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This patient with acute-onset chest heaviness and shortness of breath and ECG showing ST-segment elevation has a myocardial infarction (MI).  Localization to the lateral leads is consistent with involvement of the left ventricle.  Hypotension and cold and clammy extremities (evidence of poor tissue perfusion) suggest cardiogenic shock due to MI-induced acute left ventricular (LV) failure.

A large MI can cause profoundly decreased cardiac contractility.  The resulting LV systolic failure leads to markedly reduced cardiac output and hypotension.  In response to the hypotension, the aortic and carotid baroreceptors stimulate peripheral vasoconstriction to increase systemic vascular resistance in an effort to maintain blood pressure.  Heart rate is also increased (ie, tachycardia) to help increase cardiac output.

Failure to eject blood from the left ventricle also increases LV end-diastolic pressure, which is transmitted backward to increase pulmonary capillary wedge pressure (an estimate of left atrial pressure) and cause pulmonary edema.  This increase in pulmonary venous pressure also necessitates higher pulmonary arterial systolic pressure to maintain forward blood movement, which may precipitate acute right ventricular failure.

Educational objective:
Myocardial infarction may cause acute left ventricular (LV) failure and cardiogenic shock.  Decreased cardiac contractility leads to reduced cardiac output and hypotension.  In response, systemic vascular resistance is increased (via peripheral vasoconstriction) to maintain blood pressure.  The LV systolic failure increases LV end-diastolic pressure, which is transmitted backward to increase pulmonary capillary wedge pressure and pulmonary arterial pressure.