Coronary Artery Disease - STEMI Case #11 Answer

A 56-year-old female presents with shortness of breath, nausea and diaphoresis. She has had some “heartburn” for the last 2 days. She is afebrile with a blood pressure of 120/80 mm Hg, heart rate of 70 beats per minute and respirations 22 per minute. There is an S4 heart sound present, no murmurs and clear lungs on examination. Chest X-ray is clear. Her ECG is below:


She is treated with standard medical therapy using aspirin, clopidogrel, low molecular weight heparin, a beta-blocker, nitrates for chest pain and oxygen. Her blood pressure suddenly drops to 80/40 mm Hg. Lung exam remains clear, and she is chest pain free. Emergent left heart catheterization is performed, revealing a totally occluded proximal right coronary artery with thrombus. This is treated with primary percutaneous coronary intervention. Left ventricular angiography shows an ejection fraction of 45% with inferior hypokinesis. Right heart catheterization shows small V waves in the pulmonary capillary pressure tracing, normal right heart pressures, a right atrial saturation of 65%, right ventricle 64% and pulmonary artery 68%. Her right atrial pressure is 20 mm Hg, right ventricle 40/10 mm Hg and pulmonary artery 35/12 mm Hg. Her systemic pressure remains 80/40, even after PCI. Which of the following is the likely cause of of her hemodynamic instability?

A. Acute mitral regurgitation

B. Acute left ventricular free wall rupture

C. Acute ventricular septal defect

D. Right ventricular infarction

E. Cardiogenic shock from acute left ventricular systolic dysfunction


A right ventricular infarction can occur simultaneously with an inferior ST segment elevation myocardial infarction, as the right coronary artery supplies the right ventricle. Acute right ventricular failure can occur, leading to hypotension and cardiogenic shock. Because the right ventricle is not able to contract, the cardiac hemodynamics become “preload dependent.” If preload is high enough, blood can be “forced” through the right heart. Nitrates decrease preload by venodilation and can cause profound hypotension in the setting of right ventricular infarction. The treatment of choice is IV fluids to help increase preload. A right-sided ECG will show ST segment elevation and should be done in all patients experiencing an inferior STEMI. Below is an example of a right-sided ECG showing ST segment elevation during an inferior MI:


Choice A (acute mitral regurgitation) would reveal large V waves in the pulmonary capillary wedge pressure tracing. When a large pressure is forced into the left atrium during systole from the mitral regurgitant volume, a large pressure wave is created, which is the V wave. Normal V waves are small but become quite large with severe mitral regurgitation.

Choice B (acute left ventricular free wall rupture) causes an acute bloody pericardial effusion and cardiac tamponade. The hemodynamics of tamponade (also constrictive pericarditis) are described as “ventricular interdependence.” Normally, the pericardium can expand as the heart fills; however, with cardiac tamponade from a large pericardial effusion or constrictive pericarditis, this is not able to occur. As a person inspires, venous return is increased to the right heart, and the interventricular septum bulges to the left, impairing left ventricular filling, reducing left heart cardiac output, and thus decreasing systemic pressure (increasing the pulsus paradoxus). As a person exhales, right ventricular filling decreases, and the left heart fills, causing the interventricular septum to bulge to the right, impairing right ventricular filling. The diastolic pressures are elevated and equal because every cardiac chamber pressure influences the other, considering the heart is not able to expand as mentioned above.

Choice C (acute ventricular septal defect) causes an oxygen “step-up” in the right heart because oxygenated blood crosses through defect from the left ventricle, increasing the oxygen saturations in the right heart chambers (right ventricle and pulmonary artery). The pulmonary artery saturations would likely be in the 80% to 90% range.

Choice D (cardiogenic shock from left ventricular systolic dysfunction) is not likely because the pulmonary artery diastolic pressure (a surrogate for the left ventricular end-diastolic pressure) is essentially normal, implying no significant left heart failure is present.