Question

Difficulty: MediumCardiovascular System

A 6868-year-old male is evaluated in the intensive care unit for abrupt-onset severe respiratory distress and hypotension. Four days ago, he was admitted with an acute ST-segment elevation myocardial infarction involving the inferior leads; he subsequently received a drug-eluting stent to the right coronary artery. His medical history includes hypertension and a 4040-pack-year smoking habit. Vital signs are temperature 36.9∘C36.9^\circ\text{C} (98.4∘F98.4^\circ\text{F}), blood pressure 82/54 mm Hg82/54\text{ mm Hg}, heart rate 118/min118\text{/min}, and respirations 28/min28\text{/min}. Oxygen saturation is 84%84\% on a non-rebreather mask. Physical examination reveals cool, diaphoretic extremities and elevated jugular venous pressure. Auscultation of the chest demonstrates bilateral crackles extending halfway up the lung fields with scattered expiratory wheezes. A new, loud holosystolic murmur is heard best at the cardiac apex with radiation to the left axilla. Which of the following is the most likely cause of this patient's current clinical deterioration?

  1. A
    Rupture of the left ventricular free wall
  2. B
    Rupture of the interventricular septum
  3. Rupture of the posteromedial papillary muscleAnswer
  4. D
    Infarction of the right ventricular myocardium
  5. E
    Acute exacerbation of chronic obstructive pulmonary disease

Answer

Rupture of the posteromedial papillary muscle
The correct answer is rupture of the posteromedial papillary muscle. The patient suffered an inferior wall myocardial infarction, which typically involves occlusion of the right coronary artery. The posteromedial papillary muscle receives a single blood supply from the posterior descending artery (most often a branch of the right coronary artery), making it uniquely vulnerable to ischemic rupture. Rupture typically occurs 3 to 5 days post-infarction and presents with abrupt-onset cardiogenic shock, flash pulmonary edema, and a new, harsh apical holosystolic murmur radiating to the axilla due to acute severe mitral regurgitation.

Step-by-Step Solution

1
Identify the timeline and patient's clinical presentation.
The patient developed cardiogenic shock, severe pulmonary edema, and a new apical holosystolic murmur 4 days after an inferior myocardial infarction.
Recognizing the timeline and key physical exam findings is essential to narrow the differential diagnosis of post-myocardial infarction complications.
2
Correlate the physical exam with cardiac pathophysiology.
The new apical holosystolic murmur radiating to the axilla combined with acute pulmonary edema is classic for acute severe mitral regurgitation.
This differentiates the complication from a ventricular septal rupture (left lower sternal border murmur) or free wall rupture (tamponade with pulseless electrical activity).
3
Synthesize the vascular anatomy with the primary event.
The posteromedial papillary muscle has a single blood supply from the right coronary artery, which was involved in the patient's inferior myocardial infarction.
This explains why this specific papillary muscle ruptured, leading to flail mitral leaflet and confirming the diagnosis.

Key Concept

Mechanical complications of acute myocardial infarction
Estimated Time:1m 30s
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