A 74-year-old woman is hospitalized after an anterior ST-elevation myocardial infarction. She underwent successful percutaneous coronary intervention and has been recovering appropriately. Her medications include aspirin, ticagrelor, atorvastatin, metoprolol, and lisinopril. On hospital day 5, she suddenly becomes unresponsive while speaking with a nurse. A rapid response team is called. Temperature is 36.7°C (98.1°F), blood pressure is 72/40 mm Hg, pulse is 118/min, respiratory rate is 24/min, and oxygen saturation is 90% on a nonrebreather mask. Physical examination reveals marked jugular venous distention. Heart sounds are distant. No cardiac murmur is appreciated. Lung examination demonstrates clear breath sounds bilaterally. Telemetry shows sinus tachycardia. ECG demonstrates low-voltage QRS complexes. Troponin levels are lower than on admission. Bedside echocardiography reveals a large pericardial effusion with diastolic collapse of the right ventricle.
Which of the following is the most likely cause of this patient’s sudden deterioration?
The correct answer is:
B) Acute rupture of the left ventricular free wall causing hemopericardium
This patient has left ventricular free wall rupture, a catastrophic mechanical complication that typically occurs within the first week following a transmural myocardial infarction. The diagnosis is suggested by sudden cardiovascular collapse, elevated jugular venous pressure, distant heart sounds, hypotension, and echocardiographic evidence of cardiac tamponade.
After a myocardial infarction, inflammatory degradation of necrotic myocardium weakens the ventricular wall. Several days later, the infarcted myocardium may rupture, allowing blood to rapidly accumulate within the pericardial space. The resulting hemopericardium causes acute cardiac tamponade, which impairs ventricular filling and leads to obstructive shock.
This patient’s findings are classic for tamponade physiology. The combination of hypotension, jugular venous distention, and muffled heart sounds (Beck triad) is highly suggestive. Clear lungs are an important clue because cardiogenic pulmonary edema is often absent. Echocardiographic evidence of a large pericardial effusion with right ventricular diastolic collapse essentially confirms tamponade.
Emergency pericardiocentesis and surgical repair are required, although mortality remains extremely high.
Answer choice A: Acute rupture of the interventricular septum causing a left-to-right shunt, is incorrect.
Ventricular septal rupture usually causes a new harsh holosystolic murmur along the left sternal border, often accompanied by a palpable thrill. Patients develop pulmonary edema and cardiogenic shock due to an acute left-to-right shunt. This patient instead has tamponade physiology and no murmur.
Answer choice C: Acute rupture of the posteromedial papillary muscle causing severe mitral regurgitation, is incorrect.
Papillary muscle rupture classically causes acute severe mitral regurgitation, resulting in flash pulmonary edema, cardiogenic shock, and a new apical holosystolic murmur radiating to the axilla. The absence of pulmonary edema and the presence of a large pericardial effusion make this diagnosis unlikely.
Answer choice D: Massive pulmonary embolism due to prolonged hospitalization, is incorrect.
Massive pulmonary embolism can cause obstructive shock and elevated jugular venous pressure. However, it would not explain a large pericardial effusion with right ventricular diastolic collapse. Furthermore, the timing following a recent transmural MI should immediately raise concern for a mechanical complication.
Answer choice E: Reinfarction due to acute stent thrombosis, is incorrect.
Reinfarction usually presents with recurrent chest pain, new ischemic ECG changes, and rising cardiac biomarkers. It does not typically produce a large hemopericardium or tamponade physiology.
Key Learning Point
A patient who develops sudden hypotension, jugular venous distention, distant heart sounds, and cardiac tamponade within the first week after myocardial infarction should be presumed to have left ventricular free wall rupture causing hemopericardium until proven otherwise.
