The Wisdom of Anxiety: How Worry and Intrusive Thoughts Are Gifts to Help You Heal 1683642503, 9781683642503

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Ftplectures Cardiovascular system Lecture Notes

CARDIOLOGY

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  Ftplectures Cardiovascular system Copyright 2014 Adeleke Adesina, DO Cardiovascular system © 2012 ftplectures LLC 1133 Broadway Suite 706, New York, NY, 10010

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Future  teaching  physicians  Lectures  LLC   Medicine  made  simple             Title:  Abdominal  Aortic  Aneurysm     Objectives  for  learning:      Define  AAA,  risk  factors,  causes,  pathogensis,  diagnosis   and  treatment.     Definition:   Aneurysms  are  enlarged  blood  vessels.  Aortic  aneurysm  are  mostly  infrarenal.     Causes/  Risk  factors:     High  incidence  in  males,  Age  >  50  years,  (65-­‐70  years)   -­‐  Smoking  increases  risk  of  developing  AAA-­‐  due  deposition  of  atherosclerosis  –   deposition  of  fatty  plaques  inside  the  wall  of  the  abdominal  aorta.  This  causes  the   wall  to  weaken,  and  that  weakening  causes  that  to  balloon  out.  Atherosclerosis   pathogenesis  is  due  to  deposit  LDL  which  the  macrophages  are  getting  caught,  eat  it   up,  and  become  forming  macrophages.  They  are  going  to  cause  the  proliferation  of   the  smooth  muscle  cells,  they  are  going  to  form  a  plaque  which  is  going  to  form  in   the  walls  of  this  aorta.  And  that  plus  smoking,  hyperlipidemia,  which  means  high   LDL  and  low  HDL,  basically  is  going  to  predispose  you  to  develop  the  aneurysm.       -­‐ Hypertension,   -­‐ Vasculitis  –  inflammation  of  small  blood  vessels  in  aorta  leading  to  ischemia   and  weakening  of  aortic  walls.     -­‐ Syphilis   -­‐ Marfan  syndrome   -­‐ Fibrillin  deficiency  or  any  connective  tissue  disorder     Pathophysiology     Clinical  symptoms  and  signs   -­‐ patients  are  asymptomatic  except  when  aorta  ruptures   -­‐ palpable,  pulsating  abdominal  mass   -­‐ ruptured  AAA  is  a  life  threatening  emergency  with  a  mortality  of  90%.  The   pumping  heart  pumps  all  the  cardiac  output  into  the  abdominal  cavity   leading  to  sever  hemorrhagic  shock.     Symptoms   -­‐ severe  abdominal  or  lower  back  pain,-­‐  patient  complain  of  sudden  onset  of   abdominal  pain.     -­‐ Physical  Exam  may  show  grey  tunre  sign-­‐  flank  ecchymosis   -­‐ Cullens  sign-­‐  Periumbilical  ecchymosis-­‐  sign  of  blood  in  abdominal  cavity  

Sigs:  Triad  of  AAA-­‐  hypotension,  abdominal  pain,  and  pulsatile  abdominal  mass.     Possible  syncope  if  sever  hypotension  from  hemorrhagic  shock  and  inadequate   perfusion  to  brain.   -­‐  nausea,  vomiting.     Diagnosis   Ultrasound-­‐    100%  sensitive   CT  scan  only  for  stable  patient  with  no  hemodynamic  instability-­‐  normal  blood   pressure     Treatment   Surgery  with  synthetic  graft   Treat  risk  factors-­‐  Hyperlipidemia  with  statins,  hypertension  with  beta-­‐blockers,   thiazides,  or  ACE  inhibitors   Advice  patient  to  stop  smoking  because  it  increases  risk  of  developing  another  AAA  

Future  teaching  physicians  Lectures  LLC   Medicine  made  simple               Title:  Acute  Coronary  Syndrome     Objectives  for  learning:  Understanding  the  basic  facts  about  acute  coronary   syndromes  including  unstable  angina,  NSTEMI  and  STEMI.     Definitions:  Acute  coronary  syndrome  encompasses  unstable  angina  (USA),  non-­‐ST   elevation  (NSTEMI),  and  myocardial  infarction  (STEMI).     Causes/  Risk  factors:     • Stable  angina   • Smoking   • Diabetes   • Obesity     Pathophysiology:     Atherosclerotic  plaques  in  coronary  arteries  cause  the  initial  pathology.  The  plaque   can  rupture  which  leads  to  increased  tendency  to  increased  thrombosis.   Thrombosis  can  lower  the  blood  flow  through  the  affected  coronary  artery,  thus   causing  ischemia  to  the  regions  distal  from  the  occlusion.   • Unstable  angina  appears  on  the  basis  of  previously  developed  stable  angina.   Due  to  seriously  decreased  diameter  of  coronary  blood  vessels  caused  by   atherosclerotic  plaque  progression,  these  patients  have  increased  frequency   of  chest  pain  occurring  even  during  the  rest.   • Non-­‐STEMI  is  the  type  of  myocardial  infarction  which  is  not  big  enough  to   cause  ST-­‐elevation.       Clinical  symptoms  and  signs   • Increased  frequency  of  chest  pain  even  during  the  rest   • Prolonged  duration  of  chest  pain  (>10  minutes)     Diagnosis   • EKG  can  be  normal  in  the  case  of  unstable  angina  and  NSTEMI,  but  it  can  also   show  ST-­‐depression  and  T  wave  inversion  due  to  the  ischemia.  ST-­‐ depression  has  to  be  greater  than  0.5  mm  and  T  inversion  greater  than  2  mm   in  order  to  be  significant.   • In  order  to  distinguish  unstable  angina  and  NSTEMI,  cardiac  enzymes  are   used  (CK-­‐MB,  Troponin  I/T)  

    Treatment   • Morphine   • Oxygen   • Nitrates   • Aspirin  (COX-­‐inhibitor  which  decreases  tromboxan  A2  and  platelet   aggregation)   • Beta-­‐blockers  (decreasing  heart  frequency  and  blood  pressure)   • Glycoprotein  IIb  /  IIIa  inhibitors   • Exonoparin  (low-­‐molecular  heparin)   • Coronary  catheterization  is  performed  if  the  patient  is  not  feeling  better  after   medicamentous  treatment.     Lifestyle  modifications:   • Diet   • Exercise   • Glucose  control   • Statins   • Stop  smoking   • Lose  weight    

Future  teaching  physicians  Lectures  LLC   Medicine  made  simple               Title:  Acute  Myocardial  Infarction  (MI)     Objectives  for  learning:  Learning  the  pathophysiological  and  clinical  features  of   acute  myocardial  infarction,  as  well  as  treatment  options.     Definitions:  Acute  myocardial  infarction  is  necrosis  of  myocardium  due  to  massive   ischemia  caused  by  coronary  artery  occlusion.  It  is  the  most  common  cause  of  the   death  in  the  United  States  (30%  mortality).     Causes/  Risk  factors:     Acronym:  FLASH  –  MD   • Family  history   • Low  HDL   • Age  (men>45,  women>55)   • Smoking   • Hypertension   • Male  gender   • Diabetes     Pathophysiology:  Acute  myocardial  infarction  represents  the  necrosis  of  some   parts  of  heart  muscle  which  happens  due  to  the  massive  ischemia  caused  by   complete  occlusion  of  the  coronary  artery  responsible  for  supplying  that  region.     Clinical  symptoms  and  signs   • Chest  pain  (crushing;  radiation  to  the  neck,  jaw,  and  left  arm)   • Nausea   • Vomiting   • Diaphoresis   • Shortness  of  breath   • Weakness,  fatigue   Symptoms  last  more  than  30  minutes.   Atypical  clinical  picture  in:   • Diabetics   • Elderly   • Women   • St.  post  surgery    

Diagnosis   • EKG  changes  (ST-­‐elevation,  Q-­‐waves  (at  least  0.04s  and  25%  of  R  wave),  T-­‐ waves  inversion   o I,  aVL,  V5,  V6  –  lateral  wall   o V1,  V2,  V3  –  anterior  wall   o II,  III,  aVF  –  inferior  wall   o V1,  V2  –  Septal  wall   • Cardiac  enzyme   o CK-­‐MB  (increases  during  the  first  4-­‐8  hours;  returns  to  normal  values   after  48-­‐72  hours)   o Troponin  I/T  (increases  in  the  first  3-­‐5  hours;  returns  to  normal   values  after  5-­‐14  days)   *  CK-­‐MB  is  an  important  marker  for  reinfarction     Complications   • Ventricular  fibrillation   • Reinfarction     Treatment   • Morphine   • Oxygen   • Nitrates   • Aspirin  –  antiplatelet  (aspirin  decreases  mortality)   • Beta-­‐blockers  (reduce  mortality)   • ACE  inhibitors   • Statins   • Anticoagulant  -­‐  Low  molecular  weight  heparine   • Revascularization  

Future  teaching  physicians  Lectures  LLC   Medicine  made  simple               Title:  Acute  Pericarditis     Objectives  for  learning:  Learning  clinical  signs,  diagnostic  techniques,  and   treatment  options  for  acute  pericarditis.     Definitions:  Pericarditis  is  an  inflammation  of  pericardium.     Causes/  Risk  factors:     • Idiopathic   • Viruses  (Coxsackie  B,  HIV,  Echoviruses)   • Radiation   • Uremia   • Acute  myocardial  infarction  (Dressler’s  syndrome)   • Lupus   • Amyloidosis   • Rheumatoid  arthritis   • Sarcoidosis   • Procainamide,  hydralazine,  izoniazide  (drug  induced  pericarditis)       Clinical  symptoms  and  signs   • Retrosternal  chest  pain  (pleuritic  pain  which  radiates  to  trapezius  or   scapula)   o Leaning  forward  lowers  the  pain.   o Swallowing,  cough,  and  lying  down  increase  the  pain.   • Fever   • Pericardial  rub     Diagnosis   • EKG   o Diffuse  S-­‐T  elevation   o P-­‐R  depression  (the  most  specific  for  pericarditis)   o T  wave  inversion   • Echocardiogram       Complications   • Pericardial  effusion  

•

Pericardial  tamponade  

  Treatment   • Aspirin   • Steroids  are  given  if  the  patient  does  not  respond  well  to  aspirin  

Future  teaching  physicians  Lectures  LLC   Medicine  made  simple               Title:  Aortic  Dissection     Objectives  for  learning:  Understanding  pathophysiology,  causes,  and  clinical   features  of  aortic  dissection,  learn  how  to  diagnose  it  fast  and  what  type  of   treatment  to  apply.     Definitions:  Severe  hypertensive  emergency  where  the  blood  flow  damages  tunica   intima  and  accumulates  in  the  space  between  tunica  intima  and  tunica  media.     Causes/  Risk  factors:     • Hypertension   • Trauma   • CTD  –  Connective  Tissue  Diseases  (Ehlers-­‐Danlos  syndrome,  Marfan   syndrome)     Pathophysiology:  There  are  two  types  of  aortic  dissection  –  type  A  and  type  B.  In   type  A,  proximal  part  of  ascending  aorta  is  dissected,  so  there  is  a  risk  of  coronary   ischemia  because  the  dissection  can  reach  coronary  arteries.  In  type  B,  aortic  arch  is   dissected,  and  the  dissection  can  prolong  distally,  down  to  renal  arteries  causing   renal  ischemia.       Clinical  symptoms  and  signs   • Ripping  chest  pain  (anterior  in  proximal  dissection  and  interscapular  in   distal  dissection)   • Diaphoresis   • Aortic  regurgitation  signs  and  symptoms   • Hemiplegia  or  hemiparesis  (due  to  ischemic  stroke)     Diagnosis   • Transesophageal  echocardiogram  (TEE)   • CAT  scan  (aorta  with  two  lumens)   • AP  chest  X-­‐ray  (widened  mediastinum)     Complications   • Coronary  ischemia   • Stroke  

• Renal  ischemia   Treatment   • Beta-­‐blockers   • i.v.  Sodium  nitroprusside  (decrease  systolic  pressure  below  120  mmHg)   • Surgical  treatment  is  necessary  in  type  A  aortic  dissection    

Title:  Aortic  Stenosis    

Objectives  for  learning:  Definition,  Pathophysiology,  Causes/  Risk  factors,  Clinical  symptoms   and  signs,  Diagnosis  and  Treatment.     Definition:   Pathophysiology   Stenotic  aortic  wall  causes  left  ventricular  outflow  obstruction.  Valve  being  stenotic  becomes   unable  to  push  blood  to  left  ventricle.  Decrease  LV  outflow  leads  to  left  ventricular  hypertrophy   due  to  excessive  amount  of  force  heart  has  to  put  to  pump  the  blood.  Over  a  passage  of  time   LV  dilatation  and  then  mitral  regurgitation  develops.  Cardiac  output  becomes  decrease.     Causes/  Risk  factors:   Calcification  of  the  bicuspid  valve  (olderly  patients  most  develop  calcification  of  the  valve  due   to  deposition  of  calcium)   History  of  rheumatic  fever   Clinical  symptoms  and  signs:     Symptoms:   • • • • •

Asymptomatic  for  years   With  the  worsening  of  obstruction     Syncope   Angina   Dyspnea  due  to  CHF  

Signs:     • • • •

Murmur     Crescendo-­‐decrescendo  murmur.  Can  be  heard  at  second  intercostal  space  and  carotid   artery   S4  sound   Parvus  et  tardus  a  decreased  or  delayed  carotid  stroke    

Diagnosis  

• • •

Chest-­‐x-­‐ray   Echocardiogram  (LV  and  LA  enlargement)     Cardiac  catherization:  It  is  a  definite  diagnostic  test  and  gradient  and  valve  area  less   than  0.8  is  considered  normal.    

  Quiz       1. A  57  year  old  patient  presents  with  complaints  of  Syncope,  chest  pain  on  physical  exertion   and  malaise.  On  examination  a  murmur  is  present  over  second  intercostal  space.  S4  sound   is  also  heard.  He  has  a  previous  history  of  rheumatic  fever.  What  is  the  likely  diagnosis?   A. Aortic  stenosis   B. Aortic  regurgitation   C. Mitral  stenosis   D. Mitral  regurgitation     The  correct  answer  is:  A   The  history,  clinical  picture  and  physical  examination  all  point  towards  the  development  of   aortic  stenosis  in  this  patient.  The  murmur  of  aortic  stenosis  is  usually  heard  at  second   intercostal  space.  S4  sound  is  prominent  here.  Rheumatic  fever  is  the  most  common  cause  of   aortic  stenosis  in  the  adult  patient.   In  case  of  aortic  regurgitation  S3  sound  is  heard  whereas  the  murmur  of  aortic  regurgitation  is   heard  at  third  left  intercostal  space.     Mitral  stenosis  is  characterized  by  the  loud  first  heart  sound  and  tapping  apex  beat.  The   murmur  of  mitral  stenosis  is  heard  at  the  apical  region  and  is  low-­‐pitched.       The  murmur  of  mitral  regurgitation  is  best  heard  at  the  apex  of  the  heart.  Here  first  heart   sound  is  soft.  The  most  common  cause  of  mitral  regurgitation  is  mitral  valve  prolapsed.       2. Which  of  the  given  option  is  related  to  the  aortic  stenosis?   A. Diastolic  murmur   B. Atrial  fibrillation   C. Right  heart  failure   D. Systolic  ejection  murmur    

The  correct  answer  is:  D   Systolic  ejection  murmur  is  related  to  the  aortic  stenosis.  This  murmur  is  the  due  to  turbulent   flow  of  blood  forward  across  the  right  ventricular  outflow  tract,  aortic  valve,  or  via  the  aorta.    It   is  also  related  to  pulmonary  stenosis.     Diastolic  murmur  has  no  relation  to  the  aortic  stenosis.  Diastolic  murmurs  begin  at  or  after  S2   heart  sound  and  remains  till  at  or  before  S1.   Aortic  stenosis  does  not  lead  to  atrial  fibrillation  but  mitral  stenosis  can  cause  the  development   of  atrial  fibrillation.   Right  heart  failure  may  result  with  aortic  stenosis  but  when  disease  is  quite  old  so  best  option  is   D.       3. A  43-­‐year-­‐old  patient  presents  with  confirm  diagnosis  of  aortic  stenosis.  He  has  a  history  of   fever  and  joint  pains.  What  would  be  the  most  likely  cause  here?   A. Bacterial  endocarditis     B. Congenital  bicuspid  valve   C. Rheumatic  fever   D. Marfan’s  syndrome   The  correct  answer  is:  C   Aortic  stenosis  in  an  adult  is  usually  the  result  of  rheumatic  fever.  Rheumatic  fever  is   an  inflammatory  condition  that  precedes  an  infection  by  the  Streptococcus  pyogenes.  It  can   involve  the  skin,  heart,  brain  and  joints.     A  congenital  bicuspid  valve  is  basically  a  congenital  disease  vulnerable  to  endocarditis  and   ultimately  develops  calcification  as  well  as  symptomatic  stenosis.     Aortic  stenosis  is  usually  seen  after  the  bacterial  endocarditis.  There  must  be  a  history  of   development  of  bacterial  endocarditis.     Marfan’s  syndrome  can  cause  aortic  stenosis  but  that  adult  must  have  the  features  of  Marfan’s   syndrome.       4. Crescendo-­‐decrescendo  is  the  murmur  found  in  aortic  stenosis.  What  is  its  exact  location?   A. Fifth  intercostal  space    

B. Second  intercostal  space  and  carotid  artery   C. In  the  fourth  intercostal  space  medial  to  mid-­‐clavicular  line.   D. At  the  apex  of  the  heart   The  correct  answer  is:  B   Since  Crescendo-­‐decrescendo  murmur  occurs  due  to  stenosis  of  aorta,  so  its  location  would  be   where  aorta  is  present.  The  correct  answer  therefore  is  second  intercostal  space  and  carotid   artery.  All  other  options  are  not  correct.     5. Syphilis  is  the  infection  which  can  cause  heart  disease.  What  is  the  most  common  valve  of   the  heart  involved  by  it?   A. Mitral  valve     B. Pulmonary  valve     C. Aortic  valve   D. Tricuspid  valve     The  correct  answer  is:  C   In  the  later  stages  of  disease,  syphilis  involves  the  heart  and  remains  confined  to  the  base  of   the  aorta.  When  it  involves  the  wall  of  the  aorta,  syphilis  leads  to  loss  of  the  elastic  properties   of  the  aorta  and  even  the  formation  of  aortic  aneurysms.     Mitral  valve,  pulmonary  valve  and  tricuspid  valve  are  not  affected  by  the  syphilis.      

Title:  Atrial  Septal  Defect  (ASD)     Objectives  for  learning:  Definition,  Pathophysiology,  Clinical  symptoms  and  signs,  Physical   Exam,  Diagnosis,  Complications,  and  Treatment.       Definition:   The  defect  between  the  two  atria  is  called  atrial  septal  defect.  There  are  two  types:   Ostium  primum:  The  little  hole  at  the  top  between  the  right  and  the  left  atrium  is  called  ostium   primum.  80%  septal  defects  are  ostium  primum.     Septum  primum:  It  is  the  defect  at  the  lower  side  between  the  right  and  the  left  atrium.       Causes/  Risk  factors:       Pathophysiology   Deoxygenated  blood  normally  comes  from  the  head  and  the  lower  side  of  the  body  into  the   superior  vena  cava  (SVC)  and  inferior  vena  cava  (IVC)  respectively.  From  here  it  enters  into  the   right  atrium.  Right  atrium  now  has  deoxygenated  blood  which  enters  into  the  right  ventricle.   Right  ventricle  contracts  during  systole  and  pumps  blood  into  the  pulmonary  arteries  which   now  enters  into  the  lung.  The  pulmonary  arteries  become  smaller  pulmonary  capillaries  which   take  oxygen,  exchange  with  carbon  dioxide.  Now  oxygenated  blood  is  taken  up  by  the   pulmonary  veins  into  the  left  atrium.  The  left  atrium  always  has  oxygenated  blood.     In  case  of  atrial  septal  defect  the  left  atrium  cannot  pump  blood  into  the  left  ventricle.  The   oxygenated  blood  is  not  transferred  to  the  whole  of  the  body  through  aorta.    Thus,  oxygen  is   not  transmitted  to  the  body.     The  pressure  from  the  IVC  and  SVC  coming  into  the  right  atrium  is  always  at  low  side.  The   pressure  in  the  RV  is  25/10  mmHg,  in  the  left  atrium  is  12  mmHg  and  in  the  left  ventricle  is   130/80  mmHg.       Clinical  symptoms  and  signs   The  patients  are  normally  asymptomatic.  But  as  the  patients  reach  to  40  years  of  age,  they   develop:   • Dyspnea  at  exertion   • Exercise  intolerance   • Anemia   • Fatigue       Physical  Exam   • Mid-­‐systolic  ejection  murmur  is  heard  at  pulmonary  area.    

• Wide  fixed  split  S2  sound     • Diastolic  rumble  in  the  tricuspid  region   • Irregularly  irregular  heart  rate   • No  p  waves  on  EKG   • Atrial  fibrillation       Diagnosis   • Transesophageal  Echocardiogram  (TEE)   • Chest  x-­‐ray     • Electrocardiography  (EKG)       Complications   • Pulmonary  hypertension   • Right  ventricular  failure     • Eisenmenger's  disease     • Paradoxical  emboli   • Stroke       Treatment   Surgical  repair  –  close  up  the  valve    

Title:  Blood  Pressure  Regulation  I:  Baroreceptor  Pathway     Objectives  For  Learning:  Mean  arterial  blood  pressure,  Normal  blood  pressure,  Pathways   and  Neural  Pathways.   Mean  Arterial  Blood  Pressure   • •

Mean  arterial  blood  pressure:    2  (diastolic  blood  pressure)  +  systolic  blood  pressure  /  3.   Normal  blood  pressure  is  less  than  120/80  mmHg  i.e.  systolic  blood  pressure  over  diastolic   blood  pressure.    

Pathways     There  are  two  pathways   • •

Neural  pathways  à  fast  à  sympathetic     Hormonal  pathways  à  slow  à  Renin-­‐angiotensin,  aldosterone  pathway  

Neural  Pathways   When  someone  is  bleeding,  it  causes  decrease  in  intravascular  volume.  The  blood  pressure  also   decreases.  Normally,  the  aortic  arch  and  baroreceptors  feel  the  stretch  in  the  walls  of  the   carotid  sinus.  They  also  sense  the  decrease  in  blood  pressure.  Glossopharyngeal  nerve  of  the   hering’s  nerve  in  the  carotid  sinus  after  sensing  this  sends  signals  to  the  brainstem.   Automatically,  the  decrease  in  parasympathetic  tone  is  achieved  while  increase  of  sympathetic   tone  occurs  to  compensate  the  decrease  in  blood  pressure.  Sympathetic  nervous  system  acts   on  the  SA  nodes  and  causes:   • • •

Increase  in  the  heart  rate   Increase  in  the  contractility  of  cardiac  muscles   Increase  in  stroke  volume  

All  this  eventually  increases  the  cardiac  output  and  finally  the  BP.    The  sympathetic  system  also   activates  the  alpha  and  beta  receptors  in  the  vasculature  leading  to  vasoconstriction  and   increase  in  total  peripheral  resistance  (TPR).  Increase  in  TPR  leads  to  increase  in  BP.      

Future  teaching  physicians  Lectures  LLC   Medicine  made  simple               Title:  Cardiac  Tamponade     Objectives  for  learning:  Understanding  the  basics  of  cardiac  tamponade   pathophysiology,  clinical  features,  diagnosis,  and  treatment.     Definition:  Cardiac  tamponade  is  impaired  ventricular  filling  due  to  excessive   pericardial  effusion.     Causes/  Risk  factors:     • Penetration  of  the  chest   • Iatrogenic  damage  to  the  atrial  or  ventricular  wall  during  central  venous   catheter  placement  or  pericardiocentesis     • Pericarditis   • Myocardial  infarction     Pathophysiology:     • The  rate  of  effusion  is  important  for  the  development  of  cardiac  tamponade.   If  more  than  300  mL  of  fluid  are  rapidly  going  into  the  pericardial  space,  it   will  cause  tamponade.  On  the  other  hand,  in  cases  of  slow  filling,  the   pericardium  has  time  to  stretch  so  there  can  be  1.5  L  of  fluid  in  pericardial   space  before  developing  a  tamponade.   • Impaired  ventricular  function  leads  to  decreased  preload,  which  then  leads   to  low  cardiac  output.  Consequently,  the  blood  pressure  is  going  to  be  low.   • The  pressures  in  all  four  cardiac  cavities  is  going  to  be  equal.     Clinical  symptoms  and  signs   • Beck’s  triad:   o JVD   o Hypotension   o Muffled  heart  sounds   • Narrowed  pulse  pressure  (due  to  low  stroke  volume)   • Pulsus  paradoxus  (blood  pressure  decrease  for  >10mmHg  during   inspiration)   • Tachycardia   Diagnosis   • Echo   • Chest  X-­‐ray  

• •

o Increased  cardiac  silhouette   o Clear  lung  fields   EKG   o Electrical  alternans   Cardiac  catheterization     o Increased  intrathoracic  pressure   o RA  pressure  is  decreased  with  the  loss  of  Y  descent  

  Treatment   o If  the  patient  is  stable  and  there  is  no  blood  –  just  watch     o If  the  patient  is  unstable  –  pericardiocentesis   o Surgery  if  the  vasculature  walls  are  damaged  

Title:  Cardiac  Tumors:  Myxomas   Objectives  for  learning:  Types  Of  Cardiac  Tumor,  Most  Common  Primary  Liver  Cancer,  Most   Common  Liver  Cancer,  Most  Common  Brain  Cancer       Types  of  Cardiac  Tumor     1. Myxomas   2. Rhabdomyomas         The  most  common  primary  cardiac  tumor  of  adults  is  atrial  myxomas.  Patients  present  with   syncope  because  this  atrial  myxoma  causes  ball  valve  effect  in  the  left  atrium.  Due  to  the  tumor   blood  cannot  get  into  the  left  ventricle  because  this  tumor  seals  up  the  mitral  valve,  causing  a   decrease  in  the  left  ventricular  and  diastolic  volume.  The  cardiac  output  also  decreases,   perfusion  also  decreases  and  the  brain  gets  affected,  therefore  leads  to  syncope.       ü In  children  the  most  common  primary  tumor  of  heart  is  Rhabdomyomas.  Tuberous  sclerosis   is  the  most  common  disease  associated  with  this  tumor.     ü The  most  common  primary  liver  cancer  is  the  hepatocellular  carcinoma  from  liver  cirrhosis.     ü The  most  common  liver  cancer  is  the  metastasis  usually  from  melanoma  or  lymphoma.     ü The  most  common  brain  cancer  is  the  metastasis  usually  from  melanoma  or  lymphoma.        

Title:  Cardiogenic  Shock    

Objectives  for  learning:  Definition,  Causes,  Clinical  symptoms  and  signs,  Diagnosis,   Treatment,  Intra  aortic  balloon  pump  (IABP).    

Definition:   Cardiogenic  shock  is  the  decrease  in  cardiac  output  that  leads  to  decrease  in  tissue  perfusion.   This  is  due  to  insufficient  circulation  of  blood  owing  to  failure  of  the  ventricles  of  the  heart  to   work  effectively.     We  know  that     Mean  arterial  pressure  =  CO  x  TPR   CO=  cardiac  output   TPR=  Total  peripheral  resistance     With  decrease  in  cardiac  output,  mean  arterial  pressure  also  decreases.  Cardiogenic  shock  is  a   medical  emergency.    

Causes/  Risk  factors   • • • • •  

Acute  myocardial  infarction  (most  common  cause)   Cardiac  temponade   Tension  pneumothorax   Arrhythmias  (ventricular  tachycardia)   Massive  pulmonary  embolism  

Pathophysiology   Clinical  symptoms  and  signs   Symptoms:   • Hypotension  –Blood  pressure  can  fall  up  to  80/60   • Oliguria   • Tachycardia   • Altered  mental  status     Signs:   • Skin  appears  pale  and  cold.   • Jugular  venous  distension  is  found   • Pulmonary  congestion  or  edema  is  present.      

Diagnosis   EKG:  To  see  the  presence  of  elevated  ST  segments,  indicating  myocardial  infarction  (MI)     Echo  to  check  cardiac  temponade  

Chest  X-­‐ray  to  detect  the  presence  of  tension  pneumothorax     Hemodynamic  monitoring:   Swan-­‐Ganz  catheter  is  used  to  monitor  blood  flow  and  heart's  function.  It  measures  left  atrial   pressure  by  measuring  capillary  pulmonary  wedge  pressure.    

Treatment   The  initial  management  is  maintaining  of   Airway   Breathing     Circulation     Afterwards  following  treatment  is  started  depending  upon  the  cause.       • In  case  of  myocardial  infarction  the  following  treatment  is  given.     − Oxygen   − Beta  blocker   − Morphine   − Ace  inhibitors   − Nitroglycerin   − NG  intubation     − Statin   − Tissue  plasminogen  activator  (TPA)   − CABG   − Angioplasty     • For  cardiac  temponade  pericariocenthesis  is  performed.     • Thoracotomy  is  carried  out  for  tension  pneumothorax     • The  drug  such  as  amiodarone  is  given  for  cardiac  arrhythmias.     • Low  molecular  weight  heparin  is  given  to  manage  pulmonary  embolism.       Vasopressors  are  also  given  in  cardiogenic  shock.  They  tend  to  increase  after  and  preload  and   thus  increase  the  reduced  blood  pressure.  These  are:   − Dopamine:  It  increases  the  renal  flow  and  renal  perfusion   − Dobutamine:  It  increases  the  cardiac  output   − Norepinephrine  or  phenolepinephrine:  It  is  used  when  both  dopamine  and  dubutamine  do   not  help  to  raise  the  BP.  Norepinephrine  increases  contractility,  cardiac  output  and   eventually  the  blood  pressure.       Don’t  give  IV  (intravenous)  fluids  here  since  they  are  harmful  for  the  patient  with  cardiogenic   shock.  Left  ventricular  pressure  is  already  elevated  so  IV  fluid  should  be  avoided.      

Intra  aortic  balloon  pump  (IABP)     Intra  aortic  balloon  pump  (IABP)  is  sometimes  used  to  boost  myocardial  oxygen  perfusion.   Balloon  is  placed  in  aorta.  During  systole  this  balloon  deflates  while  during  diastole  it  inflates.   By  doing  so  it  increases  afterload  and  cardiac  output  and  consequently  the  perfusion  and   oxygen  to  the  coronary  artery  also  increases  and  myocardiac  oxygen  demand  decreases.          

Quizzes   1. A  patient  presents  with  chest  pain,  difficult  breathing  and  confusion  after  long  trip  in  an   airplane.  His  BP  was  80/40mmHg.  His  skin  is  cold.  Jugular  vein  is  distended.  Based  on  the   findings  and  history  what  is  the  likely  complication  of  pulmonary  embolism  in  this  patient?   A. Hypovolemic  shock   B. Cardiogenic  shock   C. Anaphylactic  shock   D. Neurogenic  shock     The  correct  answer  is  B.   The  most  likely  complication  pulmonary  embolism  in  this  patient  is  cardiogenic  shock.  This  is   because  massive  pulmonary  embolism  leads  to  the  development  of  cardiogenic  shock.  It  is  also   apparent  from  the  condition  of  the  patient.  He  has  developed  hypotension,  skin  is  cold  and  his   jugular  vein  is  also  distended,  pointing  toward  cardiogenic  shock.       Hypovolemic  shock  may  present  wit  hypotension,  cold  skin  but  there  is  no  chest  pain  unless   there  is  a  trauma  there.  Also,  in  this  shock  hemorrhage  or  bleeding  occurs.  Jugular  vein  is  not   distended.  The  most  important  is  that  pulmonary  embolism  does  not  lead  to  hypovolemic   shock  as  no  blood  loss  occurs  here.       Anaphylactic  shock  is  the  characteristic  of  severe  allergic  reaction.  There  may  be  a  number  of   signs  and  symptoms  such  as  itch,  swelling,  rash,  low  BP,  reduce  heart  rate,  dyspnea,  etc.  it  is   not  the  complication  of  pulmonary  embolism.       Neurogenic  shock  is  again  not  the  complication  of  pulmonary  embolism.  It  occurs  after  spinal   cord  injury.           2. In  a  patient  with  diagnosis  of  myocardial  infarction  and  cardiogenic  shock,  what  will  be  the   most  important  treatment  of  choice?     A. Intra  aortic  balloon  pump  (IABP)   B. Angioplasty     C. CABG  

D. Pericariocenthesis  

  The  correct  answer  is  A.     Intra  aortic  balloon  pump  (IABP)  is  the  most  effective  and  important  treatment  of  choice  in   patient  with  myocardial  infarction  and  cardiogenic  shock.  This  is  because  it  increases  the   perfusion  to  the  myocardium  by  increasing  the  coronary  blood  flow  as  well  as  simultaneously   decreases  the  myocardium  oxygen  demand,  which  is  important  to  prevent  re-­‐infarct  and  tissue   death.       Angioplasty  can  be  used  but  it  is  merely  used  to  open  up  the  obstructed  vessels.       Coronary  artery  bypass  grafting  (CABG)  is  basically  a  surgical  procedure  that  is  performed  to   improve  the  blood  flow.  It  is  performed  when  there  is  severe  coronary  heart  disease  (CHD).     3. Pericariocenthesis  is  not  performed  here  and  is  mainly  done  in  case  of  cardiac  temponade.     A  patient  presents  with  cardiogenic  shock  and  myocardial  infraction.  After  resuscitation  all  of   the  following  should  be  administered  based  except?     A. Beta  blocker   B. IV  fluids   C. Tissue  plasminogen  activator  (TPA)   D. Morphine     The  correct  answer  is  B.   IV  fluids  should  not  be  administered  in  the  patient  with  cardiogenic  shock.  This  is  because  they   are  harmful  for  the  patient  with  cardiogenic  shock.  They  can  raise  the  volume  and  eventually   left  ventricular  pressure  which  is  already  elevated  so  IV  fluid  should  be  avoided.     Beta  blockers  are  useful  in  patient  with  cardiogenic  shock  and  myocardial  infarction  because   they  reduce  the  size  of  infarct  as  well  as  early  mortality  when  administered  early.  Beta  blockers   also  decrease  the  incidence  of  development  of  recurrent  ischemia,  ventricular  arrhythmias,  or   reinfarction.       Tissue  plasminogen  activator  (TPA)  can  be  given  in  patient  with  cardiogenic  shock  and   myocardial  infarction.  It  helps  to  breakdown  the  thrombosis.       Morphine  is  also  used  in  myocardial  infarction  as  it  reduces  the  pain.         4. A  18-­‐year-­‐old  patient  is  admitted  to  the  hospital  because  he  presents  with  confusion,  chest   pain,  and  confusion  and  shortness  of  breath  after  a  blunt  injury  in  the  chest.  On   examination  he  is  pale  with  cold  clammy  skin.  His  BP  is  80/60  mmHg.  His  jugular  vein  is   distended  and  urinary  output  noted  is  17ml/hour.  A  diagnosis  of  cardiogenic  shock  is  made.   What  is  the  likely  cause  of  cardiogenic  shock  in  this  patient?  

 

A. B. C. D.

Acute  myocardial  infarction   Arrhythmias   Tension  pneumothorax   Massive  pulmonary  embolism  

  The  correct  answer  is  C.   History  of  blunt  trauma  with  chest  pain  and  shortness  of  breath  is  the  typical  symptoms  of   tension  pneumothorax.  It  is  the  result  of  penetrating  injury  of  the  lung  causing  development  of   one-­‐way  valve.  Tension  pneumothorax  can  further  cause  the  development  of  cardiogenic   shock,  thus  it  is  the  most  likely  cause  here.     Acute  myocardial  infarction  does  not  occur  after  trauma.    Also,  its  symptoms  are  different  such   as  here  a  person  develops  chest  pain  that  radiates  towards  neck  and  left  arm,  sweating,   palpitation,  etc.       Arrhythmias  are  the  condition  in  which  heart  beat  is  irregular.  It  is  either  too  fast  or  too  slow.  It   is  presented  with  shortness  of  breath  and  also  does  not  develop  after  trauma.       Massive  pulmonary  embolism  cannot  be  the  likely  cause  of  cardiogenic  shock  here  because  it   does  not  develop  following  a  trauma.  For  it  to  develop,  there  should  be  a  history  of  prolong  bed   rest,  deep  venous  thrombosis,  a  long  trip  in  a  car  or  aero  plane,  etc.    

Title:  Coarctation  Of  Aorta       Objectives  for  learning:  Definition,  Classification  of  Coarctation  of  Aorta,  Clinical  Symptoms  and   Signs       Definition:   It  is  the  stenosis  or  narrowing  of  the  aorta.       Classification  of  Coarctation  Of  Aorta   • Pre-­‐ductual   • Post  ductual     The  most  important  duct  is  the  ductus  arteriosum.  It  is  a  little  pipe  that  connects  the  aorta  and   the  pulmonary  artery  during  intrauterine  life.  The  ductus  arteriosum  later  becomes  ligamentum   arteriosum.  If  something  happens  before,  it  is  called  preductual  coarctation.     If  something  happens  after,  post     Preductal  coarctation  only  occurs  in  infants.   The  adult  type  is  the  post  ductual  coarctation.  By  definition  this  is  a  stenosis  of  the  aorta  past   the  ligamentum  arteriosum  or  stenosis  distal  to  the  ductus  arteriosus  is  known  as  post  ductual   coarctation.       Coarctation  of  aorta  is  associated  with  Turner  syndrome.  Aortic  regurgitation  eventually   develops.  The  murmur  of  coarctation  of  aorta  is  the  blowing  high  pitched  diastolic  murmur.       Causes/  Risk  factors:       Pathophysiology     Clinical  symptoms  and  signs   • Low  blood  pressure  in  lower  extremities  (hypotension)   • High  blood  pressure  in  upper  extremities  (hypertension)   • Notching  of  the  ribs  and  pleural  effusion  on  chest  X-­‐rays  may  be  present.     • Poor  growth       Diagnosis     Treatment    

Future  teaching  physicians  Lectures  LLC   Medicine  made  simple               Title:  Complications  of  Acute  Myocardial  Infarction     Objectives  for  learning:  Identifying  acute  and  chronic  complications  of  acute   myocardial  infarction.     1. Chronic  Heart  Failure     • The  main  symptom  is  shortness  of  breath   • Therapy:     o ACE  inhibitor  to  decrease  blood  pressure   o Diuretics  (furosemide)  to  eliminate  fluid   • It  can  progress  to  cardiogenic  shock     2. Arrhythmias   • Premature  Ventricular  Complexes  (PVCs)   • Atrial  Fibrilation   • Ventricular  tachycardia   o Therapy:   § Amjodaron   § Electrical  cardioversion  (if  hemodynamically  unstable)   • Ventricular  fibrillation   o Therapy   § Unsynchronized  defibrillation   • Paroxysmal  Supraventricular  Tachycardia  (PSVT)   • Sinus  tachycardia   • Sinus  bradycardia  (atropine  if  they  are  dynamically  unstable)   • Asystole   • AV  block  (pacemaker  is  needed  if  there  is  IIb  or  III  degree  AV  block)     3. Reinfarction   • New  ST  elevation   o Check  CK-­‐MB  level     4. Rupture   • Occurs  due  to  scar  tissue  forming  10  days  after  myocardial  infarction   • Types:   o Free  wall  rupture  (cardiac  tamponade)  –  pericardiocentesis  is  needed   o Interventricular  wall  rupture  –  surgery  is  needed  

o Papillary  muscles  rupture  (mitral  regurgitation)  –  mitral  valve   replacement  is  needed   o Ventricular  aneurysm  

  5. Pericarditis   • Inflammation  of  pericardium   • Dressler’s  syndrome  can  develop  weeks  to  months  after  myocardial   infarction   • Treatment:   o Aspirin     6. Ventricular  embolism   • Can  cause  stroke      

Title:  Congenital  Heart  Diseases   Objectives  for  learning:  Right  To  Left  Shunt,  Left  To  Right  Shunt  and   Pathophysiology.  

Definition:     1) Right  to  left  shunt  –  it  means  early  cyanosis,  blue  babies       2) Left  to  right  shunt  –  late  onset  cyanosis  also  known  as  blue  kids     Right  to  left  shunt  occurs  in     • • • • •

Tetralogy  of  Fallot  (TOF)   Transposition  of  great  vessels   Persistent  truncus  arteriosus   Tricuspid  atresia     Total  anomalous  pulmonary  venous  return  

Left  to  right  shunt   − Ventricular  septal  defect  (VSD)—the  most  common  congenital  cardiac  defect.     − Atrial  septal  defect  (ASD)   − Patent  ductus  arteriosus  (PDA)  

Pathophysiology     The  normal  pressure  inside  the  right  atrium  (RA)  is  less  than  5  mmHg   The  normal  pressure  of  the  right  ventricle  (RV)  is  25/5mmHg,  in  the  left  atrium  (LA)  is  less  than   12  mmHg,  in  the  LV  is  130/10  and  in  the  aorta  is  130/90  mmHg.     The  pressure  in  the  RA  is  less  than  5mmHg  because  this  allows  blood  to  go  into  the  heart  during   preload  because  pressure  in  the  veins  has  to  overcome  the  pressure  in  the  atrium.  The  pressure   in  the  RV  is  25  mmHg,  so  to  receive  blood;  pressure  in  it  would  be  equal  or  less  than  the   pressure  in  the  RA  during  diastole  so  that  blood  can  easily  flow  into  the  right  ventricle.    It   means  when  heart  contracts  the  pressure  the  systole  pressure  which  ejects  blood  into  the   pulmonary  artery  has  to  be  as  high  as  25mmHg  so  that  it  can  get  blood  into  the  pulmonary   artery.    Also,  blood  from  pulmonary  artery  enters  into  the  left  atrium.  The  systolic  pressure   inside  the  pulmonary  artery  is  25  and  in  the  left  atrium  is  less  than  12;  mean  high  pressure  to   low  pressure.    

The  systolic  ejection  pressure  of  130/10  in  the  LV  pushes  out  the  blood  into  the  aorta.     Initially,  blood  moves  from  higher  pressure  to  lower  pressure,  i.e.  it  shunts  from  LV  to  RV.    But   there  is  still  a  blood  to  enter  into  the  systemic  circulation.  Over  time,  the  wall  of  the  RV  gets   thick  and  thicker  the  wall  the  higher  the  diastolic  pressure.  Overtime,  pressure  in  the  RV   overcomes  the  pressure  in  the  LV,  now  we  get  deoxygenated  blood  into  the  RV.    That’s  why  it   takes  time  and  children  are  called  blue  kids  and  a  patient  is  said  to  develop  late  onset  cyanosis.     Similar  happens  when  blood  shunts  from  LA  to  RA  and  patient  develops  late  onset  cyanosis.     Same  is  with  the  PDA,  an  open  space  between  the  aorta  and  the  pulmonary  artery.    

  Clinical  symptoms  and  signs     Diagnosis     Treatment    

Future  teaching  physicians  Lectures  LLC   Medicine  made  simple               Title:  Congestive  Heart  Failure     Objectives  for  learning:  Understanding  the  pathophysiology  of  different  types  of   heart  failure,  as  well  as  risk  factors,  clinical  features,  diagnostics,  and  treatment   options.     Definition:     Heart  failure  is  a  syndrome  which  appears  when  heart  is  not  able  to  maintain   circulation  and  to  provide  adequate  perfusion  to  the  rest  of  the  body.     Causes/  Risk  factors:     − Hypertension     − Excess  salt  in  intake     Pathophysiology:   − Normally,  heart  receives  the  blood  from  the  venous  side  of  the  body,  through  the   superior  and  inferior  vena  cava  (preload).  After  the  blood  enters  the  right  atrium   and  then  right  ventricle,  the  heart  muscle  stretches,  which  is  the  stimulus  for  the   contraction.  That  way,  the  blood  is  being  pushed  from  the  ventricles,  which  is   called  stroke  volume.  Frank  –  Starling  relationship  says  that  if  the  preload  is   increased,  the  contractility  increases  too,  thus  causing  increased  stroke  volume   and  consequently  increased  cardiac  output.   − Decreased  cardiac  output  causes  the  activation  of  compensatory  mechanisms,   including  carotid  sinus  baroreceptors,  which  in  turn  increases  sympathetic   activity  (increased  heart  rate,  contractility,  increased  preload  and  afterload).   Another,  slower  compensatory  mechanism  includes  rennin-­‐angiotensin-­‐ aldosterone  system  (water  and  sodium  retention).   − The  cause  of  heart  failure  can  be  either  systolic  or  diastolic  dysfunction.   o Systolic  dysfunction  is  caused  by  lowered  contractility  of  some  parts  of   heart  muscle  due  to  myocardial  infarction,  dilated  cardiomyopathy,   myocarditis.   o Diastolic  dysfunction  appears  due  to  impaired  relaxation  of  heart  muscle.   The  common  causes  are  hypertrophic  ventricular  failure  (due  to   hypertension,  aortic  stenosis,  aortic  regurgitation,  and  mitral  stenosis)   and  restrictive  cardiomyopathy  (amyloidosis,  sarcoidosis,   hemochromatosis).    

    Clinical  symptoms  and  signs   − Shortness  of  breath  –  Dyspnea  (because  of  pulmonary  congestion)   − Orthopnea  –  breathing  difficulties  when  lying  on  the  back   − Paroxysmal  nocturnal  dyspnea   − Nocturnal  cough   − Diaphoresis   − Cold  extremities   Specific  signs  of  left-­‐sided  heart  failure  include:   − Cardiomegaly   − S3  gallop   − S4   − Crackles  (rales)  in  the  lungs   − Dullness  to  percussion  of  the  lungs   Specific  signs  of  right-­‐sided  heart  failure  include:   − Jugular  venous  distension  (JVD)   − Liver  congestion  and  hepatomegaly   − Ascites   − Peripheral  edema   − Right  ventricular  heaves   − Nocturia   Diagnosis   − Chest  X-­‐Ray  –  cardiomegaly,  Kerley  B-­‐lines,  interstitial  markings,  pleural   effusion  (blunting  of  the  costophrenic  angle)   − Echocardiogram  is  the  most  important  examination  to  make,  because  it   shows  whether  the  systolic  ejection  fraction  is  lowered.   − ECG  findings  are  not  specific.   Treatment   1. Diet  restriction  (less  than  4g  of  salt/day)   2. Diuretics     o Furosemide  –  first  line  treatment   o Thiazide  –  second  line  treatment   o Spironolactone  (can  cause  hyperkalemia!)   3. ACE  inhibitors  decrease  mortality  in  patients  with  heart  failure  by  decreasing   preload  and  afterload.  Side  effects  of  ACE  inhibitors  are:  angioedema,  cough,   and  elevated  potassium  levels.  ACE  inhibitors  can  be  replaced  with  sartans   (angiotensin  receptor  blockers)  in  patients  with  serious  cough.   4. Beta  blockers  (Carvedilol)  are  shown  to  slow  the  progression  of  heart  failure   and  decrease  mortality.   5. Group  IV  patients  (the  terminal  stadium  of  heart  failure)  should  receive   Digitalis  in  order  to  improve  cardiac  output.  Hydralazine  and  isosorbid   nitrate  can  also  be  used  to  regulate  the  blood  pressure  in  these  patients.    

Future  teaching  physicians  Lectures  LLC   Medicine  made  simple               Title:  Coronary  Circulation     Objectives  for  learning:  Define  coronary  arteries  and  their  topography,  and   explain  coronary  circulation  as  well  as  physiology  of  coronary  blood  supply.     Definition:  Coronary  circulation  is  composed  of  coronary  arteries,  the  most   proximal  branches  of  aorta.  Their  purpose  is  blood  supply  to  the  heart  muscle.     Anatomy:  Left  coronary  artery  (LCA)  and  right  coronary  artery  (RCA)  come  off  the   ascending  aorta  as  its  first  branches.  LCA  splits  into  two  arteries:  the  circumflex   artery  (CFX),  which  wraps  around  the  left  lateral  side  of  the  heart  and  finishes  on   the  posterior  side,  and  left  anterior  descending  artery  (LAD)  which  travels  down  the   interventricular  septum  and  finishes  at  the  apex  of  the  heart.  RCA  travels   downwards  giving  its  branch  –  acute  marginal  artery  (AMA).  RCA  then  curves   around  the  back  of  the  heart  forming  posterior  descending  artery  (PDA).     Blood  supply:     CFX  –  posterior  left  ventricle   LAD  –  anterior  septum  and  apex   AMA  –  right  ventricle   PDA  –  posterior  septum     Physiology:     -­‐    At  rest,  myocardium  uses  70%  of  oxygen  contained  in  the  blood  that  comes  from   coronary  blood  vessels,  while  during  exercise,  it  extracts  90%  of  oxygen  from  the   blood.     -­‐  Coronary  arteries  receive  blood  only  during  the  diastolic  phase  of  cardiac  cycle.  

Future  teaching  physicians  Lectures  LLC   Medicine  made  simple               Title:  Deep  Venous  Thrombosis     Objectives  for  learning:  Understanding  the  causes,  risk  factors,  pathophysiology,   diagnosis,  complications,  and  treatment  of  deep  venous  thrombosis.     Definition:     Deep  venous  thrombosis  is  the  presence  of  clots  in  deep  veins  of  legs.     Causes/  Risk  factors:     • Virchow's  triad   o Endothelial  damage   o Hypercoagulability   o Stasis   Risk  factors:   • Congestive  heart  failure  (CHF)   • Immobilization     • Obesity   • Estrogen  (use  of  birth  control  pills  or  pregnancy)   • Family  history  of  DVT   • Varicose  veins   Pathophysiology:   Unlike  arterial  blood  vessels,  blood  flow  in  veins  depends  only  on  muscle   contraction.  One  way  valves  enable  bringing  the  blood  up  towards  the  heart.   Endothelial  damage  can  be  caused  by:     • surgery   • stasis  (prolonged  rest  or  travel)   • malignancies   • age.   Some  hereditary  diseases  can  cause  hypercoagulability.   • Factor  V  Leiden  deficiency  –  leads  to  increased  clotting   • Protein  C  and  S  deficiency     • Antithrombin  III  deficiency   DVT  most  often  comes  from  iliac  and  femoral  veins.     Clinical  symptoms  and  signs   Signs  and  symptoms  are  very  variable  from  patient  to  patient.  Classic  findings   include:  

• • •

Lower  extremity  pain  and  swelling  (especially  while  walking)  –  non-­‐specific,   non-­‐sensitive   Homan’s  sign  –  calf  pain  with  dorsiflexion   Fever  

  Diagnosis   • Order  Doppler  ultrasound  of  the  lower  extremities  to  determine   compressibility  of  the  veins.  It  is  highly  specific  and  highly  sensitive  for  the   detection  of  blood  clots  in  proximal  parts  of  extremities,  but  not  in  the  calf.   • The  most  accurate  test  is  venography.   • D  –  Dimer  (very  specific  but  only  about  50%  sensitive)   Complications   • Pulmonary  embolism  -­‐  detached  clots  from  deep  veins  of  lower  extremities   travel  through  the  inferior  vena  cava  to  the  heart  and  are  then  towards  the   lungs.  The  result  is  pulmonary  embolism.     − Big  saddle  emboli  that  obstruct  pulmonary  artery  cause  right   ventricular  failure  and  arrhythmia  and  hypoxia.   • Postthrombotic  syndrome  appears  due  to  insufficiency  of  venous  valve   system  and  the  increase  in  hydrostatic  pressure  in  venous  capillaries.   • Phlegma  cerulea  dolens  –  severe  leg  edema  resulting  in  ischemia  which   causes  loss  of  sensitive  and  motor  neural  function.     Treatment   • Anticoagulant  treatment  is  the  most  important   − Heparin  (prolongs  PTT)   − Varfarin  (inhibits  vitamin  K)   − TPA  (Tissue  Plasminogen  Activator)   INR  should  be  maintained  between  2  and  3  for  3-­‐6  months.   • Greenfield  filter  is  used  to  prevent  pulmonary  embolism   • Surgery  post-­‐management  (leg  elevation,  compression  stockings,  early   ambulation,  pneumatic  compression  boots.      

Title:  Einsenmengers  Disease   Objectives  for  learning:   Before  studying  Einsenmengers  Disease,  first  discuss  the  diseases  that  cause  right  to  left  shunt.     • • •

Ventricular  septal  defect  (VSD)   Atrial  septal  defects  (ASD)   Patent  ductus  Arteriosus  (PDA)  

These  are  the  leading  cause  of  development  of  Einsenmengers  Disease.  A  patient  may  have   either  of  these  diseases  for  very  long  duration  and  if  not  corrected,  they  can  lead  to  the   development  of  Einsenmengers  Disease.    

Definition:   Causes/  Risk  factors:     Pathophysiology   Usually  an  uncorrected  VSD,  ASD  and  PDA  lead  to  compensatory  pulmonary  hypertrophy  which   further  results  in  progressive  pulmonary  hypertension  which  increases  pulmonary  vascular   resistance.  This  causes  reversing  of  shunt  from  left  to  right  to  right  to  left.  This  causes  late   cyanosis,  clubbing  and  polycythemia.     The  RA  pumps  blood  into  the  RV  and  from  there  to  PA  to  the  lungs.  But  when  there  is  a  space   i.e.  ventricular  septal  defect  the  pressure  in  the  LV  overcomes  pressure  in  the  RV.  This  patient   starts  pump  blood  into  the  RV.  But  with  the  passage  of  time  RV  hypertrophy  develops.  Blood   does  not  pump  into  the  lungs  and  causes  the  patient  to  become  cyanosed.     In  case  of  ASD,  lots  of  blood  goes  into  the  pulmonary  artery.  This  causes  development  of   pulmonary  hypertension  due  to  increase  blood  flow  into  the  lungs.  The  blood  again  comes  to   RV,  causing  RV  hypertrophy.     In  case  of  PDA,  there  is  an  open  space  between  the  aorta  and  the  pulmonary  artery.  This   patient  shunts  deoxygenated  blood  into  the  PA  into  the  lungs.  Overtime,  vasoconstriction   develops,  causing  pulmonary  hypertension.  If  it  is  not  corrected  the  blood  come  backs  into  the   aorta,  causing  cyanosis,  polycythemia  and  clubbing  to  develops.   Polycythemia     Poly  means  many  

Cythemia  means  cell   When  body  senses  that  it  is  not  getting  oxygen,  it  stimulates  the  production  of  erythropoietin   to  further  stimulate  the  production  of  more  red  blood  cells,  thus  causing  polycythemia.  

Clinical  Symptoms  And  Signs   • •

Cyanosis   Clubbing  

Diagnosis   Treatment      

Title:  Atrial  Fibrillation     Objectives  for  learning:  Definition,  Causes,  Pathophysiology,  Clinical  symptoms  and  signs,   Diagnosis  and  Treatment.       Definition:   It  is  the  fibrillation  or  quickering  of  the  atrium.       Causes/  Risk  factors:     • Pulmonary  embolism,  COPD     • Iatrogenic   • Rheumatic  heart  disease  /  Mitral  regurgitation   • Arthrosclerosis   • Thyroid  (Hyperthyroidism,  thyrotoxicosis)   • Endocarditis     • Sick  sinus  syndrome       Pathophysiology   Normally,  SA  nodes  fires  and  causes  depolarization  of  the  muscles.  When  atrium  depolarizes  an   atrial  contraction  occurs.    Atrium  also  squeezes  at  the  same  time,  causing  blood  to  enter  into   the  ventricles.     But  in  case  of  atrial  fibrillation,  multiple  different  ectopic  nodes  start  firing.  Not  only  atrium   contracts,  but  blood  stasis  also  occurs.       Clinical  symptoms  and  signs   • Lightheadedness   • Syncope   • Fast  heart  beat   • Hypertension       Diagnosis   On  EKG  having  atrial  fibrillation,  check   • Rate   • Regular  or  irregular  QRS  complex   • P  waves   • P:QRS  ratio   • PR  interval   • QRS  width    

  In  atrial  fibrillation,  there  are  no  P  waves  present.  The  patient  heart  rate  is  very  variable.  The   heart  beat  is  irregularly  irregular.    No  P:  QRS  ratio  since  no  P  waves  are  present.  The  normal  PR   interval  is  less  than  0.02  seconds  but  in  atrial  fibrillation,  no  P  waves  are  present  so  PR  interval   cannot  be  determined.    QRS  complex  is  usually  of  120  milliseconds.  In  atrial  fibrillation  QRS   width  is  less  than  120  milliseconds  or  normal.       Treatment   Patients  are  given:   • Anticoagulants  such  as  warfarin  (because  of  blood  stasis  and  if  anticoagulants  are  not  given   patients  with  AF  can  develop  stroke,  mesenteric  ischemia,  claudication,  myocardial   infractions,  etc.)   • Beta  blockers  such  as  methoprolol:  These  help  to  decrease  the  heart  rate.   • Calcium  channel  blockers  e.g.  nefidipine:  They  slow  down  the  heart  rate.   • Digoxin:  It  has  a  parasympathetic  effect,  stimulating  the  vagal  nerves  which  slow  down  the   firing  from  SA  and  AV  node  and  thus  allows  decreasing  the  heart  rate.          

Title:  Fetal  Red  Cell  Production     Objectives  for  learning:  Types  of  Hemoglobin  and  Organ  responsible  for  Blood  formation  during   intrauterine  life.       Fetal  hemoglobin  α2γ2   Adult  hemoglobin  α2β2       Weeks   • First  three  to  ten  weeks:  Yolk  sac  is  responsible  for  making  blood.   • 6  weeks:  Liver  is  responsible  for  erythropoises.   • 15  and  30  weeks:  Spleen  takes  on  this  responsibility.     • 22  weeks  to  adult:  Bones  becomes  responsible.         Quiz   1. Which  organ  is  responsible  for  formation  of  blood  during  6  week  of  intrauterine  life?   A. Spleen   B. Bones   C. Yolk  sac   D. Liver   The  correct  answer  is  D.   Liver  is  responsible  for  erythropoises  during  6  week  of  intrauterine  life.     Yolk  sac  is  responsible  for  making  blood  during  first  3  to  10th  week  of  intrauterine  life.     Spleen  becomes  responsible  for  erythropoises  during  15  and  30  weeks  of  life.     Bones  becomes  responsible  from  22  weeks  to  onward  in  adult  life.       Which  organ  is  responsible  for  formation  of  blood  during  25  week  of  intrauterine  life?   A. Spleen   B. Bones   C. Yolk  sac   D. Liver   The  correct  answer  is  A.   Spleen  becomes  responsible  for  erythropoises  during  15  and  30  weeks  of  life.     Liver  is  responsible  for  erythropoises  during  6  week  of  intrauterine  life.     Yolk  sac  is  responsible  for  making  blood  during  first  3  to  10th  week  of  intrauterine  life.     Bones  becomes  responsible  from  22  weeks  to  onward  in  adult  life.       During  which  stage  does  the  yolk  sac  take  part  in  erythropoises?   A. Does  not  take  part   B. 4th  week   C. 22  week   D. 15th  week  

The  correct  answer  is  B.   Yolk  sac  is  responsible  for  making  blood  during  first  3  to  10th  week  of  intrauterine  life.  So,   correct  option  is  4th  week  here.     Yolk  sac  does  take  part  in  the  formation  of  blood  during  intrauterine  life.     During  15  and  30  weeks  of  life  spleen  becomes  responsible  for  erythropoises.     Bones  becomes  responsible  from  22  weeks  to  onward  in  adult  life.       4.  What  is  the  difference  between  Fetal  hemoglobin  and  Adult  hemoglobin  with  regard  to  their   structure?   A. Fetal  hemoglobin  has  two  alpha  and  two  beta  chains.   B. Adult  hemoglobin  has  two  alpha  and  two  gamma  chains.     C. Fetal  hemoglobin  has  two  alpha  and  two  gamma  chains.   D. Both  are  same  and  have  no  difference.     The  correct  answer  is  C.   Fetal  hemoglobin  has  two  alpha  and  two  gamma  chains  while  adult  has  two  alpha  and  two  beta   chains.         Fetal  hemoglobin  has  not  two  alpha  and  two  beta  chains  but  has  two  alpha  and  two  gamma   chains.       Adult  hemoglobin  does  not  have  two  alpha  and  two  gamma  chains  but  have  has  two  alpha  and   two  gamma  chains.     Fetal  and  adult  hemoglobins  are  not  same  but  differ  structurally  as  well  as  with  respect  to  their   life.       5.  Which  organ  is  responsible  for  formation  of  blood  during  adult  life   A. Spleen   B. Bones   C. Yolk  sac   D. Liver   The  correct  answer  is  B.     Bones  are  responsible  for  formation  of  blood  from  22  weeks  to  onward  in  adult  life.     Spleen  becomes  responsible  for  erythropoises  during  15  and  30  weeks  of  life.     Yolk  sac  is  responsible  for  making  blood  during  first  3  to  10th  week  of  intrauterine  life.     Liver  is  responsible  for  erythropoises  during  6  week  of  intrauterine  life.      

Title:  Heart  Blocks   Objectives  For  Learning:  Atrio  ventricular  nodal  block,  Types,  First  degree  AV  block,  Second   degree  AV  block,  and  Third  degree  heart  block.   Atrio  Ventricular  Nodal  Block   In  AV  nodal  block  there  is  an  impairment  of  the  conduction  between  the  atria  and  ventricles  of   the  heart.  SA  node  fires  but  this  discharge  does  not  go  beyond  the  atria  to  the  ventricles.     Types   There  are  three  types  of  blocks.     1. First  degree  AV  block:     It  is  always  prolonged  in  case  of  first  degree  AV  block.  Normally,  it  is  less  than  200  mili  seconds.   But  in  first  degree  AV  block,  the  PR  interval  is  greater  than  200  mili  seconds  (greater  than  5   boxes).  This  is  because  there  is  a  block  causing  a  delay  in  the  conduction  between  the  AV  node   down  into  the  ventricle.  It  is  a  begin  condition  and  requires  no  treatment.     2. Second  degree  AV  block   It  is  of  two  types   Mobitz  type  1:  It  is  also  known  as  Wenckebach.  A  prolonged  PR  interval  until  a  p  wave  fails  to   conduct  is  known  as  mobitz  type  1.  It  is  again  a  begin  condition  and  requires  no  treatment.     Mobitz  type  2:    P  waves  here  fail  to  conduct  but  the  PR  interval  is  constant.  Here  AV  node  is   conducting  and  the  block  is  actually  in  the  bundle  of  His.  For  this  reason,  constant  PR  interval   appears.  Patients  may  have  palpitations.  They  need  pace  maker  implantation.  This  type  of   condition  can  progress  into  complete  heart  block.     3. Third  degree  heart  block   It  is  the  absence  of  conduction  of  atrial  impulses  to  the  ventricles  which  means  there  is  no   correspondence  between  P  waves  and  QRS  complexes.  The  atrial  conduction  is  doing   everything  independently.  There  is  a  complete  AV  block.  There  is  dissociation  between  atrial   impulses  and  ventricular  conduction.  Complete  heart  block  leads  to  asystole.  Patients  suffer   from  presyncope  episodes.  They  develop  lightheadedness  or  dizziness.  They  also  develop   ventricular  tachycardia  and  atrial  fibrillation.  In  EKG,  atrio-­‐ventricular  rates  are  different  from   each  other.  P  waves  are  present.  P:  QRS  ratio  is  variable.  QRS  width  is  normal.  A  pace  maker  is   needed  to  treat  third  degree  AV  block.    

Title:    Heart  Sounds  Basics     There  are  four  heart  valves   • • • •

Aortic  valve  (right  upper  sternal  border)   Pulmonary  valve     Tricuspid  valve  (left  lower  sternal  border)     Mitral  valve    

  The  apex  is  in  the  5th  and  6th  intercostal  space.     The  normal  heart  sound  is  S1  and  S2   S1  is  the  sound  heard  when  the  mitral  and  the  tricuspid  valve  close  as  the  blood  flow  from   atrium  to  the  ventricle  and  ventricle  starts  to  squeeze.     S2  heart  sound  is  due  to  closure  of  aortic  and  pulmonary  valve  and  is  heard  as  the  ventricular   systole  ends  and  the  ventricular  diastole  begins.       S3  sound  is  present  in  case  of  pregnancy  or  in  congested  heart  failure.  It  can  be  heard  in  the   apex  and  in  the  tricuspid  area.     S4  sound  is  due  to  the  atrium  contracting  against  a  non-­‐compliant  ventricle.                

Future  teaching  physicians  Lectures  LLC   Medicine  made  simple               Title:  Hypertensive  Emergency     Objectives  for  learning:  Understanding  the  basics  of  hypertensive  urgency  and   emergency,  and  learn  to  diagnose  them  and  apply  fast  and  effective  treatment.     Definitions:     • Hypertension  is  a  medical  condition  in  which  blood  pressure  is  higher  than   140/90  mmHg  in  two  separate  occasions.   • Hypertensive  urgency  –  blood  pressure  of  220/120  mmHg  or  higher  without   any  end  organ  damage.   • Hypertensive  emergency  –  blood  pressure  of  220/120  mmHg  or  higher  with   end  organ  damage.   • Hypertensive  encephalopathy  –  blood  pressure  of  240/140  mmHg  or  higher   with  neurologic  symptoms.   • Preeclampsia  –  Hypertensive  episodes  during  pregnancy  (140/90mmHg  or   higher)  with  proteinuria  and  edema  of  lower  extremities.     Causes/  Risk  factors:     Risk  factors:   • Hypertension  is  the  most  prevalent  in  African  Americans   • Men  are  more  often  affected  than  women   Causes:   • Noncompliance  to  medications   • Sympathomimetic  drugs   • Cushing’s  syndrome   • Eclampsia   • Pheochromocytoma   • Hyperaldosteronism     Pathophysiology:     − Patient  using  can  develop  hypertensive  urgency  due  to  bad  compliance  to   antihypertensive  medication  they  normally  use.   − Cocaine,  LSD,  and  phenylephrine  users  can  experience  hypertensive  urgency   due  to  sympathomimetic  effects  of  these  drugs.   Increased  blood  pressure  damages  the  endothelium  of  blood  vessels.  That  causes   the  deposition  of  proteins  in  the  walls  of  the  blood  vessels,  thus  causing  basement  

membrane  thickening.  That  thickening  narrows  the  walls  of  blood  vessels  causing   ischemia  by  decreasing  blood  flow  through  the  blood  vessels.       Clinical  symptoms  and  signs   • Head   o Headaches   o Blurry  vision  (due  to  papiloedema)   o Altered  mental  status   o Weakness  in  arms  or  legs,  numbness,  tingling,  etc.   o Retinal  hemorrhages   • Chest   o Chest  pain   o Shortness  of  breath   o Pulmonary  crackles/rales   o Jugular  venous  distension   o S3   • Kidneys   o Anuria   o Hematuria   o Increased  creatinine   • Legs   o Edema         Diagnosis   − It  is  necessary  to  take  good  history.   − Physical  exam:   o If  there  is  altered  mental  status,  rule  out  the  other  possible  causes  in   order  to  blame  hypertension.   o Full  neurological  exam   o Fundoscopic  exam   − Laboratory  techniques:   o ECG   o Electrolytes   o Creatinine   o BUN   o WBC  count   o LFTs   o Proteins  and  blood  in  urine   − Iamging:   o CT  scan  of  the  head   o Chest  X-­‐Ray      

Treatment    The  aim  is  to  decrease  the  blood  pressure  by  25%  in  first  1  –  2  hours.   *If  patient’s  blood  pressure  is  240/140  mmHg,  the  pressure  after  1  –  2  hours  should   be  180/90  mm  Hg.   Medication:   • Beta  blockers  (contraindicated  if  the  patient  used  drugs)   • Sodium  nitroprusside   • Fenoldopam   • Hydralazine   • Nitroglycerin    

Title:    Hypovolemic  Shock       Objectives  for  learning:  Definition,  Causes,  Pathophysiology,  Signs  and  Symptoms  Stages  of   hypovolemic  shock,  Diagnosis  and  Treatment     Definition:   Low  blood  volume  leads  to  decrease  cardiac  output.     Causes/  Risk  factors:     1. Hemorrhagic     • Trauma   • GI  Bleed   • Retroperitoneal  bleed     2. Non  hemorrhagic   • Burns   • Vomiting   • Massive  watery  diarrhea   • Third  space-­‐-­‐  Ascites  in  massive  liver  cirrhosis   • Low  albumin  (hypoalbuminemia)     Pathophysiology   Low  blood  volume  causes  low  cardiac  output.  The  parameters  of  hypovolemic  shock  include   decreased  cardiac  output,  increased  total  peripheral  resistance  (TPR)  and  decreased  pulmonary   wedge  pressure.       Clinical  Symptoms  And  Signs   • Hypotension   • Cold,  clammy  skin     Diagnosis   • CVP  (central  venous  pressure)   • Pulmonary  capillary  wedge  pressure  is  low.   • Systemic  vascular  resistance  is  high.     Stages  Of  Hypovolemic  Shock   Stage  1:    It  is  characterized  by  10  to  15%  (  2000ml).  The  affect  person  is  lethargic.       Treatment     • Maintain  airways,  breathing  and  circulation.  For  maintaining  airways  incubate  the  patient.       • Manual  pressure  over  bleeding  is  important  to  stop  bleeding.     • Pass  NG  tube  to  avoid  development  of  aspiration  pneumonia     • IV  fluids  Normal  saline.         Quizzes   1. A  patient  presents  with  confusion  and  lethargy.  He  sustains  a  trauma  on  his  abdomen.  On   examination  his  BP  is  80/50.  His  skin  is  cold  and  clammy.    The  jugular  venous  pressure  is   normal.  What  is  the  most  likely  diagnosis?     A. Hypovolemic  shock   B. Cardiogenic  shock   C. Aortic  aneurysms     D. Neurogenic  shock   The  correct  answer  is  A   The  most  likely  diagnosis  is  hypovolemic  shock.  This  is  because  patient  suffers  from  a  trauma  on   his  abdomen  so  it  may  have  cause  retroperitoneal  bleed.  For  this  reason,  his  BP  has  fallen  and   his  skin  is  cold.     Since  there  is  no  complaint  of  chest  pain,  so  the  cardiogenic  shock  is  unlikely  here.  The  jugular   venous  pressure  must  be  elevated  in  case  of  cardiogenic  shock.     Aortic  aneurysm  is  a  condition  in  which  aorta  is  dilated  to  greater  than  1.5  times  than  its  normal   size.  The  symptoms  of  this  problem  appear  when  aneurysm  is  ruptured.  There  may  be   abdominal  and  back  pain.  Aortic  aneurysm  rupture  is  a  serious  medical  condition.    

Neurogenic  shock  results  when  there  is  injury  to  the  spinal  cord,  affecting  the  sympathetic   system.  Skin  here  is  warm.  Bradycardia  is  also  present.       2. A  patient  is  admitted  in  the  hospital  after  a  diagnosis  of  hypovolemic  shock  is  made.  What  is   the  most  common  cause  of  this  shock?   A. Burns   B. Injury  to  spinal  cord   C. Fluid  shift   D. Blood  loss                                                 The  correct  answer  is  D.   The  most  common  cause  of  hypovolemic  shock  is  blood  loss.  Loss  of  blood  leads  to  immediate   volume  depletion.  This  depletion  further  affects  cardiac  output  which  becomes  reduced.     Burns  may  lead  to  development  of  hypovolemic  shock  but  is  not  as  common  as  blood  loss  is.   Injury  to  spinal  cord  is  the  most  common  cause  of  neurogenic  shock.   Fluid  shift  can  also  cause  hypovolemic  shock  since  it  leads  to  decrease  in  blood  pressure  to   severe  extent  but  it  occurs  rarely.         3. A  patient  is  presents  with  severe  bleeding  and  confusion  after  a  trauma.    His  BP  is   80/40mmHg.  His  heart  rate  is  120beats/min.  He  is  admitted  in  the  hospital  and  necessary   resuscitation  is  given.  It  is  however  found  that  his  urinary  output  is  15ml/  hour.  What  is  the   most  likely  stage  of  hypovolemic  shock  in  this  patient?     A. Stage  1   B. Stage  2   C. Stage  3   D. Stage  4   The  correct  answer  is  C.     The  most  likely  stage  of  hypovolemic  shock  in  this  patient  based  on  his  clinical  presentation  is   stage  3.  In  this  stage  30  to  40%  blood  loss  occurs,  leading  to  severely  dropping  of  blood   pressure  and  urinary  output.  Heart  rate  however  is  increased.  A  person  develops  lactic  acidosis  

and  consequently  altered  mental  status  and  confusion.    In  this  patient  urine  output  is  markedly   reduced.     In  case  of  Stage  1  person  does  not  have  above  mentioned  symptoms.  He  may  be  asymptomatic   because  here  only  10  to  15%  blood  loss  has  occurred.     Stage  2  is  characterized  by  20  to  30  %  loss  of  blood.  Here  systemic  BP  is  normal,  but  heart  rate   is  high.     Stage  4  is  a  severe  form  of  hypovolemic  shock  characterized  by  greater  than  40%  blood  loss.  A   person  may  be  unconscious  and  anuric.      

Title: Infective Endocarditis Objectives for learning: Definition, Causes, Classification, Complications Of Infective Endocarditis, Clinical symptoms and signs, Diagnosis and Treatment

Definition: Infection of the heart valve is called infective endocarditis.

Causes/ Risk factors: Bacteria

Classification 1. Acute Endocarditis (less than 6 weeks): The culprit is staphylococcus aureus (more common in IV drug abusers) 2. Subacute Endocarditis is caused by: • Streptococcus viridians, most prone to dentistry procedures • Enterococcus (bacteria arise from GI tract) 3. Native Valve Endocarditis • Streptococcus viridans • Haemophilus • Actinobacillus • Cardiobacterium • Ekenella • Kingella 4. Prosthetic Endocarditis The bacteria responsible here are: • Staphylococcus epidermidis (60 days of surgery) • If more than 60 days then staphylococcus aureus is responsible In blood cultures if streptococci bovi appears positive then it may probably be due to colon cancer

Complications Of Infective Endocarditis • • •

Cardiac failure Glomerulonephritis Mycotic abscess

Pathophysiology Clinical Symptoms And Signs

• • • • • • • •

Fever Roth spots (retinal lesions due to vasculitis) Osler’s nodes (painful nodes in the pads of the finger or the toes due to vasculitis) Murmur Jane way lesions (lesions on the palm and the soles due to emboli) Anemia Nail bed hemorrhages/ Splinter hemorrhages Emboli

Diagnosis • •

Blood culture Transesophageal echocardiogram

Treatment Empiric Treatment: Start with vancomycin and gentamycin and give intravenously before the results of blood culture come. Once the blood cultures come positive for particular organism, such as for streptococcus viridians then give penicillin. But if a person is allergic to penicillin then switch to ceftriaxone and gentamycin. If person is IV drug abuser, then given antibiotic against staphlococcus aureus. Nafcilin for 4 weeks is given plus gentamycin for 5 days In case of Methicillin-resistant Staphylococcus aureus (MRSA) give vancomycin for 6 weeks. And if blood culture comes positive for enterococcal bacteria give penicillin/ampicillin (for 4 to 6 weeks) If a person is allergic to penicillin then administer vancomycin + gentamycin (for 4 to 6 weeks).

Quiz 1. A 15-year-old patient presents with fever and joints pain for 3 day. A patient also complains of night sweat. On examination she is pallor. Splinter hemorrhage and painful nodules on the fingers’ pad are found. What is the most likely diagnosis? A. Polymyalgia Rheumatica B. Atrial Myxoma C. Reactive Arthritis D. Infective endocarditis The correct answer is D. The most likely diagnosis is infective endocarditis. It is characterized by low grade fever, Osler’s nodules, anemia and splinter hemorrhage. In addition, Jane way lesions and Roth’s spots are also present. It is a condition of the inflammation of the valves of the heart. Polymyalgia rheumatica (PMR) is basically a syndrome of unidentified etiology. It usually occurs in adults and is characterized by muscle pain frequently of the shoulder girdles and the hip. A patient usually complains of morning stiffness that lasts for more than one hour. Atrial Myxoma is a tumor of the heart. It is a benign tumor. Fever, joint pain, shortness of breath and weight loss occur. Painful nodules are not found here, so it is not a correct diagnosis. Reactive arthritis is an autoimmune condition which is the result of an infection. It is characterized by conjunctivitis, urethritis and arthritis. This is not correct as patient has no such complaints.

2. Which of The following is not the cutaneous involvement of infective endocarditis? A. Janeway's lesions B. Skin petechiae C. Roth's spots D. Osler's Nodules The correct answer is C. Roth's spots are not the cutaneous involvement of infective endocarditis. These are basically the retinal lesions due to vasculitis. Skin petechiae are usually found in patient with infective endocarditis.

Janeway's lesions are one of the cutaneous involvements of infective endocarditis. These are lesions on the palm and the soles and are due to emboli. Osler's Nodules are again the cutaneous manifestation of this condition i.e. infective endocarditis. These are painful nodes present in the pads of the finger or the toes due to vasculitis.

3. A person with infective endocarditis has a history of using drugs for pleasure. Which antibiotic is best for this patient? A. Nafcilin B. Vancomycin C. Amoxacillin D. Rifampicin The correct answer is A. Nafcilin is the drug of choice for the person who is a drug abuser and also suffered from infective endocarditis. Vancomycin is usually preferred for those who are allergic to penicillin. Amoxacillin has no such role in case of infective endocarditis. Likewise, rifampicin is not the drug used for patients with infective endocarditis.

4. Which of the following statements concerning infective endocarditis is not right? A. Empiric treatment of infective endocarditis includes vancomycin and gentamycin B. Splenomegaly is found to occur commonly in acute infective endocarditis than the sub acute one. C. Glomerulonephritis is one of the complications of infective endocarditis D. Infective endocarditis takes place within 2 weeks of bacteremia The correct answer is B. The incorrect option regarding infective endocarditis is A. Splenomegaly is not commonly found in case of acute infective endocarditis. It is rather present in sub acute infective endocarditis. Empiric treatment of infective endocarditis includes vancomycin and gentamycin. This treatment is generally started before the report of blood cultures come. Clinical manifestations of this condition usually take place within 2 weeks of the provocative bacteremia in approximately 80% of cases.

Glomerulonephritis is one of the complications of infective endocarditis.

5. All of the following are responsible for native valve endocarditis except A. B. C. D.

Streptococcus viridans Streptococcus viridians Haemophilus Ekenella

The correct answer is B. Streptococcus viridians do not cause native valve endocarditis instead infection by these bacteria occurs following a dentistry procedure. Streptococcus viridians are responsible for native valve endocarditis. 55-65% cases of all native valve endocarditis are caused by viridans streptococci. Haemophilus and Ekenella both are the cause behind native valve endocarditis.

Future  teaching  physicians  Lectures  LLC   Medicine  made  simple             Title:  Introduction  to  hypertension     Objectives  for  learning:      Causes,  risk  factors  and  pathophysiology  and   complications  of  hypertension.     Definition:  Hypertension  is  high  blood  pressure  (>140/90).  Essential  hypertension   is  high  blood  pressure  without  identified  cause  (95%  of  all  patients).  Secondary   hypertension  has  known  causes  (5%  of  patients).     Causes/  Risk  factors:     Risk  factors:   • Age   • Gender  (men  have  higher  risk  than  women)   • Race  (African  Americans  have  higher  risk  of  hypertension)   • Obesity   • Sedentary  lifestyle   • Increased  sodium  intake  (>4g/day)   • Alcohol     Causes:   • Secondary  hypertension   o Renal  causes   § Renal  artery  stenosis   § Chronic  renal  failure   § Polycystic  kidney  disease   o Endocrine  system   § Hyperthyroidism   § Hyperaldosteronism   § Hyperparathyroidism   § Cushing  syndrome   § Pheochromocytoma   o Medications   § Oral  contraceptives   § Decongestives   § NSAIDs   § TCAs   o Coarctation  of  the  aorta   o Illegal  drugs  

§ Cocaine   o Sleep  apnea   o Birth  control  pills     Pathophysiology:     • Decreased  perfusion  through  the  renal  artery  stimulates  rennin-­‐angiotensin-­‐ aldosterone  system,  thus  increasing  peripheral  vascular  resistance  and  blood   pressure.   • Hyperthyroidism  increases  metabolic  rate  and  consequently  the  blood   pressure.   • Hyperaldosteronism  increases  sodium  reabsorption  and  causes   hypernatremia,  thus  increasing  intravascular  volume  and  blood  pressure.   • Patients  with  Cushing  syndrome  have  excess  amount  of  cortisol  which   activates  adrenal  medulla  to  produce  more  norepinephrine  and  epinephrine,   thus  increasing  blood  pressure.   • In  pheochromocytoma,  high  amounts  of  norepinephrine  and  epinephrine  are   produced  due  to  tumor  of  adrenal  medulla.     • Decongestives  are  intended  to  make  a  local  vasoconstriction,  but  also  have   impact  on  systemic  blood  pressure  increase.     • NSAIDs  block  COX2,  thus  blocking  the  synthesis  of  vasodilatatory   prostaglandins.     • Cocaine  inhibits  the  reuptake  of  norepinephrine,  thus  increasing  its  blood   concentration  and  blood  pressure.     • Sleep  apnea  causes  respiratory  acidosis  which  provokes  hypoxia.  Hypoxia   leads  to  hypoxic  vasoconstriction  in  the  lungs  which  leads  to  pulmonary   hypertension  and  eventually  high  blood  pressure.     Increased  systemic  vascular  resistance  increases  the  afterload,  so  the  heart  has  to   work  much  harder,  which  leads  to  left  ventricular  hypertrophy.  Over  time,  heart   function  becomes  weaker  leading  towards  dilation  of  the  heart  and  heart  failure.     High  blood  pressure  accelerates  arteriosclerosis  by  damaging  endothelium  of  blood   vessels.     Complications   • Cardiac  complications   o Coronary  artery  disease  (myocardial  infarction)   o Left  ventricular  hypertrophy  and  heart  failure   o Stroke  (hemorrhagic),  TIAs,  ischemic  stroke   o Aortic  dissection   o Peripheral  arterial  disease  

•

•  

Eye  changes   o Papilloedema   o Retinal  hemorrhages   Kidneys   o Nephrosclerosis   o Renal  failure  

Title:  Kawasaki’s  Disease   Objectives  for  learning:  Clinical  Features,  Complications,  and  Treatment     Definition       Causes/  Risk  factors:       Pathophysiology     Clinical  Features     • • • • • • •

Conjunctivitis   Rash  all  over  the  body  (desquamating  rash)   Adenopathy  (cervical  lyphmadenopathy)   Strawberry  tongue   Hands  and  foot  (swelling,  erythema  and  peeling)   Burn     Uncontrolled  fever  for  more  than  5  days    

Complications   • •

Predisposed  to  coronary  artery  aneurysm   Myocardial  infraction    

Diagnosis     Treatment   •      

Intravenous  immunoglobulins  (IVIG)  +  aspirin    

Title:  MITRAL  REGURGITATION     Objectives  for  learning:  Definition,  Causes/  Risk  factors,  Pathophysiology,  Symptoms,  Diagnosis   and  Treatment.       Definition:   Blood  returns  into  left  side  of  the  heart  into  the  left  atrium  from  the  pulmonary  vein  right  back   into  left  ventricle  into  the  aorta  to  the  rest  of  the  body.     When  mitral  valve  closes  it  gives  S1.  The  blood  flows  out  through  the  aorta  during  systole  and   during  diastole  mitral  valve  opens  up  to  allow  blood  to  return  back  to  the  heart  but  at  the  same   time  aortic  valve  and  pulmonary  valve  both  close  and  it  gives  S2.    During  systole  both  tricuspid   and  mitral  valve  close  to  give  S1  sound.       During  systole  mitral  valve  blow  up  and  so  blood  goes  back  to  the  left  atrium,  increasing  the   pressure  inside  it,  causing  decrease  in  cardiac  output,  hypertension  and  cardiogenic  shock.       Causes/  Risk  factors:     Acute  causes:  Endocarditis,  S.aureus  infection,  Myocardial  infarction  (rupture  of  papillary   muscles)     Chronic  Causes:  Rheumatic  heart  disease,  Marfan  syndrome,  and  cardiomyopathy.     Pathophysiology   LA  pressure  increases  here.  The  size  of  left  atrium  is  normal  but  blood  now  backs  up,  back  to   the  pulmonary  vein,  pulmonary  capillaries,  pulmonary  edema,  congestion  and  eventually   pulmonary  hypertension.       Clinical  symptoms  and  signs   − Dyspnea   − Palpitations   − Proximal  nocturnal  dyspnea     − Pulmonary  edema     PE:  Holosystolic  murmur     Diagnosis   − Chest  x-­‐ray    shows  dilated  left  ventricle  and  pulmonary  edema     − Echo  show  presence  of  MR,  dilated  left  ventricle  and  decreased  left  ventricular  function         Treatment   Medical  therapy:  It  is  started  with  afterload  reduction  medications  such  as  ACE  inhibitors  (such   as  lisinopril)    

Decrease  salt  intake     Digoxin   For  arrhythmias  give  CCB  (calcium  channel  blocker)  to  treat  atrial  fibrillation  (AF)   Anticoagulation  therapy  (patient  may  have  AF)   Surgical  Treatment:  Patient  needs  a  mitral  valve  replacement  or  mitral  valve  repair.       Quiz     1. A  patient  presents  with  complain  of  attacks  of  severe  shortness  of  breath  and  coughing  at   night.  The  first  heart  sound  appears  soft  while  the  apex  beat  is  laterally  displaced.    There  is   a  murmur  appeared  following  first  heart  sound  and  is  of  high-­‐pitched.  Chest  x  ray  shows   enlargement  of  the  left  atrium  and  the  left  ventricle.  What  is  the  most  probable  diagnosis?   A. Mitral  regurgitation     B. Mitral  stenosis   C. Tricuspid  regurgitation     D. Tricuspid  stenosis   The  correct  answer  is:  B   The  most  probable  diagnosis  is  Mitral  regurgitation.  This  is  characterized  by  the  post  nocturnal   dyspnea,  orthopnea  and  palpitations.    Holosystolic  murmur  appears  following  first  heart  sound   and  is  of  high-­‐pitched.  Chest  x  ray  shows  enlargement  of  the  left  atrium  and  the  left  ventricle.     Mitral  stenosis  is  a  condition  characterized  by  the  narrowing  of  the  mitral  valve  orifice.  It  is   presented  with  the  same  symptoms  as  that  of  mitral  regurgitation.  Tapping  apex  beat  is  present   with  very  loud  first  heart  sound.  Chest  X  ray  shows  left  atrial  enlargement.     Tricuspid  regurgitation  is  the  consequence  of  problem  within  the  tricuspid  valve.  The  symptoms   include  those  of  right-­‐sided  heart  failure,  such  as  edema,  ascites,  jugular  venous  distension   and  hepatomegaly.    Jugular  venous  pressure  is  found  to  be  elevated.  Echo  shows  the  presence   of  enlargement  of  right  ventricle  and  right  atrium.     Tricuspid  valve  stenosis  is  a  disease  of  the  valves  of  the  heart  which  results  due  to  narrowing  of   the  tricuspid  valve  orifice.    An  abnormal  pulse  is  felt  in  the  jugular  vein  within  the  neck  during   a  physical  examination.   2. When  does  the  mitral  regurgitation  take  place?  

A. During  systole   B. During  diastole   C. During  both  systole  and  diastole   The  correct  answer  is:  A   The  mitral  regurgitation  takes  place  during  systole.  During  systole  mitral  valve  being  abnormal   could  not  propel  blood  to  the  left  ventricle  and  so  blood  goes  back  to  the  left  atrium,  increasing   the  pressure  inside  it  with  subsequent  consequences.     The  option  B  and  C  are  not  correct  since  during  diastole  pressure  exerted  on  the  walls  of  the   arteries  are  not  enough  to  proper  blood  from  left  atrium  to  left  ventricle.     3. A  46  year  old  man  with  severe  mitral  regurgitation  has  no  symptoms.  His  left  ventricular   ejection  fraction  is  approximately  45%  while  an  end-­‐systolic  diameter  index  is  about  2.9   cm/m2.  What  would  be  the  most  suitable  treatment  in  this  patient?       A. No  treatment   B. Mitral  valve  replacement  or  repair     C. ACE  inhibitor  therapy   D. Diuretic  therapy  and  digoxin       The  correct  answer  is:B   A  zurgical  treatment  is  recommended  in  case  of  severe  mitral  regurgitation  even  if  the  patient   is  asymptomatic.  This  is  because  when  the  left  ventricular  ejection  fraction  falls  down  below   60%  it  may  cause  a  progressive  dysfunction  of  left  ventricle.   If  no  treatment  is  given  patient  may  develop  cardiac  failure  and  even  death  of  the  person   ensues.     ACE  inhibitor  therapy  is  of  no  value  in  case  of  asymptomatic  patient.  It  is  however  used  when   patient  with  mitral  regurgitation  develops  hypertension.     Diuretic  therapy  and  digoxin  are  indicated  when  there  is  presence  of  hypertension  and   arrhythmias  respectively.  Since  this  patient  is  asymptomatic  therefore  both  drugs  are  not  used   here.       4. What  is  the  type  of  murmur  found  in  mitral  regurgitation  (MR)?   A. Pansystolic  murmur   B. Presystolic  murmur  

C. Holosystolic  murmur   D. Holodiastolic  murmur   The  correct  answer  is:  C.     In  mitral  regurgitation  Holosystolic  murmur  is  present.  It  is  a  high-­‐pitched  murmur  found  at  the   apex.  It  starts  from  the  end  of  S1  and  remains  till  the  beginning  of  S2.     Pansystolic  murmur  is  although  found  in  MR  but  it  is  also  present  in  other  conditions  of  the   heart.  It  starts  from  the  beginning  of  S1  and  remains  till  the  end  of  S2.   Presystolic  murmur  is  present  in  case  of  mitral  stenosis  and  appears  between  the  A  sound  and   S1.   Holodiastolic  murmur  begins  from  the  end  of  S2  and  remains  till  the  beginning  of  S1  and  is  not   present  in  MR.     5. A  55  years  old  patient  presents  with  difficulty  in  breathing  for  one  month.  He  also  suffers   from  apprehension.  He  gave  a  history  of  severe  fever  and  formation  of  lesions  on  the  hand   and  fingers.  A  diagnosis  of  mitral  regurgitation  was  made  based  on  the  clinical  examination   and  radiological  results.  What  is  the  likely  cause  of  mitral  regurgitation  in  this  patient?   A. Infective  endocarditis   B. Myocardial  infarction     C. Rheumatic  heart  disease   D. Marfan  syndrome   The  correct  answer  is:  A.   Although  all  the  options  can  cause  mitral  regurgitation  but  if  we  see  that  this  patient  gives   history  of  fever  as  well  as  lesions  on  hands  and  finger  (might  be  Roth's  spots  or  Osler's  nodes),   it  is  then  infective  endocarditis.     Myocardial  infarction  is  a  serious  condition  presents  with  chest  pain,  dyspnea,  sweating  and   palpitation.  Therefore,  this  is  not  correct  with  regard  to  this  patient’s  scenario.   Rheumatic  heart  disease  is  usually  more  common  in  children.  It  not  only  affects  the  heart,  but   also  the  joints  and  the  central  nervous  system.  It  is  the  result  of  rheumatic  fever  caused  by  a   preceding  infection  by  group  A  streptococcal.     Marfan  syndrome  is  basically  a  genetic  disorder  which  is  diagnosed  earlier.  This  syndrome  tends   to  affect  the  skeletal  system.  People  with  this  disorder  are  abnormally  tall  and  have   long  limbs  and  fingers.    

Title:  Neurogenic  Shock    

Objectives  for  learning:  Definition,  Causes,  Pathophysiology,  Parameters  of  Neurogenic   Shock,  Clinical  symptoms  and  signs  and  Treatment.    

Definition:   Neurogenic  Shock  is  defined  as  the  absence  of  sympathetic  tone  leading  to  systemic   vasodilatation.  However,  there  is  an  unopposed  vagal  nerve  activity.    

Causes/  Risk  factors:     Spinal  cord  Injury  (It  causes  loss  of  sympathetic  tone  and  unopposed  vagal  activity  vagal  nerve   tone  leads  to  hypotension).    

Pathophysiology   Systemic  vasodilatation  causes  decrease  in  systemic  vascular  resistance  and  hypotension   (80/40).  The  end  result  is  bradycardia  with  heart  rate  of  20beats/minute.    

Parameters  of  Neurogenic  Shock   Decreased  cardiac  output,  decreased  total  peripheral  resistance  (TPR)  and  decreased   pulmonary  capillary  wedge  pressure.    

Clinical  symptoms  and  signs   • • • •

Hypotensive     Bradycardia  as  sympathetic  system  is  loss     Warm  skin     Urine  output  might  be  low  or  normal  

Diagnosis   Treatment   • • • • • • • •

Maintain  Airway,  breathing  and  circulation  (ABC)   Mobilize  spine  (cover  on  neck)   IV  fluids  is  the  mainstay  of  therapy   Also  start  domapine  since  it  improves  cardiac  contractility  and  thus  the  perfusion  is   enhanced.     Administer  dobutamine  to  increase  cardiac  output.     For  braydcardia  give  atropine     For  neurodeficit  give  methylprednisolone     Try  to  maintaining  their  body  temperature    

•

Call  neurosurgery  department,  orthopaedics  and  trauma  surgeons  

  Quiz   A  patient  sustains  an  injury  in  the  back.  Now  he  is  presented  in  the  night  with  decrease  urinary   output  and  lethargy.  He  tells  that  he  has  urinated  once  in  the  morning  up  till  now.  He  has  been   urinating  twice  a  day  only  for  2  days.  On  examination  his  temperature  is  99⁰F.  BP  is   90/60mmHg.  His  heart  rate  is  50  beats/min.  What  is  the  mainstay  of  therapy?   A. B. C. D.

IV  fluids   Dobutamine   Spine  mobilization   Antibiotics  

The  correct  answer  is  A.   This  patient  is  basically  suffering  from  neurogenic  shock,  so  here  IV  fluids  are  the  mainstay  of   therapy.     Dobutamine  is  no  doubt  very  important  but  it  only  works  to  enhance  the  cardiac  output   whereas  IV  fluids  increase  blood  volume  and  also  correct  dehydration.     Spine  mobilization  is  important  too  to  prevent  further  trauma  but  it  alone  won’t  work.     Antibiotics  are  beneficial  and  mainstay  of  therapy  when  there  is  a  septic  shock.  In  this  case,   antibiotics  will  be  given  only  when  there  is  a  suspicion  of  infection.       A  36-­‐year-­‐old  injured  male  is  presented  in  emergency  with  warm  extremities,  increased   respiratory  rate,  oliguria  and  rapid  pulse.  On  examination  his  B.P.  is  70/40mmHg,  pulse  is   140/min  and  there  is  bluish  discoloration  of  tip  of  nails  and  tongue.  Which  kind  of  shock  is   developed  in  this  patient?   Hemorrhagic  Shock     A. B. C. D.

Septic  shock   Neurologic  shock   Anaphylactic  shock   Hypovolemic  shock    

The  correct  answer  is  B.  

The  clinical  findings  go  with  the  condition  of  neurogenic  shock.  Since  patient  is  injured,  it  is   possible  he  has  got  an  injury  to  his  spinal  cord.  This  causes  loss  of  sympathetic  tone  and   systemic  vasodilation  due  to  unopposed  vagal  activity.     Septic  shock  occurs  when  there  is  a  history  of  infection.  In  this  condition  peripheries  are  usually   cold.     Anaphylactic  shock  is  due  to  severe  allergic  reaction  and  is  manifested  with  a  rash,  itching,   swelling,  low  BP  and  shortness  of  breath.     Hypovolemic  shock  is  the  result  of  bleeding  or  hemorrhage  anywhere  from  the  body.  Although,   this  patient  is  injured,  injury  can  cause  internal  bleeding  but  his  peripheries  are  warm  instead  of   being  cold.       A  patient  has  devolved  neurogenic  Shock  shortly  after  getting  an  injury  to  the  spinal  cord.  How   will  he  be  presented  clinically?     A. B. C. D.

Cold  &  clammy  peripheries     Increased  heart  Rate   Increased  total  peripheral  resistance  (TPR)   None  of  these  

The  correct  answer  is  D.   The  correct  option  is  D.  The  periphery  is  usually  warm  because  of  systemic  vasodilatation.     Heart  rate  is  decreased  due  to  loss  of  sympathetic  activity  and  also  total  peripheral  resistance   (TPR)  is  decreased.    

Title: Patent Ductus Arteriosus Objectives for learning: Definition, Pathophysiology, Murmur of PDA, Clinical Symptoms and Signs, Treatment.

Definition: Patents means opened Duct means artery During fetal development, there is an open space between the pulmonary artery (PA) and the aorta. It is known as PDA. Blood actually gets shunted from PA into the aorta because lungs are not developed.

Causes/ Risk factors: Pathophysiology Normally blood goes to the right atrium to right ventricle and that blood shunts through pulmonary artery. The pulmonary artery shunts blood to the lungs which comes back to left atrium to aorta to rest of the body. When the baby borns, and takes deep breathe, the resistance inside the lungs decreases and they expand and opened up. Afterward, there is no need of ductus to shunt blood. It becomes ligamentum arteriosum. The problem arises when aorta starts to work and pumps blood into the circulations and the lungs expand as the baby borns, the resistance inside the lungs decreases, the blood starts to shunt from left aorta into the pulmonary circulation because pressure in aorta is very high i.e. blood now shunts from left to right (aorta to pulmonary artery). Now the right ventricle has to pump blood against higher pressure. Thus, a patient with patent ductus arteriosus develops right ventricular hypertrophy because the pressure gradients of the right ventricle are higher so to pump blood against the higher pressure of PA. As the blood enters into the lungs, they develop vasoconstrictions inside the lungs and therefore increasing the pulmonary pressures. Overtime the pulmonary vascular hypertension causes pulmonary vascular sclerosis inside the pulmonary vasculature. When the pressure inside the RV is high enough, the patients will now be able to reverse this flow and starts to shunt this deoxygenated blood from right side to left side. The deoxygenated blood mixes with oxygenated, causing the patient to become cyanosed and exhausted.

Murmur of PDA The murmur of PDA is machinery murmur. ü Prostaglandins (PGE) keep PDA open.

Clinical Symptoms And Signs Symptoms of cyanosis in the lower extremities

Diagnosis Treatment It is important to close this PDA. Indomathacin helps to close this PDA.

Future  teaching  physicians  Lectures  LLC   Medicine  made  simple               Title:  Peripheral  Vascular  Disease  -­‐  Atherosclerosis     Objectives  for  learning:  Learning  the  process  of  atherosclerotic  plaque  formation   and  its  consequences.     Definition:  Atherosclerosis  is  a  peripheral  vascular  disease  which  manifests  with   creation  of  atherosclerotic  plaques  inside  the  walls  of  blood  vessels.     Causes/  Risk  factors:     • Hyperlipidemia   • Bad  eating  habits     Pathophysiology:  Damage  of  the  endothelial  wall  causes  the  migration  of   macrophages.  Macrophages  then  accumulate  LDL  and  form  so  called  “foam  cells”.   That  way,  fatty  streak  is  formed  in  the  wall  of  the  blood  vessel.  Platelets  send  signals   to  fibrous  cells  and  smooth  muscle  cells  to  migrate  from  tunica  media  to  tunica   intima  producing  a  fibrous  plaque,  which  then  progresses  to  atheroma.  Narrowed   blood  vessels  than  cause  organ  ischemia.  Abdominal  aorta  is  the  most  common   place  for  artheroma  formation.     Clinical  symptoms  and  signs   •   Pain  due  to  ischemia   •   Claudications     Complications:   • Thrombosis   • Myocardial  infarction   • Stroke    

Future  teaching  physicians  Lectures  LLC   Medicine  made  simple               Title:  Prinzmetal’s  Angina     Objectives  for  learning:  Understanding  Prinzmetal’s  angina  clinical  features  and   treatment  options.     Definitions:  Transient  coronary  vasospasms  of  coronary  arteries.     Pathophysiology:  Coronary  arteries  affected  by  Prinzmetal’s  angina  usually  already   have  thrombosis  occluding  up  to  75%  of  their  lumen.  Transmural  ischemia  is   present.     Clinical  symptoms  and  signs   • Chest  pain     Diagnosis   • Transient  ST-­‐elevation   • Coronary  angiography     Treatment   • Calcium  channel  blockers   • Nitrates  

Title:  Rheumatic  Heart  Disease     Objectives  for  learning:  Definition,  Causes,  Pathophysiology,  Clinical  symptoms  and  signs,and   Diagnosis         Definition:     Rheumatic  Heart  Disease  is  the  consequence  of  the  pharyngeal  infection.       Causes/  Risk  factors:     • Group  A  beta  hemolytic  Streptococcus       Pathophysiology     This  is  a  type  II  immune  mediated  hypersensitivity.  Patients  with  this  disease  develop  a   murmur.  They  have  vegetation  and  fibrosis.  The  most  affected  valve  is  the  mitral  valve.  In  case   of  acute  disease  the  antibodies  of  the  M  protein  of  the  organism  destroy  the  valve.  The   antibodies  come  and  bind  to  M  protein  of  the  organism.  They  then  both  attack  and  destroy  the   valve  causing  an  inflammation.       In  case  of  acute  inflammatory  response  on  mitral  valve,  the  patient  suffers  from  mitral   regurgitation.  These  protein  attack  the  glycoproteins  of  the  antigen  present  on  the  valve.       In  case  of  chronic  disease,  fibrosis  of  the  mitral  valve  occurs  causing  stenosis  of  the  mitral  valve.     Not  only  mitral  valve  gets  affected  but  also  aortic  valve  can  be  affected.  Likewise,  tricuspid   valve  can  also  get  affected.  However,  mitral  and  the  aortic  valve  get  affected  more  as  compared   to  others.       Patients  with  rheumatic  heart  disease  also  develop  myocarditis.       Clinical  symptoms  and  signs   • Fever  (101.2  ⁰F)   • Erythema  marginatum  (a  red  margin  rash)   • Valvular  damage  (patients  develop  murmur  due  to  vegetation  of  the  valves.  The  most   affected  valve  which  is  affected  is  the  mitral  valve)   • Erythrocyte  sedimentation  rate  is  very  high   • Red  hot  joints  (joints  pain—migratory  polyarthritis)     • Sub-­‐cutaneous  nodules  (Ashoff  bodies:  These  are  the  granuloma  with  histocytes  with  giant   cells)   • Saint  vitus  dance  or  Sydenham's  chorea    

Sydenham's  chorea  is  due  to  the  CNS  pathology.  The  patient  has  an  immune  reaction.  The   antibodies  bind  the  neurons  in  the  brain  and  thus  affect  the  caudate  nucleus  and  subthalamic   nuclei.  Caudate  nucleus  is  important  in  the  body  movement.       Diagnosis     ASO:  antistreptolysin  O  titers       Treatment      

Title:  SEPTIC  SHOCK     Objectives  for  learning:  Definition,  Causes/  Risk  factors,  Pathophysiology,  Complications,   Symptoms,  Diagnosis  and  Treatment  of  septic  shock.       Definition:   The  sepsis  pathway   Systemic  inflammatory  response  syndrome  (SSRI)  (i.e.  inflammation  and  source)  à  sepsis  (one   organ  failure)à  severe  sepsis  (sepsis  plus  end  organ  damage)à  septic  shock  >2  àMODS     • Systemic  inflammatory  response  syndrome  is  defined  as  fever  of  more  than  38⁰C  and  higher   heart  rate.     • Sepsis  is  the  systemic  inflammatory  response  syndrome  and  the  presence  of  a  known   infection.     • Septic  shock  is  persistent  hypotension  despite  giving  IV  fluids  or  vasopressors.  It  is  the  most   common  cause  of  death  in  ICU.       Causes/  Risk  factors:     • Bacterial  infection  by  bacteria  such  as     − E.Coli     − Klebsialla   − Staph  aureus   − Pseudomonas       Pathophysiology   As  the  bacteria  enter  the  blood,  it  leads  to  activation  of  neutrophils,  monocytes,  interleukin  and   cytokines.  They  rush  the  blood  stream  to  attach  the  bacteria.  Bacteria  possess  different   endotoxins.  These  toxins  damage  the  endothelial  cells  walls  and  also  activate  the  macrophages,   interleukins,  cytokines,  and  neutrophils  leading  to  systemic  vasodilation.  This  systemic   vasodilation  further  causes  hypotension  and  underperfusion  of  the  tissues  causing  lactic   acidosis.    Coagulopathy  occurs  as  the  endothelium  of  the  blood  vessels  gets  damaged  by  the   toxins.  Eventually  body  organs  begin  to  damage  or  organ  failure  ensues.    Bacterial  infection  and   sepsis  lead  to  decrease  systemic  vascular  resistance  and  cardiac  output  increases  to   compensate  this.         Sepsis  parameters  include:    decreased  systemic  vascular  resistance,  increased  cardiac  output   and  decreased  capillary  pulmonary  wedge  pressure.       1. SIRS   IN  this  condition  following  important  findings  are  present:   • Fever  >  38⁰C  or    90  beats/min  

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Tachypnea  (develops  due  to  lactic  acidosis  and  so  to  blow  out  excess  CO2  it  leads  to   hyperventiliation)  Respiratory  Rate  is  greater  than  20  whole  PCO2  is  less  than  32  mmHg.     WBC  >  12,000  cells/ml  or    4mm/dl   • Oliguria  55)   • Smoking   • Hypertension   • Male  gender   • Diabetes     Pathophysiology:     Due  to  atherosclerotic  plaques  that  occlude  the  lumen  of  coronary  arteries,  there  is   a  higher  demand  for  oxygen  than  it  could  be  delivered  through  the  occluded   arteries.  Decreased  perfusion  to  the  heart  muscle  causes  ischemia  of  the   myocardium  presented  with  chest  pain,  especially  during  the  exercise.     Clinical  symptoms  and  signs   • Chest  pain     • Exertion   • Symptoms  can  last  for  10  –  15  min,  but  usually  1-­‐5  min.   • Symptoms  are  relieved  by  rest  and  sublingual  nitroglycerin   Diagnosis   • EKG  (normal  findings)   • Cardiac  enzyme  (no  elevation)   • Stress  test   o Exercise  (treadmill)  –  until  the  maximum  heart  rate  is  reached  (220  –   age)   § Chest  pain   § Hypotension  

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§ ST-­‐depression   § Arrhythmia   o Stress  echo   Cardiac  catheterization  –  if  stress  test  is  positive.   Pharmacologic  stress  test  (for  patients  that  are  not  able  to  perform  exercise)   o IV  adenosine  (causes  coronary  vasodilatation)   o Dipyridamol  (causes  coronary  vasodilatation)   o Dobutamine  (increases  myocardial  oxygen  demand;  increases  heart   rate,  contractility,  and  blood  pressure)  

  Complications   Progression  of  stable  angina  leads  to  acute  coronary  syndrome  (unstable  angina,   non-­‐STEMI,  and  STEMI)     Treatment   • Risk  factor  modification   o Diet  (