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. 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 sanjiv.shah@northwestern.edu 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. Test-taking tips • Use First Aid as your primary resource and write in notes in the margins • Practice test questions • Rapidly changing areas / fields / clinical trials: unlikely to be tested • Importance of clinical associations: • ~80% of questions contain a clinical vignette • Remember the ultimate goal: third-year

3. Anatomy • Carotid sheath: V-A-N • Internal jugular vein (lateral) • Common carotid artery (medial) • Vagus nerve (posterior) • Why is this important? • Need to know the anatomy for internal jugular vein cannulation (central line) • “Stick the carotid” = stroke / big bleed

4. Anatomy • Jugular venous pulsations: • V wave: venous filling of right atrium T-wave • Y descent: passive emptying of RA as tricuspid valve opens in early diastole • A wave: atrial kick P-wave • X descent: atrial relaxation • C wave: tricuspid valve closure at onset of systole QRS

5. Anatomy V A C X Y

6. Anatomy • Cardiac chambers • RV most anterior • Susceptible to trauma (RV contusion, perforation) • Left atrium most posterior • Severe enlargement can cause dysphagia or hoarseness (recurrent laryngeal nerve) • LV makes up most of the heart’s mass • That is why normal ECG axis is leftward

7. Anatomy • Cardiac chambers • CXR anatomy: • On PA film, most of what you normally see is the RV; if the heart enlarges it makes the heart wider (“cardiomegaly”) • On lateral film, RV is anterior, LV is posterior; this is used to help determine which chamber is causing cardiomegaly

8. Anatomy • Coronary anatomy: coronaries fill in diastole • Left main coronary artery • Left anterior descending (LAD) • Septal perforators • Diagonal branches • Left circumflex (LCx) • Obtuse marginals • Right coronary artery (RCA) • Acute marginals • Posterior descending artery (in 70-80%) _________

9. Anatomy • Coronary anatomy: • Left main coronary artery • Left anterior descending (LAD) ANTEROSEPTUM, APEX • Septal perforators SEPTUM • Diagonal branches ANTERIOR LV • Left circumflex (LCx) LATERAL LV • Obtuse marginals LATERAL LV • Right coronary artery (RCA) • Acute marginals RIGHT VENTRICLE • Posterior descending artery (in 70-80%) SEPTUM, INFERIOR LV, POSTERIOR LV

10. Anatomy • Coronary anatomy: • Left main coronary artery • Left anterior descending (LAD) ANTEROSEPTUM, APEX • Septal perforators SEPTUM V1, V2 • Diagonal branches ANTERIOR LV V3, V4, V5, V6 • Left circumflex (LCx) LATERAL LV I, aVL • Obtuse marginals LATERAL LV I, aVL • Right coronary artery (RCA) • Acute marginals RIGHT VENTRICLE II, III, aVF; RV4 • Posterior descending artery (in 70-80%) SEPTUM, INFERIOR LV, POSTERIOR LV II, III, aVF; V7-V9

11. Anatomy • Coronary anatomy: • Inferior LV: • Supplied by RCA in 70-80% • Supplied by LCx in 10-20% • Supplied by both RCA and LCx in 10% (co-dominant) • Why is coronary anatomy important? • Helps diagnose acute MI on ECG • Risk depends on location of MI (LAD = high-risk)

12. Cardiac auscultation • Systolic murmurs: 8 main causes • Aortic stenosis • Aortic valve sclerosis • Mitral regurgitation • Tricuspid regurgitation • Hypertrophic cardiomyopathy • VSD • Pulmonic stenosis • Flow murmur

13. Cardiac auscultation • Systolic murmurs: 8 main causes • Aortic stenosis (A, crescendo-decrescendo) • Aortic valve sclerosis (A, sounds like AS) • Mitral regurgitation (M, holosystolic) • Tricuspid regurgitation (T, holosystolic) • Hypertrophic cardiomyopathy (LSB, harsh) • VSD (LSB, harsh) • Pulmonic stenosis (P, harsh) • Flow murmur (A/P/T/M, quality varies) A = aortic, P = pulmonic, T = tricuspid, M = mitral, LSB = left sternal border

14. Cardiac auscultation • Diastolic murmurs: 4 main causes • Aortic regurgitation • Mitral stenosis • Pulmonic regurgitation • Tricuspid stenosis

15. Cardiac auscultation • Diastolic murmurs: 4 main causes • Aortic regurgitation (LSB, blowing) • Mitral stenosis (M, opening snap, rumble) • Pulmonic regurgitation (P) • Tricuspid stenosis (T) P = pulmonic, T = tricuspid, M = mitral, LSB = left sternal border

16. Cardiac auscultation • Right-sided murmurs: • Increase during inspiration • Left-sided murmurs: • Increase during expiration • Atrial septal defect (ASD): • Doesn’t cause intrinsic murmur itself b/c low velocity flow (interatrial pressures not high) • But due to increased blood returning to R heart: • Flow murmur over pulmonic valve (systolic murmur) • Flow murmur over tricuspid valve (diastolic murmur)

17. Cardiac auscultation • Murmurs you should know about: • Mitral regurgitation • Tricuspid regurgitation • Aortic stenosis • Ventricular septal defect (VSD) • Mitral valve prolapse • Aortic regurgitation • Mitral stenosis • Patent ductus arteriosus (PDA)

18. Cardiac auscultation • Mitral regurgitation – L sided heart failure • Holosystolic, apex  axilla • Etiologies: LV dilation, CAD, MVP, rheumatic • Tricuspid regurgitation – R sided heart failure • Holosystolic, left sternal border, with inspiration • Etiologies: RV dilation, endocarditis, trauma, rheumatic • Aortic stenosis – angina, syncope, CHF • Crescendo-decrescendo, later-peaking = more severe • Decreased S2, pulsus parvus et tardus • Etiologies: calcific degenerative, bicuspid • Ventricular septal defect (VSD) – L sided heart failure • Harsh, holosystolic, left-sternal border • Etiologies: congenital, post-MI

19. Cardiac auscultation • Mitral valve prolapse – atypical CP, endocarditis • Mid-systolic click, then MR • Aortic regurgitation – progressive LV dysfunction • Blowing diastolic murmur • Etiologies: bicuspid Ao valve, endocarditis, aortic root dilation • Mitral stenosis – L heart failure, pulmonary edema • Opening snap, diastolic rumble • Etiologies: rheumatic heart disease, calcific/degenerative • Patent ductus arteriosus (PDA) – L heart failure • Continuous machine-like murmur, loudest at S2

20. Cardiac auscultation • Heart sounds: • S1: mitral and tricuspid valves closing • S2: aortic and pulmonic valves closing • Splitting: • Normal: A2-P2, splitting during inspiration • Paradoxical: P2-A2, splitting during expiration (AS, LBBB) • Wide splitting: A2-P2 but splitting exaggerated (PS) • Fixed splitting: A2-P2 and fixed splitting (ASD) • S3: early diastole; increased LV filling pressures • Normal in children • S4: late diastole; increased LV stiffness • Normal in aging

21. Physiology • MAP = (SBP + (2 x DBP))/3 • Pulse pressure = SBP – DBP (≈SV) • MAP = CO x TPR • CO = HR x SV • SV = EDV – ESV • EF = SV/EDV • Resistance = pressure / flow • resistance with viscosity, length, radius • Resistance is greatest in arterioles

22. Physiology • Know the determinants of stroke volume • Contractility (), preload (), afterload () • What increases contractility? • Anything that increases intracellular calcium • How do catecholamines, digoxin do this? • What decreases contractility? • Anything that decreases intracellular calcium • Know the difference between CCBs • Dihydropyridine vs non-dihydropyridine

23. Physiology • Preload = EDV • Afterload = MAP • What drugs affect preload? • Venodilators (NTG) decrease preload • IV fluids increase preload • What drugs affect afterload? • Vasodilators (hydralazine, nitroprusside, minoxidil) decrease afterload • Vasopressors (phenylephrine, vasopressin) increase afterload

24. Physiology • Understand Starling curve • Contractility proportional to preload • In the failing heart, the LV dilates initially in order to preserve stroke volume • Eventually the failing heart will “fall off the curve” so that increasing preload will not increase contractility • Understand pressure-volume loop

25. Physiology systole AVC AVO LV pressure (mmHg) Isovolumic relaxation SV Isovolumic contraction diastole MVO MVC LV volume (mL) ESV EDV

26. Physiology

27. Physiology • Differential diagnosis of shock: • Low CVP, low CO, high SVR: hypovolemia • High CVP, low CO, high SVR: cardiogenic • Low CVP, high CO, low SVR: • Sepsis • Neurogenic • Anaphylaxis • Adrenal insufficiency

28. Electrophysiology • Action potential: • Phase 0 • Phase 1 • Phase 2 • Phase 3 • Phase 4 • Know how pacemaker action potential differs from His-purkinje system

29. Electrophysiology • Depolarization: Phase 0 • Rapid Na channels open • Slope = how fast cell depolarizes, speed of conduction • Repolarization: Phase 1-3 • Width of action potential (AP duration) • Refractory period • Plateau (Phase 2): unique to cardiac cells, due to slow Ca++ channels • Resting phase: Phase 4 • Automaticity occurs when there is leakage of cations into cell during Phase 4 (this occurs in pacemaker cells like SA and AV nodes) • Shape of action potential: • Depends on conduction velocity, refractory period, automaticity

30. Electrophysiology • Sympathetic nervous system: • Increases automaticity • Increases conduction velocity • Decreases AP duration • Parasympathetic: vice-versa • Mainly innervates SA and AV node only

31. Electrophysiology • Anti-arrhythmics: • Change shape of action potential • Alter conductivity and/or refractoriness • Class I: Na+ blockers (speed of depolarization) • Class II: beta-blockers ( sympathetic tone) • Class III: AP duration (increase refractoriness) • Class IV: Ca++ channel blockers (SA, AV node) • Class V: digoxin ( parasympathetic tone)

32. Electrophysiology • Class I: • Ia: quinidine, procainamide, disopyramide • Slow upstroke of AP (decreases conductivity) • Prolong AP duration (increases refractoriness) • Ib: lidocaine, phenytoin, tocainide, mexiletine • Shorten AP duration, decreases refractoriness • Ic: flecainide, encainide, propafenone • Marked slowing of AP upstroke (conductivity)

33. Electrophysiology • Class I: • Ia: quinidine, procainamide, disopyramide • Used to treat ventricular, atrial arrhythmias • Ib: lidocaine, phenytoin, tocainide, mexiletine • Used to treat ventricular arrhythmias • Ic: flecainide, encainide, propafenone • Used to treat atrial arrhythmias

34. Electrophysiology • Class II: • Beta-blockers • Used to treat atrial arrhythmias • Class III: • Used to treat atrial and ventricular arrhythmias • Amiodarone, ibutilide, sotalol • Amiodarone also has beta-blocker effect • Class IV: • Calcium channel blockers, affect SA / AV node • Diltiazem, verapamil • Used to treat atrial arrhythmias (a.fib, a.flutter) • Class V: • Digoxin;  parasympathetic tone so mainly affects SA / AV node • Used to treat atrial arrhythmias (atrial fibrillation)

35. Electrophysiology • Mechanisms of arrhythmias: • Automaticity, reentry, triggered activity • Anti-arrhythmic toxicity: • Ia, Ic: If you slow conduction (decrease AP upstroke), you will increase risk of reentry • Ia, III: If you increase refractoriness (increase AP duration), you prolong QT interval and increase risk of torsades de points

36. Electrophysiology • ECG pearls: • P wave: atrial depolarization • PR interval: onset of P to onset of QRS • Corresponds to A-V delay (<200 ms) • QRS: ventricular depolarization (<120 ms) • T wave: ventricular repolarization • QT interval: onset of QRS to end of T wave

37. Electrophysiology • ECG pearls: • Irregularly irregular? Think atrial fibrillation • Look for absence of P-waves • Rate control, anticoagulation, anti-arrhythmics • Atrial flutter: “saw-tooth” in inferior leads • Rate control, anticoagulation, anti-arrhythmics • Know what torsades de pointes looks like • Caused by anything that prolongs QT interval • WPW: delta wave – slurred QRS upstroke

38. Electrophysiology • ECG pearls: • AV block: • 1st degree: PR interval > 200 ms • 2nd degree: • Mobitz type I: progressive increase in PR interval, progressive decrease in RR interval until dropped P • Mobitz type II: regularly dropped P wave (PR constant) • 3rd degree: complete AV dissociation (P and QRS complexes have no relationship and are independent of each other) • Treat with pacemaker; can be seen in Lyme disease AV node problem (okay) His bundle problem (usually bad)

39. Congenital heart disease • Right-to-left shunts: • Blue babies • “Terrible Ts”: • Tetralogy, transposition, truncus arteriosus, tricuspid atresia, TAPVR • Or anything that obstructs RV + shunt • Tetralogy: PS, RVH, overriding aorta, VSD • Caused by anterosuperior displacement of infundibular septum; boot-shaped heart on CXR

40. Congenital heart disease • Left-to-right shunts: • VSD, ASD, PDA • VSD most common congenital anomaly after bicuspid aortic valve • Late cyanosis • Due to Eisenmenger’s syndrome • Development of pulmonary hypertension with reversal of shunt direction due to RV pressure

41. Congenital heart disease • Transposition • Aorta comes off of RV, PA comes off of LV • Need shunt (PFO, ASD, VSD, PDA, etc) to live • Failure of aorticopulmonary septum to spiral • Coarctation: associated with Turner syndrome • Preductal / infantile – mimics aortic stenosis • Post ductal / adult – hypertension in upper extremities • PDA • Indomethacin closes, PGE keeps it open • Normal in utero, closes only after birth • Bicuspid aortic valve • Can cause aortic stenosis or aortic regurgitation (AS occurs in 40s-50s) • Associated with coarctation, Ao root dilation

42. Congestive heart failure • Syndrome based on signs / symptoms • Differential diagnosis is broad • Dilated: systolic dysfunction • Alcohol, viral, cocaine, Chagas, chemo, peripartum • Hypertrophic: diastolic dysfunction • Septal hypertrophy = dynamic outflow tract obstruction • Treat by decreasing contractility • Restrictive: diastolic dysfunction • Amyloid, radiation, sarcoid, hemochromatosis

43. Congestive heart failure • Understand the pathophysiology behind clinical manifestations (signs/symptoms) • Dyspnea on exertion (can’t augment CO) • Pulmonary edema (increased pulmonary venous pressure) • Orthopnea (increased venous return) • Hepatomegaly (increased venous pressure) • Elevated jugular venous pressure, edema

44. Congestive heart failure • Understand how therapy works • Remember that low CO results in: • Sympathetic overload: beta-blockers, vasodilators • Renin-angiotensin-aldosterone: ACE/ARB, aldosterone antagonists • Increased ADH (increased aquaporin): vasopressin antagonists • All of the above result in increased sodium retention: diuretics

45. Congestive heart failure • Understand mechanism of action of diuretics • Acetazolamide • Na/H in proximal tubule • Loop diuretics • Thick ascending limb loop of Henle Na/K/2Cl • Thiazide diuretics • Distal convoluted tubule Na/Cl • Potassium sparing diuretics • Spironolactone vs others

46. Congestive heart failure • Digoxin: a board exam favorite… • Inhibits Na/K ATPase directly • Indirectly inhibits Na/Ca exchanger • More Ca++ in cell = increased contractility • Also stimulates vagus nerve = parasymp. • Hypokalemia = increased toxicity (more dig can bind to Na/K ATPase b/c competes w/K) • Know ECG effects (e.g., scooped ST segment)

47. Ischemic heart disease • Atherosclerosis: • Differentiate from • Monckeberg arteriosclerosis • Hypertensive arteriosclerosis • Pathogenesis • CAD / angina: • Understand pathophysiologic differences underlying different manifestations • Stable vs Prinzmetal’s vs unstable

48. Ischemic heart disease • Myocardial infarction: • Diagnosis: ECG  troponin  CK-MB • Type: transmural vs subendocardial • ST elevation vs ST depression • Complications • Arrhythmia • CHF / pulmonary edema • Cardiogenic shock • Cardiac rupture (free wall, VSD, pap muscle) • LV aneurysm • Fibrinous pericarditis (early) • Dressler’s syndrome (late)

49. Ischemic heart disease • Evolution of MI: • Day 1: release of necrotic contents into blood stream (triggers inflamm. response) • Day 2-4: acute inflammation, extensive necrosis, hyperemia: arrhythmia • Day 5-10: hyperemic border, macrophage-induced degradation: rupture • 1-2 weeks: scar formation: LV aneurysm

50. Infectious heart disease • Bacterial endocarditis: • Roth spots, Osler’s nodes, Janeway lesions, splinters • Libman-Sacks endocarditis: • Sterile vegetations of lupus: mitral • Marantic endocarditis: • Assoc with malignancy, anti-phospholipid syndrome • Usually associated with mitral valve, sterile • Syphilis: tertiary = disrupts vaso vasorum • Aortic dilation, aortic regurgitation