USMLE Step 2 CK Cardiology Questions: Acute MI – Right Ventricular Infarct, Fibrinolysis and Papillary Muscle Rupture

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Acute myocardial infarction is one of the most heavily tested topics on USMLE Step 2 CK. The exam wants you to know the next best step, which drugs to avoid, and how to recognize post-MI complications. Try these three questions, then open each explanation.

Question 1: Inferior STEMI with low blood pressure and clear lungs

A 62-year-old man comes to the emergency department with crushing chest pain that began 1 hour ago. His blood pressure is 84/50 mm Hg and pulse is 58/min. Jugular venous pressure is elevated, and the lungs are clear to auscultation. ECG shows ST-segment elevation in leads II, III and aVF, and right-sided leads show ST elevation in V4R. Aspirin has been given and the cardiac catheterization team has been called. Which of the following is the most appropriate next step to treat his hypotension?

A. Sublingual nitroglycerin
B. Intravenous furosemide
C. Intravenous normal saline bolus
D. Intravenous metoprolol
E. Intravenous morphine

Correct answer: C. Intravenous normal saline bolus

The combination of an inferior STEMI, hypotension, elevated JVP and clear lungs is the classic triad of a right ventricular infarction (ST elevation in V4R confirms it). The right ventricle is preload dependent, so the first step for hypotension is IV fluids, while arranging urgent reperfusion.

Why the other options are wrong:

  • Nitroglycerin reduces preload and can cause profound hypotension in RV infarction; it is contraindicated here.
  • Furosemide also reduces preload and would worsen hypotension.
  • Metoprolol should be avoided in hypotension, bradycardia or signs of shock.
  • Morphine causes venodilation and can drop the blood pressure further.

Question 2: Anterior STEMI far from a catheterization lab

A 58-year-old man has had substernal chest pain for 45 minutes. ECG shows ST-segment elevation in leads V1 through V4. He is at a small rural hospital, and the nearest hospital capable of percutaneous coronary intervention (PCI) is a 3-hour transfer away. He has no history of bleeding, stroke or recent surgery. Blood pressure is 142/88 mm Hg. Aspirin has been given. Which of the following is the most appropriate next step?

A. Transfer for primary PCI without fibrinolysis
B. Heparin infusion and observation
C. CT angiography of the chest
D. Exercise stress testing
E. Fibrinolytic therapy, then transfer to a PCI-capable hospital

Correct answer: E. Fibrinolytic therapy, then transfer to a PCI-capable hospital

Primary PCI is preferred for STEMI only if it can be performed within about 120 minutes of first medical contact. When the delay is longer, and symptoms began less than 12 hours ago, give fibrinolytic therapy (ideally within 30 minutes of arrival) if there are no contraindications. The patient should then be transferred to a PCI-capable center.

Why the other options are wrong:

  • Transfer for primary PCI would exceed the time goal and delay reperfusion.
  • Heparin alone does not open the occluded artery.
  • CT angiography delays treatment; the ECG already confirms STEMI.
  • Stress testing is contraindicated in an acute MI.

Question 3: New murmur and pulmonary edema 4 days after an MI

A 66-year-old man was admitted 4 days ago with an inferior wall myocardial infarction. He suddenly develops severe shortness of breath. Blood pressure is 86/52 mm Hg. There are crackles over both lung fields and a new holosystolic murmur heard best at the apex, radiating to the axilla. Which of the following is the most likely cause?

A. Ventricular septal rupture
B. Papillary muscle rupture
C. Left ventricular free wall rupture
D. Dressler syndrome
E. Left ventricular aneurysm

Correct answer: B. Papillary muscle rupture

Papillary muscle rupture usually occurs 2–7 days after an MI, most often involving the posteromedial papillary muscle, which has a single blood supply (usually from the right coronary artery) and is therefore affected in inferior MI. It causes acute mitral regurgitation: a new apical holosystolic murmur radiating to the axilla, pulmonary edema and cardiogenic shock. Treatment is urgent surgery.

Why the other options are wrong:

  • Ventricular septal rupture also causes a holosystolic murmur, but it is heard at the left lower sternal border, with a step-up in oxygen saturation from the right atrium to the right ventricle.
  • Free wall rupture causes cardiac tamponade (hypotension, JVD, muffled heart sounds), not a new murmur.
  • Dressler syndrome is an autoimmune pericarditis weeks after an MI, with pleuritic chest pain and a friction rub.
  • Ventricular aneurysm develops weeks to months later and causes heart failure, arrhythmias and mural thrombus.

Key takeaways

  • Inferior STEMI + hypotension + clear lungs = RV infarct: give fluids, avoid nitrates.
  • STEMI: primary PCI if possible within ~120 minutes; otherwise fibrinolysis within 30 minutes.
  • New apical holosystolic murmur 2–7 days after MI = papillary muscle rupture.

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Written and reviewed by Dr. Ray Makar, MD, dermatologist with 20 years of clinical practice. Last reviewed: October 2026. For exam preparation only, not medical advice.

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