A 78-year-old male presents to the ICU with chest pain, shortness of breath, and respiratory distress requiring urgent intubation. The chest radiograph shows diffuse pulmonary edema, worse in the lower lung lobes.
His vital signs are as follows:
The patient’s electrocardiogram demonstrates ST-segment elevation in lead II, III, and aVF with reciprocal changes in leads I and aVL. On physical examination, he has a systolic murmur, bilateral crackles on lung auscultation, and cold and clammy extremities. Cardiac enzymes are pending.
What interventions should be considered?
A. Intra-aortic balloon pump
Correct Answer: A
This patient developed flash pulmonary edema secondary to an acute posteromedial papillary muscle rupture in the setting of an inferior wall ST-elevation myocardial infarction. Papillary muscles are vulnerable to myocardial ischemia because they are perfused by the terminal portion of the coronary arteries. This can result in transient papillary muscle dysfunction or frank rupture. The posteromedial papillary muscle is more frequently involved because it is supplied by the posterior descending branch of the right coronary artery, whereas the anterolateral papillary muscle has a dual blood supply including the diagonal branches of the left anterior descending artery and the marginal branches of the left circumflex artery. Acute mitral regurgitation can occur because of infective endocarditis, myocardial ischemia, papillary muscle or chordae rupture, and prosthetic valve malfunction. Mitral regurgitation causes an abrupt increase in left ventricular end diastolic volume (preload) and a reduction in forward stroke volume. An important hemodynamic difference between acute and chronic mitral regurgitation is left atrial compliance. In chronic mitral regurgitation, the left atrium dilates with time and compliance increases gradually as the regurgitant volume increases. In acute mitral regurgitation, normal or decreased left atrial compliance cannot tolerate an abrupt increase in volume. This leads to pulmonary edema, pulmonary hypertension, and right ventricular failure.
Emergency surgery is indicated in patients with acute left ventricular failure due to ruptured papillary muscles. Placement of intra-aortic balloon pump may exert some beneficial physiologic effects in the setting of acute mitral regurgitation. These include improved coronary perfusion, decreased left ventricular afterload, and improved cardiac index. Afterload reduction with vasodilators such as nitroprusside will also improve forward flow; however, if the patient is in cardiogenic shock, this may not be tolerated. If hypotensive, increased inotropy with dobutamine is preferable to norepinephrine. Increased alpha-1 stimulation will increase afterload and may worsen the regurgitant volume and increase pulmonary pressures. Increased inotropy combined with afterload reduction can promote forward flow and decrease regurgitant fraction, while increasing blood pressure. Inhaled epoprostenol decreases pulmonary vascular resistance and is indicated in patients with an increased transpulmonary gradient (mean pulmonary artery pressure minus left atrial pressure); however, it has no role in case of left ventricular failure. Inhaled epoprostenol causes pulmonary arterial vasodilation, which may in fact increase the gradient between the pulmonary venous to pulmonary arterial circulation and worsen the venous congestion.
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