A 66-year-old female presents to the ED with chest pain, shortness of breath, nausea and vomiting. She has had symptoms for 3 days and thought it was indigestion; however, it is now worse. Her temperature is 99.2, blood pressure 140/90 mm Hg, heart rate 70 beats per minute, respirations 20 per minute and oxygen normal on room air. She has an S4 heart sound, but no murmurs are appreciable. Her ECG is below.
She is treated appropriately for an acute inferior wall myocardial infarction with aspirin, clopidogrel, heparin, a beta-blocker, oxygen and percutaneous coronary intervention of the right coronary artery.
On day two of her hospitalization, she becomes acutely short of breath. She remained afebrile with a heart rate of 90 beats per minute, respirations 36 per minute and blood pressure 80/40 mm Hg. Physical examination revealed once again an S4 heart sound and no murmur. Her pulsus paradoxus is 8 mm Hg. A chest X-ray showed pulmonary edema. She is brought back for coronary angiography and her stent in the right coronary artery remains patent. Right heart catheterization reveals a large V wave in the pulmonary capillary wedge tracing. The oxygen saturation measured in the right atrium was 65%, right ventricle 66% and pulmonary artery 65%.
Which of the following is the correct diagnosis?
A. Acute ventricular septal defect
B. Acute left ventricular free wall rupture
C. Acute mitral valve regurgitation
D. Right ventricular infarction
The two complications of a myocardial infarction that can cause hypotension with pulmonary edema are an acute ventricular septal defect or acute mitral valve regurgitation.
Acute severe mitral regurgitation is a life-threatening disorder. Papillary muscle rupture after acute myocardial infarction can occur as a complication of an inferior MI (right coronary artery supply), as the posteromedial papillary muscle is the most likely to rupture.
There are two papillary muscles that comprise part of the complex anatomy of the mitral valve. The anterolateral papillary muscle receives dual blood supply from the left anterior descending coronary artery and the left circumflex coronary artery in most individuals, whereas the posteromedial papillary muscle receives its sole blood supply from the right coronary artery. Complete infarction of the posteromedial papillary muscle can occur during an inferior MI, while only partial or no damage will be done to the anterolateral papillary muscle during an anterior (left anterior descending) or lateral (circumflex) infarction because there is dual blood supply to this papillary muscle. Thus, the posteromedial papillary muscle is the most likely to rupture.
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. Recall that the pulmonary capillary wedge pressure tracing is essentially a left atrial pressure tracing.
Recall that acute mitral regurgitation may not cause a murmur. The pressures of the left ventricle and left atrium equalize very quickly in systole, as there has been no time for the chambers to adapt to the acute change (dilate). This results in a very short duration of turbulent flow backward through the mitral valve, resulting in either a short early systolic murmur or no murmur at all. This differs from the murmur of chronic mitral regurgitation, which is holosystolic and frequently quite intense.
Emergent surgical repair or replacement of the mitral valve is indicated for acute mitral regurgitation. Mortality approaches 100% if not surgically fixed.
An acute VSD does not cause large V waves and frequently does create a holosystolic murmur. An acute free wall rupture results in cardiac tamponade from a rapidly accumulating pericardial effusion. This increases the pulsus paradoxus to greater than 12 mm Hg. Right ventricular infarction is a complication of inferior MI and can cause shock, but not pulmonary edema. Again, there is no V wave in this setting.