Cardiology USMLE Practice Questions
Master cardiovascular physiology, pathology, and pharmacology for USMLE.
5 free cardiology practice questions
Pick an answer and check it. After each question you get the same explanation StepGenie students see: the stem decoded clue by clue, the reasoning chain with its infographic, why every wrong option is wrong, and the trap the question was built around. Step 1 questions test mechanism; Step 2 CK questions ask for the next step.
A 52-year-old man with long-standing heavy alcohol use presents after 5 hours of recurrent vomiting of dark, granular blood with occasional bright-red streaks. He is pale, diaphoretic, and confused, oriented only to person. Temperature is 36.7°C (98.1°F), pulse is 122/min, and blood pressure is 85/59 mm Hg. Examination shows cool, clammy extremities with thready radial pulses and delayed capillary refill; multiple spider angiomata and a distended, fluid-wave–positive abdomen are noted. Compared with a healthy adult, which physiological variable is most likely decreased in this patient in response to his current condition?
Correct answer · D
Carotid baroreceptor firing activity
Decoding the stem
Step-by-step reasoning
Step 1 of 6
Upper GI bleeding from portal hypertension in a cirrhotic patient causes acute blood loss and decreased circulating volume.
Step 2 of 6
Loss of volume lowers venous return, stroke volume, and ultimately cardiac output → decreased arterial blood pressure (MAP).
Step 3 of 6
Carotid sinus baroreceptors sense arterial pressure via stretch; less stretch occurs when MAP falls.
Step 4 of 6
Decreased stretch leads to decreased baroreceptor firing along the glossopharyngeal nerve to the nucleus tractus solitarius.
Step 5 of 6
Lower baroreceptor firing disinhibits sympathetic outflow → tachycardia, vasoconstriction, cool clammy skin, and attempts to restore blood pressure.
Step 6 of 6
Therefore, compared with a healthy adult, this patient’s carotid baroreceptor firing activity is decreased in response to hypovolemic shock.
Why not the others?
C. Carotid body chemoreceptor firing activity
This option implies arterial chemoreceptor activation, which increases when perfusion and O2 delivery fall, BUT in hypovolemic shock their firing is increased, not decreased.
E. Pulmonary stretch receptor firing activity
This option implies increased lung inflation (higher tidal volumes), which would increase firing, BUT the question asks what decreases; these receptors are not the primary response in acute hypotension.
A. Atrial stretch receptor firing activity
This option implies high venous return and atrial volume (as in fluid overload), which increases stretch, BUT hypovolemia from hemorrhage reduces atrial stretch receptor firing.
B. Afferent renal baroreceptor firing activity
Renal baroreceptors in the afferent arteriole sense renal perfusion; in hypotension, their firing decreases to raise renin, BUT carotid baroreceptors are the key systemic short-term responders tested here.
F. Cardiac mechanoreceptor firing activity
These receptors respond to cardiac filling and wall stretch; hemorrhage reduces filling and thus their firing, BUT again the exam focuses on carotid sinus baroreceptors for acute MAP changes.
Exam trap
The vignette pushes you toward general ‘shock physiology.’ Many options involve receptors that increase firing in low-flow states; the key is recognizing baroreceptor vs chemoreceptor roles and that arterial baroreceptor firing falls when pressure falls.
The bottom line
Acute hypovolemic shock from upper GI bleed → low MAP → decreased carotid baroreceptor firing → sympathetic activation and tachycardia.
A 55-year-old man presents with a 6-week history of tingling pain in the sole of his right foot that occurs when he raises the foot above chest level during exercise. He began a regular exercise program 2 months ago and notes that his right calf develops cramping pain when he uses the incline feature on the treadmill, forcing him to take frequent breaks. The discomfort resolves completely within a few minutes of rest. Medical history is significant for type 2 diabetes mellitus for 8 years and long-term tobacco use (2 packs of cigarettes daily for 34 years). His only medication is metformin. Vital signs show a pulse of 82/min and blood pressure of 170/92 mm Hg. On examination, straight leg raise reproduces pallor and tingling pain in the right foot without associated back pain. Muscle strength is normal. Femoral pulses are palpable, but the right pedal pulses are absent. Which of the following is the most likely diagnosis?
Correct answer · A
Femoropopliteal artery stenosis
Decoding the stem
Step-by-step reasoning
- 1
Patient has major atherosclerotic risk factors (long-standing diabetes, heavy smoking, uncontrolled hypertension) → high risk for peripheral arterial disease (PAD).
- 2
Symptoms of exertional calf cramping pain relieved by rest define intermittent claudication, typical of PAD due to fixed arterial narrowing.
- 3
Pain and tingling in the sole when the leg is elevated reflects decreased perfusion pressure in an already stenotic arterial bed → elevation pallor sign of PAD.
- 4
Exam: femoral pulses present but right pedal pulses absent → obstruction lies distal to femoral artery but proximal to pedal arteries → in the femoropopliteal arterial segment.
- 5
Normal muscle strength and lack of back pain make neuropathic or spinal causes less likely; findings fit localized arterial stenosis → femoropopliteal artery stenosis.
Why not the others?
B. Diabetic neuropathy
This option implies chronic length-dependent sensory neuropathy causing symmetric stocking-glove numbness/burning, BUT this patient has exertional, position-dependent pain and absent distal pulses, pointing to ischemia not neuropathy.
C. Vasculitis of the right popliteal artery
This option implies inflammatory vessel disease with systemic signs (fever, elevated ESR, multisystem involvement), BUT the patient has classic atherosclerotic risk factors, chronic claudication, and segmental pulse loss without systemic inflammation.
D. Acute thrombosis of right popliteal vein
This option implies DVT, which causes limb swelling, warmth, and pain that is worse with dependency, BUT this patient has no swelling, has arterial pulse loss, and symptoms tied to exercise and elevation, not venous congestion.
E. Lumbar spinal stenosis
This option implies neurogenic claudication with pain worse with spinal extension and relieved by flexion (leaning forward), often with back pain, BUT this patient’s symptoms are clearly vascular (dependent on leg elevation and pulses are absent) and he lacks back pain or positional spine findings.
F. Aortoiliac artery stenosis
This option implies proximal PAD (Leriche syndrome) with hip/thigh claudication, diminished femoral pulses, and possibly impotence, BUT this patient’s femoral pulses are normal and symptoms localize to the calf and foot, indicating a more distal lesion.
Exam trap
The stem strongly suggests peripheral arterial disease, but the key is pulse localization: normal femoral with absent pedal pulses localizes disease to the femoropopliteal segment, not more proximal (aortoiliac) or non-arterial causes (neuropathy, spinal stenosis).
The bottom line
Peripheral arterial disease from femoropopliteal stenosis → exertional calf claudication, dependent rubor/elevation pallor, absent distal pulses in a diabetic smoker.
A 14-year-old boy is evaluated for a 3-month history of generalized fatigue and mild exertional shortness of breath. He has a history of recurrent patellar dislocations. He is at the 99th percentile for height and the 30th percentile for weight. Vital signs show a temperature of 37°C (98.6°F), pulse of 99/min, and blood pressure of 140/50 mm Hg. Physical examination reveals scoliosis, pectus carinatum, thin extremities, and pes planus. Ophthalmologic examination shows superior lens subluxation in both eyes. Cardiac auscultation reveals a grade 3/6 early diastolic murmur along the left sternal border. Further evaluation of this patient is most likely to show which of the following?
Correct answer · E
Water hammer pulse
Decoding the stem
Step-by-step reasoning
Step 1 of 6
The combination of tall, thin habitus; scoliosis; pectus carinatum; pes planus; and recurrent patellar dislocations indicates connective tissue weakness.
Step 2 of 6
Superior lens subluxation further narrows this to Marfan syndrome (fibrillin-1 defect affecting elastic tissues).
Step 3 of 6
Marfan commonly involves the aortic root, predisposing to aortic root dilation and valvular abnormalities.
Step 4 of 6
Aortic root dilation prevents proper coaptation of the aortic valve leaflets, leading to chronic aortic regurgitation.
Step 5 of 6
Aortic regurgitation causes blood to flow back into the LV in diastole → increased stroke volume and wide pulse pressure (↑ systolic, ↓ diastolic).
Step 6 of 6
The hemodynamic result is a bounding, rapidly collapsing peripheral pulse, known as a water hammer (Corrigan) pulse.
Why not the others?
A. Paradoxical splitting of S2
This option implies delayed aortic valve closure (e.g., left bundle branch block, aortic stenosis), which causes an abnormal S2 pattern, BUT this patient has clinical features and murmur classic for aortic regurgitation, not outflow obstruction or conduction delay.
B. Pulsus paradoxus
This option implies conditions like cardiac tamponade, severe asthma/COPD, or constrictive pericarditis, causing >10 mm Hg drop in systolic BP with inspiration, BUT the patient has wide pulse pressure and chronic diastolic murmur of aortic regurgitation, without signs of pericardial disease or acute respiratory pathology.
C. Pulsus parvus et tardus
This option implies severe aortic stenosis (slow-rising, low-amplitude carotid pulse) due to fixed outflow obstruction, BUT the exam shows an early diastolic murmur and wide pulse pressure, which are findings of aortic regurgitation, not stenosis.
D. Fixed splitting of S2
This option implies an atrial septal defect (ASD) with constant increased right-sided flow, BUT the murmur described is early diastolic along the left sternal border (AR), and there are no signs of right heart volume overload or ASD-related symptoms.
F. Radio-femoral pulse delay
This option implies coarctation of the aorta (delayed femoral vs radial pulses), which causes upper-extremity hypertension and diminished leg pulses, BUT there is no mention of pulse delays or differential BP; instead, the findings strongly indicate aortic regurgitation from Marfan-related aortic root dilation.
Exam trap
The exam-taker may focus only on the Marfan physical features and think of aortic dissection or MVP, missing the early diastolic murmur + wide pulse pressure that specifically indicate chronic aortic regurgitation and its classic water hammer pulse finding.
The bottom line
Marfan syndrome causing aortic root dilation → aortic regurgitation with wide pulse pressure and water hammer pulse (bounding, rapidly collapsing).
A 70-year-old man presents with acute shortness of breath at rest 3 days after undergoing cardiac catheterization and coronary angioplasty for an acute myocardial infarction. His medical history is significant for hypertension, hyperlipidemia, and type 2 diabetes mellitus. Current medications include aspirin, clopidogrel, atorvastatin, sublingual nitroglycerin, metoprolol, and insulin. He appears diaphoretic. Temperature is 37°C (98.6°F), pulse is 120/min, respirations are 22/min, and blood pressure is 100/55 mm Hg. Pulmonary examination reveals crackles at both lung bases. Cardiac examination shows a new grade 3/6 holosystolic murmur best heard at the cardiac apex. ECG demonstrates sinus rhythm with T-wave inversions in leads II, III, and aVF. Which of the following is the most likely explanation for this patient's symptoms?
Correct answer · G
Papillary muscle rupture
Decoding the stem
Step-by-step reasoning
- 1
Inferior MI (T-wave inversions in II, III, aVF) suggests right coronary artery involvement, which supplies the posteromedial papillary muscle of the mitral valve.
- 2
3 days post-MI falls in the classic 3–5 day window where infarcted tissue becomes maximally weakened due to macrophage-mediated digestion.
- 3
Papillary muscle in this setting can rupture → sudden loss of mitral valve support → acute severe mitral regurgitation.
- 4
Acute MR causes a new holosystolic murmur at the apex radiating possibly to axilla, without time for chamber remodeling.
- 5
Abrupt volume overload of the left atrium/ventricle → sharp increase in left atrial and pulmonary venous pressures → pulmonary edema, crackles, dyspnea, tachycardia, hypotension.
- 6
This explains the patient’s acute SOB, pulmonary crackles, diaphoresis, tachycardia, borderline hypotension, and new apical holosystolic murmur → papillary muscle rupture.
Why not the others?
A. Left ventricular aneurysm
This option implies a late complication of MI (weeks to months) with dyskinetic ventricular wall and risk of thrombus, BUT this patient is only 3 days post-MI with acute decompensation and new murmur, which is too early and more consistent with mechanical rupture.
B. Early infarct-associated pericarditis
This option implies pericardial inflammation causing pleuritic chest pain and friction rub, BUT the patient has dyspnea, pulmonary edema, and a holosystolic murmur rather than chest pain and rub; pericarditis does not cause acute MR or a new apical holosystolic murmur.
C. Ventricular septal rupture
This option implies a post-MI VSD causing a new holosystolic murmur best heard at the left lower sternal border with a left-to-right shunt, BUT this patient’s murmur is best heard at the apex, favoring mitral regurgitation from papillary muscle rupture.
D. Postmyocardial infarction syndrome
This option (Dressler syndrome) implies autoimmune pericarditis occurring weeks after MI with fever, pleuritic pain, and pericardial effusion, BUT this patient is only 3 days post-MI and has pulmonary edema and a new MR-type murmur, not pericarditis findings.
E. Coronary artery dissection
This option implies acute ischemia with chest pain and new ECG changes, often in young women or postpartum, BUT the patient’s acute symptoms are dominated by pulmonary edema and new holosystolic murmur after a completed MI, indicating mechanical complication rather than new dissection.
F. Ventricular free wall rupture
This option implies hemopericardium and cardiac tamponade with sudden hypotension, JVD, and pulseless electrical activity, BUT this patient has pulmonary crackles and a new holosystolic murmur without signs of tamponade or sudden cardiovascular collapse.
Exam trap
Students may see “3 days post-MI” and jump to any mechanical complication, or confuse VSD vs papillary rupture. Use both timing and murmur location: early post-MI + inferior infarct + new apical holosystolic murmur = papillary muscle rupture → acute MR, not VSD or free wall rupture.
The bottom line
Papillary muscle rupture 3–5 days post-inferior MI → acute severe MR → dyspnea, pulmonary edema, new holosystolic murmur at apex.
A 20-year-old white man comes to the clinic due to recurrent episodes of epistaxis. Further history reveals that his father died in his 40s from an intracranial hemorrhage, and 2 of his father’s 5 siblings have also had recurrent nosebleeds. Which of the following findings is most likely present in this patient?
Correct answer · C
Mucosal arteriovenous malformations
Decoding the stem
Step-by-step reasoning
Step 1 of 5
Recurrent epistaxis in a young person suggests abnormal, fragile mucosal vessels rather than acquired coagulopathy alone.
Step 2 of 5
Family history (father + paternal siblings affected) indicates an autosomal dominant vascular disorder.
Step 3 of 5
Autosomal dominant disorder with recurrent epistaxis and risk of intracranial hemorrhage is classic for hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu).
Step 4 of 5
Hereditary hemorrhagic telangiectasia is characterized by mucocutaneous telangiectasias and arteriovenous malformations (AVMs) on skin, oral, and nasal mucosa, and in organs.
Step 5 of 5
Therefore, the most likely finding in this patient is mucosal arteriovenous malformations.
Why not the others?
A. Retinal hemangioblastoma
This option implies von Hippel–Lindau disease, which causes retinal/CNS hemangioblastomas and RCC, BUT it is not characterized by recurrent epistaxis or mucosal telangiectasias.
B. Renal cell carcinoma
This option suggests von Hippel–Lindau or sporadic RCC. Those present with hematuria or flank mass, BUT they do not explain recurrent nosebleeds plus widespread family history of epistaxis/ICH.
D. Vestibular schwannoma
This implies NF2, which presents with bilateral acoustic neuromas and hearing loss, BUT NF2 is not associated with recurrent epistaxis or mucosal AVMs.
E. Cafe-au-lait spots
This suggests NF1, which features café-au-lait macules, neurofibromas, Lisch nodules, BUT NF1 typically does not cause recurrent epistaxis or intracranial hemorrhage from AVMs.
Exam trap
Nosebleeds and brain hemorrhage may tempt recall of generic bleeding disorders or aneurysms; recognizing the autosomal dominant mucosal AVM/telangiectasia pattern is key for hereditary hemorrhagic telangiectasia.
The bottom line
Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu) causes mucocutaneous telangiectasias/AVMs → recurrent epistaxis and risk of intracranial hemorrhage.
Source: StepGenie question bank. Questions are written by StepGenie, not taken from NBME or USMLE materials, and are chosen for this page by how students actually performed on them (first-attempt accuracy on StepGenie). Selection last refreshed September 5, 2026.
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About Cardiology
Comprehensive review of cardiac anatomy, electrophysiology, heart failure, arrhythmias, valvular diseases, and cardiovascular pharmacology. StepGenie helps you understand complex hemodynamic concepts through AI-powered explanations and pattern recognition.
Key Topics Covered
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Cardiology — Frequently Asked Questions
What cardiology topics are highest-yield for USMLE Step 1?
Valvular lesions and their murmurs, the cardiac and pressure-volume cycle, EKG interpretation and arrhythmias, ischemic heart disease with the infarct timeline, heart failure compensation, and congenital defects. Cardiac physiology carries disproportionate weight because it underpins pharmacology and pathology questions too, so time spent on preload, afterload and contractility pays off across several sections.
How do you tell hypertrophic cardiomyopathy from aortic stenosis on a murmur question?
Use the manoeuvres. Both produce a systolic murmur, but the HOCM murmur gets louder with Valsalva or standing because reduced preload narrows the outflow tract, while aortic stenosis gets softer. Aortic stenosis classically radiates to the carotids and pairs with a delayed, weak pulse. Squatting increases preload and does the reverse to both.
What is the fastest way to read an EKG in a timed exam question?
Work in a fixed order so nothing is missed: rate, rhythm, axis, intervals, then ST segments and T waves. Most exam EKGs hinge on one abnormality, and the stem usually tells you where to look. Reading in the same sequence every time is faster than scanning the whole tracing, because you stop as soon as the abnormality explains the vignette.
How is cardiology tested differently on Step 1 versus Step 2 CK?
Step 1 rewards mechanism: why a murmur changes with a manoeuvre, how a drug shifts the pressure-volume loop, what the infarct looks like histologically at a given hour. Step 2 CK shifts to management, asking for the next best step in diagnosis or treatment. The same disease appears on both exams with a different question stem.
Are the cardiology practice questions on this page free?
Yes. The 5 questions above come from StepGenie's question bank and can be answered here without an account, with the full explanation shown after each one. From the link under the set you can try three more Cardiology questions in the dashboard preview, also without an account; a free account is what lets you choose the system and keep going.