S C I E N T I F I C  B A S I S  O F  M E D I C I N E  2 0 0 9 USMLE Step I  Cardiovascular Boards Prep  M A Y  1 3 ,  2 0 ...
Test-taking tips <ul><li>Use First Aid as your primary resource and write in notes in the margins </li></ul><ul><li>Practi...
Anatomy <ul><li>Carotid sheath:  V-A-N </li></ul><ul><ul><li>Internal jugular  v ein (lateral) </li></ul></ul><ul><ul><li>...
Anatomy <ul><li>Jugular venous pulsations: </li></ul><ul><ul><li>V wave:  v enous filling of right atrium  T-wave </li></u...
Anatomy A C V X Y
Anatomy <ul><li>Cardiac chambers </li></ul><ul><ul><li>RV most anterior </li></ul></ul><ul><ul><ul><li>Susceptible to trau...
Anatomy <ul><li>Cardiac chambers </li></ul><ul><ul><li>CXR anatomy: </li></ul></ul><ul><ul><ul><li>On PA film, most of wha...
Anatomy <ul><li>Coronary anatomy:  coronaries fill in diastole </li></ul><ul><ul><li>Left main coronary artery </li></ul><...
Anatomy <ul><li>Coronary anatomy: </li></ul><ul><ul><li>Left main coronary artery </li></ul></ul><ul><ul><ul><li>Left ante...
Anatomy <ul><li>Coronary anatomy: </li></ul><ul><ul><li>Left main coronary artery </li></ul></ul><ul><ul><ul><li>Left ante...
Anatomy <ul><li>Coronary anatomy: </li></ul><ul><ul><li>Inferior LV:  </li></ul></ul><ul><ul><ul><li>Supplied by RCA in 70...
Cardiac auscultation <ul><li>Systolic murmurs:  8 main causes </li></ul><ul><ul><li>Aortic stenosis  </li></ul></ul><ul><u...
Cardiac auscultation <ul><li>Systolic murmurs:  8 main causes </li></ul><ul><ul><li>Aortic stenosis  (A, crescendo-decresc...
Cardiac auscultation <ul><li>Diastolic murmurs:  4 main causes </li></ul><ul><ul><li>Aortic regurgitation  </li></ul></ul>...
Cardiac auscultation <ul><li>Diastolic murmurs:  4 main causes </li></ul><ul><ul><li>Aortic regurgitation  (LSB, blowing) ...
Cardiac auscultation <ul><li>Right-sided murmurs: </li></ul><ul><ul><li>Increase during inspiration </li></ul></ul><ul><li...
Cardiac auscultation <ul><li>Murmurs you should know about: </li></ul><ul><ul><li>Mitral regurgitation </li></ul></ul><ul>...
Cardiac auscultation <ul><li>Mitral regurgitation – L sided heart failure </li></ul><ul><ul><li>Holosystolic, apex    axi...
Cardiac auscultation <ul><li>Mitral valve prolapse – atypical CP, endocarditis </li></ul><ul><ul><li>Mid-systolic click, t...
Cardiac auscultation <ul><li>Heart sounds: </li></ul><ul><ul><li>S1: mitral and tricuspid valves closing </li></ul></ul><u...
Physiology <ul><li>MAP = (SBP + (2 x DBP))/3 </li></ul><ul><li>Pulse pressure = SBP – DBP (≈SV) </li></ul><ul><li>MAP = CO...
Physiology <ul><li>Know the determinants of stroke volume </li></ul><ul><ul><li>Contractility (  ), preload (  ), afterl...
Physiology <ul><li>Preload = EDV </li></ul><ul><li>Afterload = MAP </li></ul><ul><li>What drugs affect preload?  </li></ul...
Physiology <ul><li>Understand Starling curve </li></ul><ul><ul><li>Contractility proportional to preload </li></ul></ul><u...
Physiology LV volume (mL) LV pressure (mmHg) SV diastole systole ESV EDV Isovolumic contraction Isovolumic relaxation AVO ...
Physiology
Physiology <ul><li>Differential diagnosis of shock: </li></ul><ul><ul><li>Low CVP, low CO, high SVR: hypovolemia </li></ul...
Electrophysiology <ul><li>Action potential: </li></ul><ul><ul><li>Phase 0 </li></ul></ul><ul><ul><li>Phase 1 </li></ul></u...
Electrophysiology <ul><li>Depolarization: Phase 0 </li></ul><ul><ul><li>Rapid Na channels open </li></ul></ul><ul><ul><li>...
Electrophysiology <ul><li>Sympathetic nervous system: </li></ul><ul><ul><li>Increases automaticity </li></ul></ul><ul><ul>...
Electrophysiology <ul><li>Anti-arrhythmics:  </li></ul><ul><ul><li>Change shape of action potential </li></ul></ul><ul><ul...
Electrophysiology <ul><li>Class I: </li></ul><ul><ul><li>Ia: quinidine, procainamide, disopyramide </li></ul></ul><ul><ul>...
Electrophysiology <ul><li>Class I: </li></ul><ul><ul><li>Ia: quinidine, procainamide, disopyramide </li></ul></ul><ul><ul>...
Electrophysiology <ul><li>Class II:  </li></ul><ul><ul><li>Beta-blockers </li></ul></ul><ul><ul><li>Used to treat atrial a...
Electrophysiology <ul><li>Mechanisms of arrhythmias: </li></ul><ul><ul><li>Automaticity,  reentry , triggered activity </l...
Electrophysiology <ul><li>ECG pearls: </li></ul><ul><ul><li>P wave: atrial depolarization </li></ul></ul><ul><ul><li>PR in...
Electrophysiology <ul><li>ECG pearls: </li></ul><ul><ul><li>Irregularly irregular? Think atrial fibrillation </li></ul></u...
Electrophysiology <ul><li>ECG pearls: </li></ul><ul><ul><li>AV block:  </li></ul></ul><ul><ul><ul><li>1 st  degree: PR int...
Congenital heart disease <ul><li>Right-to-left shunts: </li></ul><ul><ul><li>Blue babies </li></ul></ul><ul><ul><li>“Terri...
Congenital heart disease <ul><li>Left-to-right shunts: </li></ul><ul><ul><li>VSD, ASD, PDA </li></ul></ul><ul><ul><li>VSD ...
Congenital heart disease <ul><li>Transposition </li></ul><ul><ul><li>Aorta comes off of RV, PA comes off of LV </li></ul><...
Congestive heart failure <ul><li>Syndrome based on signs / symptoms </li></ul><ul><li>Differential diagnosis is broad </li...
Congestive heart failure <ul><li>Understand the pathophysiology behind clinical manifestations (signs/symptoms) </li></ul>...
Congestive heart failure <ul><li>Understand how therapy works </li></ul><ul><ul><li>Remember that low CO results in: </li>...
Congestive heart failure <ul><li>Understand mechanism of action of diuretics </li></ul><ul><ul><li>Acetazolamide </li></ul...
Congestive heart failure <ul><li>Digoxin: a board exam favorite… </li></ul><ul><ul><li>Inhibits Na/K ATPase directly </li>...
Ischemic heart disease <ul><li>Atherosclerosis:  </li></ul><ul><ul><li>Differentiate from </li></ul></ul><ul><ul><ul><li>M...
Ischemic heart disease <ul><li>Myocardial infarction:  </li></ul><ul><ul><li>Diagnosis: ECG    troponin    CK-MB </li></...
Ischemic heart disease <ul><li>Evolution of MI: </li></ul><ul><ul><li>Day 1: release of necrotic contents into blood strea...
Infectious heart disease <ul><li>Bacterial endocarditis: </li></ul><ul><ul><li>Roth spots, Osler’s nodes, Janeway lesions,...
Infectious heart disease <ul><li>Rheumatic heart disease: </li></ul><ul><ul><li>Aschoff bodies (granuloma with giant cells...
Etc cardiac diseases to know about <ul><li>Pericardial disease </li></ul><ul><ul><li>Acute pericarditis, constrictive peri...
Lipidology <ul><li>Understand mechanisms, effects, and side effects of lipid-lowering agents </li></ul><ul><ul><li>Best at...
Pharmacology <ul><li>A board exam favorite </li></ul><ul><li>Clinical vignette: </li></ul><ul><ul><li>Figure out the disea...
Pharmacology <ul><li>High-yield stuff: </li></ul><ul><ul><li>Anti-arrhythmics </li></ul></ul><ul><ul><li>Diuretic mechanis...
Good luck!
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S C I E N T I F I C B A S I S O F M E D I C I N E 2 0 0 9

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  • Way too long; need to know your audience (sonographers may not want to know about physiology); good talk for one hour (key points at the end is distracting on too many pages)
  • S C I E N T I F I C B A S I S O F M E D I C I N E 2 0 0 9

    1. 1. S C I E N T I F I C B A S I S O F M E D I C I N E 2 0 0 9 USMLE Step I Cardiovascular Boards Prep M A Y 1 3 , 2 0 0 9 Sanjiv J. Shah, MD Assistant Professor of Medicine Division of Cardiology, Department of Medicine [email_address] N O R T H W E S T E R N U N I V E R S I T Y F E I N B E R G S C H O O L O F M E D I C I N E
    2. 2. Test-taking tips <ul><li>Use First Aid as your primary resource and write in notes in the margins </li></ul><ul><li>Practice test questions </li></ul><ul><li>Rapidly changing areas / fields / clinical trials: unlikely to be tested </li></ul><ul><li>Importance of clinical associations: </li></ul><ul><ul><li>~80% of questions contain a clinical vignette </li></ul></ul><ul><ul><li>Remember the ultimate goal: third-year </li></ul></ul>
    3. 3. Anatomy <ul><li>Carotid sheath: V-A-N </li></ul><ul><ul><li>Internal jugular v ein (lateral) </li></ul></ul><ul><ul><li>Common carotid a rtery (medial) </li></ul></ul><ul><ul><li>Vagus n erve (posterior) </li></ul></ul><ul><li>Why is this important? </li></ul><ul><ul><li>Need to know the anatomy for internal jugular vein cannulation (central line) </li></ul></ul><ul><ul><li>“Stick the carotid” = stroke / big bleed </li></ul></ul>
    4. 4. Anatomy <ul><li>Jugular venous pulsations: </li></ul><ul><ul><li>V wave: v enous filling of right atrium T-wave </li></ul></ul><ul><ul><li>Y descent: passive emptying of RA as tricuspid valve opens in early diastole </li></ul></ul><ul><ul><li>A wave: a trial kick P-wave </li></ul></ul><ul><ul><li>X descent: atrial relaxation </li></ul></ul><ul><ul><li>C wave: tricuspid valve c losure at onset of systole QRS </li></ul></ul>
    5. 5. Anatomy A C V X Y
    6. 6. Anatomy <ul><li>Cardiac chambers </li></ul><ul><ul><li>RV most anterior </li></ul></ul><ul><ul><ul><li>Susceptible to trauma (RV contusion, perforation) </li></ul></ul></ul><ul><ul><li>Left atrium most posterior </li></ul></ul><ul><ul><ul><li>Severe enlargement can cause dysphagia or hoarseness (recurrent laryngeal nerve) </li></ul></ul></ul><ul><ul><li>LV makes up most of the heart’s mass </li></ul></ul><ul><ul><ul><li>That is why normal ECG axis is leftward </li></ul></ul></ul>
    7. 7. Anatomy <ul><li>Cardiac chambers </li></ul><ul><ul><li>CXR anatomy: </li></ul></ul><ul><ul><ul><li>On PA film, most of what you normally see is the RV; if the heart enlarges it makes the heart wider (“cardiomegaly”) </li></ul></ul></ul><ul><ul><ul><li>On lateral film, RV is anterior, LV is posterior; this is used to help determine which chamber is causing cardiomegaly </li></ul></ul></ul>
    8. 8. Anatomy <ul><li>Coronary anatomy: coronaries fill in diastole </li></ul><ul><ul><li>Left main coronary artery </li></ul></ul><ul><ul><ul><li>Left anterior descending (LAD) </li></ul></ul></ul><ul><ul><ul><ul><li>Septal perforators </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Diagonal branches </li></ul></ul></ul></ul><ul><ul><ul><li>Left circumflex (LCx) </li></ul></ul></ul><ul><ul><ul><ul><li>Obtuse marginals </li></ul></ul></ul></ul><ul><ul><li>Right coronary artery (RCA) </li></ul></ul><ul><ul><ul><li>Acute marginals </li></ul></ul></ul><ul><ul><ul><li>Posterior descending artery (in 70-80%) _________ </li></ul></ul></ul>
    9. 9. Anatomy <ul><li>Coronary anatomy: </li></ul><ul><ul><li>Left main coronary artery </li></ul></ul><ul><ul><ul><li>Left anterior descending (LAD) ANTEROSEPTUM, APEX </li></ul></ul></ul><ul><ul><ul><ul><li>Septal perforators SEPTUM </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Diagonal branches ANTERIOR LV </li></ul></ul></ul></ul><ul><ul><ul><li>Left circumflex (LCx) LATERAL LV </li></ul></ul></ul><ul><ul><ul><ul><li>Obtuse marginals LATERAL LV </li></ul></ul></ul></ul><ul><ul><li>Right coronary artery (RCA) </li></ul></ul><ul><ul><ul><li>Acute marginals RIGHT VENTRICLE </li></ul></ul></ul><ul><ul><ul><li>Posterior descending artery (in 70-80%) SEPTUM, INFERIOR LV, POSTERIOR LV </li></ul></ul></ul>
    10. 10. Anatomy <ul><li>Coronary anatomy: </li></ul><ul><ul><li>Left main coronary artery </li></ul></ul><ul><ul><ul><li>Left anterior descending (LAD) ANTEROSEPTUM, APEX </li></ul></ul></ul><ul><ul><ul><ul><li>Septal perforators SEPTUM V1, V2 </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Diagonal branches ANTERIOR LV V3, V4, V5, V6 </li></ul></ul></ul></ul><ul><ul><ul><li>Left circumflex (LCx) LATERAL LV I, aVL </li></ul></ul></ul><ul><ul><ul><ul><li>Obtuse marginals LATERAL LV I, aVL </li></ul></ul></ul></ul><ul><ul><li>Right coronary artery (RCA) </li></ul></ul><ul><ul><ul><li>Acute marginals RIGHT VENTRICLE II, III, aVF; RV4 </li></ul></ul></ul><ul><ul><ul><li>Posterior descending artery (in 70-80%) SEPTUM, INFERIOR LV, POSTERIOR LV II, III, aVF; V7-V9 </li></ul></ul></ul>
    11. 11. Anatomy <ul><li>Coronary anatomy: </li></ul><ul><ul><li>Inferior LV: </li></ul></ul><ul><ul><ul><li>Supplied by RCA in 70-80% </li></ul></ul></ul><ul><ul><ul><li>Supplied by LCx in 10-20% </li></ul></ul></ul><ul><ul><ul><li>Supplied by both RCA and LCx in 10% (co-dominant) </li></ul></ul></ul><ul><ul><li>Why is coronary anatomy important? </li></ul></ul><ul><ul><ul><li>Helps diagnose acute MI on ECG </li></ul></ul></ul><ul><ul><ul><li>Risk depends on location of MI (LAD = high-risk) </li></ul></ul></ul>
    12. 12. Cardiac auscultation <ul><li>Systolic murmurs: 8 main causes </li></ul><ul><ul><li>Aortic stenosis </li></ul></ul><ul><ul><li>Aortic valve sclerosis </li></ul></ul><ul><ul><li>Mitral regurgitation </li></ul></ul><ul><ul><li>Tricuspid regurgitation </li></ul></ul><ul><ul><li>Hypertrophic cardiomyopathy </li></ul></ul><ul><ul><li>VSD </li></ul></ul><ul><ul><li>Pulmonic stenosis </li></ul></ul><ul><ul><li>Flow murmur </li></ul></ul>
    13. 13. Cardiac auscultation <ul><li>Systolic murmurs: 8 main causes </li></ul><ul><ul><li>Aortic stenosis (A, crescendo-decrescendo) </li></ul></ul><ul><ul><li>Aortic valve sclerosis (A, sounds like AS) </li></ul></ul><ul><ul><li>Mitral regurgitation (M, holosystolic) </li></ul></ul><ul><ul><li>Tricuspid regurgitation (T, holosystolic) </li></ul></ul><ul><ul><li>Hypertrophic cardiomyopathy (LSB, harsh) </li></ul></ul><ul><ul><li>VSD (LSB, harsh) </li></ul></ul><ul><ul><li>Pulmonic stenosis (P, harsh) </li></ul></ul><ul><ul><li>Flow murmur (A/P/T/M, quality varies) </li></ul></ul>A = aortic, P = pulmonic, T = tricuspid, M = mitral, LSB = left sternal border
    14. 14. Cardiac auscultation <ul><li>Diastolic murmurs: 4 main causes </li></ul><ul><ul><li>Aortic regurgitation </li></ul></ul><ul><ul><li>Mitral stenosis </li></ul></ul><ul><ul><li>Pulmonic regurgitation </li></ul></ul><ul><ul><li>Tricuspid stenosis </li></ul></ul>
    15. 15. Cardiac auscultation <ul><li>Diastolic murmurs: 4 main causes </li></ul><ul><ul><li>Aortic regurgitation (LSB, blowing) </li></ul></ul><ul><ul><li>Mitral stenosis (M, opening snap, rumble) </li></ul></ul><ul><ul><li>Pulmonic regurgitation (P) </li></ul></ul><ul><ul><li>Tricuspid stenosis (T) </li></ul></ul>P = pulmonic, T = tricuspid, M = mitral, LSB = left sternal border
    16. 16. Cardiac auscultation <ul><li>Right-sided murmurs: </li></ul><ul><ul><li>Increase during inspiration </li></ul></ul><ul><li>Left-sided murmurs: </li></ul><ul><ul><li>Increase during expiration </li></ul></ul><ul><li>Atrial septal defect (ASD): </li></ul><ul><ul><li>Doesn’t cause intrinsic murmur itself b/c low velocity flow (interatrial pressures not high) </li></ul></ul><ul><ul><li>But due to increased blood returning to R heart: </li></ul></ul><ul><ul><ul><li>Flow murmur over pulmonic valve (systolic murmur) </li></ul></ul></ul><ul><ul><ul><li>Flow murmur over tricuspid valve (diastolic murmur) </li></ul></ul></ul>
    17. 17. Cardiac auscultation <ul><li>Murmurs you should know about: </li></ul><ul><ul><li>Mitral regurgitation </li></ul></ul><ul><ul><li>Tricuspid regurgitation </li></ul></ul><ul><ul><li>Aortic stenosis </li></ul></ul><ul><ul><li>Ventricular septal defect (VSD) </li></ul></ul><ul><ul><li>Mitral valve prolapse </li></ul></ul><ul><ul><li>Aortic regurgitation </li></ul></ul><ul><ul><li>Mitral stenosis </li></ul></ul><ul><ul><li>Patent ductus arteriosus (PDA) </li></ul></ul>
    18. 18. Cardiac auscultation <ul><li>Mitral regurgitation – L sided heart failure </li></ul><ul><ul><li>Holosystolic, apex  axilla </li></ul></ul><ul><ul><li>Etiologies: LV dilation, CAD, MVP, rheumatic </li></ul></ul><ul><li>Tricuspid regurgitation – R sided heart failure </li></ul><ul><ul><li>Holosystolic, left sternal border,  with inspiration </li></ul></ul><ul><ul><li>Etiologies: RV dilation, endocarditis, trauma, rheumatic </li></ul></ul><ul><li>Aortic stenosis – angina, syncope, CHF </li></ul><ul><ul><li>Crescendo-decrescendo, later-peaking = more severe </li></ul></ul><ul><ul><li>Decreased S2, pulsus parvus et tardus </li></ul></ul><ul><ul><li>Etiologies: calcific degenerative, bicuspid </li></ul></ul><ul><li>Ventricular septal defect (VSD) – L sided heart failure </li></ul><ul><ul><li>Harsh, holosystolic, left-sternal border </li></ul></ul><ul><ul><li>Etiologies: congenital, post-MI </li></ul></ul>
    19. 19. Cardiac auscultation <ul><li>Mitral valve prolapse – atypical CP, endocarditis </li></ul><ul><ul><li>Mid-systolic click, then MR </li></ul></ul><ul><li>Aortic regurgitation – progressive LV dysfunction </li></ul><ul><ul><li>Blowing diastolic murmur </li></ul></ul><ul><ul><li>Etiologies: bicuspid Ao valve, endocarditis, aortic root dilation </li></ul></ul><ul><li>Mitral stenosis – L heart failure, pulmonary edema </li></ul><ul><ul><li>Opening snap, diastolic rumble </li></ul></ul><ul><ul><li>Etiologies: rheumatic heart disease, calcific/degenerative </li></ul></ul><ul><li>Patent ductus arteriosus (PDA) – L heart failure </li></ul><ul><ul><li>Continuous machine-like murmur, loudest at S2 </li></ul></ul>
    20. 20. Cardiac auscultation <ul><li>Heart sounds: </li></ul><ul><ul><li>S1: mitral and tricuspid valves closing </li></ul></ul><ul><ul><li>S2: aortic and pulmonic valves closing </li></ul></ul><ul><ul><ul><li>Splitting: </li></ul></ul></ul><ul><ul><ul><ul><li>Normal: A2-P2,  splitting during inspiration </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Paradoxical: P2-A2,  splitting during expiration (AS, LBBB) </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Wide splitting: A2-P2 but splitting exaggerated (PS) </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Fixed splitting: A2-P2 and fixed splitting (ASD) </li></ul></ul></ul></ul><ul><ul><li>S3: early diastole; increased LV filling pressures </li></ul></ul><ul><ul><ul><li>Normal in children </li></ul></ul></ul><ul><ul><li>S4: late diastole; increased LV stiffness </li></ul></ul><ul><ul><ul><li>Normal in aging </li></ul></ul></ul>
    21. 21. Physiology <ul><li>MAP = (SBP + (2 x DBP))/3 </li></ul><ul><li>Pulse pressure = SBP – DBP (≈SV) </li></ul><ul><li>MAP = CO x TPR </li></ul><ul><li>CO = HR x SV </li></ul><ul><li>SV = EDV – ESV </li></ul><ul><li>EF = SV/EDV </li></ul><ul><li>Resistance = pressure / flow </li></ul><ul><ul><li> resistance with  viscosity,  length,  radius </li></ul></ul><ul><ul><li>Resistance is greatest in arterioles </li></ul></ul>
    22. 22. Physiology <ul><li>Know the determinants of stroke volume </li></ul><ul><ul><li>Contractility (  ), preload (  ), afterload (  ) </li></ul></ul><ul><li>What increases contractility? </li></ul><ul><ul><li>Anything that increases intracellular calcium </li></ul></ul><ul><ul><li>How do catecholamines, digoxin do this? </li></ul></ul><ul><li>What decreases contractility? </li></ul><ul><ul><li>Anything that decreases intracellular calcium </li></ul></ul><ul><ul><li>Know the difference between CCBs </li></ul></ul><ul><ul><ul><li>Dihydropyridine vs non-dihydropyridine </li></ul></ul></ul>
    23. 23. Physiology <ul><li>Preload = EDV </li></ul><ul><li>Afterload = MAP </li></ul><ul><li>What drugs affect preload? </li></ul><ul><ul><li>Venodilators (NTG) decrease preload </li></ul></ul><ul><ul><li>IV fluids increase preload </li></ul></ul><ul><li>What drugs affect afterload? </li></ul><ul><ul><li>Vasodilators (hydralazine, nitroprusside, minoxidil) decrease afterload </li></ul></ul><ul><ul><li>Vasopressors (phenylephrine, vasopressin) increase afterload </li></ul></ul>
    24. 24. Physiology <ul><li>Understand Starling curve </li></ul><ul><ul><li>Contractility proportional to preload </li></ul></ul><ul><ul><li>In the failing heart, the LV dilates initially in order to preserve stroke volume </li></ul></ul><ul><ul><li>Eventually the failing heart will “fall off the curve” so that increasing preload will not increase contractility </li></ul></ul><ul><li>Understand pressure-volume loop </li></ul>
    25. 25. Physiology LV volume (mL) LV pressure (mmHg) SV diastole systole ESV EDV Isovolumic contraction Isovolumic relaxation AVO AVC MVC MVO
    26. 26. Physiology
    27. 27. Physiology <ul><li>Differential diagnosis of shock: </li></ul><ul><ul><li>Low CVP, low CO, high SVR: hypovolemia </li></ul></ul><ul><ul><li>High CVP, low CO, high SVR: cardiogenic </li></ul></ul><ul><ul><li>Low CVP, high CO, low SVR: </li></ul></ul><ul><ul><ul><li>Sepsis </li></ul></ul></ul><ul><ul><ul><li>Neurogenic </li></ul></ul></ul><ul><ul><ul><li>Anaphylaxis </li></ul></ul></ul><ul><ul><ul><li>Adrenal insufficiency </li></ul></ul></ul>
    28. 28. Electrophysiology <ul><li>Action potential: </li></ul><ul><ul><li>Phase 0 </li></ul></ul><ul><ul><li>Phase 1 </li></ul></ul><ul><ul><li>Phase 2 </li></ul></ul><ul><ul><li>Phase 3 </li></ul></ul><ul><ul><li>Phase 4 </li></ul></ul><ul><li>Know how pacemaker action potential differs from His-purkinje system </li></ul>
    29. 29. Electrophysiology <ul><li>Depolarization: Phase 0 </li></ul><ul><ul><li>Rapid Na channels open </li></ul></ul><ul><ul><li>Slope = how fast cell depolarizes, speed of conduction </li></ul></ul><ul><li>Repolarization: Phase 1-3 </li></ul><ul><ul><li>Width of action potential (AP duration) </li></ul></ul><ul><ul><li>Refractory period </li></ul></ul><ul><ul><li>Plateau (Phase 2): unique to cardiac cells, due to slow Ca++ channels </li></ul></ul><ul><li>Resting phase: Phase 4 </li></ul><ul><ul><li>Automaticity occurs when there is leakage of cations into cell during Phase 4 (this occurs in pacemaker cells like SA and AV nodes) </li></ul></ul><ul><li>Shape of action potential: </li></ul><ul><ul><li>Depends on conduction velocity, refractory period, automaticity </li></ul></ul>
    30. 30. Electrophysiology <ul><li>Sympathetic nervous system: </li></ul><ul><ul><li>Increases automaticity </li></ul></ul><ul><ul><li>Increases conduction velocity </li></ul></ul><ul><ul><li>Decreases AP duration </li></ul></ul><ul><li>Parasympathetic: vice-versa </li></ul><ul><ul><li>Mainly innervates SA and AV node only </li></ul></ul>
    31. 31. Electrophysiology <ul><li>Anti-arrhythmics: </li></ul><ul><ul><li>Change shape of action potential </li></ul></ul><ul><ul><li>Alter conductivity and/or refractoriness </li></ul></ul><ul><ul><li>Class I: Na+ blockers (  speed of depolarization) </li></ul></ul><ul><ul><li>Class II: beta-blockers (  sympathetic tone) </li></ul></ul><ul><ul><li>Class III:  AP duration (increase refractoriness) </li></ul></ul><ul><ul><li>Class IV: Ca++ channel blockers (SA, AV node) </li></ul></ul><ul><ul><li>Class V: digoxin (  parasympathetic tone) </li></ul></ul>
    32. 32. Electrophysiology <ul><li>Class I: </li></ul><ul><ul><li>Ia: quinidine, procainamide, disopyramide </li></ul></ul><ul><ul><ul><li>Slow upstroke of AP (decreases conductivity) </li></ul></ul></ul><ul><ul><ul><li>Prolong AP duration (increases refractoriness) </li></ul></ul></ul><ul><ul><li>Ib: lidocaine, phenytoin, tocainide, mexiletine </li></ul></ul><ul><ul><ul><li>Shorten AP duration, decreases refractoriness </li></ul></ul></ul><ul><ul><li>Ic: flecainide, encainide, propafenone </li></ul></ul><ul><ul><ul><li>Marked slowing of AP upstroke (  conductivity) </li></ul></ul></ul>
    33. 33. Electrophysiology <ul><li>Class I: </li></ul><ul><ul><li>Ia: quinidine, procainamide, disopyramide </li></ul></ul><ul><ul><ul><li>Used to treat ventricular, atrial arrhythmias </li></ul></ul></ul><ul><ul><li>Ib: lidocaine, phenytoin, tocainide, mexiletine </li></ul></ul><ul><ul><ul><li>Used to treat ventricular arrhythmias </li></ul></ul></ul><ul><ul><li>Ic: flecainide, encainide, propafenone </li></ul></ul><ul><ul><ul><li>Used to treat atrial arrhythmias </li></ul></ul></ul>
    34. 34. Electrophysiology <ul><li>Class II: </li></ul><ul><ul><li>Beta-blockers </li></ul></ul><ul><ul><li>Used to treat atrial arrhythmias </li></ul></ul><ul><li>Class III: </li></ul><ul><ul><li>Used to treat atrial and ventricular arrhythmias </li></ul></ul><ul><ul><li>Amiodarone, ibutilide, sotalol </li></ul></ul><ul><ul><li>Amiodarone also has beta-blocker effect </li></ul></ul><ul><li>Class IV: </li></ul><ul><ul><li>Calcium channel blockers, affect SA / AV node </li></ul></ul><ul><ul><li>Diltiazem, verapamil </li></ul></ul><ul><ul><li>Used to treat atrial arrhythmias (a.fib, a.flutter) </li></ul></ul><ul><li>Class V: </li></ul><ul><ul><li>Digoxin;  parasympathetic tone so mainly affects SA / AV node </li></ul></ul><ul><ul><li>Used to treat atrial arrhythmias (atrial fibrillation) </li></ul></ul>
    35. 35. Electrophysiology <ul><li>Mechanisms of arrhythmias: </li></ul><ul><ul><li>Automaticity, reentry , triggered activity </li></ul></ul><ul><li>Anti-arrhythmic toxicity: </li></ul><ul><ul><li>Ia, Ic: If you slow conduction (decrease AP upstroke), you will increase risk of reentry </li></ul></ul><ul><ul><li>Ia, III: If you increase refractoriness (increase AP duration), you prolong QT interval and increase risk of torsades de points </li></ul></ul>
    36. 36. Electrophysiology <ul><li>ECG pearls: </li></ul><ul><ul><li>P wave: atrial depolarization </li></ul></ul><ul><ul><li>PR interval: onset of P to onset of QRS </li></ul></ul><ul><ul><ul><li>Corresponds to A-V delay (<200 ms) </li></ul></ul></ul><ul><ul><li>QRS: ventricular depolarization (<120 ms) </li></ul></ul><ul><ul><li>T wave: ventricular repolarization </li></ul></ul><ul><ul><li>QT interval: onset of QRS to end of T wave </li></ul></ul>
    37. 37. Electrophysiology <ul><li>ECG pearls: </li></ul><ul><ul><li>Irregularly irregular? Think atrial fibrillation </li></ul></ul><ul><ul><ul><li>Look for absence of P-waves </li></ul></ul></ul><ul><ul><ul><li>Rate control, anticoagulation, anti-arrhythmics </li></ul></ul></ul><ul><ul><li>Atrial flutter: “saw-tooth” in inferior leads </li></ul></ul><ul><ul><ul><li>Rate control, anticoagulation, anti-arrhythmics </li></ul></ul></ul><ul><ul><li>Know what torsades de pointes looks like </li></ul></ul><ul><ul><ul><li>Caused by anything that prolongs QT interval </li></ul></ul></ul><ul><ul><li>WPW: delta wave – slurred QRS upstroke </li></ul></ul>
    38. 38. Electrophysiology <ul><li>ECG pearls: </li></ul><ul><ul><li>AV block: </li></ul></ul><ul><ul><ul><li>1 st degree: PR interval > 200 ms </li></ul></ul></ul><ul><ul><ul><li>2 nd degree: </li></ul></ul></ul><ul><ul><ul><ul><li>Mobitz type I: progressive increase in PR interval, progressive decrease in RR interval until dropped P </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Mobitz type II: regularly dropped P wave (PR constant) </li></ul></ul></ul></ul><ul><ul><ul><li>3 rd degree: complete AV dissociation (P and QRS complexes have no relationship and are independent of each other) </li></ul></ul></ul><ul><ul><ul><ul><li>Treat with pacemaker; can be seen in Lyme disease </li></ul></ul></ul></ul>AV node problem (okay) His bundle problem (usually bad)
    39. 39. Congenital heart disease <ul><li>Right-to-left shunts: </li></ul><ul><ul><li>Blue babies </li></ul></ul><ul><ul><li>“Terrible Ts”: </li></ul></ul><ul><ul><ul><li>Tetralogy, transposition, truncus arteriosus, tricuspid atresia, TAPVR </li></ul></ul></ul><ul><ul><ul><li>Or anything that obstructs RV + shunt </li></ul></ul></ul><ul><ul><li>Tetralogy: PS, RVH, overriding aorta, VSD </li></ul></ul><ul><ul><ul><li>Caused by anterosuperior displacement of infundibular septum; boot-shaped heart on CXR </li></ul></ul></ul>
    40. 40. Congenital heart disease <ul><li>Left-to-right shunts: </li></ul><ul><ul><li>VSD, ASD, PDA </li></ul></ul><ul><ul><li>VSD most common congenital anomaly after bicuspid aortic valve </li></ul></ul><ul><ul><li>Late cyanosis </li></ul></ul><ul><ul><ul><li>Due to Eisenmenger’s syndrome </li></ul></ul></ul><ul><ul><ul><li>Development of pulmonary hypertension with reversal of shunt direction due to  RV pressure </li></ul></ul></ul>
    41. 41. Congenital heart disease <ul><li>Transposition </li></ul><ul><ul><li>Aorta comes off of RV, PA comes off of LV </li></ul></ul><ul><ul><li>Need shunt (PFO, ASD, VSD, PDA, etc) to live </li></ul></ul><ul><ul><li>Failure of aorticopulmonary septum to spiral </li></ul></ul><ul><li>Coarctation: associated with Turner syndrome </li></ul><ul><ul><li>Preductal / infantile – mimics aortic stenosis </li></ul></ul><ul><ul><li>Post ductal / adult – hypertension in upper extremities </li></ul></ul><ul><li>PDA </li></ul><ul><ul><li>Indomethacin closes, PGE keeps it open </li></ul></ul><ul><ul><li>Normal in utero, closes only after birth </li></ul></ul><ul><li>Bicuspid aortic valve </li></ul><ul><ul><li>Can cause aortic stenosis or aortic regurgitation (AS occurs in 40s-50s) </li></ul></ul><ul><ul><li>Associated with coarctation, Ao root dilation </li></ul></ul>
    42. 42. Congestive heart failure <ul><li>Syndrome based on signs / symptoms </li></ul><ul><li>Differential diagnosis is broad </li></ul><ul><li>Dilated: systolic dysfunction </li></ul><ul><ul><li>Alcohol, viral, cocaine, Chagas, chemo, peripartum </li></ul></ul><ul><li>Hypertrophic: diastolic dysfunction </li></ul><ul><ul><li>Septal hypertrophy = dynamic outflow tract obstruction </li></ul></ul><ul><ul><li>Treat by decreasing contractility </li></ul></ul><ul><li>Restrictive: diastolic dysfunction </li></ul><ul><ul><li>Amyloid, radiation, sarcoid, hemochromatosis </li></ul></ul>
    43. 43. Congestive heart failure <ul><li>Understand the pathophysiology behind clinical manifestations (signs/symptoms) </li></ul><ul><ul><li>Dyspnea on exertion (can’t augment CO) </li></ul></ul><ul><ul><li>Pulmonary edema (increased pulmonary venous pressure) </li></ul></ul><ul><ul><li>Orthopnea (increased venous return) </li></ul></ul><ul><ul><li>Hepatomegaly (increased venous pressure) </li></ul></ul><ul><ul><li>Elevated jugular venous pressure, edema </li></ul></ul>
    44. 44. Congestive heart failure <ul><li>Understand how therapy works </li></ul><ul><ul><li>Remember that low CO results in: </li></ul></ul><ul><ul><ul><li>Sympathetic overload: beta-blockers, vasodilators </li></ul></ul></ul><ul><ul><ul><li> Renin-angiotensin-aldosterone: ACE/ARB, aldosterone antagonists </li></ul></ul></ul><ul><ul><ul><li>Increased ADH (increased aquaporin): vasopressin antagonists </li></ul></ul></ul><ul><ul><li>All of the above result in increased sodium retention: diuretics </li></ul></ul>
    45. 45. Congestive heart failure <ul><li>Understand mechanism of action of diuretics </li></ul><ul><ul><li>Acetazolamide </li></ul></ul><ul><ul><ul><li>Na/H in proximal tubule </li></ul></ul></ul><ul><ul><li>Loop diuretics </li></ul></ul><ul><ul><ul><li>Thick ascending limb loop of Henle Na/K/2Cl </li></ul></ul></ul><ul><ul><li>Thiazide diuretics </li></ul></ul><ul><ul><ul><li>Distal convoluted tubule Na/Cl </li></ul></ul></ul><ul><ul><li>Potassium sparing diuretics </li></ul></ul><ul><ul><ul><li>Spironolactone vs others </li></ul></ul></ul>
    46. 46. Congestive heart failure <ul><li>Digoxin: a board exam favorite… </li></ul><ul><ul><li>Inhibits Na/K ATPase directly </li></ul></ul><ul><ul><li>Indirectly inhibits Na/Ca exchanger </li></ul></ul><ul><ul><li>More Ca++ in cell = increased contractility </li></ul></ul><ul><ul><li>Also stimulates vagus nerve =  parasymp. </li></ul></ul><ul><ul><li>Hypokalemia = increased toxicity (more dig can bind to Na/K ATPase b/c competes w/K) </li></ul></ul><ul><ul><li>Know ECG effects (e.g., scooped ST segment) </li></ul></ul>
    47. 47. Ischemic heart disease <ul><li>Atherosclerosis: </li></ul><ul><ul><li>Differentiate from </li></ul></ul><ul><ul><ul><li>Monckeberg arteriosclerosis </li></ul></ul></ul><ul><ul><ul><li>Hypertensive arteriosclerosis </li></ul></ul></ul><ul><ul><li>Pathogenesis </li></ul></ul><ul><li>CAD / angina: </li></ul><ul><ul><li>Understand pathophysiologic differences underlying different manifestations </li></ul></ul><ul><ul><li>Stable vs Prinzmetal’s vs unstable </li></ul></ul>
    48. 48. Ischemic heart disease <ul><li>Myocardial infarction: </li></ul><ul><ul><li>Diagnosis: ECG  troponin  CK-MB </li></ul></ul><ul><ul><li>Type: transmural vs subendocardial </li></ul></ul><ul><ul><ul><li>ST elevation vs ST depression </li></ul></ul></ul><ul><ul><li>Complications </li></ul></ul><ul><ul><ul><li>Arrhythmia </li></ul></ul></ul><ul><ul><ul><li>CHF / pulmonary edema </li></ul></ul></ul><ul><ul><ul><li>Cardiogenic shock </li></ul></ul></ul><ul><ul><ul><li>Cardiac rupture (free wall, VSD, pap muscle) </li></ul></ul></ul><ul><ul><ul><li>LV aneurysm </li></ul></ul></ul><ul><ul><ul><li>Fibrinous pericarditis (early) </li></ul></ul></ul><ul><ul><ul><li>Dressler’s syndrome (late) </li></ul></ul></ul>
    49. 49. Ischemic heart disease <ul><li>Evolution of MI: </li></ul><ul><ul><li>Day 1: release of necrotic contents into blood stream (triggers inflamm. response) </li></ul></ul><ul><ul><li>Day 2-4: acute inflammation, extensive necrosis, hyperemia: arrhythmia </li></ul></ul><ul><ul><li>Day 5-10: hyperemic border, macrophage-induced degradation: rupture </li></ul></ul><ul><ul><li>1-2 weeks: scar formation: LV aneurysm </li></ul></ul>
    50. 50. Infectious heart disease <ul><li>Bacterial endocarditis: </li></ul><ul><ul><li>Roth spots, Osler’s nodes, Janeway lesions, splinters </li></ul></ul><ul><li>Libman-Sacks endocarditis: </li></ul><ul><ul><li>Sterile vegetations of lupus: mitral </li></ul></ul><ul><li>Marantic endocarditis: </li></ul><ul><ul><li>Assoc with malignancy, anti-phospholipid syndrome </li></ul></ul><ul><ul><li>Usually associated with mitral valve, sterile </li></ul></ul><ul><li>Syphilis: tertiary = disrupts vaso vasorum </li></ul><ul><ul><li>Aortic dilation, aortic regurgitation </li></ul></ul>
    51. 51. Infectious heart disease <ul><li>Rheumatic heart disease: </li></ul><ul><ul><li>Aschoff bodies (granuloma with giant cells) </li></ul></ul><ul><ul><li>Anitschkow’s cells (activated histiocytes) </li></ul></ul><ul><ul><li>Elevated ASO titers </li></ul></ul><ul><ul><li>Mitral stenosis / regurgitation > Ao valve </li></ul></ul><ul><ul><li>“ Fish-mouth deformity of mitral valve” </li></ul></ul><ul><ul><li>Mitral valve leaflets tips affected </li></ul></ul><ul><li>Lyme disease: think conduction problems </li></ul><ul><li>Chagas disease: dilated cardiomyopathy, conduction problems </li></ul>
    52. 52. Etc cardiac diseases to know about <ul><li>Pericardial disease </li></ul><ul><ul><li>Acute pericarditis, constrictive pericarditis, cardiac tamponade </li></ul></ul><ul><li>Aortic disease </li></ul><ul><ul><li>Aortic aneurysms, aortic dissection </li></ul></ul><ul><li>Cardiac tumors: </li></ul><ul><ul><li>Myxoma is the most common primary cardiac tumor </li></ul></ul>
    53. 53. Lipidology <ul><li>Understand mechanisms, effects, and side effects of lipid-lowering agents </li></ul><ul><ul><li>Best at lowering LDL: statins </li></ul></ul><ul><ul><li>Best at raising HDL: niacin </li></ul></ul><ul><ul><li>Best at lowering triglycerides: fibrates </li></ul></ul><ul><ul><li>Statin + fibrate = high risk of myositis </li></ul></ul>
    54. 54. Pharmacology <ul><li>A board exam favorite </li></ul><ul><li>Clinical vignette: </li></ul><ul><ul><li>Figure out the disease </li></ul></ul><ul><ul><li>Figure out what drug to use </li></ul></ul><ul><ul><li>Question: something specific about drug mechanism or side effect </li></ul></ul>
    55. 55. Pharmacology <ul><li>High-yield stuff: </li></ul><ul><ul><li>Anti-arrhythmics </li></ul></ul><ul><ul><li>Diuretic mechanisms </li></ul></ul><ul><ul><li>Anticoagulants </li></ul></ul><ul><ul><li>Alpha-, beta-receptor subtypes and actions </li></ul></ul><ul><li>Some newer drugs to know about: </li></ul><ul><ul><li>Clopidogrel, ranolazine, nesiritide </li></ul></ul>
    56. 56. Good luck!

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