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A 69-year-old man who has hypertension and diabetes mellitus had a motor vehicle accident and suffered head trauma. He had a brief loss of consciousness. After evaluation in the emergency department, he was admitted to the neurology intensive care unit (ICU) for observation. The night of the admission, he developed severe substernal chest pain and quickly became diaphoretic. His blood pressure was 95/63 mm Hg, with a pulse rate of 60 bpm. He was in moderate distress and looked pale and clammy. The 12-lead electrocardiogram (ECG) showed acute inferolateral ST-segment-elevation myocardial infarction (STEMI) (Figure 34-1).

After consultation with the cardiologist, the patient was taken directly to the cardiac catheterization laboratory for emergent coronary angiography and angioplasty. This showed a total occlusion of a dominant proximal left circumflex (LCX) artery that was successfully opened with aspiration thrombectomy and stenting (Figure 34-2A, B). Left ventriculography showed a severe inferior and lateral wall hypokinesis with an ejection fraction of 30%.

The patient remained hypotensive despite being administered dopamine at 10 μg/kg per minute. Right heart catheterization revealed a pulmonary capillary wedge pressure of 28 mm Hg and a cardiac index of 1.8 L/min per m2.

At this point, an intra-aortic balloon pump (IABP) was placed and the patient was transferred back to the ICU. His blood pressure remained stable. The dopamine was weaned off after several hours and the IABP was discontinued 24 hours later. His echocardiogram showed severe hypokinesis of the inferior and lateral wall.

Figure 34-1.

A 12-lead electrocardiogram showing acute inferolateral ST-segment-elevation myocardial infarction.

Figure 34-2.

A. An occluded left circumflex (LCx) artery. B. LCx artery after revascularization. It was a large dominant vessel supplying a large area of myocardium. LAD, left anterior descending artery; OM, obtuse marginal branches.

This patient had acute myocardial infarction (AMI) complicated by cardiogenic shock (CS). How is CS defined?

CS is defined as persistent tissue hypoperfusion secondary to cardiac dysfunction in the presence of adequate left ventricular filling pressure. The clinical signs include hypotension, cold extremities, tachycardia, decreased urinary output, and altered mental status. Hemodynamically, there is hypotension, defined as a systolic blood pressure less than 90 mm Hg for more than 30 minutes, a low cardiac index (< 1.8 L/min per m2 without support or < 2-2.2 L/min per m2 with support), and finally an elevated filling pressure (pulmonary capillary occlusion pressure > 15 mm Hg, left ventricular end-diastolic pressure > 18 mm Hg, or right ventricular end-diastolic pressure > 10-15 mm Hg).1, 2, 3

CS, a major complication of AMI, remains the most common cause of mortality in hospitalized patients presenting with AMI. Its incidence has remained ...

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