55 If a cannula with a cuff is inserted, the cuff must first be unblocked and simultaneously suctioned out below the cannula tip 55 Then loosen the retaining strap and pull the cannula out of the tracheostoma following the bend, simultaneously aspirating 55 Place the cannula on a dry surface (e.g. compress) Tracheostomy Care: 55 Clean the skin around the tracheostoma with a compress 55 Make sure that nothing gets into the stoma, therefore only use lint-free compresses! 55 Dry the skin around the stoma well Inserting the New Tracheal Cannula: 55 To insert the new cannula, stretch the patient's head or place it in the neck 55 Spread the skin around the stoma with two fingers 55 With the other hand slowly insert the cannula following the bend 55 Tilt the head slowly forward again during insertion 55 Hold the cannula with two fingers on the holding plate and then pull out the inserter quickly 55 Then immediately fix the cannula with the retaining strap 55 Now the accessories can be attached in peace When changing the tracheal cannula, the patient must be expected to become restless, anxious or even panicky. Therefore, it must be clarified whether a mild sedation is necessary.

Furthermore, the patient is subject to frequently occurring acute shortness of breath. Therefore, the patient should be pre-­oxygenated and an Ambu-bag with O2 connection must be kept ready. The Ambubag should have a small neck mask that fits onto the tracheostoma and can be used for manual emergency ventilation. In addition, high volumes of secretion are often present. The suction system must therefore be checked and fitted with a suction catheter before changing the cannula and must be ready for operation.

4.6 

Closure of the Tracheotoma

Before final decannulation, the patient must meet the following requirements: 55 Clinical stability 55 Sufficient spontaneous breathing 55 No pronounced difficulty in swallowing 55 No tendency to aspiration 55 Effective cough expectoration 55 Ability to cooperate, no delirium In addition, there should be no obstruction of the airways and the patient should achieve a good result in the cuff leak test (7 Sect. 4.6.1).  

4.6.1 

Cuff Leak Test

Before a patient can be securely decannulated, it is advisable to perform the cuff leak test first. This test first measures how high the respiratory volume is that a patient can produce when the tracheal cannula is blocked. The measurement is performed on the respirator under ventilation. The cuff is then unblocked. Due to the resulting leakage, the respirator can be expected to measure a high leakage volume and a very reduced breathing volume. If, on the other hand, the respiratory volume is still high when the cuff is unblocked, it can be assumed that there is a pronounced constriction/obstruction.

93 Tracheotomy

>>A difference between the two breathing volumes smaller than 130 ml is an indication of a post-decannulation stridor. This stridor will also be present after removal of the tracheal cannula. Therefore, in this case, decannulation should not yet be performed.

4.6.2 

Placeholders

After decannulation, a placeholder can be inserted (. Fig.  4.16). A placeholder is a cannula with a smaller diameter and a straight shaft. It keeps the tracheostoma open. It has no ventilation function. However, tracheal secretions can be aspirated through it. The placeholder: 55 seals the tracheal wall airtight to the front, 55 enables secretion aspiration,  

..      Fig. 4.16  Placeholder (courtesy of: ANDREAS FAHL MEDIZINTECHNIK-VERTRIEB GmbH)

4

55 remains up to four days after decannulation, 55 serves the temporary preservation of the tracheostoma. >>In the event of a renewed respiratory insufficiency, the placeholder is important, as it allows for quick and easy re-­ cannulation and re-ventilation.

If there is no indication of a recurrence of respiratory insufficiency after the four days, the placeholder is removed and a dilated tracheostoma is covered with a patch. A surgically created tracheostoma must be closed surgically.

References Braune S, Kluge S (2011) Die percutane Dilatationstracheotomie. Dtsch Med Wochenschr 136:1265–1269 Braune S, Kluge S (2012) Update Tracheotomie. Med Klin Intensivmed Notfmed 107(7):543–547 De Bast Y, De Backer D, Moraine JJ et al (2002) The cuff leak test to predict failure of tracheal extubation for laryngeal edema. Intensive Care Med 28:1267–1272 Deutsche Gesellschaft Für Pflegewissenschaft E.  V. (DGP) (n.d.). http://www.­dg-­pflegewissenschaft.­ de/2011DGP/wp-­content/uploads/2012/12/Henke-­ Handlungsempfehlung-­z ur-­s ubglottischen-­ Absaugung.­pdf. Recherche 18.04.2016 Jaber S, Chanques G, Matecki S et  al (2003) Post-­ extubation stridor in intensive care unit patients. Risk factors evaluation and importance of the cuff-leak test. Intensive Care Med 29:69–74 Klemm N (ed) (2012) Kompendium der Tracheotomie. Springer, Verlag Kluge S, Schreiter D (2012) Tracheotomie DIVI:4137– 4144 Tracheotomie (n.d.). http://www.­tracheotomie-­online.­de/. Recherche 25.6.2012, Handlungsempfehlung zur subglottischen Absaugung, 3. DGP Hochschultag 7.12. 2012, Referenten: Tanja Lohr B. Sc. Gesundheit und Pflege Christine Henke B. Sc. Gesundheit und Pflege Julia Lehmann B. Sc. Gesundheit und Pflege Webop (n.d.). http://www.­webop.­de/punktionstracheotomie-­43/. Recherche 15.7.2014 Wedop (n.d.). http://www.­webop.­de/plastische-­ tracheotomie-­142/ . Recherche 1.7.2014

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NIV (Non-invasive Ventilation) Hartmut Lang Contents 5.1

Indications and Contraindications – 96

5.1.1 5.1.2

I ndications – 96 Contraindications of NIV – 97

5.2

Characteristics of the NIV – 98

5.3

Different Mask Systems – 99

5.3.1 5.3.2 5.3.3 5.3.4

 asal Mask – 99 N Full-Face Mask (Oronasal Mask) – 99 Total Face Mask – 99 Special Models – 100

5.4

Modern NIV Masks – 100

5.5

Typical Applications – 102

5.5.1 5.5.2 5.5.3 5.5.4

 OPD – 102 C Thoracic Restrictive Disorders – 102 Obesity Hypoventilation Syndrome – 102 Neuromuscular Diseases (NME) – 103

5.6

Assessment of an Adjusted Ventilation Setting – 103

5.7

Ventilation Setting of the NIV – 104 References – 104

© Springer-Verlag GmbH Germany, part of Springer Nature 2023 H. Lang (ed.), Out-of Hospital Ventilation, https://doi.org/10.1007/978-3-662-64196-5_5

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5.1 

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Indications and Contraindications

5.1.1 

5

Indications

Non-invasive ventilation as a therapy for chronic respiratory insufficiency (CRI) can be used for patients with the following diseases: 55 Chronic obstructive disease (COPD) 55 Restrictive thoracic disease 55 Obesity hypoventilation syndrome 55 Neuromuscular diseases Symptoms of chronic ventilatory insufficiency: 55 Dyspnoea/tachypnoea (during exertion and/or at rest) 55 Morning headaches 55 Lassitude 55 Limited performance 55 Psychological changes (e.g. anxiety, depression, personality changes) 55 Sleep disorders (nocturnal awakening with dyspnoea, restless sleep, daytime tiredness, tendency to fall asleep, nightmares) 55 Polyglobulia (an increased number of red blood cells in the blood) 55 Tachycardia 55 Edema 55 Cor pulmonale (disease of the heart with reduced performance due to lung disease) These symptoms can be reduced by the use of NIV.  Furthermore, an improvement of the health-related quality of life should be achieved. Ventilation in general, even under NIV, improves the quality of sleep and leads to a prolongation of life.

Possibilities of NIV Non-invasive ventilation represents an alternative to invasive ventilation. The proven advantages are:

55 Decrease in ventilator-associated pneumonia 55 Avoiding or delaying a tracheotomy if necessary 55 Shortening the intensive stay 55 Increase of the probability of survival 55 Reduction of dyspnoea 55 Avoidance of desaturation 55 Improvement or maintenance of the respiratory muscle strength 55 Patient can still communicate 55 Patient can consume food and beverages during ventilation 55 Patient is still mobile or mobilizable 55 Intermittent ventilation possibility The NIV shows high success in the case of respiratory pump failure (7 Sect. 2.1.1), breathing work is taken over. The respiratory pump is relieved. It has fewer advantages in hypoxemic lung failure (7 Sect. 2.1.2). This is accompanied by a lack of oxygen. A high tendency of the alveoli to collapse with the development of atelectasis leads to a primary failure of the lung. This leads to a disproportion between pulmonary blood flow and pulmonary ventilation and to a distributional disorder to the disadvantage of ventilation. The tendency to collapse and atelectasis can be avoided by the use of PEEP/CPAP.  However, NIV cannot maintain this PEEP reliably enough due to high leakage.  

 

Risks in the Application of NIV z Nasal Masks

Nasal masks are often prescribed because they usually offer a high degree of patient comfort. The ability to continue eating, drinking and talking cannot be overestimated. But people need to be trained for this. During sleep, high leakage through the mouth can occur. This reduces the effectiveness of nasal ventilation. This can be remedied by a chin strap, which reduces the falling of the lower jaw.

97 NIV (Non-invasive Ventilation)

z Full-Face Masks (Nose and Mouth Masks)

Leaks can be reduced by using a full-face mask. However, the acceptance is usually lower. The mask cushion of the full-face mask has a rather high dead space volume. Therefore, the previously exhaled air must not be rebreathed, because this would cause people to inhale their own exhaled air again, and thus also the exhaled CO2. However, respirator technology has long been mature. This creates a constant flow of air that "flushes" the exhaled air out of the mask. NIV ventilation can cause ventilator air to enter the stomach, which can lead to nausea and vomiting. Any vomit that gets into the mask cushion can thus be aspirated again. Coughing and secretion ejection is more difficult. It is coughed out into the mask. The mask must then be removed and cleaned. Even coughing up secretion could be aspirated. NIV ventilation can lead to increased ear pressure. However, pressure equalization is difficult to achieve. Yawning is one possibility, but it can lead to renewed leakage. This can significantly reduce acceptance by the people. Speaking is restricted and made more difficult. Human speech is unclear to the listeners. Generally speaking: 55 The high air flow can lead to drying of the nasal and oral mucous membranes. Humidification of the respiratory gas is therefore absolutely necessary. 55 The skin under the mask can sweat. This is also caused by the moisture in the exhaled air. People therefore need to be able to remove the mask to dry and care for their skin. 55 Masks that are not properly fitted can dry out the eyes and cause inflammation due to leakage. 55 The contact pressure of the mask cushions can be unevenly distributed, resulting in pressure points. They can also cause claustrophobia in those affected. The correct selection and fitting of the mask is the responsibility of the clinics or their ventilation centers.

5.1.2 

5

Contraindications of NIV

NIV cannot be offered to all persons requiring ventilation. In the following situations NIV is not a suitable therapy choice: Inability to adapt a suitable ventilatory access for NIV 55 Intolerance of NIV 55 Ineffectiveness of the NIV 55 Severe bulbar symptomatology with recurrent aspirations 55 Ineffectiveness of non-invasive secretion management 55 Failure to switch to NIV after invasive ventilation 55 Inability of the person concerned to put the mask on and take it off independently: –– patients with increasing muscular weakness –– patients with tetraplegia (full-blown neuromuscular diseases, high paraplegia) –– patients with severe respiratory centre disorders (severe stroke or severe hypoxic brain damage involving the respiratory centre) z Bulbar Symptoms

If the medulla oblongata is diseased, the so-­ called bulbar symptoms or bulbar phenomena occur. The medulla oblongata is not only the control centre for breathing (respiratory centre), but also for the coordinated movement of the tongue, lips, facial muscles, palate, pharynx and larynx. If these centres are diseased, which is usually irreversible, these patients become ill: 55 Disorders in speech formation, 55 Facial expression disorders and 55 Disorders of the swallowing reflex 55 with simultaneous increase in saliva and secretion production. The risk for the patient in this case is the lack of swallowing reflex with subsequent risk of aspiration of saliva, oropharyngeal secretions, drinks and food into the lungs.

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5.2 

Characteristics of the NIV

. Table  5.1 gives an overview of the complications and problems of invasive and non-­invasive ventilation.  

..      Table 5.1  Comparison between invasive and non-invasive ventilation (mod. according to the AWMF guideline “Non-invasive ventilation as a therapy for acute respiratory insufficiency”, 2008)

5

Complications and clinical aspects

Invasive ventilation— tracheal cannula

Non-invasive ventilation

Tracheal early and late damage

Yes

No

Intermittent application

Rarely possible

Often possible

Effective coughing possible

No

Yes

Food and drink possible

Complicated (tracheostoma)

Yes

Communication possible

Difficult (speaking essay)

Yes

Upright body position

Only limited realizable

Often possible

Difficult weaning from the respirator

10–20%

Rare

Access to the airways

Direct

Complicates

Pressure points in the facial area

No

Occasionally

CO2 rebreathing

No

Rare

Leakage

Hardly

More or less strong, mostly present

Aerophagy (air swallowing)

Hardly

Occasionally

Source: AWMF Guideline "Non-invasive ventilation as a therapy for acute respiratory insufficiency", led by DGP (Deutsche Gesellschaft für Pneumologie) (German Society for Pneumology), status 01.06.2008

5

99 NIV (Non-invasive Ventilation)

5.3 

Different Mask Systems

5.3.1 

Nasal Mask

This mask is very often used in patients with chronic respiratory insufficiency (CRI) and in the therapy of sleep apnea. It only covers the nose not the mouth (. Fig. 5.1), so that speaking and eating is possible. The nasal airways must be free. Advantages: 55 Comfortable to wear 55 Easier to use 55 Better tolerance of the patient 55 Coughing up is possible 55 Good tightness 55 Communication is possible 55 Nasal mask can be adjusted/modelled to the facial contours  

Cons: 55 Effective breathing only possible with nasal breathing 55 Good cooperation required 5.3.2 

 ull-Face Mask (Oronasal F Mask)

The full-face mask is the mask of choice for patients with acute respiratory insufficiency

..      Fig. 5.2  Full-face mask (courtesy of Prof. Dr. med. Stefan Kluge)

(ARI) (. Fig. 5.2). It covers the mouth and nose. This allows a patient to breathe through both without having to concentrate. If a nasal mask is not sufficient for ventilation, the full-face mask offers an alternative. Advantages: 55 Effective for limited cooperation 55 Sufficient function even with mouth breathing 55 Patient does not have to decide whether to breathe through the mouth or the nose  

Cons: 55 Mask must be taken off for cough ing 55 Often only limited fitting accuracy 55 Pressure points on the bridge of the nose possible 55 Air leakage that can enter the eyes and cause conjunctival irritation or inflammation 55 Subjectively felt anxiety 5.3.3 

Total Face Mask

This mask covers the entire face (. Fig. 5.3). It is the mask of choice for patients with acute respiratory insufficiency if a full-face mask cannot be fitted correctly. In this way, NIV can be performed and intubation may be avoided. This type of mask has not become established in out-of-hospital ventilation, despite the advantages listed below.  

..      Fig. 5.1  Nasal mask (courtesy of Prof. Dr. med. Stefan Kluge)

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H. Lang

if the other mask systems cannot be adapted or are not tolerated by the patient.

5.4 

5 ..      Fig. 5.3  Total face mask (courtesy of Prof. Dr. med. Stefan Kluge)

Advantages: 55 Applicable if full-face mask does not fit 55 Usually has a good seal 55 No side air flowing into the eyes 55 Patient does not have to decide whether to breathe through the mouth or the nose Cons: 55 Coughing up is possible, but only into the mask 55 It is therefore often necessary to remove the mask to clean it 55 Mask fogging from inside 55 This limits the patient's view 55 Good cooperation required 55 Communication difficult 55 Poor tolerance by the patient 5.3.4 

Special Models

Special models are mostly used for patients with chronic respiratory insufficiency or in the therapy of sleep apnea. They are often individually adapted, but there are also industrially manufactured mask systems. Ventilation via mouthpieces is an alternative

Modern NIV Masks

Requirements for modern NIV masks are 55 Comfortable to wear for the patient: –– No pressure points due to masks or retaining straps –– No sweating –– No marks on the face 55 Leakage-free seat: –– For the administration of the necessary therapy pressure –– For the avoidance of side effects 55 Easy handling and cleaning: –– Long service life –– Easy size selection and adjustment –– Clinically validated disinfection procedures for multiple use NIV masks are distinguishable between vented and non-vented masks: 55 Vented masks have an integrated exhalation port in the mask. This allows the exhaled air to escape directly. 55 Non-vented masks have no integrated exhalation ports. The exhalation valve is integrated in the ventilation hose system or there is a dual hose system. Non-­ vented masks are typically colored blue. Either at the connector to the mask or the entire mask. Modern NIV masks have a double-walled mask cushion (. Fig. 5.4). They consist of an inner and an outer cushion. The inner cushion consists of a solid membrane which is anatomically pre-shaped. It provides support and stability. The outer cushion consists of a thin membrane that fills with air.  

101 NIV (Non-invasive Ventilation)

5

This allows it to adapt to the contours of the face and the mask is securely sealed, even when the patient moves (. Fig. 5.4). Modern NIV masks have an adjustable and large-area forehead support. Advantages of the forehead support: 55 It gives support 55 Provides a very good seal around the eyes 55 At the same time, avoidance of excessive contact pressure on the root of the nose or the teeth  

. Table 5.2 gives an overview of the advantages and disadvantages of the mask systems (interfaces) used.  

..      Fig. 5.4  Double-walled mask cushion, adaptation to facial contours (courtesy of Isabel Schlütter)

..      Table 5.2  Advantages and disadvantages of common interfaces (according to: AWMF guideline "Non-invasive ventilation as a therapy for acute respiratory insufficiency, 2008) Aspect

Nose mask

Full-face mask

Mouth leakage

–

+

Volume monitoring

–

+

Initial response of the blood gases

o

+

Speak

+

–

Coughing up (expectoration)

+

–

Aspiration risk

+

o

Air swallowing (aerophagy)

+

o

Claustrophobia

+

o

Dead space (compressible volume)

+

o

Noise and irritation of the hearing

+

+

Source: AWMF Guideline "Non-invasive ventilation as a therapy for acute respiratory insufficiency", led by DGP (Deutsche Gesellschaft für Pneumologie) (German Society for Pneumology), status 1.06.2008 + Advantage o neutral – Disadvantage

102

5.5 

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Typical Applications

As described in 7 Sect. 5.1.1, NIV can be used in patients with different diseases: 55 COPD 55 Thoracic restrictive diseases 55 Obesity hyopventilation syndrome 55 Neuromuscular diseases  

5

5.5.1 

COPD

Indication for initiation of out-of-hospital NIV is when a patient is suffering from the symptoms of chronic hypercapnia (7 Sect. 5.1.1). Restriction of the quality of life is also included. However, according to the S2 guideline, at least two additional criteria must be included: 55 Permanently elevated CO2 levels in blood during the day (PaCO2 ≥ 50 mmHg/6.65 kPa) 55 During nighttime rest and sleep the CO2 content increases again (pCO2  >  55 mmHg/7.3 kPa) 55 Permanent but stable daytime hypercapnia (46–50  mmHg/6.1–6.65  kPa), but increase in CO2 level during sleep 55 Permanent but stable daily hypercapnia (46–50 mmHg/6.1–6.65 kPa), but at least two acute hospitalization-bound exacerbations with respiratory acidosis in the last 12 months (exacerbations = exacerbations of COPD requiring hospitalization; acidosis = acidification of the blood) 55 Previous exacerbation of COPD, which was so severe that artificial respiration became necessary (For the values, 7 Chap. 27 BGA blood gas analysis)  

 

5.5.2 

Thoracic Restrictive Disorders

The restrictive ventilation disorder, which causes a reduction in lung volume, is caused

by reduced compliance (ability to stretch) of the lung and thoracic wall. If the lung volume is less than 50% of normal vital capacity (VC), it is called a severe restrictive ventilation disorder. An unfavourable breathing mechanism can lead to severe desaturation. Indications for NIV: 55 Symptoms of hypoventilation (7 Sect. 5.1.1) and at least one of the following findings: 55 Permanently elevated CO2 levels in blood during the day (pCO2  ≥  45 mmHg/6.0 kPa) 55 At night (pCO2 ≥ 50 mmHg/6.65 kPa) 55 Normal CO2 values during the day, but the CO2 value increases during sleep 55 Rapid relevant decrease in vital capacity (VC) (7 Sect. 1.4.5)  

 

Targets of Ventilation in Thoracic Restrictive Diseases: 55 Elimination of hypoventilation 55 Prevention of hypercapnia 55 Taking over the breathing work 55 Supply with oxygen if necessary 5.5.3 

Obesity Hypoventilation Syndrome

The obesity hypoventilation syndrome (OHS) describes the presence of obesity with a body mass index (BMI) > 30 kg/m2. In addition, chronic alveolar hypoventilation occurs and a resulting hypercapnia (PaCO2 > 45 mmHg/6.0 kPa) in the waking state under resting respiration. Clinic and Symptoms: 55 Pronounced daytime sleepiness 55 Rapid exhaustion 55 Shortness of breath 55 Headaches 55 Sign of right-cardiac decompensation 55 Pulmonary hypertension 55 Polyglobulia (proliferation of red blood cells/red blood cells greater than standard values)

103 NIV (Non-invasive Ventilation)

Indications for NIV: 55 Persistent hypercapnia greater than 55 mmHg/7.3 kPa that persists for more than 5 min 55 Permanently elevated CO2 levels in the blood during sleep pCO2 > 10 mmHg/1.3 kPa compared to the waking state 55 Desaturation SpO2 >Where 1 mb = 1 cm H2O = 1 hPa.

8.2.2 

Flow Curve

Synonymous terms are respiratory flow curve, flow graph, air flow curve (. Fig. 8.1 second curve from above). In most cases this curve is not displayed because it is used for diagnostic purposes. Modern respirators can display it, either as a black curve or in colour.  

55 A flow-time diagram is shown, which makes statements about how the air flows into the respiratory tract and how the air flows out again. 55 The inspiratory flow is positive and goes into the upper range above the time axis. The expiratory flow is negative and goes into the lower range below the time axis. 55 With single-hose systems, only the upper area is usually displayed, with two-hose systems also the lower area. 55 A calculation of the areas indicates how much volume is administered and how much volume flows out again, the aim being that the amounts of inspiratory and expiratory volume are equal. The respirator calculates this automatically and displays the values in the measured values. 55 Deviations can be detected and provide indications of inspiratory or expiratory disorders. 55 The flow is measured with the unit 55 litres per minute (l/min) or 55 litres per second (l/s). >>1 L/s = 60 L/min

The measured values often indicate how high or fast the maximum measured air flow is, displayed as PIF = Peak Inspiration Flow. 8.2.3 

Volume Curve

This is very rarely indicated on home ventilators. However, the values are indicated in the measured values. With a single tube system, only the VTi, i.e. the inspiratory breath volume, is usually displayed. With a two-­ hose system, the VTe, i.e. the expiratory breath volume, is also displayed. 55 A volume-time-diagram is shown, which indicates how much air is administered to the lungs or how much air was given at a certain time. 55 In inspiration the curve rises, in expiration the curve sinks again.

123 Ventilation Modes

55 The measured values then indicate how much air enters the lungs during inspiration (Vt) and how much air comes out during expiration (Vte). 55 The volume is expressed in millilitres (ml) or litres (l) 8.2.4 

CO2 Curve

The CO2 curve corresponds to the expiratory CO2 measurement or the end-tidal CO2 (etCO2). However, this curve can only be displayed if additional instruments are installed to measure the exhaled CO2. This is unusual for out-of-hospital ventilation and usually not available. Nevertheless, it shall be explained to give an understanding of the exhaled CO2. The CO2 curve corresponds to the expiratory CO2 measurement or the end-tidal

8

CO2 (etCO2). A CO2-time diagram is displayed. The carbon dioxide is exhaled during expiration, therefore the CO2 curve is high during expiration, but the value of the CO2 curve during inspiration is zero. The CO2 is expressed in millimetres of mercury (mmHg). Deviations from the standard values of the CO2 curve indicate ventilation problems

References Rathgeber J (2010) Grundlagen der maschinellen Beatmung, 2. Aufl. Thieme, Stuttgart Rossaint R, Werner C, Zwißler B (2012) Die Anästhesiologie, 3. Aufl. Springer, Berlin, Heidelberg Schäfer S, Kirsch F, Scheuermann G, Wagner R (2011) Fachpflege Beatmung, 6. Aufl. Elsevier, Urban & Fischer, München Singer BD, Corbridge TC (2011) Pressure modes of invasive mechanical ventilation. South Med J 104:701–709

125

Pressure-Controlled Ventilation (PCV/A-PCV) Hartmut Lang Contents 9.1

Nomenclature – 126

9.2

Parameter Setting – 126

9.2.1 9.2.2 9.2.3 9.2.4 9.2.5 9.2.6 9.2.7 9.2.8 9.2.9

 xygen – 126 O PEEP and EPAP – 127 Inspiration ­Pressure/Respiration Pressure – 129 Frequency – 131 Inspiration Time – 131 Breathing Time Ratio I:E – 132 Ramp or Rise Time – 133 Trigger – 134 Maximum Air Pressure Limit – 135

9.3

Procedure for Pressure-­Controlled Ventilation – 135

9.4

Application of PCV Ventilation – 136

9.5

Case Study: PB 560 (Covidien) – 136 References – 137

© Springer-Verlag GmbH Germany, part of Springer Nature 2023 H. Lang (ed.), Out-of Hospital Ventilation, https://doi.org/10.1007/978-3-662-64196-5_9

9

126

9.1 

H. Lang

Nomenclature

The various respirator manufacturers usually use the term PVC or A-PCV to describe pressure-controlled ventilation. Unfortunately, the names of the individual ventilation parameters differ from respirator to respirator. A list of the parameters can be found in Table 2 in the Appendix. The individual ventilation parameters are therefore presented in general terms. Pressure-controlled ventilation is the most commonly used form of ventilation in home ventilation. The tolerance of ventilation appears to be greater in patients and it has advantages with respect to lung protective ventilation.

9

total inspiratory air. Expressed as a fraction of value 1, e.g. 0,3 (i.e. 30 % O2). The selected O2 concentration on the respirator is based on the BGA or pulse oximetry. The aim is to achieve the lowest possible O2 concentration at which the patient achieves good O2 saturation. From an O2 concentration of ≥60 % over a period of ≥24  h, the problems listed below must be expected. z Problems of High Oxygen Concentrations (Toxicity of O2 )

55 Formation of oxygen radicals 55 Release of cytokines, which are regulatory proteins produced by the human body that serve to control the immune response 55 Inactivation of surfactant 55 Depression of mucociliary clearence 55 Increase in alveolar capillary permeabil9.2  Parameter Setting ity, which means that the permeability between alveoli and capillaries in the To ventilate a patient with pressure-­ lungs for oedema water is increased controlled ventilation, the settings listed in 55 Formation of resorption atelectases, i.e. the overview are required. non-ventilated lung areas that are initially still filled with gas, but which are z Ventilation Parameters gradually resorbed 55 O2 Concentration, FiO2, Oxygen 55 This increases the intrapulmonary shunt, 55 PEEP, EPAP shunt is the blood in the pulmonary cir55 Pinsp, Pin, Pi, IPAP culation that is not filled with oxygen 55 f, AF, frequency 55 Tinsp, Ti, Thigh or breathing time ratio I : E, The oxygen in home ventilators can either Ti/Ttot be supplied through a separate inlet on the 55 Ramp, pressure ramp, curve ventilator or it can be added to the ventila55 Trigger, flow trigger or pressure trigger tion air using an additional adapter on the 55 If necessary, base flow, bias flow, flow-by inspiratory tube. 55 Pmax, Paw, pressure, Plimit The very high oxygen concentrations described above are not reached during home ventilation. The oxygen is added with an O2 9.2.1  Oxygen concentrator or a liquid oxygen tank and these usually only reach a capacity of 1–6 The O2 concentration is given in %, e.g. 30 litres per minute. This corresponds to max. %. The "Fraction of Inspired Oxygen" 44% O2. Therefore, the problems are not rel(FiO2) is the proportion of oxygen in the evant for people being ventilated at home.

127 Pressure-Controlled Ventilation (PCV/A-PCV)

9.2.2 

PEEP and EPAP

This is the ventilation pressure that is maintained during expiration. At the end of the exhalation phase, the expiration, a positive air pressure remains in the lungs. This pressure should not fall back to zero, and is called PEEP or EPAP. 55 PEEP: Positive End Expiratory Pressure or positive air pressure at the end of exhalation 55 EPAP: Exspiratory Positive Airway Pressure or positive airway pressure of the exhalation phase

Advantages of PEEP With PEEP/EPAP, the lungs and thus the alveoli always remain somewhat more distended than with normal spontaneous breathing. PEEP/EPAP thus serves the: 1. Reduction of alveoral collapse and atelectasis prophylaxis 2. Stabilization of the alveoli 3. Reopening of atelectatic areas (atelectasis  - collapsed alveoli, which are therefore no longer able to participate in gas exchange) 4. Decrease of an increased shunt volume (shunt - blood that cannot participate in gas exchange due to atelectasis) 5. Increase in functional residual capacity (FRC, 7 Chap. 1); there is always a little more air in the lungs due to the higher air pressure 6. Redistribution of the extravascular lung water into the interstitium (pulmonary edema prophylaxis) 7. Pre-stretching of the airways and the alveoli. Thereby reduced airway resistance  

The PEEP/EPAP is intended to provide open airways and open alveoli during the expiratory phase. Therefore, colloquially

9

also "hold open pressure". This is the prerequisite for secure ventilation. The PEEP/ EPAP can also be understood as "basic air pressure", because the air pressure does not drop below the set value during ventilation. The general consensus is that PEEP/ EPAP should be at least 5 mbar/cm H2O during invasive ventilation. However, it can also be lower, 3–5 mbar/cm H2O. If it is set lower, this serves to increase the tolerance for the ventilated patient who has to endure the ventilation situation for a long time. Higher PEEP/EPAP values can cause discomfort and pain for the patient. These can be caused by over-inflation caused by PEEP/ EPAP, which may not be accepted. For NIV, it is advantageous to also set a PEEP/EPAP of 5 mbar/cm H2O.  But here too, the patient's tolerance is decisive, so that it can even be reduced to the value = 0 occasionally. In general, the higher the PEEP/EPAP is set to a value of 5, the sicker the patient's lung. A higher value than 5 (sometimes even 8–10) is then necessary to keep the diseased airways and alveoli open. At values of 5–6, they would otherwise collapse and thus no longer be available for ventilation, aeration/ventilation, and thus no longer for gas exchange. A lack of oxygen (hypoxia) would be the consequence. This could be alleviated with a higher oxygen delivery, but this should only be as high as necessary. A higher oxygen delivery would also not open up the collapsed lung areas. But PEEP/EPAP can do this. If the alveoli collapse in the expiratory phase due to PEEP/EPAP that is set too low and reopen in the subsequent inspiratory phase, this quickly causes lung tissue damage. The result would be a constant cyclical collapse and opening of the alveoli, which is considered to be the cause of considerable lung damage. This makes ventilation in general risky.

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H. Lang

Adverse Effects of PEEP

z Edema Formation

The unfavourable effects can also occur at a PEEP/EPAP setting of 5 mbar. However, the advantages listed above outweigh the disadvantages. In intensive care unit clinics, there is therefore no ventilation without PEEP/EPAP.  In home ventilation, ventilation with PEEP/EPAP is therefore also ­performed.

Blood from the periphery returns to the thorax via the superior and inferior vena cava (V. cava superior and V. cava inferior) . Due to the intrathoracic pressure increase, the vena cava are compressed, which reduces the diameter. However, the amount of blood and fluid is initially the same. This quantity cannot flow through the constricted vena cava into the thorax. Thus, blood and blood fluid accumulate in the vena cava and later in all the venous vessels and capillaries of the periphery in front of it. Soon the entire blood vessels can no longer hold this amount of blood and fluid inside. The blood fluid escapes, the blood cells remain in the vessels and cause the peripheral oedema. Feet, ankles, knees and hips swell. Edema can also form in the inner abdominal organs. Oedema in the gastrointestinal tract causes a restricted food intake. Malabsorption and maldigestion with nausea and vomiting but also with diarrhoea can be the result. Blood fluid from the head and arms can also no longer flow completely back into the thorax. Oedema can also form on the fingers, arms, face and eyes. Consequences: 55 First scleral edema 55 Extension to extremities, especially back of the hand, ankles, later generalized 55 Edema in the gastrointestinal tract

z For the Cardiovascular Function

9

The PEEP/EPAP, like the ventilation pressure, causes the pressure in the thorax and lungs to rise (intrathoracic pressure increase). This pressure increase constricts the large blood vessels in the thorax, so that the blood return flow to the right heart is reduced. The cardiac output decreases. This can be a relief in heart failure. The left heart must therefore also pump less blood into the aorta. Outside the thorax the large blood vessels dilate again. The aorta leaves the thorax downwards into the abdomen, pelvis and legs and upwards through the leading aorta to the brain and arms. The diameter of the aorta increases. But the amount of blood is less, because the aorta was smaller. This lowers the systemic blood pressure. Consequences: 55 Increase of the intrathoracic pressure 55 Decrease of the heart minute volume (HMV) 55 Blood pressure drop z For the Kidney Function

This drop in blood pressure can be so severe that the mean blood pressure is no longer sufficient for the kidney blood flow. This leads to reduced diuresis and increased fluid accumulation in the blood vessel system. Consequences: 55 Hypoperfusion of the kidney 55 Reduced diuresis 55 Possible kidney dysfunction 55 ADH (antidiuretic hormone = Adiuretin).increased release 55 Reduced diuresis 55 Possible kidney dysfunction

z For the Brain

The restricted venous blood return from the brain can also cause edema there. This may result in impaired thinking, impaired cognitive receptivity, confusion and possibly clouding of consciousness. Consequences: 55 ICP increase 55 Venous outflow from the brain is obstructed z For the Lung Function

Within the lungs, the increased intrathoracic pressure can lead to an uneven distribution of air, although the application of PEEP/ EPAP has this aim. Consequences:

129 Pressure-Controlled Ventilation (PCV/A-PCV)

55 Over-expansion of areas with increased compliance 55 Possibly uneven air distribution 9.2.3 

Inspiration ­Pressure/ Respiration Pressure

55 P insp , P in , P i : Pressure Inspiration 55 IPAP: Inspiratory Positive Airway Pressure This is the ventilation pressure to be achieved during inspiration. This determines how much air the patient should receive per breath. z How High Should P insp Be Set?

9

The ventilation pressure should be set so high that the determined breathing volume can be safely administered. However, the ventilation pressure must also be adjusted again and again, e.g. after the patient has changed position. It is recommended to adjust the pressure in steps of 2-3 mbar. In general, the tidal volume administered depends on the set air pressures P insp and PEEP. The greater the pressure difference (∆ P; ∆ = Greek delta) between PEEP and Pinsp or IPAP and EPAP, the more volume is administered; the smaller the pressure difference, the smaller the volume (. Fig. 9.1).  

z Relationship Between PEEP and P insp During Pressure-Controlled Ventilation

When choosing the height of the Pinsp, the aim is to ensure sufficient ventilation. The lung tissue must not be overstretched by too much administered volume, as this can lead to damage to the lung tissue. The breath volume can be calculated with the following formula: 55 6 ml/kg bw based on the ideal body weight (IBW = Ideal Body Weight) of a person. 55 Rule of thumb for weight calculation: height in cm - 100 = normal body weight in kg. Subtract another 10-15% from this. 55 For example, for a person weighing 80 kg, you get a breathing volume of 480 ml per breath.

Depending on the ventilator, the inspiratory pressure is added to the preset PEEP or not (. Fig. 9.2). During ventilation, each value is set separately on the respirator. A PEEP setting of 8 mbar means that an air pressure of 8 mbar is built up and maintained there. Setting the PEEP to 12 mbar means that an air pressure of 12 mbar is built up and maintained. Setting the Pinsp to 12 mbar means that an air pressure of 12 mbar above the PEEP level (e.g. 8 mbar) is built up in the inspiration and maintained there. In total, a ventilation pressure of 20 mbar is achieved in inspiration. Here is the ∆ P = 12 mbar. If the Pinsp of 17 mbar is set, an air pressure of 17 mbar above the PEEP level (e.g. 8 mbar) is built

..      Fig. 9.1  Pressure difference: on the left side low pressure difference resulting in a low breathing volume and on the right side higher pressure difference

resulting in a higher breathing volume (own representation, edited by Isabel Schlütter)

 

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H. Lang

..      Fig. 9.2  Pressure setting for pressure-controlled ventilation (own diagram, edited by Isabel Schlütter)

up in the inspiration and maintained there. In total, a ventilation pressure of 25 mbar is achieved in inspiration. Here the ∆ P = 17 mbar. Practical Tip

9

PCV for Elisee 150 or VS III, ResMed: the pin is added to the PEEP or placed on it. The sum of the lower and upper air pressure is then the total air pressure in the inspiration (ventilation pressure) (. Fig. 9.2 left).  

z Connection PEEP/EPAP and Pin/Pinsp/IPAP

Just as with pressure-controlled ventilation, each value is set separately. A PEEP/ EPAP setting of 8 mbar means that an air pressure of 8 mbar is built up and maintained there. Setting the PEEP/EPAP to 12 mbar means that an air pressure of 12 mbar is built up and maintained. However, setting the Pin/IPAP to 12 mbar means that an air pressure of 12 mbar, starting from a pressure level = 0, is built up in the inspiration and is maintained there. In total, a ventilation pressure of 12 mbar is achieved in inspiration. 55 With a PEEP/EPAP = 6 mbar this is ∆ P = 6 mbar 55 With a PEEP/EPAP = 8 mbar this is ∆ P = 4 mbar If the pin/IPAP is set to 17 mbar, an air pressure of 17 mbar, starting from a pressure level = 0, is built up in the inspiration and

maintained there. In total, a ventilation pressure of 17 mb is achieved in inspiration. 55 With a PEEP/EPAP = 6 mbar this is ∆ P = 11 mbar 55 With a PEEP/EPAP = 8 mbar this is ∆ P = 9 mbar

Practical Tip

PCV for Legendair or PB 560, Covidien: the IPAP or Pinsp is set starting from the air pressure value = 0 PCV for Ventilogic LS, Weinmann: the IPAP is set from the air pressure value = 0. The IPAP or Pinsp value set then also corresponds to the air pressure in the inspiration (ventilation pressure) (. Fig. 9.2, right).  

If the respirator is changed for a ventilated patient, care must be taken to ensure that the ∆ P, i.e. the difference in air pressure between PEEP and Pinsp or EPAP and IPAP is maintained. It is therefore important to pay attention to the ventilation mode. In general, the tidal volume administered depends on the selected level of air pressures P insp and PEEP or IPAP and EPAP. With a constant pressure difference between Pinsp and PEEP or IPAP and EPAP, the lower both pressures are, the more volume is delivered (. Fig. 9.3 left):  

Example PEEP 5, Pinsp 15, pressure difference = 10. The higher both pressures are selected, the less volume is delivered (. Fig. 9.3 right).  

131 Pressure-Controlled Ventilation (PCV/A-PCV)

9

..      Fig. 9.3  Effects of the pressure level: on the left, low pressure level with larger breathing volume, on the right, higher pressure level with smaller breathing volume (own representation, edited by Isabel Schlütter)

Example Now both are increased by 5 each: PEEP 10, Pinsp 20, pressure difference of 10 remains the same. However, it is to be expected that less volume will be delivered due to the greater air filling of the lungs because of PEEP and the same pressure difference.

Example Increase both values again by 10: PEEP = 20, Pinsp = 30, pressure difference of 10 remains. The air filling of the lungs due to PEEP is even greater. An increase in pressure by 10, so that a Pinsp of 30 is reached, still results in a lower tidal volume, as the lung can hardly expand. In general, the tidal volume administered depends on the ability of the lungs to stretch (Compliance, 7 Chap. 20). 55 The greater the ability to stretch, the more volume is pumped. 55 The smaller it is, the less volume is pumped.  

In general, the tidal volume administered depends on the resistance of the airways (Resistance, 7 Chap. 20). 55 The greater the airway resistance, the less volume is delivered. 55 The smaller the airway resistance, the larger the tidal volume delivered.

If the inspiratory time is chosen too short, the time offered may not be sufficient to fill the lungs sufficiently with air. During home ventilation, it is often observed that the administered breath volume VT is greater than 6 ml/kg bw. Often the VT, which is actually optimally calculated, is not sufficient for good ventilation. Therefore, the air pressure is usually set higher and often breath volumes of 8–10 ml/kg bw or higher are achieved. The person being ventilated must also have the feeling that he or she is getting enough air. 9.2.4 

Frequency is the ventilation frequency (f, AF) per minute (bpm), e.g. 12/min. The patient should be given controlled ventilation several times per minute. The initial aim is to adjust the ventilation frequency to create a normal breathing rhythm, usually between 12-20 times/min, as is the case with a normally breathing person.

 

In general, the tidal volume administered depends on the duration of inspiration (T insp).

Frequency

9.2.5 

Inspiration Time

The inspiration duration or time, Tinsp (Time for inspiration), is given in seconds (s). It takes a certain time for a patient to be properly ventilated and for sufficient air volume to flow into the lungs. The purpose of set-

132

H. Lang

ting the inspiration time is to ensure that the volume of air to be administered reaches the lungs safely and that the ventilation pressure is only set as high as necessary, usually between 0.8 and 1.5 seconds, although variations are possible. z Relationship Between T insp and f

9

The connection between the inhalation and exhalation phase is called the breath-time ratio, inspiratory-expiratory ratio, or I:E ratio for short. Normally the inhalation phase is only half as long as the exhalation phase, or the exhalation phase is twice as long as the inhalation phase, so that all the air previously inhaled can flow out of the lungs again. This physiological status should also be achieved during ventilation. For this reason, the setting of f and Tinsp is selected to give an I:E ratio of 1:2. If one of the ventilation parameters f or Tinsp is adjusted, an additional information window opens on almost all ventilators, indicating how many seconds the Tinsp and how many seconds the Texp (exhalation time) is, and the resulting breathing time ratio.

Example I:E ratio: The ventilation rate f is 15/min, the Tinsp 1.5 s. This means that within 1 min, 15 breathing strokes are administered → Every 4 s, one ventilation stroke is administered and 1.5 s are used for inspiration: 4 s - 1.5 s = 2.5 s → 2.5 s remain for exhalation (expiration) For the calculation of the I:E the following applies: How often do 1.5 s of inspiration fit into 2.5 s of expiration? → 2.5:1.5 = 1.667 → just under 1.7 times → I:E is 1:1.7 At an f of 15/min and a Tinsp of 1.5 s, the exhalation phase is 1.7 times longer than the inhalation phase. In general, the following applies for the same inspiration time (T insp ): The faster the ventilation frequency is set, the shorter the time for expiration. The time of expiration should be sufficiently long to allow the breathing volume

to be safely exhaled! If the exhalation time were too short, less air would flow out than has flowed in during inhalation. Air accumulates and leads to over-inflation. In general, the slower the ventilation rate is set, the longer the time for expiration. The time of expiration can be intentionally long in order to safely exhale the breathing volume! Another way ofdisplaying the respiratory time ratio is made with the notation T i /T.  Ttot (Time total) describes the total duration of a breathing cycle, and is equal to 100%. T i (Time inspiration) describes the proportion of time used for inspiration. This can only be a part of the 100 %. 55 Ti/Ttot = 33 %, means that 33 % of the entire respiratory cycle is needed for inspiration. This then corresponds to a breathing time ratio I:E = 1:2 55 Ti/Ttot = 50 % , means that half of the breathing cycle is used for inspiration. I:E = 1:1

9.2.6 

Breathing Time Ratio I:E

As mentioned above, a breathing time ratio of 1:2 is often aimed for. With many respirators it is also set to this ratio. Regardless of the set ventilation frequency, the I:E ratio always remains the same. This results in a coupling between the ventilation parameters f and Tinsp. In general, the faster the ventilation rate is set, the shorter the times for inspiration and expiration become. The time of inspiration should be long enough to administer the breath volume safely! Too short inspiration times reduce the breath volume. The consequence would be hypoventilation. It can lead to a patient still actively breathing air, even if the respirator is already switched to expiration. This is stress for the patient and means a greatly increased work of breathing with increased energy consumption for work breathing.

9

133 Pressure-Controlled Ventilation (PCV/A-PCV)

In general, the slower the ventilation rate is set, the longer the times for inspiration and expiration. The time of inspiration should not be too long, because it can be felt as unpleasant! Unpleasant because a patient may already be exhaling, but the respirator is still set to inspiration. In order to get rid of his air, it can cause the patient to "press" against the ventilator. This again costs strength and energy. The same applies in the case of coupling: 55 If the Tinsp is set shorter, the ventilation rate f automatically becomes faster. 55 If the Tinsp is set longer, the f is automatically reduced. 9.2.7 

Ramp or Rise Time

The rise time or pressure ramp is the time within which the inspiratory pressure is reached. This time is given in seconds, e.g. 0.2 s, in milliseconds, e.g. 100 ms, or as a "step setting" of, e.g. 0–6. This step setting is used, for example, in the VS III (ResMed), PB 560 (Covidien) respirators. This parameter is used to determine the time within which the upper air pressure/inspiration pressure level should be reached. >>It is not possible to issue the ramp/rise time, because there must be a definition for the respirator how to build up the inspiratory pressure level. However, the value can be set to zero (= 0.0 s). However, this does not mean that the ramp is switched off.

The ramp (. Fig. 9.4) is a part of the total inspiration time Tinsp. 55 The greater the time or level set, the flatter the ramp, the slower the air flows into the lungs. The Pinsp is reached with a delay. 55 The smaller the time or stage is chosen, the steeper the ramp, the faster the air flows into the lungs. The Pinsp is reached quickly.  

..      Fig. 9.4  Ramp 0.2 s (top) and 0.0 s (bottom) (own representation, edited by Isabel Schlütter)

Example 55 Tinsp = 1.7 s, ramp = 0.2 s (200 ms) corresponds approximately to level 2 or 3. Within 0.2 s the ventilation pressure Pinsp is built up and reached. There are then 1.5 s left in which the ventilation pressure is maintained. 55 Tinsp = 1.7 s, ramp = 0.0 s (0 ms) corresponds to level 0. The ventilation pressure Pinsp is built up and reached within 0.0 s. There will then remain every 1.7 s during which the ventilation pressure is maintained. In general, the steeper the ramp/flank, the faster air flows into the airways (. Fig. 9.5). This entails the following risks: 55 Very rapid increase in inspiratory pressures with possible inhomogeneous distribution in the lungs 55 Airflow therefore not laminar (uniform) 55 Increase in airway resistance 55 Increase in shear forces with increased risk of interstitial emphysema and pneumothorax 55 Depression of mucociliary clearence  

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H. Lang

a predetermined threshold is reached, the respirator detects this and a pressure-­ controlled mechanical ventilation stroke is administered synchronously with the breath. If, for example, the flow trigger is set to 2 L/ min, the respirator will administer a breath-­ synchronized ventilation stroke as soon as the patient reaches an air flow of 2  L/min during inspiration.

Pressure Trigger

..      Fig. 9.5  Steep ramp vs. flat ramp (own representation, edited by Isabel Schlütter)

9

In general, a flat/slow ramp produces a slow flow. This entails the following risks: 55 Very slow increase of inspiratory pressures with insufficient air filling of the lungs Airflow therefore not laminar (uniform) 55 Possible incomplete filling of the lungs, as inspiration time is not sufficient to deliver full volume 55 Lack of ventilation in many lung areas 55 Inadequate ventilation leads to insufficient oxygenation and to the insufficient elimination of CO2 55 Risk of atelectasis 9.2.8 

Trigger

Trigger causes a special function. Modern respirators recognize the patient's own breathing efforts. These should be supported. The trigger function enables the patient to trigger an additional breath by himself. This can be flow- and pressure-­triggered (7 Sect. 12.2, 7 Figs. 12.2, 12.3 and 12.4).  

 

Flow Trigger The indication in is in litres/minute = L/min, e.g. 2 L/min. If the patient breathes in of his own accord, this results in an air flow. When

The indication is given in an air pressure unit or as a "step" from 1-6. With the help of the pressure trigger function, the patient himself can trigger an additional breath by creating a negative pressure. When this preset negative pressure is reached, the respirator detects this and an additional machine breath is now administered synchronously with the breath. If, for example, the pressure trigger is set to the value -2 mbar and the patient generates a negative pressure of −2 mbar through his inhalation, the respirator triggers a breathsynchronous ventilation stroke and administers it to the patient. The following applies to a pressure setting: 55 The more negative the value is set, the more difficult it is for the patient to trigger a PCV ventilation stroke. 55 The less negative the value is set, the easier it is for the patient to trigger a PCV ventilation stroke. The following applies to a step setting: 55 The smaller the value is set, the easier it is for the patient to trigger a PCV ventilation stroke. 55 The higher the value is set, the more difficult it is for the patient to trigger a PCV ventilation stroke.

Purpose of the Trigger Functions With the help of the different trigger functions, the patient can trigger one or more additional pressure-controlled ventilation strokes by his own breathing effort. The set breathing rate can thus be exceeded. A con-

135 Pressure-Controlled Ventilation (PCV/A-PCV)

9

trol is possible by reading the measured values, as ventilators differentiate between ventilation strokes delivered by the machine, and those triggered by spontaneous breathing activity. People who can do spontaneous breathing work should not be "slowed down" in their breathing efforts. Nothing seems worse than not being able to breathe in because the respirator does not allow it. All trigger functions can be deactivated. Then the patient is only ventilated at the preset ventilation rate. However, deactivation does not seem to make sense for home ventilation patients, because one of the main goals of artificial ventilation is to quickly recognize and allow spontaneous breathing.

55 Bent ventilation hose or tube 55 Patient coughs 55 Patient "presses", breathes against the device 55 Displacement/blockage of the tube/tracheal cannula by secretion

>>When the trigger function is switched on, PCV ventilation becomes A-PCV ventilation, assisted (helping) pressure-­ controlled ventilation (synonymous: (A) PCV, Ass-PCV, PCV-A).

Inspiration begins at a PEEP/EPAP level, which is intended to keep the airways and alveoli open (. Fig.  9.6). Air is delivered until a predetermined air pressure Pinsp is built up. This is set high enough to provide sufficient ventilation. The speed at which the air is delivered depends on the slope or ramp setting. When the predetermined air pressure in the airways is reached, this air pressure level is maintained for the entire duration of the inspiration. The duration of inspiration depends on the Tinsp or I:E. ratio settings. The duration of the ramp is already part of the inspiration time. Once the inspiration time has expired, the expiration valve reduces the adminis-

9.2.9 

Maximum Air Pressure Limit

The upper air pressure limit or maximum air pressure limit is abbreviated as Pmax, Paw or Plimit and is given in millibar (mbar). This air pressure limit should protect against high air pressures and should not be exceeded. High air pressures occur mainly during inspiration. Possible causes of high airway pressure:

If this maximum air pressure limit is reached, the ventilator reacts with 2 options: 55 The inspiration is terminated prematurely. 55 The air pressure is limited, the inspiration time is not interrupted.

9.3 

Procedure for Pressure-­ Controlled Ventilation

 

..      Fig. 9.6  Sequence of pressure-controlled ventilation (own diagram, edited by Isabel Schlütter)

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H. Lang

tered air back to the PEEP/EPAP level. The expiration phase begins and its duration is determined by the calculated time of the I:E ratio or by its specifications. A new ventilation cycle then begins. All parameters are calculated by the ventilator and displayed as measured values. Pressure-controlled ventilation ensures that the patient is ventilated safely. The ventilation pressure is kept constant for the duration of the inspiration time.

9

Its ventilation mode is A/C PCV, A = assisted, C = controlled. The set parameters are on the left, the air pressure bar is in the middle and the measured values are displayed on the right. The patient is ventilated 16 x/min. This ensures his/her breathing cycles per minute. This is also achieved and displayed in the measured values on the right side. Starting from the EPAP of 6 mbar, a ventilation pressure Pi of 18 mbar should be built up. The EPAP of 6 mbar does not indicate permanent lung damage, it serves to keep the airways and alveoli open. The marking lines on the air pressure bar 9.4  Application of PCV show the EPAP of 6 mbar, but the upper Ventilation mark is at approximately 22 mbar. This PCV ventilation is suitable for people whose means that the Pi of 18 mbar is currently not ability to breathe on their own is lost, such sufficient to give the patient an adequate as those with severe and complete paraple- inspiratory volume. This is achieved with the gia, or with fully developed neuromuscular target VT = 550 ml, which was previously disease. These people are tetraplegic, and determined in a ventilation center, and thus have complete respiratory insufficiency adjusted. For this purpose, a pressure of 22 mbar must be built up. The respirator can without self-breathing. A-PCV ventilation is also suitable for all calculate which pressure is necessary. The people who still have self-breathing activity. ventilation pressure is thus automatically If necessary, they should be able to trigger increased if the target VT = 550  ml is not further ventilation strokes; the respirator reached. The display on the right shows a should help them do so. This concerns peo- VTi of 612  ml. The target VT is even ple who are ventilated both continuously exceeded. The ventilation pressure is autoand intermittently. Intermittent pressure-­ matically reduced again during the next controlled ventilation is intended to bring breathing cycles. If it fits up to the set value about a recovery of the respiratory muscles, Pi = 18 mbar. From the ventilation frequency Af = 16 which is all the more pronounced the longer and the measured respiratory volume Vti, the duration of ventilation, usually during the respirator calculates the respiratory minthe night. However, people have their own ute volume M vol. of 9.7 L/min. The inhalabreathing activity both when they connect tion time (Insp. time) lasts 1.6 s. This should to ventilation, and during rest and recovery be sufficient to give the patient his adequate phases. This must be allowed. respiratory volume. The respirator calculates the respiratory time ratio I:E = 1:1.3 9.5  Case Study: PB 560 (Covidien) from the respiratory frequency (Af) and the inhalation time (Insp.Time) (display on the The patient who is ventilated with this venti- right). The exhalation time is therefore only lator (. Fig. 9.7) suffers from ALS and has 1.3 times as long as the inhalation time. been fully respiratory insufficiency in tetra- However, this corresponds to the ventilation plegia for more than 3 years. He/she is venti- requirement of the individualand was previlated invasively and continuously via a ously determined and adjusted in the ventilation center. tracheal cannula.  

137 Pressure-Controlled Ventilation (PCV/A-PCV)

9

..      Fig. 9.7  A/C PCV (own photo, courtesy of Covidien Deutschland GmbH)

The increase in air pressure from EPAP = 6 to Pi = 18 should not be too fast, but rapid. The rise time is therefore set to level 2. Now the measured Pi in the figure is approximately 22 mbar. A higher air pressure of 22 mbar should be reached just as quickly as if the Pi were at 18 mbar. If the patient still had self-breathing activity, he/she could trigger one or more additional ventilation strokes. The triggering function is activated here with the parameter Trigg I = Level 2, which is why the ventilation mode also contains the addition A = assisted. However, since the patient does not have any self-respiration, only the C = controlled function is effective; he/she is ventilated in a fully controlled manner. The A function is

nevertheless activated, because in nursing care, which also means effort for the patient, it must be possible to trigger further ventilation strokes so that the patient receives a higher M vol. (minute volume).

References Fresenius M, Heck M, Zink W (2014) Repetitorium Intensivmedizin, 5. Aufl. Springer, Heidelberg Berlin Girard TD, Bernard GR (2007) Mechanical ventilation in ARDS: a state-of-the-art review. Chest 131:921–929 Varga M et al (2014) PEEP role in ICU and operating room: from pathophysiology to clinical practice. Scient World J 852356

139

Volume Controlled Ventilation (VCV) Hartmut Lang Contents 10.1

Nomenclature – 140

10.2

Parameter Setting – 141

10.2.1 10.2.2

 reathing Volume – 141 B Flow – 141

10.3

Procedure for Volume-­Controlled Ventilation – 142

10.3.1 10.3.2 10.3.3

 hy Does the Air Pressure Drop Again? – 143 W Plateau Phase – 143 Expiration – 143

10.4

Problems of Volume-­Controlled Ventilation – 144

10.4.1 10.4.2 10.4.3 10.4.4

 isk of Unknown Air Pressures – 144 R Pendulum Air – 144 Shearing Forces – 144 Atelectasis and Emphysema – 144

10.5

Application of VCV Ventilation – 146

10.6

Case Study: Astral 150 (ResMed Company) – 146 References – 147

© Springer-Verlag GmbH Germany, part of Springer Nature 2023 H. Lang (ed.), Out-of Hospital Ventilation, https://doi.org/10.1007/978-3-662-64196-5_10

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H. Lang

10.1 

Nomenclature

The various respirator manufacturers usually use the term VCV or CV to describe Volume Controlled Ventilation. Unfortunately, the names of the individual ventilation parameters differ from respirator to respirator. A list of the parameters can be found in Table 3 in the Appendix. The presentation of the individual ventilation parameters is therefore general.

The breathing pattern of volume-­ controlled ventilation is shown as a pressure-time diagram in . Fig. 10.1. The air pressure in the airways is always in the positive range, a negative pressure is not generated. The air pressure drops to a maximum of 0 mmHg. If a PEEP/EPAP is set, the air pressure only drops to the set level. This is a time- and volume-controlled form of ventilation.  

10 ..      Fig. 10.1  VCV pressure curves, left peak pressure and plateau phase, right PLV-Pressure Limited Ventilation (own representation, edited by Isabel Schlütter)

141 Volume Controlled Ventilation (VCV)

10.2 

Parameter Setting

To ventilate a patient with volume-­controlled ventilation, the settings listed in the overview are required. Ventilation Parameters 55 O2 concentration, FiO2, oxygen 55 PEEP, Plow 55 Respiratory volume (AZV, Vt, Vti, volume tidal) 55 f, AF, frequency 55 Tinsp, Thigh or breath time ratio I:E, 55 Ti/ Ttot 55 Flow, air flow velocity 55 Flow trigger or pressure trigger 55 Pmax, Paw, pressure, Plimit

The differences in the settings are only slight compared to pressure-controlled ventilation (. Table 10.1). Most of the parameters are described in detail in 7 Sect. 9.1, so only the parameters specific to volume-controlled ventilation are discussed here.

10.2.1 

10

Breathing Volume

Data is given in millilitres (ml) per breath and indicate how much air the patient should receive per breath. Initially 6 ml/kg KG are recommended in relation to the ideal body weight of a person (IBW = ideal body weight). This ensures that the patient is sufficiently ventilated without burdening the lungs with too much air volume. Too high respiratory volumes carry the risk of lung tissue damage. During home ventilation it is often observed that the administered breath volume VT is greater than 6 ml/kg KG. Often the VT, which is actually optimally calculated, is not sufficient for good ventilation, and breath volumes of 8–10 ml/kg KG or higher are set. The person being ventilated must subjectively have the feeling that he or she is getting enough air.

 

10.2.2 

Flow

 

..      Table 10.1  Parameters for volume- and pressure-controlled ventilation Volume controlled

Pressure controlled

FiO2 Oxygen concentration

FiO2 Oxygen concentration

PEEP

PEEP

Breath volume VT

Pinsp ventilation pressure

Ventilation rate f

Ventilation rate f

I:E or Ti/Ttot

I:E or Ti/Ttot

Inhalation time Tinsp

Inhalation time Tinsp

Flow air velocity

Ramp/Flanks

Trigger

Trigger

Pmax

Pmax

The flow is also called inspiration flow or flow velocity of air. It is given in litres per minute or litres per second, e.g. 30 L/min or 0.5 L/s. 55 With a high flow, the air flows into the lungs at a high speed. 55 With a low flow, the air flows into the lungs at a slow speed. During a ventilation cycle, inspiration covers a defined period of time. The set stroke volume must be administered during this time. To achieve this, an appropriate speed is selected. The inspiratory flow is set on the ventilator, whereby 30–45 L/min is common. Exhalation is passive, no settings need to be made on the respirator. Within which time the air is administered can be calculated:

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H. Lang

Example

10.3 

Respiratory stroke volume of 700  ml and flow of 40 L/min (40,000 ml/60 s) Calculation: 40,000 ml/60 s = 700 ml/tinflat s Formed: tinflat = (700 × 60)/40,000 = 1.05 s With an I:E = 1:2 and f = 10 a breathing cycle is 6 s long. Inspiration lasts 1/3 of the breathing cycle: 2 s, expiration 2/3: that is 4 s. At 2 s inspiration and 1.05 s for one breath, 0.95 s inspiration time remains. This time after which the breath is administered is called the plateau phase/ time. The air remains in the lungs during the plateau phase. Only then does expiration begin. Modern respirators automatically calculate how fast the flow is set. The air flow should run and be maintained throughout the entire inspiration time (. Fig. 10.2).

The VCV ventilation curve (. Fig. 10.2) is explained as an example: The pressure-time ratio of volume-controlled ventilation is shown. It shows which air pressures build up in the lungs at what time. The pressure measurement in modern respirators takes place at the Y-piece. At the beginning of inspiration, air flows into the lungs at a certain flow (at a certain speed). The air pressure rises continuously, and then reaches a so-called peak pressure, the peak or PIP, which is also shown in the measured values: 55 The larger the flow is set, the faster the pressure increases. 55 The lower the flow is set, the slower the pressure rises.

 

Procedure for Volume-­Controlled Ventilation  

10

..      Fig. 10.2  Peak pressures and plateau phases at different flow rates (own representation, edited by Isabel Schlütter)

143 Volume Controlled Ventilation (VCV)

Modern ventilators design the flow in such a way that it is maintained throughout the entire inspiratory period. This prevents the development of peak pressure. When a peak pressure is reached, the predetermined and set displacement volume is applied to the lungs. The value of the peak pressure is initially unknown. After reaching the peak pressure, the pressure drops again slightly and settles at a lower level, the plateau pressure. Its level is also initially unknown. 10.3.1 

 hy Does the Air Pressure W Drop Again?

As long as the air is forced into the lungs, it cannot distribute itself evenly. Some areas of the lungs receive more air, especially the bronchial system, others receive less. The air is virtually dammed up, which is why the air pressure increases. This is measured and displayed as peak pressure (Ppeak or PIP). Once the entire stroke volume has been administered, there is usually a remaining inspiratory time (7 Sect. 10.2.2). In this phase, the air has time to distribute itself evenly in the lungs. Pendulum air (7 Sect. 10.4.2) is produced, which is detrimental to the ­ patient. The pressure in this phase drops to the level of the plateau pressure.  

 

10.3.2 

Plateau Phase

The time of plateau pressure is called plateau phase. It remains for the rest of the inspiration. The patient cannot exhale during this time because the valves are closed.

10

During the plateau phase, the inspired air is therefore held in the lungs. This gives sufficient time for the gas exchange. The duration of the plateau phase can be influenced by adjusting the flow. 55 If you want a longer plateau phase, choose a high flow. The air then flows into the airways at a faster speed, the peak pressure is reached earlier (and is usually higher), and thus the plateau phase is prolonged. 55 If you want a shorter plateau phase, choose a low flow. The air then flows into the airways at a slower rate, the peak pressure is reached later (and is usually lower) and thus the plateau phase is shortened. 55 If you do not want to have a plateau phase at all, the flow is adjusted so that the air flows into the airways for the entire duration of the inspiration. The peak pressure is therefore only reached at the end of the inspiration period, and is much lower. 10.3.3 

Expiration

When the inspiration time is over, the expiration valve opens. The air flows out of the lungs. The pressure drops continuously to its initial value-PEEP.  Exhalation is a passive process. The patient does not perform any work. The duration of the expiratory time is determined by the I:E ratio. This means that a new respiratory cycle, and thus a new inspiration is not initiated immediately upon reaching the initial pressure value, but a new respiratory cycle begins only after the expiration time has ended.

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H. Lang

10.4 

Problems of Volume-­ Controlled Ventilation  isk of Unknown Air R Pressures

10.4.1 

10

In the classic form of volume-controlled ventilation, the ventilation parameter flow is used to specify how quickly the predetermined breath volume should be administered. This can result in ventilation pressures of varying heights that are previously unknown: Neither the peak pressure level (peak or PIP) nor the plateau pressure level are known prior to ventilation. Even very high values can be achieved as peak pressure. These can also vary from breathing cycle to breathing cycle. This results in a different air pressure difference ∆P between the PEEP and the peak. However, ∆P should not exceed 15 mb, as higher pressure differences can damage the lung tissue. This cannot be guaranteed with the classic form of volume-controlled ventilation, and there is a risk of adverse effects on lung function.

Pendulum Air

10.4.2 

In volume-controlled ventilation, peak pressure occurs during inspiration. The air pressure then drops slightly and forms a plateau pressure. Since the lungs are not of equal size (7 Chap. 1, 7 Fig. 1.12), the left lung is filled with air first. The excess air, which is transported even further by the respirator, is now released to the right lung (. Fig. 10.3). The right lung is briefly overstretched and sends the air back to the left lung. The air oscillates back and forth between the lobes of the lungs until a final pressure equalization is achieved. The areas of the lungs with increased ability to stretch (compliance) are excessively stretched by the incoming air and the pendulum air, which can lead to lung damage.  

 

..      Fig. 10.3  Model of the pendulum air between the lungs (own representation, edited by Isabel Schlütter)

10.4.3 

Shearing Forces

The right lung consists of ten lung segments, the left lung consists of nine lung segments (7 Chap. 1 and . Fig. 10.4). The different compliance (stretching ability) of different segments is reinforced by pathological processes, such as pneumonic infiltrates, in which individual segments are affected. Due to the infiltrates, the segments expand to different extents during ventilation and contract unevenly during expiration. These uncoordinated movements cause the segments to rub against each other, which generates shear forces (. Fig.  10.4). This rubbing together can lead to damage to the lung parenchyma, and there is a risk of pneumothorax. This risk appears to be greater the more volume is administered and the faster the flow is adjusted.  

 

 

 

10.4.4 

Atelectasis and Emphysema

Within an acinar, the inspiratory air of the respirator does not spread evenly, as these are not equal either. Air always follows the path of least resistance. First the larger alveoli are filled, then the smaller ones. Larger

145 Volume Controlled Ventilation (VCV)

10

..      Fig. 10.5  Model of pulmonary hyperinflation (own representation, edited by Isabel Schlütter)

..      Fig. 10.6  Unknown peak pressures (own representation, edited by Isabel Schlütter)

..      Fig. 10.4  Model of the lung segments (own representation, edited by Isabel Schlütter)

alveoli generally have a better ability to stretch and therefore stretch them the farthest. Smaller alveoli may not be properly ventilated. This causes infiltrates to collect in them and the alveoli become atelectases (. Fig. 10.5). These no longer take part in the gas exchange. Larger alveoli can expand due to the inspiratory pressure to such an extent that so-called bullae are formed. These are  

large bubbles which then form emphysema. The total surface area is smaller than that of the healthy alveoli combined. This reduces the area that participates in the gas exchange. During volume-controlled ventilation, completely unknown pressure peaks occur throughout the lungs (. Fig.  10.6). Since there are areas with increased and decreased ability to stretch everywhere in the lung. The constant airflow (constant flow) that is achieved during volume-controlled ventilation ensures an uneven distribution of the respiratory air.  

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H. Lang

10.5 

Application of VCV Ventilation

The listed risks of volume-controlled ventilation have led to the fact that it is almost no longer used. However, it has the advantage of the safe administration of a predetermined breathing volume. This is used again and again in emergency situations, such as resuscitation or massive obstruction of the airways. This ventilation mode is offered to patients for whom it is important that a secured breath volume is administered, otherwise hypoventilation may occur. This is especially true for people with lung restrictions (pulmonary fibrosis, obesity hypoventilation syndrome, thoracic-restrictive diseases). But a certain degree of ventilation comfort is also important. For example, it is known that people who have been ventilated with the Respironics PLV 100 respirator find it very difficult to change devices and rarely tolerate pressure-controlled ventilation. Finding a new ventilator that offers near comfort during ventilation is a challenge for the ventilator center.

Due to the risks of volume-controlled ventilation, the flow is adjusted so that the air flows into the airway for the entire duration of inspiration. There is no plateau phase. However, if patients cannot cope with such a slow flow, it is adjusted more quickly.

10.6 

 ase Study: Astral 150 C (ResMed Company)

The patient who is ventilated with this ventilator (. Fig. 10.7) has been suffering from severe paraplegia with complete respiratory paralysis and flaccid tetraplegia for about 17 years. He/she is continuously ventilated with volume control via a tracheal cannula. There had been a switch from the PLV 100 respirator (Respironics) to the Astral 150 (ResMed). The individual could not tolerate a switch to pressure-controlled ventilation. A breath volume VT of 900 ml should be administered per breath stroke, 17 ×/min. This person would not have accepted a lower VT, and always felt shortness of breath.  

..      Fig. 10.7  Astral 150, ResMed Company (own representation, courtesy of Fd. ResMed GmbH & Co KG)

147 Volume Controlled Ventilation (VCV)

The set respiratory rate corresponds to the measured respiratory rate (below measured values). The air pressure is displayed on the left side of the air pressure bar and is 17.7 cm H2O for this breathing cycle (displayed on the top left side of the air pressure bar). This results in a respiratory minute volume of 15.3 L/min. (lower display of the measured values). The inhalation time Ti is 1.30 s and is displayed in the measured values shown below. This results in a breathing time ratio of 1:1.7 (top right measurement value display). The air speed with which the 900 ml should be administered is set with the flow curve. The air flow increases rapidly and is maintained for the entire duration of the inhalation time Ti. The air flow is nevertheless throttled during the inhalation time. When the Ti is finished, the air flow then only has a velocity of 50% of the initial value. The maximum air flow velocity PIF (Peak Inspiratory Flow) for this breathing cycle is 55 L/min. (display top right).

10

The PEEP of 5  cm H2O serves to keep the airways and alveoli open and does not indicate lung disease. The mode V(A)C is set, in the display above it is called VC, because the trigger function is switched off, as the person has no self-breathing. If it were set, VAC would also appear at the top.

References Campbell RS, Davis BR (2002) Pressure-controlled versus volume-controlled ventilation: does it matter? Respir Care 47:416–424. discussion 424–426 Kallet RH, Campbell AR, Alonso JA, Morabito DJ, Mackersie RC (2000) The effects of pressure control versus volume control assisted ventilation on patient work of breathing in acute lung injury and acute respiratory distress syndrome. Respir Care 45:1085–1096 Valta P, Takala J (1993) Volume-controlled inverse ratio ventilation: effect on dynamic hyperinflation and autoPEEP. Acta Anaesth Scand 37:323–328

149

Pressure-RegulatedVolume-­Controlled Ventilation Hartmut Lang Contents 11.1

Nomenclature – 150

11.2

Parameter Setting – 150

11.3

Independent Ventilation Pressure Level Adjustment – 151

11.3.1 11.3.2

L ung Extensibility (Compliance) – 151 Resistance – 151

11.4

Application of Pressure-RegulatedVolume-Controlled Ventilation – 152

11.5

Case Study: PB 560 (Covidien Company) – 152 Reference – 153

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Nomenclature

After the basic setting, a few "test ventilation strokes" are now performed. The resThe various respirator manufacturers usu- pirator then calculates how high the ally use the term safety Vt or target Vt to des- ventilation pressure must be (. Fig.  11.1). ignate volume-controlled-pressure-regulated The pressure is only set high enough to ventilation. It is thus less an independent ensure that the predetermined breathing form of ventilation, but rather a protective volume can be safely administered. The level of inspiratory pressure can function in pressure-controlled or pressure-­ vary from breathing cycle to breathing cycle. supported ventilation. The ventilator will automatically, autonomously, lower or raise the inspiratory pressure. This independent regulation of the 11.2  Parameter Setting inspiratory pressure takes place in small To ventilate a patient with pressure-­ steps of 2–3 mbar. This prevents unintenregulated-­volume-controlled ventilation, the tionally high pressures that could damage the lungs. settings listed in the overview are required. Setting a P max /P limit means that the ventilation pressure can only increase up to a Ventilation Parameters certain level but cannot exceed it. This serves 55 FiO2 to avoid too high ventilation pressures. The 55 PEEP ramp determines the time within which the 55 Respiratory volume, Vt ventilation pressure should be reached, 55 AF, f, frequency regardless of whether the pressure has just 55 Tinsp (the I:E results from the setting f been adjusted down or up. and Tinsp) The independent regulation of the venti55 Ramp lation pressure relieves the user from con55 Pmax/Plimit stant manual input. However, it has the disadvantage that it still produces different breathing volumes. Oxygen and PEEP are set according to the 55 For example, the respirator calculates criteria already mentioned (7 Sect. 9.2). that the pressure must be reduced. If the Depending on how long an inspiration pressure remained at the existing high stroke should last for the individual patient, level, too much breathing volume would the Tinsp is adjusted. be delivered. Slowly lowering the presThe optimal breathing volume is selected sure causes the respiratory volume to for each patient, as is a "reasonable" ventiladecrease, but not immediately. For 2–5 tion rate. The respiratory volume and ventibreathing cycles, too much volume is still lation rate result in the respiratory minute delivered. volume (RMV or MV). 11.1 

 

11

 

..      Fig. 11.1  Independent pressure regulation of the ventilator during pressure-regulated-volume-­controlled ventilation (own representation, edited by Isabel Schlütter)

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151 Pressure-Regulated-Volume-Controlled Ventilation

55 For example, the respirator calculates that the pressure must be increased. If the pressure remained at the existing low level, too little breath volume would be delivered. Slowly increasing the pressure causes the respiratory volume to increase carefully, but not immediately. For 2–5 breathing cycles the volume is still too low

11.3 

Independent Ventilation Pressure Level Adjustment

The following settings have been defined: PEEP, Vt, f, Tinsp, Ramp, Plimit (7 Sect. 11.2). Compliance and Resistance remain as regulating parameters, on which the administered breath volume depends. These are regulated independently by the respirator.  

If C  Vt  Ventilation pressure is increased automatically 

11.3.2 

Resistance

The greater the airway resistance (R), the less volume is delivered at the same ventilation pressure. Consequence for independent pressure adjustment: The ventilation pressure is slowly increased until Vt is reached again. Is R  Vt  Ventilation pressure is increased automatically  The lower the airway resistance, the more volume is delivered at the same ventilation pressure. Consequence for independent pressure adjustment: the ventilation pressure is slowly reduced until Vt is reached again (. Table 11.1).  

11.3.1 

Lung Extensibility (Compliance)

The greater the expansion capability (C), the more volume is delivered at a constant ventilation pressure. Consequence for the independent pressure adjustment: The ventilation pressure is slowly reduced until Vt is reached again. If C  Vt  Ventilation pressure is reduced automatically  The lower the Compliance, the less volume is delivered at the same ventilation pressure. Consequence for independent pressure adjustment: the ventilation pressure is slowly increased until Vt is reached again.

If R  Vt  Ventilation pressure is reduced automatically 

..      Table 11.1  Overview of independent pressure regulation To observe

Reason

Independent regulation

Vt is too high—Vt ↑

Compliance large—C ↑ Resistance low—R ↓

Ventilation pressure is reduced ↓

Vt is too low—Vt ↓

Compliance low—C ↓ Resistance high—R ↑

Ventilation pressure is raised ↑

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11.4 

Application of Pressure-RegulatedVolume-Controlled Ventilation

If the set ventilation pressure is not sufficient to administer a secured tidal volume, the set safety tidal volume is automatically administered. The ventilation pressure is increased as much as necessary to give the person the Vt. This also turns pressure-­ controlled ventilation into volume-­ controlled pressure-regulated ventilation without changing the designation on the respirator.

In this ventilation mode, a guaranteed and secured breathing volume is administered. Therefore, almost the same patients benefit from this mode, as explained in 7 Sect. 10.5. However, the risks of volume-­ controlled ventilation listed in 7 Sect. 10.4 are lower due to the automatic pressure reg11.5  Case Study: PB 560 (Covidien ulation. Thus, this comes close to pressureCompany) controlled ventilation. This ventilation mode is therefore also offered to patients for whom it is important Here the well-known example from 7 Chap. that a secured breath volume is adminis- 9. Basically it is a PCV ventilation. However, tered, as otherwise hypoventilation may a safety breath volume of at least 550  ml occur. This is especially true for people with should be administered. If the setting of the lung restrictions (pulmonary fibrosis, obe- ventilation pressure Pi = 18 mbar is not sufsity hypoventilation syndrome, thoracic-­ ficient for this, the air pressure is automatically increased so that at least a target Vt of restrictive diseases). For pressure-controlled and pressure-­ 550 ml/breathing is reached. The pressure is supported ventilation, a breath volume is automatically increased to about 22 mbar. entered in the settings for the safety of the This pressure increase happens very rapidly, patient. This is intended to protect them because this is the necessary pressure to give from receiving too little breath volume and the target Vt. It is indicated that 612 ml air thus from hypoventilating. This can happen has been administered, so in the following even though the ventilation pressure level breathing cycles the pressure is automatically reduced again (. Fig. 11.2). has been selected sufficiently.  

 

 

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153 Pressure-Regulated-Volume-Controlled Ventilation

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..      Fig. 11.2  Automatic pressure regulation—target Vt (own representation, courtesy of Covidien Deutschland GmbH)

Reference Kezler M (2006) Volume-targeted ventilation. Early Hum Dev 82:811–818

155

Pressure Support Ventilation (PSV) Hartmut Lang Contents 12.1

Nomenclature – 156

12.2

Parameter Setting – 156

12.3

Pressure Support for Breathing – 157

12.3.1 12.3.2 12.3.3

 ptimum Level of Pressure Support – 157 O Trigger – 157 Back-Up – 159

12.4

Case Study: PSV Breathing – 159

12.5

Exhalation Trigger – 160

12.6

Advantages and Disadvantages – 161

12.6.1 12.6.2

 enefits of PSV Breathing – 161 B Disadvantages of PSV: – 162

12.7

ST Mode – 162

12.7.1

Description of the ST Ventilation Mode – 162

References – 165

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Pressure support ventilation (PSV) is intended to support the patient during self-­ ventilation. The support is provided by the simultaneous administration of air pressure with the spontaneous inspiration of the patient. The patient determines how often and how deeply he/she breathes. The spontaneously breathing patient receives assistance from the respirator with each breath, an air pressure support called pressure support (PS). The patient's own inhalation work is supported by the respirator by supplying an overpressure. Even with PSV breathing, the air pressure in the lungs is always in the positive range. Nevertheless, this comes close to physiological spontaneous breathing. It is the task of the carers to ensure that the given parameters are appropriate to the patient's breathing efforts. Aspects of Observation: 55 Adequate stor age 55 Panting or effective breathing 55 Tolerance of the positioning measures by the patient 55 Stress/troubled appearance of the patient 55 States of exhaustion Signs of Exhaustion: 55 Tachypnea (high breathing rate) 55 Tachycardia 55 Saturation waste 55 Possible blood pressure fluctuations, more likely hypertension 55 Low breathing volume 55 Sweating 55 Motor restlessness 55 Patient tries to draw attention to himself non-verbally 55 Blood gas analysis: pO2 decreases, pCO2 possibly increases

12.1 

Nomenclature

The various respirator manufacturers usually use the term PSV or PSV S/T to describe pressure-supported ventilation. Unfortunately, the names of the individual ventilation parameters differ from respirator to respirator. A list of the parameters can be found in Table 4 in the Appendix. The individual ventilation parameters are therefore presented in general terms. 12.2 

Parameter Setting

The following settings are necessary for ventilating a patient with pressure-support ventilation: Ventilation Parameters 55 55 55 55

55 55 55 55

O2 concentration, FiO2, oxygen PEEP, Plow Psupport/PS Back-Up with settings: –– f, AF, frequency –– Tinsp, Thigh or –– Breath-time ratio I:E Ramp, pressure ramp, rise time Trigger, as flow trigger or pressure trigger Expiratory trigger Pmax, Paw, pressure, Plimit

Most of the parameters are described in detail in 7 Sect. 9.1, so only the parameters specific to pressure support ventilation are discussed here. The respiratory rate and Tinsp need not be set in PSV mode, as the patient has his own breathing rhythm. However, with almost all respirators it is set as a so-­ called “back-up” function!  

157 Pressure Support Ventilation (PSV)

12.3 

Pressure Support for Breathing

The basic prerequisite for using PSV mode is the patient's ability to breathe spontaneously at all. He determines his own breathing frequency, his breathing depth and whether he wants to take long or short breaths. Most of the time, however, patients are not strong enough to achieve sufficient depth of breath and a sufficient breathing volume Vt. Pressure-support ventilation is intended to support the patient in self-­ ventilation. This support is provided by the simultaneous administration of air pressure with spontaneous inspiration. A support or auxiliary pressure will be set. Usually a setting between 10 and 20 mbar or cm H2O is selected. The air pressure difference, the difference between the PEEP and the PS is called ∆ P (∆ = Greek Delta, corresponds to the air pressure difference). In general, the higher the auxiliary pressure is set, the more inspiratory volume is delivered; the lower the auxiliary pressure, the less inspiratory volume is delivered.

12.3.1 

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ramp/rise curve, the speed at which the air flows into the lungs, and the duration until the set PS level is reached is predetermined. kExhalation

Modern respirators also detect when the patient wants to exhale again. The principle of flow control is used for this purpose. This is set by an exhalation trigger. If the flow velocity of the air falls below a certain value, expiration is initiated. 12.3.2 

Trigger

The basics of the trigger were described in 7 Sect. 9.2.8.  

Flow Trigger In PS mode, an auxiliary pressure or pressure support is supplied when the flow trigger, a preset air flow of e.g. 2 L/min, is reached, This synchronous delivery of the PS pressure support is called “Demand Flow” (. Fig. 12.1). In general, the lower the flow trigger is set, the lower the inspiratory effort of the patient must be to maintain the auxiliary pressure.  

 ptimum Level of Pressure O Support

The choice of the level of pressure support depends on the patient's adequate ventilation. This is usually achieved with 6–8 ml/kg KG.  Care must be taken that the auxiliary pressure is not set too high, as this can lead to over-inflation. Setting the auxiliary pressure too low can lead to reduced ventilation. It is the task of the ventilation center to find out and set the appropriate level. kInspiration

When the patient breathes in, the respirator detects this and provides auxiliary pressure for the duration of the inspiration. This supports his own breathing. With the help of the

..      Fig. 12.1  Flow triggering, top pressure curve, bottom flow curve (own representation, edited by Isabel Schlütter)

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The flow trigger can vary between 1–15 L/min. Usually 2–5 L/min are selected at the start of PSV ventilation. If a patient breathes in, the pressure will fall slightly below the PEEP level. This negative pressure is caused by the work of the inspiratory muscles, diaphragm and external intercostal muscles (. Fig.  12.1 above). However, this small drop in pressure will very rarely be visible on the pressure curve. You may be able to tell from the air pressure bar that it moves slightly below the mark of the set PEEP. During inhalation, the patient creates a slight air flow, a flow (. Fig. 12.1 below). If the patient inhales strongly enough to generate an air flow, i.e. a flow of 2 L/min, the pressure support, PS, is triggered. The pressure increases to the set pressure level (. Fig.  12.1 above). The air flows rapidly into the patient's lungs (. Fig.  12.1 bottom).  

 

 

 

>>The danger of a too low trigger setting is a possible auto-trigger.

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z Consequences of Auto Triggering

It may be possible to unintentionally administer PS auxiliary pressure one or more times, although this pressure support was not requested by the patient. The patient can no longer breathe on his own. This creates the danger of hyperventilation. A singultus can also trigger unintentionally—with the consequences just described. z Possible Consequences of Too High a Trigger Setting

The higher the flow trigger is set, the greater the inspiratory effort of the patient must be to maintain the auxiliary pressure. The breathing effort of the patient may be too great. Too much effort in breathing can lead to exhaustion. Breathing efforts by the patient may not be responded to with PS auxiliary pressure. The patient breathes in, but not strongly enough to trigger the pres-

..      Fig. 12.2  No triggering (own representation, edited by Isabel Schlütter)

sure support (. Fig.  12.2 above pressure curve) and does not reach the flow trigger threshold (. Fig. 12.2 dashed line above the flow curve shown below). This results in hypoventilation.  

 

Pressure Trigger The indication is given in a unit of air pressure or as a “level” of 1–6. If the patient breathes in PS mode, the inhalation effort creates a negative pressure (. Fig.  12.3 above) below the PEEP level. The reaching of this negative pressure is detected and the PS auxiliary pressure or pressure support is delivered synchronously to the inspiration.  

Example The pressure trigger is set to the value −2 mbar: The patient breathes in and generates a negative pressure of −2  mbar below the set PEEP, then the respirator triggers a breath synchronous ventilation stroke and administers it to the patient. The trigger function represents a degree of difficulty that the human being must apply to trigger a PS auxiliary pressure. For a setting with an air pressure value applies: 55 It is always set with a negative value, e.g. −2 mbar/−2 cm H2O.

159 Pressure Support Ventilation (PSV)

12

order to maintain sufficient lung ventilation, a safety inspiratory volume Vt can also be set. Thus, the “Back-Up” function represents apnea ventilation and ensures ventilation for the patient.

12.4 

Case Study: PSV Breathing

The sequence of PSV breathing is shown and illustrated in . Fig. 12.4: 55 PEEP of 4 cm H2O 55 Trigger level 3, means a medium level of difficulty 55 Auxiliary pressure or PSV of +14  cm H2O above the PEEP level 55 Rise of 200 ms = 0.2 s (corresponds to the ramp, 7 Sect. 9.2.7)  

..      Fig. 12.3  Pressure trigger: top: pressure curve, bottom: flow curve (own representation, edited by Isabel Schlütter)

55 The more negative the value is set, the more difficult it is for the patient to trigger a PS auxiliary pressure. 55 The less negative the value is set, the easier it is for the patient to trigger a PS auxiliary pressure. If the pressure trigger is set to a step, the following applies: 55 The smaller the value is set, the easier it is for the patient to trigger a PS auxiliary pressure. 55 The higher the value is set, the more difficult it is for the patient to trigger a PS auxiliary pressure. 12.3.3 

Back-Up

The “Back-Up” program is a safety feature for the patient in case he or she is no longer breathing independently due to exhaustion, despite pressure support. In this case, the “Back-Up” function is automatically activated and the patient is ventilated according to the principles of pressure-controlled ventilation (7 Chap. 9). In addition, a respiratory rate and an inspiration time are set. In  

 

The starting point for breathing is the PEEP level of 4 cm H2O. The patient breathes in. This is slightly under the PEEP level. The patient must apply an inhalation force of level 3, which corresponds to a medium degree of difficulty. This level was chosen so that air pressure support cannot be triggered too easily. If a patient cannot apply this force, he/she will not receive pressure support for his inhalation (. Fig.  12.2). The correct selection of the trigger level is the task of the ventilation center. If the trigger threshold is exceeded, the patient is supplied with positive pressure, PS auxiliary pressure or pressure support parallel to his own inhalation. The rise time or ramp is set to 200 ms (=0.2  s) and means that the set PS auxiliary pressure level is reached after 200 ms. However, the patient can still breathe in further. Air is supplied for as long as he/she wants. However, a safety function is also set here: It should be ensured that the inhalation lasts at least 0.2  s (Ti Min, Min  =  minimum) and does not exceed a time of 1.5  s (Ti Max, Max = maximum). The air pressure level is not exceeded for the entire duration of the inhalation.  

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..      Fig. 12.4  PSV breathing at the Astral 150 , ResMed company (own representation, courtesy of ResMed GmbH & Co KG)

12

The total height of the air pressure level that is reached results from the PEEP = 4 plus the set PSV of 14 cm H2O. This results in a total air pressure of 18 cm H2O. This is shown on the air pressure bar on the left side of the screen. Once through the line at the height of the value 18 and at the top of the pressure bar with the value 18.7. It is thus slightly higher than calculated, but this small deviation occurs again and again and does not mean any danger for the patient.

12.5 

Exhalation Trigger

Other possible designations: 55 ETS: Expiratory Trigger Sensitivity 55 TG (E): Trigger for expiration 55 Exsp. Trigger

Inspiration eventually ends. The respirator must now recognize that the patient also wants to exhale again and must allow it immediately. The expiration trigger serves this purpose. The ventilator constantly measures the air flow generated. Relatively quickly, usually already at the beginning of the inhalation, a maximum air flow velocity is reached (a maximum flow). This value is stored by the ventilator and is set equal to 100%. The term for the maximum air flow is called PIF = Peak Inspiration Flow. The air flow decreases more and more as the inspiration progresses. Above a certain value exhalation is initiated. This value is usually 25% and means that if the air flow drops to such an extent that only 25% of the previously measured maximum air flow velocity is reached, exhalation is initiated/triggered. This value can

161 Pressure Support Ventilation (PSV)

12

..      Fig. 12.5  Expiration trigger low—high (own representation, edited by Isabel Schlütter)

be set variably. The higher the percentage, the earlier the exhalation is initiated/triggered. . Figure 12.5 left: Expiratory trigger set at 30%. Follow if ETS >The Kassenärztliche Notdienst is only available at certain times. These vary in the individual federal states. Further information can be found online on the Internet on the following homepage: 7 www.­116117info.­de  

15.2.2 

Weaning Centre

In the case of ventilation-specific problems, there is often also the possibility of contacting the last ventilation or weaning centre treating the patient by telephone. Often, problems with the ventilation or weaning centre can be clarified on the telephone and further therapeutic procedures can be discussed. The appropriate ventilation center with telephone contact details is included in the medical transfer report and should also be listed in the nursing history. On each ventilator, suction device, etc., there are also large stickers with emergency telephone numbers of the relevant providers who can be contacted in the event of technical problems. 15.2.3 

Rescue Service

In the event of an acute emergency, the rescue service is the point of contact. For the regular rescue service, the home ventilated patient is usually a rarely seen patient. Depending on the experience and level of training of the personnel, a crew may appear safe on site or may be rather unsafe. Uncertainty often leads to an unprofessional appearance and can make a situation on site more difficult. The manning of rescue equipment is regulated differently in many federal states. >>For the regular rescue service, the home ventilated patient is not a routine case!

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15.2.4 

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Qualification of Rescue Service Personnel

The personnel used in the rescue service are differently qualified. Only from 2021 on, most federal states will have regulations for the manning of an ambulance with an emergency paramedic. The emergency paramedic is a newly created job description with a three-year training and will be well prepared for medical problems. Employees who started working in the rescue service before 2016 are less extensively trained (paramedic, training usually takes 2 years). Depending on the region, paramedics may also be found (training period: 3 months). To be able to drive as an emergency doctor, you must be a licensed physician. The specialty is not decisive. Depending on the federal state, different times on wards (e.g. in an intensive care unit) are required. A special emergency doctor course (80 hours’ duration) must be completed. Afterwards, in most federal states, 50 assignments as a trainee on an emergency doctor-staffed rescue vehicle must be completed. Despite these requirements, the expertise of an emergency doctor can vary greatly. While a specialist in anaesthesia and intensive care medicine is proficient in the specialist areas of respiration and tracheostoma, it is not the everyday routine for a specialist in surgery or internal medicine to deal with these medical topics.

15.2.5 

Making an Emergency Call

In an emergency, the rescue service is alerted nationwide via the number 112. Non-urgent patient transports are sometimes called and ordered via separate telephone numbers, depending on the region. If a caller dials 112, the call will be routed to the regional emergency control centre. Depending on the region and the volume of calls, it is possible that the caller will be put on hold first.

>>If you end up in the waiting loop: DO NOT hang up, otherwise you will be re-­ listed at the last position.

As soon as a free dispatcher accepts the emergency call, modern rescue control centres will make the call from the control centre. This means that the control centre employee will ask specific questions. Nevertheless, it makes sense for the nurse on site to know the important details of an emergency call. If the control centre does not ask for something, the caller can add important information. Since the excitement in an emergency may be great, it is difficult to think clearly. Therefore, many facilities (including doctors' surgeries, clinics & emergency services) work with checklists. The standard information should be collected in a checklist, so the caller only needs to read this information. Checklist for Emergencies 55 Where is the emergency? → Information about the place, the street and the house number, the floor. 55 In nursing homes or clinics, the ward and room number must be stated. 55 CAVE: Sometimes there is a more sensible approach road than the postal address! 55 What happened? → Give the leading symptom, point out home respiration and possible infections (e.g. 3 MRGN in the tracheal secretion). 55 Who is calling? → Name and qualification 55 How many patients? → Usually it is one patient 55 Waiting for queries

15.2.6 

Transport Management

No matter whether it is an emergency or a planned transport, for the patient a trans-

181 Emergency Management

port accompaniment by the current caring nurse makes sense! This nurse usually knows her patients well and can give detailed information in the hospital. In addition, the accompaniment often prevents a change of ventilation. Finally, the caring nurse is instructed in the home ventilator. The staff in the hospital and in the rescue service is usually not. Preparation for Transport 55 Home respirator charged? Power cord and operating instructions included? 55 Reserve unit ready for use and completely present? 55 Got a full trauma kit? 55 Permanent and essential drugs packed? 55 Patient file, last hospital report, living will and power of attorney? 55 Insurance card? 55 Personal items that the patient wants to take with him/her should be kept to a minimum!

>>The patient should be suctioned endotracheally before transport. The secretion is usually massively mobilised during transport!

How the care in the hospital is to be continued is decided on site together with the treating physicians. 15.3 

Patient Assessment

z First Impression

Many colleagues know this: an experienced force expresses a feeling. “We must pay special attention to Mr. Müller. Something is wrong with him.” Sometimes this statement conceals a good “gut feeling”. But often it is the sum of the patient's impression. But this

15

cannot always be put into words. In rescue services, the first impression is often called “door threshold diagnostics”. kThe Skin of a Patient

One expects a normal, rosy and dry skin. If one notices that the patient has paleness, grey skin colour, or cyanosis, this is an indication that the disorder may be serious. kIs the Patient Moving?

Usually you observe people entering the room or talking to you. Often you can also recognize something about the mood of the person by their facial expressions. If someone does not react, has a seizure or is lying in bed completely limp, you initially assume that it is a potentially serious emergency. kIs the Patient Talking?

If the patient cannot speak, does not respond to speech, it may be an emergency. kIs the Patient Breathing?

One pays attention specifically to the rib cage. Does it rise and fall? Are the breaths even? Can you directly see a strained breathing or do you hear conspicuous breathing sounds? Of course, the general condition of the patient and the previous illnesses are decisive in determining whether a first impression really has an illness value. In a patient with paraplegia, the inability to move is “normal”. The coma patient does not fixate someone with his eyes. The patient with a severe COPD is possibly always cyanotic, etc. The nurse is therefore an important source of information for the rescue service! The same is true for new patients. If a team member has known this patient for some time, important information can be obtained. Thus, each patient must be considered individually. However, the first impression can be an easily applicable way to become aware of a problem.

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15.4 

 ed Thread of Emergency R Care

z ABCDE of Emergency Medicine

In the meantime, the ABCDE scheme has established itself as an international standard in emergency care and has been implemented in many clinics and rescue services. The ABCDE scheme provides an effective “red thread” in the care of an emergency. It is a sequence in which the patient is treated directly in an emergency. One goes through the individual points step by step. As soon as you have a problem at one point, the problem is solved and only when the problem is solved do you move on to the next point. Patients are thus treated according to the importance of the individual areas without knowing a diagnosis. Since the ABCDE scheme has its origin in the Anglo-American area, the individual word designations are in English. ABCDE Scheme

15

A: Airway

Are the airways clear?

B: Breathing

How is the ventilation of the lungs?

C: Circulation

What is the circulatory situation?

D: Disability

Are there any neurological impairments?

E: Exposure

Injuries? Pain? Heat balance disturbed?

Especially if you do not know which are the right steps to take in an emergency, a standardized procedure according to the ABCDE scheme is a good idea. This means that the helper first checks whether there is a problem in the airways.

z Signs of an A-Problem:

55 Noisy breathing 55 Airway obstruction due to foreign bodies or liquids 55 Nasal wings (especially in infants) 55 Thoracic retractions during inspiration 55 Cyanosis In a home-ventilated patient the tracheal cannula is the focus here. Is it correct? Is it blocked correctly? Can the patient be well ventilated manually? >>Avoid over-inflation of the lungs at all costs! As soon as the chest begins to lift, there is enough air in the lungs.

If the airways are secured and clear, the next step is to check the ventilation situation and improve it if necessary. z Signs of a B Problem:

55 Apnea 55 Pathologically slow/fast breathing 55 Nose wings 55 Absence or attenuation of breath sounds due to auscultation 55 Pathological breathing patterns 55 Use of the respiratory assistance musculature 55 Low oxygen saturation >There is no emergency in the world that is improved by hectic rush. In peace lies the strength. Any anxiety is transferred to the person affected. Stress increases the oxygen demand!

15

this is done under bronchoscopic control in hospital. If the patient does not breathe spontaneously, the tracheostoma must be closed with a suitable plaster (e.g. weaning plaster) or with a compress applied by a second assistant. Ventilation can then be administered via the mouth using a resuscitator bag and mask.

If the cannula cannot be inserted safely, but the patient breathes sufficiently spontaneously, no further manipulation should take place. In this case, recannulation by particularly experienced staff is indicated. Possibly

15.5.3 

Torn Cuff Tube

If a cuff tube ruptures, air will escape from the cuff and the ventilation air will no longer flow towards the lungs (. Fig. 15.1).  

Practical Tip

A classic cannula size 1 (yellow) or 2 (green) is kept ready. The cuff tube is cut diagonally with scissors, then the cannula is threaded. Now the patient can be blocked “blind” for the time being. Usually 8–10  ml of air is sufficient for this. Pay attention to the noise of secondary air and re-block if necessary. The cuff tube is then closed with a clamp. Afterwards the change of the tracheal cannula can be prepared.

185 Emergency Management

a

b

c

d

e

f

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..      Fig. 15.1 (a) Ruptured cuff tube; (b) breathing ventilation; (c) circulatory situation; (c) impairments; (e) exposure; (f) closure

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15.6 

Cerebral Seizure

Arne Raupers z Example

A patient suddenly appears confused and apathetic. He twists his eyes, is suddenly unconscious and his muscles  - arms, legs, back, shoulders, neck and also the facial muscles  - are completely tense, so much so that they tremble and twitch. One will very quickly recognize that it is a seizure and provide appropriate help. However, the fact that the working diagnosis “seizure” does not refer to a clinical pattern, but only to a symptom, behind which many different clinical patterns can be the cause, is initially ignored. Emergency medicine— unlike other faculties - is based on the symptoms and initially gets by without a diagnosis. In accordance with the many possible causes (7 Sect. 15.6.5), the symptoms and manifestations of such a seizure are also very different: from very small seizures in which only small areas of the brain are affected and, for example, only individual parts of the body cramp (focal seizures), and seizures which appear only very briefly and sometimes without unconsciousness (absences), to larger ones which, for example, have a tendency to cramping (e.g., in the case of a seizure in the brain). e.g. associated with a sudden fall (astatic seizures), up to generalized seizures that affect the whole body and are associated with unconsciousness for minutes, seizures occur in all possible manifestations. For this chapter, the grand mal seizures are interesting because they have to be classified as life-threatening.  

15

15.6.1 

Symptoms

Symptoms of a generalized seizure: 55 Aura –– The patient appears dazed and apathetic, and may even perceive abnormal sensory impressions.

55 Cramping phase –– Sudden fall, possibly with an initial cry –– Tension of the musculature (tonic cramp), trembling and twitching (clonic cramp) –– Wheezing respiration, respiratory insufficiency, cyanosis –– Salivation, “frothing at the mouth” –– Blood in the mouth as a result of a tongue bite –– Enuresis 55 Postictal phase (wake-up phase) –– Cramp stops (persists) –– Patient initially still unconscious –– Slowly coming to terms with oneself, possibly initially disorientation or drowsiness 15.6.2 

Hazards

Such a seizure must first be classified as life-­ threatening: 55 The patient can be dangerously injured, both by a fall and during the spasm, for example by repeatedly hitting his head on the floor. 55 A tracheal cannula can be disconnected during the seizure or its position can be changed. 55 Restricted breathing can lead to a lack of oxygen and thus to suffocation. 55 In the wake-up phase, the patient is initially still unconscious; accordingly, there is a risk of aspiration with the consequence of a direct airway obstruction or a life-threatening aspiration pneumonia. >>As the duration of the seizure increases, mortality increases. If the duration of a seizure is more than 30  min, mortality rises to 42%!

15.6.3 

First aid

Life Saving Measures: 1. Keep calm: with immediate help, seizures are usually controllable.

187 Emergency Management

2. Avoid injury: remove anything that is sharp-edged or dangerous. 3. Safe positioning of the patient. 4. Secure the airways! If the tracheal cannula is in danger, the home ventilator is disconnected for the duration of the attack. 5. Making an emergency call (Tel. 112) 6. Observe spasm: –– What does the cramp look like (generalized, emphasis on one half of the body, only tension or also twitching)? –– How long did the cramp last? If possible, look at the clock to tell the time. 7. Check your breathing. If normal breathing is present, the patient is placed in a lateral position to prevent aspiration. Which Measures Are Not Indicated? 55 If possible, do not hold the patient tightly, but let him or her relax as he or she does on their own, because this is the least likely way to hurt themselves. 55 Bite protection has not proved to be effective and is therefore no longer ­recommended. 15.6.4 

Extended Measures

55 Provide a suction pump, it may be necessary to suck out mucus, blood or vomit. 55 Oxygen inhalation is now only recommended if the patient is actually cyanotic. 55 The anticonvulsant benzodiazepines are particularly indicated for interruption of seizures, e.g.: –– Midazolam, which can also be administered nasally by means of a nasal applicator (MAD 300®) or, for the treatment of infantile seizures, can be simply applied into the cheek pouch (buccal application) under the trade name Buccolam. –– Lorazepam, as a fused tablet also for buccal application. CAVE: Tavor

15

Expedit® currently has no approval for the treatment of seizures. –– Lorazepam (i.v.) is the recommended drug for initial therapy according to the current study situation. –– Diazepam, as a rectiole. 15.6.5 

Causes

Only in the further treatment in the hospital an exact diagnosis with the goal of a causal therapy is to be aimed at. Possible causes: 55 Epilepsy 55 ICP due to bleeding, edema or tumors 55 Poisoning including side effects of medication 55 Withdrawal of toxins (alcohol is the main focus here) 55 Symptomatic seizures that are an expression of an undersupply of the brain and thus a symptom of a disorder of another organ system, e.g. circulatory disorders in the context of shock or cardiac arrhythmia, hypoglycaemia, lack of oxygen in the context of respiratory disorders 55 For children: fever 55 In pregnant women: eclamptic seizures If a patient is known to have a seizure disorder, it will usually not be necessary to have a clarification at the clinic. The exact procedure for this patient group will be determined with the attending physician and the treating clinic. 15.6.6 

Epidemiology

In general, about every twentieth person suffers a seizure at some point in their life for some reason. In this respect, this is one of the more frequent emergency events. Most of the time, however, these events have no further consequences. The prevalence (incidence) of permanent epilepsy is 0.5–1% of the population. It must be considered that in intensive care medicine, where people talk about ven-

188

M. Voth

tilated patients, there is already a causal disease process. In this respect, the probability of a seizure is significantly higher. The most frequent causes of seizures in intensive care medicine are 55 Encephalitis (immune reaction against central and/or peripheral nervous tissue) 55 Subarachnoid hemorrhages 55 Anoxic brain damage (7 Sect. 3.2.1)  

15.7 

15

Resuscitation

According to current guidelines (ERC 2015), resuscitation should be started if the person does not respond to speech and does not breathe normally. Palpation of pulses is no longer recommended as a standard procedure because it is associated with a high error rate. Even skilled personnel have problems sensing a correct pulse in resuscitation situations or situations associated with poor circulation. Unless a binding agreement to the contrary has been made in advance, the nurse in extra-hospital respiratory care must initiate resuscitation measures. If in doubt, resuscitation measures must be initiated. As soon as the rescue service is called, a patient is also resuscitated until the doctor can get an overview. Only when there are certain signs of death will the rescue service assistants not start the resuscitation. It is pointless to call the rescue service and then demand that no resuscitation be performed! >>Emergency call 112 means: This patient should be saved or suffering must be alleviated.

15.7.1 

Procedure

1. Address patient, touch → patient does not respond → 2. Call for help, make an emergency call (emergency number in Germany is : 112) →

3. Check breathing → no normal breathing present → 4. Start of resuscitation For adult patients, 30 cardiac pressure massages alternating with two ventilations are currently recommended. The cardiac massage should be performed at a rate of 100– 120/min. The recommended depth of pressure is at least 5 cm, but not more than 6  cm. If possible, high-dose oxygen should be given (15 L/min). Manual ventilation using a resuscitator is safer. It cannot be ruled out that a home ventilator will not perform ventilation due to a set pressure limitation, because the cardiac massage exerts a high pressure. This point should be explicitly addressed and inquired about during a device briefing. The statement of the device manufacturer must be observed. In the ideal case, manual ventilation using a resuscitator is performed via a horizontal and functioning tracheal cannula. In order not to exert unnecessary traction on the tracheal cannula, the use of a tube extension (“goose gargle”) is recommended. If it is possible to connect oxygen to the resuscitator, this possibility should also be used. The ERC Guidelines 2015 recommend high-­ dose oxygen delivery during resuscitation (15  L/min). If available, a reservoir bag should also be used. The reanimation should be carried out on a hard surface. How this is to be implemented has to be decided on site in each individual case. A light patient, e.g. a child, is relatively easy to lay on the floor. However, even with a normal-weight adult it is not so easy to lay him or her on the floor. A "resuscitation board" can help here. Some care beds have a removable footboard, which could also be used as a "hard surface". Soft-­ tissue mattresses can usually be "set hard" for a resuscitation situation. If no aids are available and the patient cannot be laid on the floor from a bed, the

15

189 Emergency Management

rescuer should start resuscitation on the spot. If the patient is in a wheelchair or e-rollie and is in a sitting position, it is also important to lay him/her on the floor. This procedure should be practised in emergency courses. >>Before any emergency relocation, always secure the airway and other access routes (e.g. a bladder catheter)! The ventilator is disconnected for this purpose.

15.7.2 

Advanced Resuscitation Measures

If a defibrillator or AED (automated external defibrillator) is available, it should be fetched by another nurse at the start of resuscitation and made ready for use during basic resuscitation. Early defibrillation can be life-saving in case of ventricular fibrillation. Every minute that defibrillation is not performed reduces the probability of survival by 8–12%. A drug therapy is only carried out by a ­present, specially trained doctor or a specially trained nurse. As a rule, this is the task of the rescue service. Decisive for the resuscitation result (outcome) are well executed and quickly initiated basic measures. This is because brain cells die after only 3 min without oxygen. The access routes for the alarmed rescue service must be opened. If the caregiver is alone on site, it is recommended that this be done while the emergency call is being made. In a home care situation, relatives may also be able to do this. 15.7.3 

 he Resuscitation Result T (Outcome)

The outcome depends on the rapid and effective start of the basic measures and the cause of the circulatory arrest. Of course,

the previous illnesses also influence a possible survival. Home-breathed patients are usually already seriously ill. Therefore, the nurse, as well as the relatives of this patient group, must always assume a poor resuscitation result. When starting care for a patient, management personnel should specifically address the question of resuscitation and the patient's will. The subject of living wills (7 Sect. 34.3) must be addressed directly in advance and the outcome of the discussion must be documented accordingly. The will of the patient must be documented in the medical record, a living will and a power of attorney must be kept in the medical record as an additional copy. The doctor in charge makes the decision to terminate resuscitation. The criteria are individual. The following aspects are taken into account: 55 Was the event observed (time of circulatory arrest)? 55 What was the probable reason for the circulatory arrest? 55 How long did the resuscitation measures last? 55 What was the first heart rhythm and which one is now present in the patient? 55 Which underlying diseases are present? 55 What is the (presumed) patient will?  

Depending on the patient's underlying disease, the requirements for technically correct cardiac massage can vary. Patients with a changed anatomy of the body have worse conditions due to the changes. All persons involved must be aware of this fact.

15.8 

Child Resuscitation

15.8.1 

Procedure

1. Address patient, touch → patient does not respond → 2. Call for help →

190

M. Voth

3. Check your breathing → no normal breathing present → 4. 5 × initial ventilation 5. Any life signs? → if no: 6. 15 chest compressions: 2 ventilations 7. If the rescuer is alone, the rescue service should only be called after one minute of basic resuscitation Initially, 5 initial ventilations should be performed on a child. The reason is that in children, an A or B problem is usually the cause of circulatory arrest. In adults, the cause is usually a C problem (e.g. heart attack). If there is no reaction to these initial breaths 15 cardiac pressure massages alter-

nating with 2 breaths are recommended for medical personnel. The pressure depth is 1/3 of the thorax. If possible, high-dose oxygen should be given (15 L/min). For children, a suitable resuscitator must be used. In the resuscitation guidelines, a child is considered a child until the beginning of puberty. Depending on the underlying disease and the child's stage of development, the nurse on site will decide on the further procedure. The differences in resuscitation in ­children are summarized in . Table 15.1. It is important here to start resuscitation measures early on.  

.       Table 15.1  Child resuscitation

15

Newborn (directly after birth

Infant (day 1 until end of 1st year of life)

Child until puberty (beginning of 2nd LJ until puberty)

HDM/ ventilation ratio

5 initial breaths (inspiration time 1–1.5 s) then 3:1

5 initial breaths (inspiration time 1–1.5 s) 15:2

5 initial breaths (inspiration time 1–1.5 s) 15:2

Pressure point

Lower third of the sternum

Lower third of the sternum

Lower third of the sternum

Pressure technique

Two-finger compression (one hand) for 1 assistant Two-thumb compression (embrace the thorax) for 2 assistants

Two-finger compression (one hand) for 1 assistant Two-thumb compression (embrace the thorax) for 2 assistants

One-hand or two-hand method (depending on the helper) The correct pressure depth is decisive

Pressure depth

1/3 of the diameter of the ribcage

1/3 of the diameter of the ribcage

1/3 of the diameter of the ribcage

Frequency

120

100–120

100–120

Ventilation volume

Ventilation should result in a moderate lifting of the rib cage No hyperventilation Highly dosed oxygen

Ventilation should result in a moderate lifting of the rib cage No hyperventilation Highly dosed oxygen

Ventilation should result in a moderate lifting of the rib cage No hyperventilation Highly dosed oxygen

Pulse buttons (for experienced personnel)

Brachial artery

Brachial artery

Carotid artery

Start of resuscitation

In the absence of circulation or pulse 50 years. kInteractions

Potentiation of tricyclic antidepressants (imipramine, trimipramine, opipramine, amitriptiline, doxepin), haloperidol, phenytoin, carbamazepine, diazepam and lithium salts, triptans and dextromethorphan. kContraindication

Simultaneous use of MAO inhibitors.

 SNRI (Selective Serotonin/ S Noradrenaline Reuptake Inhibitor) These drugs are substances that inhibit the absorption of serotonin and norepinephrine from the synaptic cleft at the nerve endings. Their concentration is thus increased there, and the effect of the messenger substances

.       Table 16.18  SSRI - selective serotonin reuptake inhibitors Drug substance

Medium dosage

Miscellaneous

Citalopram

20 mg/d

Cipramil® Generic citalopramHalf-­life 36 h

Escitalopram

10 mg/d (max. 20 mg 1 × daily)

Cipralex® tablets and drops (drops can be taken in water, apple or orange juice)

Fluoxetine

20 mg/d

Half-life 4days generics

Paroxetine

20–40 mg/d

Half-life 24 h Seroxat® and generics

Sertraline

50 mg/d

Half-life 26 h Gladem® and generics

Fluvoxamine

100–200 mg/d

Half-life 15 h Fevarin® and generics

220

B. Behrens

..      Table 16.19  SSNRI - selective serotonin/ noradrenalin reuptake inhibitors

..      Table 16.20  NaSSA—Noradrenaline and specifically serotonergic antidepressants

Drug substance

Medium dosage

Miscellaneous

Drug substance

Medium dosage

Miscellaneous

Venlafaxine

2 × 37.5–75 mg/d or 1 × 75–150 mg/d as retarded form

Trevilor® Generic Venlafaxine

Mirtazapine

15–30 mg/d

Remergil® and generics

Duloxetine

30–60 mg/d (120 mg max.)

Cymbalta® Duloxetine generics

at the receptors themselves is altered. The drugs have an activating rather than a sedative effect (. Table 16.19).  

kSide Effects

kApplication

For inhibited depression, social phobias, resistance to therapy of tricyclic antidepressants. The antidepressive effect begins after about 2 weeks.

Nausea, dizziness, sleep disturbances, tremor, nervousness, sweating, potency disorders.

kSide Effects

kContraindications

kInteractions

Do not take MAO inhibitors at the same time, caution with ciprofloxacin, fluvoxamine and enoxacin, and severe liver and kidney disorders.

NaSSA (Norepinephrine and Specifically Serotonergic Antidepressants)

16

moclobemide mainly inhibits type B of the enzyme reversibly. As an effect, the amount of transmitter at the synapses is increased.

Mirtazapine represents this mechanism of action. In a dosage of up to 30 mg mirtazapine has a sedative effect, in higher dosages it has a stimulant effect (. Table 16.20).  

 AO inhibitors (Tranylcypromine, M Moclobemide) kEffect

MAO inhibitors block the breakdown of monoamines (dopamine, norepinephrine, serotonin and adrenaline) by inhibiting the enzyme monoamine oxidase. This enzyme occurs as type A and type B. Tranylcypromine irreversibly inhibits type A and B, while

Sleep disturbances, nausea, headaches; with moclobemide additionally dry mouth. Amphetamines, levodopa, sumatriptan, alcohol. In the case of tranylcypromine, foods containing tyramine (e.g. ripe cheese, yeast, meat extract, canned fish) can lead to an increase in blood pressure, up to a hypertensive crisis (danger to life possible!) kContraindications

Severe heart and circulatory diseases, pheochromocytoma, thyrotoxicosis, suicidal tendency, confusion, simultaneous intake of opioids (especially pethidine), clomipramine, sympathomimetic drugs and tricyclic antidepressants (SSRI + SNRI) (. Table 16.21).  

16.2.6 

Anticoagulants

The occlusion of vessels, especially arterial vessels, by the formation of blood clots (thrombi) and the resulting thrombo-­ embolic diseases, such as heart attack and

221 Pharmacology

16

.       Table 16.21  MAO inhibitors Drug substance

Medium dosage

Miscellaneous

Tranylcypromine

5–20 mg

Inhibits type A + B irreversibly Requires special diet (without thyramine) Half-life 1–2 h, but with longer duration of action Jatrosom® and generics

Moclobemide

300–600 mg

DDD 300 mg Only inhibits type A reversible Aurorix® and generics

DDD defined daily dose

stroke, are among the most frequent causes of death in western industrialized nations. The accumulation of thrombocytes leads to the formation of thrombi, which normally close defects or injuries in tissue for repair. In the case of vascular changes, e.g. pathological deposits within the vessels (arteriosclerosis), changes in the flow properties of the blood (slowing of the flow due to immobilization, turbulence of the blood due to diseased heart valves or venous valves), accelerated coagulation or after surgical interventions, the risk of thrombus formation is increased. Various drugs can be used to intervene in or prevent the pathological processes (prophylaxis).

Antiplatelet Aggregation Inhibitor Acetylsalicylic acid (ASA), clopidogrel and dipyridamole are platelet aggregation inhibitors. They inhibit or reduce the aggregation of thrombocytes z ASS

Irreversibly inhibits the enzyme cyclooxygenase 1  in the blood platelets, thereby inhibiting the synthesis of thromboxane A2 and preventing clumping. ASA is used in unstable angina pectoris, for primary and secondary prophylaxis of myocardial infarction and stroke. The dosage is 30–100 mg/d (preparations: Aspirin® 100 mg, ASS 100 mg generic drugs)

kSide Effects

Gastrointestinal disorders, increased bleeding tendency, iron deficiency. kInteractions

Glucocorticoids, allopurinol, NSAIDs, other anticoagulants (except low-dose heparin) kContraindications

Gastrointestinal ulcers, bronchial asthma, analgesic asthma, kidney damage, ­pregnancy. kClopidogrel

Selectively inhibits the binding of ADP (adenosine diphosphate) to the platelets, preventing them from cross-linking and preventing the formation of clots. The dosage is 75 mg/d (preparations: Iscover®, Plavix®, generic clopidogrel). kSide Effects

Increased bleeding tendency, changes in blood count, headache, dizziness. kInteractions

Other anticoagulants, NSAIDs. kContraindications

Severe liver dysfunction, acute bleeding in the gastrointestinal tract or intracranial, fresh heart attack.

222

B. Behrens

z Dipyridamole

kDosage

Enhances the anti-aggregation action of adenosine and prostaglandin E and inhibits platelet phosphodiesterase, an enzyme that suppresses the release of messenger substances from the platelets so that they do not cross-link and do not clump. It is usually used in combination with ASS. Dosage: 2 × daily 1 retard capsule 200 mg/25 mg (ASA), (preparation: Aggrenox®).

2–5 h before the operation and 5–10 days after the operation in 6 h, 8 h later 12 h intervals 3000–5000 IU standard heparin or equivalent dose of low-molecular heparin.

Direct and Indirect Anticoagulants z Heparins

The main mechanism of action of heparins is the activation of antithrombin, which inhibits thrombin and other blood clotting enzymes. Heparin forms a complex with these substances and thus reduces the blood's ability to clot. Heparins have the advantage that they act immediately after administration. The effect of standard heparin can, for example, be quickly neutralised with protamine sulphate and is therefore relatively easy to control. Depending on the molecular weight, a distinction is made between 55 Standard heparin: 5000–30,000 molecular weight, Ø 15,000, 1  mg corresponds to 170 I.U. 55 Low molecular weight heparin: 4000– 6000 molecular weight, half-life 4–6 h with subcutaneous application, preparations: Clexane®, Fragmin®,Clivarin®, Innohep®

16

kApplication

Pre- and postoperative prophylaxis of thrombosis and embolism, unstable angina pectoris, acute phase of myocardial infarction.

kSide Effects

Bleeding into the skin or mucous membranes, heparin-induced thrombocytopenia (HIT) type I and II (if type II occurs, another group of substances must be used), allergic reactions kContraindications

Bleeding tendencies, gastrointestinal ulcers, severe liver, kidney and pancreatic diseases. kInteractions

Antiplatelets and antibiotics (penicillins, cephalosporins) increase the tendency to bleed. Antihistamines, digitalis and tetracyclines reduce the effect z Coumarin Derivatives (Phenprocoumone and Warfarin)

Effect These drugs are vitamin K antagonists which intervene in the formation of coagulation factors within the liver and block the normal course of blood clotting. The effect only occurs after a certain latency period of 1–3 days. During this time warfarin has a medium-long effect (40 h) and phenprocoumon is long-acting (150 h). Application The drugs are used for long-term therapy as prophylaxis and therapy of thromboembolism. At the beginning of the therapy, the drugs are always combined with a parenteral anticoagulant until all other signal sub-

223 Pharmacology

stances within the blood clotting system that promote blood clotting have normalised. Dosage The dosage is adapted to the patient, as the metabolism varies individually. Blood coagulation is closely monitored by determining the INR value (International Normalized Ratio). This blood value should be 2.5–3.5 and should not exceed 4.5. Phenprocoumon is dosed between 1.5–6 mg/d and warfarin between 5–15 mg/d. Antidote Vitamin K is used as an antidote, but has a delayed onset of action of 6–12  h. Transfusions and coagulation factors are administered in cases of heavy bleeding. Side effects Bleeding, with prolonged clotting time. Contraindications Pregnancy and lactation. Interactions The coumarin derivatives are very susceptible to interactions, the effect can be weakened or strengthened. 55 Reinforcement of the bleeding tendency by: allopurinol, thyroid hormones, NSAIDs (salicylates!) sulfonylureas, chloramphenicol, long-term sulfonamides, quinidine, tetracyclines, anabolic steroids 55 Attenuation of the effect: barbiturates other enzyme inducers, vitamin K-containing preparations and foodstuffs z Anti-Xa factors (Direct Thrombin Inhibitors) (Dabigatran, Rivaroxaban, Apixaban, Edoxaban)

Effect These drugs intervene directly in the coagulation cascade, i.e. they are direct anticoagu-

16

lants with a rapid onset of action and, after discontinuation, with a rapid attenuation of action. Application Atrial fibrillation, increased risk of venous thromboembolism (prophylaxis of stroke and pulmonary embolism), postoperative knee and hip joint surgery. Regular use, i.e. the patient's adherence to therapy, is very important with these drugs. Under no circumstances should a forgotten dose then be taken as a double dose. Interactions For dabigatran and edoxaban: amiodarone, verapamil, clarithromycin Contraindication For dabigatran and edoxaban: simultaneous use of dronedarone, itraconazole, ciclosporin. Interactions For rivaroxaban and apixaban: phenytoin, carbamazepine, St. John’s wort! reduces the effect Contraindications Artificial heart valves, kidney dysfunction, certain coagulation disorders. Since mid-2016, there has also been a specific antidote, an antibody called idarucizumab, for the drug dabigatran, Pradaxa® , which cancels the effect of dabigatran. After 24 h, treatment with Pradaxa® can be started again. The preparation is called Praxbind® 2.5  g/50 ml, it is an infusion solution used exclusively for emergency treatment in hospitals. The effect starts immediately after the infusion (. Table 16.22).  

224

B. Behrens

.       Table 16.22  Anti-Xa factors Drug substance

Medium dosage

Miscellaneous

Dabigatran

1 × 220 mg/d (2 capsules of 110 mg each) 1 × 150–300 mg/d for 28–35 days after joint replacement surgery 1 × 300 mg (2 capsules of 150 mg) for deep vein thrombosis, pulmonary embolism 1 × 150 mg/d (2 capsules of 75 mg each) in patients > 75 years, impaired renal function

Pradaxa® 75, 110, 150 mg capsules. Antidote: Praxbind® 2.5 mg/50 ml infusion solution

Apixaban

2 × 2.5-10 mg/d

Eliquis® 2.5 mg and 5 mg

Edoxaban

1 × 15–60 mg/d

Lixiana® 15, 30.60 mg DDD 60 mg

Rivaroxaban

1 × 10 mg/d joint surgery 1 × 20 mg/d breath prophylaxis 2 × 15 mg for 3 weeks then 1 × 20 mg/d for deep vein thrombosis and pulmonary embolism 2 × 2.5 mg/d as a combination with ASS or ASS + clopidogrel or ticlopidine

Xarelto® 2.5 mg, 10 mg, 15 mg, 20 mg

Further Reading DAZ (2014), Nr. 1, Artikel S. 52, 09.01.2014 DocCheck Flexicon Online Kirchner W (2000) Arzneiformen richtig anwenden Gelbe Liste Online 2016 Rote Liste Online 2016 Mutschler (2001) Arzneimittelwirkungen Pharmazeutische Zeitung Ausgabe 05/12 Artikel Neu auf dem Markt Pharmazeutische Zeitung Ausgabe 22/12 Artikel Bluthochdruck – Ausnahmen von der Regel Pharmazeutische Zeitung Ausgabe 39/11 Artikel Runter mit dem Blutdruck Pharmazeutische Zeitung Ausgabe 47/11 Artikel Damit aus akut nicht chronisch wird

16

Onlineartikel PZ 28/13 Ulrike Viegener, Metaanalyse bringt neue Ordnung rein Onlineartikel PZ 46/13 Hintergrundwissen für den Patienten Onlineartikel PTA Forum Ausgabe 01/07 Den quälenden Reiz stillen und den zähen Schleim lösen Onlineartikel Ursula Sellerberg PTA Forum 07/12 Beratungshinweise bei Psychopharmaka Onlineartikel PTA Forum Ausgabe 16/15 Blutgerinnung-­ Neue Wirkstoffe mit Beratungsbedarf Onlineartikel PTA Forum Ausgabe 02/16 Neue Arzneistoffe Scholz H, Schwabe U (2000) Taschenbuch der ­Arzneibehandlung

225

Oxygen Therapy Hartmut Lang Contents 17.1

Respiratory Tasks – 226

17.1.1 17.1.2

 bsorption of Oxygen and Release of Carbon Dioxide – 226 A Oxygen and Carbon Dioxide – 226

17.2

Symptoms of Oxygen Deficiency – 228

17.3

Measuring Methods for Oxygen Measurement – 229

17.3.1 17.3.2

T ranscutaneous Oxygen Saturation – 229 Pulse Oximetry – 229

17.4

Indications for Oxygen Administration – 230

17.4.1 17.4.2 17.4.3

L ong-Term Oxygen Therapy (LTOT) – 231 Intermittent Oxygen Administration – 231 Basic Diagnostics – 231

17.5

Devices for Oxygen Supply – 232

17.5.1 17.5.2 17.5.3 17.5.4

 xygen Concentrator – 232 O Oxygen Cylinders – 233 Liquid Oxygen – 235 Selection of an Appropriate Mobile System – 236

17.6

Application Systems – 236

17.7

Safety Against Fire – 237 References – 238

© Springer-Verlag GmbH Germany, part of Springer Nature 2023 H. Lang (ed.), Out-of Hospital Ventilation, https://doi.org/10.1007/978-3-662-64196-5_17

17

226

H. Lang

17.1 

Respiratory Tasks

17.1.2 

Being able to breathe is for us humans a basic requirement for our life. Without breathing no life is possible. Oxygen is a component of the air that we breathe and need in order to live, so that the metabolic processes can be kept going, so that energy and heat can be gained. 17.1.1 

Absorption of Oxygen and Release of Carbon Dioxide

The basic prerequisite of human life is its ability to absorb oxygen and release carbon dioxide through respiration. Oxygen is the element needed for all metabolic processes in our body. Carbon dioxide is the end product of these metabolic processes and must be excreted by the body. The carbon dioxide (CO2) is breathed out. The proportion of CO2 in the exhaled air is significantly higher than in the inhaled air. Components of our breathing air . Table 17.1 For unrestricted breathing to function properly, two conditions must be met in humans: 55 Functioning breathing pump 55 Functioning gas exchange (7 Chap. 2)

Oxygen (O2) Oxygen is essential for life, and is needed so that our food components can be "burned". From this we obtain the energy for all metabolic processes in the body. In addition, heat is released, which is 37 °C in humans. CO2 (carbon dioxide) is produced as a metabolic end product. z Example

Combustion of dextrose: C6H12O6 + 6 O6 → 6 CO2 + 6 H2O + Energy (ATP) + Heat z How much oxygen are we breathing?

Nitrogen

78

78

Oxygen

21

16

Carbon dioxide

0.03

4

Example Example of an adult: Respiratory rate/min = 16× Breathing volume = 500 ml (≙105 ml O2) → Respiratory minute volume = 8 L/min (≙1.68 L O2) → Respiratory volume/hour (h) = 480 L/h (≙100.8 L O2) → Respiratory volume/day = 11520  L/ day (≙ 2419.2 L O2) 21% of this is oxygen. Example Example of a newborn baby (3  kg weight): Respiratory rate/min = 50× Breathing volume = 18 ml → Respiratory minute volume = 900 ml/ min (≙189 ml O2) → Respiratory volume/h = 54000  ml = 54 L/h (≙11.34 L O2) → Respiratory volume/day = 1296000 ml = 1296 L/day (≙272.16 L O2) 21% of this is oxygen.

Other/noble gases

1

1

z How much oxygen do we need?

 

 

..      Table 17.1  Composition of air during inhalation and exhalation Inhalation (%)

17

Oxygen and Carbon Dioxide

Exhalation (%)

The following information refers to people with healthy cardiovascular and pulmonary systems.

227 Oxygen Therapy

17

Oxygen Binding Capacity (Hüfner Number): 55 Maximum amount of oxygen (O2) that can bind 1 g haemoglobin (Hb). 55 1 g haemoglobin (Hb) can bind 1.34 ml oxygen O2.

55 Approximately 25% of the O2 transported in arterial blood is consumed in the periphery and absorbed by the tissue 55 Approximately 75% remain in the venous blood “oxygen reserve”

Oxygen Content (CaO2 = oxygen content of arterial blood): 55 Amount of oxygen (O2) in the arterial blood, depends on: –– Hb concentration –– Oxygen saturation 55 Amounts to approximately 18–20  ml O2/100 ml blood, or 180–200 ml O2/1 L blood

Oxygen Supply: 55 Amounts to approximately 1500  ml under physiological conditions

Oxygen Supply (DO2 = oxygen delivery): 55 The amount of oxygen (O2) transported per minute from the lungs to the capillaries depends on: –– Hb concentration –– Oxygen saturation –– Cardiac output per minute 55 Amounts to approximately 1000  ml O2/ min Oxygen Consumption (VO2): 55 Amount of oxygen (O2) absorbed by the tissue per minute 55 Amounts to approximately 250–300  ml O2/min, or 3–4 ml/kg KG However, oxygen consumption is increased during physical exertion, such as physical work or sports, and can easily double or quadruple. The healthy body can also react to this and increase the supply of oxygen by increasing the breathing frequency and depth. In addition, the heart beats faster during physical exertion; this increases the cardiac output per minute. However, the increased workload cannot usually be sustained in the long term, and phases of recovery are required after exertion. Oxygen Extraction Rate: 55 Ratio of oxygen consumption (VO2) and oxygen supply (DO2)

At a consumption of 250 ml/min, the oxygen supply is thus sufficient for approximately 6 min. If a person is oxygenated with 100% oxygen, the oxygen supply increases to approximately 4200 ml and is thus sufficient for approximately 15 min (therefore important in emergency situations).

Carbon Dioxide (CO2)

z How much carbon dioxide do we produce?

Through our metabolic processes our organism produces CO2, the CO2 production is dependent on our nutrition: 55 It is higher for carbohydrates 55 It is lower for fats Carbon dioxide production (VCO2): Through our metabolic processes our organism produces CO2, namely approximately 250 ml CO2/min or 3 ml/kg KG. CO2 diffuses through the membranes about 20 times faster than oxygen. Respiratory Quotient (RQ): 55 Relationship between CO2 production and O2 consumption –– VCO2 = 250 ml/min –– VO2 = 300 ml/min –– RQ = 0.8 Interpretation of the respiratory quotient (RQ): The production of CO2 is reduced in the case of pure fat burning and tends towards the value 0.7. It is increased in the case of pure carbohydrate burning and tends towards the value 1.0. An increased supply of fats seems to be advantageous during ventilation, because not so much CO2 is produced.

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Terms 55 Hypoxaemia: too little oxygen in the blood 55 Hypoxia: too little oxygen in the tissue 55 Normoxie: sufficient oxygen in blood and tissue 55 Hyperoxia: too much oxygen in the blood and tissue 55 Hypocapnia: too little carbon dioxide in the body/blood 55 Normocapnia: sufficient CO2 in body/ blood 55 Hypercapnia: too much CO2 in the body/blood

17.2 

Symptoms of Oxygen Deficiency

The first signs of oxygen deprivation: 55 Tiredness 55 Fatigue, listlessness 55 Loss of vitality 55 Performance drop 55 Mental and physical exhaustion 55 Decrease in the ability to concentrate 55 Headaches

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These are rather unspecific symptoms, which usually do not need treatment yet. In the following symptoms, it is appropriate to be concerned about the person. If they persist for a long time, urgent medical attention is indicated: 55 Shortness of breath 55 Shortness of breath (dyspnea) 55 Exhaustion at low physical strain 55 Cyanosis (blue coloration of the skin) 55 Pallor of the oral mucosa z Diseases Associated with Oxygen Deficiency

Slowed, Obstructed or Interrupted Blood Flow Through the Blood Vessels: 55 Thrombosis

55 Arterial occlusive disease pAVK (shop window disease) 55 Pulmonary embolism Lung Disease: 55 Chronic bronchitis 55 Bronchial asthma 55 Emphysema of the lungs 55 Pneumonia 55 Pulmonary fibrosis 55 Chronic obstructive pulmonary disease (COPD) 55 Pulmonary embolism 55 Possible lung tumours 55 Cystic fibrosis (cystic fibrosis) Neuromuscular and Thoracic Wall Diseases: 55 Spinal muscular atrophy 55 Amyotrophic lateral sclerosis 55 Post-polio syndrome 55 Polyneuroradiculitis 55 Guillain-Barré Syndrome 55 Phrenic nerve paresis (usually bilateral) 55 Progressive muscular dystrophy 55 Congenital myopathies 55 Polymyositis 55 Myasthenia gravis pseudoparalytica 55 Kyphosis 55 Scoliosis 55 Ankylosing spondylitis 55 Restrictive pleural diseases Diseases of the Heart: 55 Congenital heart defects (Fallot tetralogy) 55 Flap defects (stenoses, insufficiency) 55 Coronary heart disease (CHD) 55 Heart failure (cardiac insufficiency) 55 Heart rhythm disturbances (bradycardia, tachycardia) 55 Inflammations (e.g. endocarditis) 55 Tumours Not all the above-mentioned diseases lead to a permanent lack of oxygen, which requires permanent oxygen therapy. However, very many of the above-mentioned illnesses result in people requiring permanent oxygen therapy.

229 Oxygen Therapy

17.3 

Measuring Methods for Oxygen Measurement Transcutaneous Oxygen Saturation

17.3.1 

For example, a TCM 5 monitor can be used to measure transcutaneous oxygen saturation (. Fig. 17.1). The oxygen diffusing through the skin and through the membrane of the sensor changes the voltage between a + pole and a  - pole, which are located in the sensor (. Fig. 17.2, far right). The instrument can measure and convert this, and gives the value of the oxygen saturation.  

 

17.3.2 

Pulse Oximetry

The oximetry of the pulse (or pulse oximetry) is the measurement of the oxygen saturation of the blood using a sensor attached to the pulsating blood vessels. Common abbreviations: 55 SpO2 55 O2 sat. z Measurement Method

The colour of the blood depends on the oxygen saturation of the haemoglobin. Oxygen-rich blood absorbs less light than oxygen-poor blood. In the recipient, the light is emitted by two diodes. After passing through the collection point (fingers, earlobes, etc.) the light is absorbed by a photodetector. This continuously transmits the intensity of the absorbed light to the device. The device measures the difference between the minimum and maximum absorption over several cardiac cycles and calculates an average value, the so-called oxygen saturation level of the arterial blood (. Fig. 17.3). Oxygen saturation indicates the percentage of oxygen saturation of the available haemoglobin. It is an indication in %: 55 It should be >96% in young people with healthy lungs. 55 In older healthy people >93%. 55 In healthy infants ~94–96%  

..      Fig. 17.1  TCM 5 monitor for transcutaneous measurement (courtesy of Radiometer)

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..      Fig. 17.2  TC blood circulation (courtesy of Radiometer)

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17.4 

..      Fig. 17.3  Pulse oximeter (courtesy of Medtronic GmbH)

Values < 90 % in adults and in children/ infants >The service life of a disinfectant means the period of time during which it can be used under the same application conditions (spectrum of action, concentration and exposure time).

Das Landesamt für Gesundheit und Soziales (The State Office for Health and Social Affairs) (LAGuS) M-V has issued a specification for the various medical products as to how long the individual products may be used. These are not fixed hygiene regulations, but rather serve as an orientation (. Table 20.1). In case of doubt, always pay attention to what the manufacturer specifies!  

20.2.2 

Aqua

The service life of humidifier liquids for humidifying oxygen, nebuliser solutions and active respiratory gas humidification such as Aqua (sterile water) varies in the home and (in hospitals) in inpatient facilities. In hospital, the aqua packs (Aqua-Pack) for ventilation remain for 7  days, while oxygen humidification can remain for 30 days. This means that the changeover takes place either after the specified time has elapsed, or when the pack is used up or a new patient uses the ventilator. >>Specified time periods of the materials can be different, this i0s due to the manufacturer’s specifications. For Aqua-­ Packs, for example, manufacturers specify 30–35  days. Average values are used which have no specifications for the practical procedure.

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.       Table 20.1  Service life specifications Product

Service life

Special note

Ventilation system (dry)

7 days

In case of infectious diseases, these may have to be changed in consultation with the hygiene department.

Ventilation system (moist)

48 h

Aqua (sterile water)

7–30 days

Change with the new patient, here observe the manufacturer’s instructions, the interval depends on the product used.

Suction

24 h

Closed systems can remain on the patient for up to 7 days.

Ventilation filter (HME)

24 h

Inhalations/ nebulisers

24 h to 6 weeks

20.2.3 

This difference is due to the individual components, for example filters have a service life of 7 days, connecting pieces 6 weeks and nebuliser chambers only 24 h.

Hose Systems

In the homecare sector, other standing times apply, since at home people live in their own germ environment. His body knows these germs and he is prepared for them. This is why tubes that are changed in hospital after 7 days can be left in place for a month. 20.2.4 

Disinfection

Where disinfectants are used in hospitals, cleaning at home with a standard cleaner, preferably curd soap, is sufficient. However, the manufacturer’s instructions must also be observed here. Why curd soap? Curd soap does not contain perfumes and has a pH-value of 8–10. The absence of perfumes has the advantage that plastics are not attacked but are protected. The fatty acids contained in the soap have a disinfecting effect (7 nurse.­com). Surgeons also recommend the use of curd soap for inflammations (Gesellschaft für Fußchirurgie— Society for Foot Surgery). This disinfecting effect can be used well in the homecare sector without having to resort to “chemistry”.  

20

>>Curd soap is to be preferred, as it does not contain any perfumed additives. Good curd soap is available in pharmacies.

20.3 

Dry Breathing Systems

These are the ventilation hoses from the ventilator to the HME filter. Other principles apply to the HME filter and the goose gargle, which are dealt with separately after the ventilation systems (7 Sect. 20.5).  

20.3.1 

Reusable Breathing Tube

In the past, multi-way ventilation systems were used in the clinical intensive care area. Today, single-use systems are used (7 Sect. 20.3.2). However, these multiway breathing tubes are still used in some areas of medicine today. These multiple breathing tubes had to be prepared separately. Two procedures in particular are used, which should also be considered in the homecare sector. 1.  Cleaning by Hand (Manual Cleaning)  

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The first procedure is to place the breathing tubes in a disinfectant solution. In this solution, the respiratory systems remain in place for at least one hour.

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>>After cleaning, check that all hoses and accessories are in perfect condition. Be careful in case of leakages! These can lead to complications such as breathing difficulties when changing the system.

Practical Tip

Disassemble the hose system completely before cleaning. Some hoses are plugged together with connectors due to insufficient length. The complete disassembly is ­important for cleaning. After disassembling, you will generally get the two hose legs, the Y-piece and the goose gargle (this also applies to the homecare area).

The systems must be completely disassembled to ensure that the disinfectant solution reaches everywhere. Before insertion, all the material is roughly pre-cleaned so that residues, for example of blood, are removed. >>Any gross contamination reduces the success of cleaning with disinfectant!

The problem with this method is that disinfectants have an unpleasant smell and (some) continue to outgas for quite some time afterwards. It is therefore very important to rinse the hoses well afterwards or to water them in clear water. Only when the odour has abated as far as possible can the hoses be welded in and sterilised. 2.  Mechanical Cleaning Mechanical cleaning is similar to manual cleaning. The breathing hoses must also be completely disassembled, as the dishwashers only clean where the rinsing solution reaches. The hoses are disinfected by the cleaning and disinfection machine. In addition to disinfection, the machine also rinses and dries the hoses. The user only has the task of inserting the hoses properly into the machine. After machine cleaning, the hoses are then prepared for sterilization, packed and then stored.

20.3.2 

Disposable Hose Systems

Disposable hose systems are intended for single use only. There are the very classic hose systems with two legs. Inspiration and expiration have separate legs. They separate at the Y-piece behind the goose gargle. Another group of disposable systems is the tube-in-tube method. Here, the tube for inspiration is contained as an inner tube in the expiratory leg. In addition, there are also hose systems that can be extended to the required length like an accordion. There is no need to reprocess these hoses, as they are disposable materials. They are disposed of properly after the system change. The disposal mainly influences whether the patient lies in the isolation area or not. These disposable systems are now mandatory in the homecare sector. 20.3.3 

Standing Times

The service life for ventilation tubes is approximately 7 days in the clinical area. It does not matter whether they are intensive care or home care devices. These service lives are specified by the companies and are supported by hospital hygiene. The situation is different in the home ventilation area, however: As already mentioned above, the patient is in his own environment here and is familiar with the germs. Here, there are different standing times. According to the manufacturer, disposable systems should normally be changed once a month. If, as for example in the CPAP area, the hose systems are made of durable mate-

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M. Thoms

rials, there are also significantly different change intervals. These tubes can be used at home for up to 1 year. 20.3.4 

System Change

Hygienic working when changing systems is a prerequisite for avoiding infections. The basic rules apply here: 55 The system must not be placed in the patient bed after preparation. There could be germs in patient beds that the patient does not yet have in the airways. 55 The hoses must not come into contact with the ground. Especially, the floors in stationary facilities and hospitals often contain a multitude of germs. >>Any system that has been contaminated may no longer be used, but must be disposed of immediately.

In the hygienically correct procedure, the new system is first assembled and then either placed on a sterile surface or held in the hand so that contamination does not occur. Then the system to be changed is removed and the new system is connected. In addition to the hygienic work, time plays a role here. The system should be changed quickly and smoothly. Hectic system changes often lead to contamination. Patient information also contributes to quiet working and conveys safety. 20.3.5 

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Reusable Systems

In the homecare sector, hoses are often used that are cleaned once a week. Here, it is sufficient to rinse the tubes under warm running water and then hang them up to dry. So it is best to start in the morning so that the tubes are dry until the next use. External coarse impurities can be removed with curd soap. But always pay attention to the manufacturer’s instructions!

Practical Tip

Always remove the hose system first from the patient and then from the device. The new system is then connected first to the device and only then to the patient. It is important to work calmly and to inform the patient about the procedure.

20.4 

Tubes with Humidifier

These have almost completely disappeared in the hospital. The problem was that aqua had to be warmed up and then be given to the patient during inspiration. This was to prevent the patient’s pulmonary system from becoming too dry and to avoid pneumonia. The problem, however, was the improper handling. Warm water vapour could be generated, which could damage the lungs, but could also lead to contamination, as germs feel very comfortable and multiply abundantly, especially in a moist and warm environment. And respiratory humidifiers meet these requirements. Especially in hospitals, where there is a large number of germs, these can multiply very strongly with only the slightest degree of uncleanliness. >>It is important that no HME filters are used when using ventilation systems with humidifiers. HME filters would obstruct the humidified breathing gas and the moisture would collect in the filter.

20.4.1 

Hose Systems

Basically, the same procedures apply to these hose systems with regard to cleaning and changing. However, there are some special features. On the one hand, it makes a difference which system is used, on the other hand, it plays a role whether the systems are heatable hoses or not.

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z Without Heatable Hoses

The problem with this type of tubing is that the respiratory gas cools down considerably on the way from the humidifier to the patient. In the process, the water from the breathing gas collects at the lowest point of the system. For this reason, these tubing systems have water traps in which the condensate should collect. However, since the hoses do not always hang in such a way that the water traps are at the lowest point, accumulations can occur in the hose system. These are then in turn sources of infection, as the germs find a good environment in them to multiply. >>Water traps must always hang at the lowest point in the ventilation system. In this way, the condensation water runs off directly and reduces the risk of contamination.

z Heatable Hoses

There are essentially three types of system. The first two are disposable systems, which are treated in the same way as all other disposable hoses in terms of hygiene. These systems have 55 a heater wrapped around the hose, 55 or a heating wire that is already drawn into the hose. 55 With the reusable system, the heating wire must still be pulled in, as the tube and heating wire can fuse during sterilisation. Threading requires a very hygienic procedure. Under sterile conditions, a guide rod is inserted into the inspiratory leg of the tube system and the heating wire is then pulled through the system with the help of the rod. The measuring adapter is then placed in front of the Y-piece of the inspiratory leg. Its tip must also be sterile as it is in contact with the breathing gas. Heatable hose systems are preferred, since damp chambers in the hose system form less often. This cannot be completely

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ruled out, but the probability is significantly lower. This also significantly reduces the risk of microbial contamination. Nevertheless, these hose systems also have water traps that must be suspended at the lowest point of the ventilation system. >>If water does form, it must be removed as soon as possible, as the heat causes germs to form even more quickly. Then you should find out why the water has formed. Practical Tip

Humidified systems are not so susceptible to faults. The main fault is the temperature regulation, where too little heat was set. Another common error is defective sensors.

20.4.2 

Changing the Heatable Hose Systems

Essentially, the same rules apply here again as when changing from dry systems: sterile working without contaminating the hoses. Always first remove them close to the patient and then on the device, and vice versa when attaching them. With humidified systems, however, the following applies in addition: since it takes longer to change systems with humidifiers and not every patient can manage without respiratory gas for as long as this takes, the humidified system should first be changed to a dry system. To do this, the humidifier is switched off, then the hoses are removed from the humidifier and the patient is given dry respiratory air for a short period of the change. Then the humidifier chamber with the connecting hose to the respirator is replaced, but not yet connected. After preparing the rest of the system, the patient is disconnected from the device, then the connection hose of the humidifier chamber is

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connected to the inspiratory part of the ventilator and then the rest of the ventilation system. Practical Tip

It is important to work calmly and to inform the patient. Speed has nothing in common with hectic pace. Fast and calm is best!

z Change Intervals

The RKI recommends changing the humidification systems every 7  days. Only these systems have a device protection filter before the expiratory part of the ventilator, together with a water trap. The change interval is always the same, as the systems are considered closed systems. 20.4.3 

20

Humidifying Liquids

The liquid used in the humidifiers is mainly Aqua. Self-regulating humidifiers are also used in the homecare sector. Here, an Aqua-­ Pack or an infusion bottle with Aqua is connected to the humidifier. The connecting hoses belong to the humidifier chambers. Here, a float checks the Aqua level and always replenishes so much that overheating of the humidifier is avoided. Overheating would result in excessive heating of the breathing gas, which could lead to combustion. The shelf life is 7  days and would be changed with the humidifier system at the latest. Otherwise, a change should always be made when the container is empty. Medical aqua must be used in the homecare sector. Aqua from hardware stores is often used, this is not permitted! Medical Aqua is purified and comes on the market as a sterile solution. Normal aqua is not subjected to these requirements and can therefore be contaminated. This is not important in the craft sector, where it is otherwise used,

but it should never be used, especially in the ventilation area at home. >>Always use only medically approved aqua!

20.5 

 ME Filters and Goose H Gargle

For HME filters and goose gargles, the change interval and handling are identical. HME stands for Heat and Moisture Exchanger. The task of the filters is to clean, humidify and warm up the breathing air in the inspiration. The moisture and heat is retained in the expiration and returned to the breathing air in the next inspiration phase. The goose gargle is a connecting tube between the tracheal cannula (endotracheal tube) and the ventilation system. This tube is called goose gargle because it is very flexible and cannot be bent. z Replacement Intervals

The HME filter and the goose gurgles are changed according to the manufacturer’s instructions, if they are not dirty, in a 24-h  cycle. If they are dirty, they must be changed immediately to prevent infection (this also applies to the homecare sector). Practical Tip

Here, too, observe the change direction so that the patient does not have too much dead space.

>>If the patient has a ventilation system with humidifier, do not use HME filters. These would only retain the humidity of the respiratory air. In this case, the filters would become blocked or the moisture would migrate back into the ventilator during expiration (current and wetness).

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20.6 

Ventilation Masks

There is a wide range of ventilation masks available in the homecare sector. From the simple nasal mask to the full-face mask, the total face mask or the respiratory helmet. No matter which system is used, all of them have to be cleaned and the same requirements apply to all of them. z Homecare Area

Today, respiratory masks are used in sleep medicine and also in home respiration. The masks are prescribed in hospital and given to the patient at home. These masks have to last there for 1 year, as health insurance companies only replace them once a year. Cleaning must therefore take place at home at a fixed interval, and here too the manufacturer’s instructions must be observed. It is recommended to clean them once under running water with curd soap. For cleaning, the masks are carefully disassembled into their individual parts and a small bottle brush is used to clean the individual components. Then rinse well and lay them out to dry. >>Only use curd soap or cleaning agents specified by the manufacturer. The perfume components in normal household detergents can destroy the tubes and masks and deposit in the lungs. Get small brushes, sponges or cloths for cleaning, which are only used here.

If a mask is damaged, which is unavoidable with plastic and regular use, you should contact the dealer immediately. In most cases, health insurance companies will cover a new mask, otherwise many masks can be repaired by the dealer. Some clinics offer a mask consultation hour, this can also be a good place to go. Never patch the masks in any way that could impair their function!

20

Practical Tip

A well-maintained mask lasts much longer and is much more comfortable for the patient to wear.

20.7 

Tracheal Cannula Management

Tracheal cannula management is the cleaning and general care of a tracheal cannula. Here, however, it is not a matter of the procedure for changing a cannula, but rather of the period of time how often the cannulas should be changed. Various factors play a role in the period of time: the material of which the cannula is made must be taken into account, but also the question of whether the tracheal cannula is freshly inserted. 20.7.1 

Lay Days

The length of time the tracheal cannulae are in place depends on many factors: is it defective or can it still be easily blocked? Is it encrusted with secretion from the inside? Does it have inner souls that can be changed and thus cleaned? Is it the first change after installation or has the patient had it for a longer time? And finally, what does the manufacturer and the treating doctor say at home and/or in the clinic? To give an idea, here are some indicative figures: 55 Representatives of companies indicate lay days of 3–7 days and 1–2 weeks. 55 Doctors in the homecare sector specify a stay of 2–4 weeks. 55 In the intensive area, periods of between 14  days and 2.5  months after the first change are traded. Here, however, it usually remains at 4 weeks.

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Ultimately, the attending physician must decide according to the circumstances and manufacturer’s specifications. 20.7.2 

Cleaning of Cannulae

With tracheal cannulas, only the removable inner cannulas, also called the soul, are cleaned. The cleaning of these souls is again subject to the manufacturer’s instructions. The hygiene institutes refer to the manufacturers’ cleaning materials. They offer special disposable brushes and solutions for cleaning the inner cannulas. Each manufacturer has its own agents, if possible these should be used. Practical Tip

The removed core is thoroughly cleaned of coarse dirt with a brush under running water. Afterwards, the core is placed in a special tin with the cleaning solution. Coarse soiling prevents disinfection of the core. This is known as a protein defect, as it involves protein structures (secretion residues). >>In some areas, cleaning tablets like the one for third teeth are used. This is strictly discouraged, as the manufacturers of the cleaning tablets and the manufacturers of the tracheal cannulas refuse any responsibility!

20.8 

20

Equipment Maintenance

The care of the equipment in the ventilation area is an aspect that is all too often not given sufficient consideration. Whether in the clinic or at home, a clean device is less susceptible to malfunction and the transmission of germs is also reduced.

20.8.1 

Ventilators

For ventilators, there are two essential aspects to be considered, both in the inpatient and outpatient sector: first, cleaning the equipment and second, changing the equipment filter. z Cleaning

In the clinical area, the devices are cleaned daily with a disinfectant solution to prevent the transmission of germs. In the homecare area, the devices should be cleaned at weekly intervals. Since disinfectants are not necessarily required, cleaning with curd soap is also recommended here. Coarse impurities must be removed promptly. Contamination can lead to long-term functional impairment and/or germination. Hygienic work is of enormous importance, especially for patients who are invasively ventilated in the homecare sector. Here, it is recommended to adapt to the standards of the clinics. >>Purity is the first step in preventing disease, even if it is only the outer shell of a ventilator.

z Device Filter Change

Many ventilators in the homecare sector have a timer that indicates when a device protection filter needs to be changed. In some series, the devices have a coarse dust filter, in others a fine dust filter. The coarse dust filter must be cleaned between once a week and once a month, depending on the manufacturer’s instructions. The dust is beaten out and then rinsed under running water. The homecare appliances usually have a replacement filter that is used in exchange. The coarse dust filter is completely replaced between once a month and once a year. The fine dust filter is usually a filter cassette. But regardless of whether it is a cassette or a fleece, the device often specifies the replacement interval. Otherwise, as every-

285 Hygiene

where else, the manufacturer’s specifications apply, which usually specify a monthly rhythm. >>Never use damp fine dust filters!

20.8.2 

Cough Assist

The Cough Assist is a device designed to assist patients with coughing. This device is designed for patients who are no longer on an intensive care ventilator. It is mainly used in the homecare sector. Cleaning and hygienic preparation with system change has the same basic rules as with the ventilator. The system change is easier, because it is not a continuous use of equipment, but an intermittent one. Since the Cough Assist also has an HME filter and a goose gargle, the intervals and specifications already mentioned are also valid here. The actual hoses can be left in place for between 1 month and 1  year, depending on the manufacturer’s specifications. 20.8.3 

Oxygen Equipment

There are two modes of operation for the oxygen devices: the oxygen concentrators and the supply of liquid oxygen. Both systems have to be cleaned and both systems have hoses for changing. z Oxygen Concentrators

Oxygen concentrators are the most commonly used devices for administering oxygen to patients at home. These devices filter the oxygen from the surrounding room air and then pass it on to the patient. This is only possible up to a certain litre quantity. The devices work with filters that need to be changed regularly, just like the fine and coarse dust filters of the ventilators. A dirty

20

filter cannot fully retain dust and other particles, so that these can then enter the device and thus reach the patient. Replacement of fire flow stop valves and other technical parts may only be carried out by trained medical personnel. As with the respirators, the best way to clean the equipment is to use curd soap. Here too, coarse impurities should be removed promptly. The oxygen lines from the device to the patient should be changed once every 6  months as a disposable material, but the manufacturer’s instructions apply here as well. A (clear) advantage of concentrators is that they are not so sensitive to moisture. Only the filters are to be used dry only, so that no moisture gets into the device. The Aqua units should be replaced once a month or as soon as they are empty. Only medically approved Aqua may be used for refill systems. The nasal cannula should also be cleaned and changed regularly. Here, the specifications are valid between 1 month and 1 year. Here too, the manufacturer’s specifications specify the relevant times. z Liquid Oxygen

The tanks of liquid oxygen are refilled by the supplying company regularly or as required by the patient. At the same time, the company carries out a check of the most important parts. If something is contaminated or defective, remedial action is taken immediately. Otherwise, cleaning in the homecare sector is similar to that of oxygen concentrators. The main advantage is that more oxygen can be administered. The disadvantage is that there is a lot of condensation water due to the cold of the oxygen. Care must be taken that the tank is tight! Work here with as little liquid as possible, as ice formation can occur. >>Never use fire at the same time during oxygen therapy!

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20.8.4 

Suction Devices

As in the clinical sector, special guidelines apply in the homecare sector, especially for the suction units. Since many germs collect and multiply in the containers with the aspirated secretion, these must be renewed daily. The suction catheters, on the other hand, are exclusively disposable and are disposed of after each use. An exception is also made here for the so-­called closed suction systems. These suction units are firmly attached to the tracheal cannula and connected to the suction system. According to the manufacturer’s instructions, they should be changed every 3–4 days at the latest. >>With a few exceptions, suction material is disposable material that is disposed of and not cleaned.

The holders of the extraction units should be cleaned daily. Curd soap is also the product of choice in the homecare sector.

20.9 

Washing Hands

An important area of hygiene is hand washing. Soap dissolves the germs and ensures that they can be rinsed off under running water. Die Bundeszentrale für Gesundheitliche Aufklärung (The Federal Centre for Health Education) has issued a recommendation on this. Hands should be thoroughly soaped with soap for about 30–40  s, especially between the fingers, as germs like to hide here. Then rinse thoroughly under running water and dry thoroughly. Washing hands is not only important after going to the toilet or before eating; before contact with patients, thorough hand cleaning is a good way of preventing illness.

20

z Hand Disinfection

Various hand disinfectants are availablein pharmacies for hand disinfection. It is particularly important for patients ventilated with tracheal cannula at home: Even if they live at home in a known germ milieu, they can still be infected with germs from outside. Furthermore, self-protection also applies to the nursing staff. The RKI recommends the following procedure for hand disinfection: 1. Apply disinfectant to the palm of your hand and rub in. 2. Palm on back of the hand alternately for both hands. 3. Palm on palm with crossed, spread fingers. 4. Exterior side of fingers to opposite palm with interlaced fingers. 5. Circular rubbing of the thumbs in the closed palm for both hands. 6. Circular rubbing back and forth with closed fingertips in the hollow hand for both hands. >>A ventilated patient is always immunocompromised. Ventilation makes it much easier for germs to penetrate even deep areas of the lungs. That is why hygiene and hygienic work start with washing your hands. >>Hygiene is not only disinfection in the hospital, but the best prevention for the health of the patient and protection of the material.

Conclusion Hygiene is a factor that is often neglected, especially in the homecare sector, but with which every family member and the employees of the intensive care services play an important role in the prevention of diseases. As disinfectants are not avail-

287 Hygiene

able at home like in hospitals, soap water made with curd soap is recommended for cleaning. Since original curd soap does not contain perfumes or other fragrances, it does not damage the equipment or accessories. Thus, improper use becomes almost the only source of damage to the respiratory equipment.

References Aerogen—Informationsmaterial (Hygiene und Umgang im Krankenhaus) (n.d.) Bode—Informationsmaterial (Risikobewertung im Krankenhaus) (n.d.) Bundeszentrale für Gesundheitliche Aufklärung (2016). www.­infektionsschutz.­de Covidien—Informationsmaterial (Heimbeatmungslösung, Schlauchsysteme, Reinigung von Shiley-Kanülen, Respi Flow, Standzeiten Aerodyne Omega, Standzeiten Masken, Brillen und Schläuche, Wiederaufbereitung von Flutter) (n.d.) Deutsche Gesellschaft für Krankenhaushygiene e.V. (DGKH) und Deutsche Gesellschaft für Anästhesiologie und Intensivmedizin e.V. (DGAI) (Infektionsprävention) (n.d.)

20

Deutsche Gesellschaft für Pneumologie und Beatmungsmedizin e. V.—Nichtinvasive und invasive Beatmung als Therapie der chronischen respiratorischen Insuffizienz (n.d.) Deutsche Gesellschaft für Sterilgutversorgung—Informationsmaterial (Leitlinie zur Validierung maschineller Reinigungs—Desinfektionsprozesse zur Aufbereitung thermolabiler Endoskope) (n.d.) Dräger—Informatinsmaterial (Handbuch zur Aufbereitung von Geräten und Zubehör) (n.d.) Kassenärztliche Vereinigung Bayern (Hygienische Aufbereitung von Medizinprodukten, Verpackung von Medizinprodukten) (n.d.) Landesamt für Gesundheit und Soziales (LAGuS) M-V, Abteilung 3, Dezernat Krankenhaushygiene (n.d.) Pflegewiki.de—Händedesinfektion (n.d.) Robert Koch Institut (2016), www.­rki.­de Robert Koch Institut—Händehygiene Richtlinien (n.d.) Robert Koch Institut—Informationsmaterial (Empfehlung Medizinprodukte) (n.d.) Robert Koch Institut—Prävention der nosokomialen beatmungsassoziierten Pneumonie (n.d.) Spectaris (Groß et al. 2012), Hygienische Aufbereitung von Hilfsmitteln der respiratorischen Heimtherapie Weinmann—Informationsmaterial (Poster Hygienische Aufbereitung) (n.d.) Wilamed—Informationsmaterial (Atemgasbefeuchtung) (n.d.)

289

Resistance and Compliance Hartmut Lang Contents 21.1

Resistance – 290

21.1.1 21.1.2

S tandard Values – 290 Effect of the Resistance – 291

21.2

Compliance – 293

21.2.1 21.2.2

S tandard Values – 294 Impact of Compliance – 295

21.3

Resistance and Compliance – 297 References – 297

© Springer-Verlag GmbH Germany, part of Springer Nature 2023 H. Lang (ed.), Out-of Hospital Ventilation, https://doi.org/10.1007/978-3-662-64196-5_21

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21.1 

Resistance

Resistance R stands for flow resistance of the airways. It is a measure of the resistance that must be overcome by the airflow during inhalation. The corresponding calculation formula is R=

Pressure difference ∆P mbar = in l Flow Flow s

. Figure  21.1 shows the airway resistance in an intubated patient. Air flows through the tube at a certain flow rate. A tube represents a constriction, an airway resistance. In front of the constriction and behind the constriction the air pressures are measured, called P1 and P2. You will notice that the air pressure P1 before the constriction is higher (20 mbar) than the air pressure P2 after the constriction (15 mbar). The air accumulates in front of the constriction, it is more difficult for it to pass through the constriction and thus the air pressure P1 increases. Behind the constriction the air that has passed through can unfold, because there is enough space there. The air pressure P2 is lower. This results in a pressure difference,  

called ΔP, calculated by P1 − P2. It is given in millibar (mbar). Here is: ∆P = 20 – 15 = 5 mbar The greater the flow resistance R, the higher the pressure difference ΔP at constant flow. Behind the bottlenecks, turbulences form, there is no linear air flow. Air particles are swirled around and a reverse flow can occur, which in turn increases the flow resistance R again. The displayed measured value R corresponds to the pressure loss or ΔP (pressure difference). The higher the value, the greater the airway resistance. The smaller the value, the lower the airway resistance. The tube or tracheal cannula is essential factors that increase the flow resistance R. The resistance can be explained relatively easily by the fact that it is much more difficult to breathe permanently through a thin straw than with a thick straw. The longer and narrower in diameter the ventilation access, the greater/higher the airway resistance, for example tube ID 6.5. The shorter and wider in diameter the ventilation access, the lower the airway resistance, for example tracheal cannula ID 11.0. Therefore, in practice, the largest possible tracheal cannula is selected. It is often observed that patients breathe more easily spontaneously than before after the creation of a tracheostoma and insertion of a large tracheal cannula. 21.1.1 

. Table 21.1 An increase in resistance occurs when the airways are narrowed, regardless of the cause. Possible causes for an increased resistance are 55 Endotracheal tube. 55 Hypersecretion of the airways. 55 Bronchospasm. 55 Emphysema. 55 Stenoses of the respiratory tract.  

..      Fig. 21.1  Schematic representation of airway resistance (Courtesy of Isabel Schlütter)

Standard Values

21

291 Resistance and Compliance

.       Table 21.1  Resistance—standard values Age

Flow resistance R

Non-intubated adults

1–2

Intubated adults

4–6

10-year-old

Approximately 5–20

Newborns

Approximately 25–40

Tube

Approximately 25

21.1.2 

Effect of the Resistance

Pressure Controlled Ventilation In pressure-controlled ventilation, the ventilation pressures Pinsp and PEEP are set. The same pressures are always achieved from breathing cycle to breathing cycle. If the airway resistance R increases due to a narrowing of the airway (secretions, bronchoconstriction, obstruction), the respiratory volume and minute volume will decrease while the ventilation pressures remain constant (. Table 21.2).  

R ↑→ Airways are narrow. If the respiratory volume drops, hypoventilation is imminent. This in turn is measured by an increased pCO2 value in the blood gas analysis or expiratory as increased etCO2. R ↑→ Vt ↓ and MV ↓ and etCO 2 ↑ If the cause of the airway constriction can be eliminated (aspiration, inhalation with bronchodilators), the airway resistance R will decrease. If the cause cannot be eliminated at first, the Pinsp should be increased carefully until an adjusted respiratory volume is obtained for the patient. R ↑→ Vt ↓ and MV ↓→ Pinsp ↑ If the cause of the airway constriction can be eliminated later after increasing the Pinsp, the airway resistance R will decrease and the airway volume Vt will increase again, even

more than appropriate. Now the Pinsp can be lowered again.

Volume-controlled Ventilation In classic volume-controlled ventilation, a predetermined breathing volume is set for the patient. Initially, it is not known how high the ventilation pressure will rise. If the airway resistance R increases due to a narrowing of the airway (secretions, bronchoconstriction, obstruction), the ventilation pressure will increase while the inspiratory volume Vt remains constant (. Table 21.2).  

R ↑→ Airways are narrow. This can be so high that there is a risk of lung damage. The pressure must be limited to a maximum (Pmax, Plimit) to avoid this. This results in pressure-limited ventilation. This, in turn, can lead to a decrease in the respiratory volume and minute volume. R ↑→ Vt still the same but pressure ↑→ Plimit If the cause of the airway constriction can be eliminated by suction or inhalation with bronchodilatatives, the airway resistance R drops and the ventilation pressure also falls.

Pressure-supported Ventilation During pressure-supported ventilation, the ventilation pressures ASB/PS and PEEP are set. The same pressures are always achieved from breathing cycle to breathing cycle. If the airway resistance R increases due to a narrowing of the airway (secretions, bronchoconstriction, obstruction), the respiratory volume and minute volume will decrease with the same distance between ventilation pressures (. Table 21.2).  

R ↑→ Airways narrow If the respiratory volume drops, hypoventilation is imminent. This can be recognized by the elevated pCO2 value in blood gas analysis or expiratory as increased etCO2. R ↑→ Vt ↓ and MV ↓ and etCO 2 ↑

292

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.       Table 21.2  Effect R on ventilation Effect R on ventilation

Vt

MV

etCO2 pCO2

etCO2 ↑ pCO2 ↑

Additionally to observe

Consequences for treatment

Risk involved

Raise Pinsp

High ventilation pressure

High ventilation pressure

Plimit Pmax

VP and MV decrease Hypoventilation

Pressure controlled

R↑

Airways narrow

Vt ↓

MV ↓

Volume controlled

R↑

Airways narrow

Vt same

MV still the same

Pressure supported

R↑

Airways narrow

Vt ↓

MV ↓

etCO2 ↑ pCO2 ↑

Breathing accelerated Panting?!

PASB Psupp raise

High ventilation pressure

Volume-­ controlled-­ pressure-­ regulated

R↑

Airways narrow

Vt ↓

MV ↓

etCO2 ↑ pCO2 ↑

Automatic adjustment of the Pinsp ↑

Plimit Pmax

Vt and MV remain humiliated

PEEP

R↑

Airways narrow

pO2 ↓

Increase PEEP

Over-inflation

Possible effect on the patient: the affected patient experiences the increased airway resistance as strenuous. Taking a breath becomes difficult. To compensate, the patient will breathe faster and fall into tachypnea. Tachypnea may be able to compensate for hypoventilation. However, this will take energy and the patient may become exhausted, anxious or panicky. Breathing becomes “asynchronous”, the patient “struggles” with the respirator. R ↑→ Accelerated breathing, frequency ↑ If the cause cannot be eliminated at first, the ASB/PS should be carefully increased until an adapted breathing volume is obtained for the patient. R ↑→ Respiration accelerated , frequency ↑→ ASB / PS ↑ If the cause of the airway constriction can be eliminated later after increasing the ASB/ PS, the airway resistance R will decrease and

the airway volume will increase again, possibly even higher than appropriate. Now the ASB/PS can be lowered again. In addition, the patient needs increased attention to avoid fear and panic. States of exhaustion must be detected.

Volume-controlled-pressure-­ regulated Ventilation In volume-controlled-pressure-regulated ventilation, the respiratory minute volume is determined directly (ASV) or indirectly by setting the respiratory rate and respiratory volume (AVAPS). If the airway resistance R increases, the ventilation pressure is automatically raised in steps of 2–3  mbar. The user does not need to make any settings (. Table 21.2).  

R ↑→ Airways narrow R ↑→ Vt ↓ and MV ↓→ automatic adjustment of Pinsp ↑

293 Resistance and Compliance

Unfortunately, this can also be so high that there is a risk of lung damage. The pressure must therefore also be limited to a maximum (Pmax, Plimit). This can lead to a decrease in the respiratory volume and respiratory minute volume. The risk of very high ventilation pressures with damage to lung tissue is too great, so that reduced ventilation is temporarily accepted. R ↑→ Vt still the same, but pressure ↑→ Plimit If the cause of the airway constriction can be eliminated (aspiration, inhalation with bronchodilators), the airway resistance R will decrease, and airway volume and minute volume will increase again, possibly even more than appropriate. Now the ventilation pressure is automatically lowered in small steps of 2–3 mbar until an appropriate inspiratory volume and minute volume is reached. Again, no adjustment by the user is ­necessary.

PEEP An increase in airway resistance R can also be caused by the collapse of the airways or alveoli. If the alveoli collapse, ventilation is disturbed and no air containing O2 can enter the alveoli. This means that no oxygen can be absorbed; this can be recognised by the drop in O2 saturation or, in the BGA, by the drop in pO2 value (. Table 21.2).  

R ↑→ Airways narrow , ventilation ↓ R ↑→ pO 2 ↓

21

PEEP serves to stabilize and keep the alveoli and airways open. Therefore, an increase in PEEP can help to keep the alveoli and airways open. Ventilation would be restored and O2 can be absorbed again through the alveoli. pO 2 ↓→ PEEP ↑ Conclusion If the airway resistance is high, the airways are constricted. The Vt and the MV decrease. Airway resistance should be low. A value R >The measured value C indicates how flexible our lungs are. The higher the C value, the greater the stretching capacity. The lower the C value, the lower the stretching ability.

21.2.1 

Standard Values

Age-dependent standard values of elongation are given in . Table 21.3. A decrease in the compliance value indicates a reduced stretching ability. The period of time during which the change takes place provides an indication of the underlying cause (. Table 21.4).  

 

.       Table 21.3  Compliance—standard values Age

Elasticity of the lungs C

Adults

>50–100 mL/mbar

10 years old

Approximately 25

Newborns

Approximately 2.5

.       Table 21.4  Change in compliance Change

Reference to

Within a short time

–  Rigid thorax for coughing –  Unfavourable positioning of the patients –  Pain

For hours or days

–  Pulmonary fluid –  Infiltrates –  Alveolar Collapse –  Increased intra-abdominal pressure

Longer term

–  Structural remodelling of the lungs

∆P = Pinsp − PEEP = −1mbar − +1mbar = 2 mbar ∆V 700 mL mL C= = = 350 ∆P 2 mbar mbar

21

295 Resistance and Compliance

21.2.2 

Impact of Compliance

C ↓→ Vt ↓ and MV ↓ and etCO 2 ↑

Pressure Controlled Ventilation In pressure-controlled ventilation, the ventilation pressures Pinsp and PEEP are set. The same pressures are always achieved from breathing cycle to breathing cycle. If compliance C, the lung’s ability to expand, decreases, for example due to “poor” storage, infiltrates or pulmonary fluid, the lung’s ability to expand will be reduced. If the interval between ventilation pressures remains the same, respiratory volume and minute volume will decrease (. Table 21.5).  

C ↓→ Lung insufficiently expandable If the respiratory volume drops, hypoventilation is imminent. This can be measured by means of an elevated pCO2 value in blood gas analysis or expiratory as elevated etCO2. If the cause of the reduced ability to stretch can be eliminated, compliance C will increase, breath volume and minute volume will increase again.

If the cause cannot be eliminated at first, the Pinsp should be carefully increased until an adapted breathing volume is achieved for the patient. C ↓→ Vt ↓ and MV ↓→ Pinsp ↑ If the cause of the reduced stretching ability can be eliminated later after increasing the Pinsp, compliance C will increase. Also the breathing volume, even higher than appropriate. Then the Pinsp should be lowered again.

Volume-controlled Ventilation In classic volume-controlled ventilation, a predetermined breathing volume is set for the patient. Initially, it is not known how high the ventilation pressure will rise to ensure that the respiratory volume is maintained. If the compliance C decreases, the lung’s ability to expand is reduced and the ventilation pressure increases while maintaining the same breath volume (. Table 21.5).  

.       Table 21.5  Effect C on ventilation Effect C on ventilation

Vt

MV

etCO2 pCO2

MV ↓

etCO2 ↑ pCO2 ↑

Pressure controlled

C ↑ Lungs Vt ↓ insufficiently flexible

Volume controlled

Vt same MV C ↑ Lungs insufficiently still the flexible same

Pressure-­ supported

C ↑ Lungs Vt ↓ insufficiently flexible

Volume-­ C ↑ Lungs Vt ↓ controlled-­ insufficiently pressure-­ flexible regulated PEEP

C ↑ Lungs insufficiently flexible

Additionally to observe

ConseRisk involved quences for treatment Raise Pinsp

High ventilation pressure

High ventilation pressure

Plimit Pmax

Vt and MV decrease, hypoventilation

MV ↓

etCO2 ↑ Breathing pCO2 ↑ accelerated Panting?!

PASB Psupp raise

High ventilation pressure

MV ↓

etCO2 ↑ automatic pCO2 ↑ adjustment of the Pinsp ↑

Plimit Pmax

Vt and MV remain humiliated

Increase PEEP

Over-­inflation

pO2 ↓

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H. Lang

C ↓→ Lung insufficiently expandable C ↓→ Vt same, but print ↑ Unfortunately, this can also rise so high that there is a risk of lung damage. To avoid this, the pressure must be limited (Plimit). This results in pressure-limited ventilation. This can lead to a decrease in the respiratory volume and respiratory minute volume. C ↓→ Vt same, but pressure ↑→ Plimit If the cause of the reduced ability to stretch can be eliminated, compliance C increases and the ventilation pressure decreases.

Pressure-supported Ventilation In pressure-supported ventilation, the ventilation pressures ASB/PS and PEEP are set, which are achieved in each breathing cycle. If the compliance C drops, the lung’s ability to expand is reduced. Therefore, with the same distance between the ventilation pressures, respiratory volume and minute volume will decrease (. Table 21.5).  

an adapted breathing volume is obtained for the patient. C ↓→ Respiration accelerated , frequency ↑→ ASB / PS ↑ If the cause of the reduced ability to stretch can be eliminated later after increasing the ASB/PS, Compliance C will increase and the breathing volume will increase again, possibly more than appropriate. Now the ASB/ PS should be lowered again. In addition, the patient needs increased attention to avoid fear and panic. Exhaustion must be detected.

Volume-controlled-pressure-­ regulated Ventilation In volume-controlled-pressure-regulated ventilation, the respiratory minute volume is determined directly (ASV) or indirectly by setting the respiratory rate and respiratory volume (AVAPS). If the compliance C drops, the ventilation pressure is automatically raised in steps of 2–3 mbar. No adjustment by the user is necessary (. Table 21.5).  

C ↓→ Lung insufficiently expandable C ↓→ Vt ↓ and MV ↓ If the respiratory volume drops, hypoventilation is imminent. This is measured by means of an elevated pCO2 value in the blood gas analysis or elevated etCO2 end expiratory. C ↓→ Vt ↓ and MV ↓ and etCO 2 ↑ The affected patient cannot breathe in sufficiently deeply due to the reduced ability to stretch. It becomes difficult to take a breath and the patient breathes faster to compensate. He becomes tachypneic. The tachypnea may compensate for the hypoventilation. This takes energy and the patient may become exhausted. He is afraid or panicky. Breathing becomes “asynchronous”, the patient “struggles” with the respirator. C ↓→ Respiration accelerated , frequency ↑ If the cause cannot be eliminated at first, the ASB/PS should be carefully increased until

C ↓→ Lung insufficiently expandable C ↓→ Vt ↓ and MV ↓→ automatic adjustment of Pinsp ↑ The Pinsp can increase to such an extent that there is a risk of lung damage. The pressure must be limited to a maximum (Plimit). C ↓→ Vt still the same, but pressure ↑→ Plimit The pressure limitation can lead to a decrease of the respiratory volume and respiratory minute volume. But the risk of damage to lung tissue due to the high ventilation pressures is high, so that temporarily reduced ventilation is accepted. If the cause of the reduced ability to stretch can be eliminated, compliance C will increase, and respiratory volume and minute volume will increase again, even more than appropriate. Now the ventilation pressure is automatically lowered in small steps of

297 Resistance and Compliance

2–3 mbar until an appropriate breath volume and minute volume is reached. Again, no adjustment by the user is necessary.

PEEP A reduction in the stretching ability C of the lungs can also be caused by the collapse of the alveoli. This disrupts the ventilation. No air containing O2 can enter the lungs. This means that no oxygen can be absorbed via the alveoli. This can be seen from the drop in O2 saturation or, in the BGA, from the drop in the pO2 value (. Table 21.5).  

C ↓→ Lung insufficiently expandable, ventilation ↓ C ↓→ pO 2 ↓ PEEP serves to stabilize and keep the alveoli and airways open. It should be checked whether increasing the PEEP helps to keep the alveoli and airways open. Ventilation would then be restored and O2 can be absorbed again through the alveoli. pO 2 ↓→ PEEP ↑ Conclusion If the compliance drops, the ability of the lungs to stretch decreases, Vt ↓ and MV ↓. The compliance values should be high. A value C >50 would be favourable for the patient.

21.3 

Resistance and Compliance

An increase in resistance and a decrease in compliance can usually be observed simultaneously. The patient must be observed to find out the cause of the change. While it is correct to simply rely on the numerical values, the correct interpretation is valuable for the patient. Then therapeutic measures can be taken to help eliminate the cause. With the certainly simple lifting of Pinsp or ASB/PS or, if necessary, the lifting of

21

PEEP, it is possible to temporarily increase the respiratory volume Vt, so that the respiratory minute volume MV, possibly a reduction of the respiratory frequency during spontaneous breathing and an improvement of oxygenation can be achieved. But caring for ventilated patients is more than just adjusting ventilation parameters. The following considerations are also important: 55 Is the patient correctly positioned? –– Or did the patient slip down towards the end of the bed? This reduces compliance! –– Is his upper body elevated 30–45°? This increases compliance! –– Is the patient positioned at hip level for OK elevation? This increases compliance! 55 Does he need to be suctioned? Possibly under bronchoscopic control? Displaced airways increase the resistance! 55 Should bronchodilative inhalation be performed? Obstructive airways increase the resistance! 55 Is the tube/trach tube snapped? Increase the resistance! 55 Is the tube/tracheal cannula continuous? Increase the resistance! 55 Does the patient feel fear, panic, pain? –– If YES: when, permanently or according to specific tasks? Can increase resistance and decrease compliance! 55 Does the patient have a cough? –– If YES: why? –– If YES: when, after which performance does cough occur? Can increase resistance and decrease compliance!

References Larsen R (2012) Anästhesie und Intensivmedizin für die Fachpflege, 8. Aufl. Springer, Heidelberg Berlin Ullrich L, Stolecki D, Grünewald M (2010) Intensivpflege und Anästhesie, 2. Aufl, Thieme Stuttgart

299

Control Mechanisms and Types of Control Hartmut Lang Contents 22.1

Ventilation Control Mechanisms – 300

22.2

Ventilation Control Modes – 300

22.3

Ventilation Modes of Practical Relevance – 301 Reference – 301

© Springer-Verlag GmbH Germany, part of Springer Nature 2023 H. Lang (ed.), Out-of Hospital Ventilation, https://doi.org/10.1007/978-3-662-64196-5_22

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H. Lang

22.1 

Ventilation Control Mechanisms

Depending on the ventilation mode, individual variables are kept constant by the respirator (. Table 22.1).  

22.2 

Ventilation Control Modes

Control modes refer to the respiratory cycle, that is when inspiration and expiration begin and end. Control variables are limiting variables for the course of inspiration (. Table  22.2). Upper limits are specified for pressure, volume and time, which cannot be exceeded. For flow control, a lower limit terminates the inspiration.  

.       Table 22.1  Control mechanisms Volume controlled

Pressure controlled

Synonym: Constant volume or volume guarantee The breathing volume is kept constant by the device, the same volume is always given. If this volume cannot be administered, the respirator displays the alarm message “Volume inconstant”. Synonym: Pressure constant The set ventilation pressure is kept constant, a certain pressure level is not exceeded.

.       Table 22.2  Control types Print control

During inspiration the pressure is built up until a certain value is reached. Once this pressure is reached, the ventilator switches from inspiration to expiration. There is no inspiratory pause.

Volume control

The ventilator switches from inspiration to expiration as soon as the predetermined volume has been administered, without an inspiratory pause. Danger: The inspiratory phase ends when a pre-set volume has been delivered, regardless of where the volume remains, for example in case of a leakage. The volume is delivered, but only part of it reaches the patient. This results in a risk of hypoventilation (→ volume-controlled ventilation is no longer used today, but is often confused with volume-controlled ventilation).

Time control

Inspiration and expiration are in a certain temporal relationship. VCV and PCV work with a time control. It is indicated by the breathing time ratio I:E or T insp, respectively.

Flow control

If the flow rate falls below a certain speed, a certain flow, inspiration is stopped and expiration is initiated. In modern respirators, only works in spontaneous breathing mode, not in mandatory ventilation mode and only after triggering. Trigger mechanisms detect that the patient wants to inhale. The flow control recognizes that the patient wants to exhale again.

301 Control Mechanisms and Types of Control

22

Ventilation Modes of Practical Relevance

55 PSV is a pressure-controlled flow-­ controlled form of ventilation. A ­predetermined air pressure level is not exceeded. The inspiration ends dependThis results in the mixed formulations for ing on the speed of the inspiratory airthe individual ventilation modes: flow. 55 VCV is a volume-controlled, time-­ 5 5 AVAPS/IVAPS is a hybrid of volume-­ controlled form of ventilation, that is a guaranteedtime-­cycled ventilation and pre-determined volume is administered pressure-controlled flow-controlled venwith each breath and inspiration stops tilation after a pre-determined time. 22.3 

55 PCV is a pressure-controlled, time-­ controlled form of ventilation. Here too, the duration of inspiration is predeter- Reference mined. A predetermined air pressure level is not exceeded with each breath. Larsen R (2012) Anästhesie und Intensivmedizin für die Fachpflege, 8. Aufl. Springer, Heidelberg The amount of air is variable. ­Berlin

303

Flow and Flow Curves Hartmut Lang Contents 23.1

Sinus Flow, Constant Flow, Decelerating Flow – 304

23.1.1 23.1.2

S tatements of Flow Curves – 305 Advantages of the Decelerating Flow – 305

23.2

Flow During Volume-controlled Ventilation – 305

23.3

Flow During Pressure-controlled Ventilation – 307

23.3.1 23.3.2 23.3.3 23.3.4 23.3.5 23.3.6 23.3.7

F low Behaviour with Different Steep Ramps – 307 Flow Behaviour at Different Pinsp – 307 Flow Curve for Too Short Expiratory Time – 307 Flow Curve with Too Short Inspiration Time – 308 Flow Trigger – 309 Pressure Trigger – 309 Flow Trigger Versus Pressure Trigger – 310

23.4

Flow Curve in PSV – 311

23.4.1 23.4.2 23.4.3

F low Trigger – 311 Rise or Ramp – 311 Expiratory Trigger – 313

Reference – 314

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304

 inus Flow, Constant Flow, S Decelerating Flow

curve shows that physiological breathing has a breathing time ratio of about 1:2 or 1:1.5. In volume-controlled ventilation, the air Ventilation modes have so far only been preflows at a constant flow rate determined by sented using pressure–time diagrams. On the the user (. Fig. 23.1 centered). An inspiradisplays of modern respirators, however, an tory flow is selected for the ventilation additional airflow curve, the flow curve, can parameters, for example 45  L/min. At this be shown. This chapter is intended to show speed, the air is introduced into the patient the relationship between pressure and flow from the start of inspiration until the predecurves, which is why they are shown one termined volume is administered. The volabove the other in the illustrations. ume is administered when the peak pressure First, the various flow curves are preis reached. The inspiratory air flow curve sented, as they occur during spontaneous has the shape of a square or rectangle and is breathing, volume-controlled and pressure-­ called constant flow. Once the volume has controlled ventilation (. Fig.  23.1). The been administered, the flow curve falls back pressure curve (P = Pressure) is shown at the top and the corresponding flow curve (Flow) to 0, that is no more air flows, either in the tube system or into the patient. This phase is at the bottom of the illustrations. During spontaneous breathing, the air- called the zero flow phase. It lasts until the flow is quite even (. Fig.  23.1 left). The inspiration time is over and the expiration inspiratory airflow curve has the shape of an time begins. With pressure-controlled ventilation, the arc and is called sinus flow. The inhalation is inspiratory airflow curve no longer appears uniform. It begins slowly at first. But the airrectangular. It is more rounded and falls off flow increases rapidly and reaches a maxito the right side. This shape is called decelermum point or speed. Then the airflow is ating flow (. Fig.  23.1 right). The inspirathrottled until it stops completely. The inhatory flow results from the Pinsp and Inspiration lation is complete, the inhalation ends. If Ramp settings. Initially, the airflow is very inhalation is faster, the airflow follows the high, the air flows quite fast at first because dotted curve. At the beginning of the exhathere is a lot of space in the lungs and the lation, the air flows out very quickly at first, airway resistance is low. When the upper air because the lungs are filled with air. In the pressure level is reached, the airflow curve course of time, this airflow also slows down reaches a maximum speed. This is called until the exhalation is complete. The flow 23.1 

23

H. Lang

 

 

 

 

..      Fig. 23.1  Sinus flow with left spontaneous breathing (rapid inspiration: dotted line); constant flow in the middle with volume-controlled ventilation; decel-

erating flow on the right with pressure-­controlled ventilation (Own presentation, edited by Isabel Schlütter)

305 Flow and Flow Curves

PIF (Peak Inspiration Flow). From this point on, the flow speed is reduced, airway resistance is present. The flow speed gradually decreases. If enough air is administered to maintain the upper air pressure level, the flow = 0. The expiratory air flow curve shows a similar shape in all ventilation modes. During expiration, the air flows out of the patient. The flow curve is in the negative or lower range. Since only the valve is opened during expiration, the expiratory flow is very high at the beginning. However, it quickly approaches 0. From the time when the flow is zero again, this phase is also called the zero flow phase. >>If single-hose ventilation systems are used, only the inspiratory flow curve is usually displayed because there is no sensor measuring the expiratory airflow.

23.1.1 

Statements of Flow Curves

The flow curves supplement the information of the pressure curve and allow a more comprehensive assessment of the ventilation situation. The statements of flow curves are: 55 Flow curves show how the air flows into the airways. 55 Flow curves indicate how the air flows out again. 55 The inspiratory flow is positive or in the upper range. 55 The expiratory flow is negative or in the lower range. 55 A calculation of the areas enclosed by the flow curves indicates how much volume is administered and how much volume flows out again. 55 The aim is that the inspiratory and expiratory volumes are equal. 55 Deviations can be detected and give indications of inspiratory or expiratory flow disturbances.

23.1.2 

23

Advantages of the Decelerating Flow

Artificial respiration attempts to simulate physiological respiration in some areas. Pressure-controlled ventilation modes that generate a decentralized flow are closer to physiological breathing than volume-­ controlled ventilation modes with constant flow. Therefore, there are several advantages of the decelerating flow: 55 Peak pressure is avoided. 55 Observance of resistance and compliance. 55 Over-expansion of well ventilated alveoli is reduced. 55 Preventing pendulum air in areas of the lungs with reduced ability to stretch (7 Sect. 10.4.2). 55 In lung areas with reduced compliance, the alveolar opening pressure is reached at the beginning of inspiration.  

23.2 

Flow During Volume-controlled Ventilation

z Peak Pressures and Plateau Phases

The faster you set the flow, the higher and narrower the rectangle of constant flow appears. This means, in relation to the pressure curve, that also the peak pressure is reached earlier and is higher. The zero flow phase during inspiration is longer. Relative to the pressure curve, the plateau phase is also longer (. Fig. 23.2). Conversely, the slower you set the flow, the flatter and wider the rectangle of constant flow appears. This means that the peak pressure is reached later and is lower. The zero flow phase during inspiration is shorter. In relation to the pressure curve, the plateau phase is also shorter. In contrast, there are no differences in flow during expiration.  

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..      Fig. 23.2  Peak pressures and plateau phases at different flow rates (Own representation, edited by Isabel Schlütter)

Practical Tip

Since high pressure peaks should be avoided, it is recommended to set the flow more slowly. The air will then flow more evenly. There is less turbulence, which also increases the airway resistance.

Modern ventilators design the flow in such a way that it is maintained upright throughout the entire inspiratory period. This prevents the development of peak pressure.

307 Flow and Flow Curves

23.3 

Flow During Pressure-controlled Ventilation

23.3.1 

23.3.2 

Flow Behaviour with Different Steep Ramps

23

 low Behaviour at Different F Pinsp

The height of the Pinsp is adjusted to create an adequate breathing volume for the patient. The Pinsp is therefore individually different in height. The higher the Pinsp is set, the faster the flow will be (. Fig. 23.4 left). The flow is promoted quickly and reaches its maximum very quickly. A high air flow is generated. The lower the Pinsp is set, the lower the flow will be (. Fig. 23.4 right). The flow will also increase rapidly, but its maximum will be lower. This will result in an air flow that is slower overall.  

The ramp defines the time within which the ventilation pressure Pinsp should be reached. This can be done quickly, for example within 0.0–0.1 s or if a low level is set (levels 1 and 2, 7 Chap. 9) (. Fig.  23.3 left). Then the flow is conveyed very quickly and reaches its maximum very quickly. This results in a fast and high air flow. The ramp can also be flatter, the increase is slower, for example within 0.3–0.5 s or if a higher level is set (levels 3–5, 7 Chap. 9) (. Fig.  23.3 right). Then the flow will increase more slowly, its maximum will be reached a little later. This results in a flow of air whose overall increase is slower and lower.  

 

 

23.3.3 

 low Curve for Too Short F Expiratory Time

 

 

If the expiration time is too short, the flow does not return to 0 (. Fig.  23.5 dashed line). The expiratory time is too short for complete expiration. This results in an “intrinsic PEEP”.  

..      Fig. 23.3  Flow behaviour with ramps of varying steepness. Steep ramp or fast rise → fast high flow (left) and flat ramp or slow rise → slow low flow (right) (Own representation, edited by Isabel Schlütter)

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..      Fig. 23.4  Flow behavior with different Pinsp. High Pinsp, fast high flow (left), low Pinsp, fast but low flow (right) (Own representation, edited by Isabel Schlütter)

Release Ventilation) ventilation mode makes use of this, because there the expiratory phases are intentionally kept short in order to produce a therapeutically higher PEEP. Be Careful When Setting the Parameters, Because This Flow Behavior Occurs: 55 Increase in respiratory rate with the same time for Tinsp. 55 Reduction of the expiration time. 55 Risk if the I:E ratio is less than 1:1.5 or even with reversed I:E, where the inhalation time is longer than the exhalation time. ..      Fig. 23.5  Flow if expiratory time is too short, dashed line end expiratory flow (Own representation, edited by Isabel Schlütter)

23.3.4 

Not all the air in the lungs is exhaled, but a residual volume remains. This is added to the volume of air administered during the next inspiration. A permanent positive internal air pressure is created, the so-called “intrinsic PEEP” or “intrinsic PEEP”, also called “Auto-PEEP”. The difference to the set PEEP is that it is achieved by means of ventilation. The clinically relevant APRV (Airway Pressure

The decelerating flow is maintained during the whole time of inspiration. At the end of inspiration, however, it does not decrease towards 0 (. Fig.  23.6 dotted line), but remains positive. Then expiration begins and the air is released. A “landing” appears in the inspiratory flow curve. In this case, the duration of the inspiration time was too short. It is not sufficient to administer the volume achievable with the

 low Curve with Too Short F Inspiration Time

 

309 Flow and Flow Curves

..      Fig. 23.6  Flow curve with too short inspiration time, dotted line end inspiratory flow (Own ­representation, edited by Isabel Schlütter’s)

set pressure → lung areas with reduced ability to expand are not sufficiently ventilated. Be Careful When Setting the Parameters, Because This Flow Behavior Occurs: 55 Increase of the respiratory rate with constant I:E. 55 Reduction of the time for Tinsp. 23.3.5 

Flow Trigger

Modern respirators recognize the patient’s own breathing efforts. These should also be supported. The patient must generate a certain amount of self effort in breathing. If he does so, an air flow is created. When a predetermined threshold is reached (. Fig.  23.7 dashed line in the lower flow curve), the respirator detects this and the Pinsp ventilation pressure is now administered synchronously with the patient’s breathing. This flow curve is exaggerated for better recognition, because a flow trigger of 2–5 L/ min is usually set on the respirator. This is usually not visible on the displayed flow curve on the ventilator. It is also possible to set a level that reflects a degree of difficulty, for example levels 1 and 2 are rather easy, levels 3 and 4 are rather medium to difficult.  

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..      Fig. 23.7  Flow trigger. Trigger threshold is shown as a dashed line in the lower flow curve (Own display, edited by Isabel Schlütter)

The flow trigger function enables controlled ventilation and spontaneous breathing to be synchronized. This is implemented in almost all ventilation modes: 55 In pressure-controlled PCV ventilation, a patient can trigger an additional ventilation stroke using the flow trigger. This means that the number of measured ventilation strokes exceeds the number of ventilation strokes set in the menu. 55 The same applies to the volume-­ controlled-­pressure-regulated ventilation mode. 55 With SIMV and BIPAP or BiLevel, the flow trigger can be used to adapt the administration of the ventilation strokes to the patient’s spontaneous breathing and thus synchronize them. As a result, the respiratory time ratio I:E may change slightly. 55 The same applies to MMV and ASV (clinical modes). 23.3.6 

Pressure Trigger

Modern respirators recognize the patient’s own breathing efforts. These should also be supported. The patient must generate a cer-

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..      Fig. 23.8  Pressure trigger. Trigger threshold: dashed line in the upper pressure curve (Own representation, edited by Isabel Schlütter)

tain amount of self effort in breathing. If he does so, a slight negative pressure is created. When a predetermined threshold is reached (. Fig.  23.8 dashed line in the upper pressure curve), the respirator detects this and the Pinsp ventilation pressure is now administered synchronously with the patient’s breathing. This pressure curve is exaggerated for better recognition, because a pressure trigger of −1 to −2  mbar is usually set on the respirator. This is usually not visible on the displayed pressure curve. It is also possible to set a trigger level which then reflects the degree of difficulty, for example levels 1 and 2 are rather easy, levels 3 and 4 are rather medium to difficult. This is usually not visible on the pressure curve. If a patient breathes in spontaneously, a slight negative pressure is created, which falls slightly below the PEEP level. This simultaneously triggers an air flow, a flow. This flow is also shown exaggeratedly above for better recognition. The pressure trigger enables a synchronization of controlled ventilation and spontaneous breathing. This is realized in some ventilation modes: 55 With volume-controlled VCV, a patient can trigger an additional ventilation  

stroke using the pressure trigger. This means that the number of measured ventilation strokes exceeds the number of ventilation strokes set in the menu. 55 In many older home ventilation devices, the pressure trigger in A-PCV mode performs the same function. 55 With volume-controlled SIMV, the pressure trigger is used to adapt the administration of the ventilation strokes to the patient’s spontaneous breathing and thus synchronize them. This may cause a slight change in the I:E respiratory time ratio. Here too, it is mostly older intensive care ventilators that have the pressure trigger but no flow trigger function yet. 23.3.7 

Flow Trigger Versus Pressure Trigger

A pressure trigger works by the ventilator still keeping the inspiration valve closed when the patient starts to breathe. The patient therefore initially breathes in against a closed valve. The air flow is interrupted. This enables the device to measure the negative pressure that is created during spontaneous breathing. The valve only opens when a set threshold is reached. The inhalation can be perceived as “chopped off ” or interrupted. This triggers asynchrony. The patient “draws in” the air and must fight for it, “fight”. This in turn increases the effort of breathing and can lead to rapid respiratory exhaustion. A flow trigger enables a patient to breathe more easily spontaneously. The inspiration valve is open at all times and air can flow. During inspiration, the patient does not have to “pull” the air strongly. The air flow during inspiration is not interrupted, but continuous. The transition until the flow trigger threshold is reached and the transition to administering the inspiratory stroke is almost seamless.

311 Flow and Flow Curves

Conclusion The following applies to both trigger types: the sensitive setting of the respective trigger threshold determines the success of synchronicity of spontaneous breathing and controlled or assisted ventilation. If the respective threshold is set too high, the patient cannot generate either the flow or the negative pressure that leads to the triggering of the ventilation stroke or air pressure support (PS) during spontaneous breathing (PSV). Consequently, the patient does not receive a ventilation stroke. Hypoventilation is the risk here. Breathing effort is increased and leads to respiratory exhaustion.

23.4 

Flow Curve in PSV

The further possibility of a “stair landing” in the flow curve is available in PSV.  Here, the duration of the inspiration is not too short, as this is not predetermined in PSV, but the stair descent is intentional. The reason is the control mode of the ventilation. Types of control determine the breathing cycle, that is when the inspiration begins and when it ends. ASB or PSV is a flow-­controlled form of ventilation. The different influencing factors are shown below. 23.4.1 

Flow Trigger

In ASB/PSV, the respirator detects the patient’s inhalation efforts. These should be supported. The patient must breathe in vigorously until a flow is generated that corresponds to the set trigger threshold, for example 5 L/min. If the patient reaches this threshold, he receives the PS for his inhalation (. Fig.  23.9). If the patient  

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does not reach this threshold, he will not receive PS. 23.4.2 

Rise or Ramp

It is determined how fast the air PS should be reached, or how fast the high air pressure level of the PS should be reached. This is set with the ventilation parameter rise or ramp (. Fig. 23.10). Usually a short time is set, for example 0–200 ms or 0.0–0.2 s. This makes it easier for a patient with weakened, exhausted respiratory muscles to breathe. The shorter the time for the rise or ramp is selected, the faster the air pressure level of the PS is reached. And the faster the air flow generated by the ventilator. Definitely up to 60–80 L/min (1–1.3 L/s). 55 Advantage for the patient: Facilitation of breathing work, important in cases of respiratory distress. 55 Disadvantage: Sometimes the patient feels the support as: “too much pressure”.  

The longer the time for the rise or ramp is selected, the slower the air pressure level of the PS is reached and the slower the air flow (flow) generated by the ventilator. Advantage for the Patient: 55 Air does not come that fast. 55 Is perceived as more pleasant. 55 Air can be distributed more evenly in the lungs. 55 Patients with “restrictive” lung diseases may benefit. Downside: 55 Patient must inhale with exertion, “draw air”. 55 Airtight feeling. 55 Can cause renewed exhaustion.

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..      Fig. 23.9  Flow trigger at PSV (Own display, edited by Isabel Schlütter)

..      Fig. 23.10  Rise or ramp. Fast rise (left) and slow rise (right) (Own representation, edited by Isabel Schlütter)

313 Flow and Flow Curves

23.4.3 

Expiratory Trigger

The expiration trigger is named differently depending on the device: 55 Exsp. Trigger 55 Tg (E) 55 ETS A patient breathes spontaneously in ASB or PSV mode and receives air PS. The ventilator must also recognize when the patient’s own inhalation is complete and exhalation should begin. The ventilation parameter expiration trigger is available for this purpose. z Functional Principle Expiration Trigger

The ventilator constantly measures the air flow generated. Relatively quickly, usually at the beginning of inspiration, a maximum airflow velocity (a maximum flow), the PIF,

23

is reached. This value is stored by the ventilator and is set equal to 100%. In the further course of inspiration, the air flow decreases more and more. From a certain value, which is set with the parameter TgE/ETS E, exhalation is initiated (. Fig. 23.11). This value can be variably adjusted and in practice is usually 25% and means that if the air flow drops to such an extent that only 25% of the previously measured maximum air flow velocity PIF is reached, exhalation is initiated. The higher the % number is, the earlier the exhalation is initiated/triggered.  

kTgE/ETS Set with Low % Number

If TgE is real 40% in real terms, inhalation is shorter and exhalation may be easier. This offers the patient (also experienced in self-experiments!) the advantage of easier exhalation, during which he does not have to exert pressure and exhale without strain.

Reference Rittner F, Döring M (2013) Kurven und Loops in der Beatmung. http://www.­draeger.­com/sites/assets/ PublishingImages/Products/rsp_evita_infinity_ v500_sw2/DE/9097420Kurven-­Loops-­Fibel-­DE-­ 230513.­pdf. Recherche 20.05.2015

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Alarms and Alarm Settings Hartmut Lang Contents 24.1

Alarm Message Levels – 316

24.2

Special Alarms – 316

24.2.1 24.2.2 24.2.3 24.2.4 24.2.5

Airway Pressure/Pmax – 316 Minute Volume – 317 Breathing Volume – 317 Respiratory Rate – 318 Apnea Time/Apnea Ventilation/Back-up Setting – 319

Reference – 319

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24.1 

Alarm Message Levels

There are usually three levels of alarm messages, which are indicated both visually and acoustically. 55 Alarm messages with the highest priority: usually with red optical signals and a longer, constantly repeating, very urgent tone sequence. 55 Alarm messages with medium priority: usually with red or yellow optical signals and tone sequences that are not as intrusive. 55 Low priority alarms: usually with yellow visual signals and a single tone sequence. Possible selectable alarms: 55 Airway pressure (Paw). 55 Low airway pressure (PEEP). 55 Minute volume low. 55 Minute volume high. 55 Breath volume deep. 55 Breath volume high. 55 Respiratory frequency high. 55 Low breathing frequency. 55 Apnea time. The user must set limits for these alarms. These should also be checked by the employee at the beginning of each shift. If necessary, they can be adapted to the conditions of the patient. They are therefore not rigid. When selecting the alarm limits, they should give the user a timely indication if an alarm situation occurs and the patient is endangered. The alarm limits should not be too far apart, otherwise there is a risk that an alarm situation will not be detected in time. However, the alarm limits should also not be too close together. Otherwise, alarm notices could be shown that do not endanger the patient at all. The result would only be an unbearable acoustic burden, especially for the patient who is lying directly next to the ventilator.

Modern ventilators also initially set the alarm limits for the user, but the alarm limits are set by the ventilation center. These must be re-checked and adjusted after a final ventilation setting has been made. 24.2 

Special Alarms

24.2.1 

Airway Pressure/Pmax

This airway pressure limit (Paw, Pmax, Ppeak) should protect against unintentionally high air pressures and should not be exceeded, because high air pressures can damage lung tissue and lead to barotrauma. High air pressures are reached in inspiration. >> Usually, an air pressure limitation between 30 and 40 mbar or cm H2O is selected.

There are two possibilities how this limit works: 1. If an air pressure exceeds the set limit, the air pressure is limited, that is the air pressure cannot rise above the set limit. However, this does not necessarily mean that the inspiration phase is interrupted. It can be maintained according to the set inspiration time (Tinsp). 2. Function with volume-­controlled ventilation: However, if air pressure exceeds the set limit by more than 10 mbar, inspiration is interrupted. The overpressure valve or expiration valve is opened, the air is released and the air pressure in the lungs drops back to the set PEEP. Possible causes of the “Airway pressure too high” alarm: 55 Alarm limit was exceeded. 55 Patient coughs. 55 Patient “presses”, breathes against the device. 55 Secretion transfer of the tube/tracheal cannula. 55 Bent ventilation accesses.

317 Alarms and Alarm Settings

Possible causes for the “Airway pressure too low” alarm: 55 No tightness of the hose system. 55 Leakage. 55 Cuff sleeve is not sufficiently blocked  resulting in leakage. 55 Disconnection. 55 Tracheoal cannula dislocated. Airway pressure low/PEEP low: This alarm is intended to warn the user when the air pressure in the ventilation system is too low. >>Setting: approximately 2–3  mbar/cm H2O below the PEEP level.

The PEEP setting determines the minimum air pressure that should be maintained. If the air pressure falls below this minimum pressure, an alarm is triggered. Low air pressures are reached in the exhalation phase. Possible causes for too low air pressure: 55 Ventilation hose system has a defect or leak. 55 Ventilation hose system is not properly connected, too loosely attached. 55 Cuff sleeveof the tracheal cannula not sufficiently blocked, resulting in air leakage 55 Dislocation of the tracheal cannula. 55 Patient triggers, breathes in and thereby generates a lower pressure than the PEEP level, adjust the alarm limit here! 24.2.2 

Minute Volume

The minute volume (MV) is calculated from the respiratory frequency (f) and the respiratory volume (Vt): f × Vt = MV. z Example

14 × 500 mL = 7 L/min Within certain ranges, the ventilation and ventilation of patients is not endangered. Below a limit, however, there is a risk that patients are not adequately ventilated. There is a risk of hypoventilation and, as a

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result, insufficient exhalation of CO2. This results in the threat of CO2 anaesthesia. Above a limit there is a risk of hyperventilation. This can result in hypocapnia with possible tetanic spasms. Possible causes for alarm “Minute volume too high”: 55 Patient breathes too fast, he hyperventilates. 55 Unintentional hyperventilation due to incorrect parameter setting. 55 In the A-PCV also both possible. >>Recommendation for the alarm setting: average MV + 50%, in the above example 7 L/min + 50%, that is at 10.5 L/min.

Possible causes for “Minute volume too low” alarm: 55 Hypoventilation of the patient. 55 Unintentional hypoventilation due to incorrect parameter setting. 55 Airway obstruction. 55 Relocation of the tube. 55 Airway obstruction. 55 Leakage in the hose system. >>Recommendations for the alarm setting: average MV − 50%, in the above example 7 L/min − 50%, that is at 3.5 L/min.

24.2.3 

Breathing Volume

For adequate ventilation, a patient should be given a respiratory volume (Vt, AZV) of 6  mL/kg KG based on his or her ideal weight. In home ventilation, however, people also aim for higher RVs, as otherwise their lung ventilation is insufficient. This is the case for people with restrictive lungs (OHS, high cross-section, thoracic-­ restrictive diseases). They must be given a guaranteed breathing volume. Here too, a certain amount of variation is permitted without endangering the patient. The RV is a proportion of the minute volume, so the risks correspond to those

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already described for the minute volume (7 Sect. 24.2.2). Possible causes for the “Breathing volume too high” alarm: 55 Patient breathes too deeply because the PS support is too high. 55 Air pressures too far apart because the distance between PEEP and Pinsp is too great (with pressure-controlled ventilation). 55 Vt selected too high (with volume-­ controlled ventilation).  

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>>Recommendations for the alarm setting: average RV + 50%.

Possible causes for the “Breathing volume too low” alarm: 55 Hypoventilation of the patient: –– Patient breathes too shallowly, for example if the dressing dosage is too low or the positioning is unfavourable. –– Possibly too little PS support. 55 Air pressures set too tight, that is the distance between PEEP and Pinsp is too small (with pressure-controlled ventilation). 55 Vt set too low (with volume-controlled ventilation). 55 Airway obstruction. 55 Relocation of the tracheal cannula or tube. 55 Airway obstruction. 55 Leakage in the hose system. >>Recommendations for the alarm setting: average AZV − 50%.

For people who need to be administered a guaranteed minimum respiratory volume, this is set in the setting parameters. In the case example from 7 Chaps. 9 to 7 11, the patient should receive at least 550  mL air per breath. If this is not achieved with the  

pressure settings, the mode changes automatically to volume-controlled and pressure-regulated ventilation. However, this is not shown in the display of the respirator. In the above example, the ventilation mode is still called A/C-PCV. 24.2.4 

Respiratory Rate

An adult person breathes at a frequency (f or AF) of approximately 12–20×/min. When ventilating, comparable breathing frequencies are usually chosen. Here too, a certain variation is permitted without endangering the patient. The respiratory rate is a proportion of the minute volume, so the risks are the same as those already described for minute volume (7 Sect. 24.2.2). Possible causes for the “Respiratory rate too high” alarm: 55 Patient breathes too quickly (tachypnea): –– Patient has fear or pain or both and breathes faster because of it. –– Possibly trigger in PS too low, thus auto triggering with resulting frequency increase. –– Patient threatens to exhaust himself. 55 Ventilation frequency f selected too high  

>>Alarm setting recommendations: 30–35 breaths/min.

Possible causes for the “Respiratory rate too low” alarm: 55 Patient breathes too slowly (bradypnoea), for example: –– If analgosedation is too deep. –– Patient is already exhausted. 55 Ventilation frequency f selected too low.

 

>>Recommendations for alarm setting: 8 breathing cycles/min.

319 Alarms and Alarm Settings

24.2.5 

Apnea Time/Apnea Ventilation/Back-up Setting

Nearly all ventilators display the “Apnea time” or “Apnea ventilation” alarm and leave the choice up to 60 s. Values between 15 and 30 s are usually selected. Often modern ventilators are pre-configured with an apnea time of 15 s as the start setting. The device thus gives an alarm, one with a very high priority, if the apnea time is set to longer than 15 s. If the time is set to 30 s, the alarm will not go off until after 30 s. On some ventilators, apnea ventilation must first be activated, others have always been active for safety reasons. This means that apnea ventilation does not always follow automatically when an apnea alarm is displayed. It makes sense that active apnea ventilation is always activated on the device. This is especially true for patients who breathe completely on their own with PS support. This is usually done with the back­up settingwhere a minimum breathing rate, a Tinsp or an I:E ratio is entered. These patients may become tired or exhausted and thus stop breathing. Apnea ventilation is intended to enable them to breathe. Apnea ventilation starts after a certain time (can be set as an apnea time). It is often accompanied by visual and acoustic alarms of the highest priority. However, if people in PSV mode are often unlikely to breathe on their own, the back-up setting becomes active. Very rarely is this coupled with an alarm, as people are

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expected to stop breathing. This often happens during rest periods, for example at night. The patients should then not be awakened by alarm sounds. Apnea ventilation is performed as volume or pressure controlled ventilation. The settings of the ventilation parameters are usually preconfigured by the ventilator, sometimes they must be set separately. If a back-up setting is active because the patient is no longer breathing, the ventilation mode will automatically change to pressure-­ controlled ventilation without being shown in the ventilator display. The level of pressure support PS automatically becomes the ventilation pressure. If the person actively breathes on his own again after his resting phase, it becomes PSV breathing again. z Combination of Back-up and Breath Volume and Breathing Rate

In order to ensure ventilation during apnea and the respiratory volume deemed necessary, it is very often observed that all inputs have already been made by the ventilation center. They are therefore not alarms at all, but ventilation settings. Patients are expected to be exhausted and/or hypoventilating. This is prevented by the combined ventilation settings.

Reference Schäfer S, Kirsch F, Scheuermann G, Wagner R (2011) Fachpflege Beatmung, 6. Aufl. Urban & Fischer, Elsevier München

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Ventilation Measured Values Hartmut Lang Contents 25.1

Measured Values – 322

25.1.1 25.1.2 25.1.3 25.1.4

 ressure Values – 322 P Volumes – 323 Frequency Values – 323 Further Measurement Parameters – 324

25.2

Ventilation Protocol – 325 References – 327

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25.1 

Measured Values

25.1.1 

Pressure Values

z Peak Pressure

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This is the maximum air pressure measured during a breathing cycle, also called pressure peak (Ppeak) or PIP (Peak Inspiration Pressure). As a rule, this should correspond to the Pinsp during pressure-controlled ventilation and to the PEEP plus PS during PSV ventilation. However, there are always small deviations, which are not dangerous for the patient. z Minimum Pressure

The minimum air pressure measured during a breathing cycle, also called “pressure minimum” (Pmin). As a rule, this should correspond to the PEEP during ventilation. However, there are always small deviations, which occur especially at the onset of spontaneous breathing. The contraction of the respiratory muscles during spontaneous breathing and triggering causes a brief drop in pressure even below the PEEP level. This value is then measured and displayed (. Fig. 25.1).  

z PEEP

The “PEEP”, the positive air pressure at the end of the exhalation phase (expiration phase), checks whether the set PEEP corresponds to the measured PEEP.  Mostly it matches, sometimes there are small deviations that are not dangerous for the patient. z Respiratory Fluid Pressure

The ventilator calculates the respiratory medium pressure, or “pressure mean” (Pmean), for each breathing cycle. It is the mean value of the peak pressure Ppeak /Pinsp and the PEEP. z Example

Pinsp = 20 mbar PEEP = 8 mbar Calculation of the mean value: 20 + 8 = 28:2 = 14 mbar. In the ventilation of adults, this measured value has a subordinate role. While it is of great importance in the ventilation of premature and newborn infants and provides information on whether the airways remain open during the entire respiratory cycle. 55 The higher the mean pressure, the more likely it is that the airways will remain open. 55 The lower the mean pressure, the greater the risk of respiratory collapse.

..      Fig. 25.1  Pmin with triggering (Own display, edited by Isabel Guckes)

323 Ventilation Measured Values

25.1.2 

Volumes

z Respiratory Minute Volume

The ventilation or breathing volume that reaches the patient’s lungs within 1 min is also called MV. It is calculated from the respiratory volume (Vt) × respiratory rate (f/AF). z Spontaneous Respiratory Minute Volume

This is the MV inhaled through spontaneous breathing (MV spontaneous). Many forms of breathing allow spontaneous breathing, such as PS or AVAPS. The proportion of the total MV is measured as described above. The proportion of MV achieved by spontaneous breathing activity is shown separately in the measured values. In the case of augmented ventilation modes, there are indications of how large the proportion of spontaneous breathing currently is. z Inspiratory Volume

The respiratory volume (AZV) or tidal volume “volume tidal” (Vt or Vti) measures how many milliliters (ml) of air enters the patient during inspiration. The patient should receive an appropriate volume of air per breath. In pressure-controlled and pressure-­ regulated ventilation, this is achieved indirectly by the difference between Pinsp and PEEP. In volume-controlled ventilation, the set volume should correspond to the measured inspiratory volume. In PSV ventilation, a corresponding Vt is achieved indirectly by the difference between PS and PEEP. z Expiratory Volume

The volume tidal expiration (Vte) indicates how many millilitres (ml) of air comes out of the patient’s lungs during expiration. There will be variations between Vt and Vte. These deviations occur rather rarely during controlled ventilation and are small. However, greater deviations may occur during spontaneous breathing. Inhaled and exhaled air volumes do not always corre-

25

spond in one breathing cycle. In the course of a minute, however, they usually balance out. Caution is required if the inhaled (inspired) air volume is always greater than the exhaled (expired) air volume. This can lead to unwanted air accumulation in the lungs, which increases the air pressure inside the lungs. This contributes to the development of “intrinsic PEEP”. This would then also increase the PEEP and pmean readings (7 Sect. 25.1.1).  

>>The Vte is only measured if a two-hose system is used.

25.1.3 

Frequency Values

z Ventilation Frequency

The ventilation frequency, fmand or AFmand is given in “breaths per minute” (bpm) or AZ/ min (=breathing cycles per minute). It is measured and counted how often a patient is ventilated per minute in controlled ventilation. This should correspond to the set ventilation frequency f or AF. z Spontaneous Breathing Rate

During A-PVC ventilation, a patient can trigger further ventilation strokes. The proportion of the frequency that is generated by the patient’s own spontaneous breathing is indicated in the measured values (spontaneous breathing phases, fspontaneous or AFspontaneous). Only the respiratory frequency that the patient generates through spontaneous breathing or through his own breathing per minute is measured. In pressure-­supported PSV breathing, the number of times the patient breathes on his own is measured and counted. z Respiratory Rate

For the respiratory rate (f or AF), it is measured and counted how often a patient is ventilated per minute. Since the patient can

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trigger further ventilation phases in A-PCV mode and can also breathe spontaneously in PSV mode, it can happen that the measured respiratory rate is higher than the set ventilation rate. Here, mandatory and spontaneous frequency are usually added together. 25.1.4 

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Further Measurement Parameters

z Breath–Time Ratio I:E

The inspiratory–expiratory ratio (I:E or Ti / Ttot) indicates the temporal relationship between the inhalation and exhalation phases. In controlled ventilation, this value is determined by the setting of ventilation rate and Tinsp. This means that it is usually the same. However, if the patient triggers further ventilation phases, the breathing time ratio also changes. The most commonly used breathing time ratio of 1:2 will then be changed, for example 1:1.5. In PSV ventilation, the ventilator recalculates the ­ breathing time ratio with each breath of the patient. Therefore, this value may vary considerably, for example 1:1.3 but sometimes also 2.1:1. kBreath–Time Ratio Ti/Ttot

In this variant of measuring the breath–time ratio, the entire respiratory cycle, consisting of inspiration and expiration, is referred to as Tdead and assigned the value 100% or the integer 1. The portion used for inspiration Ti is therefore always only a part of the 100%, for example 30%. This value is displayed. The portion used for inspiration Ti is therefore always only a part of the integer 1, for example, 0.3. This value is displayed. z Inspiration Phase, Inspiration Time

The duration of the inhalation phase, “time inspiration” (Tinsp or Ti) is given in seconds. In controlled ventilation, this value is fixed, so the set value and measured value corre-

spond. In ASB/PSV ventilation, almost every breath of the patient is different from the previous one. How long the inhalation phase lasts for the patient’s spontaneous breathing is measured by the ventilator anew with each breath. Therefore, there can also be strong variations. z Expiration Phase, Expiration Time

The duration of the exhalation phase, “time exspiration” (Texsp or Te) is given in seconds. This is only a measured value, as normally no predetermined expiration phase is set on the respirator. The duration of the exhalation phase results either from the settings f or AF and the inspiration time Tinsp or Ti. Or it results from the setting of the respiration time ratio I:E or Ti/Ttot. z Resistance

Section 7 21.1  

z Compliance

Section 7 21.2  

z Rapid Shallow Breathing Index (Sect. 7 30.6)  

The RSB or RSBI or f/Vi is displayed in spontaneous breathing mode PSV and is a quotient between spontaneous breathing rate and measured inspiratory volume. It gives an indication of the respiratory capacity (Sect. 7 2.1.1 Muscular capacity and exertion) of a patient. 55 The smaller the value, the stronger the patient is. 55 The higher the value, the less strength and endurance a patient has for spontaneous breathing.  

>>The RSBI is also displayed in A-PCV mode on the Respirator Astral (ResMed). However, the RSBI will be constant. It is only a display value which does not make any statement about the breathing capacity of the patient.

325 Ventilation Measured Values

z % Trigger

With A-PCV it is measured how often the person triggers an additional ventilation stroke and is displayed as a % value. z Example

15 ventilation cycles/min and additionally 3 triggered breathing cycles  =  18 measured breathing cycles. Then a calculation of three sets: 18 AZ = 100%. How many % is 3 AZ then? % trigger = 16.6% In PSV mode, you would expect to get 100% trigger. However, if the person is exhausted and can no longer breathe independently, the back-up ventilation function is automatically activated and the person is fully ventilated. In this way, a 0% trigger can also occur in PSV mode. z Oxygen Concentration

With the O2 concentration, a comparison of the set with the real measured O2 concentration is carried out. >>If there is a large deviation, permanently greater than 3%, there will be a fault in the respirator. The device may no longer be used and must be replaced. The technical service must be informed.

25.2 

Ventilation Protocol

A ventilation log is usedfor documentation and thus for recording the measured values of the ventilation settings (. Fig.  25.2). Such a protocol could be supplemented by the ventilation settings specified by the ventilation center or the attending physician. The recorded measured values should also be used to assess the ventilation. The protocol is assigned to a patient. It records which respirator he is supplied with and whether there is a second device. This is required for patients whose ventilation dura 

25

tion is greater than 16 h/day. The ventilation duration is documented in hours during the day and at night. In this way, it is possible to assess whether the duration changes over time. As a rule, the ventilation duration is also specified by the ventilation center or the attending physician as a medical prescription (AVO). It is recorded with which ventilation access the patient is provided with, invasively with tracheal cannula and size of TK or non-invasively with NIV mask and size. The manufacturer of the ventilation accesses could also be listed here. The type of respiratory gas humidification is indicated, active humidification or passive humidification with an HME filter. A ventilation should always have a respiratory gas humidification. The corresponding systems have been prescribed by a doctor. The individual measured values are written down with date and time. Not all values mentioned in 7 Sect. 25.1 need to be documented. The values listed in the example are sufficient to be able to assess ventilation. The temporal documentation interval can be arranged variably. For people whose ventilation is not stable and regular, for example in the case of fever and respiratory tract infections, a tighter time interval seems to be appropriate. The interval should depend on the patient’s state of illness and can be 2 h if necessary. If ventilation is stable, documentation at each shift change will be sufficient. People’s sleep should not be disturbed by over-motivated documentation. In addition, there is memory in the respirator, so that it is possible to add the measured values. The measured values will vary, so the respective documentation is only a snapshot of the ventilation. However, if the values move within a range, the changes are not critical. This frame is also determined by the alarm limits (7 Chap. 24). It is possible that a change can be observed over days, weeks or months. It is also the responsibility of  

 

Ventilation Protocol

SIMV

EPAP PEEP

Frequency or Respiration Rate

time

P peak PIP PEEP

Frequency or Respiration Rate

T insp

Spont. Freq.

I:E

Trigger

T insp Ti (inspiration time)

(level) or declaration in l / min.

AVAPS

I:E

V ti

or Ramp (level)

(in sec)

Rise time

Andere

..      Fig. 25.2  Example of GHP Pflegedienst Hamburg and surroundings (Courtesy of GHP Pflegedienst in Hamburg and surroundings)

Date

Measured values /data (essential to be documented) :

IPAP P insp

Ventilation-settings the doctor or the hospital made: (please fill in) :

PSV

25

A-PCV

Ventilation-Mode the doctor or the hospital made: (please mark):

Desease of patient that leads to ventilation: ___________________________________________________

Name of Ventilator (Name): _____________________________

V te

O2 ( l / min) O2 ( % )

326 H. Lang

327 Ventilation Measured Values

25

professional carers to determine and assess these changes. This documented information must be passed on to the treating physician.

goal could even be to achieve a large degree of spontaneousization and weaning from the respirator.

Examples of Measured Value Changes: 55 If the values deteriorate, the AZV and AMV may decrease, although the ventilation pressures have not changed. If this occurs within a short period of time (hours, days), the patient’s ventilated lungs or general condition may have deteriorated acutely. 55 But values could also improve. If, for example, AZV and AMV increase with constant pressure over time, this could indicate an improvement in the lungs. The physician would have to decide whether the ventilation pressures could be reduced. 55 If, for example, the spontaneous breathing rate increases, this could indicate that the patient’s own breathing is increasing and the patient may need fewer ventilation hours during the day. The treatment

Conclusion Measured values alone provide an indication of whether ventilation is running regularly or not. Changes can be observed and interpreted. This applies to all values that are collected and documented, including pulse, RR, consciousness, etc. However, this does not replace the general observation of people by the nursing staff, but rather complements it.

References List WF, Metzler H, Pasch T (1995) Monitoring in Anästhesie und Intensivmedizin. Springer, Berlin Heidelberg Rathgeber J (2010) Grundlagen der Maschinellen Beatmung, 2. Aufl. Thieme, Stuttgart Storre JH, Dellweg D (2014) Monitoring des Beatmungspatienten. Pneumologie 68:532–541

329

Monitoring Malte Voth Contents 26.1

Clinical View/Clinical Monitoring – 330

26.2

Pulse Oximetry – 330

26.3

Capnometry – 331

26.4

Circulation, Pulse and Blood Pressure – 331 References – 332

© Springer-Verlag GmbH Germany, part of Springer Nature 2023 H. Lang (ed.), Out-of Hospital Ventilation, https://doi.org/10.1007/978-3-662-64196-5_26

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M. Voth

26.1 

Clinical View/Clinical Monitoring

Monitoring does not only have to do with devices. The “clinical view” of a nurse is much more important. She uses her senses to detect changes in the patient, his excretions, or in catheters, probes and, for example, cannulas: Clinical Monitoring

26

55 Vision (inspection), for example skin and mucous membranes, coloration of urine, breathing excursions. 55 Feeling (palpation), for example temperature, breathing, abdominal tension, muscle tension. 55 Hearing (auscultation), for example breath sounds, bowel sounds. 55 Smell (Olfacio), for example infections, ketoacidosis.

tant to observe the condition of the skin very closely and to recognise a developing decubitus ulcer at an early stage and treat it professionally. A frequent complication in homebreathed patients is generally ventilation-­ induced pneumonia. The early detection of an infection of the respiratory tract can be life-saving in this case. Therefore, every nursing staff member must learn the auscultation and practice it regularly. Pneumonia can only be diagnosed if one knows how different breath sounds differ. >>Hygienic standards and deviations in standardised care activities can be noticed in the monitoring process and must be discussed in the team.

You can collect information during any routine activity.

In addition, various technical aids are available: starting with the clinical thermometer, the stethoscope, pulse oximetry and blood gas analysis. Which technical devices are used depends on the individual patient’s condition and the underlying disease. The most important ones are presented below, even if they are not used on every patient.

z Example

26.2 

Visual analysis of the aspirated secretion: the aspirated secretion is assessed according to colour and viscosity: 55 Odourless and transparent secretion is normal. 55 Yellow or greenish mucus with an unpleasant odor indicates an infection. 55 Is there blood in the secretion? A few strips of blood are harmless. However, if there is more light red or dark, old blood in the secretion, the treating doctor should be informed. The nurse must deal with the underlying disease of the patient entrusted to her/him and consider the individual risk potential. For example, tetraplegia patients have an increased mortality due to a decubitus ulcer. In this case, it is therefore extremely impor-

Pulse Oximetry

A sensor is used to measure the percentage of saturated hemoglobin in total Hb. Normally this is oxygen. In the case of smoke poisoning, a pulse oximeter cannot distinguish which gases are bound to the red blood cells and thus gives a false high saturation value with oxygen. Error Sources for Incorrect Measured Values 55 Lacquered fingernails (black, blue, green lacquer, NOT with red or purple lacquer). 55 Artificial acrylic fingernails. 55 Reduced blood flow to the extremities (hypothermia, shock).

331 Monitoring

55 55 55 55

Venous pulsations. Ambient light interference. Severe anemia. Pronounced oedema.

In healthy young people, the measured value is about 97–98%. Depending on disease and age, a different saturation is “normal” for the patient. From a saturation of less than 90% one already speaks of hypoxia (7 Chap. 27).  

26.3 

Capnometry

By means of capnometry, the carbon dioxide content in the exhaled air can be measured. This measured value provides an overview of “internal respiration”, also known as “cell respiration”. The values determined should be in correlation with the blood gas analysis. This method is mainly used in hospitals and rescue services and is one of the most important monitoring parameters for ventilated patients. >>The standard value is 35–45  mmHg. If deviations occur, the treating team should intervene quickly.

Control Options 55 Selecting the ventilation pattern. 55 Control of the respiratory minute volume. 55 Adjusting the ratio of inspiration to expiration. 55 For the medicinal control of the pH-­ value or the acid–base balance.

If a high CO2 content is measured in the exhaled air, a lot of CO2 is present in the

26

blood. The patient is therefore hypoventilating. If this condition is not changed quickly, the consequence will be the development of respiratory acidosis. The first step is to increase the respiratory minute volume. The patient receives more respiratory air per minute. The situation is different with a lower CO2 content in the exhaled air. Now the patient is hyperventilated. The result will be a respiratory alkalosis. To counteract this, the respiratory minute volume is reduced. For patients requiring resuscitation, the quality of the cardiac massage can be read from the CO2 content in the exhaled air. If the person performing the cardiac massage is exhausted, the CO2 content drops. It is therefore time to take turns.

26.4 

 irculation, Pulse and Blood C Pressure

A simple way to monitor patients is to collect their pulse rate. This is usually palpated at the radial artery. A distinction is made here between the frequency and the quality (strong or weak) of the pulse wave. Furthermore, the question arises whether the pulse is regular or irregular. If a pulse wave can be felt at the radial artery, the blood pressure is at least 80 mmHg systolic. If no pulse can be felt at the radial artery, the pulse can be felt on one side of the carotid arteries. In children, the pulse is palpated at the brachial artery (upper arm artery). The blood pressure is usually measured auscultatorily. A palpatory measurement (i.e., only feeling, without the use of a stethoscope) should only be taken for quick orientation after the first auscultatory measurement. In the case of a palpatory measurement, we only record the systolic blood pressure value. The values obtained must be documented accordingly.

332

26

M. Voth

The cycle reacts to various influences. As compensation mechanisms, patients develop tachycardia in hypoxia. If the problem is not corrected, the adult patient suffers cardiac arrhythmia and later a drop in blood pressure. Circulatory signs are very rare in children. These show no clinical signs for a long time, but decompensate very quickly. The relevance of blood pressure and heart rate is therefore less relevant in children than in adult patients. The monitoring device of choice here is the pulse oximeter (7 Chap. 27).  

References Heck M, Fresenius M (2007) Repetitorium Anästhesiologie. 5. Auflage. Springer, Berlin Hinkelbein J, Genzwuerker HV, Sogl R, Fiedler F (2007a) Effect of nail polish on oxygen saturation determined by pulse oximetry in critically ill patients. Resuscitation 72(1):82–91 Hinkelbein J, Koehler H, Genzwuerker HV, Fiedler F (2007b) Artificial acrylic finger nails may alter pulse oximetry measurement. Resuscitation 74(1):75–82 S.  Hirschfeld, G.  Exner, S.  Tiedemann, R.  Thietje: Langzeitbeatmung querschnittgelähmter Patienten: Trauma und Berufskrankheit >Ausgabe 3/2010, S. 177–181

333

Blood Gas Analysis (BGA) Hartmut Lang Contents 27.1

Assessment of a BGA – 334

27.2

Oxygen and Carbon Dioxide – 335

27.2.1 27.2.2 27.2.3 27.2.4 27.2.5 27.2.6 27.2.7

Oxygen (O2) – 335 Carbon Dioxide (CO2) – 336 Partial Pressure of Oxygen and Carbon Dioxide (pO2 and pCO2) – 337 Oxygen Saturation – 340 Oxygen Fixation Curve – 341 Central Venous Oxygen Saturation (ScvO2) – 344 Horowitz Quotient – 344

27.3

Acid–Base Balance – 345

27.3.1 27.3.2 27.3.3 27.3.4 27.3.5

 H Value – 345 p Buffers and Buffer Systems – 346 Regulation of the Acid–Base Balance – 347 Disturbances of the Acid–Base Balance – 349 Base Excess (BE) – 350

27.4

Effects of Acidosis and Alkalosis – 357

27.5

Reading a BGA – 358 References – 359

© Springer-Verlag GmbH Germany, part of Springer Nature 2023 H. Lang (ed.), Out-of Hospital Ventilation, https://doi.org/10.1007/978-3-662-64196-5_27

27

334

H. Lang

27.1 

Assessment of a BGA

The following explains which values are represented in the blood gas analysis (BGA), how each of them comes about and how these values can be interpreted (. Table  27.1). The collection points for blood samples are shown in . Table 27.2. What is assessed with the BGA? 55 State of oxygenation The values pO2, the oxygen saturation SO2 and the oxygenation quotient pO2/FiO2 (Horrowitz quotient) are used for this purpose. 55 Ventilation With the help of the pCO2. 55 Acid–base balance (SBH) With the help of the values pH, HCO3-, BE and the pCO2.

Capillary blood collection is the preferred method in out-of-hospital ventilation and intensive care, as it involves comparatively low risks for humans and is quite easy to handle. The other collection options do not play a role in extra-hospital care.

 

 

27

.       Table 27.2  Points of acceptance Arterial

Blood collection directly from an arterial vessel access

Capillary

After hyperemia from the earlobes, not quite, but largely corresponds to an arterial harvest

Venous/ central venous

In front of or from the right atrium, distal leg of a multi-­ lumen CVT

Mixed venous

Blood collection from the pulmonary artery Is only possible with a horizontal pulmonary artery catheter

.       Table 27.1  Standard values BGA Displayed values

Standard values, arterial

Standard values, capillary

Standard values, venous/mixed venous

pO2

70–105 mmHg 9.3–14 kPa

>80 mmHg >10.5 kPa

35–40 mmHg 4.5–5.3 kPa

pCO2

35–45 mmHg 4.5–6 kPa

35–45 mmHg 4.5–6 kPa

41–55 mmHg 5.4–7.3 kPa

pO2/FiO2

>450/60 kPa

pH

7.36–7.44 (7.35–7.45)

7.36–7.44 (7.35 to −7.45)

7.33–7.43

HCO3

21–25 (26) mmol/L

21–25 (26) mmol/L

21–25 mmol/L

BE

±2 (±3) mmol/L

±2 (±3) mmol/L

±2 (±3) mmol/L

Conversion: 1 mmHg = 133 Pa or 1 mmHg = 0.133 kPa → 1 kPa = 7.5 mmHg

27

335 Blood Gas Analysis (BGA)

27.2 

Oxygen and Carbon Dioxide

.       Table 27.3  Composition of air

Important Terms 55 Hypoxemia: too little oxygen in the blood. 55 Hypoxia: too little oxygen in the tissue. 55 Normoxie: sufficient oxygen in blood and tissue. 55 Hyperoxia: too much oxygen in blood and tissue. 55 Oxygenation: uptake of oxygen from the alveolus into the blood. 55 Hypocapnia: too little carbon dioxide in the body or blood. 55 Normocapnia: sufficient CO2 in the body or blood. 55 Hypercapnia: too much CO2 in the body or blood. 55 Decarboxylation: release of carbon dioxide from the blood into the alveolus.

27.2.1 

Oxygen (O2)

Oxygen is essential for life and is needed so that our food components can be “burned”. From this, we obtain the energy for all metabolic processes in the body. In addition, heat is released, 37 °C in humans. Carbon dioxide (CO2) is produced as a metabolic end product. z Example

Combustion of glucose Glucose has the structural formula C6H12O6 C6 H12 O6 + 6 ½ O 2 → 6 × CO 2 + 6 × H 2 O The reaction produces energy (as molecule ATP  =  adenosine triphosphate, the energy carrier of our body) and heat.

Inhalation

Exhalation

Nitrogen

78%

78%

Oxygen

21%

16%

Carbon dioxide

0.03%

4%

Others, for example noble gases

1%

1%

z Oxygen Supply

Room air consists (. Table 27.3).

of

21%

oxygen

 

z Example

Example of an adult: 55 Respiratory rate/min = 16× 55 Respiratory volume  =  500  mL (O2 content 21% ≙ 105 mL O2) –– Respiratory minute volume = 8 L/min (≙ 1.68 L O2) –– Respiratory volume/hour  =  480  L/h (≙ 100.8 L O2) –– Respiratory volume/day  =  11,520  L/ day (≙ 2419.2 L O2) z Example

Example of a newborn baby weighing 3 kg: 55 Respiratory rate/min = 50× 55 Respiratory volume = 18 mL (O2 content 21% ≙ 3.8 mL O2) –– → Respiratory minute volume = 900 mL/min (≙ 189 mL O2) –– → Respiratory volume/h = 54,000 mL = 54 l/h (≙ 11.34 L O2) –– → Respiratory volume/day = 1,296,000 mL = 1296 L/day (≙ 272.16 L O2) z Oxygen Demand

Oxygen Binding Capacity The maximum amount of oxygen that can bind 1 g haemoglobin (Hb). Also known as the Hüfner number.

336

27

H. Lang

1 g haemoglobin (Hb) can bind 1.34 mL oxygen. Oxygen Content (CaO2) The amount of oxygen in arterial blood (CaO2—arterial oxygen content). This depends on the Hb concentration and oxygen saturation. CaO2 is approximately 18–20 mL O2 per 100  mL blood (=180–200  mL O2 per 1  L blood). Oxygen Supply (DO2) The amount of oxygen transported per minute from the lungs to the capillaries (DO2—oxygen delivery). This depends on the Hb concentration, the oxygen saturation and the cardiac output per minute/cardiac output. DO2 is approximately 1000 mL O2/min. Oxygen Consumption (VO2) The amount of oxygen absorbed by the tissue per minute (VO2—oxygen consumption, oxygen uptake) VO2 is approximately 250–300  mL O2/ min or 3–4 mL/kg KG. The oxygen consumption VO2 is increased during physical exertion, for example during physical work or sports, and can easily increase to double or quadruple. A healthy body can react to this and increase the supply of oxygen by increasing the breathing frequency on the one hand and the breathing volume on the other. In addition, the heart beats faster during physical exertion. This increases the cardiac output per minute. However, we cannot sustain the increased load in the long term and need phases of recovery after exertion. Oxygen Extraction Rate The O2 extraction rate describes the relationship between oxygen consumption (VO2) and oxygen supply (DO2). This is approximately 25% of the amount of O2 transported in arterial blood, which is consumed in the periphery and absorbed by the tissue. In total, 75% of the oxygen remains in the venous blood as “O2 reserve”. Oxygen Supply

Under physiological conditions the oxygen supply is approximately 1500  mL.  At a consumption of 250  mL/min, the oxygen supply is sufficient for approximately 6 min. If a person is oxygenated with 100% oxygen, the oxygen supply increases to approximately 4200 mL. Thus it is sufficient for approximately 15  min. Oxygenation is therefore important in emergency situations. z Symptoms of Oxygen Deficiency

The first signs of an oxygen deficiency usually show up in: 55 Tiredness. 55 Fatigue, listlessness. 55 Loss of vitality. 55 Performance drop. 55 Mental and physical exhaustion. 55 Decrease in the ability to concentrate. 55 Headaches. These are rather unspecific symptoms, which usually do not need treatment yet. In the following symptoms, concern for the person is appropriate: 55 Shortness of breath (dyspnea). 55 Exhaustion at low physical strain. 55 Cyanosis (blue coloration of the skin). 55 Pallor of the oral mucosa. If these symptoms persist, urgent medical attention is indicated. 27.2.2 

Carbon Dioxide (CO2)

z Carbon Dioxide Production

Carbon Dioxide Production (VCO2) Through our metabolic processes our organism produces CO2 (VCO2—rate of elimination of carbon dioxide), approximately 250 mL CO2/min or 3 mL/kg KG. The production of CO2 is dependent on our diet: 55 It is higher for carbohydrates. 55 It is lower for fats.

337 Blood Gas Analysis (BGA)

>>CO2 diffuses through the membranes about 20 times faster than oxygen. Therefore, even people suffering from shortness of breath may be lacking in oxygen, but a normal or even lower CO2 value can still be measured.

..      Table 27.4  Partial pressures of atmospheric air

>>Conversely, oxygen has 20 times more difficulty than CO2 in diffusing through the membranes. Therefore, a lack of oxygen will show up earlier, for example by a reduction of the oxygen saturation (SpO2).

Gas

Composition

Partial pressure

Nitrogen

78%

pN2 = 600 mmHg 80 kPa

Oxygen

21%

pO2 = 159 mmHg 21.2 kPa

Carbon dioxide

0.03%

pCO2 = 0.28 mmHg 0.024 kPa

Together

100%

Approximately 760 mmHg/101.1 kPa

Respiratory Quotient (RQ) The ratio (the quotient) between CO2 production and O2 consumption (RQ) RQ =

VCO 2 250 mL / min = = 0.8 300 mL / min VO 2

..      Table 27.5  Partial pressures of humidified breathing air

The production of CO2 is decreased in the case of pure fat burning and the RQ tends towards the value 0.7. It is increased in the case of pure carbohydrate burning and the RQ tends towards the value 1.0. An increased supply of fats seems to be advantageous during ventilation because less CO2 is produced. A pure carbohydrate diet increases CO2 production and can lead to hypercapnia. 27.2.3 

 artial Pressure of Oxygen P and Carbon Dioxide (pO2 and pCO2)

z Standard Values of Partial Pressure

Air consists not only of oxygen (. Table  27.3), but of all gases present in the atmosphere. The individual gases do not only form a mixture of air. Each of the gases has its share, its part in the total air pressure. This is called partial pressure. The atmospheric pressure is usually 760  mmHg or 101.1  kPa. The individual gases have their respective shares of the total air pressure (. Table 27.4).  

 

27

Gas

Composition

Partial pressure

Nitrogen

74%

pN2 = 563 mmHg 75 kPa

Oxygen

19.7%

pO2 = 149–150 mmHg 19.9 kPa

Carbon dioxide

0.03%

pCO2 = 0.28 mmHg 0.024 kPa

Steam

6.2%

pH2O = 47 mmHg 6.2 kPa

Together

100%

Approximately 760 mmHg/101.1 kPa

When the air is inhaled, it is warmed through the mucous membranes of the nasopharynx, freed from dust particles and moistened. This moistening is done by means of water vapour, which evaporates from the mucous membranes. The respiratory air is completely saturated with water vapour. This also changes the composition of the inspiratory breathing air and thus the partial pressures change (. Table 27.5).  

338

H. Lang

The inhaled air does not yet correspond to the alveolar air (. Table 27.6). This air is not completely exchanged with each breath, but there are still parts of the dead space air remaining. In addition, the alveoli also contain CO2, which was absorbed from the blood by the alveolus. At the same time, oxygen always flows from the alveoli into the blood. The partial pressures in pulmonary capillary blood that are of interest in gas exchange are pO2 and pCO2. These two gases are exchanged. The diffusion, that is the migration of the gases, occurs from the location of higher partial pressures to the location of lower partial pressures. Along this pressure gradient oxygen flows from the  

27

.       Table 27.6  Partial pressures of alveolar air Gas

Composition

Partial pressure

Nitrogen

74.9%

pN2 = 569 mmHg 75 kPa

Oxygen

13.6%

pO2 = 100–105 mmHg 13.8 kPa

Carbon dioxide

5.3%

pCO2 = 40 mmHg 5.3 kPa

Steam

6.2%

pH2O = 47 mmHg 6.2 kPa

Together

100%

Approximately 760 mmHg/101.1 kPa

alveoli into the blood and carbon dioxide from the blood into the alveoli (. Table 27.7 and . Fig. 27.1). In the pulmonary arteries the pO2 is very low, that is the blood is poor in oxygen, which is used up by the metabolic processes. The pCO2 in turn is very high, that is the blood is rich in carbon dioxide, which is the end product of metabolism (. Table  27.7 right venous/mixed venous).  

 

 

z Differences in Oxygen and Carbon Dioxide Partial Pressure

Oxygen Partial Pressures In the bronchioli there is a high pO2 of about 150  mmHg/19.9  kPa and almost no pCO2. In the alveolus there is a reduced pO2 of about 100  mmHg/13.8  kPa. Why is this so? The air in the alveolus is not completely exchanged. A larger amount of air remains in the alveoli after exhalation. This amount of air is the functional residual capacity (FRC). Old air thus mixes with new, ventilated air. Therefore, there is a lower pO2 in the alveoli compared to the bronchioli. The FRC guarantees gas exchange even during expiration. Nevertheless, this reduced pO2 is sufficient for a sufficient pressure difference between intraalveolar and intracapillary. Therefore oxygen diffuses (migrates) from intra-alveolar to intra-capillary. After passage of the blood at the alveolus, the blood is saturated with oxygen, it is oxygenated. If the respiratory air is enriched with oxygen (e.g., O2 concentration of 100%—760

.       Table 27.7  Overview of partial pressures and diffusion directions Gas

Partial pressure in the alveoli

Diffusion direction

Partial pressure in the venous blood of the pulmonary arteries

Partial pressure in arterial blood

Oxygen

100–105 mmHg 13.8 kPa

→→→→→→→

35–40 mmHg 4.5–5.3 kPa

→

70–105 mmHg 9.3–14 kPa

Carbon dioxide

40 mmHg

←←←←←←←

41–55 mmHg 5.4–7.3 kPa

→

35–45 mmHg 4.5–6 kPa

27

339 Blood Gas Analysis (BGA)

..      Fig. 27.1  Gas exchange mmHg (left) and kPa (right) (Own representation, edited by Isabel Schlütter)

..      Fig. 27.2  Gas exchange under O2-therapy in a healthy lung patient (left) and a lung patient (right) (Own presentation, edited by Isabel Schlütter)

mmHg (101.1  kPa), a considerably higher pressure gradient between intra-­ alveolar and intra-capillary results. This results in better diffusion (. Fig. 27.2). If we are “lung healthy”, this results in a pO2 of about 500  mmHg or 66.5  kPa (. Fig. 27.2 left). If we are “lung sick”, we hope for a pO2 of at least 60–70 mmHg or 8–9.3 kPa (. Fig. 27.2 right). Carbon Dioxide Partial Pressures There is almost no pCO2 in the bronchiolus. However, in the alveolus there is an increased pCO2 of approximately 40 mmHg/5.3 kPa. Why is this so? The air in the alveolus is not completely exchanged. A larger amount of air remains in the alveoli after exhalation. This amount of air is the  

 

 

FRC. Old air thus mixes with new ventilated air. Therefore, there is an increased pCO2 in the intra-alveolar space. CO2 diffuses through the membranes about 20 times faster than oxygen. Therefore, such a high pressure difference is not necessary for the CO2 to diffuse. The diffusion direction is from intracapillary to intraalveolar. After passage of the blood at the alveolus, the blood contains less CO2. This is the decarboxylation (. Fig. 27.3 left). Hypoventilation If the patient breathes too little, the pCO2 also increases intracapillary (. Fig.  27.3 right). After passage of the blood at the alveolus, the blood still contains a lot of CO2. The pCO2 also rises in the bronchioli  

 

340

H. Lang

..      Fig. 27.3  Gas exchange carbon dioxide (left) and during hypoventilation or hypercapnia (right) (Own illustration, edited by Isabel Schlütter)

27

because no CO2 is exchanged by respiration, but is permanently produced in the metabolism. This high CO2 content can be measured with the exhaled air as “etCO2” (end-tidal CO2). 27.2.4 

Oxygen Saturation

Oxygen saturation (SO2) indicates the percentage of oxygen saturation of the hemoglobin present. It is an indication in %. It should be age dependent: 55 In lung healthy young people >96%. 55 In older healthy people >93%. 55 In healthy infants ~94–96%. Values If the saturation drops, concerns for the patient’s well-being are justified, as pO2 decreases disproportionately to the drop in O2 saturation and the risk of hypoxia increases accordingly!

Right Shift ..      Fig. 27.4  Oxygen saturation: differences in the individual organ systems, left half of the figure venous and right arterial (in %) (Own illustration, edited by Isabel Schlütter)

is slightly lower than the mixed venous saturation. A determination of the O2 saturation after venous blood collection from the femoral vein therefore only represents the O2 saturation of the lower half of the body. This is higher because the O2 consumption of the lower organs, that is abdominal organs and legs, is not as high as in the upper half of the body. The saturation is accordingly higher at 80%.

The right shift means an increased pO2 in relation to SO2. A right shift of the oxygen fixation curve (. Fig.  27.6) occurs in the following situations: 55 Decrease of the pH value, thus increase of the H+ ions ↑ → acidosis. 55 Retention of CO2, thus increase in pCO2 ↑ → Hypercapnia. 55 Fever or hyperthermia ↑. 55 Increase in 2.3-BPG concentration ↑.  

2,3-BPG  The molecule “2,3-bisphosphoglyc-

erate” (2,3-BPG) is formed during a by-path of glycolysis (process of energy production). It reduces the binding capacity (affinity) of oxygen to haemoglobin and thus ensures a better release of oxygen into the tissue.

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H. Lang

27

..      Fig. 27.5  Physiological S-shaped O2 binding curve (Own representation, edited by Isabel Schlütter)

With the same pO2, less oxygen is thus bound to hemoglobin. This can be recognized by a lowered O2 saturation. Or vice versa, a lowered O2 saturation still results in an increased pO2. 2,3-BPG in particular facilitates the delivery of O2 to the tissue, that is at low SO2, increased O2 is still delivered to the tissue. 55 Thus, at a saturation of 100%, the pO2 is certainly also at 100 mmHg/13.5 kPa. 55 At a saturation of 90% one has a pO2 of only about 70–75 mmHg/9.3–9.9 kPa. 55 At a saturation of 80% one has a pO2 of only approximately 60 mmHg/7.9 kPa. 55 At a saturation of 70% one has a pO2 of only about 50 mmHg/6.65 kPa. Situations like acidosis, hypercapnia and fever are common in ventilated people. But

a lowered O2 saturation does not necessarily mean tissue hypoxia, as the release of oxygen is facilitated under the above-mentioned circumstances. >>In fever, acidosis or hypercapnia, however, an apparently sufficient pO2 shows a lowered O2 saturation.

Left Shift The left shift indicates a decreased pO2 in relation to SO2. A left shift of the oxygen fixation curve (. Fig.  27.7) occurs in the following situations: 55 Increase of the pH value → thus decrease of the H+ ions ↓ → Alkalosis. 55 Hypocapnia (with hyperventilation) → Decrease in pCO2 ↓.  

343 Blood Gas Analysis (BGA)

..      Fig. 27.6  Right shift of the oxygen binding curve (Own representation, edited by Isabel Schlütter)

..      Fig. 27.7  Left shift of the oxygen binding curve (Own representation, edited by Isabel Schlütter)

27

344

H. Lang

55 Hypothermia ↓. 55 Waste of the 2.3-BPG concentration ↓.

27

A too low concentration of the molecule “2,3-BPG “) strengthens the O2-bond to the haemoglobin. Less oxygen is released to the tissue. With the same pO2, more oxygen is bound to hemoglobin. This can be recognized by an increased O2 saturation. Or vice versa, an increased O2 saturation still results in low pO2. The O2 delivery to the fabric is therefore heavier, that is despite high SO2, less O2 is delivered. 55 At 100% saturation the pO2 is certainly at 100  mmHg/13.5  kPa. However, it could also be much lower, at 50–60 mmHg or 6.65–8 kPa. 55 At a saturation of 90% one has a pO2 of only about 35–40 mmHg/4.65–5.3 kPa. 55 At a saturation of 80% one has a pO2 of only about 30 mmHg/3.9 kPa. Situations such as alkalosis, hypocapnia and hypothermia are also very common in patients. The delivery of oxygen to the tissue is difficult and tissue hypoxia is imminent. Therefore, alkalosis should be treated by buffering, hypocapnia by possibly reduced ventilation and hypothermia by warming up the patient. >>Alkalosis, hypocapnia and hypothermia “pretend” that we have good O2 saturation.

27.2.6 

Central Venous Oxygen Saturation (ScvO2)

The standard value of central venous oxygen saturation (ScvO2) for healthy people is 75%. Deviations can occur both upwards and downwards (. Table 27.8).  

27.2.7 

Horowitz Quotient

The quotient (oxygenation quotient) of arterial O2 partial pressure and inspired oxygen is used to assess the oxygenation function of the lungs, that is the extent to which the lungs are able to saturate the flowing blood with oxygen. Oxygenation index in mmHg: 55 pO2 = 70 mmHg and FiO2 = 0.21 → 70/ 0.21 = 335 mmHg 55 pO2  =  60  mmHg and FiO2  =  0.60  → 60/0.6 = 100 mmHg 55 pO2 = 100 mmHg and FiO2 = 0.21 → 10 0/0.21 = 476 mmHg (for healthy lungs) In kPa: 55 pO2 = 9.31 kPa and FiO2 = 0.21 → 9.31: 0.21 = 44.3 kPa 55 pO2 = 8.0 kPa and FiO2 = 0.60 → 8.0:0.60 = 13.33 kPa 55 pO2 = 14 kPa and FiO2 = 0.21 → 14:0.21 = 66.6 kPa (for healthy lungs) The Horowitz quotient should: 55 in young lung-healthy people over 450 mmHg or 60 kPa and 55 in older lung-healthy people are above 350 mmHg or 46.5 kPa. According to the “Berlin Definition” of the ARDS, that is acute respiratory failure, from 2012, the following applies 55 Horowitz quotient below The pH value is defined as the “negative decadic logarithm” of the hydrogen ion concentration. The numbers 10−1, 10−2, 10−3  …  10−12 are composed of the base number 10 and a superscript with a negative sign. This is called the “negative decadic logarithm”.

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H. Lang

In pure water, some water molecules break down into their individual components: H 2O → decays to → H + + OH − ( hydrogen and hydrogen ions ). Chemically correct is that 2 water molecules react with each other and then decompose into their ions: H 2O + H 2O → H3O + + OH − ; the H3O + ions are called hydronium ions.

27

In 1  L of chemically pure water (with neutral reaction) there are 1/10,000,000  g (=10−7 gs) of H+ ions. And the same number of OH-ions. For simplification, only the digit “7” of the value 10−7 is given— that is pH 7. The starting point of the scale is neutral water, which always has a pH value of 7. >>Values below pH value 7 indicate acids, values above pH value 7 alkalis. The lower the pH value, the stronger the acid present. The higher the pH value, the stronger the lye present (. Table 27.9).  

..      Table 27.9  Relationship between pH value and H+ ions pH value

Grams of H+ ions

pH 7.0

1/10,000,000

pH 7.1

1/12,589,254

pH 7.2

1/15,848,931

pH 7.3

1/19,952,623

pH 7.36

1/22,908,676

pH 7.4

1/25,110,864

pH 7.44

1/27,542,287

pH 7.5

1/31,622,776

pH 7.6

1/39,810,717

pH 7.7

1/50,118,723

pH 7.8

1/63,095,734

pH 7.9

1/79,432,823

pH 8.0

1/100,000,000

To simplify matters, the 9 from the superscript is placed after the designation pH → pH 9 (. Table 27.10). To sum up: 55 The lower the pH value, the greater the number of H+ ions. The solution is “acidic”.  

In principle, the pH value has to do with incredibly small amounts of hydrogen ions, but the effects they have are considerable. The following are examples of acids and alkalis. In both examples, the pH value has been rounded for simplification. z Example

Acidity: Acids have a pH value 7. The pH value of intestinal juice is 9, that is in 1  L of intestinal juice there are 1/1,000,000,000 g of H+ ions (10−9 g).

pH ↓→ H + ↑ 55 The higher the pH value, the lower the number of H+ ions. The solution is “alkaline or basic”. pH ↑→ H + ↓ 27.3.2 

Buffers and Buffer Systems

The hydrogen ion concentration of the blood is kept constant within narrow limits. The blood has a pH value between 7.36 and 7.44. The body is independently able to keep this narrow pH value constant, because only within this blood pH value can the bio-

347 Blood Gas Analysis (BGA)

27

.       Table 27.10  pH value of individual acids and alkalis Hydrochloric acid 35

pH = −1

Beer

pH = 5

Hydrochloric acid 3.5

pH = 0

Urine

pH = 5

Hydrochloric acid 0.35

pH = 1

Skin surface

pH = 5.5

Gastric acid

pH = 1

Mineral water

pH = 6

Lemon juice

pH = 2

Pure water

pH = 7

Vinegar essence

pH = 2

Blood

pH = 7.4

Vinegar

pH = 3

Clean seawater

pH = 8.3

Coca Cola

pH = 3

Gut juice

pH = 8.3

Wine

pH = 4

Detergent solution

pH = 10

Sour milk

pH = 4.5

Caustic soda 3%

pH = 14

Bowel movement infants

pH = 4.5–5

Caustic soda 30%

pH = 15

Source: 7 http://www.­seilnacht.­com/Lexikon/pH-­Wert.­htm, Research from October 28, 2014  

chemical reactions in the body take place correctly. In order for the body to keep its blood pH value constant, it uses so-called buffers and buffer systems. z Buffer

Buffers are solutions (e.g., blood) whose pH value does not change significantly when an acid or base is added. The buffers can bind H+ ions when an acid is added and release H+ ions when a base is added. Most acids are formed during metabolism. This results in large amounts of CO2. CO2 is then exhaled as a so-called “volatile acid”.

27.3.3 

Regulation of the Acid–Base Balance

There are three systems of regulation: 1. Carbon dioxide bicarbonate buffer system, it consists of carbon dioxide and bicarbonate (75% of the buffer system). 2. Kidney. 3. Lung (kidney and lung together 25% of the buffer system).

The acid–base balance can be represented by means of the CO2 dissociation equation: H 2O + CO 2  H 2CO 3  H + + HCO 3 − The reaction is in constant equilibrium. Water reacts with carbon dioxide to form carbonic acid, which quickly breaks down into the components hydrogen ion and hydrogen carbonate. Conversely, hydrogen ions react with hydrogen carbonate to form carbonic acid. This then decomposes into water and carbon dioxide. The body constantly contains too much or too little hydrogen ions, carbon dioxide or bicarbonate. The imbalances are constantly compensated by our buffer system. The reaction always runs in both directions, indicated by the double arrows. Thus the body is always able to react to imbalances in the acid–base balance. Another model to understand: If the pH is low, it is an acid. An acid contains many H+ ions. To reduce this excess of H+ ions, a buffer substance is needed, a substance that is able to bind the H+ ions and thus neutralize them. This is the hydrogen carbonate/

348

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H. Lang

bicarbonate (HCO3−). The kidney regulates the concentration of HCO3− in the body. pH ↓  →  H+ ↑ (HCO3− is required for buffering). If the pH is high, it is a lye. Very few H+ ions are present in a caustic solution. To compensate this lack of H+ ions, CO2 and H2O (carbon dioxide and water) are needed as buffer substances. This is because when CO2 and H2O react with each other, H+ can be released and thus compensate for a lack of H+ ions. The lungs regulate the concentration of CO2 in the body. pH ↑ → H+ ↓ (CO2 + H2O are required for buffering)

 arbon Dioxide Bicarbonate Buffer C System z Decrease of the pH-Value

A drop in the pH value means an increase in hydrogen ions (H+), the blood becomes “acidic”. pH ↓ → H + ↑ Bicarbonate (HCO3−) is required to ensure that sufficient H+ ions are bound. It is released sufficiently by the kidney, binds with the H+ ions and reacts according to the dissociation equation (7 Sect. 27.3.3) to carbonic acid, which in turn decomposes into water H2O and carbon dioxide CO2. CO2 is breathed out and water remains. This happens until the H+ ion concentration has dropped again and the blood is no longer acidic but has reached its normal pH value. Chemical reaction formula:  

H + ↑↑↑ ( increased ) + HCO 3 − → H 2CO 3 → H 2O + CO 2 ( exhaled ) z Increase in pH Value

An increase in the pH value means a decrease in hydrogen ions (H+), the blood becomes alkaline (or basic).

pH ↑→ H + ↓ Water and carbon dioxide react so that sufficient H+ ions are available. If the body needs more CO2, breathing is slower and less CO2 is breathed out. The carbonic acid decomposes again into bicarbonate (HCO3−) and hydrogen ions (H+). The reaction continues until sufficient hydrogen ions are available again and the pH value has reached its normal range. Chemical reaction formula: H 2O + CO 2 → H 2CO 3 → HCO 3 − + H + ↑↑↑ ( increasing )

Regulation Via the Kidney There are two mechanisms of regulation of hydrogen ion concentration: 55 Increase of the bicarbonate concentration in the blood: This results in increased binding of H+ ions and balancing of “acidic” conditions. 55 Decrease of the bicarbonate concentration in the blood: As a result, fewer H+ ions are bound and “alkaline” conditions are balanced. The formation of bicarbonate and H+ ions is catalysed by the enzyme carbonic anhydratase.

 egulation via the Lungs R and Respiration The blood pH value is kept constant by breathing. Here, the correlation between CO2 concentration and pH value is considered. z Increased CO2 Concentration

If the CO2 concentration in the body is increased, the pH value drops. The organism becomes “acidic”, too many H+ ions are present. CO 2 ↑→ pH ↓→ H + ↑

27

349 Blood Gas Analysis (BGA)

If the CO2 concentration increases, more CO2 can react with water to form carbonic acid, which decomposes again. This causes the H+ concentration to rise. The blood pH value decreases. CO 2 ( concentration increases )

↑↑↑ + H 2O → H 2CO3 → HCO3− + H + ↑↑↑ ( increases )

Now the self-regulation of the buffer system occurs. The body reacts to this by accelerating breathing. The patient hyperventilates and breathes more CO2. The H+ ions combine with bicarbonate to form carbonic acid. Carbonic acid breaks down into H2O and CO2. The CO2 is breathed out. The pH value returns to normal. >>If the organism becomes “acidic”, the breathing becomes compensatory faster, hyperventilation is performed.

z Reduced CO2 Concentration

If the CO2 concentration in the body decreases, the pH value increases. The organism becomes “alkaline”, there are too few H+ ions. CO 2 ↓ → pH ↑→ H + ↓ If the CO2 concentration drops, the reaction of CO2 with water to form carbon dioxide does not take place. Consequently, carbonic acid cannot decompose to bicarbonate and H+ ions. The concentration of H+ ions decreases and the blood pH increases. CO 2 ( concentration decreases ) ↓↓↓ + H 2O ( noreaction closed ) → H 2CO3

( no reaction closed ) → HCO3− + H + ↓↓↓ ( decreases )

Now the self-regulation of the buffer system occurs. The body slows down breathing, the patient hypoventilates. This increases the CO2 concentration because less is breathed out. CO2 reacts more with water to form carbonic acid. Carbonic acid dissociates

(breaks down) into H+ and HCO3−. H+ ions are released again and the pH value drops again. >> If the organism becomes “alkaline”, breathing is compensatory slower, hypoventilation is performed.

27.3.4 

Disturbances of the Acid–Base Balance

The disturbances of the acid–base balance are called: 55 Acidosis: Increase of H+ ions in the blood pH 7.44. The cause of the imbalance can be respiratory and metabolic. Thus, a distinction is made between: 55 Respiratory acidosis. 55 Respiratory alkalosis. 55 Metabolic acidosis. 55 Metabolic alkalosis. 55 Combined appearance. A BGA is necessary to differentiate respiratory or metabolic causes (. Table 27.11). 55 Respiratory component: CO2 partial pressure (pCO2) changed, 55 Metabolic component: Standard bicarbonate (HCO3−) and base excess (BE = base excess) changed.  

The Henderson–Hasselbalch equation gives an indication whether an acid–base disorder has a respiratory or metabolic cause.  metabolic component,  HCO3−   mainly through the kidney   pH ~  respiratory component,  pCO 2    especially through the lungs  more precisely: pH = 6.1 + log

HCO3− . 0.03 × pCO 2

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H. Lang

.       Table 27.11  Changes in metabolic and respiratory values Standard bicarbonate (HCO3−) indicates a metabolic component (standard value: 21–25 mmol/L) Alkalosis

HCO3−↑

pH↑

Acidosis

HCO3−↓

pH↓

The base deviation BE behaves like HCO3− and indicates a metabolic component (standard value: ±2 mmol/L) Alkalosis

BE↑

pH↑

Acidosis

BE↓

pH↓

Alkalosis

CO2↓

pH↑

Acidosis

CO2↑

pH↓

The CO2 refers to a respiratory disturbance

27

This equation states that the pH value depends on the amounts of CO2 and HCO3−. HCO3− is the metabolic cause and CO2 is the respiratory cause of acid–base disorder. 27.3.5 

..      Table 27.12  Exemplary BGA for respiratory acidosis

Base Excess (BE)

The BE is a calculated value and indicates how many mmol of a strong acid or base are required to titrate a blood sample to the normal pH of 7.4. The most important buffer bases in blood are bicarbonate, hemoglobin, negatively charged proteins and inorganic phosphate. Bases are capable of binding and neutralizing H+ ions. Bicarbonate is a proportion of the total bases. Therefore HCO3− and BE usually develop in the same direction: 55 Excess of bases  →  positive base deviation (BE). 55 Lack of bases → negative base deviation (BE). If non-volatile acids are accumulated in the metabolism or the body loses bicarbonate, standard bicarbonate and base deviation decrease. A lack of bases develops and the BE decreases. This leads to a negative base

pH

7.30 ↓

pCO2

48 ↑

pO2

95

BE

+2

HCO3−

25

deviation in the measured value, for example BE = −5. If the body loses non-volatile acids or if bicarbonate is accumulated, standard bicarbonate and base deviation increase. An excess of bases is formed, the BE increases. This leads to a positive base deviation in the measured value, for example BE = +5.

Respiratory Acidosis Respiratory acidosis is caused by increased pCO2 due to reduced CO2 exhalation through the lungs (hypoventilation) (. Table 27.12).  

>>The main characteristic of respiratory acidosis is a low pH and a high pCO2:

27

351 Blood Gas Analysis (BGA)

>>pH ↓ and pCO2 ↑

Hypoventilation is assessed on the basis of respiratory minute volume (MV). If the MV decreases, the partial pressure (pCO2) increases. If pCO2 increases, acidosis develops and the pH value decreases. A low pH value means a high number of hydrogen ions.

PEEP. The smaller the distance between Pinsp and PEEP, the smaller the Vt. MV ↓→ f ↓ +Vt ↓=

PEEP The cause of respiratory acidosis is hypoventilation. Which means the MV is too low. Summarized using the symbols/formula:

MV ↓ → pCO 2 ↑→ pH ↓ → H + ↑ Cause of a low MV: 55 Insufficient respiration/ventilation frequency and/or 55 Too low breathing volume Vt The respiratory volume (Vt) is determined during pressure-controlled ventilation using the ventilation parameters Pinsp and

Pinsp ↓

MV ↓→ f ↓ +Vt ↓=

Pinsp ↓

PEEP ↑→ pH ↓→ H ↑

→ pCO 2

+

Respiratory treatment also means finding out the cause of the disturbed ventilation, the hypoventilation. Various causes (. Table  27.13) can lead to a reduction in breathing, for example obstruction of the airways with mucus and secretions, an  

.       Table 27.13  Respiratory acidosis Cause

Setting of too low AMV during ventilation 2:1 ventilation (ventilation with inverse breathing time ratio) airway obstruction respiratory depression, through deep analgosedation Lung diseases (COPD) Rib fractures, phrenic paresis Exhaustion of breath Pressure support set too low

BGA

pH 45 mmHg Bicarbonate normal, slightly elevated

Compensation

Body tries to balance it metabolically. Kidney increases H+ excretion with urine Kidney increases bicarbonate production, because HCO3− is the buffer substance that can bind and neutralize an excess of H+ ions Problem: in acute or chronic renal insufficiency the kidney is unable to compensate

Compensated BGA

pH almost normal pCO2 >45 mmHg Bicarbonate >25 mval/L ↑↑↑

Therapy

Respiratory treatment by increasing respiration An increase in respiration means an increase in the respiratory minute volume MV↑, this can be achieved by increasing the ventilation frequency f and/or increasing the respiratory volume Vt, in pressure controlled ventilation the Vt is increased by raising the Pinsp This reduces the CO2 concentration, the pH normalizes and the number of H+ ions also decreases.

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H. Lang

occurring bronchospasm, unfavourable positioning of the patient or bent or misplaced tracheal cannulae and breathing tubes. If these causes can be eliminated immediately (aspiration, inhalation with bronchodilator drugs, elevation of the patient, etc.), hypoventilation will be quickly eliminated. If the causes of hypoventilation cannot be eliminated immediately (Sect. 7 2.1.1), it is necessary to consider which ventilation parameters lead to an increase in ventilation, the MV. Common practical experience is to increase the ventilation rate, because this increases the MV.  If this is set to 10 or 12 strokes/min, it may be useful to increase it. However, if a ventilation rate is already set quite high, e.g. 20 strokes/min., a further increase will not be very promising. It is equally important to consider the breath volume (Vt) in the measured values. A good reference point for assessing whether an adapted Vt is achieved for the patient is the formula 6–8 mL/kg KG in relation to the ideal body weight IBW.  

27

z Example

For a patient weighing 80 kg a Vt of approximately 430–580  mL should therefore be expected. If this is permanently too low in the measured values, the set value for the respiratory volume Vt must be increased for volume-controlled ventilation. For pressure-­ controlled ventilation, the value Pinsp must be increased, but carefully in steps of 2–3 mb/ cm H2O. It must always be checked whether the target volume is administered after increasing the Pinsp. After a given time, approximately ½–1 h after adjusting the ventilation parameters, a new BGA should be performed. Success will then consist of a decrease in pCO2 and an increase in pH value. Nursing staff in home ventilation usually do not have permission to adjust ventilation parameters. This restricts their options for

action. However, the focus is on identifying and eliminating the actual causes. Some ventilation centers use the criteria mentioned above to determine which ventilation parameters should be adjusted for a person and to what extent. If respiratory treatment is not carried out, the body attempts to compensate, that is metabolic compensation (. Table 27.14). But only if the kidney can still work. The increase of bicarbonate/hydrogen carbonate leads to a slight increase of the pH value. However, it remains apparent that respiratory acidosis exists.  

Respiratory Acalosis Respiratory alkalosis is caused by reduced pCO2 due to increased CO2 exhalation through the lungs (hyperventilation) (. Table 27.15).  

>>The main characteristic of respiratory alkalosis is an increased pH and a low pCO2: pH ↑ and pCO2 ↓

..      Table 27.14  Compensated BGA for respiratory acidosis pH

7.35–7.37 ↓

pCO2

48 ↑

pO2

95 +6 ↑

BE HCO3

−

28 ↑

..      Table 27.15  Exemplary BGA for respiratory alkalosis pH

7.52 ↑

pCO2

30 ↓

pO2

95

BE HCO3

+2 −

23

27

353 Blood Gas Analysis (BGA)

Hyperventilation is assessed on the basis of MV.  If the MV increases, the partial pressure (pCO2) decreases. If the pCO2 decreases, an alkalosis develops and the pH value increases. A high pH value means a low number of hydrogen ions. MV ↑→ pCO 2 ↓→ pH ↑→ H + ↓

The cause of respiratory alkalosis is hyperventilation. Which means the MV is too high. Summarized using the symbols/formula: MV ↑→ f ↑ + Vt ↑↓→ ↓→ pH ↑→ H + ↓

Pinsp ↑ PEEP

→ pCO 2

Respiratory treatment means finding out the cause of hyperventilation. Various causes are listed in . Table 27.16. However, therapeutically controlled hyperventilation is indicated for some clinical pictures and should not be changed. If these causes can be eliminated immeThe Vt is determined during pressure-­ diately (tachypnea in case of anxiety, pain, controlled ventilation using the ventilation followed by mild sedation), hyperventilaparameters Pinsp and PEEP. The greater the tion will be quickly eliminated. If the causes distance between Pinsp and PEEP, the greater of hyperventilation cannot be eliminated the Vt. immediately, it is necessary to consider which ventilation parameters lead to a Pinsp ↑ MV ↑→ f ↑ + Vt ↑= reduction in ventilation, the MV. PEEP If the MV is too high, this could be the cause: 55 too high respiration/ventilation frequency and/or 55 respiratory volume too high Vt

 

.       Table 27.16  Respiratory alkalosis Cause

Compensatory hyperventilation for lung diseases Controlled hyperventilation during ventilation Incorrect respirator setting Compensatory hyperventilation for craniocerebral trauma, as long as the person can breathe Pulmonary embolism Psychic excitement, like fear, excitement, anger

BGA

pH >7.44 pCO2 25 mmol/L BE >+2 mmol/L

Compensation

Attempt of respiratory compensation through reduced CO2 exhalation (hypoventilation) The reduced excretion of CO2 means slower breathing, hypoventilation There is already a shortage of H+ ions; this must be supplemented This requires CO2 and H2O; hypoventilation increases the amount of CO2 retained in the body, which in turn increases the pCO2 value. CO2 can react with water and thus produce H+ ions. The H+ deficiency can thus be compensated However, HCO3− is also increasingly produced, this value then rises further Problem: in acute or chronic lung failure, the lungs are unable to compensate

Compensated BGA

pH almost normal Bicarbonate increased ↑ positive BE further increased ↑ pCO2 increased ↑

Therapy

Acid addition at pH >7.5–7.6 Electrolyte control Na+, K+, Cl−

 

27

357 Blood Gas Analysis (BGA)

losis exists. The same applies here: however, if a person has chronic ventilatory insufficiency, he cannot attempt to compensate for metabolic acidosis by breathing. In this case, artificial respiration may be able to partially compensate for the acidosis.

Effects of Acidosis and Alkalosis

27.4 

The effects of acidosis and alkalosis are shown in . Tables 27.26 and 27.27. . Table 27.28 summarizes how individual values change when the acid–base balance is disturbed. With metabolic disorders, the display parameters develop in the same direction.  

 

.       Table 27.26  Effects of acidosis

.       Table 27.27  Effects of alkalosis ZNS

hyperexcitability of the peripheral nervous system Tetanyia → tonic spasms of the musculature

Cardiovascular

Blood pressure fluctuations Cardiac arrhythmia

Breathing

Attenuated in metabolic alkalosis Increased for respiratory alkalosis

Oxygen binding capacity of haemoglobin

With the same pO2, more oxygen is bound to the haemoglobin and the O2 delivery is more difficult, less oxygen is delivered to the tissue

..      Table 27.28  Overview acid–base imbalance

Damping of the CNS

Confusion Muscular weakness Coma

Fault

Bicarbonate and base deviation

pH value

pCO2

Cardiovascular

Blood pressure fluctuations Cardiac arrhythmia Reduced responsiveness to circulatory support drugs

Respiratory acidosis

↑

↓

↑↑↑

Breathing

Increased for metabolic acidosis Attenuated for respiratory acidosis

Respiratory alkalosis

↓

↑

↓↓↓

Metabolic acidosis

↓↓↓

↓

↓

Metabolic alkalosis

↑↑↑

↑

↑

Oxygen binding capacity of haemoglobin

With the same pO2, less oxygen is bound to the haemoglobin and the O2 delivery is easier, more oxygen is delivered to the tissue

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H. Lang

27.5 

Reading a BGA

The following logarithm is helpful for respiratory and metabolic disorders (. Fig. 27.8).  

27

..      Fig. 27.8  Logarithm for respiratory disorders (Own representation, edited by Isabel Schlütter)

359 Blood Gas Analysis (BGA)

References Anonymous (n.d.). http://www.­intensivcareunit.­de/bga.­ html: Recherche 01.10.2014 Boemke W, Krebs MO, Rossaint R (2004) Blutgasanalyse, Weiterbildung, zertifizierte Fortbildung. Anaesthesist 53:471–494

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Rehm M, Conzen PF, Peter K, Finsterer U (2004) Das Steward-Modell. „Moderner“ Ansatz zur Interpretation des Säure-Basen-Haushalts. Anaesthesist 53: 347–357

361

Breathing Gas Conditioning Hartmut Lang Contents 28.1

Tasks of the Airways – 362

28.2

Absolute and Relative Humidity – 362

28.3

Active Respiratory Gas Humidification – 364

28.3.1 28.3.2

 ass-over Evaporator – 364 P Countercurrent Method – 364

28.4

Ventilation Filter – 365

28.4.1 28.4.2

 echanical Filters – 365 M Electrostatic Filters – 366

28.5

Passive respiratory Gas Humidification – 366

28.5.1 28.5.2 28.5.3

 eneral Operation – 366 G Physical and Chemical HME Elements – 366 HMEF – 368

28.6

Active Versus Passive Humidification – 368 Further Reading – 369

© Springer-Verlag GmbH Germany, part of Springer Nature 2023 H. Lang (ed.), Out-of Hospital Ventilation, https://doi.org/10.1007/978-3-662-64196-5_28

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Tasks of the Airways

The consequences of invasive ventilation with insufficient respiratory gas conditionEven during normal breathing, the respira- ing are: tory tract has four functions, . Table 28.1. 55 Toughness of bronchial secretion increases. These functions of the respiratory tract 5 5 Cilia lose their mobility. are described by the term breathing gas con5 5 secretion accumulates in the respiratory ditioning. The term respiratory tract humidtract. ification is synonymous. The humidification 5 5 Airways become narrower, breathing systems used in artificial respiration are resistance increases. intended to ensure and maintain respiratory 5 5 Patients have to exert themselves more gas conditioning. when breathing. The conditioning of the respiratory gas 5 5 Secretion blockage of the bronchi leads through the airways has the effect of mainto atelectasis. taining the self-cleaning system, the so-­ 5 5 BGA deteriorates. called mucociliary clearance, the mobility of 5 5 Susceptibility to infections is increasing. the cilia (7 Sect. 1.2.4) and the function of the surfactant (7 Sect. 1.2.7). The mucociliary clearance ensures that Heating and humidifying the air must thereinhaled foreign bodies are removed from the fore be artificial, regardless of whether the respiratory tract. If the air humidity is insuf- patient is breathing spontaneously or is ficient and the temperature too low, the being ventilated. The ventilation air must cleansing mechanism is hindered. The sur- always be clean. factant ensures open alveoli by reducing their surface tension. If the air is insufficiently conditioned, the surfactant loses its 28.2  Absolute and Relative activity and alveoli collapse and form atelecHumidity tases. Invasive ventilation with a tracheal cannula can have this effect and the respira- The air is able to absorb moisture without tory tract can no longer perform its tasks. the water condensing. The lower the air temperature, the less water the air can absorb, and the warmer the air becomes, the more water it can absorb. .       Table 28.1  Tasks of the upper airways 55 At 37 °C, 1 L of air can absorb 44 mg of water. Heating Inhaled air is heated and can 5 5 Thus air is 100% saturated with water. therefore absorb more water 28.1 

 

 

 

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vapour Humidification

With aqueous secretion from the glands of the upper respiratory tract; self-cleaning mechanism is thus maintained

Filtering

Interception of larger particles through nasal hairs and through the mucus coating of the nasal and tracheobronchial mucosa

Turbulence

Causes the greatest possible contact between air and mucous membrane

kAbsolute Humidity

It indicates how many milligrams of water per liter of air have been absorbed at a certain temperature. According to the above example, it is 44 mg at 37 °C. kRelative Humidity

It is an indication in % and indicates the proportion of water in the air. According to the above example, the air is 100% saturated with water.

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363 Breathing Gas Conditioning

..      Fig. 28.1  Dependence of absolute humidity on temperature (Own representation, edited by Isabel Schlütter)

. Figure  28.1 is intended to show how the ratio of absolute and relative humidity is dependent on temperature. 55 37  °C warm air can absorb 44  mg of water per litre of air, so it has a relative humidity of 100%. 55 At a relative humidity of 90%, it contains only about 39 mg of water per litre of air. 55 At a relative humidity of 80%, it contains only about 35 mg of water per litre of air, etc. 55 30  °C warm air can absorb 30  mg of water per litre of air, so it has a relative humidity of 100%. 55 At a relative humidity of 90%, it contains only about 27 mg of water per litre of air. 55 At a relative humidity of 80%, it contains only about 24 mg of water per litre of air, etc. 55 20  °C warm air can absorb 17  mg of water per litre of air, so it has a relative humidity of 100%.  

55 At a relative humidity of 90%, it contains only about 16 mg of water per litre of air. 55 At a relative humidity of 80% it contains only about 14 mg of water per litre of air, etc. 55 At a relative humidity of 40–50% in living spaces, it contains only about 7–8.5 mg of water per litre of air. (Source of the calculations: 7 http://www.­ wetterochs.­de/wetter/feuchte.­html, research June, 11, 2016) The respiratory tract can compensate for this heat and moisture deficit. And artificial humidification systems should also compensate for this deficit during ventilation. During normal spontaneous breathing in humans, the inspiratory air is heated to 37  °C and saturated with 100% water vapour. The physiological loss of water during exhalation is about 7  mg water per litre of air.  

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28.3 

 ctive Respiratory Gas A Humidification

Active humidification of the respiratory gas is also known as “heated humidification”, or HH for short. The device that performs active respiratory gas humidification is therefore called a “Heated Humidifier”. These terms express more clearly that the respiratory air is heated and humidified. Two principles are applied.

The warming of the breathing air should also be 37  °C for invasively ventilated patients. This temperature corresponds to the body core temperature, higher temperatures are not recommended. 28.3.2 

Countercurrent Method

In this process, the water flows against the air or gas flow. There is a large exchange surface between air and water (. Fig.  28.3). Heat and moisture are transferred to the air. High temperatures are unnecessary and so the air is heated up to 37  °C and 100% ­saturated with humidity. The countercurrent method offers further advantages: 55 Temperature and humidity of the gas administered to the patient are largely independent of the actual gas flow and the gas temperature at the humidifier inlet. 55 Changes in ventilation settings or changes in the patient’s respiratory activity or lung function have essentially no effect on the humidification performance. 55 Due to the possibility of patient-specific settings, the target humidity can be optimally adapted to the patient and his individual situation (e.g., body core temperature). 55 Low work of breathing for the patient due to minimal resistance (flow resistance) of the entire humidification system.  

28.3.1 

28

Pass-over Evaporator

The respiratory air is passed through a water-filled container in which the water is heated to 40–85 °C (. Fig. 28.2). The respiratory air, which flows over the heated water, absorbs the evaporated water. The air is heated to approximately 37  °C and can therefore absorb 44 mg of water as moisture per litre of air. Humidification by evaporation of water and the extent of evaporation depends on three factors: 55 With rising temperature more water evaporates. 55 With a large surface area, more water evaporates. 55 The greater the air movement above the water surface, the greater the evaporation.  

..      Fig. 28.2  Pass-over evaporator (Courtesy of Gründler, ResMed)

365 Breathing Gas Conditioning

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..      Fig. 28.3  Counterflow method (Courtesy of ResMed)

In both humidification systems, water is released to the respiratory air in the form of water molecules. This has a hygienic advantage because no germs are released into the air. Heatable ventilation hose systems are used to prevent the water from condensing on the way to the patient.

28.4 

Ventilation Filter

Respiratory filters serve to prevent infections. Inhaled gases are filtered during ventilation, thus protecting the patient and the ventilation system including accessories. A distinction is made between mechanical and electrostatic filters.

28.4.1 

Mechanical Filters

In the mechanical filter, a pleated membrane (usually made of glass-fibre paper or ceramic-coated fleece) is used for screening, so here the pore size is the limiting factor. The mechanical filter has a higher retention value than electrostatic filters. Retention value is the value that describes at which pressure the filter membrane is broken by liquid, causing it to be irreversibly damaged and no longer have any protective function. For mechanical filters, this value is usually in the range of 140 cm H2O. The reason for this high retention value lies in the pleated membrane, which has water-­ repellent (hydrophobic) properties.

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28.4.2 

Electrostatic Filters

The electrostatic filter takes advantage of the fact that the surface of bacteria and viruses has different electrical charges. A type of cotton wool pad is used, the fibres of which are permanently electrostatically charged, which means that the virtual pore size (the electrical field around the fibres) is much smaller than the fibre spacing. This generates a much lower airway resistance than with a mechanical filter. The retention value of electrostatic filters is only about 20 cm H2O.

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28.5 

 assive respiratory Gas P Humidification

The passive humidification of the respiratory gas is done with heat and moisture exchangers, the HME filters. The HME filters are colloquially called ventilation filters. The HME filter is usually placed between the breathing tube system and the goose gargle (. Figs. 28.4 and 28.5). However, it can also be placed directly onto the tracheal cannula.  

..      Fig. 28.5  Ventilation filter single tube system

28.5.1 

During the expiration phase, the patient’s heat and water vapor are bound by the HME element and thus temporarily stored (. Fig. 28.6). During the subsequent inspiration, the bound heat and moisture is released to the patient with the air (. Fig. 28.7).  

 

28.5.2 

..      Fig. 28.4  Respiratory filter with two hose system

General Operation

 hysical and Chemical HME P Elements

HME elements work according to different principles. There are physical filters that have a hydrophilic (water-attracting or water-­ loving) HME membrane and thus absorb the moisture of the patient’s exhaled air. There are chemical filters that have a hygroscopic (water-repellent or waterrepellent) surface. This surface can be the hygroscopic salt calcium chloride, which absorbs moisture from the gas. Calcium chloride is applied in the manufacturing process.

367 Breathing Gas Conditioning

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..      Fig. 28.6  Expiration with HME (Courtesy of Intersurgical)

..      Fig. 28.7  Inspiration with HME (Courtesy of Intersurgical)

The HME element can be made of different materials, from a rolled up strip of blotting paper but also polyurethane sponges soaked

with the hygroscopic salt calcium chloride. The product should deliver approximately 30 mL H2O per litre of breathing gas at 30 °C.

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28

HMEF

2. Rate of Fan Associated Pneumonia The rate of pneumonia occurring in patients as a result of artificial ventilaHMEF (Heat and Moisture Exchange tion is described as approximately 11 Filters) combine a filter medium with an elecases per 1000 ventilation days. The ment for heat and moisture exchange. The highest rate of pneumonia occurs after HME element can be located in front or 6–10 days of ventilation. The most combehind the filter element. An electrostatic mon cause of pneumonia is microaspiramembrane is also hydrophobic to a certain tion of bacteria from the oropharynx. degree. Exogenous factors such as insufficient hand disinfection of hospital staff also >>No joint use of active humidification play a role. system and HME filter! The formation of condensate and an increased suction frequency in active humidifiers increase the risk of germs 28.6  Active Versus Passive entering the respiratory tract. Insufficient Humidification return of heat and moisture from HME filters reduces the rate of suction freWhen comparing the two humidification quency and increases the risk of secremethods, five aspects are usually considered. tion thickening with increased 55 Humidifier output. susceptibility to infection. 55 Rate of Ventilator Associated PneumoModern HME filters are equipped nia. with a filter system that protects patients 55 Airway resistance. from contamination by germs. At pres55 Dead space increase. ent, however, neither the Robert Koch 55 Costs. Institute (Robert-­Koch-­Institut, RKI) nor the Center for Disease Control 1. Humidifier Output (CDC/USA) gives any recommendation Active respiratory humidifiers are for the use of HME filters. There are, able to saturate the inspiratory air 100% however, a number of studies and obserwith moisture, that is 1  L of air can vations that describe a reduction in fan-­ absorb 44  mg of water vapour at associated pneumonia using an HME 37 °C. However, there is also the danger filter. that the humidifiers are set too hot, that 3 . Airway Resistance is higher than 37  °C.  This leads to the The conditions for increased airway formation of condensate and over-­ resistance have already been described. humidification. This can result in an HME filters increase airway resistance increased suction frequency. just as much as the diameter and length Passive humidification systems, soof a tube. Patients who begin to breathe called HME filters store the heat and on their own will have to compensate moisture from the expiratory air and for the increased airway resistance with release it again during the following an increased workload. Modern respirainspiration. The absorption capacity is tors therefore offer the possibility that described differently in the literature, the active or passive humidification sysbetween 25 and 34 mg water per litre air. tem must be selected at the start of venNewer filters guarantee a water loss of tilation to compensate for airway max. 7 mg water per litre air, which corresistance. responds to the physiological water loss. 28.5.3 

369 Breathing Gas Conditioning

4. Dead Space Increase The physiological dead space is approximately 140–150  mL air in adult humans. An increase in dead space is suspected through the use of tracheal cannulas, goose gargling and HME filters. However, it is almost equal to the anatomical dead space. HME filters with a high internal volume carry the risk of increased dead space and that the pCO2 content can increase when ventilating with lower tidal volumes. They also carry the risk that spontaneously breathing patients will have to overcome this increased dead space through increased breathing effort, which can quickly lead to states of exhaustion if the performance of the respiratory pump is reduced. Modern HME filters are now offered with smaller internal volumes, which are smaller than 50 ml. 5. Costs With regard to the replacement intervals of the entire hose systems, it is not necessarily possible to speak of a cost advantage. If the recommendations of the RKI are followed, the replacement intervals can be 7  days, regardless of whether an HME filter is used or not. However, there may already be clinics that have increased the change interval of the hose systems when using an HME filter. When using an HME filter, the suction rate may decrease. A lower suction rate means fewer suction catheters and therefore lower costs. When using active airway humidification with the risk of hypersecretion, the suction rate may increase. An increased suction rate car-

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ries the risk of germs being introduced into the respiratory tract. This also increases the risk of pneumonia and other infections. Possible antibiotic administration and an extended patient stay increase the costs. Since recent studies have shown a reduction in the rate of ventilator associated pneumonia when using an HME filter, the length of time patients are hospitalized and their ventilation time has also been reduced, thus reducing the cost of treatment.

Further Reading Kramer et  al (2010) Infektionsprävention bei der Narkosebeatmung durch Einsatz von Atemsystemfiltern (ASF): Gemeinsame Empfehlung der Deutschen Gesellschaft für Krankenhaushygiene e.V. (DGKH) und der Deutschen Gesellschaft für Anästhesiologie und Intensivmedizin e.V. (DGAI). GMS Krankenhaushygiene Interdisziplinär 5(2). ISSN: 1863–5245 Leitlinie der US-amerikanischen American Association for Respiratory Care (n.d.). http:// www.­guideline.­gov/content.­aspx?id=36911 Prävention der nosokomialen beatmungsassoziierten Pneumonie (2013) Empfehlung der Kommission für Krankenhaushygiene und Infektionsprävention (KRINKO) beim Robert Koch-Institut. Bundesgesundheitsbl 56:1578–1590, Online publiziert: 16. Oktober 2013, © Springer-Verlag Berlin Heidelberg 2013 Restrepo RD, Walsh BK (2012) Humidification during invasive and noninvasive mechanical ventilation: 2012. Respir Care 57(5):782–788 Tablan OC et  al (2004) Guidelines for preventing health-care—associated pneumonia, 2003: recommendations of CDC and the Healthcare Infection Control Practices Advisory Committee. MMWR Recomm Rep 53(RR-3):1–36

371

Secretary Management Hartmut Lang

Contents 29.1

Ability to Cough – 372

29.1.1 29.1.2

 oughing Procedure – 372 C Problems with Reduced Cough – 372

29.2

Support for Coughing – 373

29.2.1 29.2.2

 easures to Increase the Intrathoracic Volume – 373 M Measures for Intensified Expiratory Air Flow – 375

29.3

Endobronchial/Endotracheal Suction – 377

29.3.1 29.3.2

 losed Versus Open Suction – 379 C Subglottic Suction – 379

29.4

Inhalation Therapy – 381

29.4.1 29.4.2 29.4.3 29.4.4

 eposition – 381 D Types of Deposition – 382 Metered Dose Inhalers – 383 Nebuliser Systems – 384

References – 388

© Springer-Verlag GmbH Germany, part of Springer Nature 2023 H. Lang (ed.), Out-of Hospital Ventilation, https://doi.org/10.1007/978-3-662-64196-5_29

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29.1 

Ability to Cough

The ability to cough is vital. With the cough it is possible to transport secretions and foreign bodies out of the airways. The removal of secretions from the airways by coughing is called secretion clearance. In order for a person to be able to cough, a number of conditions are necessary: 55 Sufficient inspiration (at least 1.5  L of air). 55 Ability to close the epiglottis (glottis closure). 55 Building up sufficient pressure within the airways (high intrathoracic pressure). 29.1.1 

29

Coughing Procedure

The coughing process takes place in four phases (. Fig. 29.1). 55 Phase 1: Inspiration phase → deep inhalation with a pause in breathing. 55 Phase 2: Inspiratory break. 55 Phase 3: Compression phase → creation of a high intrathoracic pressure (compression) by pressing against the closed epiglottis (glottis closure). 55 Phase 4: Ejection phase → abrupt opening of the epiglottis; this causes the air to flow out at a high speed (air speed approx. 360 L/min.)  

For a coughing shock to be effective, a minimum air flow of 270 L/min is required. The cough becomes critical when the flow is less than 160  L/min, which would no longer guarantee effective secretion clearance. Coughing, clearing your throat or sneezing is in principle a very quick exhalation. As a result, the secretions are carried along by the very fast exhaled air stream and are transported out of the airways. Coughing or clearing the throat occurs several times in succession, not just once. 29.1.2 

Problems with Reduced Cough

Patients with reduced coughing are particularly at risk of suffering complications. These are especially people with 55 a weakened respiratory pump, 55 neuromuscular diseases, 55 constricted and swollen airways, 55 restricted ciliary mobility or 55 bronchopulmonary diseases that impede secretion clearance. People with a weakened respiratory pump have the following problems, among others: 55 Reduced ventilation (hypoventilation). 55 This reduces the ability of the lung tissue to stretch.

..      Fig. 29.1  Coughing procedure (Courtesy of Philips GmbH Respironics)

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373 Secretary Management

55 Thereby clearly weakened coughing impulse. 55 Thereby reduced or lacking secretion elimination. People with narrowed and swollen airways, for example in the case of COPD, also have problems with the mobilisation of secretions: 55 Their secretions are very viscous. 55 These are difficult to mobilize due to the narrowed airways. 55 This means that they accumulate preferentially in the lowest airways. People with limited ciliary mobility have problems with mobilisation of secretions: 55 Mucus is still produced by the mucus-­ forming cells of the respiratory tract. 55 However, mucus and secretions are not transported away by the cilia’ flickering activity and accumulate in the lowest airways.

Complications of a Lack of Secretion Clearance 55 Obstruction or blockage of the airways due to accumulation of secretions. 55 These can affect whole lung areas, for example segmental and trunk b ­ ronchi. 55 This results in reduced ventilation of these areas. 55 Often there is no ventilation at all. 55 A lack of ventilation leads to a lack of oxygen supply, the consequence is oxygen deficiency (hypoxia). 55 Accumulations of secretions are an ideal breeding ground for pathogenic germs, the result is an infection or even pneumonia. 55 Pneumonia can lead to complete respiratory failure in patients with a weakened respiratory pump. 55 This often leads to invasive artificial respiration.

29.2 

Support for Coughing

The support of the coughing process should include the inhalation phase, the inspiration pause with compression and the expulsion phase. People who cannot perform these phases alone due to muscular weakness require both manual and technical assistance. These aids are effective if they are applied 2–5 times in a row and not just once. 29.2.1 

Measures to Increase the Intrathoracic Volume

The measures to increase the inhalation volume in preparation for coughing can be carried out manually or with technical aids. The aim of all measures is to achieve a sufficient inspiratory volume (Phases 1 and 2) and that the air is then held and compressed intrathoracally (Phase 3). To mobilize mucus, air must be present distally (behind) the obstruction (mucus) (. Fig.  29.2). Only then can the secretion be transported by the outflowing air or by the increase in pressure behind the obstruction (“air behind the plug”). In order for the air to pass behind the constricting mucus plug in the inhalation phase, it should flow slowly. For machine ventilation, this means that the inspiratory flow must be slow, approxImately 25–30 L/ min or 0.3–0.5 L/s. During regular ventilation, flow rates of 40–80  L/min or 0.6–1.2  L/s are achieved. This would transport the secretion plugs further into the bronchial system (. Fig. 29.3). Mobilization to the outside is thus more difficult.  

 

Manual Measures 55 Mobilisation: mobilisation means increased physical effort and causes an increased depth of inhalation. This is not hindered, but allowed even in artificial ventilation with the ventilation modes A-PCV and PSV.

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..      Fig. 29.2  Slow and steady inspiration (Own representation, edited by Isabel Gucke’s)

55 Contact exercises: here, a therapist or a nurse places his hand on a region of the lung, for example left dorso-lateral (facing the back, outside back). This hand contact is intended to ensure that the air is directed to the lung regions during the inhalation phase. However, the patient must concentrate on this, which will be difficult with artificial respiration. People who breathe spontaneously can do this well under guidance. 55 Packing and stimulating handles: the purpose of this breathing exercise is to consciously direct the breath into a region of the lungs. This therapeutic measure also works with artificially ventilated people. The pack and stimulus grips are applied by the therapist during the inspiration phase (. Fig. 29.4). Skin contact is maintained during the expiration phase. –– These grips are also used to reduce tissue resistance, for general relaxation and, in people who breathe spontaneously, they can reduce the breathing rate.  

29

..      Fig. 29.3  Quick inspiration (Own representation, edited by Isabel Schlütter)

>>Caution, these exercises may be painful as skin folds are “grabbed” and pulled. People with sensitive skin should not undergo these breathing exercises.

..      Fig. 29.4  Packing and stimulus handles (Own representation, edited by Isabel Schlütter)

375 Secretary Management

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Mechanical Support Measures

z VCV

All measures serve to increase the depth of inhalation as preparation for coughing. It is hoped that the large amount of inhaled air will be expelled from the lungs at an increased speed and bronchial secretions will be carried out. As a further effect of these measures, the lung is recruited, that is unventilated lung areas are reopened and thus recovered for gas exchange.

Volume-controlled ventilation (VCV) can be set as the second mode in many ventilators. In this mode, the patient’s lung is carefully over-inflated with a predetermined breathing volume, and usually twice or three times the breathing volume otherwise administered. Here too, the setting is made by the ventilation center.

z Air Stacking with Ambu Bag

29.2.2 

The person is carefully over-inflated with the help of an Ambu bag. This is possible with tracheotomized and also with spontaneously breathing people. As a rule of thumb, how much volume should be allowed to enter the lungs can be taken as twice to three times the normal breathing volume. An Ambu bag for adults has a possible filling volume of 1.5–1.7 L. Once the lungs are filled with the increased volume, the elastic properties of the thorax and lungs are used. The Ambu bag is removed and the air flows out of the lungs at a higher speed. Due to the increased exhalation speed, bronchial secretions should be transported out with it. The process can be repeated up to five times, several times a day and if necessary at night. z LIAM for Ventilogic Respirators

The Lung Insufflation Assist Maneuver (LIAM) of the Ventilogic respirators (Weinmann company) also follows the principle of cautious over-inflation of the lungs. However, a predetermined air pressure is set which is approximately twice the ventilation pressure that would otherwise be set. This overinflation maneuver is triggered by pressing the so-called LIAM button on the ventilator. The setting of the pressure level is done by the ventilation center, which also determines how often the maneuver is performed. Usually, it is performed 3–5 times a day, if necessary also at night.

Measures for Intensified Expiratory Air Flow

Manual Cough Support If the expiratory force is insufficient, the expiratory flow can be increased synchronously with the cough by using sheets or cloths wrapped around the patient’s trunk. If the patient does not tolerate this measure, manual support can also be provided by a light handshake in the epigastrium. With manual support measures, care must be taken to ensure that the pressure is mainly applied to the abdomen and that the pressure is applied synchronously with the cough (. Fig. 29.5).  

Mechanical Cough Support z Cough Assist devices (. Fig. 29.6)  

Deployment A cough assistant device is a mechanical inand exsufflator that simulates a natural cough. For this purpose, during inhalation—similar to normal deep breathing—a large amount of air is gradually released into the respiratory tract (positive pressure) and then switched to negative pressure so that secretion deposits are transported out of the lungs (negative pressure/suction). A coughing cycle is imitated. As a rule, 3–6 cough cycles are used, as with the normal cough. These form a coughing sequence. Indications The in- and exsufflator is suitable for patients who have no or only an insufficient

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..      Fig. 29.5  Manual expiratory aid (Own representation, edited by Isabel Schlütter)

Contraindications 55 Secured bullous emphysema. 55 Known susceptibility to pneumothorax or pneumomediastinum. 55 Severe heart disease. 55 Fresh operations on thorax or lungs. 55 Fresh abdominal operations. 55 Condition after barotrauma.

29

kBasic Application Principle of Cough Assist

..      Fig. 29.6  Cough Assist (Courtesy of Phillips Respironics)

cough. These are usually patients with neuromuscular diseases, injuries of the spinal cord, but also with caution and restrictions, also in COPD.  The procedure is also suitable for acute infections of the respiratory tract if other air stacking measures (air stacking 7 Sect. 29.2.1) are not sufficient and to reduce the invasive suctioning of secretions.  

The Cough Assist can be applied with the help of a face mask, a mouthpiece or a tracheal cannula. If possible, patients should sit upright during treatment. For tracheal cannulas, the pressure of the cuff can be increased. The ventilation center determines which application method is to be used, how high the insufflation pressure is to be built up and how long a pause phase should last before exsufflation, suction (the PEF—Peak Exspiratory Flow) is generated. The application can be manual or automatic: 55 When used manually, the coughing cycle is started by a switch or foot pedal. The manual procedure is suitable for patients

377 Secretary Management

with a preserved cough drive, so the beginning and the course of the cough cycle can be discussed with the patient. The pause time and exsufflation are also performed manually. 55 For automatic application, in addition to the above parameters, the duration of the insufflation, pause and exsufflation phases is defined. These values are then shown on the Cough-Assist display. An extended application of the automatic function is triggering, that is patients can trigger the sequences when they are ready for them. However, patients without their own respiratory drive cannot use this function.

29.3 

Endobronchial/Endotracheal Suction

Normally, it is possible to cough up and expectorate secretions that accumulate in the respiratory tract. The mechanisms as described in the chapter “Respiratory gas humidification” can help here. Intubated and ventilated patients do not have the possibility of coughing up. The elimination of secretions is not possible for them. Although it is desired that their cough reflex is maintained, they need help to expel the secretions. Reasons for Extraction: 55 Maintaining the patency of the tracheal cannula. 55 Avoid laying due to secretions. 55 Reduced cough reflexes in case of too deep sedation or coma. 55 Tough mucus with exsiccosis. 55 Preventing infections. Basic Procedure: 55 Informing patients. 55 Keep the procedure as short as possible, max. 20  s, otherwise there is a risk of hypoxia.

29

Preparation: 55 Position patients so that the tracheal cannula can be easily reached; this does not have to be the supine ­position. Suction can also be performed in the lateral or prone position 55 Meanwhile, turn on suction and attach suction catheter. 55 Use suction catheters that are as “atraumatic” as possible; they do not adhere to the mucous membranes, but form an air cushion during suction, which protects the tissue. 55 Put on gloves, face mask and safety goggles. 55 Put on sterile gloves. Implementation: 55 Disconnect patient from the ventilator → place “goose gargle”/connector on a sterile surface (the inside of the sterile glove packaging is suitable for this purpose). 55 Grasp the sterile suction catheter with a sterile glove. 55 Hold and fix the tube with your unsterile hand all the time, the suction is also activated with your unsterile hand → so hold the suction hose firmly. 55 Use your sterile hand to insert the sterile suction catheter into the tube. 55 Insert the suction catheter without suction. 55 Atraumatic suction catheters must be inserted with suction! 55 Insert until resistance is encountered. 55 Do not overcome the resistance with force → in this case do not insert the suction catheter any further! 55 Insertion with rotating movement of the catheter can overcome resistance. 55 Slowly pull out with suction. 55 Pull out the suction catheter with rotating movements. 55 No “poke”, no sudden movements!

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55 If necessary, repeat the procedure if secretion is still present. 55 Then reconnect the “goose gargle”/connector to the tracheal cannula. 55 Final check of the cuff pressure and position of the tracheal cannula.

29

Important to Note: 55 There may be tracheal lesions of the inner wall → risk of bleeding. 55 The suction catheter may injure the carina → risk of bleeding. 55 So-called atraumatic suction catheters are often recommended. 55 The risk of bleeding is higher the more anticoagulants the patient receives. 55 Danger: due to the bleeding and seepage of blood, the tube, trachea and bronchial tubes can be repositioned 55 Have an Ambu bag ready, if necessary use it for positive pressure ventilation. 55 Then reconnect the patient to the respirator. 55 Observe respirator → is sufficient volume administered? Under pressure-controlled ventilation (PCV), it is quite possible that pressure is built up but no volume is delivered. 55 →Note on airway obstruction. 55 →Reference to bronchospasticity. Modern respirators then also give an “apnea alarm”, because no air flows within the tube system. Therefore no breathing cycle can be registered. The display “f” (frequency) therefore also decreases until the apnea alarm is triggered. As a rule, backup ventilation will then take over. If the volume is insufficient, the ventilator will also administer the safety Vt. During this period, the ventilation pressure will increase (see 7 Sect. 9.5).

55 Vagus stimulus can be triggered → bradycardia and RR drop. 55 Sympathetic stimulus can be triggered → tachycardia and RR increase. 55 Therefore observe pulse oximetry during aspiration. 55 If the stimuli are triggered, stop aspiration immediately, usually the bradycardia will also stop. 55 Continuous monitoring of oxygen saturation before, during and after aspiration. 55 Other dangers of endobronchial suctioning: Alveolar collapse and new f­ ormation of atelectases. 55 Evaluation and documentation of the secretions according to composition, consistency, smell and colour. z Insertion Depth of the Suction Catheter

Due to the risks involved, the suction catheter should only be inserted deeper by trained and experienced nursing staff. These are summarized once again in the overview: Risks During Suctioning 55 Suction of the catheter at the bronchial wall –– → thereby injuries or lesions on the bronchial wall 55 Irritation of the carina –– → thereby triggering a very strong cough stimulus 55 Injury of the carina –– → thereby lesions up to necroses at the carina 55 Triggering of bradycardia or tachycardia, drop in oxygen saturation –– → thereby risk of hypoxia

 

Important to Note: 55 The probability that the right main bronchus is more likely to be aspirated, as it falls more steeply than the left

If these risks become more frequent during the suction procedure or are constantly present, the suction catheter should only be inserted as deep as the shaft of the tracheal cannula is long.

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z Subsequent Oral and Nasal Care

55 In addition to endotracheal suction, oral and nasal care should be performed in one step. Here too, all secretions are aspirated orally and nasally. They are assessed according to their consistency, consistency, odour and colour. 55 Secretions of the nasopharynx always represent a reservoir for germs. They form a moist chamber, the environment in which pathogenic germs grow. Accumulated secretions in the nasopharynx hold the danger of silent aspiration. 55 It is obligatory to remove bark, food remains, coatings, etc. from the oral cavity, to cleanse the nose of scabs and dried secretions or blood, and to subsequently care for the skin of the nasal mucosa and lips. 29.3.1 

Closed Versus Open Suction

Discussions on the various advantages and disadvantages of closed versus open suction are still ongoing. These relate, among other things, to the rate of pneumonia or its reduction, change intervals, PEEP and monitoring losses and manageability. In general, closed suction systems are recommended for 55 High oxygen supply, O2 concentration >50%. 55 PEEP >8 mbar. 55 Patients with problem germs (MRSA, AIDS, Tb, 3 or 4 MRGN). 55 Prevention of cross-infections. 55 Infection prophylaxis. With regard to the pneumonia rate, neither the open nor the closed suction system could bring about a significant reduction. One problem of closed suction systems is the accumulation of water in the plastic sleeve, which forms damp chambers and thus reservoirs for germs. Closed suction catheters are rapidly microbially colonised

at the tip. The germs are reintroduced into the respiratory tract during each suction procedure. A change interval of 24–48 h is therefore recommended. The problem with open suction systems is the disconnection of the ventilation tube from the tube. This increases the risk of germ migration. Disconnecting also often results in the personnel being exposed to a wet and humid air stream. This wet and humid air stream, which can also be contaminated with germs, is then poured onto their hands and onto the upper body of the patient. A further problem of disconnection is the loss of PEEP, which can lead to the formation of new atelectases, which only have to be reopened with the reconnection. This impairs oxygenation. Although a negative pressure is automatically generated by the closed suction, the PEEP is at least regionally suctioned. However, closed suction prevents a general loss of PEEP. Ventilation is not interrupted. Disconnections cause a loss of monitoring: there is no monitoring of respiratory rate and volume by the ventilator. Opinions are likely to be divided on manageability. In closed systems, it is often complained that suction cannot be performed so effectively because the catheter is only inserted rigidly. In addition, there is a lack of tactile sensitivity through the plastic sleeve. However, these concerns should diminish with increasing practice and familiarity (. Fig. 29.7).  

29.3.2 

Subglottic Suction

Subglottic suction is used to aspirate secretions that pass through the larynx and glottis and onto the cuff (7 Sect. 4.3.2). Through a small suction tube inserted in the cannula shaft, the secretions that lie on the cuff can be specifically aspirated. The suction can be done with the help of a syringe or a suction device (. Figs. 29.8 and 29.9).  

 

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a

b

c

d

e

f

29 ..      Fig. 29.7  Closed suction

a

b

..      Fig. 29.8  Subglottic suction with suction unit

c

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a

b

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c

..      Fig. 29.9  Subglottic suction manual with syringe

The suction with a syringe is always intermittent. The suction with suction device can be done intermittently or continuously.

29.4 

Inhalation Therapy

Advantages of inhalation therapy compared to systemic application: 55 High local concentration of active ingredients. 55 Low total dose. 55 Favourable effect—side effect ratio. 55 Rapid onset of effect. . Table 29.1 gives an overview of the average particle size that can be inhaled. In a therapeutic inhalation, the inhaled particles should be directed to the place where they can also develop their effect. For this purpose, the respiratory tract is roughly divided up to simplify matters (. Table 29.2 and . Fig.  29.10). Particles that are to be inhaled specifically must be small, the smaller the distance to the airways. Particles to be therapeutically inhaled have a size of 2–6 μm. The optimal particle size is  

 

 

3 μm in the middle. Oscillating diaphragm and nozzle nebulizers produce 3–6  μm. Nonventilated, unventilated lung areas cannot be reached by inhalation, for example atelectasis, emphysema, cystic fibrosis. 29.4.1 

Deposition

The deposition or separation of an inhaled active substance, an inhaled aerosol, in the respiratory tract is called deposition. The deposition is dependent on: 55 Particle size (the place of separation). 55 The breath volume, the inspired air volume. 55 The respiratory flow, the inhalation velocity. 55 Airway geometry and morphology. 55 Influence of the breathing volume. 55 The deeper the breath, the more aerosol is inhaled. 55 With deep breathing the functional dead space has less effect (oral cavity, hypopharynx, trachea = 150 mL). 55 The deeper and slower the inhalation, the more active substance is deposited.

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Influence of the respiratory flow: 55 Slowly inhaled particle follows the respiratory tract. 55 Particle inhaled too quickly already hits proximal airway walls. 55 At a respiratory flow of 30 L/min particles 10 μm.

Central

Trachea, truncal bronchi

5–10 μm

kSedimentation

Intermedial

Bronchia

3–5 μm

Peripherals

Bronchioles and alveoli

0.5–3 μm

..      Table 29.2  Respiratory tract inhalation sites

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Types of Deposition

Is the deposition of particles/aerosols on the mucous membrane following gravity. This deposition depends on the particle size and the residence time in the large and middle airways. The particles follow the inspiratory airflow. The slower and deeper the inhalation, the better the deposition. Particle size 3–10 μm. kDiffusion

Is the deposition of particles/aerosols on the bronchial or alveolar wall. It increases if the particle remains on the wall for a long time. The particles follow the “Brown molecular movement”. They virtually float in the air. Particle size > Die Deutsche Atemwegsliga (The German Respiratory League) has published various videos that illustrate the correct use of the various inhalation systems and techniques. Here, the internet address: 7 https://www.­ youtube.­com/results?search_query=deutsc he±atemwegsliga  

z Application of a Metered Dose Aerosol During Tracheotomy or Machine ­Ventilation

..      Fig. 29.12  Adapter for dosing aerosol (e.g., with kind permission of the company Medisize)

There are several options for the administration of MDIs. Various adapters are available for this purpose, which are shown in . Figs.  29.11, 29.12, 29.13, 29.14, 29.15. They ensure that the inhalate can be safely administered into the airways through the tracheal cannula. However, a slight loss of the active ingredient quantity must be expected. The MDI should be triggered synchronously with inspiration. People with spontaneous breathing should be encouraged to deepen their inhalation and, if they have the capacity, hold their breath a little.  

z Application with Closed Suction

Machine ventilated people also receive the DA synchronously with inspiration. However, the ventilation rhythm is fixed.

..      Fig. 29.13  Use of the adapter for metered dose inhaler (Courtesy of Medisize)

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..      Fig. 29.14  Application location with closed suction (Courtesy of P.J. Dahlhausen & Co. GmbH)

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The spray must be applied at the time of inspiration. It would be advantageous if the inspiratory air could be held for a few seconds, for example by an “inspiration hold” installed on various ventilators. 29.4.4 

Nebuliser Systems

There are three systems available for nebulization of drugs, which are used in outpatient ventilation (. Table 29.3 and . Fig. 29.16). The aerosols generated in this way reach the lungs with the mechanical inspiratory current. This type of inhalation is usually carried out for 5–15 min. Since the aerosols are liquids, the nebulisers must be aligned vertically (. Figs. 29.17, 29.18, 29.19, 29.20 and 29.21). If they are placed at an angle or upside down, the liquid will be lost (. Figs. 29.22a and 29.23a). Most users recommend the use of nebulizers without HME filter (. Figs.  29.17  

..      Fig. 29.15  DA application with closed suction (Courtesy of P.J. Dahlhausen & Co. GmbH)

The application of the high inspiratory ventilation pressure produces the administration and the PEEP of the subsequent expiratory phase should produce an even distribution of the inhalation. However, the problem remains that part of the administered amount of metered dose aerosol is deposited in the system on the walls.

 

 

 

 

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.       Table 29.3  Nebuliser systems Nozzle nebulizer

Aerosol generation by compressed air via compressors according to the Venturi principle (. Fig. 29.16 above)  

Ultrasonic nebulizer

Aerosol generation by low-­ frequency ultrasound, membrane vibration (. Fig. 29.16 middle) Generate the aerosol by electrically driving and vibrating a piezo crystal

Membrane nebulizer

Also calledmesh nebulizer (. Fig. 29.16 below) They use an ultrasonic head to generate vibrations in the inhalation solution and push the droplets through the static mesh disc

 

 

..      Fig. 29.17  Nozzle nebuliser used correctly

..      Fig. 29.18  Nozzle nebuliser correct mounting with HME filter

..      Fig. 29.16  Nebulizer systems (Own representation, edited by Isabel Schlütter)

and 29.20): it would not be wrong to use inhalation with HME filter. However, there is a risk that the pores of the HME filter would be blocked by the inhalation. This would then again impair ventilation (. Figs. 29.18 and 29.21).  

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..      Fig. 29.19  Vibrating diaphragm nebuliser (Aeroneb Pro®) (With friendly permission: INSPIRATION Medical GmbH)

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..      Fig. 29.20  Aeroneb solo nebulizer correctly applied

However, the risk of incorrect application also lies in the wrong order of ­composition. First the nebuliser system and then the HME filter. This way the aerosol is captured by the HME and does not reach the lungs (. Figs.  29.22b and 29.23b). If  

the HME filter is removed for inhalation, it must be stored cleanly in case it is to be used again afterwards. When using the nebulizers with an active humidification system, this remains active and in operation. When using the

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..      Fig. 29.21  Aeroneb solo nebulizer correct installation with HME filter

a

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..      Fig. 29.22  Nozzle nebuliser incorrect application

b

..      Fig. 29.23  Aeroneb solo nebuliser incorrect use

nebulizers with an active humidification system, no HME filter is used either. Inhalation can therefore be performed without any problems. It can be recommended to disconnect the nebulizer system after use. Nebulization should be performed 4–8 times a day, depending on the doctor’s instructions. When the nebulisation interval is over, the HME filter must be replaced for breathing air conditioning. Usually, the nebulizer is removed and the HME filter is put back in in one step. However, this means the repeated dis- and reconnection of the ventilator and thus may involve hygienic risks.

The nebuliser should be stored clean and dry. It can then be used during the subsequent intervals. If the nebuliser remains in the breathing tube system, this increases the dead space, especially if the nebulisation is carried out with HME filter. The ventilation of the lungs may then be too low. Hypoventilation would be the consequence. If the nebuliser remains, residual fluids can accidentally enter the lungs via the goose gargle and tracheal cannula. This corresponds to an aspiration. This in turn increases susceptibility to infection. The comfort for people is generally impaired, because even more equipment is “attached” to the person.

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References Anonymous (n.d.). http://www.­atemwegsliga.­de/ empfehlungen-­positionspapiere.­html?file=tl_files/ eigene-­dateien/empfehlungen/empfehlungen_physiotherapeutischen_atemtherapie.­pdf.­ Recherche 14.12.2014 Empfehlungen für die Auswahl von Inhalationssystemen (2001) Arbeitsgruppe Aerosolmedizin in der Deutschen Gesellschaft für Pneumologie. Pneumologie 55:579–586 Kasper M, Kraut D (2000) Atmung und Atemtherapie. Verlag Hans Huber, Ein Praxishandbuch für Pflegende

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Schill Medizintechnik—Animationsfilm zu Inhalations systemen (n.d.). http://www.­multisonic.de/flash/ D_01_Navigation_03_why.­swf. Recherche 14.12.2014 Schütz A et al (2017) Vergleich verschiedener mechanischer Hustenhilfen durch Messung der exspiratorischen Spitzenflüsse. Pneumologie 71:166–172 Schwabbauer N, Riessen R (2010) Sekretmanagement in der Beatmungsmedizin, UNI-MED Van Gestel A, Teschler H (2014) Physiotherapie bei chronischen Atemwegs- und Lungenerkrankungen: Evidenzbasierte Praxis, 2. Aufl. Springer Verlag Weise S, Kardos P, Pfeiffer-Kascha D, Worth H (2008) Empfehlungen der Deutschen Atemwegsliga, Empfehlungen zur physiotherapeutischen Atem­ therapie, 2. Aufl. Dustri Verlag

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Weaning Hartmut Lang Contents 30.1

Weaning Process – 390

30.2

Weaning Classification – 390

30.3

Conditions for Successful Weaning – 391

30.4

 ursing Measures to Strengthen the Respiratory N Musculature – 393

30.5

Weaning Strategies – 393

30.5.1 30.5.2

 iscontinuous Weaning – 393 D Continuous Weaning – 394

30.6

Weaning Index (RSB Index) – 395

30.7

Weaning of Long-Term Ventilated Patients – 396

30.7.1 30.7.2 30.7.3 30.7.4 30.7.5

 onditions – 396 C Weaning Process – 397 Carrying Out the Spontaneous Breathing Test – 397 Weaning – 398 Closure of the Tracheotomy – 399

Further Reading – 399

© Springer-Verlag GmbH Germany, part of Springer Nature 2023 H. Lang (ed.), Out-of Hospital Ventilation, https://doi.org/10.1007/978-3-662-64196-5_30

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30.1 

Weaning Process

An international working group (task force) consisting of five international professional societies has described six different phases of the weaning process (Boles et al. 2007a, b): 1. Intubation or tracheal cannula supply, ventilation and treatment of respiratory insufficiency of the patient. 2. Considering whether a patient is ready for weaning, weaning off the ventilator. 3. Carrying out tests, using criteria for assessing whether the patient is weanable; these should confirm or reject weanability. 4. Carrying out a spontaneous breathing test (SBT  =  self breathing trial): the patient should be able to breathe reliably and spontaneously for a long time. 5. Extubation or decannulation if the spontaneous breathing test is successful. 6. If necessary, re-tubation or recanalization in case of subsequent failure. According to the Task Force, a patient is considered successfully weaned if he or she can breathe spontaneously for at least 48 h after extubation or decannulation without further ventilatory support. Weaning failure is defined as the following events occurring within the first 48 h: 1. Failed spontaneous breathing test. 2. Reintubation or recannulation with resumption of ventilatory support. 3. Death.

30.2 

Weaning Classification

The same task force divides the weaning patients into three groups (. Table 30.1) The patients of group 3 (prolonged weaning) are further differentiated (. Table  30.2). The further subdivision is shown in the S2K guideline “Prolonged Weaning” of the DGP under the direction  

 

..      Table 30.1  Weaning classification (According to Boles et al. 2007a, 2007b and Funk et al. 2010) Group

Category

Definition

1

Simple weaning

Successful weaning after a first spontaneous breathing trial (SBT = self breathing trial) and the first extubation This is almost 60% of all intubated patients

2

Difficult weaning

Weaning does not succeed immediately A first SBT fails Weaning succeeds however at the latest with the third SBT Or: Weaning succeeds within 7 days after the first SBT failed Proportion 26% of patients

3

Prolonged or extended weaning

Weaning only succeeds after the third SBT, all before that all fail Or: Weaning only succeeds after 7 days, after the first SBT failed Share 14% of patients

Source of classification: Boles et al. (2007a, b) Source via percentage distribution: Funk et al. (2010)

of Prof. Schönhofer. It refers to patients who are ventilated for a long time and have difficulties in weaning. Non-invasive ventilation (NIV) has become an integral part of ventilation weaning. Patients who are successfully extubated or decannulated but do not yet have sufficient spontaneous breathing (primary weaning failure) can benefit from NIV. Reintubation or recannulation can be avoided by NIV. Secondary weaning failure may occur in patients who have been successfully extu-

391 Weaning

..      Table 30.2  Subgroups of prolonged weaning (According to Schönhofer et al. 2014) 3a

3b

Prolonged or extended wine without NIV

Prolonged wine with NIV

Successful vinification with extubation or decannulation only after at least three unsuccessful SBTs Or: Ventilation for more than seven days after the first unsuccessful SBT without the use of NIV Successful vinification with extubation or decannulation only after at least three unsuccessful SBTs Or: Ventilation longer than seven days after the first unsuccessful SBT and only by means of NIV, if necessary with continuation of NIV as extra-clinical ventilation

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55 Sufficient ventilation. 55 Intact central respiratory drive. 55 Strengthen respiratory musculature. kSufficient Oxygenation

It is reached when pO2 >60 mmHg (8 kPa) is reached with an O2 content