Common misconceptions

Common mistake
Wrong: Nitrates are safe in RV infarction because they are used in most ACS presentations.
Right: Nitrates are contraindicated in RV infarction because the RV is preload-dependent and venodilation causes catastrophic hypotension.
Nitrates work by causing venodilation, which reduces preload — that's useful when the LV is volume-overloaded, but catastrophic when the RV is already failing and preload-dependent. In RV infarction, the only thing keeping cardiac output up is adequate filling; drop the preload and you drop the output. Giving nitrates here can precipitate severe hypotension within minutes, and this is a classic USMLE Step 1 'wrong drug' scenario.
Common mistake
Wrong: Inferior ST elevation on standard ECG is sufficient to diagnose RV infarction.
Right: RV infarction requires right-sided leads (ST elevation in V4R is most sensitive) because standard leads miss the RV free wall.
Standard 12-lead ECG views the LV, not the RV free wall. Inferior ST elevation (II, III, aVF) tells you there's an RCA-territory event, but it doesn't confirm RV involvement. You must place right-sided leads, and ST elevation in V4R is the most sensitive single finding for RV infarction. Missing this means missing the diagnosis — and potentially giving contraindicated drugs.
Common mistake
Wrong: RV infarction results from LAD occlusion because the LAD supplies most of the heart.
Right: RV infarction results from proximal RCA occlusion, which supplies the RV free wall via the right marginal branch.
The LAD supplies the anterior LV and most of the interventricular septum — it doesn't supply the RV free wall. The RV free wall is supplied by the right marginal branch of the RCA. When the proximal RCA is occluded (proximal enough to cut off the right marginal branch before the posterior descending artery), you get both an inferior MI and RV infarction simultaneously. LAD occlusion causes anterior MI, not RV infarction.
Common mistake
Wrong: IV fluids are harmful in RV infarction because they worsen pulmonary edema.
Right: IV fluids are the cornerstone of RV infarction management because the failing RV requires high preload to maintain output across the pulmonary circuit.
The reflex to avoid fluids in MI comes from LV failure, where a stiff, overloaded ventricle backs up into the pulmonary circulation and causes pulmonary edema. RV infarction is the opposite scenario: the lungs are clear because the RV can't push blood forward. The LV is actually underfilled. IV fluids increase RV filling pressure, which by Starling's law improves RV stroke volume and restores forward flow. Withholding fluids here starves an already failing circuit.
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What the exam tests

  1. Recognize the classic bedside triad of RV infarction: hypotension, jugular venous distension, and clear lung fields in the context of an inferior MI.
  2. Identify which ECG leads are required to diagnose RV involvement — specifically ST elevation in right-sided lead V4R — and why standard 12-lead ECG is insufficient.
  3. Know which therapies are contraindicated in RV infarction (nitrates, diuretics, morphine) and which are required (IV fluids, early reperfusion), and explain the hemodynamic rationale for each.
  4. Explain why the failing RV is preload-dependent: loss of RV contractility means cardiac output across the pulmonary circuit depends on filling pressure, not pump function.

Can you avoid these mistakes?

A patient with acute inferior MI becomes hypotensive after receiving sublingual nitroglycerin in the ED. JVP is elevated and lungs are clear. What is the diagnosis, what mistake was made, and what should be given instead?
You suspect RV infarction in a patient with inferior ST changes on standard 12-lead ECG. What specific additional test do you order, and what finding confirms the diagnosis?
Explain in one or two sentences why IV fluids improve hemodynamics in RV infarction but would worsen hemodynamics in left ventricular failure.
A patient presents with hypotension, clear lungs, and elevated neck veins. Which coronary artery is most likely occluded, and at what level of that artery must the occlusion occur to produce this syndrome?

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