ASTHMA EDUCATION principles and practice for the asthma educator. [2 ed.] 9783030778965, 3030778967

357 80 15MB

English Pages [660] Year 2021

Table of contents :
Preface
References
Acknowledgments
Contents
Abbreviations
Part I: Asthma: The Fundamentals
1: Asthma and Asthma Education: The Background
1.1 Introduction
1.2 What Is Asthma?
1.2.1 Symptoms
1.2.2 Definitions
1.3 Significance of Asthma
1.3.1 Overview
1.3.2 Morbidity
1.3.3 Mortality
1.3.4 Costs
1.4 Etiology of Asthma
1.4.1 Allergy and Asthma
1.5 Genetics and Environment
1.5.1 Phenotype and Genotype Correlation
1.5.2 Environmental Issues
1.6 Approaches to Asthma
1.6.1 Guidelines
1.6.2 NHLBI Guidelines
1.6.3 Pediatric Guidelines
1.6.4 COVID-19 and Asthma
1.6.5 Organization of Care
1.6.5.1 General Approach of Health Systems
1.6.5.2 Healthcare Professionals
1.6.5.3 Personal Responsibility
1.7 Education of Persons with Asthma
1.7.1 The Issues
1.7.2 Role of the Asthma Educator
1.7.3 Skills of the Asthma Educator
1.7.4 Essential Qualities of the Educator
References
2: Lung Structure and Function
2.1 The Respiratory Tract
2.2 Parts of the Respiratory Tract
2.2.1 Nose
2.2.2 Mouth and Pharynx
2.2.3 Larynx
2.2.4 Tracheobronchial Tree Including Alveoli
2.2.5 Histology of the Airways
2.2.6 Rib Cage and Diaphragm
2.3 The Nervous System and the Lungs
2.4 Control of Breathing
2.5 Defense Mechanisms of the Lungs
2.5.1 Specific Defenses: Immunological Mechanisms
2.6 Lung Changes and Pathophysiology of Asthma
2.7 Conclusion
2.8 Background Reading
References
3: Measurements of Lung Function
3.1 Overview
3.2 Lung Volumes and Capacities
3.2.1 Volumes
3.2.1.1 Tidal Volume (VT, Sometimes Shown as TV)
3.2.1.2 Inspiratory Reserve Volume (IRV)
3.2.1.3 Expiratory Reserve Volume (ERV)
3.2.1.4 Residual Volume (RV)
3.2.2 Lung Capacities
3.2.2.1 Total Lung Capacity (TLC)
3.2.2.2 Inspiratory Capacity (IC)
3.2.2.3 Functional Residual Capacity (FRC)
3.2.2.4 Vital Capacity (VC)
3.2.2.5 Forced Vital Capacity (FVC)
3.2.2.6 Forced Expiratory Volume in One Second (FEV1)
3.2.2.7 Integrating Capacities
3.2.3 “Normal” or “Predicted” Values
3.3 Spirometry
3.3.1 FEV1, FVC, and FEV1/FVC
3.3.1.1 Forced Expiratory Flow Maximum (FEFmax)
3.3.1.2 Forced Expiratory Flow25-75 (FEF25-75)
3.3.1.3 Expiratory Flow200-1200 (FEF200-1200)
3.3.2 Flow-Volume Loops
3.3.2.1 Volume-Time Curves
3.3.2.2 Technical Requirements for Spirometry
3.3.2.3 Criteria for Acceptability
Individual Factors
The Technologist
Factors Affecting Reproducibility
Body Position
3.3.3 Bronchodilators in Pulmonary Function Testing
3.3.4 A Pulmonary Function Test and Its Interpretation
3.4 Measures of Lung Function
3.4.1 Peak Flow Measurement
3.4.1.1 Calculating Reversibility
3.4.1.2 Diurnal Variation
3.4.1.3 Calculating Diurnal Variability
3.4.1.4 Consistency in Obtaining PEF Readings
3.4.1.5 PEF and Adherence
3.4.2 Other Measures of Lung Function
3.4.2.1 Fraction of Exhaled Nitric Oxide (FeNO)
3.4.2.2 Dilution Techniques: Helium and Nitrogen
3.4.2.3 Plethysmography
3.5 Bronchial Challenge Testing
3.5.1 Methacholine and Histamine Challenge
3.5.2 Exercise Testing
3.5.3 Inspired Cold Air
3.5.4 Ultrasonic Distilled Water
3.5.5 Adenosine 5’-Monophosphate (AMP)
3.6 Other Testing Methods
3.6.1 Bronchoalveolar Lavage (BAL)
3.6.2 Induced Sputum
3.6.3 Exhaled Breath Condensate (EBC)
3.7 Oxygen Saturation
3.8 Pulmonary Function Testing in Infants and Preschool Children
3.8.1 Pulmonary Function Testing in Infants
3.8.2 Pulmonary Function Testing in Preschool Children
3.8.2.1 Forced Oscillation Technique (FOT)
3.8.2.2 Interrupter
3.9 Pulmonary Function Testing of Adults Unable to Do Standard Spirometry
3.10 Quality Control
3.11 Application
References
4: Clinical Presentation of Asthma
4.1 Introduction
4.1.1 Symptoms: Overview
4.1.2 Detailed History
4.1.3 Physical Examination
4.1.3.1 Palpation
4.1.3.2 Percussion
4.1.3.3 Auscultation
4.1.3.4 Other Components of Examination
4.2 Investigations: Spirometry
4.2.1 Other Investigations
4.2.2 Trial of Therapy
4.3 Asthma Severity
4.3.1 Classification of Severity Before Treatment
4.3.2 Risk Domain
4.4 Patterns of Asthma
4.4.1 Important Factors Contributing to Severity
4.4.1.1 Phenotypes of Asthma
4.4.1.2 Exercise-Induced Asthma
4.4.1.3 Nocturnal Asthma
4.4.1.4 Allergies, Asthma, and Seasonal Changes
4.4.2 Occupational Asthma
4.5 Life-Threatening Asthma
4.5.1 Severe Acute Asthma (Status Asthmaticus)
4.5.2 Brittle Asthma, Catastrophic Asthma
4.6 Differential Diagnoses
4.6.1 Wheeze and Lung Disease
4.6.2 COPD and Asthma
4.6.3 Hyperventilation
4.6.4 Vocal Cord Dysfunction (VCD)
4.6.5 Bronchial Obstruction
4.7 Time Course of Events in Asthma
4.7.1 Response to Exercise
4.7.2 Response to Allergens
4.7.3 Response to Viral Infection
4.8 Diagnostic Problems in Asthma
4.8.1 Age-Related Asthma
4.8.1.1 Less Than One Year of Age
4.8.1.2 One to Five Years
4.8.1.3 Five to Twelve Years
4.8.1.4 Twelve to Twenty-Five Years
4.8.1.5 Twenty-Five to Thirty-Five Years
4.8.1.6 Thirty-Five to Sixty Years
4.8.1.7 Sixty Years and Above
4.9 Sex and Gender Differences in Asthma
4.10 Avoiding Delays in Diagnosis
4.11 Monitoring Asthma
4.11.1 Fraction of Exhaled Nitric Oxide (FeNO)
4.12 Referral to a Specialist
4.13 Application
References
5: Environmental Issues in Asthma Management
5.1 Introduction
5.2 Environmental Issues and Common Triggers of Asthma
5.2.1 Outdoor Allergens
5.2.1.1 Pollen
5.2.1.2 Molds
5.2.2 Indoor Allergens
5.2.2.1 Dust Mites
5.2.2.2 Cockroaches
5.2.2.3 Rodents
5.2.2.4 Pets
5.2.2.5 Mold
5.2.2.6 Ladybugs
5.2.2.7 Latex
5.2.2.8 Cannabis
5.2.3 Irritants
5.2.3.1 Air Pollution
5.2.3.2 Tobacco
5.2.3.3 Other Irritants
5.3 Ingested Allergens
5.3.1 Oral Allergy Syndrome
5.3.2 Food Additives
5.3.2.1 Sulfites
5.4 Non-allergenic Triggers or Irritants
5.4.1 Cold Air
5.4.2 Exercise
5.4.3 Emotion
5.4.4 Viral Infections
5.4.5 Medication Sensitivity
5.5 Exposure Reduction and Avoidance Techniques
5.5.1 Pollen
5.5.2 Mold
5.5.2.1 Outdoor Mold
5.5.3 Dust and Dust Mites
5.5.4 Cockroach Allergen
5.5.5 Pet Allergen
5.5.6 Rodent Allergen
5.5.7 Food Allergen
5.5.8 Medications
5.5.9 Insect Allergen
5.5.10 Irritants
5.5.11 Viral Infections
5.5.12 Cold Air
5.5.13 Exercise
5.5.13.1 Asthma and the Athlete
5.5.14 Latex
5.5.15 Conclusion
5.6 Identification of Triggers
5.7 Home Assessment
5.7.1 Smoking
5.7.2 Vaping
5.8 Application
References
6: Medications Used in Asthma Management
6.1 Introduction
6.2 Principles of Medication Use
6.3 Available Medications: Broad Categories of Use
6.4 Quick-Relief Medications (“Rescue Medications”)
6.4.1 Short-Acting Beta-Agonist (SABA) Bronchodilators
6.4.2 Short-Acting Anti-cholinergic Bronchodilators
6.4.3 Systemic Corticosteroids
6.4.3.1 Side Effects of Systemic Corticosteroids: Some Comments
6.4.3.2 Use of Systemic Corticosteroids in Severe Acute Asthma
6.5 Long-Term Asthma Control Medications
6.5.1 Inhaled Corticosteroids (ICS)
6.5.2 Long-Acting Beta-Agonists (LABA)
6.5.3 Long-Acting Muscarinic Antagonists (LAMA)
6.5.4 Combination Products
6.5.5 Leukotriene Receptor Antagonists (LTRA)
6.5.6 Immunomodulators and “Precision Health”
6.5.7 Long-Term Systemic Corticosteroids
6.5.8 Theophylline
6.5.9 Cromolyn and Nedocromil
6.6 Other Medications Used in Asthma
6.7 Immunotherapy in Asthma (“Allergy Shots”)
6.8 Low Evidence-Based Medications as Treatment Options
6.8.1 Approach to the Use of These Medications
6.9 Role of Bronchial Thermoplasty in Treatment
6.10 Concern About Side Effects: General Approach
6.11 Classification of Severity After Treatment
6.12 Step Approach to Asthma Management
6.13 Goals of Therapy
6.14 Quality-of-Life Scores
6.15 Conclusion
6.16 Application
References
7: Inhalation Devices Used in Asthma
7.1 Introduction
7.1.1 Metered Dose Inhalers (MDIs)
7.1.1.1 Technique
Open Mouth Technique
Closed Mouth Technique
Cleaning
7.1.1.2 Spiriva Respimat
Initial Priming
Use, Care, Cleaning, and Replacement
7.1.1.3 MDI Replacement
7.1.1.4 Storage
7.1.1.5 Priming the HFA Inhaler
7.1.1.6 Common Errors with MDIs
7.1.1.7 Disadvantages of the MDI
7.1.2 Spacers and Valved Holding Chambers
7.1.2.1 Valved Holding Chambers
7.1.2.2 Requirements of a Chamber or Spacer
Using an AeroChamber with Mask
Using an AeroChamber with Mouthpiece
Cleaning
7.1.3 Dry Powder Inhalers (DPIs)
7.1.3.1 Common Errors with DPIs
7.1.3.2 Aerolizer
7.1.3.3 Diskus
7.1.3.4 Ellipta
7.1.3.5 RespiClick
7.1.3.6 Digihaler
7.1.3.7 Twisthaler
7.1.3.8 Turbuhaler
7.1.3.9 Flexhaler
7.1.3.10 Wixela Inhub
7.1.4 Nebulizers
7.1.4.1 Advantages and Disadvantages
7.1.4.2 Technique
Steps in Using a Nebulizer
7.1.4.3 Ultrasonic Nebulizers
7.1.4.4 Substitute Devices
7.1.5 Choice of Inhaler Devices
7.1.5.1 Considerations in Choosing a Device
7.1.5.2 Choosing a Device
7.1.6 Application
References
8: Special Situations in Asthma
8.1 Special Situations in Asthma
8.2 Pregnancy
8.3 Asthma in Older Adults
8.4 Diabetes
8.5 Surgery and Anesthesia
8.6 Occupational Asthma
8.7 Obesity
8.8 Immunization/Vaccination
8.9 Smoking
8.10 Competitive Athletes
8.11 Non-asthma Medications and Asthma
8.11.1 Aspirin Sensitivity
8.11.2 Sulfite Sensitivity
8.11.3 Antihistamines
8.11.3.1 Adverse Effects of Antihistamines
8.11.3.2 Excipients
8.11.4 Over-the-Counter Medications
8.12 Direct-to-Consumer Advertising (DTCA): Advantages and Disadvantages
References
9: Comorbidities in Asthma
9.1 Comorbidities and Their Treatment
9.2 Contact Dermatitis
9.3 Atopic Dermatitis and Eczema
9.4 Rhinitis, Sinusitis, and Rhinosinusitis
9.4.1 Rhinitis
9.4.2 Sinusitis
9.5 Nasal Polyps
9.6 Gastroesophageal Reflux
9.7 Vocal Cord Dysfunction (VCD)
9.8 Asthma-COPD Overlap (ACO)
9.9 Obstructive Sleep Apnea
9.10 Bronchopulmonary Aspergillosis (ABPA)
9.11 Depression
9.12 Acute, Severe Acute, and Life-Threatening Asthma
9.12.1 Classification of Severity of Acute Asthma
9.12.1.1 Assessing an Attack
9.12.1.2 The Life-Threatening Attack
9.12.2 Treating Asthma in the Home
9.12.3 Treating Asthma in the Office
9.12.4 Cardiopulmonary Resuscitation (CPR)
9.13 Anaphylaxis: Type 1 Allergy
9.13.1 Definition
9.13.2 Causes
9.13.3 Risk Factors for Anaphylaxis
9.13.4 Symptoms
9.13.4.1 Biphasic Reactions
9.13.5 Differential Diagnosis of Anaphylaxis
9.13.6 Management of Anaphylaxis
9.13.7 Education for Anaphylaxis
9.14 Application
References
Part II: The Role of Education
10: An Integrated Approach to Asthma Management
10.1 Overview
10.2 Asthma Management: A General Approach
10.2.1 Steps Taken by Healthcare Provider
10.2.2 Approach to Management: Role of Educator
10.2.3 Educational Visits
10.2.3.1 Initial Visit
10.2.3.2 Follow-Up Interview
10.2.3.3 Further Follow-up Appointments
10.3 Management of Problems by Age
10.3.1 Less than 1 Year
10.3.2 From 1 to 5 Years
10.3.3 From 5 to 12 Years
10.3.4 From 12 to 25 Years
10.3.5 From 25 to 35 Years
10.3.6 From 35 to 60 Years
10.3.7 Over 60 Years
10.4 Home Monitoring
10.4.1 The Peak Flow Meter
10.4.2 Calculating Diurnal Variability: Other Methods
10.4.2.1 Method 1
10.4.2.2 Method 2
10.4.2.3 Method 3
10.4.3 New Personal Best Readings
10.4.4 Checking PEF Technique
10.4.5 The Peak Flow Diary
10.4.6 Observing Symptoms and Using the Diary
10.4.7 The Asthma Action Plan
10.4.7.1 Acute Asthma
10.4.7.2 Other Approaches
10.5 Severe, Acute, and Chronic Asthma
10.6 Potentially Fatal Asthma
10.7 Application
References
11: Adherence
11.1 Overview
11.2 Healthcare Providers and Self-Management
11.3 Adherence: Common Issues
11.3.1 Asthma as a Chronic Condition
11.3.2 Medication Regimens
11.3.3 Avoidance of Triggers
11.3.4 Recognition of Deterioration
11.3.5 Reaction to Emergency Situations
11.3.6 Impact of Asthma
11.3.6.1 Effect on the Individual
11.3.6.2 Effect on the Family
11.3.7 Coping Strategies
11.3.8 Psychosocial Factors
11.4 Adherence
11.4.1 Definition
11.4.2 Physician and Healthcare Provider Adherence to Guidelines
11.4.3 Nonadherence
11.4.4 Patterns of Nonadherence
11.4.5 Identifying Nonadherence
11.4.6 The Team Approach
11.5 General Approach to Adherence
11.5.1 Strategies for Chronic Illness
11.5.2 Anticipatory Guidance
11.5.2.1 Short-Term Counseling
11.5.2.2 Long-Term Counseling for Parents
11.5.2.3 Counseling for Adolescents
11.5.2.4 Long-Term Counseling for Adults
11.5.3 Skills Required by the Educator
11.6 Specific Aids to Adherence
11.6.1 Self-Management of Asthma
11.6.1.1 Attack Management Skills
11.6.1.2 Prevention Skills
11.6.1.3 Social Skills
11.6.2 Health Education
11.7 Cultural and Religious Differences
11.8 Suggested Reading
11.9 Application
References
12: Complementary and Alternative Medicine in Asthma
12.1 Introduction
12.2 Specific Types of Care
12.2.1 Relaxation
12.2.2 Meditation
12.2.3 Yoga
12.2.4 Biofeedback
12.2.5 Breathing Exercises
12.2.6 Hypnosis
12.2.7 Imagery
12.2.8 Therapeutic Touch
12.2.9 Religion
12.3 Professions
12.3.1 Osteopathy
12.3.2 Chiropractic
12.3.3 Acupuncture
12.3.4 Homeopathy
12.3.5 Massage Therapy
12.3.6 Naturopathy
12.4 Self-Help CAM
12.4.1 Herbs
12.4.2 Nutrition and Nutritional Supplements
12.4.3 Exercise as Treatment
12.4.4 Electromagnetic Treatment
12.4.5 Aromatherapy
12.4.6 Reflexology
12.5 Approach of the Educator
12.6 Application
References
13: Frequently Asked Questions
13.1 Introduction
13.2 Asthma: Symptoms and Control
13.3 Triggers
13.4 Fatal Asthma
13.5 Exercise and Asthma
13.6 Medications
13.7 Testing and Devices
13.8 Spacers
13.9 The Peak Flow Meter
13.10 Allergies
13.11 School and Camp
13.12 Pregnancy
13.13 Travel
13.14 Coping
13.15 Immunizations
13.16 Other Questions
Part III: The Effective Asthma Educator
14: Learning: Theories and Principles
14.1 Introduction
14.1.1 How Is Learning Achieved?
14.2 Learning and Teaching Definitions
14.2.1 Learning
14.2.2 Teaching
14.3 The Learning Process
14.4 Theories of Learning
14.4.1 Behaviorism
14.4.1.1 Relevance of Behavioral Theory to Asthma Education
14.4.2 Gestalt or the Cognitive Theory of Learning
14.4.2.1 Relevance of Gestalt Theory to Asthma Education
14.4.3 The Humanistic Theory
14.4.3.1 Relevance of Humanistic Theory to Asthma Education
14.4.4 Information Processing
14.4.4.1 Relevance of Information Theory to Asthma Education
14.5 Online Learning: Some Considerations
14.6 Personality Development
14.6.1 Infancy: Trust Versus Mistrust
14.6.2 Early Childhood: Autonomy Versus Shame and Doubt
14.6.3 Middle Childhood: Initiative Versus Guilt
14.6.4 Elementary School Age: Accomplishment Versus Inferiority
14.6.5 Adolescence: Identity Versus Confusion
14.6.6 Young Adulthood: Intimacy Versus Isolation
14.6.7 Adulthood: Generativity Versus Stagnation
14.6.8 Old Age: Integrity Versus Despair
14.6.9 Application of Theories to Asthma Education
14.7 Age-Related Learning
14.7.1 Learning Styles
14.7.2 Children
14.7.3 Adolescents
14.7.4 Adults
14.7.5 Older Adults
14.7.6 Implication of Learning Styles
14.7.7 Types of Learning
14.8 Barriers to Learning
14.8.1 Environment
14.8.2 Physical Factors
14.8.3 Individual Factors
14.8.4 Sociological and Emotional Factors
14.9 Principles of Learning
14.10 Application
References
15: Teaching the Person with Asthma
15.1 Introduction
15.2 Teaching Approaches for Different Audiences
15.2.1 Parents
15.2.1.1 Attitude
15.2.1.2 Asthma Diary
15.2.1.3 Parents Are the Child Experts
15.2.1.4 Warning Signs
15.2.1.5 Asthma Plan
15.2.2 Children
15.2.3 Adolescents
15.2.3.1 Independence
15.2.3.2 Rebellion
15.2.3.3 Peer Pressure
15.2.3.4 Adherence
15.2.3.5 Teaching Approach
15.2.3.6 Adolescent Concerns
15.2.4 Adults
15.2.5 Low-Literacy Individuals
15.2.6 The Older Adult
15.2.7 Response to Education
15.2.8 Cultural Competency
15.2.9 Mobile Applications for Asthma
15.3 Teaching Methods
15.3.1 The Individual
15.3.2 The Small Group
15.3.3 The Large Group
15.4 The Process of Education
15.4.1 The Cognitive Domain
15.4.2 The Affective Domain
15.4.2.1 The Affective Domain and Chronic Illness
15.4.3 The Psychomotor Domain
15.5 Planning for Teaching
15.5.1 Assessment
15.5.2 Planning
15.5.3 Planning for the Affective Domain
15.5.4 Planning for the Cognitive Domain
15.5.5 Planning for the Psychomotor Domain
15.5.6 Implementation
15.5.7 Evaluation
15.5.8 Sample Teaching Plans
15.6 The Role of the Educator
15.6.1 Principles of Communication in a Consultation
15.6.2 Setting the Climate for Teaching
15.6.3 Ways of Teaching That Can Cause Problems
15.7 Teaching Strategies
15.8 The Team Approach to Teaching
15.9 Application
References
16: Clinic Management and Evaluation
16.1 Introduction
16.2 Running an Asthma Clinic
16.2.1 Facilities
16.2.2 Time
16.2.3 Equipment and Materials
16.2.3.1 Peak Flow Meters
16.2.3.2 Placebo Devices
16.2.3.3 Peak Flow and Symptom Diaries
16.2.3.4 Asthma Action Plans
16.2.3.5 Quality of Life (QOL) Scores
16.2.3.6 Information Leaflets
16.2.3.7 Books and Internet Materials
16.2.3.8 Visual Aids
16.2.3.9 Computer-Assisted Learning (CAL)
16.2.3.10 Records
16.2.4 Telemedicine
16.2.5 Resources
16.2.6 Evaluation of Teaching Materials
16.2.7 Education Programs
16.2.8 Planning
16.2.9 Costs
16.2.10 Data Collection
16.2.11 Standards
16.3 Teaching in the Home
16.3.1 Assessing the Environment
16.3.2 The Home Teaching Kit
16.4 The School Environment
16.4.1 Classroom Assessment
16.4.2 Within the School
16.4.3 Outside the School
16.4.4 School Policies
16.4.5 Physical Education
16.4.6 General Education for School Staff
16.4.6.1 Parents and School
16.5 Evaluation of Education Programs
16.5.1 Designing an Evaluation Program
16.5.2 Establishing Standards
16.5.3 Data Collection
16.5.4 Data Analysis and Evaluation
16.5.5 Review
16.5.6 Confidentiality
16.6 Self-Evaluation
16.6.1 Using the Self-Evaluation Checklists
16.7 Self-Evaluation Checklists
16.7.1 Checklist 2
16.8 Application
Appendix 16.1
Reading Material for Patients
Appendix 16.2
Internet Addresses
General Interest
For Asthma Educators (Not for Patients)
Appendix 16.3
Suggested Reading for Asthma Educators
References
Part IV: Case Studies
17: Case Studies
17.1 Introduction
17.2 Instructions for Case Studies 1 to 14
17.3 Additional Case Studies
17.4 Case Study 1
17.5 Case Study 2
17.5.1 Response to Case Study 1
17.5.2 Response to Case Study 2
17.6 Case Study 3
17.7 Case Study 4
17.7.1 Response to Case Study 3
17.7.2 Response to Case Study 4
17.8 Case Study 5
17.8.1 Response to Case Study 5
17.9 Case Study 6
17.9.1 Response to Case Study 6
17.10 Case Study 7
17.10.1 Response to Case Study 7
17.11 Case Study 8
17.11.1 Response to Case Study 8
17.12 Case Study 9
17.12.1 Response to Case Study 9
17.13 Case Study 10
17.14 Case Study 11
17.15 Case Study 12
17.16 Case Study 13
17.17 Case Study 14
Glossary
Index

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Asthma Education Principles and Practice for the Asthma Educator Ian Mitchell Gaynor Govias Second Edition

123

Asthma Education

Ian Mitchell • Gaynor Govias

Asthma Education Principles and Practice for the Asthma Educator Second Edition

Ian Mitchell University of Calgary Calgary, AB Canada

Gaynor Govias Edmonton, AB Canada

1st edition: © Authors 2005 ISBN 978-3-030-77895-8 ISBN 978-3-030-77896-5 (eBook) https://doi.org/10.1007/978-3-030-77896-5 © The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Switzerland AG 2005, 2021 This work is subject to copyright. All rights are solely and exclusively licensed 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 Nature Switzerland AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland

Preface

To educate educators! But the first ones must educate themselves! And for these I write. (Friedrich Nietzsche)

Much has changed since 2005 in the fields of asthma and asthma education, when this book was first published as Asthma Education – Principles and Practice [1]. While the principles and theory underlying asthma remain much the same today, new equipment, guidelines, and medications have since appeared, and so we felt it appropriate to release this second edition. Some of the new medications belong to the paradigm of precision health and promise to be as great a revolution in asthma care as inhaled corticosteroids when they were introduced. We aimed for clarity in our writing, using all the tools of the English language. We used American spellings and American trade names for medications and devices. Sadly, manufacturers, selling the same medication and device, often use different names in different countries. If you find some of the spelling unfamiliar, we suggest you consult a national medical organization. The first edition was ahead of its time – it was published when the profession of asthma education was in its infancy. Regulatory organizations were just being set up, and only a handful of trained asthma educators existed in America. There are more educators today, as well as institutions that formally train asthma educators, but comprehensive texts written specifically for asthma educators are still rare. Asthma Education – Principles and Practice remains the only text written specifically for asthma educators on asthma education. This second edition – which we call “Asthma Education: Principles and Practice for the Asthma Educator” – has been updated and made comprehensive, and now includes a part on COVID and asthma. We believe it is still the only textbook an asthma educator will require. It provides the necessary medical knowledge, describes medications and equipment in use, and – most importantly – answers the vital question that conscientious asthma educators everywhere ask themselves: “I have all this knowledge. Now how do I communicate it effectively to my patients?” The cooperative relationship between those with asthma and their professional advisers – which we have long advocated – is becoming the norm in all areas of healthcare.

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If you are an experienced asthma educator, and now have the immensely rewarding job of teaching new educators, we hope this book will make your job a little easier. We believe it will also make an excellent text and reference source. The goal of education is to meet the needs of the individual. In asthma, the goal is to help those with asthma to self-manage their illness. But the educator also has an unstated goal. Dr. Richard S. Irwin [2], in a convocation speech to the American College of Chest Physicians, read aloud their pledge on patient-focused care (PFC). It states that: PFC is compassionate, is sensitive to the everyday and special needs of patients and their families, and is based on the best available evidence. It is interdisciplinary, safe and monitored. To ensure the provision of PFC in my professional environments, I shall willingly embrace the concepts of lifelong learning and continuous quality improvement.

It is a pledge that we believe every aspiring asthma educator should take and strive to meet, for it will make the difference between being merely competent – and being outstanding and effective.

References 1. ISBN 1-896291-19-8. 2. Irwin RS. Patient-focused care: the 2003 American College of Chest Physicians Convocation Speech. Chest 2004;1125: 1910–12.

Calgary, AB, Canada Edmonton, AB, Canada

Ian Mitchell Gaynor Govias

Acknowledgments

This book could not have been written without the guidance and support of many individuals over many, many years. The authors welcome the opportunity to specially thank the people who helped them along the sometimes- difficult path from inspiration to publication. The influence of wise mentors, whether at the start of a career or at some stage during it, cannot be over-emphasized. Ian Mitchell’s interest in asthma was stimulated, first by Drs. Ian Grant and Hamish Simpson in Edinburgh, and then by Dr. Henry Levison in Toronto, all of whom provided a first-rate grounding in the scientific aspects of lung disease and asthma. Further education came from the nurse educators and the psychosocial team at the Alberta Children’s Hospital, Calgary, Canada. Gaynor Govias was encouraged and supported by Dr. G Fred MacDonald, an early advocate for patient education who set a very high standard in the field. The advice and encouragement she received from Dr. Tom Plaut, Dr. Elliot Ellis, Dr. Kathy Conboy-Ellis, and Dr. Stanley Galant was also invaluable. A special thank you to Kenneth Govias who looked after the technical aspects of the manuscript; offered helpful advice, support, and wise counsel; read and re-read much of the text; and kept us on schedule. For the use of their diagrams, photographs, and tables, our thanks go to the Asthma Education Clinic Ltd., AstraZeneca Canada Inc., Boehringer- Ingelheim Canada, Medical International Research, Merck Canada Inc., Mylan Pharmaceuticals ULC, Pari Respiratory Equipment, and Teva Canada. For both authors, some of the best teachers were the people with asthma and their families. Because of them, both authors improved (and continue to improve) their knowledge and skills, and have come to appreciate that patients are unique individuals whose medical treatment must be compatible with their goals in life. Our special thanks to them.

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Contents

Part I Asthma: The Fundamentals 1 Asthma and Asthma Education: The Background �� 3 1.1 Introduction�� 4 1.2 What Is Asthma? �� 5 1.2.1 Symptoms �� 5 1.2.2 Definitions�� 7 1.3 Significance of Asthma �� 8 1.3.1 Overview�� 8 1.3.2 Morbidity�� 9 1.3.3 Mortality �� 11 1.3.4 Costs�� 12 1.4 Etiology of Asthma �� 15 1.4.1 Allergy and Asthma�� 15 1.5 Genetics and Environment�� 16 1.5.1 Phenotype and Genotype Correlation �� 16 1.5.2 Environmental Issues�� 17 1.6 Approaches to Asthma�� 20 1.6.1 Guidelines �� 20 1.6.2 NHLBI Guidelines�� 20 1.6.3 Pediatric Guidelines�� 23 1.6.4 COVID-19 and Asthma�� 24 1.6.5 Organization of Care�� 25 1.7 Education of Persons with Asthma �� 27 1.7.1 The Issues�� 27 1.7.2 Role of the Asthma Educator�� 29 1.7.3 Skills of the Asthma Educator�� 30 1.7.4 Essential Qualities of the Educator �� 31 References�� 33 2 Lung Structure and Function �� 39 2.1 The Respiratory Tract �� 40 2.2 Parts of the Respiratory Tract �� 40 2.2.1 Nose�� 40 2.2.2 Mouth and Pharynx�� 41 2.2.3 Larynx �� 41 2.2.4 Tracheobronchial Tree Including Alveoli �� 41 ix

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2.2.5 Histology of the Airways�� 43 2.2.6 Rib Cage and Diaphragm�� 44 2.3 The Nervous System and the Lungs �� 45 2.4 Control of Breathing �� 46 2.5 Defense Mechanisms of the Lungs �� 48 2.5.1 Specific Defenses: Immunological Mechanisms�� 48 2.6 Lung Changes and Pathophysiology of Asthma �� 50 2.7 Conclusion�� 54 2.8 Background Reading�� 54 References�� 54 3 Measurements of Lung Function�� 55 3.1 Overview�� 57 3.2 Lung Volumes and Capacities�� 57 3.2.1 Volumes�� 58 3.2.2 Lung Capacities�� 59 3.2.3 “Normal” or “Predicted” Values �� 59 3.3 Spirometry�� 62 3.3.1 FEV1, FVC, and FEV1/FVC�� 65 3.3.2 Flow-Volume Loops�� 66 3.3.3 Bronchodilators in Pulmonary Function Testing�� 70 3.3.4 A Pulmonary Function Test and Its Interpretation�� 71 3.4 Measures of Lung Function�� 71 3.4.1 Peak Flow Measurement�� 71 3.4.2 Other Measures of Lung Function�� 77 3.5 Bronchial Challenge Testing�� 80 3.5.1 Methacholine and Histamine Challenge �� 80 3.5.2 Exercise Testing�� 81 3.5.3 Inspired Cold Air�� 83 3.5.4 Ultrasonic Distilled Water�� 83 3.5.5 Adenosine 5’-Monophosphate (AMP)�� 83 3.6 Other Testing Methods�� 83 3.6.1 Bronchoalveolar Lavage (BAL)�� 83 3.6.2 Induced Sputum�� 84 3.6.3 Exhaled Breath Condensate (EBC)�� 84 3.7 Oxygen Saturation�� 85 3.8 Pulmonary Function Testing in Infants and Preschool Children �� 85 3.8.1 Pulmonary Function Testing in Infants�� 85 3.8.2 Pulmonary Function Testing in Preschool Children�� 86 3.9 Pulmonary Function Testing of Adults Unable to Do Standard Spirometry �� 86 3.10 Quality Control �� 87 3.11 Application�� 88 References�� 90

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4 Clinical Presentation of Asthma �� 95 4.1 Introduction�� 96 4.1.1 Symptoms: Overview�� 97 4.1.2 Detailed History�� 97 4.1.3 Physical Examination�� 99 4.2 Investigations: Spirometry�� 103 4.2.1 Other Investigations�� 103 4.2.2 Trial of Therapy�� 104 4.3 Asthma Severity�� 104 4.3.1 Classification of Severity Before Treatment �� 107 4.3.2 Risk Domain �� 108 4.4 Patterns of Asthma�� 109 4.4.1 Important Factors Contributing to Severity�� 112 4.4.2 Occupational Asthma�� 115 4.5 Life-Threatening Asthma�� 116 4.5.1 Severe Acute Asthma (Status Asthmaticus)�� 116 4.5.2 Brittle Asthma, Catastrophic Asthma�� 117 4.6 Differential Diagnoses�� 117 4.6.1 Wheeze and Lung Disease�� 117 4.6.2 COPD and Asthma�� 118 4.6.3 Hyperventilation �� 118 4.6.4 Vocal Cord Dysfunction (VCD)�� 119 4.6.5 Bronchial Obstruction�� 119 4.7 Time Course of Events in Asthma�� 120 4.7.1 Response to Exercise�� 120 4.7.2 Response to Allergens�� 120 4.7.3 Response to Viral Infection�� 120 4.8 Diagnostic Problems in Asthma�� 121 4.8.1 Age-Related Asthma �� 121 4.9 Sex and Gender Differences in Asthma�� 124 4.10 Avoiding Delays in Diagnosis�� 125 4.11 Monitoring Asthma �� 126 4.11.1 Fraction of Exhaled Nitric Oxide (FeNO)�� 127 4.12 Referral to a Specialist�� 127 4.13 Application�� 128 References�� 128 5 Environmental Issues in Asthma Management�� 131 5.1 Introduction�� 132 5.2 Environmental Issues and Common Triggers of Asthma�� 133 5.2.1 Outdoor Allergens�� 133 5.2.2 Indoor Allergens�� 135 5.2.3 Irritants�� 139 5.3 Ingested Allergens�� 140 5.3.1 Oral Allergy Syndrome �� 142 5.3.2 Food Additives�� 142 5.4 Non-allergenic Triggers or Irritants�� 143 5.4.1 Cold Air�� 143 5.4.2 Exercise�� 144

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5.4.3 Emotion�� 144 5.4.4 Viral Infections�� 144 5.4.5 Medication Sensitivity�� 144 5.5 Exposure Reduction and Avoidance Techniques�� 146 5.5.1 Pollen�� 146 5.5.2 Mold�� 148 5.5.3 Dust and Dust Mites�� 149 5.5.4 Cockroach Allergen�� 151 5.5.5 Pet Allergen�� 151 5.5.6 Rodent Allergen�� 153 5.5.7 Food Allergen�� 153 5.5.8 Medications�� 154 5.5.9 Insect Allergen�� 154 5.5.10 Irritants�� 155 5.5.11 Viral Infections�� 156 5.5.12 Cold Air�� 156 5.5.13 Exercise�� 157 5.5.14 Latex �� 158 5.5.15 Conclusion�� 158 5.6 Identification of Triggers�� 159 5.7 Home Assessment �� 159 5.7.1 Smoking�� 161 5.7.2 Vaping �� 162 5.8 Application�� 163 References�� 164 6 Medications Used in Asthma Management �� 175 6.1 Introduction�� 176 6.2 Principles of Medication Use�� 178 6.3 Available Medications: Broad Categories of Use �� 179 6.4 Quick-Relief Medications (“Rescue Medications”) �� 180 6.4.1 Short-Acting Beta-Agonist (SABA) Bronchodilators�� 180 6.4.2 Short-Acting Anti-cholinergic Bronchodilators�� 181 6.4.3 Systemic Corticosteroids�� 181 6.5 Long-Term Asthma Control Medications �� 183 6.5.1 Inhaled Corticosteroids (ICS) �� 183 6.5.2 Long-Acting Beta-Agonists (LABA)�� 185 6.5.3 Long-Acting Muscarinic Antagonists (LAMA)�� 185 6.5.4 Combination Products�� 186 6.5.5 Leukotriene Receptor Antagonists (LTRA)�� 186 6.5.6 Immunomodulators and “Precision Health” �� 188 6.5.7 Long-Term Systemic Corticosteroids �� 193 6.5.8 Theophylline �� 194 6.5.9 Cromolyn and Nedocromil �� 196 6.6 Other Medications Used in Asthma�� 197 6.7 Immunotherapy in Asthma (“Allergy Shots”)�� 197 6.8 Low Evidence-Based Medications as Treatment Options�� 206 6.8.1 Approach to the Use of These Medications�� 206

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6.9 Role of Bronchial Thermoplasty in Treatment �� 206 6.10 Concern About Side Effects: General Approach�� 207 6.11 Classification of Severity After Treatment�� 209 6.12 Step Approach to Asthma Management�� 211 6.13 Goals of Therapy�� 214 6.14 Quality-of-Life Scores�� 215 6.15 Conclusion�� 217 6.16 Application�� 217 References�� 217 7 Inhalation Devices Used in Asthma�� 223 7.1 Introduction�� 224 7.1.1 Metered Dose Inhalers (MDIs) �� 225 7.1.2 Spacers and Valved Holding Chambers�� 230 7.1.3 Dry Powder Inhalers (DPIs)�� 235 7.1.4 Nebulizers �� 245 7.1.5 Choice of Inhaler Devices�� 248 7.1.6 Application�� 250 References�� 251 8 Special Situations in Asthma�� 255 8.1 Special Situations in Asthma�� 256 8.2 Pregnancy�� 256 8.3 Asthma in Older Adults�� 261 8.4 Diabetes�� 265 8.5 Surgery and Anesthesia�� 265 8.6 Occupational Asthma�� 266 8.7 Obesity�� 268 8.8 Immunization/Vaccination�� 272 8.9 Smoking�� 272 8.10 Competitive Athletes�� 276 8.11 Non-asthma Medications and Asthma�� 277 8.11.1 Aspirin Sensitivity�� 277 8.11.2 Sulfite Sensitivity�� 278 8.11.3 Antihistamines�� 279 8.11.4 Over-the-Counter Medications �� 281 8.12 Direct-to-Consumer Advertising (DTCA): Advantages and Disadvantages�� 283 References�� 284 9 Comorbidities in Asthma�� 291 9.1 Comorbidities and Their Treatment�� 292 9.2 Contact Dermatitis�� 292 9.3 Atopic Dermatitis and Eczema �� 293 9.4 Rhinitis, Sinusitis, and Rhinosinusitis�� 293 9.4.1 Rhinitis�� 293 9.4.2 Sinusitis�� 297 9.5 Nasal Polyps�� 299 9.6 Gastroesophageal Reflux�� 299 9.7 Vocal Cord Dysfunction (VCD)�� 302

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9.8 Asthma-COPD Overlap (ACO)�� 304 9.9 Obstructive Sleep Apnea�� 305 9.10 Bronchopulmonary Aspergillosis (ABPA)�� 307 9.11 Depression�� 309 9.12 Acute, Severe Acute, and Life-Threatening Asthma�� 310 9.12.1 Classification of Severity of Acute Asthma�� 312 9.12.2 Treating Asthma in the Home �� 316 9.12.3 Treating Asthma in the Office�� 317 9.12.4 Cardiopulmonary Resuscitation (CPR)�� 318 9.13 Anaphylaxis: Type 1 Allergy�� 318 9.13.1 Definition�� 318 9.13.2 Causes �� 319 9.13.3 Risk Factors for Anaphylaxis�� 321 9.13.4 Symptoms �� 321 9.13.5 Differential Diagnosis of Anaphylaxis�� 322 9.13.6 Management of Anaphylaxis�� 322 9.13.7 Education for Anaphylaxis�� 323 9.14 Application�� 324 References�� 324 Part II The Role of Education 10 An Integrated Approach to Asthma Management�� 335 10.1 Overview�� 336 10.2 Asthma Management: A General Approach �� 336 10.2.1 Steps Taken by Healthcare Provider �� 336 10.2.2 Approach to Management: Role of Educator �� 337 10.2.3 Educational Visits �� 337 10.3 Management of Problems by Age�� 345 10.3.1 Less than 1 Year�� 345 10.3.2 From 1 to 5 Years�� 346 10.3.3 From 5 to 12 Years�� 346 10.3.4 From 12 to 25 Years�� 346 10.3.5 From 25 to 35 Years�� 348 10.3.6 From 35 to 60 Years�� 348 10.3.7 Over 60 Years�� 348 10.4 Home Monitoring�� 348 10.4.1 The Peak Flow Meter�� 348 10.4.2 Calculating Diurnal Variability: Other Methods�� 351 10.4.3 New Personal Best Readings�� 352 10.4.4 Checking PEF Technique�� 352 10.4.5 The Peak Flow Diary�� 353 10.4.6 Observing Symptoms and Using the Diary�� 354 10.4.7 The Asthma Action Plan �� 355 10.5 Severe, Acute, and Chronic Asthma�� 362 10.6 Potentially Fatal Asthma �� 363 10.7 Application�� 364 References�� 365

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11 Adherence �� 369 11.1 Overview�� 370 11.2 Healthcare Providers and Self-Management�� 371 11.3 Adherence: Common Issues �� 372 11.3.1 Asthma as a Chronic Condition�� 373 11.3.2 Medication Regimens �� 374 11.3.3 Avoidance of Triggers�� 375 11.3.4 Recognition of Deterioration�� 375 11.3.5 Reaction to Emergency Situations�� 375 11.3.6 Impact of Asthma�� 376 11.3.7 Coping Strategies�� 378 11.3.8 Psychosocial Factors�� 381 11.4 Adherence �� 385 11.4.1 Definition�� 385 11.4.2 Physician and Healthcare Provider Adherence to Guidelines�� 386 11.4.3 Nonadherence �� 388 11.4.4 Patterns of Nonadherence �� 389 11.4.5 Identifying Nonadherence�� 390 11.4.6 The Team Approach�� 391 11.5 General Approach to Adherence �� 392 11.5.1 Strategies for Chronic Illness�� 393 11.5.2 Anticipatory Guidance�� 394 11.5.3 Skills Required by the Educator �� 397 11.6 Specific Aids to Adherence �� 398 11.6.1 Self-Management of Asthma�� 401 11.6.2 Health Education�� 406 11.7 Cultural and Religious Differences�� 407 11.8 Suggested Reading�� 414 11.9 Application�� 414 References�� 414 12 Complementary and Alternative Medicine in Asthma �� 421 12.1 Introduction�� 422 12.2 Specific Types of Care�� 426 12.2.1 Relaxation �� 427 12.2.2 Meditation �� 427 12.2.3 Yoga�� 427 12.2.4 Biofeedback�� 427 12.2.5 Breathing Exercises�� 428 12.2.6 Hypnosis �� 428 12.2.7 Imagery �� 428 12.2.8 Therapeutic Touch�� 428 12.2.9 Religion�� 429 12.3 Professions�� 429 12.3.1 Osteopathy�� 429 12.3.2 Chiropractic�� 429 12.3.3 Acupuncture�� 431

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12.3.4 Homeopathy�� 432 12.3.5 Massage Therapy�� 433 12.3.6 Naturopathy�� 433 12.4 Self-Help CAM�� 434 12.4.1 Herbs �� 434 12.4.2 Nutrition and Nutritional Supplements�� 436 12.4.3 Exercise as Treatment �� 437 12.4.4 Electromagnetic Treatment �� 438 12.4.5 Aromatherapy �� 438 12.4.6 Reflexology �� 438 12.5 Approach of the Educator �� 438 12.6 Application�� 440 References�� 440 13 Frequently Asked Questions �� 445 13.1 Introduction�� 446 13.2 Asthma: Symptoms and Control�� 446 13.3 Triggers �� 449 13.4 Fatal Asthma �� 453 13.5 Exercise and Asthma�� 453 13.6 Medications�� 454 13.7 Testing and Devices�� 458 13.8 Spacers�� 459 13.9 The Peak Flow Meter�� 460 13.10 Allergies�� 461 13.11 School and Camp�� 463 13.12 Pregnancy�� 464 13.13 Travel�� 465 13.14 Coping�� 466 13.15 Immunizations�� 470 13.16 Other Questions�� 471 Part III The Effective Asthma Educator 14 Learning: Theories and Principles �� 477 14.1 Introduction�� 478 14.1.1 How Is Learning Achieved?�� 479 14.2 Learning and Teaching Definitions �� 479 14.2.1 Learning�� 479 14.2.2 Teaching�� 479 14.3 The Learning Process�� 479 14.4 Theories of Learning�� 480 14.4.1 Behaviorism�� 480 14.4.2 Gestalt or the Cognitive Theory of Learning�� 483 14.4.3 The Humanistic Theory�� 486 14.4.4 Information Processing �� 488 14.5 Online Learning: Some Considerations�� 491 14.6 Personality Development�� 493

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14.6.1 Infancy: Trust Versus Mistrust�� 493 14.6.2 Early Childhood: Autonomy Versus Shame and Doubt�� 493 14.6.3 Middle Childhood: Initiative Versus Guilt�� 494 14.6.4 Elementary School Age: Accomplishment Versus Inferiority�� 494 14.6.5 Adolescence: Identity Versus Confusion�� 494 14.6.6 Young Adulthood: Intimacy Versus Isolation �� 494 14.6.7 Adulthood: Generativity Versus Stagnation�� 494 14.6.8 Old Age: Integrity Versus Despair�� 494 14.6.9 Application of Theories to Asthma Education�� 495 14.7 Age-Related Learning�� 496 14.7.1 Learning Styles �� 496 14.7.2 Children�� 497 14.7.3 Adolescents �� 497 14.7.4 Adults�� 498 14.7.5 Older Adults�� 499 14.7.6 Implication of Learning Styles�� 499 14.7.7 Types of Learning �� 502 14.8 Barriers to Learning�� 503 14.8.1 Environment�� 503 14.8.2 Physical Factors�� 504 14.8.3 Individual Factors �� 504 14.8.4 Sociological and Emotional Factors �� 506 14.9 Principles of Learning�� 508 14.10 Application�� 512 References�� 512 15 Teaching the Person with Asthma�� 515 15.1 Introduction�� 517 15.2 Teaching Approaches for Different Audiences �� 517 15.2.1 Parents�� 517 15.2.2 Children�� 520 15.2.3 Adolescents �� 522 15.2.4 Adults�� 525 15.2.5 Low-Literacy Individuals�� 527 15.2.6 The Older Adult�� 528 15.2.7 Response to Education�� 530 15.2.8 Cultural Competency�� 530 15.2.9 Mobile Applications for Asthma�� 532 15.3 Teaching Methods�� 534 15.3.1 The Individual�� 535 15.3.2 The Small Group�� 536 15.3.3 The Large Group�� 537 15.4 The Process of Education�� 538 15.4.1 The Cognitive Domain�� 539 15.4.2 The Affective Domain�� 540 15.4.3 The Psychomotor Domain�� 543

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15.5 Planning for Teaching �� 544 15.5.1 Assessment�� 544 15.5.2 Planning�� 546 15.5.3 Planning for the Affective Domain �� 546 15.5.4 Planning for the Cognitive Domain�� 547 15.5.5 Planning for the Psychomotor Domain�� 547 15.5.6 Implementation �� 548 15.5.7 Evaluation �� 548 15.5.8 Sample Teaching Plans �� 550 15.6 The Role of the Educator�� 551 15.6.1 Principles of Communication in a Consultation �� 551 15.6.2 Setting the Climate for Teaching�� 552 15.6.3 Ways of Teaching That Can Cause Problems �� 554 15.7 Teaching Strategies �� 556 15.8 The Team Approach to Teaching�� 562 15.9 Application�� 564 References�� 564 16 Clinic Management and Evaluation�� 569 16.1 Introduction�� 571 16.2 Running an Asthma Clinic�� 571 16.2.1 Facilities�� 572 16.2.2 Time�� 572 16.2.3 Equipment and Materials�� 572 16.2.4 Telemedicine �� 576 16.2.5 Resources�� 577 16.2.6 Evaluation of Teaching Materials �� 579 16.2.7 Education Programs�� 580 16.2.8 Planning�� 580 16.2.9 Costs�� 581 16.2.10 Data Collection �� 581 16.2.11 Standards�� 581 16.3 Teaching in the Home �� 584 16.3.1 Assessing the Environment�� 584 16.3.2 The Home Teaching Kit�� 586 16.4 The School Environment�� 587 16.4.1 Classroom Assessment�� 587 16.4.2 Within the School�� 588 16.4.3 Outside the School�� 588 16.4.4 School Policies�� 589 16.4.5 Physical Education�� 590 16.4.6 General Education for School Staff�� 590 16.5 Evaluation of Education Programs �� 591 16.5.1 Designing an Evaluation Program�� 592 16.5.2 Establishing Standards�� 595 16.5.3 Data Collection �� 596 16.5.4 Data Analysis and Evaluation �� 596 16.5.5 Review�� 597

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16.5.6 Confidentiality�� 599 16.6 Self-Evaluation�� 599 16.6.1 Using the Self-Evaluation Checklists �� 600 16.7 Self-Evaluation Checklists�� 601 16.7.1 Checklist 2�� 603 16.8 Application�� 604 Appendix 16.1�� 605 Reading Material for Patients�� 605 Appendix 16.2�� 605 Internet Addresses�� 605 General Interest�� 606 For Asthma Educators (Not for Patients)�� 606 Appendix 16.3�� 606 Suggested Reading for Asthma Educators�� 606 References�� 607 Part IV Case Studies 17 Case Studies�� 613 17.1 Introduction�� 614 17.2 Instructions for Case Studies 1 to 14�� 614 17.3 Additional Case Studies�� 614 17.4 Case Study 1 �� 614 17.5 Case Study 2 �� 614 17.5.1 Response to Case Study 1 �� 615 17.5.2 Response to Case Study 2 �� 615 17.6 Case Study 3 �� 615 17.7 Case Study 4 �� 615 17.7.1 Response to Case Study 3 �� 616 17.7.2 Response to Case Study 4 �� 616 17.8 Case Study 5 �� 616 17.8.1 Response to Case Study 5 �� 617 17.9 Case Study 6 �� 617 17.9.1 Response to Case Study 6 �� 618 17.10 Case Study 7 �� 619 17.10.1 Response to Case Study 7 �� 620 17.11 Case Study 8 �� 620 17.11.1 Response to Case Study 8 �� 621 17.12 Case Study 9 �� 621 17.12.1 Response to Case Study 9 �� 622 17.13 Case Study 10 �� 622 17.14 Case Study 11 �� 623 17.15 Case Study 12 �� 623 17.16 Case Study 13 �� 624 17.17 Case Study 14 �� 625 Glossary�� 627 Index�� 635

Abbreviations

AAP AARC AAT ABPA ACCI ACE ACO ACQ ACT ACTH AE-C ALB AMP APGAR AR ARIA ASA ATAQ ATS BAL BHR BMI BT CAM CC CDC CNS CO CO2 CO2e COLD COPD CORE CPR DPI

Asthma Action Plan American Association for Respiratory Care Alpha 1-anti-trypsin Allergic Bronchopulmonary Aspergillosis Asthma Control and Communication Instrument Angiotensin Converting Enzyme Asthma-COPD Overlap Asthma Control Questionnaire Asthma Control Test Adrenocorticotrophic Hormone Certified Asthma Educator Asian Ladybug Adenosine 5’ Monophosphate Activities, Persistence; triGGers, Asthma medications, Response to therapy Allergic Rhinitis Allergic Rhinitis Impact on Asthma Acetylsalicylic Acid Asthma Therapy Assessment Questionnaire American Thoracic Society Bronchoalveolar Lavage Bronchial Hyper-Reactivity/Hyper-Responsiveness Body Mass Index Bronchial Thermoplasty Complementary and Alternative Medicine Conventional Cigarette Centers for Disease Control and Prevention (USA) Central Nervous System Carbon Monoxide Carbon Dioxide Carbon Dioxide Equivalents Chronic Obstructive Lung Disease, also called COPD Chronic Obstructive Pulmonary Disease, also known as COLD Cough, Obstructive Sleep Apnea, Rhinosinusitis and Esophageal Reflux. Cardio Pulmonary Resuscitation Dry Powder Inhaler xxi

xxii

DTCA EBC EC ED EIA EMR EPR-3

Direct to Consumer Advertising Exhaled breath condensate Electronic Cigarette, E-cigarette Emergency Department Exercise Induced Asthma Electronic Medical Records Expert Panel Report 3 (by the National Asthma Education and Prevention Program) ERV Expiratory Reserve Volume ETS Environmental Tobacco Smoke EVALI E-cigarette Vaping Use Associated Lung Injury FDA Food and Drug Administration (U.S.) FeNO Fraction of Exhaled Nitric Oxide FEV1 Forced Expiratory Volume in One Second FOT Forced Oscillation Technique FRC Functional Residual Capacity FVC Forced Vital capacity GERD Gastroesophageal Reflux Disease GINA Global Initiative for Asthma GRAS Generally Regarded as Safe HCP Health Care Professional HDM House Dust Mites He Helium HEPA High Efficiency Particulate Air HFA Hydrofluoroalkane HIPPA Health Insurance Portability and Accountability Act HMO Heath Maintenance Organization HPA Hypothalamic Pituitary Adrenal (axis) HRCT High Resolution C T HRQoL Health-Related Quality of Life IC Inspiratory Capacity ICS Inhaled Corticosteroids ICU Intensive Care Unit IgE Immunoglobulin E IOC International Olympic Committee IRV Inspiratory Reserve Volume JCAHO Joint Commission on Accreditation of Healthcare Organizations LABA Long-Acting Beta Agonists LAMA Long-Acting Muscarinic Agent LTRA Leukotriene Receptor Antagonist MAO Monoamine Oxidase Inhibitors MDI Metered-Dose Inhaler N Nitrogen NAEPP National Asthma Education and Prevention Program NCCLS National Committee for Clinical Laboratory Standards NCES National Center for Educational Statistics NCICAS National Co-operative Inner City Asthma Study NHANES National Health and Nutrition Examination Survey III

Abbreviations

Abbreviations

xxiii

NHLBI National Heart, Lung and Blood Institute NIH National Institutes of Health NP Neuropsychiatric NRT Nicotine Replacement Therapy NSAID Non-Steroid Anti-Inflammatory Drug O2 Oxygen OCL Online Collaborative Learning OCS Oral Corticosteroids OLD Occupational Lung Disease OR Odds Ratio OSA Obstructive Sleep Apnea OTC Over-the-Counter PaCO2 Partial Pressure of Carbon Dioxide PCC Patient-Centered Care (also known as PFC) PDR Physicians’ Desk Reference PEF Peak Expiratory Flow PEFM Peak Expiratory Flow Meter PEFR Peak Expiratory Flow Reading PFA Potentially Fatal Asthma PFC Patient-Focused Care PFM Peak Flow Meter PPD p-Phenylenediamine PSG Polysomnography QALY Quality-Adjusted Life Years QOL Quality of life RAD Reactive Airway Disease RAW Airway Resistance RCT Randomized Controlled Trials REM Rapid Eye Movement RS Rhinosinusitis RSV Respiratory Syncytial Virus RTI Respiratory Tract Infection RV Residual Volume SABA Short-Acting Beta Agonists SCIT Subcutaneous Immunotherapy SIDS Sudden Infant Death Syndrome SLIT Sublingual Immunotherapy SPD Serious Psychological Distress SPO2 Oxygen Saturation TGV Thoracic Gas Volume TLC Total Lung Capacity TRACK Test for Respiratory and Asthma Control in Kids TSP Tri-sodium Phosphate TV Tidal Volume UAO Upper Airway Obstruction UNDW Ultrasonically Nebulized Distilled Water UNESCO United Nations Educational Scientific and Cultural Organization URI Upper Respiratory Infection

Abbreviations

xxiv

VC VCD VOC WHO

Vital Capacity Vocal Cord Dysfunction Volatile Organic Compounds World Health Organization

Part I Asthma: The Fundamentals

1

Asthma and Asthma Education: The Background

Contents 1.1 Introduction

4

1.2 What Is Asthma? 1.2.1 Symptoms 1.2.2 Definitions

5 5 7

1.3 Significance of Asthma 1.3.1 Overview 1.3.2 Morbidity 1.3.3 Mortality 1.3.4 Costs

8 8 9 11 12

1.4 Etiology of Asthma 1.4.1 Allergy and Asthma

15 15

1.5 Genetics and Environment 1.5.1 Phenotype and Genotype Correlation 1.5.2 Environmental Issues

16 16 17

1.6 Approaches to Asthma 1.6.1 Guidelines 1.6.2 NHLBI Guidelines 1.6.3 Pediatric Guidelines 1.6.4 COVID-19 and Asthma 1.6.5 Organization of Care 1.6.5.1 General Approach of Health Systems 1.6.5.2 Healthcare Professionals 1.6.5.3 Personal Responsibility

20 20 20 23 24 25 25 26 27

1.7 Education of Persons with Asthma 1.7.1 The Issues 1.7.2 Role of the Asthma Educator 1.7.3 Skills of the Asthma Educator 1.7.4 Essential Qualities of the Educator

27 27 29 30 31

References

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© The Author(s), under exclusive license to Springer Nature Switzerland AG 2021 I. Mitchell, G. Govias, Asthma Education, https://doi.org/10.1007/978-3-030-77896-5_1

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1 Asthma and Asthma Education: The Background

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Key Points

• Asthma is a significant and common condition. • Definitions and symptoms are provided, together with an impact on health, including costs and the fact that it may cause premature death. • Asthma is closely related to allergy. –– Allergy and asthma have common genetic and environmental factors. –– The relevance of phenotype- genotype correlations are described. –– Factors relevant to the less common but important non-allergic asthma are described. • Guidelines are important to all approaches to asthma. –– These require organization of care and system-wide measures. –– Those with asthma have a personal responsibility in their care. • Health professionals—and especially the Asthma Educator—have a specific and important role in the education of people with asthma. –– The skills and essential qualities of the asthma educator are described in detail.

Chapter Objectives

After reading this chapter, you should be able to: 1. List the warning signs and symptoms of asthma. 2. Explain the definitions of asthma. 3. Describe the current guidelines for asthma. 4. Discuss the organization of care for a person with asthma. 5. Explain the importance of education and the role of educators in asthma management.

1.1

Introduction

This chapter is intended to serve as an introduction to the world of asthma education—to the various facets of knowledge and skills needed by the successful asthma educator. It hence provides only brief overviews of the many components that make up asthma education, and its purpose is to paint a “big picture” to help place various asthma- and education-related topics in perspective. Points to Ponder

If physicians, or healthcare providers and others, assume that wheeze is essential for the diagnosis of asthma, then the diagnosis will often be missed.

While other chapters in the book each address a single topic in detail and may be read in part or in whole or in the order that meets a specific need, this chapter should be read first, in its entirety. The effective asthma educator requires a good understanding both of asthma in all its aspects and of the teaching process. Teaching is a form of empowerment—in this case, empowerment of people with asthma. The asthma educator must know how to effectively transfer knowledge about asthma and its treatment methods and management techniques to the person with asthma, thereby empowering and helping him or her to effectively self-manage his or her asthma. The aim of the asthma educator is to help people with asthma stay well. When writing about these people, we are unsure what term to use. When they get sick, they are correctly designated as patients. But much of the time, perhaps most of the time, they are well and the word “patient” seems inappropriate. This discussion pervades all aspects of healthcare, with alternative language of “client” or “consumer” suggested [1, 2]. We understand this discussion, but want the empowered person with asthma to enjoy a good and full life. We will talk about asthma and people with

1.2 What Is Asthma?

asthma throughout this book, using other designations when appropriate. However, we will never use “asthmatic,” for it is a term that defines an individual solely by a medical problem and thus removes individuality and perhaps humanity. While this book contains the information needed to prepare for the Asthma Educator’s Certification (AE-C) examination, it goes much further: it is intended as an ongoing reference, and it presents supplementary information and discussions that can enrich the educator’s practice. It will also, hopefully, show that the goal of effective teaching is to present information in such a way that that information is easily remembered, that its value is understood, and that it is then used (by people with asthma) for personal benefit. This chapter will also indicate the directions that our collective understanding of asthma will take. These will be speculative to some extent and based on the authors’ extrapolation and interpretation of current knowledge. Such information is clearly not needed for asthma educators to be successful in their work, but it will enhance their knowledge of various trends and in turn will enrich the understanding they bring to their education of those with asthma. This book is written as the COVID-19 pandemic rages. Healthcare practitioners have all had to change their practice and learn new skills. One specific skill that is likely to persist when the pandemic is over is the ability to help those with asthma using virtual techniques. At the least, this might involve using a phone with both the educator and the person with asthma looking at a website. But much more elaborate online educational programs are currently available and will be developed even further. There will not be a return to “life as before.” This, in brief, is the purpose of the book. Now let us proceed and define its subject.

1.2

What Is Asthma?

1.2.1 Symptoms Symptoms are “what is felt.” They are the main impetus in seeking healthcare advice. They are

5

therefore the logical starting point for this chapter. Some people with asthma have symptoms throughout their lives and others at one life stage only and still others have symptoms in more than one life stage, but with long periods of remission. For those in the first category, the symptoms do not necessarily remain the same at all life stages. Hence, a broad division of asthma into “pediatric” and “adult” is insufficient for the knowledgeable educator, who needs to understand the special characteristics of the disease at different ages. For example, the symptoms of an infant are likely to be different from those of a 9-year-old or of a teenager, although all three are considered to have “pediatric” asthma. Similarly, the predominant symptoms of adults aged, say, 25, 50, or 70 may differ considerably. The major common symptoms of asthma are: • • • •

Cough Wheeze Shortness of breath Chest pain or chest tightness

Variations and differences in these symptoms occur at different ages; they will be discussed in later chapters. Some people will complain of wheeze, but this is unusual as a presenting complaint and indeed, most persons with asthma will report cough or shortness of breath. Shortness of breath is thus the most common complaint and the one which interferes most with the quality of life for individuals with asthma. It is not usually constant, unless the asthma is particularly severe, but occurs in episodes. The shortness of breath may start suddenly during the night, with attendant fear and extreme anxiety, or it may come after exercise or exposure to triggers. In some instances, chronic breathlessness may develop, but without the feeling of distress. While the lack of distress may reduce stress, it simultaneously increases the danger; there may be no realization of the degree of deterioration that exists. Cough is the most common symptom. It is most often dry and irritating and generally worse at night, although occasionally sputum is pro-

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duced. Cough may follow exercise or exposure to allergenic triggers. In children, cough may be the only symptom reported by parents, and this cough is often confused with croup. In adults, cough is often confused with pneumonia. Wheeze is found at the same time that a person presents with cough or shortness of breath. It may be heard by the person but may also be an objective finding on physical examination by a healthcare professional. Louder wheezes can be heard by bystanders. While the presence of wheeze strongly suggests asthma, its absence does not mean that asthma itself is absent. And the contrary is also true; asthma might be the most common cause of wheeze, but many other conditions may cause it. Aaron et al. [3] suggest up to a third of those diagnosed with asthma may turn out to have some other condition. Of those who do have asthma, many never wheeze, or wheeze so occasionally that this is never heard by a healthcare provider during a physical examination. They may have cough, particularly at night. In severe acute asthma, wheeze may be absent since there is insufficient airflow to produce the noise. This so-called silent chest is a marker of severity and requires urgent action. If it is assumed that wheeze is essential for the diagnosis of asthma, then the asthma will often be missed, and the diagnosis will be incorrect. Other symptoms do exist. For instance, chest tightness is very common and will disappear with treatment. Others will complain of chest pain, and care must be taken to distinguish this from other causes of chest pain, such as problems with the heart or with the chest wall itself–in other words, strain involving the muscles of the rib cage. Chest pain is a symptom that seems to be particularly common in adolescents and is perhaps related to changes in the configuration of the chest wall that occur with growth. Vomiting, by itself, is not a symptom of asthma, but at least one-third of children with asthma will vomit at some time. Vomiting is so common that there is an old belief that inducing vomiting will lead to improvement in the asthma. While this is incorrect, the vomiting remains unexplained. It is associated with coughing and

1 Asthma and Asthma Education: The Background

deterioration in asthma, such as with a common cold. It may occur after a cough, but can also occur without a cough. Vomiting usually subsides as the asthma improves. People with asthma may also present with other symptoms that are caused by or due to asthma. These include fatigue, reduced activity, and disturbed sleep. Other signs and symptoms are listed in Table 1.1. It is important to remember that these will vary from person to person. Some young children may have cough as their only symptom, especially at night or during the early hours of the morning, while others may not cough at all. However, all persons with the disease—and more particularly the parents of young children with asthma—should be made aware both of the signs and the symptoms, with particular emphasis on the danger signals of asthma. When asked, most people will usually describe only their symptoms to a healthcare provider. However, they will also have their own personal ideas and anxieties about their asthma and the significance of their symptoms. Healthcare providers must pay attention to these anxieties when they ask for a description of the symptoms, as they will often describe the effect asthma has on their quality of life. For example, they may worry about the regular use of expensive medications, interference with exercise and with sleep, prob-

Table 1.1 Signs and symptoms of asthma Warning signs Danger signs Skin retracted at base of throat Suddenly becomes and between ribs quiet or withdrawn Nostrils flared Looks distressed Breathing rate is above normal Coughs (adults: 25 or more; children: Wheezes 30 or more) Feels breathless Blue tinge on lips, and nail Coughs at night, after beds exercise or in cold air Cannot say a complete Has tightness or pain sentence in one breath in chest Takes longer to breathe Rapid pulse (adults: 110 or more; children: 120 or more) out than breathe in Peak flow readings 33% to Vomits 50% below normal levels Says or feels that medication is ineffective Pulsus paradoxus >10mmHg

1.2 What Is Asthma?

lems with relationships, embarrassment with noisy breathing, and so on. Surveys [4–7] show that persons with asthma have a high incidence of symptoms and disturbance in their lives, affecting mobility, school attendance, work, leisure, sleep, and medication usage and causing avoidance of everyday activities such as sports, social gatherings, and even mild exercise. The healthcare provider must guard against superficial inquiry about symptoms, even if the person being examined states that they live normal lives. Their definition of “normal” may be far removed from the normal lives led by healthy persons without asthma and be based on the restrictions and adjustments they have already incorporated into their lives. This redefinition may be a form of coping mechanism that enables them to emphasize the positive aspects of their lives, thus permitting them to develop and extend their current coping skills and avoid dealing with the problems of chronic illness [8, 9]. Similarly, when they talk about “exercise,” it is important to understand what they mean by the term. For many individuals, exercise is a special activity carried out in a gymnasium, on a sports field, or at a fitness club. Everyday activities such as walking, using stairs, vacuuming, and housework are often not considered exercise. Hence, when asking about asthma symptoms, exercise, or the response to treatment, specific questions must be included about daily routine or everyday activities. In the case of children, parental perception of asthma severity in a child may differ from objective measures of severity, but both must be considered when evaluating the child’s ability to function [10]. Individuals with asthma may overestimate or even underestimate the severity of their symptoms. And older sufferers may have greater limitations and symptoms that are negated by familiarization and the development of coping strategies [4].

1.2.2 Definitions Asthma has literally been around for a very long time! It was described thousands of years ago in the time of Hippocrates. Despite this long famil-

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iarity with the disease, an easy definition that fits all situations remains elusive. Educators should be familiar with the definition of asthma by the National Institute of Health (NIH) Expert Panel Report on Guidelines for the Diagnosis and Management of Asthma. It is complex and comprehensive, and states that: Asthma is a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role, in particular mast cells, eosinophils, T lymphocytes, macrophages, neutrophils and epithelial cells. In susceptible individuals this inflammation causes recurrent episodes of wheezing, breathlessness and coughing, particularly in the night or early morning. These episodes are usually associated with widespread but variable airflow obstruction that is reversible either spontaneously or with treatment. The inflammation also causes an associated increase in the bronchial hyperresponsiveness to a variety of stimuli. Reversibility of airflow limitation may be incomplete in some patients with asthma [11].

Despite the comprehensive nature of this definition, other special use definitions also exist. Some are created for research purposes, others for clinical practice, and still others for administrative purposes. It is worth examining these other definitions, since each provides a different viewpoint and different information about the disease. Points to Ponder

A definition of asthma should: • Allow for the recognition of asthma • Enable meaningful tests to be used in the diagnosis of asthma • Be of use in assessing severity

The conventional medical definition, which has been used for many years, is that asthma is “reversible airways obstruction.” This confirms that asthma is in the airways, is concerned with airflow, and is variable. In other words, asthma may improve or deteriorate, sometimes over a surprisingly short time. To use this particular definition, there needs to be a measurement of

1 Asthma and Asthma Education: The Background

8

airflow that can then give an indication of the degree of obstruction in the airways. There are many different ways of applying the definition, such as by history, by measurement, or by pathology [12]. Professionals and scientists view and describe asthma in terms quite different from those used by those who actually have asthma. The Global Initiative for Asthma (GINA) [13] defines asthma as: a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role. The chronic inflammation causes an associated increase in airway hyperresponsiveness that leads to recurrent episodes of wheezing, breathlessness, chest tightness, and coughing, particularly at night or in the early morning. These episodes are usually associated with widespread but variable airflow obstruction that is often reversible either spontaneously or with treatment.

Both these definitions—by NIH and GINA— stress the fact that asthma is a chronic inflammatory disorder of the airways, with the emphasis being on both the chronicity and its inflammatory nature. These are two very important aspects, both of which must be understood by the healthcare provider and the individual with asthma in order to manage the disease. The “reversibility” component in the definition is essential for the diagnosis of asthma. Despite difficulties in reaching agreement on a precise definition of asthma, the presence of asthma is recognized by most individuals and healthcare providers. The definition exists to allow the recognition of the asthma, to enable meaningful tests to be used in its diagnosis, and for use in assessing severity.

1.3

Significance of Asthma

1.3.1 Overview In dealing with definitions of asthma and its assessment, there is considerable concentration on the acute situation, with widespread use of words such as “episode,” “exacerbation,” or “attack.” While the medical conditions described by these words all occur, this should not obscure the fact that asthma is a chronic condition, which

implies that it will continue for many months or years, in some perhaps for a lifetime, while in others it may come and go over surprisingly long periods. It is not a progressive condition that proceeds over time from mild to severe; rather, its clinical course is one of exacerbations and remissions [14]. Individuals with asthma may have it at one stage in their lives; it may then remit, only to recur many years later. It is common for adults to present with asthma for what appears to be the first time, only to discover or remember that they had had it in childhood. Thus, the chronic nature of asthma is one reason why education and individual involvement are extremely important [15]. Asthma is the second most common major chronic disease found in Americans, the most common being dental decay. It was one of the 27 focus areas defined by the US Department of Health in Healthy People 2020 [16] through which improvements to the health of the nation were monitored and for which objectives were defined. It continues to be a focus area in Healthy People 2030 [17]. Another very common chronic disease is rhinitis. In most people, it can have less of an impact on quality of life than asthma. This is not invariably true; for example, chronic upper airway obstruction may lead to obstructive sleep apnea. Thus, it is easy to see the toll taken by upper and lower respiratory diseases together. While its exact incidence is difficult to obtain, asthma affects about 1 in 13 Americans (at least 7.8% of adults, and 7.5% of children) [18]. An estimated 42.7 million Americans have asthma [19]. As there may be more than one individual in a family with the disease, perhaps one-quarter to one-third of all families are affected by asthma at one time or another. As mentioned earlier, the severity of asthma varies considerably, both between individuals and in any one individual at different ages. The range of severity is wide. At one extreme, for example, are persons with one or two episodes of wheezing that follow a very specific exposure, such as exercise in combination with a cold, and who have no symptoms at any other time. At the other extreme are persons who have severe daily wheezing which does not fully respond even to

1.3 Significance of Asthma

major environmental change and medication therapy. However, defining what is severe asthma is complex. FitzGerald et al. [20] point out the importance of distinguishing uncontrolled and severe asthma. Taking measures to improve health in these variants requires very different approaches. Uncontrolled asthma might be due to inadequate asthma management, whereas severe asthma may already have optimal management, usually with high-dose inhaled corticosteroids plus a second controller and/or systemic corticosteroids. These latter individuals should be considered for one of the new biologics [21]. In both cases, it is assumed a full diagnostic workup has been performed and environmental exposures have been identified and minimized prior to determining whether the asthma is severe and/or uncontrolled. Asthma has an impact not only on the individuals concerned but also on their families, the healthcare system, healthcare professionals, hospital usage, and medication costs. Performance at work and at school also suffers.

1.3.2 Morbidity Morbidity, briefly, is the incidence of the condition “asthma.” It can be extended to include the lack of wellness, all the effects of illness, and the consequent reduction in quality of life of the person with asthma. The World Health Organization (WHO) defines health as a state “of complete physical, mental and social well-being and not merely the absence of disease or infirmity.” The educator has an important role in helping those with asthma achieve the highest level of well-being. Many individuals with asthma do not enjoy good health in the fullest sense of the term. Many children, and many adults, accept a surprising degree of correctable ill health. This includes tolerating disturbed sleep, avoiding sports, and taking time off from work or school for preventable illnesses. Both the asthma educator and the healthcare provider must remember that persons with asthma often accept ill health as a “normal state” and must take extra care to determine the effects of the disease on those they advise.

9

While asthma affects millions of Americans, it has a very high impact on specific racial and ethnic groups. Race and ethnicity refer to different personal qualities, but are often considered together, and the language to refer to them is still evolving. “Hispanic” is less used, having been replaced by “Latino” and “Latina,” words in turn superseded by “Latinx.” “African-American” and “black” American may mean different things, but are often used interchangeably. It is not clear what is meant by the descriptor “white.” The confusion is not surprising, as stereotyping the enormous diversity of human appearance and ancestry is an impossible task even as smaller subgroups are formed. The 2020 election of Senator Kamala Harris as Vice-President of the USA encapsulates much of the discussion. Is she African-American? Black? Asian? Isn’t she all of these?! In general, when we cite studies, the language used will be that of the author, even if it feels limiting. In addition, race and ethnicity may gain relevance in large because of socioeconomic factors. These are the so-called social determinants of health, the many background factors in our personal lives, our social connections, our economic status, and our home and work environments, that are relevant to our health. There is a growing recognition of the importance of the social determinants of health; medical care alone, even of the highest quality, is not enough to ensure good health. For example, inner-city African-American, Hispanic, and Puerto Rican communities have high rates of asthma. Puerto Ricans have the highest rates of asthma in the USA. Overall, racial and ethnic minority populations have higher rates of asthma and visit emergency department (ED) and physicians’ offices more often for treatment than do whites. Among children, more non-Hispanic black children have asthma compared with Hispanic and non-Hispanics. Black Americans are more likely to be hospitalized and placed in intensive care for asthma than whites. They are also two to three times more likely to die from asthma than any other group [18, 22–27]. Factors such as poverty, substandard housing, increased exposure to allergens, lack of

1 Asthma and Asthma Education: The Background

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education, inability to follow prescribed regimen, and limited access to continuous medical care all contribute to elevated morbidity, increased severity, uncontrolled asthma, and even death. This ethnic or racial variation in health status is the result both of exposure or vulnerability to environmental, behavioral, and psychosocial factors and also due to a lack of resources [28–32]. Most of these may be considered “downstream” effects, but these effects are shaped by “upstream” effects. Upstream effects can only be changed by political actions, such as addressing poverty and improving educational standards. Even if these changes are made, they will not translate into immediate improvements in health. Hence, when professionals interact with someone with asthma, they will do their best to help in amelioration of factors, such as reducing allergen exposure that if possible and successful will have an immediate impact on asthma. We hope all healthcare professionals, including asthma educators, understand that many important factors are not under any degree of control of the person with asthma or his or her family. An understanding of the social determinants of health helps to explain why morbidity is elevated in those who come from inner-city neighborhoods. Increased severity of asthma is associated with greater feelings of stigmatization, more negative attitudes towards healthcare providers, and reduced self-confidence in the ability to manage asthma [33]. Socioeconomic status, as one of the social determinants of health, is related to health outcomes [26, 33]. In low-income and black populations, it is the major cause of medical emergencies, increased ED visits, and hospitalizations [25, 35]. Females, low socioeconomic groups, and ethnic minorities in particular have a poorer quality of life because of their asthma [4, 24, 36, 37]. Asthma morbidity is thus governed by the four major risk factors [38] of: • • • •

Genetics Environment Socioeconomic status Psychosocial determinants

A combination of the following contributes to the increased risk of asthma morbidity [39]: • Poor problem-solving skills • Multiple caregivers (many of whom are extended family members) • Adjustment problems, both behavioral and emotional • The caregiver’s high level of stress in caring for a child with a chronic illness while coping with the burdens of poverty [40–42] Asthma also accounts for the greatest number of absences from school and is the cause of [34, 43]: • Low self-image in some individuals • Poor school or work performance [44] • Disruption of family life [35] Absence from school due to asthma has a negative impact on educational achievement and also later in life [43]. Thus, such absence may be a marker of asthma severity and a consideration in treatment outcomes. Children with asthma also have more disturbed sleep; perform less well on tests of memory and concentration; and tend to have more psychological and behavioral problems [41, 45, 46]. The more severe the symptoms, the greater the psychiatric morbidity [33]. It seems from the evidence that psychiatric morbidity is a consequence of the severe asthma, rather than the reverse, but this of course is difficult to prove absolutely. Lack of sleep in children impinges on their cognitive abilities during the day and affects mood, behavior [47], and sense of well-being. This also applies to caregivers and adults. At the same time, some of the changes are very difficult to quantify. For example, if children have inadequate education because of disturbed sleep or poor morale, it may affect their career choices and their lifestyle as adults. Limitations because of allergies or asthma may also affect the choice of geographic area in which they can live. The use of quality-of-life (QOL) measures is part of a general trend that supplements tradi-

1.3 Significance of Asthma

tional medical outcomes with individual or family- centered outcomes. In asthma, these include sleep quality; ability to exercise; time lost from work because of personal asthma or to look after children with asthma; career opportunities missed or taken; and forced alterations in the home to change the environment. All have a severe impact on the family’s quality of life, particularly that of the caregivers [48–50]. Some items, such as time lost from work, may also have a financial impact. There are other monetary aspects that must be borne in mind when taking a comprehensive view of asthma, such as the cost of medications, of environmental changes or modifications that may be needed to living spaces, of additional cleaning or housekeeping requirements, and so on.

1.3.3 Mortality Deaths from asthma continue to occur, with the numbers varying over time. There have been well-documented epidemics of asthma deaths in the USA, England, Australia, New Zealand, and many other countries. During these epidemics, the death rate has risen; after a period, it has fallen, but never to zero. There has been (and is) much speculation on the cause of these epidemics, and many new interventions are tried during each epidemic. It is never clear whether the interventions have led to improvement in the mortality rate or whether the natural history of the epidemics of asthma deaths tends towards spontaneous improvement. Between 1960 and 1998, the prevalence of asthma, and death rates for the disease, increased both nationally and regionally in the USA for all races, sexes, and ages [22]. In the year 2000, the actual number of deaths fell to 4,497 (from an earlier high of 5,400). According to a recent Center for Disease Control (CDC) report, the death rate has continued to fall. Currently ten Americans die every day from asthma. 3,564 people died from asthma in 2017 [51]. Adults die from asthma at five times the rate that children do. African-Americans had two to three times the death rate of whites [18, 23, 25]. Together

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with Hispanics they are three times more likely to die from asthma than whites. Why this is so has not been explained, though the incidence of asthma among the African-American and Hispanic population is much higher than among the white. Asthma mortality shows a high correlation with race and low socioeconomic status [23, 25, 52]. It is surmised that because impoverished individuals lack access to continuous medical care, they neglect their illness until an acute exacerbation forces a visit to an ED [53]. The result is partial recovery before the next exacerbation. This unrelenting cycle can deplete the person’s physical resources and increase the impact of the disease. Most deaths occur in those who have severe asthma and whose disease has been inadequately controlled over a long period [54, 55]. While some deaths are related to overwhelming and sudden allergen exposure, this is not common. A number of detailed studies have been done on the cause of the deaths and the life circumstances of those who die [52, 54, 56–62]. Deaths have been associated with depression, denial of the disease, anxiety, family conflicts, life crises, and social isolation. Many deaths were found to be related to poor adherence and also to poor physician understanding of the disease [63]. In short, they were preventable. As far as physicians are concerned, there was a failure of management [13] in that: • Deterioration was often not recognized early enough, and clinical status was not adequately assessed. • Objective measures of severity were not used. • The use of both inhaled and systemic corticosteroids was not begun soon enough. GINA states that underdiagnosis and inappropriate treatment were major factors contributing to asthma mortality and morbidity, although in line with the comments above, some people have severe asthma that may continue with apparent appropriate conventional treatment. Thus, undertreatment and under-assessment can be fatal [54, 56, 59].

1 Asthma and Asthma Education: The Background

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Individuals with asthma very often:

ance or some form of government plan, but may also be covered in part, sometimes wholly, by the • Did not understand the use of medications and person with asthma. preventive medication [59] Direct costs are determined using severity of • Failed to recognize symptoms of deterioration asthma, adherence to prescribed medication regi[54] mens, the prevalence of the disease, and the • Unable to follow advice on changes in their actual cost of healthcare in the country. Illiteracy environment adds to these costs [65]. • Relied on symptomatic treatment such as a Indirect costs include days absent from school, bronchodilator loss of work both in and outside the home, and • Avoided preventative treatment with inhaled economic costs due to premature death. Indirect corticosteroids or similar medications [58] costs are those borne in the main by the individ• Delayed getting medical help [58, 63, 64] ual or family. A significant percentage of the indirect costs relate to children. This is a clear It has been assumed until recently that the indication of the increasing prevalence of asthma only hope for changing these factors is by educat- and the loss of resources, including time taken off ing people about their symptoms and teaching from work to care for children in the home. them how to manage the asthma through environBy 2013, the estimate of the total annual cost mental control and appropriate medication usage. of asthma stood at $88.4 billion. Published in the Primary care-based interventions such as health Annals of the American Thoracic Society, the figeducation can be effective in teaching individuals ures were considered low since they were based with asthma how to achieve guided self- on an assumed prevalence of asthma of about management of a troublesome condition that can 5%, though the National Health Survey put the unnecessarily end in death. That statement prevalence at 8% [18]. Further, the costs were remains true, but there is a subset of people with based only on individuals who were actually severe asthma for whom one of the new biologi- receiving treatment through visits to providers, cal agents is essential. Choosing which “bio- pharmacists, ED, or hospitals. logic” is best for any one individual with asthma Assuming that the prevalence of asthma in all will require detailed assessment of the biochemi- age and gender groups remains unchanged, in cal and genetic features of that person’s 2019 Yaghoubi and colleagues [66] projected the condition. excess costs of uncontrolled asthma for the next 20 years. Excess direct costs were estimated to be $300.6 billion. With the addition of indirect costs, 1.3.4 Costs this raised the estimated excess total economic costs to $963.5 billion. They also calculated that Many attempts have been made to estimate the individuals with asthma would lose 14.46 million cost of asthma, but it has proven difficult to get a quality-adjusted life years. precise estimate. However, there is little doubt The projected excess cost estimates were that this one condition accounts for a significant based only on uncontrolled asthma in adults. percentage of overall healthcare spending. Pediatric costs were not included. As opposed to US estimates are divided into direct and indi- the excess costs, the estimate of direct costs of rect costs, with the major elements of direct costs uncontrolled asthma in adults over the same being inpatient care, emergency visits, physician 20-year period was over $1.5 trillion. However, services, and medications. Other direct costs if all the adults had well-controlled asthma, then include nursing and ambulance services, devices, the saving in the USA would be an estimated research, and community health education. In $300.6 billion in direct costs and a further other words, what we refer to “direct costs” are $66.2 billion in indirect costs. See Tables 1.2 costs to the system that may be covered by insur- and 1.3.

1.3 Significance of Asthma

While it is important to estimate dollar costs, they do not take into account loss of enjoyment of life and other intangible costs, including the negative emotional impact; the fear, pain, unhappiness, and grief that result from a chronic illness [67–71]; the loss of potential resulting from children missing school due to the disease; and the reduction in career choices available to adults. A detailed knowledge of costs can be helpful when planning asthma-related services and when devising measures to control costs. Costs can be reduced by careful assessment that results in a limited number of medications being prescribed, by the use of generic medications where available, and, if necessary, by recourse to the individual’s insurance or prescription plans. And obviously, fewer exacerbations translate into much lower personal costs, to say nothing of a better life and less suffering. Educators are the professionals who can make the greatest impact on costs in both routine care and emergencies. A person with asthma who really understands his or her own condition will need fewer admissions to hospital and fewer emergency visits, with resultant cost savings [72–74]. A study by Clark et al. [75] showed that education did make a significant difference, with $11.22 being saved for every $1 Table 1.2 Projected excess costs of uncontrolled asthma in adults 20-year Projected Excess Costs of Uncontrolled Asthma ($m, rounded) Direct Costs Indirect Costs Age (Years) Males Females Males Females 15–30 40 44 99 188 30–65 76 91 188 228 >65 20 30 19 25

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spent on educating families. Lewis et al. [76] estimated a saving of $180 per child per year subsequent to an education program. Bolton and colleagues [77] found that for an educational investment of $85 per person, there was a reduction in ED charges of $628 per person. In dealing with a group of adult women with a history of repeated hospitalizations, Castro and others found that an investment of $186 per person could result in a saving of both direct and indirect costs of $6,462 per person, when the investment involved appropriate education, support, and counseling [78]. Nurmagambetov et al. [79] found the individual costs of asthma in 2013 to be • • • • •

$1,830 for prescription medications $640 for office visits $529 for hospitalizations $176 for hospital outpatient visits $105 for emergency room visits

Suh and colleagues [80] showed that a targeted asthma intervention program which actually increased individual asthma medication costs by one dollar ($1) could reduce individual costs by • $149 for hospitalizations • $16 for emergency room visits • $82 for physician visits The numbers are in, and they show conclusively that effective asthma education can, on average, save each person with asthma $725 in direct and $1,239 in indirect costs and lower the annual number of missed work days from 10.8 to 2.6 [81].

Table 1.3 Projected excess costs of uncontrolled asthma according to age and gender 20-year Projected Excess Costs of Uncontrolled Asthma ($m, rounded) Direct Costs Indirect Costs Age Males Females Males Females 15–30 40 44 99 108 30–65 76 91 188 225 >65 20 30 19 25 Total 301 664 Quality-Adjusted Life Years Lost (‘000)

a

QALY Losta Males 2,060 3,907 1,022 15,461

Females 2,260 4,686 1,526

1 Asthma and Asthma Education: The Background

14

Another way to analyze costs is to consider the costs of controlling asthma (through scheduled physician or healthcare provider visits, prophylactic medications, and education) against the costs of uncontrolled asthma (unscheduled healthcare provider visits, ED use, hospital admissions, and so on). The costs of asthma have been linked with lack of control over the disease, with increasing costs directly related to the increase in prevalence and severity. The definition of what constitutes effective therapy has undergone many changes. It is no longer assumed that improvement in a laboratory test is synonymous with real-life improvement, particularly from the point of view of the person with asthma. Much recent research has related the clinical outcomes to what the person with asthma actually feels, and tests have been develFig. 1.1 Some references for quality- of-life scores

oped to measure day-to-day function on a physical, social, and emotional level. While these QOL scores have been developed for research purposes and for studying new treatments, the concepts behind them are more generally applicable and are useful for educators to understand. Some QOL principles are not specific for asthma and provide an overall profile of how a person is functioning in terms of health. There are also disease-specific QOL evaluation forms, as generic forms will not suit all purposes. Some are designed to show differences between individuals and others to evaluate changes in an individual over time. The scores are realistic rather than theoretical, and the rigorous method of development emphasizes their relevance. See Fig. 1.1. Individuals are asked to estimate the issues important to them; and, as the score is applied to many people, it is refined. One

Wilson SR, Mulligan MJ, Ayala E, Chausow A, Huang Q, Knowles SB et al. A new measure to assess asthma's effect on quality of life from the patient's perspective. J Allergy Clin Immunol. 2018 Mar; 141(3):1085-1095. doi: 10.1016/j.jaci.2017.02.047 Wilson SR, Rand CS, Cabana MD, Foggs MB, Halterman JS, Olson S, et al. Asthma outcomes: quality of life. J Allergy Clin Immunol. 2012 Mar;129(3 Suppl):S88-123. doi: 10.1016/j.jaci.2011.12.988 Nishimura K, Hajiro T, Oga T, Tsukino M, Sato S, Ikeda A. A comparison of two simple measures to evaluate the health status of asthmatics: the Asthma Bother Profile and the Airways Questionnaire 20. J Asthma. 2004. 41(2):141-6. doi: 10.1081/jas-120026070 Blanco-Aparicio M, Vázquez I, Pita-Fernández S, Pértega-Diaz S, VereaHernando H. Utility of brief questionnaires of health-related quality of life (Airways Questionnaire 20 and Clinical COPD Questionnaire) to predict exacerbations in patients with asthma and COPD. Health Qual Life Outcomes. 2013 May 27;11:85. doi: 10.1186/1477-7525-11-85. Grammatopoulou E, Skordilis E, Koutsouki D, Baltopoulos G. An 18-item standardized Asthma Quality of Life Questionnaire-AQLQ(S). Qual Life Res. 2008 Mar;17(2):323-32. doi: 10.1007/s11136-007-9297-y Osborne RH, Elsworth GR, Whitfield K. The Health Education Impact Questionnaire (heiQ): an outcomes and evaluation measure for patient education and self-management interventions for people with chronic conditions. Patient Educ Couns2007;66:192-201

1.4 Etiology of Asthma

of those (the Asthma Quality of Life Score) deals with symptoms, emotions, exposure to environmental stimuli, and activity levels. Each item is scored on a seven-point scale. A separate score is used for children, to assess their stress levels and quality of life [82–84]. There are other QOL scores based on race, culture, or literacy, and some used specifically for research. It seems likely that many persons with asthma can, by following a carefully negotiated and prescribed regimen, reduce the cost to themselves and to society. They can lower their personal cost by achieving as good control as possible and avoiding triggers that lead to sharp deterioration. Such management also reduces societal costs by reducing healthcare provider and ED visits and hospital admissions and even the number of deaths from asthma [36, 85, 86]. The aim of all those involved in managing asthma, whether educators, healthcare providers, or individual and family members, should be to use the most effective therapy at the least cost.

1.4

Etiology of Asthma

Simple observation makes it clear that asthma is a heterogeneous condition; in turn, that observation suggests there may be more than one underlying pathological mechanism. In fact, in asthma there seems to be a complex interaction between allergies, genetic predisposition, and the physical and psychosocial environment. Described in outline here, these are explored in detail in later chapters. Words used here, such as genotype, phenotype, endotype, and atopy, require definition. Genotype is a person’s genetic constitution and relates to all the genes possessed by that individual. This is becoming increasingly well understood as more large-scale genome-wide association studies become available [87]. Phenotype is what we see in an individual with asthma. For example, one phenotype might be early-onset disease with severe exacerbations [88]. There are of course many phenotypes, and it is usually assumed that they are due to the interaction of genotype and environment. Endotype is a subgroup of a phenotype that is not easily dis-

15

cerned without detailed pathological study [89]. Atopy refers to the propensity, usually genetic, for developing allergic responses to common environmental allergens, usually via immunoglobulin E (IgE). In other words, the features of asthma seen in atopic persons are the product of their genes and their environmental exposures.

1.4.1 Allergy and Asthma Most of the time, a strong association can be observed between allergy and asthma. People with asthma may belong to a family in which many members have other allergic disorders such as hay fever or eczema (atopic dermatitis). The person with asthma may have rhinitis, eczema, or even anaphylaxis (a severe life-threatening allergic reaction) in addition to the asthma. Such people are described as atopic. Most persons with asthma also have evidence of allergy, as indicated by positive skin tests, an increase in the overall level in the blood of IgE and specific increases in IgE to specific allergens, and increased eosinophils in the blood and the airways. Allergic asthma is by far the most common form of asthma. In individuals with this form of the disease, the asthma is due to IgE-type hypersensitivity reaction, usually to inhaled allergens. This commonly has onset during childhood and usually persists or recurs in adult life. See Fig. 1.2. Non-allergic asthma is found in some adults and, very rarely, in children. Even in adults, it is much less common than allergic asthma [90, 91]. Persons with non-allergic asthma usually exhibit the following characteristics. They: • Have definite asthma, but without IgE hypersensitivity • Generally do not have seasonal variation in symptoms • Often experience the onset in adult life • Tend not to remit, but to persist with symptoms • Do not show the same variation with time as exhibited by allergic asthma • Show a poor response to treatment other than with the use of systemic corticosteroids

1 Asthma and Asthma Education: The Background

16 Fig. 1.2 The interrelationship between asthma and allergy

1.5

Genetics and Environment

1.5.1 Phenotype and Genotype Correlation The recognition that genetic factors are important in asthma is not new. Asthma runs in families. It would be more accurate to say that allergies run in families, and in any particular family, some members may have hay fever, some dermatitis or eczema, and some asthma. Individuals within the family structure may have more than one of those conditions at any given time. A child who has an atopic parent is twice as likely to have asthma as a child who has neither parent atopic. The risk is slightly higher of having an atopic tendency with an atopic mother than with an atopic father. Atopy is a risk factor for asthma. Yet the wide variation in manifestations and severity from one person to another (a variation which is seen even when they are closely related) has made precise estimation of genetic risk difficult. As noted earlier, some of

this may become clearer with genome-wide analysis. Developments in molecular biology overall, but specifically in genome analysis, are beginning to provide an understanding of some of these issues. It seems that there are many different relevant genes, present on different chromosomes, but in different proportions in different families. The precise genes present in an individual will be one of the major determinants of the pattern of asthma. Researchers are attempting to identify these, and it may well be that genes for allergy, for airway reactivity, and for asthma are all related. Their precise mix in an individual will determine how the asthma presents and behaves. This latter feature, seen in the individual, is the phenotype or clinical expression of the gene. Confusion exists because the asthma phenotype may be mimicked by nongenetic disorders. Bronchial hyperreactivity (BHR) is an example of phenotype-genotype confusion. At one time BHR was thought to be specific for asthma, but it is now recognized that BHR is seen in other diseases including the common chronic obstructive

1.5 Genetics and Environment

pulmonary disease (COPD). In other words, the previous belief that asthma and COPD were separate entities that could be readily differentiated is simply not true. Rather, there is considerable overlap between them. Pharmacogenetics, the study of the “genetic determinants in the variable response to therapy,” is an important new area of asthma research that will eventually help in prescribing the most effective remedy for an individual with asthma [92]. For example, some people with asthma, with specific genetic traits, have a poor response to inhaled corticosteroids [93]. Tests that would provide such information are not presently readily available: knowledge will however help us understand so-called nonresponders, rather than assuming that they are not following recommendations. For practical purposes, at the present time, a family history from first-degree relatives is extremely important to identify this genetic predisposition. This history must include occurrences of asthma, eczema, hay fever/allergic rhinitis, and anaphylaxis. Care must be taken to explore the childhood history of adult relatives. For example, parents will often indicate in their history that they themselves had “bronchitis” as a child and sincerely believe they do not have a history of asthma. If it is possible to get information from the previous generation about those episodes of “bronchitis,” it will often turn out that this should have been diagnosed as asthma. Other markers of genetic predisposition, such as IgE levels in umbilical cord blood, are useful in research studies.

1.5.2 Environmental Issues Genetic predisposition is not the only issue of concern. For children, there may be an environmental cause in addition to the genetic predisposition, and this has only recently been recognized. In the past, focus was placed on environmental triggers, which were defined as anything that could lead to an episode of asthma.

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In infancy and childhood however, what would be considered a trigger in an older child or adult may actually be a cause of asthma and may interact with the genetic factors to set the scene for continuing asthma. In other groups, strong environmental exposure—such as through occupational exposure to Western Red Cedar, for example— may cause asthma with minimal or no genetic predisposition. This is an example of the asthma phenotype mimicked by a nongenetic cause.

Points to Ponder

Common triggers of asthma • • • •

Allergens Infections Irritants Emotions

The main identified environmental causes of asthma are exposure to allergens such as cat dander and house dust mites in infancy [94], exposure to passive cigarette smoke during pregnancy and infancy [95, 96], and poor socioeconomic circumstances [23, 54, 97]. Some food allergies have recently been shown to be important in the development of asthma in infancy and childhood, for example, to milk [98] and hen’s eggs [98–100]. While the relevance of early life events to the onset of asthma has been well recognized for many years, the specifics have been elusive. A common confounder has been recall bias by studies in later childhood or early adult life that focus on events from many years earlier. Recently, large cohort studies (began in infancy and continued with follow-up for many years) have helped to resolve some difficulties. For example, Sears et al. [101] followed 613 children born in New Zealand from April 1972 through March 1973 all the way through to age 26. This unselected birth cohort completed questionnaires, pulmonary function testing, bronchial-challenge testing, and allergy testing. About one in four had wheezing in adult life.

1 Asthma and Asthma Education: The Background

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Those with persistent or relapsing symptoms were more likely to: • • • • •

Be sensitized to house dust mites Have airway hyperresponsiveness Be female Smoke Have early onset of wheeze

Despite similar information in other studies, no universal strategy for prevention of asthma has emerged. It is common to find that exposure to dust mites is one of the most potent asthma-producing allergens and that this exposure is a risk factor for bronchial hyperresponsiveness or BHR [94, 102, 103]. The National Heart, Lung, and Blood Institute (NHLBI) guidelines [11] note that exposures to high levels of house dust mite antigen and environmental tobacco smoke are associated with increased incidence of asthma among infants. A study of 696 newborns in Europe at increased risk of atopy showed a reduced incidence of sensitization to dust mite allergens at 1 year with the use of mattresses that were impermeable to house dust mites [104]. Unfortunately, it has not yet been shown that reduction in exposure to house dust mites in infancy will prevent the onset of asthma. As far as pets are concerned, there is apparent confusion in the current literature between their roles, firstly in the onset of asthma and, secondly, in the persistence of the disease [103, 105]. There is a clear association in adolescents and adults between sensitization to pets and both current wheezing and BHR. Yet cohort studies have shown a lower risk of asthma in children exposed to pets in early life, in effect suggesting that pets might be protective. In a review of these studies, it is speculated that it is not the pets that are protective, but some associated factor. For example, bacteria produce toxins, and endotoxins in the cell wall are released when those walls disintegrate. Toxins can harm. For an example outside asthma, the deadly disease botulism is caused by a toxin. Exposure to bacterial toxins is thought to be a major factor in developing immune responses other than the

Th2 response characteristic of asthma [106]. Thus toxins brought into the home by pets may protect against the development of allergy. Other studies have shown a possible reduced risk of asthma in children who spend their early life on farms, again perhaps due to endotoxin exposure [107]. Viral infections may also have paradoxical effects. In preschool children, viral infections are the most common trigger of an episode of wheezing. Some specific respiratory infections are correlated with asthma severity and linked to susceptibility of later infections which are potent triggers of asthma [108]. Then again, recent evidence suggests that exposure to older siblings and in daycare facilities may lessen the likelihood of asthma in genetically predisposed children [109–111]. These findings, interpreted against the background of a general increase in asthma in the western world, have led to speculation that lifestyle issues may be relevant. The potential role of exposure to bacterial endotoxin and viral infections in protecting against asthma has been described as the “Hygiene Hypothesis” [107, 108, 112, 113]. This hypothesis is one explanation for the increase in the incidence of asthma in developed countries. It assigns a causal role to “improvements” in society, particularly changes in early childhood with an emphasis on cleanliness and smaller family size. The suggestion is that fewer infections and less exposure to dirt and endotoxins impair immune development. This hypothesis explains some, but not all, of the recent data, and it is not yet proven. It is possible that advances in genetic knowledge may allow better understanding of genetic/environmental interactions. Perhaps some children, with one genotype, when exposed to infection or endotoxin will exhibit heightened susceptibility to allergy. Others may be harmed by too much infection in infancy or by one or two specific infections. The educator must move carefully when reviewing the complex literature relating to the onset and persistence of asthma. For persons with asthma, or infants with recurrent wheezing, attention to the environment remains important.

1.5 Genetics and Environment

Allergic sensitization requires assessment, and where exposure can be reduced, such as to pets, it should be. The benefits of such reduction are clear. It is possible that the paradox of exposures being protective at one age and then harmful at another will be explained in the future by detailed genetic analysis. Cohort studies give invaluable information on populations, but their findings must be interpreted cautiously in individuals. Non-allergenic triggers [114] also exist, such as cold air, exercise, tobacco smoke, wood and industrial smoke, and many different environmental exposures. Only tobacco smoke exposure has been shown to be causal for the onset of asthma, although the others are very relevant to its persistence. Outdoor pollutants can trigger asthma and worsen symptoms [115–117], but whether outdoor pollutants can cause asthma is a different question. In a systematic review, Gowers et al. [118] concluded that some forms of outdoor air pollution might play a role in susceptible individuals in the causation of their asthma. The conclusion was very cautious, stating that this was a small effect on a small proportion of the population. The fact that asthma is a combination of genetic and environmental factors [119–121] does pose some practical implications. There is little that can be done about the genetic tendency, but where there is a known genetic predisposition, it is important to offer counseling, for example, during pregnancy, with a focus on reducing exposure to tobacco smoke. It is tempting to suggest that pregnant women avoid those foods that might lead to allergies, but this may not be helpful for the child. An extensive review concluded that an antigen avoidance diet for a high-risk woman during pregnancy is unlikely to reduce substantially her risk of giving birth to an atopic child. Moreover, such a diet may have an adverse effect on maternal and/or fetal nutrition (122). There should be strong encouragement and support for breastfeeding. However, infants can be sensitized to potent food allergens in breast milk. Counseling should be maintained after birth. Despite theoretical confusion, it is possible for anticipatory guidance to make a difference.

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An example would be Wickman’s study of children whose families were provided with guidelines that recommended breastfeeding, no exposure to tobacco smoke, and homes without dampness and with good ventilation. Families that followed these guidelines had a 12.6% incidence of wheezing and 6.8% of asthma when compared with 24.1% and 17.9%, respectively, for families that did not follow them. Further, for children without allergic parents, there was a twofold reduction in asthma, while children with allergic parents reduced their risk of asthma by a factor of 3 when these guidelines were followed [123]. In another study, the parents of 58 infants at increased risk of asthma and allergy were given advice on feeding and avoidance of house dust mite. The outcome, in terms of allergy and asthma in the children, was compared to 62 children whose parents were not given this specific advice. It was confirmed that allergic diseases could be reduced [124]. The risk factors for asthma are: • A parental history of atopy • Nature of the allergen • Respiratory illness before age 2 GINA lists the risk factors in two categories, host and environmental, and further groups the latter into causal and contributing factors with allergens and occupational sensitizers included in causal factors. See Table 1.4.

Table 1.4 Genetic and environmental risk factors for asthma [13] Host: predisposing Atopy Genetic Airway hyperresponsiveness Gender Ethnicity

Causal Allergens • Indoor • Outdoor Occupational sensitizers

Contributing Respiratory infections Small size at birth Diet and medications Obesity Air pollution • Indoor • Outdoor Smoking • Active • Passive

1 Asthma and Asthma Education: The Background

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1.6

Approaches to Asthma

Before treating a person who has asthma, every healthcare practitioner (HCP) must be familiar with the latest recommendations for diagnosis and treatment of this condition. The recommendations are summarized and published as “guidelines”.

1.6.1 Guidelines Guidelines exist for a number of diseases, and they tend to be updated at different times. Asthma guidelines have been updated fairly recently, and this section provides a brief overview of their major emphases. “Guidelines” exist under a wide variety of names, such as Clinical Practice Guidelines, Care Maps, Care Plans, and so on. There are differences, often subtle, between the various titles, the intended audiences, and how they might be used. Guidelines were first developed when it became clear that there was a huge gap between the scientific knowledge available about a medical condition and the implementation of that knowledge in everyday practice. They were intended to serve as a way to quickly translate scientific research into clinical actions with the aim of benefiting individuals with asthma. It is assumed that no physician or other healthcare professional can be an expert in every aspect of care. Guidelines allow access to a succinct statement of the evidence available at one moment in time. Guidelines are an important part of “knowledge transfer” in ensuring the results from research are available to those with asthma as soon as possible. Guidelines can become obsolete as new evidence becomes available. Typically, they usually list areas of agreement and also identify areas of disagreement and areas for further study. Further, they are not intended to control every detail of care. It is recognized that while there is commonality from one person to another, yet there are so many individual differences that, within limits, it is important that healthcare professionals and individuals have some freedom to make choices.

The process of guideline development varies. In general, the first step is to identify all the relevant evidence and to discuss its significance. Participants in the discussion are regarded as “experts,” and there should be a very open process for identifying them and a wide range of latitude in determining who is considered an “expert”. Conflicts of interest in those developing guidelines should be declared. Some committees producing guidelines will assume that consumers are experts, while others will not make this assumption. The authors of this book believe that consumers are always experts on how disease and treatments affect their lives. Developers of guidelines will vary in their attitude to evidence. They will also vary in their attitude towards implementation. Sometimes they will assume that the very development and publishing of guidelines is of itself a sufficient start towards implementation. At other times, very detailed steps will be developed and published to help with the implementation. One final important topic in guideline development is the funding of the process. The costs associated with the extensive literature required, the meetings of experts, the discussion groups, and publishing have all to be borne by one group or another. If industry provides the funding, then the extent of its influence over the final product needs to be clearly articulated and evaluated. This is a completely separate issue from the declaration of individual conflicts of interest mentioned above.

1.6.2 NHLBI Guidelines The National Heart, Lung, and Blood Institute (NHLBI) is one of the federally funded National Institutes of Health. NHLBI Guidelines are immediately relevant to all healthcare professionals planning to obtain their AE-C designation. The first NHLBI Expert Panel Report on Asthma was released in 1991 and has been updated from time to time. The most recent comprehensive document, the Expert Panel Report 3 (EPR-3) cited earlier, was published in September

1.6 Approaches to Asthma

2012 [11]. Since then there have been focused updates on specific topics, most recently in 2020 [125]. Other bodies have also produced helpful reports, particularly GINA [2]. Reference will be made to relevant and useful parts of all these documents. It is important that the reports from official bodies and healthcare organizations summarize evidence fully and fairly and base their recommendations on that evidence. The orderly process followed in the 2012 publication is a model. Here is the process in sequence: (1) Completing a comprehensive search of the literature (2) Conducting an in-depth review of relevant abstracts and articles (3) Preparing evidence tables to assess the weight of current evidence with respect to past recommendations and new and unresolved issues (4) Conducting thoughtful discussion and interpretation of findings (5) Ranking the strength of evidence underlying the current recommendations that are made (6) Updating text, tables, figures, and references of the existing guidelines with new findings from the evidence review (7) Circulating a draft of the updated guidelines through several layers of external review, as well as posting it on the NHLBI web site for review and comment by the public and the NAEPP Coordinating Committee (8) Preparing a final report based on consideration of comments raised in the review cycle The evidence that justified the recommendations was ranked as follows: A ─ Randomized controlled trials (RCTs) with rich data B ─ RCTs with limited data C ─ Non-randomized trials and observational studies D ─ Panel consensus judgment

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The Panel listed these key points: • Asthma is a chronic inflammatory disorder of the airways. • Immunohistopathologic features are important. • Inflammation leads to airway hyperresponsiveness, airflow limitation, respiratory symptoms, and disease chronicity. • Some of those with asthma have permanent structural changes to the airway. • Importance of gene-environment interactions. • Atopy is the strongest identifiable predisposing factor for developing asthma. The key differences from previous reports are (and we quote again): • The critical role of inflammation has been further substantiated, but evidence is emerging for considerable variability in the pattern of inflammation, thus indicating phenotypic differences that may influence treatment responses. • Gene-by-environmental interactions are important to the development and expression of asthma. Of the environmental factors, allergic reactions remain important. Evidence also suggests a key and expanding role for viral respiratory infections in these processes. • The onset of asthma for most patients begins early in life with the pattern of disease persistence determined by early, recognizable risk factors including atopic disease, recurrent wheezing, and a parental history of asthma. • Current asthma treatment with anti- inflammatory therapy does not appear to prevent progression of the underlying disease severity. In the report, asthma management is seen as consisting of four components: careful assessment and monitoring; education as a partnership; environmental control and treatment of comorbidities; and medications. The concepts of severity (the intrinsic intensity of the disease process) and control (degree to which manifestations of

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asthma are minimized) are closely linked. In turn, both are linked to responsiveness, which is the ease with which the asthma is controlled by therapy. Severity and control should be assessed initially and then later, after therapy has shown benefit. Previously, comorbidities that might interfere with asthma management were identified as rhinitis, sinusitis, and gastroesophageal reflux. To this list, the report adds as important comorbidities allergic bronchopulmonary aspergillosis (ABPA), obesity, obstructive sleep apnea (OSA), and stress. The type of asthma also affects management, with “type” being broadly described as intermittent and persistent. The classification “mild intermittent” has been removed, as persons with intermittent asthma, even if generally mild, can have severe exacerbations on some occasions. Persistent is subdivided into mild, moderate, and severe. Attention to environmental aspects is still considered important, but the 2012 report noted that the new evidence strengthens recommendations that asthma control is improved with reduced exposure to indoor allergens. A multifaceted approach to environmental control is essential. Medications are placed in two broad categories: long-term control and quick relief. The main aim of such therapy is to “prevent and control asthma symptoms, improve quality of life, reduce the frequency and severity of asthma exacerbations, and reverse airflow obstruction.” Medications used in long-term control are inhaled corticosteroids (ICS), long-acting beta agonists (LABAs), leukotriene modifiers, immunomodulators, and methylxanthines. Newer medicines are being developed, and some are in use that help people with asthma by altering the immune response. These have been described as immunomodulators, and currently the one used most frequently is omalizumab that blocks IgE action. At one time, cromolyn sodium and nedocromil were in use for mild asthma, but it was always recognized that their potency was low. Today, ICS are the mainstay of management and may be combined with a LABA. The latter are never used on their own. Leukotriene modifiers may be used as adjunctive therapy, along with ICS, and possibly

1 Asthma and Asthma Education: The Background

as an alternative therapy to ICS in mild persistent asthma. There are an increasing number of immunomodulators [126], still mainly monoclonal antibodies such as omalizumab. Each agent seems to be particularly useful with specific phenotypes and is used with persistent symptoms despite full therapy with other agents and good environmental control. Methylxanthines are another long-standing treatment for mild persistent asthma. They are no longer a preferred treatment given their high incidence of side effects, requiring both symptom monitoring and regular measurement of blood levels. They may have a limited use as adjunctive therapy with ICS. The main medications for quick relief are the SABAs. Anticholinergics provide an additive benefit to a SABA: the SABAs relax the muscles, while the anticholinergics prevent the muscles from tightening. SABA drugs are safe, but increasing or increased use indicates poor control and the need for more effective long-term therapy. While systemic corticosteroids are not rapid- acting, they are used along with SABA in moderate and severe exacerbations. Most of the medicines (SABA, LABA, and ICS) are given by the inhaled route. For those delivered by metered-dose inhaler (MDI), a “spacer” is required. The spacer or holding chamber extends the MDI away from the mouth and retains the large particles of medication, allowing a greater proportion of small particles to enter the airway. Many persons with asthma, or their families, will ask about complementary and alternative medicines. None of these compounds is a substitute for any medicine mentioned above, and there is no, or insufficient, evidence to make recommendations. Acupuncture is not recommended for asthma. Herbal preparations may contain substances that are harmful and/or interfere with the action of prescribed medications. The severity of the asthma will determine the initial prescription (the medications, doses, and schedules). The level of asthma control will determine how these are adjusted. This is done in steps, following a six-step approach. Therapy is then stepped down (i.e., reduced) to the point

1.6 Approaches to Asthma

where the disease remains controlled with the minimum amount of medication. The overall aim is to reduce impairment. Specific aims are to prevent symptoms, have only infrequent use of SABA (2 days a week or less), maintain normal pulmonary function, and maintain normal activity. All of this should be achieved to the satisfaction of the person with asthma and his or her families. Monitoring and follow-up is essential. It should be remembered that because asthma is a chronic disease, persistent asthma will require daily therapy. This group of recommendations differs in a number of ways from previous iterations. Management recommendations for those below 12 years are no longer grouped together; they are now subdivided, into 0–4 years and 5–11 years. The decision on choice of initiation therapy is based on assessment of both impairment and risk components of severity. A number of other changes will be mentioned in detail later, including the need to consider separately both QOL and functional issues. In addition to some racial and ethnic disparities, there is a constant reminder of the importance of identifying and treating comorbidities. The 2020 report [125] was asked to focus on six specific topics and not to revise all of the previous recommendations. Hence in Chaps. 5 and 6, material from both reports will be used to guide evidence-based practice. The 2020 topics include: 1. Use of fractional exhaled nitric oxide testing in diagnosis and management 2. Indoor allergen mitigation in management 3. Use of intermittent inhaled corticosteroids in treatment 4. Use of long-acting muscarinic antagonists 5. The role of subcutaneous and sublingual immunotherapy in the treatment of allergic asthma 6. Use of bronchial thermoplasty to improve outcomes The inclusion of an item does not mean support; rather, it indicates that clarification of the evidence was needed. For example, the evidence

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on the use of bronchial thermoplasty was not strong, and a very limited role was envisaged. Similarly, many cautions are placed around the use of immunotherapy. One item that drew attention was the use of intermittent inhaled corticosteroids in the treatment of intermittent asthma. This break from the mantra of “ICS every day for everyone with asthma” was welcome and also realistic in the expectations we have of people with asthma. The 2020 Focussed Updates provided details on “the need to integrate the new evidence-based recommendations into a comprehensive approach to asthma care using the EPR-3 step diagrams.” One important new topic—that of the role of immunomodulators—is addressed in the GINA update. That update provides details on those currently available, all of them being monoclonal antibodies. This is both an important topic and an exciting development and is described in detail in Sect. 6.4.6. However, all of the compounds available are new, so their use requires both discernment and care and avoidance of the tendency to “jump on the band wagon.”

1.6.3 Pediatric Guidelines The US Guidelines for the Diagnosis and Management of Asthma are applicable to children and adults and recognize that asthma affects all ages [11]. As noted, the issues affecting children are subdivided into those for children aged 0–4 years and those aged 5–11 years. The differential diagnosis of asthma in children, especially those under 4 years, is wider than in older children and young adults. However, additional care is required with children, both to improve their quality of life throughout childhood and to ensure that they reach adulthood in good health. Help with the specific issues pertaining to pediatric asthma is available in a recent review of guidelines from a variety of sources [127]. Many adult pharmacologic therapies are used in children, with only minor variation in dosage. The dose should be tailored more to the assessed severity than to the physical size of the child.

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The onset of asthma most often occurs in childhood, and between 50% and 80% of asthma develops before the age of 5 years. In the USA, there are about 5.5 million children (7.5%) below 18 years with asthma, with approximately 744,000 (about 3.8%) of them less than 5 years old [18, 128]. Asthma is responsible for extensive time lost from school and is particularly prevalent in areas of poverty and in inner cities. It affects the child’s life at home, but may also reduce ability to participate in sports, attend school trips, participate in physical education or playground activities, or play a musical wind instrument. Once good control is achieved, all these activities are possible for children with asthma. Asthma is often overlooked in children. The criteria for diagnosis, and the wide differential diagnoses in younger children, are described in Chap. 4. When assessing children with asthma, a full environmental history should be done. While this will obviously look at the child’s home, it must include school, daycare facilities, and friends and family whom the child visits frequently. ICS are the mainstay of treatment of asthma, but there are specific concerns with these drugs because of the paucity of formal studies in children. While the impact of inhaled corticosteroids on the child’s growth appears to be minimal, the evidence is however confusing [129]. Decreases in the growth rate appear to be temporary and unlikely to have an effect on final growth height. However, atopy itself has an effect on growth and can increase the risk of short stature by two to five times [130]. Nevertheless, linear growth should be monitored in children on inhaled corticosteroids. Once the asthma is under control, the dose of medication should be reduced to the lowest effective level. Formal assessment using spirometry should be done as soon as possible, possibly as early as 3 or 4, but more likely at 6 or 7. Where the 2020 update applies to children, details are given. The relevance of the use of intermittent inhaled corticosteroids in children, whose asthma is often intermittent, is noted. The newer biologic immunomodulators are relevant to children with severe persistent asthma, although currently limited to those over 6 years of age.

1 Asthma and Asthma Education: The Background

1.6.4 COVID-19 and Asthma The COVID-19 pandemic has caused extreme anxiety in those with asthma and also among educators and healthcare personnel. It has also meant services have been limited and often provided online. How much these new ways of providing education will be used in the future remains to be seen. It is safe to conclude that when the pandemic is over, there will not be a return to the old way of doing things—some of the new procedures will remain in place, while others, possibly less cost-effective, may be discarded. GINA has provided some guidance [131]. It clearly states that “People with asthma are not at increased risk of acquiring COVID-19.” The evidence supporting this statement is that: • Systematic reviews have not shown an increased risk of COVID-19 in people with asthma. • Handwashing, masks, and social/physical distancing have reduced the incidence of other respiratory infections, including influenza, in 2020. The role of the educator remains important in the life of people with asthma. Overall, people with asthma are not at increased risk of death related to COVID-19, but the risk of death was increased in those who recently had oral steroids [132]. “Therefore, it is important to continue good asthma management (as described in the GINA report), with strategies to maintain good symptom control, reduce the risk of severe exacerbations and minimise the need for oral corticosteroids.” Other COVID-related advice: 1. Medications a) Advise patients to continue taking their prescribed asthma medications, particularly inhaled corticosteroids. b) For patients with severe asthma, continue biologic therapy or oral corticosteroids if prescribed. Make sure that all patients have a written asthma action plan, advising them to:

1.6 Approaches to Asthma

Increase controller and reliever medication when asthma worsens Take a short course of OCS when appropriate for severe asthma exacerbations Avoid nebulizers where possible, to reduce the risk of spreading virus Preferably, use pressurized metered dose inhaler via a spacer except for life- threatening exacerbations Add a mouthpiece or mask to the spacer if required 2 . Infection control a) Avoid spirometry in patients with confirmed or suspected COVID-19, or if community transmission of COVID-19 is occurring in your region. b) Follow aerosol, droplet, and contact precautions if spirometry is needed. c) Consider asking patients to monitor PEF at home, if information about lung function is needed. d) Follow strict infection control procedures if aerosol-generating procedures are needed, such as nebulization, oxygen therapy (including nasal prongs), sputum induction, manual ventilation, noninvasive ventilation, and intubation. Above all GINA advises us all to “Follow local health advice about hygiene strategies and use of personal protective equipment, as new information becomes available in your country or region.”

1.6.5 Organization of Care There will always be some people who prefer to attend the ED for urgent care—possibly because they do not have a regular healthcare provider, or do not want to deal with the same healthcare provider on a regular basis since that person might give them unwelcome advice about asthma control. Such persons will always have many reasons for preferring a visit to emergency. However, others will prefer to achieve a productive long-term professional relationship with one or more healthcare providers (such as a phy-

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sician, healthcare provider, nurse, pharmacist, and others) and will view this relationship as an effective way to help them manage their chronic conditions. Individuals seldom think about how healthcare providers will relate to one another or how well they are educated in current trends and in a specific disease and how the arrangements of their personal healthcare plan, or the healthcare system as a whole, relate to their disease. Some of these issues will be dealt with in the next section.

1.6.5.1 General Approach of Health Systems For the most part, early twentieth-century healthcare consisted of physician visits followed by a trip to a pharmacy. In some cases, the pharmacy visit was not needed as the physicians may also have dispensed the medications. For serious illnesses, a nurse may have visited the home, or the individual may have been admitted to a local hospital. As the twentieth century progressed, there were improvements both in the effectiveness of specific medical treatments and many organizational changes. Within medicine, there was less reliance on family physicians and an increase in the number and types of specialists. Nursing, the one profession traditionally associated with medicine, was joined by many other healthcare professions, including physiotherapists, occupational therapists, respiratory therapists, physiologists, social workers, and therapists of many different skills; and they all have an important role in healthcare. These groups have increased in number and significance, and there has also been specialization within groups. For example, some respiratory therapists specialize in a specific area of medicine, such as care of children, while others work in intensive care units (ICUs). Asthma educators are a new type of healthcare professional, with background training in one of many healthcare disciplines, together with additional specialized knowledge of asthma that is supplemented by training in patient education. They may be found in any healthcare setting and may confine practice to asthma education or may

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combine asthma education with the more general practice of their discipline. They may also work more widely as respiratory educators. While these changes in the professions were occurring, treatments, including medications, increased both in effectiveness and in cost and are now very expensive. These dual increases led to many changes in insurance coverage, including the introduction of national schemes such as Medicare and Medicaid. The final decades of the twentieth century have seen the evolution of many varieties of health maintenance organizations (HMOs). “The delivery, organization and financing of healthcare is a complexly adapting system” [133]. The current trend is to focus designated resources on specific diseases. Disease management programs have been developed with the twin aims of improving outcomes and reducing costs. Thus, the emergence of cardiac centers, which include both cardiac surgery for end-stage disease, and cardiac rehabilitation centers; of diabetes centers with a focus on education; and so on. A system-wide approach to asthma fits into this scenario. In the twenty-first century, all of the centers, including those for asthma, will make extensive use of virtual and online resources. As an unanticipated result of COVID-19, those living in rural areas, if they have high-speed Internet coverage, will have the same access to high- quality health education as those living next door to a prestigious medical center. Where there is such system-wide support, there is great hope for everyone with asthma. Even when such support is absent, there is great hope that health outcomes can be improved, wherever both the agency providing healthcare and individual healthcare providers accept the responsibility to include prevention and education.

1.6.5.2 Healthcare Professionals As mentioned earlier, traditional healthcare has concentrated on the roles of the physician and the hospital for inpatient and emergency department care. There is a growing recognition that healthcare has a far wider scope—many other healthcare providers are involved, and healthcare is

1 Asthma and Asthma Education: The Background

delivered in many sites other than a physician’s office or a hospital. In addition to the healthcare providers, it is necessary to consider also those with asthma, their families, and their whole social network in the overall organization of care. A conventionally structured healthcare team set up to deal with a chronic condition might include a physician or nurse practitioner (a nurse who prescribes and does primary care), nurse, pharmacist, therapist (respiratory therapist for asthma), social worker, psychologist, physiotherapist, and others. As described, the team implies that the person being treated is a passive participant rather than an active member. However, experience suggests that this person should, instead, be an active and participating member of the team. Thus, a proper team to deal with a chronic condition, such as asthma, would include: • The person with asthma and his/her family • A physician and/or another healthcare provider • Healthcare providers such as an asthma educator and a pharmacist • Other healthcare providers, as needed Other healthcare providers may be involved in some cases, depending on severity. They will include, among others, respiratory therapists, psychologists, social workers, physiotherapists, teachers, and specialists in allergy, pulmonology, sports, and exercise activity. The person at the center of this team is the person with asthma and the family. The team will recognize the person’s importance and will offer a variety of professional expertise. Since each professional will view the individual’s problem from a different point of view, the advice given will be multifaceted and comprehensive. However, it must be noted that the major (and final) responsibility for taking and adjusting medications, and for making any needed changes, rests with the person and his or her family. In asthma, an organized system for provision of care will lead to a number of benefits including:

1.7 Education of Persons with Asthma

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• Improved assessment and diagnosis 1.7.1 The Issues • A methodical approach to treatment • Education and development of self-Asthma is a chronic condition. Strategies used by management plans for those with the both those with asthma and by healthcare profescondition sionals in managing a chronic condition are quite • Access to information different from those for an acute situation. In a • Regular follow-up to maintain and reaffirm chronic condition, the complicated interaction the need for long-term treatment between the family/person with the condition, the • Further regular follow-up to determine the condition itself, and other healthcare providers need for changes in treatment becomes fundamentally different from the inter• Modification of treatment with advances in action that occurs in an acute disease. Those with knowledge a chronic condition may additionally be very knowledgeable and rightly demand more control 1.6.5.3 Personal Responsibility over their treatment. The person with asthma, and the family, must be Healthcare in North America has had most responsible for monitoring the severity of the success in dealing with acute diseases. Those asthma. This becomes even more important with with long-term conditions or disabilities meet a chronic long-term condition. They will know various barriers in the system and in the attitude when their loved one with asthma is in trouble of some healthcare providers. Insurers may quesand will be able to take early corrective action tion the provision of expensive medication for rather than later crisis reaction. They will be ambulatory care. The issue of “pre-existing conable to make minor adjustments in treatment, to ditions” is currently under political review in the plan appropriate interventions themselves, and USA in terms of overall healthcare coverage, to deal with situations such as exercise. They including medication coverage. will be able to assess the effect of a new enviIndividuals with a chronic condition may not ronment and be full partners in the valuable see themselves as having a disease and may go assessment of treatment. They will be able to do for long periods without giving much thought to all of these things if they are educated about their healthcare. This desire to “get on with life,” their condition and the way it affects them. often referred to disparagingly as “denial” by Individuals need to be made aware of their roles professionals, can actually be healthy. Those with and responsibilities in the management of chronic conditions themselves realize there is asthma. Hence the educator has a role to play in much more to life than their condition. However, helping everyone with asthma become self-reli- in almost every chronic condition, there is a need ant and self-managed with guidance from the for daily discipline: to take medications, to avoid asthma care team. situations which will cause deterioration, and to consider specific conditions when dealing with such issues as changes at work, relocating, choosing a house, and dealing with family structure. 1.7 Education of Persons There may also be long-term reduction in income. with Asthma Some of the words used when discussing The process of educating people about their dis- chronic conditions are pejorative. These include ease used to be done by healthcare providers “normal,” “disability,” and “handicap.” The word (HCPs). Today, the asthma educator works, along “normal” is often used by physicians and other with the HCP and other members of the medical scientists in a statistical sense, but individuals team, to provide much of that education and with chronic conditions find its opposite, “abnorongoing support. The educator’s functions are mal,” to be an offensive word. The words “disability” and “handicap” have their own negative briefly described here.

1 Asthma and Asthma Education: The Background

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connotations. In addition to this, many persons with chronic conditions, including those with asthma, exhibit quite a wide variation in the degree to which they may be affected. Chronic disorders abound in medicine, and one of them, diabetes mellitus, has useful parallels to asthma. Diabetes mellitus requires: • Daily medication, sometimes involving injections • A need for lifestyle changes (particularly in diet) • A quick response to a sudden change, such as that caused by an acute illness In diabetes mellitus, experience shows that educated—i.e., knowledgeable and empowered—individuals achieve a better degree of disease control, and a vastly improved quality of life, than those who simply follow instructions. Disease control and quality of life are poorer still in those who ignore instructions. Much has been made in recent medical literature of the re-recognition that asthma has an inflammatory basis. This provides support for the avoidance of environmental factors which may lead to chronic inflammation and for the use of effective medications such as inhaled steroids, which can deal with the inflammation when taken on a regular prophylactic (preventive) basis. The recognition that asthma is based on airway inflammation is at least as important as the recognition that it is chronic. Many factors need to be considered in management in addition to an appropriate prescription for a chronic condition. These include: • • • • • • • • • •

Perception [134] Understanding Attitude Literacy overall and health literacy Education Individual treatment regimen Identification of triggers Avoidance of triggers Objective assessment Follow-up

A key component in long-term management includes a partnership with the person who has the condition. This requires a full exchange of information, an understanding of expectations by both sides, and the responsibilities of each party [135, 136]. People with chronic conditions, including those with asthma, require education and help in order to live a normal life. Some restrictions, such as avoidance of vulnerable situations and the regular use of medication for prevention, may be necessary. They will also need to develop the skills to recognize the signs of deterioration and to cope with it. They must also be able to recognize when they are sick enough to need professional help. Poor treatment adherence is a major problem with asthma. Studies often focus on subtle differences between one anti-inflammatory medication and another and ignore the larger issue of why people with asthma will or will not take prophylactic treatment. The addressing of this issue is extremely important in improving the outcome of individuals with asthma. Many barriers militate against adherence. One of the easiest to overcome is a lack of knowledge about why certain medications are necessary and how they should be taken. Other barriers include cost, the inconvenience of regular treatment, and fear of side effects of some medications. All these can be addressed in an educational program. Even with adherence, a major barrier to achieving control of the asthma lies in the incorrect use of the various devices designed for inhalation of asthma medications. Individuals with asthma need frequent teaching and monitoring in the correct use of the many devices available. There is definite evidence of the benefits to be obtained from patient education [63, 67, 72, 135, 137–139] whether in self-management and coping [35, 140, 141], in school attendance or reduced ER visits or hospitalizations [33, 62, 141–144]. Education reduces the fear and builds confidence in the individual’s ability to manage the disease [140].

1.7 Education of Persons with Asthma

1.7.2 Role of the Asthma Educator

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ing optimal pharmacologic therapy.” It should be noted this has the highest level of supporting eviWhy educate people with asthma? As far back as dence. GINA [13] lists “education of patients to 1975, the American Nurses Association stressed develop a partnership in asthma management” as that patient education is both the professional and the first and most important part of a six-part legal duty of a nurse [145]. By 1988, the NHLBI, management plan. in a workshop entitled Asthma Education: A Many early attempts at education sought to National Strategy [146], strongly emphasized teach the concepts of self-management by stressasthma education as a prerequisite for manage- ing a detailed knowledge of asthma [145]. But it ment of this condition. This included not only soon became clear that an increase in knowledge individual/public education but also professional did not lead to acquisition of the skills necessary education and a national coalition of agencies for self-management and that, often, what was and organizations, both professional and volun- learned was not translated into practice. In a teer, to promote a national education plan. The review session, those with asthma would list Joint Commission on Accreditation of Healthcare what had to be done during an asthma episode, Organizations (JCAHO) listed individual and but seemed unable to actually do what was family education as a priority in 1993. In every required when confronted with a crisis situation. report after that, JCAHO has emphasized educaInitial “education” sessions were done by phytion of the individual. It is a critical component in sicians who tried to educate persons with asthma their criteria for Disease-Specific Care through information packages, brochures, and Certification. JCAHO standards also require leaflets. This did not have the necessary and interdisciplinary collaboration [147, 148]. expected impact. The time required to teach peoIn its 1993 publication, Healthy People 2000 ple with asthma was often a disincentive to physiReview 1992 (PHS#93-1232-1 August 93), the cians. When nurses took over the job of education, US Department of Health and Human Services it was noted that the response was far better stated that one goal towards improving the health towards nurses who themselves had asthma than to of the nation should be to increase to 50% the nurses who did not [95, 152]. But again, the results number of persons with asthma receiving formal did not meet the hoped-for expectations. Education asthma education. In hindsight, this proved to be seminars were conducted for healthcare providers too ambitious, since subsequent research found involved in working with people with asthma, but that only 8% of persons with asthma had received those too were found to be insufficient. The semisuch education. In Healthy People 2010, the goal nars resulted in an increase in knowledge for the was to have 50% of people with asthma receive healthcare provider, but did little to advance an formal asthma education. In the most recent understanding of the triggers of asthma and how to biennial report, that goal was revised from the avoid them. Nor did they have a lasting effect on baseline in 2008 of 12.1% to a more realistic those who actually had asthma [153]. 14.5% [149]. Time and a better understanding of the task International Consensus Guidelines [150] also brought change and an appreciation of the role of emphasize asthma education and self-the educator. Then came the realization that it management as integral components of asthma required a specially trained healthcare profesmanagement. The NIH publication Nurses: sional [64, 154, 155] who not only understood Partners in Asthma Care (1995) [151] featured asthma and its pathology but was able to impart education of those with asthma as one of the four that knowledge in an appropriate, customized, components of asthma management. The NHLBI and effective manner. That person could teach, Expert Panel Report on Asthma [11] states that provide support and counseling, and encourage “Therapeutic strategies should be considered in using a systematic approach that was tailored to concert with clinician-patient partnership strate- individual patterns of learning and behavior. gies; education of patients is essential for achiev- Thus was born the asthma educator.

1 Asthma and Asthma Education: The Background

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1.7.3 Skills of the Asthma Educator The asthma educator has to be well-versed and proficient not only in the field of healthcare but also that of education. As with any healthcare professional, the basic requirement for an asthma educator is appropriate knowledge [43]. With special reference to asthma, the educator must understand the: • • • • • • • • • • • • • • •

•

Pathophysiology of asthma Methods of diagnosis Spectrum of severity Morbidity from asthma Medications used in treatment Side effects of medications and how to minimize them Lead time to effectiveness for the different medications Selection, use, and care of the various asthma medication devices Methods of monitoring and assessment Goals of asthma therapy Rationale behind various treatment options Psychology of chronically ill individuals Reasons underlying noncompliance or non-adherence Asthma triggers Effect that allergies have on the person with asthma and methods for coping with, as well as avoiding, allergen exposure Environmental controls required for control of the disease and how to implement them in a practical, low-cost way

And, as mentioned earlier, the educator is also required to know how to educate [156, 157]. This requires: • An assessment of attitudes, beliefs, concerns, and educational needs of those with asthma in dealing with psychosocial, socioeconomic, cultural, and age-specific requirements and limitations [134] • A sensitivity and understanding of ethnic and religious differences • An awareness of all possible reasons for non-adherence

• Strategies for dealing with individuals of different ages, developmental stages, and backgrounds • An understanding of how people learn and methods to motivate them • A knowledge of educational theories and principles • Recognition of maladaptive patterns of behavior in individuals or families [158] • Strategies for dealing with non-adherence • A focus on a variety of health-related behaviors that include adherence to medical regimens • Teaching skills that range from active listening to interviewing and communication skills [159] • Good time management and record keeping skills • The ability to establish rapport with the person with asthma and the family • Creation and maintenance of a suitable learning environment that is encouraging, supportive, and non-judgmental • Devising an individualized education program to meet the needs of the person with asthma and adapting it as needed to meet changing needs • Preparing educational objectives and establishing instructional goals • Preparing suitable educational materials • Supervising the practice and application of the necessary skills • Providing education in a variety of settings • Evaluating the effectiveness of teaching • Evaluating the outcomes in terms of the perspective of the person as related to quality of life • Providing feedback, reinforcement, individualization, facilitation, and relevance in educating both those with asthma and caregiver(s) • Being a mentor to those with asthma and caregivers [160] • Working with a team of healthcare professionals An essential addition skill is being adept at facilitating online learning.

1.7 Education of Persons with Asthma

The function of the educator [37, 145] is therefore to assess the person with asthma, assist in defining needs, plan the sequence of learning, create the conditions conducive to learning, use effective methods of teaching, provide resource material, and finally evaluate or measure the results of learning. The educator who recognizes the person with asthma as an individual and who provides assistance can markedly and significantly reduce the suffering and costs of this chronic disease [161]. The implication in this process is that as the self-confidence of the person with asthma increases, his or her dependency on the educator will be progressively decreased. In time the person with asthma will no longer need the educator. This then is the goal of guided self-management.

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the most confident “student” will require support from time to time, the goal of guided self- management is to bring them to the point where they no longer need constant help. An asthma educator must therefore be credible, competent, confident, courteous, compassionate, and an excellent communicator. Credibility will be judged by their students, who will expect the most current (and accurate) information. But they will not expect their educator to know everything and will be much more accepting if the educator frankly admits, when necessary, that the answer to a particular question is not known. People with asthma will be even more appreciative if the educator then makes the effort to find the required information. Points to Ponder

1.7.4 Essential Qualities of the Educator The asthma educator on occasion may be the primary healthcare provider for those with asthma, but more often, another professional will perform this function. In the latter situation, the educator should serve as a liaison between the primary healthcare provider and the person with asthma. In general, when a physician or healthcare provider is consulted, all too often there are feelings (on the part of the individuals with asthma) that the connection and communication could be improved. The asthma educator hence has a primary task—to explain asthma in ways that can be understood—this will be welcomed by those with asthma. It is the educator’s job to explain their asthma, the diagnosis, and the recommended treatment in terms to which they can relate. Whenever it is necessary to use technical terms, the educator must always explain them clearly. They must also help the person with asthma devise an asthma action plan. Then the educator can help the person follow the plan at every exacerbation until such time as the person is willing and confident enough to carry it out without ongoing support from the educator. At that point, the educator will have some certainty that the teaching has been effective. While even

Qualities of an asthma educator • • • • • •

Credibility Courtesy Competence Compassion Confidence Communication

Competency in asthma education will come from knowledge of asthma coupled with the ability to do an individual assessment and devise a teaching program based on a particular person’s specific needs and concerns. Competency will also make itself evident in all dealings with those with asthma; in the asthma action plans that the educator helps them devise; in the solutions that the educator helps them find for their problems; and in the educational methods that are chosen depending on the age, development, and specific learning pattern of the person being taught. Competency will also be reflected in: • The skill used in dealing with those with asthma and their problems • The flexibility demonstrated when faced with unusual situations

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• The ability to find creative solutions • The methods used to help those with asthma devise appropriate solutions to problems • Techniques used to help them set goals and adapt to changing situations • Assessment of outcomes • The provision of appropriate feedback to those with asthma and/or caregivers • On-going evaluation of the effectiveness of teaching methods used • Adaptation of teaching methods to meet changing goals and needs Confidence will show in the selection of what is to be taught, the actual teaching, the techniques used, and particularly the educator’s ability to dispel fears. It will be most evident in the type of learning environment that the educator provides and in how well-organized the educator is. Courtesy requires that every person be treated with respect, in a nonjudgmental manner that recognizes cultural and ethnic differences and does not discriminate in any way or for any reason. Courtesy is also an awareness of potential cultural conflicts and linguistic barriers. It is the result of the educator’s attitude and motivation to provide those with asthma with the opportunity to participate in their own healthcare. It will show in the preparations made and in interdisciplinary cooperation. It will be revealed in the degree of acceptance of decisions that may foster selfdefeating behaviors—even decisions that (in the opinion of the educator) are likely to lead to further harm. Acceptance of those decisions is also important in such extreme situations, and those with asthma are more likely to accept advice when it is accompanied with a respect for their point of view. Compassion will be evident in the empathy displayed towards those with asthma, in the sensitivity shown to their feelings, the support and encouragement provided, and the amount of time spent with them. Given an allotted amount of time, the asthma educator must focus first and foremost on the person’s fears and needs and be willing to jettison and adjust planned teaching

1 Asthma and Asthma Education: The Background

that would interfere with allaying those fears and needs, so that the person being taught does not feel that the educator is rushed and unable to pay attention to their concerns. The compassionate educator will see things from the perspective of the person with asthma, understand the person’s difficulties, help find solutions, and accept their decisions, however unsatisfactory those decisions might be. The educator’s ability to communicate effectively with the person with asthma will manifest itself in the choice of teaching aids and in the use of simple and clear explanations. It will show in the written instructions provided and the answers given to questions. It will also show in the skill with which those with asthma are drawn into the teaching process, encouraged to build on what they already know, and helped to set and achieve realistic goals. The asthma educator is the coach for the team, the mentor [159], and the person who helps those with asthma learn, experiment, and develop skills. It is through education and support that their fears, as they move from diagnosis to acceptance to control, can be reduced. This also requires that the asthma educator make the effort to stay current with recent advances, the newest medications, and the latest asthma devices. This in turn implies a consistent and continual effort to learn [162]. Staying up to date requires time and effort. To the primary healthcare provider, the asthma educator is a member of the team that provides asthma education. To the team, the educator is a colleague. To those with asthma, the educator will be a lifeline. When the educator has built a close relationship with those with asthma, those persons will confide the most intimate details of their lives, knowing that that confidence will not be betrayed. They will come for help knowing that it will be provided. They will be comfortable communicating with the educator. They will regard the educator as a source of information and for help in medical, social, and financial contexts. They will depend on, and trust, the educator. The educator will be their teacher, their confidant, and, above all, their mentor and guide.

References

References 1. Deber RB, Kraetschmer N, Urowitz S, Sharpe N. Patient, consumer, client, or customer: what do people want to be called? Health Expect. 2005;8(4):345–51. https://doi. org/10.1111/j.1369-7625.2005.00352.x. 2. Costa DS, Mercieca-Bebber R, Tesson S, Seidler Z, Lopez AL. Patient, client, consumer, survivor or other alternatives? A scoping review of preferred terms for labelling individuals who access healthcare across settings. BMJ Open. 2019;9(3):e025166. https://doi.org/10.1136/bmjopen-2018-025166. 3. Aaron SD, Vandemheen KL, FitzGerald JM, Ainslie M, Gupta S, Lemiere C, et al. Reevaluation of diagnosis in adults with physician-diagnosed asthma. JAMA. 2017;317(3):269–79. https://doi. org/10.1001/jama.2016.19627. PMID:28114551 4. Schmier JK, Chan KS, Leidy NK. The impact of asthma on health-related quality of life. J Asthma. 1998;35(7):585–97. https://doi. org/10.3109/02770909809048961. 5. Anderson HR, Butland BK, Strachan DP. Trends in prevalence and severity of childhood asthma. BMJ. 1994;308:1600–3. https://doi.org/10.1136/ bmj.308.6944.1600. 6. Winders TA, Wilson AK, Fletcher MJ, McGuinness A, Price DB. A patient-centered description of severe asthma: patient understanding leading to assessment for a severe asthma referral (PULSAR). Patient. 2019;12(5):539–49. https://doi.org/10.1007/ s40271-019-00371-0. 7. Yamasaki A, Burks CA, Bhattacharyya N. Cognitive and quality of life-related burdens of illness in pediatric allergic airway disease. Otolaryngol Head Neck Surg. 2020:194599820908202. https://doi. org/10.1177/0194599820908202. 8. Nocon A. Social and emotional impact of childhood asthma. Arch Dis Child. 1991;66(4):458–60. https:// doi.org/10.1136/adc.66.4.458. 9. Mailick MD, Holden G, Walther VN. Coping with childhood asthma: caretakers. Views. Health Soc Work. 1994;19(2):103–11. https://doi.org/10.1093/ hsw/19.2.103. 10. Perrin JM, MacLean WE, Perrin EC. Parental perceptions of health status and psychologic adjustment of children with asthma. Pediatrics. 1989;83(1):26– 30. PMID:2909973 11. National Asthma and Education Prevention Program Expert Panel Report 3. Guidelines for the diagnosis and management of asthma. NHLBI Bethseda MD. NIH pub #12-5075. Revised September 2012. 12. Guidotti TL. Consistency of diagnostic criteria for asthma from Laennec (1819) to the National Education Program (1991). J Asthma. 1994;31(5):329–38. https://doi. org/10.3109/02770909409061312. 13. Global Initiative for Asthma: Global strategy for asthma management and prevention. 2020. Available from www.ginasthma.org. Accessed 23 Mar 2020.

33 14. McFadden ER Jr, Gilbert IA. Asthma. N Eng J Med. 1992:1928–36. https://doi.org/10.1056/ NEJM199212313272708. 15. Oswald H, Phelan PD, Lanigan A, Hibbert M, Bowes G, Olinsky A. Outcome of childhood asthma in mid-adult life. BMJ. 1994;309:95–6. https://doi. org/10.1136/bmj.309.6947.95. 16. Centers for Disease Control and Prevention. Sleeping, breathing, and quality of life: a healthy people 2020 progress review. https://www.cdc.gov/ nchs/healthy_people/hp2020/hp2020_rd_and_sh_ progress_review.htm. Accessed 20 Mar 2020. 17. Office of Disease Prevention and Health Promotion. Healthy People 2030. https://health.gov/healthypeople/objectives-a nd-d ata/browse-o bjectives/ oral-conditions 18. Centers for Disease Control and Prevention. Most recent national asthma data.https://www.cdc.gov/ asthma/most_recent_national_asthma_data.htm Accessed 20 Mar 2020. 19. American Lung Association. Asthma trends and burden. https://www.lung.org/our-initiatives/research/ monitoring-trends-in-lung-disease/asthma-trends- brief/trends-and-burden.html. Accessed 24 Mar 2020. 20. FitzGerald JM, Lemiere C, Lougheed MD, Ducharme FM, Dell SD, Ramsey C, et al. Recognition and management of severe asthma: A Canadian Thoracic Society position statement. Canadian Journal of Respiratory, Critical Care, and Sleep Medicine. 2017;1(4):199–221. https://doi.org/10.1080/247453 32.2017.1395250. 21. Chung KF, Wenzel SE, Brozek JL, Bush A, Castro M, Sterk PJ, et al. International ERS/ATS guidelines on definition, evaluation and treatment of severe asthma. Eur Respir J. 2014;43(2):343–73. https://doi. org/10.1183/09031936.00202013. PMID:24337046 22. National Center for Health Statistics. Health, United States, 2018. Hyattsville, MD 2019. https://www. cdc.gov/nchs/data/hus/2018/012.pdf. Accessed 20 Mar 2020. 23. Siber JH, Rosenbaum PR, Calhoun SR, Reiter JG, Hill AS, Guevara JP, et al. Racial disparities in Medicaid asthma hospitalizations. Pediatrics. 2017;139(1):e20161221. https://doi.org/10.1542/ peds.2016-1221. 24. Lang DM, Polansky M. Patterns of asthma mortality in Philadelphia from 1969 to 1991. N Engl J Med. 1994;331(23):1542–6. https://doi.org/10.1056/ NEJM199412083312302. 25. Centres for Disease Control and Prevention. National Asthma Control Program https://www.cdc. gov/nceh/information/asthma.htm Accessed 25 Mar 2020. 26. Moorman JE, Rudd RA, Johnson CA, King M, Minor P, Bailey C, et al. Centres for disease control and prevention. National Surveillance for asthma – United States, 1980-2004. MMWR SurveillSumm. 2007;56(8):1–54.

34 27. Mehta NK, Lee H, Yitalo KR. Child health in the United States: recent trends in racial/ethnic disparities. Soc Sci Med. 2013;95:6–15. https://doi. org/10.1016/j.socscimed.2012.09.011. 28. Chronic Health Conditions. Annual Report of the Robert Wood Johnson Foundation. Princeton: Robert Wood Johnson Foundation; 1993. 29. Williams DR, Lavizzo-Mourey R, Warren RC. The concept of race and health status in America. Public Health Rep. 1994;109(1):26–41. 30. Trivedi M, Fung V, Kharbanda EO, Larkin EK, Butler MG, Horan K, et al. Racial disparities in family- provider interactions for pediatric asthma care. J Asthma. 2018;55(4):424–9. https://doi.org/1 0.1080/02770903.2017.1337790. 31. Smith LA, Hatcher-Ross JL, Wertheimer R, Kahn RS. Rethinking race/ethnicity, income and childhood asthma; racial/ethnic disparities concentrated among the very poor. Public Health Rep. 2005;120(20):109– 16. https://doi.org/10.1177/003335490512000203. 32. Kitsantas P, Kornides ML, Cartiello J, Wu H. Chronic physical health conditions among children of different racial. ethnic backgrounds. Public Health. 2013;127(6):546–53. https://doi.org/10.1016/j. puhe.2013.02.006. 33. Garden GMF, Ayres JG. Psychiatric and social aspect of brittle asthma. Thorax. 1993;48(5):501–5. https://doi.org/10.1136/thx.48.5.501. 34. Adler NE, Boyce T, Chesney MA, Cohen S, Folkman S, Kahn RL, et al. Socioeconomic status and health: the challenge of the gradient. Am Psychol. 1994;49(1):15–24. https://doi. org/10.1037//0003-066x.49.1.15. 35. Clark NM. Asthma self-management education research and implications for clinical practice. Chest. 1989;95(5):1110–3. https://doi.org/10.1378/ chest.95.5.1110. 36. Tougaard L, Krone T, Sorknaes A, Ellegard H. Economic benefits of teaching patients with chronic obstructive pulmonary disease about their illness. The PASTMA Group Lancet. 1992;339(8808):1517–20. https://doi. org/10.1016/0140-6736(92)91274-c. 37. Knowles A. The modern practice of adult education. New York: Association Press; 1970. 38. Malveaux FJ, Houlihan D, Diamond EL. Characteristics of asthma mortality and morbidity in African-Americans. J Asthma. 1993;30(6):431– 7. https://doi.org/10.3109/02770909309056751. 39. Wade S, Well C, Holden G, Mitchell H, Evans R 3rd, Kruszon-Moran D, et al. Psychosocial characteristics of inner-city children with asthma: a description of the NCICAS psychosocial protocol. Ped Pulmonol. 1997;24:236–76. https://doi.org/10.1002/(sici)1099- 0496(199710)24:43.0.co;2-l. 40. Butz AM, Alexander C. Anxiety in children with asthma. J Asthma. 1993;30(3):199–209. https://doi. org/10.3109/02770909309054518. 41. Lavoie KL, Bacon SL, Barone S, Cartier A, Ditto B, Labrecque M. What is worse for asthma control and

1 Asthma and Asthma Education: The Background quality of life – depressive disorders, anxiety disorders, or both? Chest. 2006;130:1039–47. https://doi. org/10.1378/chest.130.4.1039. 42. Valero-Morena S, Perez-Marin M, Montoya- Castilla I, Castillo-Corullón S, Ramírez-Aguilar A, Escribano-Montaner A. Emotional distress in family caregivers of adolescents with bronchial asthma: analysis of its predictors. Arch Argent Pediatr. 2018;116(2):e234–40. https://doi.org/10.5546/ aap.2018.eng.e234. Abstract 43. Clark NM, Gotsh A, Rosenstock IR. Patient, professional and public education on behavioral aspects of asthma. J Asthma. 1993;30(4):241–55. https://doi. org/10.3109/02770909309054524. 44. Fowler MG, Davenport MS, Garg R. School functioning of US children with asthma. Pediatrics. 1992;90(6):939–44. PMID:1437438 45. Calam R, Gregg L, Simpson B, Morris J, Woodcock A, Custovic A. Childhood asthma, behavior problems, and family functioning. J Allergy Clin Immunol. 2003;112:499–504. https://doi. org/10.1016/s0091-6749(03)01606-3. 46. Kavanagh J, Jackson DJ, Kent BD. Sleep and asthma. CurrOpinPulm Med. 2018;24(6):569–73. https://doi.org/10.1097/MCP.0000000000000526. 47. Stores G, Ellias AJ, Wiggs L, Crawford C, Thomson A. Sleep and psychological disturbance in nocturnal asthma. Arch Dis Child. 1998;78:413–9. https://doi. org/10.1136/adc.78.5.413. 48. Chen SH, Huang JL, Yeh KW, Tsai YF. The stress of caring for children with asthma: a quantitative study of primary caregivers. J NursRes. 2015;23(4):298–307. https://doi.org/10.1097/ JNR.0000000000000083. 49. Dean BB, Calimlim BM, Kindermann SL, Khandker RK, Tinkelman D. The impact of uncontrolled asthma on absenteeism and health-related quality of life. J Asthma. 2009;46(9):861–6. https://doi. org/10.3109/02770900903184237. 50. Stanescu S, Kirby SE, Thomas M, Yardley L, Ainsworth B. A systematic review of psychological, physical health factors, and quality of life in adult asthma. NPJ Prim Care Respir Med. 2019;29(1):37. https://doi.org/10.1038/s41533-019-0149-3. 51. Xu JQ, Murphy SL, Kochanek KD, Arias E. Mortality in the United States, 2018. NCHS Data Brief, No 355. January 2020. https://www.cdc.gov/ nchs/products/databriefs/db355.htm Accessed 22 Apr 2020. 52. Sly RM. Changing asthma mortality. Ann Allergy. 1994;73(3):259–68. PMID:8092562 53. Haire-Joshu D, Fisher EB, Munro J, Wedner HJ. A comparison of patient attitudes toward asthma self- management among acute and preventive care settings. J Asthma. 1993;30(5):359–71. https://doi. org/10.3109/02770909309056740. 54. McFadden ER, Warren EL. Observations on asthma mortality. Ann Int Med. 1997;127(2):142–7. https://doi. org/10.7326/0003-4819-127-2-199707150-00009.

References 55. Targonski PV, Persky VW, Ramakrishnan V. Effect of environmental molds on risk of death from asthma during the pollen season. J Allergy Clin Immunol. 1995;95:955–61. https://doi.org/10.1016/ s0091-6749(95)70095-1. 56. British Thoracic Association. Death from asthma in two regions of England. Br Med J (Clin Res Ed). 1982;285(6350):1251–5. 57. Robertson CF, Rubinfeld AR, Bowes G. Deaths from asthma in Victoria: a 12 month survey. Med J Aust. 1990;152(10):511–7. PMID:2338923 58. Strunk RC. Asthma deaths in childhood: identification of patients at risk and intervention. J Allergy Clin Immunol. 1987;80:472–7. https://doi. org/10.1016/0091-6749(87)90078-9. 59. Bucknall CE, Robertson C, Moran F, Stevenson RD. Management of asthma in hospital: a prospective audit. BMJ. 1988;296:1637–9. https://doi. org/10.1136/bmj.296.6637.1637. 60. Mao Y, Semenciw R, Morrison H, MacWilliam L, Davies J, Wigle D. Increased rates of illness and death from asthma in Canada. CMAJ. 1987;137(7):620–4. 61. Burr ML, Davies BH, Hoare A, Jones A, Williamson IJ, Holgate SK, et al. A confidential inquiry into asthma deaths in Wales. Thorax. 1999;54:985–9. https://doi.org/10.1136/thx.54.11.985. 62. Robertson CF, Rubinfeld AR, Bowes G. Pediatric asthma deaths in Victoria: the mild are at risk. PediatrPulmonol. 1992;13(2):95–100. https://doi. org/10.1002/ppul.1950130207. 63. British guideline on asthma management. Revised 2019. https://www.sign.ac.uk/assets/sign158.pdf. Accessed 20 Mar 2020. 64. Patterson R, Greenberger PA, Patterson DA. Potentially fatal asthma: the problem of noncompliance. Ann Allergy. 1991;67(2 Pt 1):138–42. PMID:1867451 65. Morgan PP. Illiteracy can have major impact on patients’ understanding of health care information. Can Med Assoc J. 1993;148(7):1196–7. PMC1490866 66. Yaghoubi M, Adibi A, Safari A, FitzGerald JM, Sadatsafavi M. The projected economic and health burden of uncontrolled asthma in the United States. Am J Respir Crit Care Med. 2019;200(9):1102–12. https://doi.org/10.1164/ rccm.201901-0016OC. 67. Barnes PJ, Jonasson B, Klim JB. The costs of asthma. Eur Resp J. 1996;9:636–42. https://doi.org /10.1183/09031936.96.09040636. 68. Nunes C, Pereira AM, Morais-Almeida M. Asthma costs and social impact. Asthma Res Pract. 2017;3:1. https://doi.org/10.1186/s40733-016-0029-3. eCollection 2017 69. Sullivan PW, Ghushchyan VH, Slejko JF, Belozeroff V, Globe DR, Lin SL. The burden of adult asthma in the United States: evidence from the Medical Expenditure Panel Survey. J Allergy Clin Immunol. 2011;127(2):363–369.e1–3. https://doi. org/10.1016/j.jaci.2010.10.042.

35 70. Miller GF, Coffield E, Leroy Z, Wallin R. Prevalence and costs of five chronic conditions in children. J Sch Nurs. 2016;32(5):357–64. https://doi. org/10.1177/1059840516641190. 71. Sullivan PW, Ghushchyan VH, Campbell JD, Globe G, Bender B, Magid DJ. Measuring the cost of poor asthma control and exacerbations. J Asthma. 2017;54(1):24–31. https://doi.org/10.1080/0277090 3.2016.1194430. 72. Boulet LP, Chapman KR. Asthma education: the Canadian experience. Chest. 1994;106(4):206S–10S. https://doi.org/10.1378/ chest.106.4_supplement.206s. 73. O’Brien KP. Managed care and the treatment of asthma. J Asthma. 1995;32(5):325–34. https://doi. org/10.3109/02770909509082757. 74. Gallefoss F, Bakke PS. Cost-effectiveness of self-management in asthmatics: a 1 year followup randomised, controlled trial. Eur Respir J. 2001;17(2):206–13. https://doi.org/10.1183/090319 36.01.17202060. 75. Clark NM, Feldman CH, Evans D, Levison MJ, Wasilewski Y, Mellins RB. The impact of health education on frequency and cost of health care use by low-income children with asthma. J Allergy Clin Imunol. 1986;78(1):108–15. https://doi. org/10.1016/0091-6749(86)90122-3. 76. Lewis CE, Rachelefsky GS, Lewis MA, de la Sota A, Kaplan M. A randomised trial of A.C.T. for kids. Pediatrics. 1984;74:478–86. PMID:6384911 77. Bolton MB, Tilley BC, Kuder J, Reeves T, Schultz LR. The cost and effectiveness of an education program for adults who have asthma. J Gen Intern Med. 1991;6:401–7. https://doi.org/10.1007/ bf02598160. 78. Castro M, Zimmermann NA, Crocker S, Bradley J, Leven C. Schechtman KB. Asthma intervention program prevents readmissions in high healthcare utilizers. Am J Respir Crit Care Med. 2003;168(9):1095–9. https://doi.org/10.1164/ rccm.200208-877OC. 79. Nurmagambetov T, Kuwahara R, Garbe P. The economic burden of asthma in the United States, 2008- 2013. Ann Am Thorac Soc. 2018;15 https://doi. org/10.1513/AnnalsATS.201703-259OC. 80. Suh DC, Shin SK, Okpara I, Voytovich RM, Zimmerman A. Impact of a targeted asthma intervention program on treatment costs in patients with asthma. Am J Manag Care. 2001;9:897–906. PMID:11570023 81. Bunting BA, Cranor CW. The Asheville project: long-term clinical, humanistic, and economic outcomes of a community-based medication therapy management program for asthma. J Am Pharm Assoc. 2006;46(2):133–47. https://doi. org/10.1331/154434506776180658. 82. Mishoe SC, Baker RR, Poole S, Harrell LM, Arant CB, Rupp NT. Development of an instrument to assess stress levels and quality of life in children with asthma. J Asthma. 1998;35(7):553–63. https:// doi.org/10.3109/02770909809048958.

36 83. Osman L, Silverman M. Measuring quality of life for young children with asthma and their families. Eur Respir J Suppl. 1996;21:35S–41S. PMID:8962616 84. Creer TL, Wigal JK, Kotses H, Hatala JC, McConnaughy K, Winder JA. A life activities questionnaire for childhood asthma. J Asthma. 1993;30(6):467–73. https://doi. org/10.3109/02770909309056756. 85. Creer TL, Stein RE, Rappaport L, Lewis C. Behavioural consequences of illness: childhood asthma as a model. Pediatrics. 1992;90:808–15. PMID:1437411 86. Lozano P, Sullivan SD, Smith DH, Weiss KB. The economic burden of asthma in US children. Estimates from the National Medical Expenditure Survey. J Allergy Clin Immunol. 1999;104(5):957– 63. https://doi.org/10.1016/s0091-6749(99)70075-8. 87. Zhu Z, Hasegawa K, Camargo CA Jr, Liang L. Investigating asthma heterogeneity through shared and distinct genetics: insights from genome- wide cross-trait analysis. J Allergy Clin Immunol. 2020;18:S0091–6749(20)30966-0. https://doi. org/10.1016/j.jaci.2020.07.004. 88. Deliu M, Fontanella S, Haider S, Sperrin M, Geifman N, Murray C, et al. Longitudinal trajectories of severe wheeze exacerbations from infancy to school age and their association with early-life risk factors and late asthma outcomes. Clin ExpAllergy. 2020;50(3):315– 24. https://doi.org/10.1111/cea.13553. 89. Zhao N, Smith BM, Olivenstein R, Martin JG, Lemiere C, Hamid Q. Asthma and fixed airflow obstruction: long-term trajectories reveal distinct endotypes. InA32. Asthma: Clinical Studies II 2019 May (pp. A1334–A1334). American Thoracic Society). 90. Weiss ST, Sparrow D, O’Connor GT. The interrelationship among allergy, airway responsiveness and asthma. J Asthma. 1993;30(5):329–49. https://doi. org/10.3109/02770909309056738. 91. Levy M, Hilton S. Asthma in practice. Royal College of General Practitioners; 1993. 92. Palmer LJ, Silverman ES, Weis ST, Drazen JM. Pharmacogenetics of asthma. Am J Respir Crit Care Med. 2002;165:861–6. https://doi.org/10.1164/ ajrccm.165.7.2109096. 93. Perez-Garcia J, Espuela-Ortiz A, Lorenzo-Diaz F, Pino-Yanes M. Pharmacogenetics of pediatric asthma: current perspectives. Pharmacogenomics Pers Med. 2020;13:89–103. https://doi.org/10.2147/ PGPM.S201276. 94. Sporik R, Holgate S, Platts-Mills TAE, Cogswell JJ. Exposure to house-dust mite allergen (Der p 1) and the development of asthma in childhood. N Engl J Med. 1990;323:502–7. https://doi.org/10.1056/ NEJM199008233230802. 95. Fielder HM, Lyons RA, Heaven M, Morgan H, Govier P, Hooper M. Effect of environmental tobacco smoke on peak flow variability. Arch Dis Child. 1999;80:253–6. https://doi.org/10.1136/ adc.80.3.253.

1 Asthma and Asthma Education: The Background 96. Cook DG, Strachan DP. Summary of effects of parental smoking on the respiratory health of children and implications for research. Thorax. 1999;54:357–66. https://doi.org/10.1136/thx.54.4.357. 97. Seth D, Saini S, Poowuttikul P. Pediatric inner-city asthma. Pediatr Clin N Am. 2019;66(5):967–79. https://doi.org/10.1016/j.pcl.2019.06.012. 98. Rhodes HL, Sporik R, Thomas P, Holgate ST, Cogswell JJ. Early life risk factors for adult asthma: birth cohort study of subjects at risk. J Allergy Clin Immunol. 2001;108:720–5. https://doi.org/10.1067/ mai.2001.119151. 99. Tariq SM, Matthews SM, Hakim EA, Arshad SH. Egg allergy in infancy predicts respiratory allergic disease by 4 years of age. Pediatr Allergy Immunol. 2000;11:162–7. https://doi. org/10.1034/j.1399-3038.2000.00077.x. 100. Nickel R, Kulig M, Forster J, Bergmann R, Bauer CP, Lau S, et al. Sensitization to hen’s egg at the age of twelve months is predictive for allergic sensitization to common indoor and outdoor allergens at the age of three years. J Allergy Clin Immunol. 1997;99:613–7. https://doi.org/10.1016/s0091-6749(97)70021-6. 101. Sears MR, Greene JM, Willan AR, Wiecek EM, Taylor DR, Flannery EM, et al. A longitudinal, populationbased, cohort study of childhood asthma followed to adulthood. N Engl J Med. 2003;349(15):1414–22. https://doi.org/10.1056/NEJMoa022363. 102. Woolcock AJ, Dusser D, Fajac I. Severity of chronic asthma. Thorax. 1998;53:442–4. https://doi. org/10.1136/thx.53.6.442. 103. Mendy A, Wilkerson J, Salo PM, Zeldin DC, Thorne PS. Endotoxin clustering with allergens in house dust and asthma outcomes in a U.S. national study. Environ Health. 2020;19(1):35. https://doi. org/10.1186/s12940-020-00585-y. 104. Halmerbauer G, Gartner C, Schierl M, Arshad H, Dean T, Koller DY, et al. SPACE collaborative study team. Study on the prevention of allergy in children in Europe (SPACE): allergic sensitization at 1 year of age in a controlled trial of allergen avoidance from birth. Pediatr Allergy Immunol. 2003;14(1):10–7. https://doi.org/10.1034/j.1399-3038.2003.02069.x. 105. Gehring U, Bishof W, Fahlbusch B, Wichmann H-E. Heinrich J for the INGA study group. House dust endotoxin and allergic sensitization in children. Am J Respir Crit Med. 2002;166:939–44. https:// doi.org/10.1164/rccm.200203-256OC. 106. Martinez FD. Toward asthma prevention ─ does all that really matter happen before we learn to read? N Engl J Med. 2003;349:1473–5. https://doi. org/10.1056/NEJMe030041. 107. Braun-Fahrlander C. Environmental exposure to endotoxin and other microbial products and the decreased risk of childhood atopy: evaluating developments since April 2002. CurrOpin Allergy Clin Immunol. 2003;3(5):325–9. https://doi. org/10.1097/00130832-200310000-00001. 108. Sarafino EP, Dillon JM. Relationships among respiratory infections, triggers of attacks and asthma

References severity in children. J Asthma. 1998;35(6):497–504. https://doi.org/10.3109/02770909809071003. 109. Martinez FD, Stern DA, Wright AL, Taussig LM, Halonen M. Association of non-wheezing lower respiratory tract illnesses in early life with persistently diminished serum IgE levels. Thorax. 1995;50:1067– 72. https://doi.org/10.1136/thx.50.10.1067. 110. Von Mutius E, Martinez FD, Fritzsch C, Nicolai T, Reitmeir P, Thiemann HH. Skin test reactivity and number of siblings. BMJ. 1994;308:692–5. https:// doi.org/10.1136/bmj.308.6930.692. 111. Von Mutius E, Martinez FD, Fritzsch C, Nicolai T, Roell G, Thiemann HH. Prevalence of asthma and atopy in two areas of West and East Germany. Am J Respir Crit Care Med. 1994;149:358–64. https://doi. org/10.1164/ajrccm.149.2.8306030. 112. Hall IP. The future of asthma. BMJ. 1997;314:45– 53. https://doi.org/10.1136/bmj.314.7073.45. 113. Van Tilburg BE, Arrieta MC. Hygiene hypothesis in asthma development: is hygiene to blame? Arch Med Res. 2017;48(8):717–26. https://doi.org/10.1016/j. arcmed2017.11.009. 114. Khot A, Burn R, Evans E, Lenney W, Storr J. Biometerological triggers in childhood asthma. Clin Allergy. 1988;18:351–8. https://doi. org/10.1111/j.1365-2222.1988.tb02882.x. 115. Landau LI. Risks of developing asthma. PediatrPulmonol. 1996;22:314–8. h t t p s : / / d o i . o r g / 1 0 . 1 0 0 2 / ( S I C I ) 1 0 9 9 - 0496(199611)22:53.0.CO;2-K. 116. Herbert C, Kumar RK. Ambient air pollution and asthma. EurRespir J. 2017;49:1700230. https://doi. org/10.1183/13993003.00230-2017. 117. Gehring U, Wijga AH, Brauer M, Fischer P, de Jongste JC, Kerkhof M, et al. Traffic-related air pollution and the development of asthma and allergies during the first 8 years of life. Am J Respir Crit Care Med. 2010;181:596–603. https://doi.org/10.1164/ rccm.200906-0858OC. 118. Gowers AM, Cullinan P, Ayres JG, Anderson HR, Strachan DP, Holgate ST, et al. Does outdoor air pollution induce new cases of asthma? Biological plausibility and evidence; a review. Respirology. 2012;17(6):887–98. https://doi. org/10.1111/j.1440-1843.2012.02195.x. 119. Chang CC, Phinney SD, Halpern GM, Gershwin EM. Asthma mortality: another option - is it a matter of life and .... bread? J Asthma. 1993;30(2):93–103. https://doi.org/10.3109/02770909309054503. 120. Gilliland FD, Islam T, Berhane K, Gauderman WJ, McConnell R, Avol E, et al. Regular smoking and asthma incidence in adolescents. Am J Respir Crit Care Med. 2006;174(10):1094–100. https://doi. org/10.1164/rccm.200605-722OC. 121. Morales E, Duffy D. Genetics and Gene-environment interactions in childhood and adult onset asthma. Front Pediatr. 2019;7:499. https://doi.org/10.3389/ fped.2019.00499. 122. Kramer MS. Maternal antigen avoidance during pregnancy for preventing atopic disease

37 in infants of women at high risk. Cochrane Database Syst Rev. 2000;2:CD000133. https://doi. org/10.1002/14651858.CD000133. 123. Wickman M, Melen E, Berglind N, Lennart Nordvall S, Almqvist C, Kull I, et al. Strategies for preventing wheezing and asthma in small children. Allergy. 2003;58(8):742–7. https://doi. org/10.1034/j.1398-9995.2003.00078.x. 124. Arshad SH, Bateman B, Sadeghnejad A, Gant C, Matthews SM. Prevention of allergic disease during childhood by allergen avoidance: the Isle of Wight prevention study. J Allergy Clin Immunol. 2007;119(2):307–13. https://doi.org/10.1016/j. jaci.2006.12.621. 125. 2020 Focused updates to the asthma management guidelines. A report from the national asthma education and prevention program coordinating committee expert panel working group. NIH publication No. 20-HL-8140. December 2020. 126. Dimov VV, Stokes JR, Casale TB. Immunomodulators in asthma therapy. Curr Allergy Asthma Rep. 2009;9:475. https://doi. org/10.1007/s11882-009-0070-x. 127. Tesse R, Borrelli G, Mongelli G, Mastrorilli V, Cardinale F. Treating pediatric asthma according guidelines. Front Pediatr. 2018;6:234. https://doi. org/10.3389/fped.2018.00234. 128. Zahran HS, Bailey CK, Damon SA, Garbe PL, Breysse PN. Vital Signs: Asthma in children – United States, 2001–2016. MMWR Morb Mortal Wkly Rep. 2018;67:149–55. https://doi.org/10.15585/ mmwr.mm6705e1. 129. Price J, Hindmarsh P, Hughes S, Efthimiou J. Evaluating the effects of asthma therapy on childhood growth: what can be learned from the published literature? Eur Respir J. 2002;19:1179–93. https://doi.org/10.1183/09031936.02.00288702. 130. Allen DB, Bielory L, Derendorf H, Dluyh R, Colice G, Szefler SJ. Inhaled corticosteroids: past lessons and future issues. J Allergy Clin Immunol. 2003;112:S1–40. https://doi.org/10.1016/ s0091-6749(03)01859-1. 131. https://ginasthma.org/wp-content/uploads/2020/12/ GINA-i nterim-g uidance-o n-C OVID-1 9-a nd- asthma-20_12_20.pdf 132. Williamson EJ, Walker AJ, Bhaskaran K, Bacon S, Bates C, Morton CE, Curtis HJ, et al. Factors associated with COVID-19-related death using OpenSAFELY. Nature. 2020;584(7821):430–6. https://doi.org/10.1038/s41586-020-2521-4. 133. Kongstvedt PR. Essentials of managed health care. 4th ed. Aspen; 2001. 134. Hopp JW, Gerken CM. Making an educational diagnosis to improve patient education. Respir Care. 1983;28(11):1456–61. PMID:10315478 135. Partridge MR. Delivering optimal care to the person with asthma. Eur Respir J. 1995;8:298–305. https:// doi.org/10.1016/0738-3991(95)00738-l.

38 136. Mullen DP. Compliance becomes concordance. BMJ. 1997;314:691–2. https://doi.org/10.1136/ bmj.314.7082.691. 137. Millins RB. Asthma education: a national strategy. Am Rev Resp Dis. 1989;140(3):577–8. https://doi. org/10.1164/ajrccm/140.3.577. 138. Osman LM, Abdalla MI, Beattie JAG, Ross SJ, Russel IT, Friend JA, et al. on behalf of GRASSIC. Reducing hospital admission through computer supported education for asthma patients. BMJ. 1994;308:568–671. https://doi.org/10.1136/ bmj.308.6928.568. 139. Lahdensuo A, Haahtela T, Herrala J, Kava T, Kiviranta K, Kuusisto P, et al. Randomised comparison of guided self-management and traditional treatment of asthma over one year. BMJ. 1996;312:748–52. https://doi.org/10.1136/ bmj.312.7033.748. 140. Brook V, Mendelberg A, Heim A. Increasing parental knowledge of asthma decreases the hospitalization of the child: a pilot study. J Asthma. 1993;30(1):45– 9. https://doi.org/10.3109/02770909309066379. 141. Clark NM, Feldman CH, Evans D, Duzey O, Levison MJ, Wasilewski Y, et al. Managing better: children, parents and asthma. Patient Educ Couns. 1986;8(1):27–38. https://doi. org/10.1016/0738-3991(86)90024-8. 142. Detwiler DA, Boston LM, Verhulst SJ. Evaluation of an education program for asthmatic children ages 4 to 8 and their parents. Resp Care. 1994;39(3):204– 12. PMID:10145989 143. Fireman P, Friday GA, Gira C, Vierthaler WA, Michaels L. Teaching self-management skills to asthmatic children with their parents in an ambulatory care setting. Pediatrics. 1981;8(3):341–8. PMID:6792585 144. Boulet LP, Boutin H, Cote J, Leblanc P, Laviolette M. Evaluation of an asthma self-management education program. J Asthma. 1995;32(3):199–206. https://doi.org/10.3109/02770909509089508. 145. Rankin S, Stallings K. Patient education: issues, principles, practices. 3rd ed. Lippincott; 1996. 146. Parker SR, Mellins RB, Sogn DD. Asthma education: a national strategy. NHLBI workshop summary. Am Rev Respir Dis. 1989;140(3):848–53. https://doi.org/10.1164/ajrccm/140.3.848. 147. Joint Commission on Accreditation of Healthcare Organizations. Framework for improving performance. Oakbrook Terrace; 1994. 148. Joint Commission on Accreditation of Healthcare Organizations. Criteria for Disease Specific Care. (Internet) (cited 2020 April 23) Available at https://www.jointcommission.org/ en/accreditation-a nd-c ertification/certification/ certifications-b y-s etting/hospital-c ertifications/ disease-specific-care-certification/

1 Asthma and Asthma Education: The Background 149. Office of Disease Prevention and Health Promotion. Healthy People 2020. https://www.healthypeople. gov/2020/topics-o bjectives/topic/respiratory- diseases/objectives. Accessed 22 Apr 2020. 150. International consensus report on the diagnosis and treatment of asthma. NHLBI #92-3091. 1992 Eur Respir J 1992, 5, 601-641 https://erj.ersjournals. com/content/erj/5/5/601.full.pdf. Accessed 22 Apr 2020. 151. Nurses: partners in asthma care. NHLBI-NAEP. NIH publication 1995: #95-3308. Update October 1998. 152. Maiman LA, Green LW, Gibson G, MacKenzie EJ. Education for self-treatment by adult asthmatics. JAMA. 1979;241(18):1919–22. PMID:430774 153. Henry RJ, Hazell J, Halliday JA. Short interventions can improve knowledge about childhood asthma in nursing staff. J Asthma. 1993;30(2):127–33. https:// doi.org/10.3109/02770909309054507. 154. Charlton I, Charlton G, Broomfield J, Campbell M. An evaluation of a nurse run asthma clinic in general practice using an attitude and morbidity questionnaire. Fam Prac. 1992;9:154–60. https://doi. org/10.1093/fampra/9.2.154. 155. Boulet LP. Asthma education: what has been its impact? Can Respir J. 1998;5(Suppl A):91A–6A. PMID:9841114 156. AARC. Clinical practice guidelines: providing patient and caregiver education. Respir Care. 2010;55(6):765–0. 157. Green LW, Frankish CJ. Theories and principles of health education applied to asthma. Chest. 1994;106(4):219S–30S. https://doi.org/10.1378/ chest.106.4_supplement.219s. 158. Miller BD, Wood B. Childhood asthma in interaction with family, school and peer systems: a developmental model for primary care. J Asthma. 1991;28(6):405–14. https://doi. org/10.3109/02770909109110622. 159. Bitsko MJ, Everhard RS, Rubin BK. The adolescent with asthma. Paediatr Respir Rev. 2014;15(2):146– 53. https://doi.org/10.1016/j.prrv.2013.07.003. 160. Snadden D, Brown JB. The experience of asthma. SocSc Med. 1992;34(12):1351–61. https://doi. org/10.1016/0277-9536(92)90144-f. 161. Partridge MR, Hiss SR. Enhancing care for people with asthma: the role of communication, education, training and self-management. 1998 World asthma meeting education and delivery of care working group. Eur Prespir J. 2000;16(2):333–48. https://doi. org/10.1183/09031936.00.16233400. 162. Hanania NA, Witttman R, Kesten S, Chapman KR. Medical personnel’s knowledge of and ability to use inhaling devices: metered dose inhalers, spacing chambers, and breath-activated dry powder inhalers. Chest. 1994;105(1):111–6. https://doi.org/10.1378/ chest.105.1.111.

2

Lung Structure and Function

Contents 2.1 The Respiratory Tract

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2.2 Parts of the Respiratory Tract 2.2.1 Nose 2.2.2 Mouth and Pharynx 2.2.3 Larynx 2.2.4 Tracheobronchial Tree Including Alveoli 2.2.5 Histology of the Airways 2.2.6 Rib Cage and Diaphragm

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2.3 The Nervous System and the Lungs

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2.4 Control of Breathing

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2.5 Defense Mechanisms of the Lungs 2.5.1 Specific Defenses: Immunological Mechanisms

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2.6 Lung Changes and Pathophysiology of Asthma

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2.7 Conclusion

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2.8 Background Reading

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References

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© The Author(s), under exclusive license to Springer Nature Switzerland AG 2021 I. Mitchell, G. Govias, Asthma Education, https://doi.org/10.1007/978-3-030-77896-5_2

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2 Lung Structure and Function

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Key Points

• The Respiratory Tract—From the Nose to the Tracheobronchial tree –– Histology of the airways –– Rib cage and diaphragm • The nervous system and the lungs • Control of breathing • Defense mechanisms of the lungs –– Specific defenses—Immunological mechanisms • Lung changes in asthma and the pathophysiology of asthma

Fig. 2.1 The respiratory system

2.2 Chapter Objectives

After reading this chapter, you should be able to: 1. List the parts of the respiratory tract, explain their function, and describe how each is affected by asthma. 2. Explain the role of allergy in asthma.

2.1

The Respiratory Tract

The respiratory tract, which starts at the nose and lips and continues through the air passages to the alveoli (air sacs), should be considered as one unit. See Fig. 2.1. Much of it is contained within a specific area of the body, the thorax, with the ribs and diaphragm forming the boundaries. The heart is also within the thorax, and blood vessels to the lung come from both the right side (through the pulmonary artery) and left side (the bronchial artery, via aorta) of the heart. The lining of the respiratory tract, from the nose all the way to the alveoli, forms an interface between the outside world and the human body. Thus the detailed structures of the surface lining of the respiratory tract, both in the nose or in the lower airway, share many common features. Diseases affecting this lining, such as allergic rhinitis (hay fever) of the nose, have much in common with asthma.

Parts of the Respiratory Tract

2.2.1 Nose This is the normal route for outside air to enter the body. A septum divides the nose into right and left nostrils, and posteriorly the nose opens into the pharynx through two choanae. The front of the nasal cavity is the nasal vestibule, which extends from the face to the nasal valve. It is supported by cartilage that keeps it open during the negative pressure of inspiration. The nasal vestibule is lined with skin from which hairs grow. These hairs filter inspired air and are the first of many defense mechanisms that protect the lungs from harmful inhaled materials. The nasal septum itself is not always precisely midline and may be deviated to one or the other side. This can lead to significant narrowing of a nostril and consequent problems in breathing. On the side wall of the nasal cavity are three horizontal downward-sloping, scroll-shaped bones pointing towards the septum. These are the conchae that create three passages—the inferior, middle, and superior meatus. The conchae are also called turbinates since they help increase turbulence within the nasal cavity. They significantly increase the surface area of the nasal cavity and allow greater contact between the unfiltered inspired air (which has not yet been humidified) and the nasal mucosa. Four paired sinuses—frontal, maxillary, sphenoid, and ethmoid—drain into the nasal cavity

2.2 Parts of the Respiratory Tract

under the nasal turbinates. When healthy, the sinuses contain air, but infection may occur within them. When there is an allergic disease of the nose, swelling of the mucosa may narrow the opening from the sinuses into the nasal cavity known as the ostiomeatal complex and make drainage of normal mucus difficult. The mucus then accumulates in the sinuses. The nose performs three functions: filtration, humidification, and heat exchange. The inner shape of the nose promotes air turbulence. The turbulence presents a greater volume of air to the mucosal lining of the nose than would a “smooth” inhalation, enabling the mucosal lining to trap many dust particles. The mucosal lining thus hinders the progress of dust into the lower airways. Turbulence within the nose increases with accelerated or rapid breathing. The nose’s ability to filter and absorb particles varies with individuals and tends to be lower in children.

2.2.2 Mouth and Pharynx The mouth and pharynx contain the tongue, palate, and teeth. This is not the usual route for breathing, as air passing through the mouth does not get the same degree of filtering as air passing through the nose. During vigorous exercise, when large breaths are taken, air is taken in through the mouth. Air also passes through the mouth whenever the nose is blocked. Common causes for blockage include allergic rhinitis on a long-term basis or a common head cold in the short-term.

2.2.3 Larynx The larynx or voice box can be felt under the skin—as thyroid cartilage, commonly called Adam’s apple. The larynx contains the vocal folds (vocal cords) which open and close during inspiration and expiration. The width of the opening controls the amount of air that enters the trachea. Vibration of the vocal folds produces sound. The larynx is given some protection by a cartilaginous structure, the epiglottis, which sits

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immediately in front of it. Behind, and to some extent on each side of the larynx, is the esophagus (gullet) which leads to the abdomen. The diaphragm is the major muscle of respiration. It is controlled by the phrenic nerve, while the vocal cords are controlled by the laryngeal nerves. During breathing, the body automatically coordinates the diaphragm’s movement with the opening and closing of the vocal cords. The vocal cords have to be closed when eating, so that food can pass smoothly behind the larynx, into the esophagus, and onto the stomach. When breathing, though, the vocal cords must be open. When the vocal cords are irritated, for example, with acid coming back up from the stomach, they will close in spasm, and again this is protection against such substances passing through the larynx into the lungs.

2.2.4 Tracheobronchial Tree Including Alveoli The first part of the tracheobronchial tree is the trachea. The trachea is partly outside the chest and partly inside. It starts immediately below the vocal folds and continues to the carina when it divides into the right and left main stem bronchi. The trachea is not round in cross section, but varies in shape. Most of the time, it is U-shaped, but where blood vessels leaving the heart cross the front of the trachea, it may be slightly flattened. The main supports for the trachea are horseshoe-shaped cartilaginous structures that are open at the back and vary in number between 8 and 20. Without the cartilage, the trachea would readily collapse during inspiration or expiration, thereby preventing any movement of air. Also, if the cartilage were not present, cough would become totally ineffective, as the trachea would readily collapse during coughing. The two main stem bronchi branch off from the trachea at slightly different angles at the carina. The right main stem bronchus varies just a little, about 20°, from a straight line, and the right upper lobe bronchus branches off immediately after the right main stem bronchus leaves the trachea. Further down the right side is the

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bronchus intermedius, after which the middle lobe bronchus moves off anteriorly, while the rest of the right main stem bronchus proceeds to the right lower lobe. The opening to the middle lobe (which exists only on the right) is slightly elliptical and is easily plugged by secretions. When this occurs, the middle lobe can collapse as air in the lobe is absorbed, a condition known as atelectasis. The left bronchus at the carina is set at an angle of almost 45° from the straight and divides into branches that go to the lower lobe and to the upper lobe. There are thus five main lobes arising from these bronchi, three on the right (upper, middle, and lower) and two on the left (upper and lower). Each lobe forms a unit in terms of airway supply and blood supply. On both sides, the upper lobe is not only higher than the lower lobe but tends to be in front, with the lower lobe behind. The middle lobe is situated to the front and to the right side. Each of the main stem bronchi also has cartilage supporting the wall. Within the lobes, the airways keep dividing, and there are up to 23 subdivisions or generations of airway. No gas exchange takes place in the airways. The bronchi divide into segmental and sub- segmental bronchi. After the third generation of airway divisions, the bronchi are within the lung parenchyma, which is the functional part of the lung. Within the parenchyma, each airway moves on through different generations until it reaches the alveoli, but each airway is also part of the supporting structure for other airways. All of the airways, from the carina to the alveoli, are known as conducting airways. In contrast to alveoli, they do not increase in number throughout childhood. The smallest airways (bronchioles) lead to alveolar ducts and then to the alveoli themselves. The small bronchioles have no cartilage. By the time air reaches the respiratory unit, it is already at body temperature and fully (100%) saturated with water. The process of saturation starts the instant air enters the nose and continues until complete saturation has been achieved by the time it reaches the alveoli. Airflow is generally laminar (layered), with discrete streamlines or layers moving at different speeds. The layer of air next to the airway wall is stationary, while air

2 Lung Structure and Function

in the center is at highest velocity. Airways are asymmetrical and irregular, and this changes the pattern of flow to one of turbulence, which is chaotic and has many swirling currents. In this area, turbulence may move the air towards the airway wall as well as towards the alveoli or the mouth. If the airways are generally irregular or partially obstructed, then respiration is noisy and an increased pressure is required to move the turbulent air. The time it takes for air to flow from any one alveolus to the mouth varies because of the asymmetry in the airways and the mixture of turbulent and laminar flow encountered by the gas molecules. The alveoli are part of the gas exchange area. The terminal respiratory unit, consisting of a terminal bronchiole, alveolar duct, alveolar sac, and alveoli, is called an acinus. The numbers of alveoli increase through adolescence until there are about 300 million in an adult. Gas exchange occurs at the surface of the alveoli, and the total surface area available for this gas exchange has been calculated as being between 50 and 100 square meters. Gas exchange takes place at the alveolar capillary membrane, through type I and type II cells. Type I cells comprise most of the surface area. Type II cells are shorter and more complex, producing surfactant. Capillaries are embedded in the walls of the alveoli. Gas exchange takes place, with oxygen moving from the alveoli into a capillary which eventually goes to the left atrium and thence to the body via the left ventricle and aorta. Carbon dioxide is removed from capillaries as they enter the alveoli, these capillaries being the smallest vessels arising from the pulmonary artery. Thus, the movement of blood, both from and to the heart via the capillaries of the alveoli, is key to respiration. Blood returning from all parts of the body (apart from the lung, with one small exception) does so via the inferior and superior venae cavae to the right atrium. The blood passes through a valve into the right ventricle and is then pumped via a large artery (the pulmonary artery) to the lungs. The pulmonary arteries run alongside the airways, branching as the airways branch, becoming progressively smaller. They become

2.2 Parts of the Respiratory Tract

arterioles, and then capillaries, the smallest blood vessels. Oxygen is transferred to the capillaries from the alveoli. The capillaries then join together and run alongside the arteries and the airways, but they are now the pulmonary veins. Eventually the right and left pulmonary veins flow into the left atrium of the heart. Blood then flows through a valve into the left ventricle of the heart. It is pumped into the aorta and then around the body, this time with oxygen which it has picked up from the lungs. The lungs have an additional blood supply from the aorta via the bronchial arteries. These supply the airway walls and supporting tissue of the lung—from the major bronchi down to respiratory bronchioles—with the oxygen the lung requires to do its work. Once oxygen has been removed from the blood in the bronchial arteries to meet the needs of the lungs, the blood circulates toward the heart. Some of this blood drains back via the bronchial veins into the right atrium. However some of the blood from the bronchial arteries drains directly into the pulmonary veins, thus diluting the oxygen-rich blood coming from the capillaries of the alveoli with a small amount of oxygen-poor blood.

2.2.5 Histology of the Airways Histology describes the fine structure of the airways, which may be seen under a microscope using special stains. The nose is lined with epi-

Fig. 2.2 Functional anatomy of the bronchial mucosa

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thelium, at first without, and then with, cilia. Cilia are small hair-like structures that move mucus along by beating in a coordinated manner. Cilia are an important component of the defense mechanism of the lung. Underneath the epithelium is an extensive capillary network with blood vessels lying deeper in the mucosa. These vessels can widen or narrow, thereby changing the amount of blood underneath the lining of the nose and providing a way for air passing through the nose to be warmed. The structure of the lower airway wall is much more complex than that of the nose. Epithelium lines the airways and contains cells that secrete mucus. There are also cilia on the epithelium throughout most of the bronchi and bronchioles. Immediately below the epithelium is a basement membrane below which are layers containing smooth muscle, elastic fibers, blood vessels, and nerves. Below this is a layer of cells, the submucosa, which again contains glands with mucus. Finally, there is the supporting tissue that surrounds the airways and blood vessels, called adventitia, although this particular sheath does not go beyond the bronchioles. See Fig. 2.2. The epithelium initially contains cilia and goblet cells, but further down the airway, the layers become thinner and flatter and near the alveoli lose the cilia. Cartilage disappears at the same time, and goblet cells become fewer as the air passage moves down towards the alveoli. The layer of cilia is covered with mucus secreted by a variety of glands, and the movement of these cilia

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is coordinated. This movement, which allows the layer of secretions to move from the most peripheral airways towards the pharynx, is called the “ciliary escalator.” Mucus production by the airway is important both in health and disease. Mucus is produced by the goblet cells in the surface epithelium, by serous cells in the surface epithelium, by Clara cells in the bronchioles, and by serous and mucus cells in the submucosal gland. Mucus itself is a mixture of substances—about 95% water, 1% salts, and between 1% and 3% proteins, mainly glycoprotein and mucins. Mucins are peptides of high molecular weight with sugar side chains, and also within the mucus are some non-mucus proteins such as albumen and immunoglobulin. The function of mucus in health is to clear inhaled particles and debris and to form a barrier against bacteria and viruses. If mucus is overproduced or becomes too thick, it may participate in disease processes such as asthma, and this will be discussed in more detail later. Smooth muscle is also important for airway function, both in health and disease. The exact location of the smooth muscle varies with the size of the airways. In the trachea and large bronchi, a band of muscles bridges the opening of the reversed U-shaped cartilage. In the next largest airways, the muscle bundle connects the tips of the cartilage. As the airway size decreases, the muscle shifts along the inside of the cartilage until it is detached completely and forms a separate layer between the cartilage and the epithelium. In the medium and small bronchi, when the smooth muscle contracts, it causes a reduction in both the thickness and the length of the bronchus. This increases the rigidity of the airway. Smooth muscle receives nerves both from the sympathetic (excitatory) and the non-adrenergic (inhibitory) pathways.

2 Lung Structure and Function

through the diaphragm. Twelve pairs of ribs make up the front, back, and sides of the chest wall. The ribs are hinged at the vertebrae in the back and are connected by muscle. Some of the ribs are joined to cartilage in the front. The chest wall with the ribs forms an ellipse rather than a circle. It has its greatest diameter at the level of the 8th or 9th rib; it narrows slightly below that level until it reaches the abdomen. The chest wall narrows rather more above the 9th rib towards the level of the thoracic inlet and the boundary of the first rib. The bottom boundary of the rib cage is the diaphragm. This is a very large and powerful muscle, with right and left parts. It consists of both muscle and a central tendon. Its nerve supply is the phrenic nerve, which starts in the neck at the level of the fifth cervical nerve and then runs down through the neck, through the chest close to the heart until it reaches the diaphragm. In normal quiet breathing, inspiration depends on contraction of the diaphragm. When it contracts, the diaphragm pulls around the rib margin and on the central tendon and thus flattens itself. It pushes down on the abdomen and pushes the abdominal wall outwards. At the same time, the ribs move and become more horizontal, causing the rib cage to become larger and rise slightly. Other muscles of breathing, called the accessory muscles, also exist. The most important of these is the intercostal muscles that lie between the ribs. See Fig. 2.3. In quiet breathing the inter-

2.2.6 Rib Cage and Diaphragm The lungs are enclosed within what is effectively a cage, which has openings towards the neck and

Fig. 2.3 Primary muscles of ventilation

2.3 The Nervous System and the Lungs

costal muscles are used minimally. As breathing increases in depth and frequency, the intercostal muscles are used more, and their activity can be observed by watching a person breathe. Other accessory muscles reside in the neck, and again, when respiration increases in depth, these muscles are used to lift the ribcage up and increase the volume of air that can be inspired. Expiration is generally a passive movement that is a result of the recoil of the various muscles and the ribs, but there may also be some active movement of some of the intercostal muscles to empty the lungs at the end of each breath.

2.3

he Nervous System T and the Lungs

The nervous system has two parts: somatic and autonomic. The former deals with skeletal muscle and with nerves coming from the central nervous system directly to the muscle. A synapse connects the nerve ending and the muscle. Myelin surrounds the nerve, and acetylcholine is the neurotransmitter substance. The autonomic nervous system deals with the smooth muscle in the bronchial wall (and also with cardiac muscle, and the activity of the various glands in the airway). It is nonvoluntary, and target tissues may be either stimulated or inhibited. Nerve endings have two neurons in series: a preganglionic neuron, which connects the nervous system to an autonomic ganglion, and a postganglionic neuron, which goes from the ganglion to the target tissue. The preganglionic neuron cell bodies are in the cranial nerves and in the spinal cord. They have myelin cover; thereafter there is no myelin cover. The preganglionic neurons release acetylcholine, while the postganglionic neurons release either acetylcholine or norepinephrine. When the somatic sensory nerves in the chest wall sense that the muscles are being stretched, they inhibit expansion of the chest wall and then initiate contraction. A neural message about the expansion of the chest wall

45

is sent to and processed by the brain, and the return “instruction” is then delivered via somatic nerves. The main somatic nerve for breathing is the phrenic nerve that emerges from the spinal cord at cervical levels 3–5. This passes through the chest, close to the heart, and then divides into numerous small branches when it reaches the diaphragm. The intercostal nerves are nerves that come from the spinal cord directly to the various intercostal muscles. The movements of these muscles are coordinated, along with the main nerve to the vocal cord, which is the recurrent laryngeal nerve. This nerve is a branch of the vagus nerve. The right recurrent laryngeal nerve enters the chest, loops around the aorta, and then returns to the larynx. The autonomic nerve fibers enter the lung at the hilum (or opening) and run along the same general course that has already been described for the airways and blood vessels. The autonomic system is divided into sympathetic and parasympathetic components. See Fig. 2.4. There is a third system, a non-adrenergic, non-cholinergic system, whose functions are not fully understood. The parasympathetic fibers go to airway smooth muscle and also to the mucus glands. They secrete acetylcholine. The activity of the parasympathetic nerves ensures there is constant, low-level, smooth muscle contraction resulting in a “tone” to the airways. Unlike skeletal muscle, such as the diaphragm, the structure of smooth

Fig. 2.4 Subdivision of the central nervous system

2 Lung Structure and Function

46

muscle permits prolonged contraction. Increased activity of the parasympathetic nerve leads to more intense contraction of the smooth muscle, called bronchospasm. Parasympathetic nerve activity also increases the production of mucus glycoproteins. Nerves in the sympathetic nervous system are called adrenergic fibers. They secrete norepinephrine. Stimulation of the adrenergic receptors in the airway causes the smooth muscle to relax. This is called bronchial dilation or bronchodilation. The receptors themselves are, for the most part, specialized areas of cell surfaces that interact with various natural compounds of the body and also with drugs. The interaction of the transmitter substance or drug with the receptor precipitates a chain of biochemical events. Agonists regulate receptors and can bind to receptors. Some agonists, known as antagonists, can prevent other agonists from attaching themselves to receptors and thus block their function. This antagonistic blocking action can be partial or complete, reversible or irreversible. The receptors mentioned earlier are very important in asthma and relevant to medication use. The transmitter that affects the sympathetic nervous system is norepinephrine or epinephrine. The receptors involved are called adrenergic receptors. There are two general types, named alpha and beta, with the numbers and types varying according to the tissues in which they are found. Adrenergic receptors are important in asthma. The main ones are the beta-adrenergic receptors that are divided into two groups, beta-1 and beta- 2. Beta-1 receptors are found primarily in the heart and cause tachycardia (rapid heartbeat) when stimulated. Beta-2 receptors are found primarily in the airways. When stimulated, both beta-1 and beta-2 receptors cause: • Smooth muscle relaxation • Inhibition of mediator release by mast cells and basophils • Reduction in mucosal edema • Increased mucus clearance • Decreased airway reactivity

Table 2.1 Action of epinephrine Location of effect Mast cells

Receptors Beta-2

Bronchial smooth muscle Heart

Beta-2

GI tract Blood vessels of skin and gut Blood vessels of skeletal muscle Eye

Beta-2

Effect Inhibits secretions Relaxes

Beta-2

Increases rate and force Decreases motility Causes constriction Dilates

Alpha

Constricts pupils

Alpha and beta-2 Alpha-1

Beta-2 receptors are also responsible for dilation of blood vessels and relaxation of the uterus. They are responsible for tremor in the skeletal muscles of the extremities. They act metabolically and lead to an increase in serum concentration of glucose. See Table 2.1.

2.4

Control of Breathing

The fundamental function of respiration is to supply adequate oxygen to support normal human activity and to ensure the removal and excretion of carbon dioxide. The lungs work very efficiently under the varying workloads that occur when individuals are in good health. Blood levels of oxygen and carbon dioxide are maintained within narrow and consistent limits. The components that play an important role in the control of breathing are described as controllers, effectors, and sensors. The controllers are the: • Cerebral cortex, which permits some voluntary control over breathing • Brain stem, which provides automatic control • Spinal cord The effectors are the nerves leading to the muscles of respiration and to the lungs. The sensors are nerves in the lungs, chest wall, and receptors (chemoreceptors present in the carotid body) which measure and respond to blood gases in the body.

2.4 Control of Breathing

Breathing is regulated from moment to moment. It varies with exercise, sleep, and disease. Breathing when a person is asleep is very different from that when awake. When asleep, breathing also varies with the different stages of sleep. For example, during REM (rapid eye movement) sleep, breathing is irregular, with brief periods of apnea lasting between 15 and 20 seconds. When oxygen levels fall, a condition called hypoxemia occurs. An acute shortage of oxygen causes extreme distress. Various body mechanisms are activated, and they work to restore oxygen levels to normal. When the shortage of oxygen is long term, as may occur in disease, there may be some adaptation, leading to less distress. Because the body strives to maintain normal blood gas levels, exercise causes an increase in the rate and volume of ventilation. If the exercise is either very hard or prolonged, blood oxygen levels may drop. At the same time, carbon dioxide may increase, and this leads to a small fall in pH and therefore an increase in blood acidity. As carbon dioxide (CO2) accumulates, respiration automatically becomes more rapid and deep, causing CO2 levels in the blood to be lowered. The various sensory reflexes provide some control over the depth of breathing and the amount of chest expansion. These reflexes are affected by other factors such as the air temperature.

Points to Ponder

Main regulators of ventilation • Carbon dioxide • Reflexes • Psychogenic factors, since part of ventilation is under voluntary control • Other factors, such as temperature

Ventilation is mainly automatic, but it is also voluntary and may be influenced by psychogenic factors. In panic, for example, there is an increase

47

in both the rate and depth of breathing. This also occurs in anxiety. Central and peripheral chemoreceptors also play a role in the control of respiration. The central chemoreceptors are nerve cells in the medulla (a subdivision of the brain stem). These nerve cells are very sensitive to changes in pH (hydrogen ions), which reflect changes in CO2 levels. The central chemoreceptors are surrounded by cerebrospinal fluid which is separated from the blood by a membrane called the blood-brain barrier. When CO2 accumulates in the body, it passes rapidly through this barrier into the cerebrospinal fluid and forms hydrogen ions. The central chemoreceptors then sense the increase in acidity, reflexively increase the rate and depth of breathing, and are thus the ongoing minute-to-minute controller of ventilation. Peripheral chemoreceptors are located in very small structures in the arteries called the carotid and aortic bodies. There is a carotid body on each side in the common carotid arteries, while the aortic bodies are in the arch of the aorta. Impulses from these receptors travel to the respiratory control center in the medulla. Whereas the central chemoreceptors respond rapidly to changes in CO2 and hydrogen ions but not to oxygen, the peripheral chemoreceptors are the oxygen sensors as they respond to changes in oxygen (O2) levels in the blood. Stretch receptors in the lung and chest wall, while important in respiration, have a lesser impact than the chemoreceptors. Within the lung there are several receptors, all of which use the vagus nerve to send information to the central nervous system. Slow-adapting stretch receptors exist within the smooth muscle of the airway, and these are stimulated by a deep breath. A deep breath will inhibit parasympathetic activity, and this, as mentioned earlier, leads to smooth muscle relaxation and bronchial dilation. Rapid-adapting receptors, called the irritant receptors, also exist, in the larynx, trachea, and main stem bronchi. When stimulated by foreign substances, they act very quickly, and this, in turn, leads to a number of protective responses: narrowing of the larynx, cough, deep breathing, mucus secretion, and bronchial constriction.

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48

Stretch receptors are also contained in the intercostal muscle and the diaphragm. As part of the somatic system, they pass impulses to the spinal cord. They are important in terminating inspiration. Receptors called C-fibers are located in the lung parenchyma, conducting airways, and pulmonary blood vessels. C-fibers seem to be involved in the bronchial constriction that occurs, for example, after breathing cold air, which cools the airway, or after exercise, which also cools the airway. Based on the physiological information provided so far, we can now make a preliminary examination of changes that occur to airway diameter with breathing and of factors that may affect airway resistance. This section will deal only with the airways inside the thorax. Individual airways proceed through more than 20 divisions, narrowing after each division. Although the individual air passages at the end of these divisions are very small, the total diameter of all of the small airways taken together is greater than the total diameter of the larger airways. Thus, although there may be high resistance in an individual small airway, overall resistance is lower in the peripheral airways than in the central airways. Resistance is affected by the size of the airway, the amount and activity of elastic tissue, the tone of the smooth muscle, and also the recoil pressure as a person breathes in and out. Smooth muscle tone is affected by autonomic nervous system activity, which is in turn affected by O2 and CO receptors. In quiet breathing, the pressure in the airway is less than the pressure in the supporting tissue around the airway, leading to some compression of the airway on expiration. When the rate of breathing increases, and when expiration is forced to empty the lungs, a higher pressure is generated, and the intrathoracic airway is compressed further. Although effort is initially important in this compression, at higher pressures the compression of the airway becomes independent of effort. This is particularly true at high lung volumes, that is, at the start of, rather than at the end of, expiration.

2.5

Defense Mechanisms of the Lungs

The lungs offer multilayer in-depth defense against airborne particles and other potential irritants, and some of the reflexes involved have already been described. Other defenses exist too. They include: • The physical structure of the lungs • The physical structure of the airways • Non-specific defense mechanisms such as cilia, cough, and mucus • Specific immunological mechanisms Particles are prevented from reaching the lower airway by the normal filtering that occurs in the nose or throat, and these particles may sometimes stimulate a sneeze. Particles that reach the vocal cords will stimulate their abrupt closure, an effective but uncomfortable protective mechanism. If they manage to get past the vocal cords, they will stimulate irritant receptors, leading to increased production of mucus that may engulf the particles, following which ciliary activity will move them towards the throat. It may also be enough to stimulate an explosive cough. Cellular defenses include the phagocytic cells that incorporate particles (including bacteria and viruses) and then engulf and kill them. Phagocytic cells include macrophages, and these mechanisms are also supplemented by a number of biochemical factors. These are described next.

2.5.1 Specific Defenses: Immunological Mechanisms Many of the lung’s defenses lie in immunological mechanisms that are latent until activated by exposure to foreign material. The stimuli and responses associated with each mechanism may be very specific. See Fig. 2.5. For example, an antigen produces an immune response in many different ways:

2.5 Defense Mechanisms of the Lungs

49

Fig. 2.5 Process of antibody formation following exposure to a pathogen

• The body clearly differentiates the antigen from a non-antigen. • The antigen is taken up by cells called dendritic cells and pulmonary macrophages, which process and deliver the antigen to reactive lymphocytes, which differentiate into cells known as T or B cells. • Lymphocytes have an effective response that includes synthesis and release of antibodies by B cells, or production of potent soluble products such as cytokines by T cells . Antibodies formed by B cells are of five different classes: IgG, IgA, IgM, IgD, and IgE. These differ in their structures and biological properties. The IgG antibodies represent about 80% of the total immunoglobulin family and have primarily a protective function against bacteria and certain viruses. IgA antibodies are found predominantly in respiratory tract secretions where they provide immunity on mucosal surfaces. IgE antibodies, which are present in the body in exquisitely small numbers, have no protective function as far as is known, but cause allergic diseases including hay fever (allergic rhinitis), many cases of asthma, anaphylaxis (a life-threatening allergic reaction), and a variety of other allergic disorders. About 20% of the human population has a genetically determined predisposition to produce IgE antibodies against substances found in the environment, such as pollen, dust mites, and other irritants. These “irritants,” however, do not bother the other 80%. Individuals who form IgE antibodies are known as atopic. The mechanism by which atopic people become sensitized or allergic to foreign substances is unknown.

Type 1 IgE-mediated allergic reactions are the most important in asthma and will be discussed in detail. Under the influence of interleukin 12 (Il12) secreted by macrophages, so-called naïve or immature T helper cells differentiate or develop into so-called Th1 cells. The Th1 cells secrete a cytokine known as interferon gamma (IFNy). IFNy inhibits production of IgE antibodies by B cells, and this is referred to as the nonatopic profile. On the other hand, other naïve T helper cells, under the influence of interleukin 4 (Il-4) from T cells, differentiate into Th2 cells. Th2 cells secrete Il-4 and Il-13, which in turn influence B cells to produce IgE antibodies. This is the atopic profile. In the IgE allergic pathway, antigen-presenting cells, both dendritic or macrophages, process antigen and deliver it to the uncommitted naïve T helper cells which stimulate B cells according to the above paradigm. Then B cells develop in the plasma cells which are the end-stage cells that actually produce the IgE antibodies. Once produced locally in the tissues of the respiratory tract, such as the nasal mucosa, the IgE antibodies spill over into the circulation and “home in” onto tissue mast cells and circulating basophils, binding to the IgE receptors on the surface of these target cells. These cells are now “sensitized.” Upon exposure to an antigen (allergen), such as ragweed, which stimulated the formation of the IgE antibodies to begin with, bridging of two adjacent cell-bound IgE antibodies occurs. This leads to a series of biochemical reactions which culminate in the release of chemical mediators, such as histamine, from preformed granules in the mast cells and basophils. New synthesis and

2 Lung Structure and Function

50

release of other mediators (such as leukotrienes) also occur from the mast cells. Release mediators are hence responsible for tissue injury and other signs and symptoms, for example, of allergic rhinitis or asthma. The reaction described above is known as an immediate or early reaction and is depicted in Fig. 2.6. Other mediators that are released attract inflammatory cells, such as eosinophils and neutrophils. This attraction process is known as chemotaxis. Once attracted to the site of the original reaction, these inflammatory cells release tissue-destroying substances such as eosinophil major basic protein. This secondary reaction, which does not require exposure to allergen, takes between 2 and 8 hours to develop and is known as the late reaction. The late reaction manifests in the lung as biphasic symptoms and also in the skin and nasal mucosa. In asthma, the late phase reaction occurs in about 50% of persons with asthma, primarily in those with moderate to severe forms of the disease. It is often persistent and more difficult to treat than the initial reaction. The biphasic response is clearly observable in experimental studies. In such studies, only one trigger is used, and careful measurements are made over a long time period. In real life, issues are rarely so simple or clear-cut. Identification with certainty of triggers that cause a late response is unusual. Most individuals with asthma are exposed to a variety of triggers by day, and thus many individual early and late responses will blend together into overall deterio-

ration of the asthma. These responses are described in more detail in the next section.

2.6

Lung Changes and Pathophysiology of Asthma

Eosinophils have long been known to be present in the lungs of persons with asthma. They can be seen in sputum, which is coughed up and can be stained specifically to detect their presence. Modern techniques have confirmed this observation. For example, biopsy of part of the lung via a bronchoscope, or lavage (production of secretions after instilling saline), confirms the presence of a large number of eosinophils in the air passages of the lungs. The eosinophils, mast cells, and basophils all show increased levels. There is a large migration of lymphocytes to the airway epithelium. All of these inflammatory cells produce cytokines, growth factors, and mediators such as histamine and leukotrienes. They lead to movement of water into the cells and swelling of the mucosal lining of the airway. Taken together this leads to narrowing of the airway. See Tables 2.2 and 2.3 and Fig. 2.7.

Table 2.2 Phases of the allergic response Phase 1 Ig E produced

Phase 2 Mast cell activated

Fig. 2.6 The allergic reaction leading to the early phase of the response in asthma

Phase 3 Mediators released

Phase 4 Mediators take effect

2.6 Lung Changes and Pathophysiology of Asthma

51

Table 2.3 Effects of mediators in the allergic response

The smooth muscle surrounding the airway may constrict in response to a variety of stimuli. Some of this constriction will be direct, such as when the airway is exposed to very dilute (hypotonic) or concentrated (hypertonic) saline, both of which will dramatically change the exchange of water between the airway lumen and the airway mucosa. Similarly the drying or cooling of the airway that occurs during severe exercise produces airway smooth muscle constriction because of similar fluid shifts. Some of the action of the smooth muscle will be indirect, in response to changes to the autonomic nervous system and perhaps also in response to various irritants such as sulfur dioxide or particles inhaled in the airway. If the mucosa of the airways is damaged, as in infection or in acute asthma, inhalants may have more direct access to the nerve fibers and may thereby stimulate more severe bronchial constriction. Mucus plugs are also an important part of the asthma picture and are seen in almost all cases of

Substance Histamine

Platelet activating factora Leukotrienesb

Prostaglandin D2 Kallikrein

Action Constricts bronchi Opens blood vessels Leaking from blood vessels Nerve endings Mucus production Narrows airways Opens blood vessels Narrows airways Leakage from blood vessels Mucus production Narrows airways Opens blood vessels

Released from granules Lipid

a

b

Effect Wheeze Redness (If widespread leads to shock) Swelling Itch and pain Wheeze and cough

Wheeze Redness (If widespread leads to shock) Wheeze Swelling Wheeze and cough

Wheeze Wheeze Bronchospasm

Fig. 2.7 Formation of mast and inflammatory cells that instigate the early and late-phase reaction

52

individuals who die from asthma. Mucus plugs may also occur in acute severe and in chronic severe asthma. Once mucus accumulates and forms a plug, it decreases the space available for airflow. This narrow airway then exaggerates the effect of the smooth muscle contraction, so that a lesser degree of shortening of the smooth muscle is able to close the airway. Airway hyperresponsiveness is one of the cardinal features of asthma, and it arises from a combination of all the previously described effects of inflammation, smooth muscle contraction, and mucus plugs. It is intensified by cells sloughed from the surface and also by changes in the lung as a whole. On receipt of a stimulus, individual changes of inflammation, smooth muscle contraction, or mediator production will be initiated, or some combination of these factors. The net result will be narrowing of the airways. The degree of narrowing, and the time frame over which it occurs, will depend on the severity of the insult or strength of the stimulus. The response will be greater if there are any p receding abnormalities such as mild inflammation, some smooth muscle contraction, or some production of mucus, or two or indeed all three at the same time. Hyperresponsiveness is also seen in the normal morning-to-evening variation in airway caliber, with the caliber being narrower overnight and wider during the day. The variability in asthma is usually considered reversible, but in persons with severe asthma, it may be quite marked and not easily reversible. Intensive treatment may need to continue for some time before lung function improves. The overall effect of all of these changes is decreased flow rates through the narrower airways. Given the asymmetrical structure of airways, there will be asymmetrical closure. This will be exaggerated with mucus plugs and bronchial constriction. Therefore some units of the lung will not be able to empty at the end of expiration. Over time this will lead to a significant number of units being unable to empty and an increase in the air remaining in the chest at the end of expiration. This volume of air remaining is called the residual volume. In turn, this leads to

2 Lung Structure and Function

further consequences, including a reduction in lung elasticity. The result is that the lung becomes “stiffer,” and the diaphragm is no longer dome-shaped. When the lungs are hyperinflated with an increased residual volume, the diaphragm will tend to be flat during expiration, and therefore the body will have to work harder to contract the diaphragm and flatten it further with inspiration. This will lead to increased diaphragmatic work and some mechanical disadvantage. There will also be an increase in the “dead space” of the lung (that part of the respiratory tract that does not participate in gas exchange). Typically, air in the mouth, trachea, large airways, and a few of the alveoli does not participate in gas exchange. When residual volume is increased, the volume of air in the alveoli is increased. Gas exchange still takes place but only at the alveolar surface. The larger amount of air (dead space) is still moving with each breath but does not contribute to effective oxygen intake by the body. This contributes to making respiration more inefficient. Ventilation becomes very uneven as asthma increases in severity. Blood flows through the pulmonary arteries to the capillaries, going both to those parts of the lungs that are ventilated and to those parts that are not. Capillaries in the ventilated parts of the lung pick up oxygen and return it to the lungs. Blood going to capillaries of those alveoli not ventilated does not pick up oxygen. When these capillaries eventually connect to a large vein, the non-oxygenated blood mixes with blood containing a high level of oxygen. This ventilation/perfusion mismatch is important in asthma as it lowers the overall level of oxygen returning to the heart for distribution to the body. As these changes progress and oxygen levels fall in the blood, there will be an increase in respiratory drive, which increases the rate of breathing. This hyperventilation will then lead to a fall in carbon dioxide. The combined changes of slightly low levels of oxygen and carbon dioxide are seen in the early stages of severe acute asthma. Inflammation is probably the most important underlying pathological feature of

2.6 Lung Changes and Pathophysiology of Asthma

asthma, and chronic inflammation will cause tissue injury with subsequent changes in structure. These longer-term changes are referred to as “remodeling.” The changes wrought by remodeling are not a new discovery but have received recent attention with the increasing recognition that not all persons with asthma have well-marked reversibility. Remodeling affects the airway wall, smooth muscle, mucus-producing cells, the subepithelial layers, production of myofibroblast, changes in the blood vessels, and possible changes in the matrix composition. Remodeling seems to affect a subgroup of those people with asthma with airflow obstruction that is at best only partially reversible [1]. Remodeling of the airways has been described in detail [1]. Its changes include an increase in the thickness of the airway wall. Almost all components of the airway wall are thickened—smooth muscle, connective tissue and mucus glands—and these changes extend to the submucosa and adventitial tissues. The proportionate increase in smooth muscle mass is much greater than the increase in total airway thickness. Some of the increase is due to formation of additional muscle cells, while some is chronic thickening of the existing muscles. The number of mucus glands increases, and they are larger than the mucus glands in non-affected airways. There is also an increase in collagen immediately below the bronchial epithelium, leading to subepithelial fibrosis. At one time, this was thought to be “basement membrane thickening,” but it is now known that there are only minor changes in the basement membrane. Myofibroblast are specialized cells that increase in tissues undergoing repairs, and these cells are increased in the submucosa of people with asthma. They are a source of interstitial collagen that may contribute to some of the other abnormalities. The blood vessels, which travel alongside the airways, also have vascular congestion, some increased thickening of the walls, and perhaps formation of new vessels. A number of other substances are also deposited in the airway wall, including collagen, matrix

53

glycoprotein, proteoglycans, and other substances. Investigations to date point to the small airways (2–6 microns) as the major site of these abnormalities in most individuals with asthma. There are changes in epithelial cells with shedding of some cells, loss of ciliated cells, and hyperplasia of goblet cells. Airway epithelial proliferation may be another contributor to airway wall thickening. In summary, changes occur because of ongoing inflammation, injury, and repair. The sum total of remodeling is that the airway responds poorly to treatment. It has difficulty in reverting to normal, and there is a chronic increase in the work of breathing. Aggressive and meticulous treatment may reduce the impact of remodeling, although the evidence for this is not clear. The prevalence of remodeling can only be estimated using indirect measures. Much of the knowledge described in the preceding paragraphs comes from bronchial biopsies or specimens taken at autopsy. There are obvious difficulties in obtaining such specimens on a large scale, or even in a small population, and in doing so repeatedly over a number of years. Indirect measures such as computed tomography of airway wall thickness, positron emission tomography scans, or measurement of lung function have also been used. One longitudinal study, which followed 1037 children (born between April 1, 1972, and March 31, 1973) for two decades, provides important information on the impact of childhood asthma, airway hyperreactivity, atopy, sex, and smoking on remodeling [2]. The investigators used the ratio of the forced expiratory volume in one second and the functional vital capacity FEV1/FVC, (described in more detail in the next chapter) as a measure of remodeling. A ratio that was low after use of a bronchodilator, at age 18 or 26, was used as a marker of airway remodeling. The investigators justified this measurement on the assumption that structural abnormalities in the airway wall prevent full reversibility. The low ratio was found in 4.6% of the population at both 18 and 26 years. This group had low lung function throughout childhood. Low ratios were independently asso-

2 Lung Structure and Function

54

ciated with male sex and airway hyperresponsiveness but not with smoking or atopy. This study provides data indicating that airway remodeling begins in childhood and continues into adult life. This study does not provide evidence that remodeling can be prevented. However, it does identify a marker of disease (FEV1/FVC) that educators can review at intervals, say annually, for individuals with asthma. Those with low FEV1/FVC, particularly if the trend is declining, need extra care to identify the best treatment regimen and must be encouraged to adhere to it. This is only one of many cohort studies that add to our understanding of changes in the lungs of people with asthma over time.

2.7

Conclusion

In conclusion, asthma educators must understand the lung, its normal structure, and the functions underlying lung changes when asthma is present. This chapter has provided the essential medical background they need. In turn, this understanding is essential in understanding current therapeutic approaches and why new approaches are needed.

2.8

Background Reading

Thomson NC, Rodger IW, Barnes PJ, editors. Asthma: basic mechanisms and clinical management. Academic; 1998. Barnes PJ, Drazen JM, Rennard SI, Thomson NC, editors. Asthma and COPD: basic mechanisms and clinical management. Elsevier; 2009 Mar 19. Clark TJH, Godfrey S, Lee TH, Thomson NC. Eds. Asthma, 4th Ed. Arnold, London; 2000. Beachey W. Respiratory care anatomy & physiology foundations for clinical practice. 563 St Louis, Mo. Elsevier; 2013:159–67.

References 1. Shifren A, Witt C, Christie C, Castro M. Mechanisms of remodeling in asthmatic airways. J Allergy. 2012;2012:316049. https://doi. org/10.1155/2012/316049. 2. Rasmussin F, Taylor DR, Flannery EM, Cowan JO, Green JM, Herbison GP, et al. Risk factors for airway remodeling in asthma manifested by a low postbronchodilator FEV1/Vital capacity ratio. A longitudinal population study for childhood to adulthood. Am J Respir Crit Care Med. 2002;165(11):1480–8. https:// doi.org/10.1164/rccm.2108009.

3

Measurements of Lung Function

Contents 3.1 Overview

57

3.2 L ung Volumes and Capacities 3.2.1 Volumes 3.2.1.1 Tidal Volume (VT, Sometimes Shown as TV) 3.2.1.2 Inspiratory Reserve Volume (IRV) 3.2.1.3 Expiratory Reserve Volume (ERV) 3.2.1.4 Residual Volume (RV) 3.2.2 Lung Capacities 3.2.2.1 Total Lung Capacity (TLC) 3.2.2.2 Inspiratory Capacity (IC) 3.2.2.3 Functional Residual Capacity (FRC) 3.2.2.4 Vital Capacity (VC) 3.2.2.5 Forced Vital Capacity (FVC) 3.2.2.6 Forced Expiratory Volume in One Second (FEV1) 3.2.2.7 Integrating Capacities 3.2.3 “Normal” or “Predicted” Values

57 58 58 58 58 58 59 59 59 59 59 59 59 59 59

3.3 Spirometry 3.3.1 FEV1, FVC, and FEV1/FVC 3.3.1.1 Forced Expiratory Flow Maximum (FEFmax) 3.3.1.2 Forced Expiratory Flow25-75 (FEF25-75) 3.3.1.3 Expiratory Flow200-1200 (FEF200-1200) 3.3.2 Flow-Volume Loops 3.3.2.1 Volume-Time Curves 3.3.2.2 Technical Requirements for Spirometry 3.3.2.3 Criteria for Acceptability 3.3.3 Bronchodilators in Pulmonary Function Testing 3.3.4 A Pulmonary Function Test and Its Interpretation

62 65 65 66 66 66 67 69 69 70 71

3.4 M easures of Lung Function 3.4.1 Peak Flow Measurement 3.4.1.1 Calculating Reversibility 3.4.1.2 Diurnal Variation 3.4.1.3 Calculating Diurnal Variability 3.4.1.4 Consistency in Obtaining PEF Readings 3.4.1.5 PEF and Adherence

71 71 75 75 75 76 76

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2021 I. Mitchell, G. Govias, Asthma Education, https://doi.org/10.1007/978-3-030-77896-5_3

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3 Measurements of Lung Function

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3.4.2 Other Measures of Lung Function 3.4.2.1 Fraction of Exhaled Nitric Oxide (FeNO) 3.4.2.2 Dilution Techniques: Helium and Nitrogen 3.4.2.3 Plethysmography

77 77 78 79

3.5 Bronchial Challenge Testing 3.5.1 Methacholine and Histamine Challenge 3.5.2 Exercise Testing 3.5.3 Inspired Cold Air 3.5.4 Ultrasonic Distilled Water 3.5.5 Adenosine 5’-Monophosphate (AMP)

80 80 81 83 83 83

3.6 Other Testing Methods 3.6.1 Bronchoalveolar Lavage (BAL) 3.6.2 Induced Sputum 3.6.3 Exhaled Breath Condensate (EBC)

83 83 84 84

3.7 Oxygen Saturation

85

3.8 P ulmonary Function Testing in Infants and Preschool Children 3.8.1 Pulmonary Function Testing in Infants 3.8.2 Pulmonary Function Testing in Preschool Children 3.8.2.1 Forced Oscillation Technique (FOT) 3.8.2.2 Interrupter

85 85 86 86 86

3.9 P ulmonary Function Testing of Adults Unable to Do Standard Spirometry

86

3.10 Quality Control

87

3.11 Application

88

References

90

Key Points

• Measurements of lung function allow objective values to be used in understanding asthma. –– They supplement what those with asthma tell us, but do not replace individual experience of asthma. • Understanding of lung function testing implies a knowledge of the meaning of lung volumes and capacities, spirometric values, and interpretation of spirograms. –– The peak flow is less accurate than spirometry, but can be done frequently at home, in the workplace and at leisure. –– Oxygen saturation can now be readily measured and is essential in the management of acute asthma. • In severe chronic asthma and in research, other tests can expand our understanding of asthma.

–– These include exhaled fraction of nitric oxide, dilution techniques, plethysmography, and exercise testing and challenges. –– Challenges with inspired cold air, ultrasonic distilled water, and adenosine 5’-monophosphate (AMP) are used in some situations. • Examining cell type and counts and other alveolar substances can help in describing the asthma phenotype. –– These include bronchial lavage, induced sputum, and exhaled breath condensate. • Special techniques and tests are needed in infants and preschool children and of those adults unable to do spirometry. • Measurements of lung function are only as good as the quality control used.

3.2 Lung Volumes and Capacities

Chapter Objectives

After reading this chapter, you should be able to: 1. Explain spirometry, FEV1, and PEF and their use in the diagnosis and control of asthma. 2. Explain the significance of objective lung function measurements. 3. Identify the technical requirements of spirometry. 4. List the different tests used in measuring lung function. 5. Calculate diurnal variability using peak flow readings.

3.1

Overview

Asthma and lung function measurements go hand in hand—an accurate appraisal of the latter is an essential component of the assessment process when dealing with persons who have asthma and an important objective addition to other measures of disease severity. In people with asthma, healthcare providers, including physicians, often underestimate or overestimate the severity of asthma, especially on initial assessment. Pulmonary function tests—which provide an indication of lung function—can aid in accurate diagnosis and, consequently, in the management of asthma [1].

3.2

Lung Volumes and Capacities

When measuring lung function, the focus is on the effects of breathing on gas exchange. In all measurements, there are two volumes that must be differentiated, ventilated air that participates in gas exchange and a smaller volume that does not participate in gas exchange. This latter volume is called “dead space.” In turn, there are two types of dead space. The anatomical dead space is represented by the volume of air that fills the

57

conducting zone of respiration made up by the nose, trachea, and bronchi. In adults this is about 150 ml. Physiologic or total dead space is equal to anatomic plus alveolar dead space, the volume of air in the respiratory bronchioles, alveolar duct, alveolar sac, and alveoli—the respiratory zone that does not take part in gas exchange. Anatomic dead space is fairly constant, while physiological dead space is commonly increased in disease. Equipment used in lung function testing will have additional dead space, that of the tubing that connects the person being tested to the device. This is almost always minimal. It is only relevant when equipment designed for adults is used in children. Some measures of lung function (see Fig. 3.1) are easy and repeatable; some are difficult; and a few can be conducted only in a research laboratory. Measures of airflow and lung volumes using spirometry are by far the most useful and repeatable measurements. Other measurements, such as resistance (by plethysmography), residual volume (by dilution techniques or plethysmography), or carbon monoxide diffusion, can be helpful in specific situations. All these tests, however, require the full cooperation of the person being tested; where this is not available (as, e.g., with children, the elderly, or in those who also have other severe diseases), testing is not possible. New tests under development, such as forced oscillation or interrupter techniques, may enable some information to be gathered from such persons [2, 3]. Lung function is assessed by measuring the amount of air in the lungs at various stages of the respiratory cycle. These amounts are converted into percentages and ratios that a healthcare provider can use to make a meaningful assessment. Much of the terminology associated with lung function pertains to volumes [4] in the lung, and an understanding of this terminology is essential for an understanding of lung function testing. Figure 3.1 shows both the basic measures and those that involve the sum of two of more volumes, referred to as capacities. While both the diagram and the terminology may appear daunt-

3 Measurements of Lung Function

58 Fig. 3.1 Lung volumes and capacities

ing at first glance, they are in fact extremely logical and very easily understood.

3.2.1 Volumes 3.2.1.1 Tidal Volume (VT, Sometimes Shown as TV) This is the amount of air inhaled and exhaled during normal breathing. It is typically only 10% of the lung’s total capacity. In other words, under normal conditions, the lungs take in just a fraction of the volume that can be inhaled. 3.2.1.2 Inspiratory Reserve Volume (IRV) IRV is the difference between the volume inhaled with a normal breath and the volume that can be inhaled on maximal inspiration.

3.2.1.3 Expiratory Reserve Volume (ERV) This is the difference between the volume exhaled with a normal breath and the volume that can be exhaled after a forced exhalation. 3.2.1.4 Residual Volume (RV) It is physically impossible for a person to expel all the air from the lungs. RV is the amount of air that remains in the lungs even after a “maximum” forced exhalation. RV is usually about 25% of the total lung capacity. A normal exhalation leaves more air in the lungs—about 40% of total lung capacity—than a forced exhalation. In long- standing asthma, the RV may increase. RV is calculated as

RV FRC ERV

3.2 Lung Volumes and Capacities

(where FRC is the functional residual capacity, that is, the amount of air left in the lungs after a normal exhalation. See below for more details.)

3.2.2 Lung Capacities 3.2.2.1 Total Lung Capacity (TLC) TLC is the volume of air in the lungs after the maximum possible inhalation. 3.2.2.2 Inspiratory Capacity (IC) This is the total volume that can be inhaled. It is comprised of two components: tidal volume (normal breathing) and the inspiratory reserve volume (IRV), which is the additional amount of air that can forcefully still be inhaled after a normal breath.

IC TV IRV

3.2.2.3 Functional Residual Capacity (FRC) FRC is the amount of air left in the lungs after a normal exhalation.

3.2.2.6 Forced Expiratory Volume in One Second (FEV1) FEV1 is actually a measurement of volume. It is described here because it is a subdivision of FVC. FEV1 is the amount of air expelled in one second (the very first second) through forceful expiration after maximal inspiration. In persons who do not have asthma, TLC is between 6 and 7 liters for men and 5 and 6 liters for women. FRC is between 2 and 3 liters for both men and women. FVC will be about 4 liters for men and 3 liters for women. In persons with asthma, FEV1 will be less than 80% of FVC, but FVC will be maintained at the normal values mentioned above. 3.2.2.7 Integrating Capacities Without asthma, TLC is between 6 and 7 liters for men and between 5 and 6 liters for women. FRC is between 2 and 3 liters for both men and women. FVC will be about 4 liters for men and 3 liters for women. With asthma that is not fully controlled, FEV1 is less than 80% of FVC, but FVC will be maintained at the normal values mentioned above.

FRC TLC IC

3.2.2.4 Vital Capacity (VC) VC is the maximum amount of air that can be breathed out after breathing in to the maximum extent.

59

VC TLC RV

3.2.2.5 Forced Vital Capacity (FVC) This is the amount of air that can be expelled forcefully after a maximal inspiration. FVC is affected by both environment and by occupation. Athletes and individuals in physically demanding occupations will have FVCs that are higher than normal (normal being the predicted values for an individual of certain height, age, weight, and race). FVC also indicates the degree of lung and chest expansion, since it measures the total amount of air that can be blown out as quickly as possible after inhaling as deeply as possible.

3.2.3 “Normal” or “Predicted” Values Before reviewing the various lung function tests in common use today, it is necessary to understand what the “normal” values are and how they were derived. The normal or predicted values for the tests described here were derived from specific samples within the population. This is done to help assess whether or not there is an abnormality and the degree of abnormality in comparison to what are deemed normal values. Cross-sectional studies are typically used to develop normal or predicted values from cross- sectional data, using a certain segment of the population—for example, boys aged 10 or women aged 40. These persons will have their pulmonary function tested, and their height, weight, and ethnic origin recorded. Their health needs will be established through questionnaires,

3 Measurements of Lung Function

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examinations, and perhaps X-rays. While smokers past and present will be excluded, it will be difficult to take into account (or compensate for) unpredictable factors such as brief environmental exposures, passive exposure to smoke, or brief illnesses. The values for the whole population under study will then be analyzed to obtain a mean and a standard deviation. Longitudinal studies, where a population is identified, defined, then followed, and studied at pre-defined intervals for a number of years, may give more accurate results than cross-sectional studies. The values and readings obtained are most useful for documenting changes that occur over the years—at times of growth, for example, or with aging [5, 6]. However, while results from longitudinal studies are preferred, those from

cross-sectional studies may be the ones actually in use. Care should hence be taken when using, at the same time, data that has been acquired through both methods. Determination of normal lung function values for a specific individual is hence not easy. Most laboratories arbitrarily assume that a person has abnormal readings if these are less than 80% of the predicted values. It would be much more accurate and useful to assume that the lowest 5% of population values are abnormal, but such an approach is overly complex for routine use. On the other hand, tracking the lung function values of any one individual over time will provide an idea of their “normal.” Table 3.1 provides definitions, abbreviations, an overview of the terminology, and the methods

Table 3.1 Measures of pulmonary function Lung volumes Four primary volumes do not overlap. They are measured in liters Abbreviation Name Definition VT

Tidal volume

IRV

Inspiratory reserve volume

ERV

Expiratory reserve volume

RV

Residual volume

Volume of gas inspired or expired during each respiratory cycle Maximal amount of gas that can be inspired from the end- inspiratory position Maximal volume of gas that can be expired from the end expiratory level Volume of gas remaining in the lungs at the end of a maximal expiration

How measured Spirometer

Clinical application in asthma Limited use

Spirometer

None

Spirometer

None

He dilution, plethysmograph

Lung volumes Each includes two or more of the primary volumes, measured in liters Abbreviation Name Definition How measured VC or FVC

Vital capacity

TLC

Total lung capacity

IC

Inspiratory capacity

FRC

Functional residual capacity

Maximal volume of gas that can be expelled from the lungs by forceful effort following a maximal inspiration (IRV+ VT + ERV) Amount of gas contained in the lung at the end of a maximal inspiration Maximal volume of gas that can be inspired from the resting expiratory level (IRV + VT) Volume of gas remaining in the lungs at resting expiratory level (RV +ERV)

Spirometer

He dilution, plethysmograph Spirometer

He dilution, plethysmograph

May be useful, but generally used in referral laboratories

Clinical application in asthma Common, useful

Special situations

Rarely used

Special situations

(continued)

3.3 Spirometry

61

Table 3.1 (continued) Forced expiratory volumes and flows Abbreviation Name Definition FEV1

FEF25-75 or MMEF

FEFmax or PEF

MEFV

Clinical application in asthma Spirometer and liters Most useful test in Volume of air exhaled in 1 Forced both diagnosis and second starting from a full expiratory continuing inspiration volume in one assessment second Spirometer and liters Wide range of Volume of air in mid-flow, that Forced values limits mid-expiratory is, the first 25% and last 25% are usefulness. See text “discarded” in the last flow for details measurement Can be easily and Maximal flow in forced Spirometer and liters FEF Maximal exhalation Peak flow meter (PFM) in frequently forced measured. Wide liters/min expiratory flow/ range of normal Spirometer/Can be easily and frequently measured, wide range of normal PEF/Peak expiratory flow rate/fastest rate air leaves lungs after full inspiration/Can be easily and frequently measured, wide range of normal Useful in giving a Spirometer with Maximal visual impression of simultaneous expiratory obstruction, and in measurement of flow flow-volume differential curve diagnosis

Ratios Abbreviation Name FEV1/FVC Ratio of FEV1 and FVC

How measured Spirometer

Other measures of pulmonary function Abbreviation Name How measured Raw Dco SaO2

Airway resistance Diffusion capacity O2 saturation

Plethysmography and pneumotachograph Inhaled CO (carbon monoxide) is measured in expired air Pulse oximetry

How measured

Clinical application in asthma Very useful. Lung size varies considerably, mainly due to age, gender, and height, and this allows partial corrections Unit Cm/H20/liters/sec

Clinical application In asthma Special situations only

MICO/min/mmHg None

Useful in acute asthma and exercise testing

3 Measurements of Lung Function

62

used for assessment and measurement of lung function. It also indicates the practical usage of each measurement.

3.3

Spirometry

Spirometry is a laboratory test that has stood the test of time. It was invented in 1844 by John Hutchinson, a British surgeon. He published his first paper on the subject in 1846 after he had measured 2,130 individuals. He also coined the phrase “vital capacity” and related it to disease [7]. Today, FEV1 and FVC measured with a modern spirometer, either physically or electronically, are the most useful measures of lung function. Traditional spirometers are machines that measure inhaled and exhaled volumes of air. They combine mechanical components (which measure volumes of air) and computer software (which performs the various calculations). In the best spirometers, the software includes tested and reliable predictive algorithms. The technologist enters the necessary data (age, gender, height, race, whether or not a smoker), and the software then computes a normal predicted value for that individual, given the available information. It should be remembered that a number of factors are not fully considered by the equipment and the predictive equation, including genetic characteristics; past and present general health; environmental exposures other than smoking; present or former occupation; type of residential premises with exposure to airborne environmental hazards; and socioeconomic status [8, 9]. The use of spirometry has been revolutionized by the availability of fully electronic spirometers. These can calculate airflow rates in the channel into which the person blows using a transducer or by measuring pressure differences in the channel. These devices are very accurate as they do not have moving parts and hence no resistance errors. In essence, the software is the spirometer. As will be discussed later, they are ideal for home monitoring and detecting trends over time [10].

Airflow varies with a number of factors, of which the dominant one is height. Hence, as children grow, airflow increases. In adulthood, pulmonary function tends to peak between the age of 30 and 35 in men and around 30 in women and then declines. This change in age is independent of health. It can be hastened by a number of diseases, including asthma, genetic factors, and adverse exposures, the most important of which is smoking [11]. Differences in pulmonary function also exist between ethnic groups, but these are not easy to estimate or even to understand [12, 13]. For example, studies have shown that the reference values for Caucasians can be satisfactorily used for American Indians [14]. The National Health and Nutrition Examination Survey (NHANES) III provides predicted readings for males and females between the ages of 6 and 75 for Caucasians, African-Americans, and Mexican Americans in the USA [15]. However, reference equations need to be adjusted for different ethnic groups, for instance, by 12% for Asian-Americans [16]. It is also not easy to define clearly what is meant by “ethnic group,” and differentiating between one group and another can be difficult. In addition, although some ethnic differences are related to lung size (i.e., to the ratio of trunk length to total height), part of the ethnic differences will also be explained by differences in socioeconomic status. All of these factors are particularly important when considering African-Americans. Ethnic differences do exist between this group and Caucasians, but even without intermingling between populations, genetic differences are extremely minute. Much of the difference between Caucasians and African-Americans is due to the greater incidence of socioeconomic problems in the latter. The same consideration of genetic difference and socioeconomic difference applies to other apparently “distinct” populations. The position is even more confused with individuals who reside in North America but were born elsewhere. Because of the interconnections and complexities, the standard used for peak flow meter

3.3 Spirometry

readings is the individual’s own personal best [17]. As will be mentioned later, it is one measurement that depends on the effort expended by the person with asthma, but there is, unfortunately, no real way to control or assess that effort. A successful spirometry test demands a great deal of cooperation from the person being tested. For this reason, it can be difficult to perform when other illnesses are present or the individual is very young or elderly. In terms of lower age limits, most pulmonary function laboratories expect that children above the age of 6 will be able to do the test with minimal guidance, and they may use the same equipment for them as for adults. However, if “adult” equipment is used in children, the dead space may introduce inaccuracies. It requires a great deal of effort to obtain accurate readings from the very young. Reproducible spirometric results have been obtained from carefully coached children aged between 3 and 6 years by technologists trained and experienced in testing children [18]. However they require more teaching and more time to become comfortable with the equipment and to practice blowing through unattached mouthpieces. Special techniques, such as incentive games [19], can help bring about success, but even with these aids, only a minority of children successfully manage spirometry [20] (Figs. 3.2, 3.3 and 3.4). Today’s spirometers measure flow and calculate volumes electronically and are very accurate. Less expensive portable devices are also available for office use. Spirometry can be used for [8, 21–23]: Diagnosis • To evaluate symptoms, signs, or abnormal laboratory test results • To measure the physiologic effect of disease or disorder • To screen individuals at risk of having pulmonary disease • To assess preoperative risk • To assess prognosis

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Fig. 3.2 Child performing spirometry

Fig. 3.3 Portable digital spirometer. (Spirometer © Medical International Research. Used with permission)

Fig. 3.4 Handheld digital spirometer. (Spirometer © Medical International Research. Used with permission)

Monitoring • To assess response to therapeutic intervention • To monitor disease progression • To monitor patients for exacerbations of disease and recovery from exacerbations • To monitor people for adverse effects of exposure to injurious agents

3 Measurements of Lung Function

64

• To watch for adverse reactions to drugs with known pulmonary toxicity Disability/impairment evaluations • To assess patients as part of a rehabilitation program • To assess risks as part of an insurance evaluation • To assess individuals for legal reasons Other evaluations • • • •

For research and clinical trials For epidemiological surveys To derive reference equations For preemployment and lung health monitoring for at-risk occupations • To assess health status before beginning at- risk physical activities In its Expert Panel Report 3, the National Asthma Education and Prevention Program (NAEPP) [17] recommends spirometry both in initial assessment of asthma and later, after symptoms and peak flows have stabilized. It also suggests that while a handheld peak flow meter can be used as a diagnostic tool, the meter, with all its drawbacks, is best employed for monitoring changes in asthma in one individual over time. EPR-3 recommends that spirometry be done every 1 to 2 years to monitor and provide an ongoing assessment of airway function [17, 24]. Baseline spirometry provides a very accurate snapshot of the degree of airway obstruction caused by asthma and hence its severity at that specific moment. The likelihood of dying from asthma is increased among those who underestimate their personal degree of airway obstruction [23]. Hence routine pulmonary function testing should be a part of both the assessment and monitoring of acute asthma. It should also be used on a periodic basis to assess lung function in all people with asthma [1, 17]. Ruppel and Enright [24] point out that accurate results depend on three factors: having a spirometer that is accurate and precise; a person

who can perform “acceptable and reproducible measurements”; and “a motivated technologist to elicit maximum performance from the patient.” At the beginning of the lung function test, the technologist enters all necessary personal and environmental data, such as date of birth, both height and weight without shoes, race, smoking status, time of day, humidity, air pressure, and room temperature [8, 9, 25]. The technologist will then coach and encourage the person through several steps. The following sequence must be observed. The person must • Take several normal breaths. • Inspire, as deeply as possible, to maximal inspiration. • Place the mouth around the tube connected to the spirometer. • Exhale with maximum effort, blowing as hard as possible. • Keep exhaling (“squeezing”) till no more air can be exhaled. • Take a hard, deep breath. A noseclip is optional. In closed-circuit spirometers, the individual may take five tidal breaths before taking a maximal inspiration from the reservoir and then blowing out rapidly till the end-of-test criteria are met. With the smaller, computerized portable machines, test results are available only after the test has been completed; larger laboratory machines tend to provide progressive results in real time, as they become available. The technologist watches the subject and decides whether the test is acceptable or not. If it is, the technologist obtains a printed report that shows the results in both numerical and graphical form. This report is a spirogram. Two graphs are usually available, and both should be requested: • The Flow-Volume Loop • The Volume-Time Graph. Spirometry measurements of lung volumes are expressed in liters or milliliters at normal body temperature (37° C), and ambient pressure

3.3 Spirometry

and saturated with water vapor [4]. The spirometry readings most frequently requested for a diagnosis of asthma are listed and explained next.

65 Table 3.2 Pulmonary function in asthma FEV1 ↓ PEF ↓

TLC ↑ RV ↑

3.3.1 FEV1, FVC, and FEV1/FVC The FEV1, FVC, and the ratio FEV1/FVC ratio should be considered together and are the most important measurements in both initial and continued assessment of asthma. The concept of FEV1or “degree of narrowing of air passages” is readily understood by most people with asthma. The ratio FEV1/FVC is always a fraction (less than 1.0) and is a useful crosscheck on the accuracy of FEV1 normal values. FEV1values require careful scrutiny. An FEV1 of 100%, while within the predetermined normal limits for FEV1, may still indicate obstruction. In this example, if the FVC is 130, then the FEV1/ FVC ratio is 100/130, which is 0.77, or 77% when expressed as a percentage. Because it is a ratio, FEV1/FVC provides an automatic correction for lung volume. No “normal” or predicted values exist for the FEV1/ FVC. Further, the American Thoracic Society (ATS) has not set a lower “normal” limit since both values are directly affected by both the age and the height of the person [24]. The FEV1/FVC ratio is generally above 80%, and values below this may well be indicative of obstruction. In severe airway obstruction, many airways will close prematurely and FVC will be reduced. While the FEV1/FVC is reliable, even here caution is needed. The FEV1 and the FVC are inversely related to age and height. If a fixed value is used, older individuals are more likely to be considered abnormal [24]. Most modern spirometers measure additional volumes during the forced expiratory maneuver. In asthma, both the residual volume (RV) and the functional residual capacity (FRC) tend to be higher than normal predicted values [26]. See Table 3.2. Some general points are worth mentioning.

• A healthy adult will exhale about 83% of the FVC in the first second, 94% in 2 seconds, and about 97% in the third second [27]. In asthma, these volumes are all reduced. • For people without lung disease, FEV1 is greater than 3.0 liters for men and greater than 2.0 liters for women [28]. However, any value must take into consideration the age (age causes a reduction in FEV1 due to decreased elastic recoil), ethnicity [23], and whether the person smokes tobacco. Smokers often have airway obstruction, and FEV1 values may well be about 15% lower than nonsmokers, if they feel well [26]. • In asthma FEV1will be reduced when there is airway obstruction, but FVC is maintained unless the asthma is particularly severe. (There may be difficulties in exhaling due to narrowed airways.) Typically, an FEV1 of 80% or less is considered indicative of airway obstruction. • In moderate airway obstruction, expiratory airflow is decreased. When air is trapped in the lungs, the FVC will have a higher value than predicted. The FVC normally declines with age, so that elderly persons without airway obstruction will have a ratio below 70% to 80%. FVC is indicative of both lung and chest expansion with maximal inhalation and rapid maximal exhalation. It is a good indicator of individual effort. • Children may have ratios greater than 90% [23].

3.3.1.1 Forced Expiratory Flow Maximum (FEFmax) This measurement is often represented as the peak expiratory flow (PEF) which is the highest instantaneous flow achieved during the FVC maneuver.

66

3.3.1.2 Forced Expiratory Flow25-75 (FEF25-75) This is a subset of FEFmax. FEV25-75 is the average flow rate over the middle 50% of the FVC. It is usually calculated electronically by excluding the first and last 25% of the FVC (hence the “25-75”). At the start of a forced exhalation, air is expelled from the lungs and trachea. At the end of the forced exhalation, the individual attempts to “squeeze” all the air out of the lungs. The first 25% is an approximation of anatomical dead space, and the value of the last 25% from the smaller airways becomes difficult to interpret in moderate to severe airway disease because of the asymmetric closure of the smallest airways. It has been suggested that this particular measurement provides some idea of small airway function, but this is a questionable assumption, and it probably adds little in the way of useful information [29]. The FEV25-75 is most useful in research and in cases where there are equivocal values in the FVC. The FVC is always effort-dependent. FEV1, FVC, and their ratio remain the primary guide to disease severity. It is recommended that FEV25-75 “should not be used to diagnose small airway disease in individual patients” [8]. 3.3.1.3 Expiratory Flow200-1200 (FEF200-1200) This is also a subset of FEFmax. The first 200 ml exhaled during the FVC maneuver and any gas exhaled after 1200 ml are not included in the calculation. This measurement is very similar to the FEF25-75 in its intent and provides similar help in interpreting results. It is probably not required in most cases, but computerized spirometers generally compute and display this and other values automatically.

3 Measurements of Lung Function

individuals a visual depiction of their reading. It does not give a numerical value. The characteristic shape of this curve, with obstruction in mainly medium-sized airways as in asthma, is shown in Fig. 3.5. Some abnormalities have a characteristic pattern, and the flow- volume loop may also provide clues to the presence of other diseases such as vocal cord disease or large airway obstruction due to tumor. A normal flow-volume loop should show the expiratory flow rate as a rapid rise with a gradual decline in flow back to zero. The inspiratory section of the loop is shown in the negative area of the flow axis as a deep U-shaped curve. In airway obstruction both the inspiratory and the expiratory section of the flow-volume loop changes. See Fig. 3.5. There is a rapid peak expiratory flow (PEF), but the gradual decline is replaced by a curve with a concave shape indicative of a marked decrease in FEF25-75. The inspiratory flow, shown below the x-axis, is shallower, indicative of a reduction in inspiratory volume. In more severe cases of asthma, the peak becomes sharper, and the expiratory flow line drops precipitously. The concavity of the downward slope is an indication of the severity of obstruction. See Fig. 3.6. The flow-volume loops provide information about the effort involved. The two figures above show a well-defined peak indicative of good

3.3.2 Flow-Volume Loops The flow-volume loop provides visual representation of flow. It can help in determining whether a valid test has been done and additionally gives Fig. 3.5 Flow-volume loop for person with asthma

3.3 Spirometry

Fig. 3.6 Spirogram showing severe obstruction

Fig. 3.7 Unacceptable spirogram (example 1)

effort [29]. Unacceptable efforts (see Figs. 3.7, 3.8, and 3.9) are usually indicated by: • Lack of normal early peak, indicative of variable effort • Sharp, abrupt downward slope in the expiratory curve, indicative of premature termination • Sharp spikes in the downward portion of the expiratory curve that indicate cough Spirograms are not acceptable when they have been terminated early due to cough, or if a full inspiration was not taken at the start of the procedure, resulting in inconsistent forced exhalation. An examination of the flow-volume loop provides a good indication of the quality of the spirogram.

67

Fig. 3.8 Unacceptable spirogram (example 2)

Fig. 3.9 Unacceptable spirogram (example 3)

3.3.2.1 Volume-Time Curves The normal volume-time curve shows a rapid upslope that peaks and flattens (reaches a plateau) shortly after exhalation. Figures 3.10, 3.11, 3.12, and 3.13 depict differences between volume-time curves for normal airways and for airways that have either mild or severe obstruction and restrictive disease. Sample FEV1 and FVC values have been provided without reference to age or height. In asthma, the slope is milder or less steep, with a gradual increase to the point of maximum volume. Figures 3.14 and 3.15 show acceptable and unacceptable volume-time curves. Figure 3.14 depicts an acceptable effort and shows the curve both before and after bronchodilator use, with the FEV1 marked. Figure 3.15, on the other hand, shows a delay in exhalation, which makes the

3 Measurements of Lung Function

68

Fig. 3.10 Volume-time curve for person without asthma

Fig. 3.13 Volume-time curve showing severe restriction

Fig. 3.11 Volume-time curve showing mild obstruction

Fig. 3.14 Volume-time curve showing both pre- and post-bronchodilator volumes

Fig. 3.12 Volume-time obstruction

Fig. 3.15 Unacceptable volume-time curve

curve

showing

severe

3.3 Spirometry

result unacceptable. Figure 3.15 may indicate that too much air had escaped prior to the maximal effort being made. D’Angelo and others showed that in normal subjects, a 4- to 6-second delay after inhalation and prior to exhalation caused a reduction of 4 to 5% in both FEV1 and PEF [30].

3.3.2.2 Technical Requirements for Spirometry The asthma educator may or may not perform spirometry themselves on people with asthma. Nonetheless, it is essential that they understand the technical aspects of this particular test. As pointed out earlier, the results obtained by spirometry are only as good as the equipment, the effort of the individual, and, most importantly, the skill and expertise of the technologist who supervises the test and coaches the person. Results are always effort-dependent, and it is important that there be a good relationship between the technologist and the person being tested. 3.3.2.3 Criteria for Acceptability The American Thoracic Society (ATS) and the American Association for Respiratory Care (AARC) have developed specific criteria for acceptability [8] of spirometry tests: • Number of trials. A minimum of three acceptable trials is required. • Acceptability. To be considered acceptable, each trial must meet all three of the following conditions: 1. There must be no false start, hesitation, coughing, or early termination of exhalation unless the individual can exhale no further. 2. The extrapolated volume must be less than or equal to 5% of FVC, or 150 ml, whichever is greater. 3. A rapid rise to start time is also required, and the test should last at least 6 seconds and give evidence of maximum effort by the individual [31]. • Reproducibility. The two largest FVC and FEV1 readings should not vary by more than 0.2 liters. The largest values for FVC and FEV1 should be selected, regardless of the test used.

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Individual Factors At times, individuals with asthma will be unable to meet these criteria for a number of reasons. They may: • Be physically unable to carry out the instructions • Not understand the instructions • Have poor motivation, general ill health, or physical impairment • Be at the extreme age limits (too young or too old) Differences in environment (including air pollution), nutrition, physical activity, and socioeconomic factors all affect lung function [8]. So does smoking, which reduces FEV1 and causes an annual rate of decline greater than caused by normal aging [32, 33]. Hence, for each test, information on the person’s gender, age, height, weight, race, and smoking status must be provided. The Technologist Spirometry is not yet at the point where the equipment operates autonomously (by itself). The technologist needs skills, both interpersonal and technical, in order to obtain accurate spirograms. The technologist must: • Help the subject perform the test correctly. This can require interpersonal skills, patient coaching, encouragement, and similar supportive actions. • Be able to assess the individual’s effort, since the test is effort-dependent. In addition, the technologist requires certain technical skills. These include [8] the ability to: • Demonstrate the FVC maneuver to the individual. • Coach the person so that the onset of the maneuver begins with an exhaled “blast.” • Observe the person through the entire maneuver. • Provide positive feedback to encourage the individual to provide a maximal effort.

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• Monitor the various attempts and select the best of them for use. • Calibrate and maintain the test equipment according to the manufacturer’s directions. • Ensure that all necessary health precautions are taken. Factors Affecting Reproducibility Consistent and reproducible results require consistent and proper technique. There will be a lack of reproducibility if the individual’s efforts are inconsistent; there is an air leak in the equipment; or the mouthpiece is obstructed. Reproducibility may deteriorate after repeated efforts due to fatigue or bronchospasm (tightening of the airways). In any case, after eight attempts to perform a single acceptable maneuver, the test should be discontinued. The technologist must be able to judge the quality of the tests and decide whether or not more teaching is desirable, depending on the person’s condition and tolerance. Body Position Body position affects air volumes. Readings drop by 7 to 8% when supine and by a 1% to 2% loss when sitting as compared to standing. For obese individuals, standing is particularly helpful [8]. Persons with asthma may sit or stand, but whatever the choice, the same position should be used through the test. They should preferably stand and begin with a deep full inhalation; then, with maximal effort, they should provide a full and forceful exhalation. The exhalation should proceed from a normal “blowing out” to a “squeezing out” for a complete FVC maneuver without coughs and/or extra breaths. Lack of a full inspiration, a less than maximal effort, excessive variability between efforts, and too short an effort are also considered unacceptable. As an aside, it is worth noting that prior to 1994, the AARC considered instrumentation to be the major source of variability; since then, the major source of variability has been attributed to improper performance. AARC’s Clinical Practice Guidelines recommend that spirometry be administered by trained technologists under the direction of a healthcare

3 Measurements of Lung Function

professional specifically trained in pulmonary function testing. Interpretation of the results demands careful attention to the equipment used, the person’s performance, and the reference values that are chosen [28, 31–35]. Unlike measures of peak expiratory flows, spirometry is a useful tool for assessing progress, particularly in those persons whose lung function is compromised, or in the elderly, or in individuals with a chronic obstructive lung disease (COLD) such as emphysema or chronic bronchitis. In these cases peak flows tend to be higher than their corresponding reduced spirometric values [23].

3.3.3 Bronchodilators in Pulmonary Function Testing Since asthma is characterized as having reversible airway obstruction, use of spirometry over time may indicate whether or not the disease can be reversed. It is standard practice in most laboratories to administer a bronchodilator if the FEV1/FVC ratio or FEV1 is below a predetermined value, perhaps 10% below predicted normal. Spirometry is repeated between 5 and 10 minutes after the bronchodilator has been given, and the degree of change (in the result) is used to determine whether or not the person is responding to the bronchodilator. However, the exact type and degree of change that should be observed is a matter of some debate. This is not surprising, as bronchodilator response depends not only on changes in smooth muscle but also on activity in the airway epithelium and nerves and on mediator production and blocking. Further, individual bronchodilators may vary in their effectiveness from person to person. Values obtained from the post-bronchodilator test may be expressed as a percentage of initial spirometric values (FVC and FEV1 expressed as a volume), as a percentage of initial predicted baseline, or as an absolute change. Most often, the reading provided shows the percent change against the initial predicted baseline value. Here again, there is debate on how

3.4 Measures of Lung Function

big the change should be. Values of 8% or less are within the normal tolerances of the equipment. The ATS suggests 12–15% [8] as a meaningful change, while the American College of Chest Physicians has suggested 15–25% [36]. Also, the reason for the test may affect the criteria: bronchodilator reversibility may be done as a diagnostic test or, in someone with known asthma, to see if a bronchodilator will improve pulmonary function. Reversibility is the hallmark of asthma. If someone has poor lung function, specifically a low FEV1 or FEV1/FVC, and exhibits an improvement after bronchodilator, reversibility has been demonstrated. This usually confirms a clinical diagnosis of asthma. The initial measurement is done before bronchodilator. Bronchodilators may give immediate systematic relief, but most laboratories wait 15 minutes after inhalation of a bronchodilator before repeating spirometry or peak flow. Reversibility after inhalation is not shown when the inhaled drug is a corticosteroid and is not seen with the long-acting beta-2 agonist salmeterol, although it is seen with the long-acting beta-2 agonist formoterol. Reversibility should not be measured if a bronchodilator has been taken immediately before the test. A number of hours must elapse before the test can commence. AARC guidelines suggest the following waiting times for various drugs: • • • • •

Salmeterol 12 hours Ipratropium 6 hours Terbutaline 4–8 hours Albuterol 4–6 hours Metaproterenol 4 hours

Most laboratories use either albuterol or the subject’s personal bronchodilator. While an improvement in the range of 15–20% is usually accepted as satisfactory [37], it is important to look at as much information as possible. In other words, the FEV, the FEV1/FVC, and shape of the flow-volume curves should all be examined. Changes in any one of these may help to identify those individuals with reversibility.

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3.3.4 A Pulmonary Function Test and Its Interpretation Figure 3.16 presents the results of a pulmonary function test. These are interpreted in Fig. 3.17.

3.4

Measures of Lung Function

The various measures of lung function used in asthma are presented below.

3.4.1 Peak Flow Measurement FEFmax (or peak expiratory flow) is the maximum rate at which an individual can expel air from the lungs. It can be measured using either an electronic spirometer or a handheld peak flow meter (PFM). The spirometer measures FEFmax in liters per second, while the PFM measures peak expiratory flow (PEF) in liters per minute; therefore, conversion from FEFmax to PEF requires multiplication by 60. Given the difference in sophistication between the two types of equipment, however, and the marked differences in technique, the translation of PEF (taken by a handheld PFM) to FEFmax is not advisable [23, 38–40]. The PFM gives values at ambient temperature, while spirometers correct values to body temperature. In addition, reference values would need to be correlated with the specific brand of peak flow meter; currently, these values are not available [17]. Where spirometry is unavailable, serial measurement of peak flow over 1 to 2 weeks may be used to demonstrate variability, particularly in those individuals where asthma is suspected but the spirogram was normal [17]. While changes in PEF may parallel changes in FEV1, PEF is less sensitive in detecting bronchoconstriction, is more effort-dependent, and is less reproducible [41]. Being essentially mechanical devices, individual PFMs lose their accuracy over time. FEFmax may be compared against a PFM reading to determine whether the PFM is working correctly or needs replacing.

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Fig. 3.16 Pulmonary function test results

3 Measurements of Lung Function

3.4 Measures of Lung Function

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Interpretation of Pulmonary Function Test Results (Letters shown below refer to corresponding entries in the charts) A sample Pulmonary Function Test (PFT) result is shown on in Figure 3-14. The results sheet is explained below. Preliminary Information A, B, C, F and G This information is used to calculate normal values. D

Location at which the diagnosis was made

E

The date is extremely important and often over-looked when scanning reports.

G

This is the patient’s age.

[2,3] Items marked [2] are actual pre-measures and are also given as a percentage in [3]. This adolescent female therefore has severe obstruction with an FEV1 of 23% of predicted before bronchodilator, FEV1/ FVC at 50 %, and FEF25-75 at 8%. The PEF is given for comparison, but this should not be used for general PEF values. Instead, a Peak Flow meter should be used. [4, 5] The post-bronchodilator measures [4] and the post-bronchodilator percentage values [5] show the improvement. However, they do not reach normal since FEV1 is still only 52%, and the FEV1/FVC has only risen to 60%.

Flow Volume Curves [6] It is worthwhile examining the time volume curve and the flow volume curve. The time volume curve shows the prolonged expiration, and the difference pre-and post-bronchodilator. The flow volume curve shows the characteristic scooped shape of airflow obstruction. Although there is improvement after administering the bronchodilator, the forced curve covers the circle in the center (the tidal breath), showing that some obstruction remains after treatment.

Post-bronchodilator [6], impressive changes have occurred, but their size reflects the fact that the baseline was so low. Explaining the PFT Unless qualified to do so, the asthma educator may not interpret the findings of the test. However, the asthma educator should explain the following to the patient: •

• Technologist’s comments The technologist’s comments (9, 10, and 11) are also very important. They are entered after the test has been completed. Lung Mechanics [1] These items give the reference volume in liters for someone of this weight, height, gender and age.

Fig. 3.17 Interpretation of pulmonary function test results

• •

•

the PFT shows that the patient has asthma and that it is currently severe persistent (FEV1 is 60%). the test is a ‘snapshot’. It shows how the lungs are functioning at the time the test was conducted. the test is the basis for determining the medication that will be prescribed. the test will be kept on file, and will be Compared against subsequent PFTs to see how well the prescribed medication is working, and how well the patient is responding. if the medication is taken, then there is hope for improvement.

3 Measurements of Lung Function

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Despite its limitations, the PEF may be a useful measurement in strictly limited circumstances. Nowadays spirometry can be done with a portable electronic device such as a laptop. Results of PEF are most likely to be valid when the person is confident, makes a full effort, and can be followed over time. A successful effort with a PFM is one that is both effort- and volume- dependent [42]. The individual must be encouraged to take a full inspiration and to then exhale as vigorously as possible since optimal peak flow is achieved in about one-tenth of a second. Hence a prolonged exhalation is not necessary. The peak flow meter measures how fast, not how long, an individual can exhale (Fig. 3.18). PEF usage should be taught by a person who is skilled in the procedure; in addition, the individual’s PEF technique and readings should be reviewed at every visit. Single measurements may miss clinically important changes in function, particularly in children [43–45]. Performance of a peak flow maneuver initially requires both an explanation and a demonstration by a trained person such as the asthma educator. The sequence of steps includes: • • • •

Setting the indicator on the PFM to zero Standing up straight Taking a rapid and complete inhalation Placing the PFM between the teeth, on the tongue, with lips sealed around the mouthpiece

Fig. 3.18 (from left to right) Pediatric, youth, and adult peak flow meters

• • • •

Exhaling with maximal force Noting the pointer’s new position Recording the reading (PEF) Repeating the maneuver for a total of three attempts and recording each reading

PEF readings can easily be manipulated in many ways by individuals with asthma. These include: • Spitting into the device • Flicking the pointer quickly with a finger • Flicking the tongue or blocking the mouthpiece with the tongue • Incorrectly placing the mouthpiece in front of the teeth and tongue They may also fail to reset the pointer before taking a reading. And there exists the possibility that the numbers recorded on the chart may be a figment of the imagination. Ideally, the person using a PFM should be conscientious and honest. Despite the known problems that can occur with PEF, the test can be performed with low- cost equipment in the office, clinic, or home, provided the potential for loss of accuracy is recognized and accepted. While tables of normal rates exist (see Figs. 3.26 and 3.27 at the end of this chapter), they were measured for Caucasians, and other ethnic groups will have different rates [12, 46]. There can be a very wide variation from one person to another, and each individual’s PEF reading (PEFR) needs to be reviewed periodically to determine his or her best reading. When individuals with asthma are followed over time and know their best PEFR, such factors diminish in importance. Consider, for instance, the case of a 16-year-old male student, 5 feet 10 inches (180 cm) in height, with a predicted peak flow of 475±75 l/m. This young man went to a clinic complaining of shortness of breath and chest tightness. When tested, he blew 480 l/m on his peak flow meter, which was higher than the predicted 475±75 l/m. However, further questioning revealed that his normal PEFR was 650 l/m and that he played soccer, ice hockey, and a

3.4 Measures of Lung Function

(musical) wind instrument. Thus this student was at 74% of his personal best and experiencing symptoms, and this was indicative of loss of control of asthma. Hence the need to obtain some personal background information and to determine the individual’s personal best reading, before making a judgment. The educator must seek immediate medical help for any adult whose PEFR is less than 180 l/m and must ensure that the individual understands the severity of the situation with such a low PEFR.

3.4.1.1 Calculating Reversibility The degree of reversibility may be calculated using readings obtained through a peak flow meter. A PEFR should be taken, following which a short-acting bronchodilator should be administered. After a 15-minute wait (which is sufficient time for it to work and achieve maximum effectiveness), a second reading should be taken. The degree of reversibility is then calculated by dividing the second PEFR by the first PEFR. The answer should be greater than 1 and in the form “1.xx”. The number in front of the decimal point should be ignored. The two digits after the decimal point give the percentage of reversibility. For instance, a person who blows 320 l/min before and 360 l/min after the bronchodilator would have a degree of reversibility of:

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this twice-daily testing is done over a period of time, those with asthma will show an exaggerated morning to evening variation and other variabilities in PEF throughout the day and from one day and another. See Fig. 3.19. Ambulatory monitoring through peak flows is a useful diagnostic tool, with PEF recorded in a diary preferably for 2 weeks. When there is a variability of >13% in children and >10% in adults, requirements for physiologic reversibility have been met. These changes are in keeping with asthma. Peak flow readings will often show a distinct and helpful pattern. Those with poorly controlled asthma will show at least 20% variability between morning and afternoon readings (with “afternoon” defined as being between noon and 2 p.m.) [17].

3.4.1.3 Calculating Diurnal Variability Diurnal variability is calculated using a formula recommended by the NAEPP [6]. It is expressed as the daily amplitude percent mean. That is,

max daily PEF min daily PEF 100

Mean PEF

The educator can easily perform this calculation. For example, a person reports a morning PEF of 370 and evening PEF of 330. Using the formula above, the diurnal variability is calculated as

360/320 = 1.125, that is, 12.5%. If the “after” PEF is 380, then the degree of reversibility would be 380/320, which is 1.1875, or 18.75%.

3.4.1.2 Diurnal Variation Pulmonary function varies throughout the day, whether or not there is lung disease, being lowest overnight and highest between noon and 4 p.m. [40]. This daily variation is exaggerated in asthma. The diurnal variation can be shown when individuals with asthma use PFM at home, measure PEF in the morning, record results in a diary, and repeat the measurement in the evening. When

Fig. 3.19 Peak flowchart showing daily variation

3 Measurements of Lung Function

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370 330 100 4000 11.43% 370 330 2 350

A variability of 12% or less in daily readings is acceptable. However, if the lower reading is 320, then the diurnal variability changes:

370 320 100 5000 14.49% 370 320 2 345

This is close to 15%, which is indicative of asthma that is not in control. If the lower reading were 300, then the formula would give a diurnal variability of 20.9%, which indicates uncontrolled asthma.

3.4.1.4 Consistency in Obtaining PEF Readings PEF tends to peak in the middle of the waking day. As mentioned earlier, it is important for individuals with asthma to take two or three PEF readings each time and to record the best, but it is equally important not to exceed three, since multiple attempts at PEF may induce reactivity and lead to a sharp fall in PEF readings. PEF readings should also be taken at the same times each day. For most individuals, this means a morning measurement, prior to any medication being taken, followed by an evening measurement, after a reliever medication has been taken [17]. Evening readings tend to be more convenient for most people. However, since the highest PFR occurs between noon and 2 p.m., an evening reading will tend to underestimate the diurnal variation. 3.4.1.5 PEF and Adherence While PEF readings are not as reliable as FEV1 [47], they can be very useful since they provide measurements over a period of time (days to weeks) of the person’s airway lability (openness and degree of obstruction) while in their natural setting. The readings can demonstrate the effects of allergens or viral infections and show the improvement in asthma with drugs such as inhaled steroids or oral corticosteroids. They can also be used in action plans to guide the individual’s response to deterioration, by being

used to indicate when to seek medical help and when to intensify treatment [43, 48]. Wide diurnal variability and significant bronchodilator reversibility can be used in the estimation of asthma control. Many individuals, however, will see the measurement exercise as a chore or nuisance and will not be enthusiastic about doing it regularly or frequently [49]. PEF use should hence be encouraged when there is a specific reason, so that they are more likely to cooperate. Figures 3.20, 3.21, and 3.22 illustrate typical real-life scenarios that the educator will encoun-

Fig. 3.20 Peak flowchart for person under good control, who gets a cold and develops symptoms after some days. There is a slow response after treatment is doubled

Fig. 3.21 Peak flowchart for a person with some degree of control who is exposed to a trigger, catches a cold, takes prednisone (an oral steroid), and then shows some improvement

3.4 Measures of Lung Function

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3.4.2 O ther Measures of Lung Function

Fig. 3.22 Peak flowchart of a person with poorly controlled asthma who responds to inhaled corticosteroids over several days

ter. Persons with asthma should be taught to recognize these situations, so that they can self-assess their health and the effectiveness (or otherwise) of their medication regime. Each diagram shows a distinctive pattern that starts with a decline in PEF values over a period of a few days. Intervention then occurs, after which an increase in consecutive PEF readings is observed. This is typical for an exacerbation due to an allergen exposure or viral infection. For many individuals, the PFM is a valuable and useful tool. For others, it is yet another irritating reminder of asthma and an additional burden on their lives. Hence, the educator should discuss PFM use with each person, rather than recommend it to everyone. It is worth remembering that people may be compliant in their use of the PFM in the short term, but not for prolonged periods of time [35]. In cases of mild to moderate asthma, the PFM does not provide helpful information when the person is well. When the person is ill, equally useful information may be gained by counting the number of extra doses of rescue medication used as by doing a PEF. Nevertheless PEF may be helpful for a limited time in some individuals [38, 50, 51]. The NAEPP Guidelines [13] strongly encourage the use of peak flow meters in individuals with moderate to severe asthma.

3.4.2.1 Fraction of Exhaled Nitric Oxide (FeNO) Nitric oxide is a biologic mediator produced by the lung. It plays a role in the pathophysiology of asthma and is present in exhaled breath. Measurement of nitric oxide, expressed as fraction of exhaled nitric oxide (FeNO), can be helpful in determining the degree of inflammation within the lungs. The FeNO test is noninvasive, simple, safe, and easily repeatable in individuals with severe airflow limitation. It can also be used in children. Normal FeNO levels are dependent on race, age, height, and sex, being higher in males [52– 54]. Levels of FeNO are lower in children, but increase as they age. Levels are also affected by atopy, disease severity, current therapy, smoking status, measurement technique, obesity, and other diseases. Higher levels are found in atopic individuals and lower levels in tobacco smokers [55]. FeNO correlates significantly with peripheral blood eosinophil counts in people with asthma; it can hence be used to distinguish between asthma and COPD [56]. FeNO is measured in parts per billion (ppb) using chemiluminescence analysis of exhaled breath. It is helpful in caring for individuals with asthma in that it can: • Aid in the diagnosis of asthma especially in those >5 years who are unable to perform spirometry • Detect eosinophilic airway inflammation –– therefore, a step in identifying the phenotype • Predict and monitor response to therapy • Evaluate a current exacerbation • Predict a future exacerbation • Evaluate adherence to medication regimen • Monitor response to anti-inflammatory therapy • Aid in titrating type and dose of medication to improve asthma control

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FeNO can also be used to screen people suspected of having asthma or individuals with nonspecific symptoms. It can also be a guide to further testing since those with asthma have increased exhaled NO levels compared to those without asthma [57, 58]. However, FeNO levels can be difficult to interpret, because they will depend on the individual’s age and weight, level of atopy, use of ICS or oral steroids, and asthma phenotype [59]. FeNO levels can also be used to determine the degree of sensitization of persons prone to occupational asthma. A prospective study by Wild and colleagues [60] of apprentices in 2-year programs for baking, pastry-making, and hair dressing found that in comparison with non-sensitized individuals, FeNO levels were • 83% higher in highly sensitized individuals • 30% higher in mildly sensitized subjects They concluded that the levels of sensitization were “early markers of airway inflammation.” The most recent recommendations [61] make it clear that FeNO has “a supportive role when the diagnosis of asthma is uncertain.” FeNO results should never be used on their own to diagnose asthma, but is a relevant adjunct test. The update comments on specific levels of FeNO: • FeNO levels of < 25 ppb (or < 20 ppb in children ages 5–12 years) are inconsistent with T2 inflammation and suggest a diagnosis other than asthma (or that the individual has asthma but their T2 inflammation has been managed with corticosteroids or they have non-T2 inflammation or non-eosinophilic asthma). • FeNO levels > 50 ppb (or > 35 ppb in children ages 5–12 years) are consistent with elevated T2 inflammation and support a diagnosis of asthma. Individuals who have T2 inflammation are more likely to respond to corticosteroid treatment. • FeNO levels of 25 ppb to 50 ppb (or 20–35 ppb in children ages 5–12 years) provide little information on the diagnosis of asthma and should be interpreted with caution and attention to the clinical context.

3 Measurements of Lung Function

• The specificity and sensitivity of the FeNO testing process depend on the clinical situation. However, in corticosteroid-naïve individuals with asthma, FeNO measurement is most accurate for ruling out the diagnosis of asthma when the result is less than 20 ppb. In this situation, the test has a sensitivity of 0.79, a specificity of 0.77, and a diagnostic odds ratio (OR) of 12.25. • Inhaled corticosteroid treatment should not be withheld solely based on low FeNO levels.

3.4.2.2 Dilution Techniques: Helium and Nitrogen As noted, there is always some air remaining in the lung, no matter how forcible or prolonged the expiration. This is residual volume (RV). RV is increased in poorly controlled asthma and creates mechanical disadvantages in respiration and hence an increase in the work of breathing. It cannot be measured by spirometers that give information about tidal volume, inspired and expired volume, vital capacity, and inspired capacity. Residual volume measurements require the use of either dilution techniques using helium (He) or nitrogen (N) or a plethysmograph. Dilution techniques using He or N work well if the gas in the lung communicates with major airways and hence with the gas in the mouth. They permit functional residual capacity measurement; when combined with inspiratory capacity from the spirometer, they also allow total lung capacity to be measured. If parts of the lung are blocked, such as by a mucus plug, and there is gas behind the mucus plug, then the dilution techniques will not give accurate values. Helium is an insoluble gas. It is not absorbed by the body and is not present in the lungs in life. For the dilution test, the individual breathes through the spirometer in a closed circuit. Then a known amount of He is inhaled, and then breathing continues until equilibrium is reached. During the process of reaching equilibrium, the volume of gas in the system remains constant as oxygen is abstracted in the alveoli. Oxygen is added to the mixture being breathed to replenish the amounts being removed by the alveoli, and carbon dioxide (CO2) is removed from the exhaled gas as it

3.4 Measures of Lung Function

appears. At the start, the volume and the concentration (percentage) of He in the spirometer are known, and therefore the amount of He can be calculated. At the end of the test, the percentage of He is measured, and this will be lower than the starting percentage because of dilution by FRC. FRC is then calculated using a simple formula. In the nitrogen washout test, the basic assumption at the start of the test is that air in the lung has the normal concentration of 21% oxygen (O2) and 79% nitrogen (N). The test commences with the individual breathing 100% O2 until the nitrogen in the lung is washed out, a process that usually takes between 6 and 8 minutes. The percentage of N is measured continuously in exhaled air, and therefore the amount of N in FRC is known. Since this is 80% of total FRC, FRC can be readily calculated.

3.4.2.3 Plethysmography The plethysmograph, or body box, gives very accurate information, not only on volumes and capacity but also on airway resistance. Its main component is the body box, which is a sealed, airtight chamber. The individual sits inside the body box wearing a noseclip and breathing through a tube passing out of the box. A known volume of gas is injected into the box at the start of the test, and the resultant pressure change is noted. At the end of exhalation, the breathing tube is shut by a valve. At this point the pressure at the person’s mouth is atmospheric and therefore known. The respiratory muscles try to work, but the closed shutter means that air cannot be breathed in and therefore the thorax enlarges. This simultaneously lowers the pressure inside the thorax and increases the pressure in the box around the person (because the individual’s body volume increases). To obtain its results, the plethysmograph relies on Boyle’s Law, which relates pressure to volume. The equation for Boyle’s Law is:

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V1 is the FRC and is the unknown that is to be measured. P2 is the final pressure at the mouth and is equivalent to alveolar pressure. V2 is FRC plus the change in lung volume (V). The plethysmograph can also be used to measure resistance. In any tube, including the airways, the driving pressure is related to the difference in pressures between one end of the tube and the other. This driving pressure overcomes resistance, which in the case of a gas that is made up of the viscosity of the gas and the tube size. Resistance is calculated as the pressure difference (between the inlet and outlet) divided by the flow rate. It is measured in centimeter H2O/L/sec. In normal adults at FRC, this varies between 0.5 and 1.5. Lung volume affects airway resistance, and airway resistance (RAW) is measured at FRC (Fig. 3.23). Conductance is the reciprocal measure of RAW and is also related to lung volume. Conductance is highest at high lung volume, is usually measured at known lung volumes, and is then called the specific conductance. Plethysmography is not required for routine diagnosis or assessment of individuals with asthma but can give useful information in special situations. It should be requested in those with airflow limitation and air trapping to check FRC and thoracic gas volume (TGV) or for a diagnosis of restrictive lung disease [8].

P1V1 = P2 V2

where

P1 is the pressure in the mouth, is atmospheric pressure, and is known.

Fig. 3.23 Plethysmograph, with child

3 Measurements of Lung Function

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3.5

Bronchial Challenge Testing

Challenge testing, also known as bronchial provocation [62], is used in diagnosis and research. It is essentially the opposite (or reverse) of the test for reversibility after the use of a bronchodilator. In challenge testing of individuals with normal or near-normal spirometric values, an inhaled substance (generally, methacholine) or a respiratory maneuver is used with the intention of causing some deterioration. For deterioration to be observable, a baseline reading or assessment must be present. Hence, it is important that any challenge test be done after an adequate clinical and spirometric assessment. Challenge tests are not only not needed in those with clear abnormalities on spirometry; they may be dangerous in this situation. While the procedure is safe in those with normal or near-normal pulmonary function, facilities should be available for treatment should there be unexpected severe deterioration [63]. Individuals should not be left alone during the test and a healthcare provider, skilled and able to treat bronchospasm, should be close at hand. Therapist safety is also a concern, and care is necessary to prevent staff exposure to the methacholine. Absolute contraindications to methacholine challenge include severe airway obstruction, such as FEV1< 50% predicted (although the challenge will give no useful information if FEV1 is 1000 ng/mL Central (proximal) bronchiectasis Elevated IgE and IgG to A. fumigatus

Not all of the above criteria need to be present to make a diagnosis. ABPA is usually suspected when there is pulmonary eosinophilia, or mucus impaction (mucus plugs containing A. fumigatus), or after skin and serologic testing. Repeated exposure and inhalation to A. fumigatus can activate the immune system to initiate the inflammatory cascade with immediate airway constriction and reduced lung capacity [129]. The long-term result could be chronic bronchitis, asthma, alveolitis, farmers’ lung, or mushroom workers’ lung. It is essential to begin treatment as early as possible because delays will result in

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irreversible pulmonary damage. Left untreated, what begins as local inflammation can, due to recurrent exacerbations, cause irreversible bronchiectasis and pulmonary fibrosis. During acute attacks, there may be loss of lung function due to mucoid impaction of the airways. In time, central bronchiectasis and pulmonary fibrosis develop. IgE levels can be used as markers for exacerbations and to assess the response to therapy. In later stages, CT scans are helpful to track changes within the lungs. The disease has been divided into five stages, though not all individuals progress through all five stages [130]: • Stage 1 is called the acute stage. It is rarely diagnosed in the first stage which is marked by asthma, elevated IgE levels, peripheral eosinophilia, pulmonary infiltrates, and both IgE and IgG antibodies to A. fumigatus. • Stage 2 is the remission stage. • Stage 3 is the exacerbation phase where IgE levels are double that at baseline. • Stage 4 occurs when the person who has been treated with corticosteroids attempts to reduce the corticosteroid therapy but sees a worsening of symptoms and the development of pulmonary infiltrates. They are now corticosteroid-dependent. Serum IgE levels tend to be normal or elevated, while the CT scan will show central bronchiectasis. Regretfully, it is at this stage that they are usually diagnosed with APBA. • Stage 5 is attained by a minority of individuals. This stage is typical of end-stage lung disease with dyspnea, low SpO2, cor pulmonale, and clubbing. The staging system is helpful to gauge a person’s response to therapy, to assess the progression of the disease, to identify exacerbations, and to suggest treatment. Not all follow the five stages, and predictions based on the above staging are uncertain for much depends on the individual and their response to therapy. The four goals of treatment in ABPA include symptoms control, prevention of exacerbations of ABPA, reduction of pulmonary inflammation,

9 Comorbidities in Asthma

and prevention of disease progression to bronchiectasis and permanent lung damage [128–131]. The mainstay of treatment for ABPA is oral, not inhaled, corticosteroids that suppress the immune system and minimize the secondary inflammatory consequences. This reduces bronchoconstriction and pulmonary infiltrates and decreases both IgE levels and peripheral eosinophilia. The recommended dosage is 0.5 mg/kg/d for 2 weeks. Next, the oral corticosteroids (OCS) should be given on alternate days for 6–8 weeks and then slowly reduced over 3–6 months. Caution should be observed in reducing the OCS, and the person should be closely monitored as the dosage is reduced. Remission is said to be achieved when no oral corticosteroids have been needed for 6 months and without any symptoms. However, during this stage, the disease progression should be monitored with serial chest radiographs, serum IgE levels, and pulmonary function testing. This is also helpful in identifying potential exacerbations. At Stage 4, when corticosteroid therapy cannot be discontinued, the lowest dose of OCS should be used to minimize side effects and toxicity. In addition, adjunct therapies, including antifungal agents, should be considered. Antifungal agents such as itraconazole (200– 400 mg/d) and voriconazole can help reduce the dosage of OCS while improving both exercise tolerance and pulmonary function. In those who are stable, they reduce eosinophilic airway inflammation, systemic immune activation, and exacerbations [132]. They should be prescribed for a duration of 16 weeks. Omalizumab has also been found to be helpful [129]. In the end stage of the disease, treatment recommendations are scarce. The prognosis is poor and individuals often develop recurrent infections. Early treatment of ABPA can prevent the progression of the disease into its further stages of recurrent exacerbations, further bronchiectatic changes, and, finally, respiratory compromise and end-stage fibrosis. Individuals should be monitored for loss of lung function to avoid further deterioration, and as always, the goal of treatment should be prevention of loss and maintenance of good respiratory function.

9.11 Depression

9.11 Depression Chronic illness lends itself to depression. In the USA, adults with asthma have more than double the rates of anxiety and depression compared with adults without asthma [133]. It is estimated that two out of three individuals with asthma may suffer from depression, and researchers have linked depression with increased severity of asthma [134]. Depression may exacerbate asthma and asthma in turn can exacerbate depression [135]. Oraka and colleagues [133] analyzed data from 186,738 adults for the prevalence and risk factors for serious psychological distress (SPD) and their health-related quality of life (HRQOL). Among adults with asthma, the prevalence of SPD was 7.5%, and no matter their asthma status, there was a negative association between HRQOL and SPD. An inverse dose-response relationship was seen between serious psychological distress and health-related quality of life. Risk factors for SPD included lower socioeconomic status, smoking, alcohol use, and more comorbid conditions. Adults with asthma have a higher prevalence of frequent mental distress [136]. Research has clearly linked asthma and mental disorders [137]. Depression, particularly in adolescents with asthma, can result in potentially fatal asthma [11]. Asthma in adolescence and early adulthood increases the likelihood of major depression, panic attacks, and any anxiety disorder [138]. Depression in the elderly is linked to lower medication adherence and poor asthma control and quality of life [139]. Individuals who are obese and depressed have poor asthma control. A study of 798 adults found an inverse association with BMI and asthma control after adjusting for age, sex, education, cohabitation, and ICS use [140]. Children with asthma who are overweight or obese and have depressive symptoms have predicted lower baseline FEV1 [141]. A study of data from the 2007–2012 National Health and Nutrition Examination Survey involving 20,272 adults between the ages of 20 and 79 years found that individuals with major depression had 3.4 times higher odds of asthma

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than those with either minimal or no depressive symptoms. Further, unlike adults without asthma, in adults with asthma and major depression, there was a 4.3% reduction in bronchodilator response [142]. Depression can lead to suicide. A study by Clarke and colleagues [143] found that there is a link between chronic respiratory diseases, depression, suicide ideation, and suicide attempts. Analysis of data from 5692 adults found that while 4.2% of adults attempt suicide, the ratio for adults with asthma who attempt suicide is 12%. The difference between non-asthma and asthma individuals remained significant even after adjustment for confounders such as smoking, nicotine dependence, age, sex, and race/ethnicity, depression, panic disorder, and alcohol abuse. The factors that were associated with an increased likelihood of suicide attempts included: • • • • • •

Female sex Current smoking Nicotine dependence Depression Anxiety Alcohol abuse

Goodwin [144] found a statistical interaction between pulmonary disease, depression, and suicidal ideation in that the odds increased with depression: • Pulmonary disease without depression—OR 1.9 • Depression without pulmonary disease—OR 7.4 • Pulmonary disease with depression—OR 9.6 A study of youth hospitalized for asthma found higher than expected levels of suicide ideation [145]. An analysis of 6584 adults whose data was drawn from the Third National Health and Nutrition Examination Survey (NHANES III) found an association between current asthma and suicide ideation (Odds Ratio 1.77) and suicide attempt (OR 3.26), after adjusting for confounders such as mood disorder, poverty, smoking, and demographics [146].

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Of all the physical illnesses studied, while suicide was linked primarily to epilepsy, asthma ranked second with a relative risk of 1.8 after epilepsy at 2.9 (followed by psoriasis, diabetes, and eczema). Psychiatric illness is closely linked to self-harm and suicide [147]. When it came to asthma management, anxiety/depression leads to decreased adherence to medication, monitoring, and smoking cessation. The results of anxiety/depression were reduced self-care and functioning with increased symptoms burden, healthcare utilization, and medical costs, all of which have long-term implications [148]. Hence, any treatment modality for asthma, in order to minimize the possibility of suicide in those with asthma, must incorporate • • • • •

Asthma treatment Smoking cessation Alcohol surcease Behavior modification Treatment for depressive disorders

sure to known triggers and inadequate adherence to regular treatment. There is a continuum of acute asthma: • Wheeze might present for a few minutes after exercise, followed by spontaneous recovery. • Deterioration might occur for several days after a viral head cold and eventually benefit from treatment at home. • There may be deterioration severe enough to require aggressive treatment in the ED. • Hospitalization may be needed. • Assisted ventilation in an intensive care unit (ICU) may be required. Those individuals with the most severe episodes, such as life-threatening asthma in the ICU, were previously described by the term “status asthmaticus. “While this phrase is still used to indicate severe acute or life-threatening asthma, it does not convey the full range of severity.

Points to Ponder

It is clear that there is a significant association between asthma, depression/anxiety, and suicide. Hence, educators and healthcare professionals should work with individuals to identify associations between depression and asthma in order to increase control and reduce the severity of asthma. Those with asthma must be constantly assessed not only for physical health but also for psychological morbidity.

9.12 A cute, Severe Acute, and Life-Threatening Asthma Deterioration of asthma from time to time is a reality, no matter how well-controlled the disease or how much attention is paid to avoiding environmental triggers. Sometimes this deterioration is unexpected and sudden. More often, warning signs are not identified by the individual or healthcare provider or are compounded by expo-

Respiratory induced changes in asthma • • • • • • • •

Interference with speech Increase in respiratory rate Intercostals indrawing Wheeze on auscultation Changes in breath sounds Increase in heart rate Use of accessory muscles of respiration Pulsus paradoxus

Despite the existence of a continuum of severity, individuals do not generally go through a complete sequence of events. They have particular patterns, and in some cases, the deterioration progresses from onset to severe very quickly. Thus, it is important to know their previous response to help predict their course during new episodes of deterioration. Action plans, described in Chap. 10, can help them identify when they need to seek help from a clinic or hospital.

9.12 Acute, Severe Acute, and Life-Threatening Asthma

However, asthma plans will only help if the person: • Understands the plan • Has the action plan readily at hand when deterioration occurs • Is prepared to follow the directions in the plan Some individuals will have normal or near‑normal lung function and will have smooth muscle contraction during exercise. More commonly, with acute deterioration, there will already be some preexisting abnormality of lung function, due to mild inflammation, an increase in secretion, or perhaps airway remodeling. With acute deterioration, these changes are exacerbated, and secretions start to block the airway. The combination of inflammatory edema, smooth muscle contraction, and airway secretions leads to closure of a number of medium to small airways. The difficulty in breathing occurs in both expiration and inspiration but is more marked in expiration. As the attack progresses, the amount of gas trapped in the lung increases, together with an increase in the anteroposterior diameter of the chest. There is marked ventilation/perfusion inequality—that is, perfusion of under-ventilated areas of the lung leads to the development of hypoxemia. With more severe and prolonged episodes of deterioration, functional loss of many airways can also occur [149]. The general approach to acute asthma is to: • Identify deterioration. • Assess severity. • Take action as soon as possible. The aims of treatment are to achieve recovery as rapidly as possible; break the vicious circle of downward deterioration and prevent future episodes of acute asthma. The mainstays of treatment are a beta‑2 agonist delivered by inhalation, systemic corticosteroids, and oxygen. All three are not always required and because the route, delivery, and detailed dose will vary from person to person; a detailed assessment is important.

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Episodes are identified by increased symptoms, such as wheeze or cough, particularly when they occur at night. One of the most important indicators of deterioration is increased bronchodilator use. Increased use of an inhaled bronchodilator is an important warning sign. It is a sign that calls for urgent self-assessment followed by appropriate changes in asthma care. Further action might include stopping activity, such as exercise, or taking environmental precautions (such as removing themselves from a harmful environment). An increase in ICS is no longer routinely advised. If advised to use intermittent ICS, as indicated in the following paragraph, now is the time to act. Systemic corticosteroids might be needed but only with professional direction. When to go to the hospital or call for an ambulance must be well understood. One recent change in the Updates to the Asthma Management Guidelines [150] is that in some situations, ICS are not used regularly but only with exacerbations. The specifics are: • Children aged 1–4 years, recurrent wheezing triggered by respiratory tract infection (RTI) and no wheezing between infections –– Short course of daily ICS at onset of infection + as needed SABA • Twelve years and over, mild persistent asthma –– As needed ICS and SABA as choice (Also allowed low-dose regular ICS + as needed SABA) • Four years +, moderate to severe persistent asthma –– ICS-formoterol in a single inhaler as both daily controller and reliever therapy (Also allowed higher dose ICS + SABA as needed, or ICS-LABA + SABA as needed) There has also been a marked change in the guidelines recommendations on how to handle an asthma attack. Since the danger posed by increased inflammation is clear, speedy reduction of inflammation is the goal. The emphasis now is to regain control of the asthma as quickly as

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possible with the use of oral corticosteroids (OCS). Frequent exacerbations are known to impair lung function and accelerate the decline in lung function [151–154]. Exacerbations/attacks are defined as a worsening of asthma of sufficient severity to require intervention of a medical professional or self- administration of oral corticosteroids. The frequency of deterioration may be an indication of greater severity or poor compliance with therapy. Comorbidities may play a significant role, particularly psychosocial dysfunction and severe chronic sinusitis. While there are many causes for attacks, the major cause tends to be viral, particularly rhinovirus infection [155]. About 80% of all exacerbations are triggered by viral infections with two-thirds due to the rhinovirus. Bacterial infections, increased exposure to fungal spores, allergy, extreme weather conditions, psychological stress, and exposure to high levels of air pollution, including ozone, nitrogen dioxide, and living close to roads, are all contributors to exacerbations [15, 153, 156–158]. It is rarely a single trigger that results in an exacerbation but rather the combined effects of many triggers or repeated exposures to a few triggers. Some triggers, such as air pollution, work synergistically with viral infections and allergic sensitization to provoke an exacerbation.

9.12.1 Classification of Severity of Acute Asthma Severity requires: • Assessment of the respiratory system • Assessment of the cardiovascular system • Objective measurements, including peak flow and oxygen saturation • Assessment of blood gases (note that this measurement becomes more important the longer the episode lasts) Respiratory changes can be noted as the clinician listens to the individual. Episodes of acute asthma interfere with speech, and it should be

9 Comorbidities in Asthma

noted whether the person can speak in sentences, phrases, or only syllables. Other important findings include an increase in respiratory rate, an increase in tracheal tug or intercostal indrawing, use of accessory muscles of respiration, or evidence of wheeze on auscultation. Findings such as persistent crackles in one area of the lung should be noted, since they may indicate alternate pathology such as pneumonia. Marked asymmetry in the intensity of breath sounds may indicate a complication of the severe attack, such as pneumothorax, atelectasis, pneumonia, or inhaled foreign body. Inspection may also show an increase in anteroposterior diameter. The major cardiovascular effect is an increase in heart rate. Another well‑recognized cardiovascular finding is pulsus paradoxus. In normal healthy individuals, systolic blood pressure drops by about 5 mm of mercury during inspiration. In pulsus paradoxus, this is exaggerated, with systolic blood pressure falling by 10 mm of mercury or more during inspiration, together with an obvious decrease in the size of the pulse. This is an important sign of severe airflow limitation. The marked hyperinflation of lung in acute asthma leads to major changes in pulmonary pressure, which limits return of blood to the heart during inspiration, and subsequently affects cardiac emptying. Pulsus paradoxus requires blood pressure to be measured during both inspiration and expiration. Although it is potentially useful as a sign of severity, it may be absent even in severe asthma. Moreover, many healthcare professionals may not perform this measurement because they think it is not easy to do. The importance of accurate assessment of the person with asthma during attack is emphasized from the realization that some of them will die. Death of course is rare, but not unknown, and when the circumstances of death are examined, almost always errors are found. The errors may be on the part of the person with asthma themselves, in not maintaining regular anti-asthma therapy or not escalating therapy at the early stages of deterioration. The errors may be on the part of healthcare professionals in not recognizing early enough the severity of the attack. While there may be errors in recognition of deteriora-

9.12 Acute, Severe Acute, and Life-Threatening Asthma

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Fig. 9.2 Death not due to asthma Fig. 9.3 Death from asthma

tion, or management of deterioration, almost always there is a long history of poorly controlled asthma before the fatal event. When individuals die due to severe asthma, the lungs show evidence of chronic illness. The illustrations that follow (Figs. 9.2, 9.3, and 9.4) are casts of the lung prepared after postmortem examination. They were obtained as part of a prospective study of asthma mortality [159, 160]. In this study, all asthma deaths in three Canadian provinces were reported to the study investigators. The next of kin was asked for permission to remove and study the lungs. The casts were prepared using a novel procedure described by Perry et al. [159]. In summary, a silicon component was inserted into the lungs under negative pressure. The casts shown are representative of three groups of individuals studied. Figure 9.2 was obtained from an individual who had a history of asthma but in whom the cause of death was unrelated to the asthma. The branching pattern is normal, and there was filling of the airway with the compound to the level of the respiratory bronchioles. Figure 9.3 is from someone whose cause of death was clearly asthma. There are irregular segments, tapering, and areas of constriction. The

Fig. 9.4 Changes in the lungs due to asthma

airway constriction means that many of the segments are truncated. Figure 9.4 is from an individual who did not die because of asthma but did have a history of asthma. This cast does not show the extreme changes of Fig. 9.3 but does show some of the changes of faithful asthma, with some changes due to mucous plugs and some airway truncation.

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Examination of these casts will help to understand the pathophysiological changes described earlier in this section and the possible complications of severe acute asthma. They also point the way to the need for objective measures wherever possible early in the period of deterioration. Measurement of peak expiratory flow, particularly if the previous best is known, can guide therapy at home, in the educator’s office, at the clinic, or in the hospital. The educator should remember, however, that individuals in an acute exacerbation may not be able to do a peak flow maneuver. When a reading is obtained, it is compared against their normal “best” reading. Below normal readings (50–80% of normal best, or less than 50%) indicate a severe, or impending severe, attack. If facilities are available in a clinic or hospital, FEV1 may be done with some help. For more severe attacks pulse oximetry should be performed although normal oxygen saturation does not indicate the episode is mild. Deterioration in oxygen saturation is a very serious sign, and

such patients require oxygen therapy. Measurement of blood gases including pH and PaCO2 (partial pressure of carbon dioxide) is essential for those individuals with severe episodes. In more severe episodes, or when there are atypical features such as asymmetry of clinical findings of chest sounds, a chest X‑ray is required. The X‑ray should be scrutinized for areas of mucus plugging involving major airways, areas of pneumonia, or evidence of a pneumothorax. A chest X‑ray should not be requested in other less severe attacks, because the findings can be misleading. The usual findings are minor changes such as patchy infiltrates representing areas of atelectasis. Table 9.5 shows an overall classification of severity during an exacerbation, based on the NHLBI Expert Panel Report 3 Guidelines [15]. Most individuals with mild asthma can be managed at home easily, but when seen by the educator, a number of simple measurements are

Table 9.5 Classification of severity and treatment of an asthma exacerbation Signs and symptoms Dyspnea Speech Conscious level Respiratory rate (RR) Accessory muscles Wheeze

Severity Mild With activity Sentences Agitated

Moderate Limits activity Phrases Agitated

Severe At rest Words Agitated >30a

No

Yes, some

Usually

End expiration

Expiration

Heart rate (HR) Pulsus Paradoxus PEF as % of personal best SpO2%

25 mm Hg May be absent