USMLE STEP 2/3: CARDIOLOGY (DAY 1)

MOHAMED ELNAGDY (MD, MS): ECFMG CERTIFIED, PATHOLOGY RESIDENT AT WMC/NYMC (NEW YORK, USA)

CONCISE YET COMPREHENSIVE REVIEW FOR CLINICAL MEDICINE REQUIRED FOR USMLE STEP 2/3
 ISCHEMIC HEART DISEASES - INTRODUCTION

 The 1° cause of ischemic heart disease is atherosclerotic occlusion

of the coronary arteries
 Most significant RF: Early coronary artery disease (CAD) in a first-degree relative,
as defined by significant disease in male relatives before age 55 or in female
relatives before age 65.
ISCHEMIC HEART DISEASES - INTRODUCTION
 ISCHEMIC HEART DISEASES - PRESENTATION

 May be asymptomatic or present as follows:

■ Stable angina: Typical substernal chest pressure or shortness of breath that is exacerbated by exertion and relieved
by rest or nitroglycerin. Reflects a stable, flow-limiting plaque.
■ Unstable angina or MI (acute coronary syndrome): Chest pressure and/or shortness of breath that occur at rest or
with minimal exertion, often with a duration of > 20 minutes. Pain tends not to improve markedly with nitroglycerin or
recurs soon after its use. Reflects plaque rupture with the formation of a clot in the lumen of the blood vessel.
■ Not all patients present with typical anginal symptoms. Ask about other symptoms that are considered “anginal
equivalents,” such as dyspnea, nausea, and diaphoresis. Some patients may complain of indigestion.
 ISCHEMIC HEART DISEASES - PRESENTATION

 Exam may be normal when patients are asymptomatic.

 During episodes of angina, a left ventricular S4 or a mitral regurgitation murmur may occasionally be heard on
cardiac auscultation.
 Signs of heart failure (e.g., ↑ jugular venous pulse [JVP], inspiratory crackles, hepatomegaly, lower extremity edema)
that could be due to prior MI and may be causing left ventricular dysfunction.
 Vascular disease elsewhere (e.g., carotid, abdominal, and femoral bruits; asymmetric or diminished pulses; and
lower extremity ischemic ulcers).
 Diaphoresis and the Levine sign (clenched right fist held over the chest when describing pain).
ISCHEMIC HEART DISEASES - PRESENTATION
 ISCHEMIC HEART DISEASES - MANAGEMENT

 + / − ECG changes (ST-segment elevation/depression/Q waves) in the distribution of the coronary arteries
 ISCHEMIC HEART DISEASES - MANAGEMENT

 + / − ECG changes (ST-segment elevation/depression/Q waves) in the distribution of the coronary arteries
 ISCHEMIC HEART DISEASES - MANAGEMENT

 + / − ECG changes (ST-segment elevation/depression/Q waves) in the distribution of the coronary arteries

 Cardiac biomarkers (troponin, creatine kinase [CK], CK–MB fraction) ➔ Non-ST-segment-elevation MI (NSTEMI) can
be distinguished from unstable angina by the presence of elevated cardiac biomarkers
 Stress testing (if stable): Exercise, dobutamine, or vasodilator stress; ECG, echocardiography, or radionuclide
imaging to assess perfusion

 Cardiac catheterization (if unstable): Defines anatomy and the location and severity of lesions; can also be used for
reperfusion
 ISCHEMIC HEART DISEASES - MANAGEMENT

 Acute coronary syndrome:

■ Initial treatment: Anticoagulation (low molecular weight heparin [LMWH], unfractionated heparin), aspirin,
nitroglycerin, supplemental O2 , and a β -blocker in hemodynamically stable patients. Antiplatelet agents (clopidogrel,
prasugrel, ticagrelor) are often used as well if a percutaneous stent is placed. Glycoprotein IIb/IIIa antagonists
(abciximab, eptifibatide, tirofiban) or bivalirudin may be used in the catheterization laboratory when angioplasty is
pursued.

■ STEMIs or NSTEMIs with high-risk features should be managed by percutaneous coronary intervention (PCI) if
available at that hospital. If PCI is unavailable or cannot be initiated within 90 minutes, tPA should be given. If possible,
an angiotensin converting enzyme inhibitor (ACEI) should be started before discharge.
ISCHEMIC HEART DISEASES - MANAGEMENT
 ISCHEMIC HEART DISEASES - MANAGEMENT

 Angina: β -blockers ↓ HR, ↑ myocardial perfusion time, and ↓ cardiac workload, which ↓ exertional angina. If
symptoms arise on a β -blocker, a long-acting nitrate or calcium channel blocker (CCB) can be added. Ranolazine
can be added for refractory angina.
ISCHEMIC HEART DISEASES – EKG CHANGES IN MI
ISCHEMIC HEART DISEASES – EKG CHANGES IN OLD MI
ISCHEMIC HEART DISEASES – CARDIAC ENZYMES
 ISCHEMIC HEART DISEASES - COMPLICATIONS

 Arrhythmia: VF and VT are the most common complications and the most common causes of sudden death
following acute MI. Sinus bradycardia and third-degree (complete) heart block are also very common.
 Less common complications include reinfarction, left ventricular wall rupture, VSD, pericarditis, papillary muscle
rupture (with mitral regurgitation), left ventricular aneurysm or pseudoaneurysm, and mural thrombi (with
subsequent acute limb ischemia, TIA, or stroke).
 A timeline of common post-MI complications:
■ First day: Heart failure.
■ 2–4 days: Arrhythmia, pericarditis.
■ 5–10 days: Left ventricular wall rupture (acute pericardial tamponade causing electrical alternans,
pulseless electrical activity, and JVD), papillary muscle rupture (severe mitral regurgitation, pulmonary
edema), septal rupture (lower left sternal border murmur, increase in O2 saturation in the right ventricle).
■ Weeks to months: Ventricular aneurysm (CHF, arrhythmia, persistent ST-segment elevation, mitral
regurgitation, thrombus formation).
 ISCHEMIC HEART DISEASES - COMPLICATIONS

 Dressler’s Syndrome - Patients with Dressler's syndrome present weeks after a myocardial infarction with chest pain that is
improved by leaning forward. EKG shows ST segment elevations in all limb and precordial leads except in aVR, where ST
depression is seen. NSAIDs are the treatment of choice. Corticosteroids can be used in refractory cases or when NSAIDs are
contraindicated.
 Right ventricular infarction: Caused by the occlusion of the RCA. Presents with hypotension, JVD, and clear lungs.
Treat with high-volume fluid replacement (preload dependent), and avoid nitrates and diuretics.

 Ventricular remodeling in the weeks to months following myocardial infarction can lead to dilatation of the
ventricle. This process is lessened by ACE inhibitors.
ISCHEMIC HEART DISEASES – COCAINE INDUCED
 VALVULAR HEART DISEASES – CARDIAC EXAMINATION

■ Jugular venous distention (JVD > 4 cm above the sternal angle): Most typically from volume overload, stemming from conditions such as
right heart failure or pulmonary hypertension.
■ Hepatojugular reflux (distention of neck veins upon applying pressure to the liver): Seen in the same conditions as JVD.
■ Kussmaul sign (↑ in jugular venous pressure [JVP] with inspiration): Often seen in constrictive pericarditis.
■ Gallops:
■ S3 gallop: A sign of fluid overload (ie, heart failure, mitral valve disease); often normal in younger patients and in high-output states (eg,
pregnancy).
■ S4 gallop: A sign of decreased compliance (ie, hypertension, aortic stenosis, diastolic dysfunction); usually pathologic but can be normal
in younger patients and in athletes.
■ Edema:
■ Pulmonary: Left heart failure (fluid “backs up” into the lungs).
■ Peripheral: Right heart failure and biventricular failure (fluid “backs up” into the periphery), nephrotic syndrome, hepatic disease,
lymphedema, hypoalbuminemia, and drugs.
■ Hands:
■ Finger clubbing: Congenital cyanotic heart disease; endocarditis.
■ Infective endocarditis: Splinter hemorrhages; Osler nodes, Janeway lesions.
 VALVULAR HEART DISEASES – CARDIAC EXAMINATION

■ Peripheral pulses:
■ Increased: Compensated aortic regurgitation (bounding pulses); coarctation (greater in arms than in legs); patent ductus
arteriosus.
■ Decreased: Peripheral arterial disease; late-stage heart failure.
■ Collapsing (“waterhammer”): Aortic incompetence; AV malformations; patent ductus arteriosus; thyrotoxicosis, severe
anemia.
■ Pulsus paradoxus (↓ systolic BP > 10 mm Hg with inspiration): Cardiac tamponade; pericardial constriction; also seen in
obstructive lung diseases (eg, severe asthma), tension pneumothorax, and foreign body in airway.
■ Pulsus alternans (alternating weak and strong pulses): Cardiomyopathy; impaired left ventricular systolic function (LVF).
Poor prognosis.
■ Pulsus parvus et tardus (weak and delayed pulse): Aortic stenosis.
■ Jerky: hypertrophic obstructive cardiomyopathy (HOCM).
■ Pulsus bisferiens (bifid pulse/“twice beating”): Aortic regurgitation; combined aortic stenosis and aortic regurgitation,
HOCM
VALVULAR HEART DISEASES – CARDIAC AUSCULTATION
VALVULAR HEART DISEASES – CARDIAC
AUSCULTATION
VALVULAR
HEART
DISEASES
VALVULAR
HEART
DISEASES
VALVULAR
HEART
DISEASES
 VALVULAR HEART DISEASES – MURMURS & MANEUVERS

Cardiac Murmur Workup - Diastolic and continuous murmurs as well as loud systolic murmurs revealed on cardiac
auscultation should always be investigated using transthoracic Doppler echocardiography. Midsystolic soft murmurs (grade
1-11/ VI) in an asymptomatic young patient are usually benign and need no further work-up.
VALVULAR HEART DISEASES – ANTITHROMBOTIC
THERAPY IN MECHANICAL HEART VALVES
 HEART FAILURE - INTRODUCTION

The inability of the heart to pump adequate blood to meet the demands of the body. One categorization scheme
includes:
■ Systolic heart failure.
■ Diastolic heart failure.
■ Heart failure related to valvular disease.
■ Heart failure related to arrhythmias.
 SYSTOLIC HEART FAILURE – DEFINITION & CAUSES

■ Weakened pump function of the heart. Sometimes referred to as “heart failure with reduced ejection fraction”
(HFrEF).
■ Common causes include ischemic heart disease, long-standing hypertension, toxins (eg, alcohol), and viral or
idiopathic cardiomyopathy in younger patients.
SYSTOLIC HEART FAILURE – CLINICAL CLASSIFICATION
 SYSTOLIC HEART FAILURE – MANIFESTATIONS

■ Poor exercise tolerance, exertional dyspnea, and easy fatigability.

■ Orthopnea or paroxysmal nocturnal dyspnea, poor appetite, RUQ pain, and ankle swelling (due to volume
overload).
■ Exam often reveals inspiratory crackles (may be absent in chronic heart failure); a diffuse left-displaced point of
maximal impulse (PMI), reflecting cardiomegaly; an S3 gallop, ↑ JVP; and lower extremity edema. Cool extremities
and/or confusion may suggest low cardiac output.
 SYSTOLIC HEART FAILURE – MANAGEMENT
■ The history and exam are suggestive, but the determination of the EF via an imaging study (eg, echocardiography,
radionuclide imaging, cardiac MRI) confirms the diagnosis.
■ Look for the cause of the low EF:
■ Perform a stress test or cardiac catheterization to look for CAD; evaluate for thyroid and renal disease.
■ Look for a history of alcohol use or exposure to offending cardiotoxic medications such as doxorubicin.
■ Consider dilated cardiomyopathy in postpartum women.
■ Consider myocardial biopsy in selected cases to evaluate for infiltrative disease or other rare causes when other
evaluations are inconclusive.
 SYSTOLIC HEART FAILURE – MANAGEMENT

■ Optimize cardiac output via the following mechanisms:

■ ↓ Preload (reducing cardiac filling pressures).
■ ↓ Wall stress and optimization of cardiac contractility.
■ ↓ Afterload (making it easier for the heart to pump systemically).
■ Maintenance medications include:
■ Preload reduction: Diuretics (furosemide, bumetanide, torsemide).
■ ↓ Wall stress: β-blockers (metoprolol, bisoprolol, carvedilol).
■ Optimization of contractility: Digoxin (may lower the frequency of hospitalizations and improve symptoms but
does not ↓ mortality).
■ Afterload reduction: Renin-angiotensin-aldosterone antagonists (ACEIs/ ARBs; spironolactone if potassium and
creatinine are not ↑ and the patient is on optimal dosages of β-blockers and ACEIs/ARBs). Hydralazine and nitrates
may be useful additions to ACEIs/ARBs in African American patients or an alternative to ACEIs/ARBs in patients
with kidney disease/hyperkalemia.
SYSTOLIC HEART FAILURE – MANAGEMENT
 SYSTOLIC HEART FAILURE – MANAGEMENT

■ Exacerbations: Give loop diuretics such as furosemide when the patient is volume overloaded. These are given
first in IV form and then transitioned to oral form once the patient is closer to euvolemia. β-blockers and afterload
reduction agents can be initiated once the patient is euvolemic.
■ Implantable cardiac defibrillators (ICDs) are associated with ↓ mortality from ventricular tachycardia and
ventricular fibrillation (VT/VF) in heart failure patients who are symptomatic and have a ↓ EF (< 35%).

■ Advanced pharmacologic therapy:

■ Sacubitril/valsartan: angiotensin receptor-neprilysin inhibitor (ARNI) is a new drug class used in patients who
continue to be dyspneic despite using the initial pharmacologic regimen. Provides mortality benefit for systolic
dysfunction.
■ Ivabradine: Reduces heart rate through SA nodal inhibition of the “funny channels.” Indicated in patients with
systolic dysfunction if pulse is > 70 bpm or β-blockers are contraindicated.
 DIASTOLIC HEART FAILURE – DEFINITION & CAUSES

■ During diastole, the heart is stiff and does not relax well, resulting in ↑ diastolic filling pressure. However, the EF is
often normal, so diastolic heart failure is sometimes referred to as “heart failure with preserved ejection fraction”
■ Hypertension with left ventricular hypertrophy (LVH) is the most common cause; other causes include
hypertrophic cardiomyopathy and infiltrative diseases.
 DIASTOLIC HEART FAILURE – MANAGEMENT

■ Echocardiography shows preserved EF, often accompanied with ventricular hypertrophy. Biopsy may be needed to
establish the underlying diagnosis if infiltrative disease is suspected. Cardiac MRI is becoming an increasingly popular
modality for this purpose.
■ Control hypertension. Give diuretics to control volume overload and symptoms, but avoid overdiuresis, which can
↓ preload and cardiac output.
■ Manage arrhythmias (eg, AF) that are frequently associated with diastolic dysfunction.
■ Control renal and vascular disease, both of which are thought to be associated with diastolic heart disease
 DIASTOLIC HEART FAILURE – MANIFESTATIONS

■ Signs and symptoms are the same as those of systolic heart failure.
■ Exam findings are like those of systolic heart failure. Listen for an S4 rather than an S3 (if the rhythm is regular) or
an irregular rhythm (atrial fibrillation [AF] is commonly associated with diastolic dysfunction).
 CARDIOMYOPATHY

1st step ➔ Echocardiography

CARDIOMYOPATHY
 PERICARDITIS – DEFINITION & CAUSES

 Inflammation of the pericardial sac. Acute (< 6 weeks; most common), subacute (6 weeks to 6 months), or
chronic (> 6 months).
 Causes include bacterial or viral infection (especially enterovirus), mediastinal radiation, post-MI (Dressler
syndrome), cancer, rheumatologic diseases (systemic lupus erythematosus [SLE], rheumatoid arthritis [RA]),
uremia, tuberculosis (TB), and prior cardiac surgery. May also be idiopathic (the most common cause of
acute cases).
 PERICARDITIS – MANIFESTATIONS

■ Presents with chest pain that is often improved with sitting up or leaning forward. The pain may radiate to the
back and to the left trapezial ridge.
■ If a large effusion is present, the patient may be short of breath.
■ Exam may reveal a pericardial friction rub (a leathery sound that can be present in multiple stages of the cardiac
cycle).
 PERICARDITIS – DEFINITION & CAUSES

■ First diagnostic test: ECG

 PERICARDITIS – DEFINITION & CAUSES

■ First diagnostic test: ECG

 PERICARDITIS – MANAGEMENT

■ First diagnostic test: ECG

■ Echocardiography may reveal an associated pericardial effusion.
■ Search for an underlying cause (ie, take a history for viral illness, radiation exposure, and malignancy). Check
antinuclear antibody (ANA), PPD, blood cultures if febrile, and renal function.
■ Treat the identified underlying disorder (eg, SLE, advanced renal failure).
■ For viral or idiopathic pericarditis, give NSAIDs, colchicine, or aspirin.
■ Avoid NSAIDs or steroids in early post-MI pericarditis, as they may interfere with scar formation.
 PERICARDIAL EFFUSION/TAMPONADE – DEFINITION &
MANIFESTATIONS

■ Accumulation of fluid (usually chronic) or blood (usually acute and posttraumatic/postsurgical) in the pericardial
cavity surrounding the heart.
■ Symptomatology often depends on the rate of fluid accumulation. If acute, patients may present with shock. If
chronic, patients may present with shortness of breath and heart failure (if gradual, several liters of fluid may
accumulate).
■ In patients with pericardial effusions and tamponade physiology, exam
classically reveals distant or muffled heart sounds, ↑ JVP, and pulsus
paradoxus (a drop of > 10 mm Hg in systolic BP [blood pressure] during inspiration).
 PERICARDIAL EFFUSION/TAMPONADE – MANAGEMENT

■ Initial test: Echocardiography is needed to confirm the diagnosis.

■ CXR may reveal an enlarged cardiac silhouette, and ECG may show low voltages
and electrical alternans (beat-to-beat variation in R-wave amplitude)
■ Consider emergent pericardiocentesis for patients with
post–chest trauma shock as well as for those whose echocardiogram
shows evidence of tamponade physiology.
■ Also, consider a pericardial window for those with recurrent or
malignant effusions. While evaluation with echocardiography is being pursued,
give IV fluids to maintain preload and systemic BP.
SYNCOPE