JM is in cardiogenic shock from an ST elevation MI secondary to an occlusion of his proximal left anterior descending (LAD) artery (ST elevation is in LAD distribution). His profound hypotension and...

JM is in cardiogenic shock from an ST elevation MI secondary to an occlusion of his proximal left anterior descending (LAD) artery (ST elevation is in LAD distribution). His profound hypotension and CHF is secondary to two processes: (1) ischemic systolic dysfunction; and (2) ischemia-induced papillary muscle rupture, resulting in a flail mitral leaflet (4/6 murmur on exam). Although his clinical presentation, low-grade fever, leukocytosis, and ECG are consistent with ST elevation MI, the troponin and CK were negative on admission because 4 to 6 hours must elapse from infarction onset before significant elevation of these biochemical markers may be observed. JM subsequently developed ventricular fibrillation requiring electrical defibrillation before he was brought to the cardiac catheterization laboratory, where his LAD artery was successfully opened with angioplasty and stenting.