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

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 CardiovascularBoards Prep

M A Y 1 3 , 2 0 0 9

Sanjiv J. Shah, MDAssistant Professor of Medicine

Division of Cardiology, Department of Medicine

[email protected]

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


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


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


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


Anatomy

AC

V

XY


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


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


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%) _________


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


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


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)


Cardiac auscultation

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



• 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



• Diastolic murmurs: 4 main causes» Aortic regurgitation » Mitral stenosis» Pulmonic regurgitation» Tricuspid stenosis



• 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



• 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)



• 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)



• 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



• 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



• 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


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


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


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


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


Physiology

LV volume (mL)

LV pressure (mmHg)

SV

diastole

systole

ESV EDVIs

ov

olu

mic

con

trac

tio

n

Isov

olu

mic

relaxation

AVO

AVC

MVCMVO


Physiology


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


Electrophysiology

• Action potential:» Phase 0» Phase 1» Phase 2» Phase 3» Phase 4

• Know how pacemaker action potential differs from His-purkinje system


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


Electrophysiology

• Sympathetic nervous system:» Increases automaticity» Increases conduction velocity»Decreases AP duration

• Parasympathetic: vice-versa»Mainly innervates SA and AV node

only


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)


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)


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


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)


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


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


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


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)


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



• 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



• 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


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



• 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



• 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



• 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



• 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)


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



• 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)



• 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


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


Infectious heart disease

• Rheumatic heart disease:» Aschoff bodies (granuloma with giant cells)» Anitschkow’s cells (activated histiocytes)» Elevated ASO titers» Mitral stenosis / regurgitation > Ao valve» “Fish-mouth deformity of mitral valve”» Mitral valve leaflets tips affected

• Lyme disease: think conduction problems• Chagas disease: dilated cardiomyopathy,

conduction problems


Etc cardiac diseases to know about

• Pericardial disease» Acute pericarditis, constrictive

pericarditis, cardiac tamponade

• Aortic disease» Aortic aneurysms, aortic dissection

• Cardiac tumors:» Myxoma is the most common primary

cardiac tumor


Lipidology

• Understand mechanisms, effects, and side effects of lipid-lowering agents» Best at lowering LDL: statins» Best at raising HDL: niacin» Best at lowering triglycerides: fibrates» Statin + fibrate = high risk of myositis


Pharmacology

• A board exam favorite• Clinical vignette:

» Figure out the disease» Figure out what drug to use» Question: something specific about drug

mechanism or side effect


Pharmacology

• High-yield stuff:» Anti-arrhythmics» Diuretic mechanisms» Anticoagulants» Alpha-, beta-receptor subtypes and

actions

• Some newer drugs to know about:» Clopidogrel, ranolazine, nesiritide

Good luck! Good luck!

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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