USMLE Step 1 Quiz: Cardiac Pathophysiology

What this quiz covers

This quiz focuses on Cardiac Pathophysiology, giving you a quick way to practice the rules, question types, and explanations that matter most for USMLE Step 1.

How to use this quiz

Try each quiz question before looking at the correct answer. Use the explanations to review missed ideas, then come back to similar questions until the pattern feels familiar.

Question 1

1. Low cardiac output and high systemic vascular resistance
2. High cardiac output and low systemic vascular resistance (correct answer)
3. Low cardiac output and low systemic vascular resistance
4. High cardiac output and high systemic vascular resistance

Explanation: Septic shock is a form of distributive shock characterized by widespread vasodilation due to inflammatory mediators. This leads to a profound decrease in systemic vascular resistance (SVR), causing hypotension. In the early 'warm shock' phase, the heart compensates for the low SVR by increasing heart rate and stroke volume, resulting in a high or normal cardiac output. This contrasts with cardiogenic shock, which is defined by a primary pump failure leading to low cardiac output and a compensatory, reflexive increase in SVR (causing cool, clammy skin).

Question 2

1. Rupture of the plaque with superimposed thrombosis
2. A thick, intact fibrous cap covering a lipid core (correct answer)
3. Coronary artery vasospasm at the site of the plaque
4. Erosion of the endothelial surface without cap rupture

Explanation: This patient's presentation is classic for stable angina, which is characterized by exertional chest pain due to a mismatch between myocardial oxygen supply and demand, relieved by rest. The underlying pathology is a stable atherosclerotic plaque with a thick, intact fibrous cap that narrows the coronary lumen but does not rupture. This fixed obstruction limits blood flow during times of increased demand. Plaque rupture with thrombosis is characteristic of acute coronary syndromes like unstable angina or myocardial infarction. Vasospasm is the mechanism of Prinzmetal angina. Plaque erosion is another cause of acute coronary syndrome.

Question 3

1. Myocardial hibernation
2. Myocardial stunning (correct answer)
3. Ventricular remodeling
4. Coronary no-reflow phenomenon

Explanation: Myocardial stunning refers to the temporary loss of contractile function in myocardial tissue that persists for hours to days after reperfusion, even though the tissue is viable. It is thought to be caused by oxidative stress, calcium overload, and inflammation associated with reperfusion. Myocardial hibernation is a state of chronic, but reversible, contractile dysfunction in response to chronic ischemia. Ventricular remodeling is a long-term process of changes in ventricular size, shape, and function after an MI. The no-reflow phenomenon is a failure to perfuse the microvasculature despite an open epicardial artery.

Question 4

1. Natriuretic peptide system
2. Renin-angiotensin-aldosterone system (correct answer)
3. Kallikrein-kinin system
4. Parasympathetic nervous system

Explanation: In systolic heart failure, decreased cardiac output leads to reduced renal perfusion, which activates the renin-angiotensin-aldosterone system (RAAS). Angiotensin II causes vasoconstriction and stimulates aldosterone release. Aldosterone acts on the renal distal tubules and collecting ducts to increase sodium and water reabsorption, leading to volume expansion, which is initially compensatory but becomes maladaptive, causing systemic and pulmonary congestion. Natriuretic peptides (ANP, BNP) are released in response to stretch and promote vasodilation and natriuresis, counteracting RAAS, but their effects are often overwhelmed in advanced heart failure.

Question 5

1. Impaired myocardial relaxation and increased ventricular stiffness (correct answer)
2. Decreased myocardial contractility and stroke volume
3. Eccentric hypertrophy with ventricular dilation
4. Excessive preload due to renal failure

Explanation: This patient has heart failure with preserved ejection fraction (HFpEF), also known as diastolic heart failure. The primary mechanism is impaired diastolic function. Long-standing hypertension causes pressure overload, leading to concentric hypertrophy. This hypertrophied ventricle is stiff and relaxes poorly during diastole, impairing ventricular filling and leading to elevated left ventricular end-diastolic pressure. This pressure is transmitted backward to the left atrium and pulmonary circulation, causing pulmonary congestion and dyspnea. Systolic function (contractility) is preserved, as indicated by the normal ejection fraction.

Question 6

1. Myocardial contractility (correct answer)
2. Diastolic relaxation
3. Pericardial compliance
4. Valvular competence

Explanation: This patient's presentation is highly suggestive of viral myocarditis leading to dilated cardiomyopathy (DCM). The primary pathophysiologic defect in DCM is impaired myocardial contractility (systolic dysfunction). The viral infection and subsequent immune response damage myocytes, leading to a dilated, thin-walled, and poorly contracting ventricle. This results in a reduced ejection fraction and symptoms of systolic heart failure. While diastolic dysfunction can also be present, the defining feature is the profound impairment of systolic function.

Question 7

1. Increased systemic vascular resistance
2. Reduced total blood volume
3. Rapid diastolic runoff of blood from the aorta (correct answer)
4. Decreased left ventricular contractility

Explanation: This patient has aortic regurgitation (AR). The wide pulse pressure (systolic minus diastolic pressure) is a hallmark of chronic AR. The left ventricle ejects a large stroke volume (forward flow plus regurgitant volume from the previous beat) into the aorta, causing a high systolic pressure. During diastole, blood flows backward from the aorta into the left ventricle through the incompetent aortic valve. This regurgitant flow, or 'diastolic runoff,' causes a rapid decline in aortic pressure, leading to a very low diastolic pressure and thus a wide pulse pressure.

Question 8

1. Spontaneous closure of the ventricular septal defect
2. Development of severe pulmonary vascular obstructive disease (correct answer)
3. Progressive left ventricular hypertrophy and failure
4. Acquired tricuspid valve regurgitation

Explanation: A large VSD initially causes a left-to-right shunt, leading to excessive blood flow through the pulmonary circulation. Over time, this chronic volume and pressure overload causes medial hypertrophy and intimal proliferation of the pulmonary arterioles, a process known as pulmonary vascular obstructive disease. This leads to a progressive increase in pulmonary vascular resistance and pulmonary artery pressure. Eventually, the pressure in the right ventricle exceeds the pressure in the left ventricle, causing the shunt to reverse (right-to-left). This reversal, known as Eisenmenger syndrome, results in deoxygenated blood entering the systemic circulation, causing cyanosis.

Question 9

1. A sudden increase in pulmonary blood flow
2. Dynamic infundibular spasm increasing right ventricular outflow obstruction (correct answer)
3. Acute closure of the ventricular septal defect
4. A paradoxical embolism to a coronary artery

Explanation: A hypercyanotic or 'tet' spell in Tetralogy of Fallot is caused by an acute increase in the right-to-left shunt. The primary trigger is often a sudden decrease in systemic vascular resistance (SVR) or an increase in right ventricular outflow tract (RVOT) obstruction. Dynamic spasm of the hypertrophied infundibular muscle is a key mechanism that acutely worsens the RVOT obstruction. This makes it harder for blood to enter the pulmonary artery, shunting more deoxygenated blood from the right ventricle across the VSD into the aorta, leading to profound cyanosis. Squatting increases SVR, which helps to reverse the shunt and improve oxygenation.

Question 10

1. An accessory pathway connecting the atria and ventricles
2. Multiple chaotic atrial impulses
3. Enhanced automaticity of a focus in the His-Purkinje system
4. A reentrant circuit involving two distinct pathways within the AV node (correct answer)

Explanation: This clinical presentation is classic for atrioventricular nodal reentrant tachycardia (AVNRT), the most common type of paroxysmal supraventricular tachycardia (PSVT). The underlying mechanism is the presence of dual AV nodal pathways (a fast pathway and a slow pathway) with different conduction velocities and refractory periods. This allows for the formation of a micro-reentrant circuit within the AV node, leading to a rapid, regular tachycardia. Vagal maneuvers, like bearing down (Valsalva), increase parasympathetic tone to the AV node, which can block the circuit and terminate the arrhythmia.

Question 11

1. Exaggerated interventricular septal motion towards the left ventricle during inspiration
2. A significant decrease in right atrial pressure during systole
3. Equalization of diastolic pressures in all four cardiac chambers (correct answer)
4. A large pressure gradient between the pulmonary artery and the right ventricle

Explanation: This patient's presentation is classic for cardiac tamponade, a potential complication of an invasive cardiac procedure. In tamponade, the accumulation of fluid in the pericardial space compresses the heart, restricting diastolic filling. As the intrapericardial pressure rises, it limits the extent to which the chambers can expand. This external constraint causes the diastolic pressures in the right atrium, right ventricle, pulmonary artery, and left ventricle to equilibrate at the level of the elevated intrapericardial pressure. This equalization of diastolic pressures is a pathognomonic hemodynamic finding.

Question 12

1. Thyroid hormone-induced myocardial toxicity causing systolic dysfunction
2. Inability of the heart to meet the body's supranormal metabolic demands (correct answer)
3. Autoimmune-mediated myocarditis secondary to Graves' disease
4. Severe reduction in systemic vascular resistance leading to distributive shock

Explanation: This patient has high-output heart failure secondary to thyrotoxicosis. In this condition, the heart function is normal or even supranormal (high cardiac output, preserved EF), but it is insufficient to meet the body's pathologically elevated metabolic demands. Thyroid hormone increases basal metabolic rate and causes peripheral vasodilation, which decreases systemic vascular resistance and increases venous return. The heart must pump an exceptionally large volume of blood to satisfy the tissues' need for oxygen. Eventually, the heart cannot keep up with this chronic demand, leading to symptoms of congestion (pulmonary edema) despite the high cardiac output.

Question 13

1. Systolic contractility
2. Diastolic filling (correct answer)
3. Atrioventricular conduction
4. Coronary blood flow

Explanation: This patient has restrictive cardiomyopathy, most likely from amyloid deposition. The key pathophysiology is severe diastolic dysfunction. The infiltration of the myocardium by the rigid amyloid protein makes the ventricular walls stiff and noncompliant. This severely impairs the ability of the ventricles to relax and fill during diastole, leading to very high diastolic filling pressures. These high pressures are transmitted backward to the atria (causing biatrial enlargement) and the pulmonary and systemic venous circulations, resulting in dyspnea and peripheral edema. Systolic function is often preserved until late in the disease.

Question 14

1. Rheumatic fusion of the mitral valve commissures
2. Myxomatous degeneration of the mitral valve leaflets (correct answer)
3. Calcific stenosis of a bicuspid aortic valve
4. Bacterial endocarditis causing leaflet perforation

Explanation: The mid-systolic click and late systolic murmur are pathognomonic for mitral valve prolapse (MVP). The underlying pathology is myxomatous degeneration of the mitral valve leaflets and chordae tendineae, making them redundant and floppy. During systole, the leaflet billows back into the left atrium (the 'click' occurs when the chordae abruptly tense). If the prolapse is severe enough, mitral regurgitation occurs late in systole (the murmur). Standing decreases venous return and reduces left ventricular volume, causing the prolapse to occur earlier in systole and the murmur to lengthen.

Question 15

1. Delayed conduction through the atrioventricular node
2. An ectopic atrial pacemaker firing faster than the SA node
3. An accessory atrioventricular conduction pathway (correct answer)
4. Intraventricular conduction delay in the bundle branches

Explanation: This patient's ECG shows the classic findings of Wolff-Parkinson-White (WPW) syndrome: a short PR interval and a delta wave (the slurred upstroke of the QRS). The underlying pathophysiology is an accessory atrioventricular pathway (Bundle of Kent) that bypasses the AV node. This accessory tract conducts the atrial impulse directly to the ventricle, bypassing the normal physiologic delay in the AV node. This pre-excitation of the ventricle results in a short PR interval and the delta wave. This pathway can also serve as one limb of a reentrant circuit, leading to paroxysmal supraventricular tachycardias.

Question 16

1. Depletion of intracellular glycogen stores
2. Swelling of mitochondria and the sarcoplasmic reticulum
3. Clumping of nuclear chromatin
4. Disruption and fragmentation of the sarcolemmal membrane (correct answer)

Explanation: The transition from reversible to irreversible ischemic injury in myocytes is marked by profound membrane damage. Disruption of the sarcolemma (cell membrane) leads to a massive influx of calcium and the leakage of intracellular proteins (like troponin and creatine kinase) into the circulation. This loss of membrane integrity is the hallmark of cell death (necrosis). Glycogen depletion, cellular swelling, and nuclear chromatin clumping are all early changes that occur during the reversible phase of ischemic injury.

Question 17

1. Increased pressure gradient between the left atrium and left ventricle during diastole (correct answer)
2. Decreased pressure gradient between the aorta and left ventricle during systole
3. Equalization of left and right ventricular end-diastolic pressures
4. Increased left ventricular end-systolic volume

Explanation: The patient's history of rheumatic fever and clinical findings are classic for mitral stenosis. The stenotic mitral valve obstructs blood flow from the left atrium (LA) to the left ventricle (LV) during diastole. To maintain cardiac output, the LA pressure must rise significantly higher than the LV diastolic pressure, creating a large pressure gradient across the mitral valve. This elevated LA pressure leads to LA enlargement, atrial fibrillation, and transmission of pressure back to the pulmonary circulation, causing dyspnea and hemoptysis.

Question 18

1. Sinoatrial node
2. Atrioventricular node
3. Myocardial sleeves of the pulmonary veins (correct answer)
4. Right atrial appendage

Explanation: The pathophysiology of atrial fibrillation involves both triggers and a susceptible substrate. The most common triggers are ectopic foci that fire rapidly and erratically. Electrophysiologic studies have demonstrated that these foci are most often located within the myocardial sleeves that extend from the left atrium into the pulmonary veins. Ablation procedures for atrial fibrillation often target the isolation of these pulmonary veins to eliminate the source of these ectopic beats.

Question 19

1. Fixed subaortic stenosis from a fibrous membrane
2. Calcification and immobility of the aortic valve leaflets
3. Systolic anterior motion of the mitral valve leaflet (correct answer)
4. Abnormal papillary muscle insertion causing mitral regurgitation

Explanation: In hypertrophic cardiomyopathy (HCM), the key pathophysiologic feature is asymmetric septal hypertrophy. During systole, the anterior leaflet of the mitral valve is pulled toward the hypertrophied septum due to Venturi effects, causing a dynamic obstruction of the left ventricular outflow tract (LVOT). Maneuvers that decrease preload, such as Valsalva, decrease the LV cavity size and worsen the obstruction, making the murmur louder. This phenomenon is known as systolic anterior motion (SAM) of the mitral valve.

Question 20

1. Massive peripheral vasodilation leading to relative hypovolemia
2. Severe depression of myocardial contractility leading to inadequate tissue perfusion (correct answer)
3. Obstruction of right ventricular filling due to pericardial effusion
4. Loss of intravascular volume due to capillary leak syndrome

Explanation: This patient is in cardiogenic shock. The primary insult is a severe reduction in myocardial contractility due to the extensive myocardial infarction. This 'pump failure' leads to a drastic decrease in cardiac output and stroke volume (reflected by the low cardiac index), resulting in systemic hypotension and hypoperfusion (cool extremities, confusion). The failing left ventricle is unable to pump blood forward, causing blood to back up into the pulmonary circulation, leading to a high pulmonary capillary wedge pressure (a surrogate for left atrial pressure) and pulmonary edema.