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  • Tissue hypoperfusion: Depressed mental status, cool extremities, decreased urinary output.
  • Hypotension: Systolic blood pressure < 90 mm Hg.
  • Reduced cardiac output: Cardiac index < 2.2 L/min/m2.
  • Adequate intravascular volume: Pulmonary artery wedge pressure > 15 mm Hg.


A diagnosis of cardiogenic shock has historically conferred a very high mortality. Despite recent advances in treating this condition, nearly 50% of patients with cardiogenic shock still do not survive to hospital discharge. In a strict sense, cardiogenic shock develops as a result of the failure of the heart in its function as a pump, resulting in inadequate cardiac output. This failure is most commonly caused by extensive myocardial damage from an acute myocardial infarction (MI), but other mechanical complications of an acute MI, valve lesions, arrhythmias, and end-stage cardiomyopathies can also lead to cardiogenic shock.


A number of definitions for cardiogenic shock have been proposed. Although these definitions differ in some ways, there is general agreement that both hemodynamic and clinical parameters should be included. There should be evidence of a reduced cardiac output without hypovolemia. Clinical signs of decreased peripheral perfusion should be present and include cool and clammy skin, weak distal pulses, altered mental status, and diminished urinary output (less than 30 mL/h). A commonly used set of hemodynamic criteria for cardiogenic shock are (1) a systolic blood pressure of less than 90 mm Hg for at least 30 minutes (or the need for vasopressor or intra-aortic balloon pump support in order to maintain a systolic blood pressure 90 mm Hg), (2) a pulmonary capillary wedge pressure (PCWP) of greater than 15 mm Hg, and (3) a cardiac index less than 2.2 L/min/m2. Using a combination of clinical and hemodynamic criteria means that fewer patients are given an inappropriate diagnosis of shock.


Acute MI accounts for most cases of cardiogenic shock. Acute MI results in cardiogenic shock in 5–10% of patients; however, it is likely that cardiogenic shock develops in many more patients following an acute MI, but they do not survive to receive medical attention. Cardiogenic shock may occur in a patient with a massive first infarction, or it may occur with a smaller infarction in a patient with an already substantially infarcted myocardium. “Mechanical” complications of acute MI can also cause shock, and these include ventricular septal rupture, acute mitral regurgitation as a result of papillary muscle rupture, and myocardial free wall rupture with tamponade. Right ventricular infarction in the absence of significant left ventricular infarction or dysfunction can lead to shock. Refractory tachyarrhythmias or bradyarrhythmias, usually in the setting of preexisting left ventricular dysfunction, are occasionally a cause of shock and can occur with either ventricular or supraventricular arrhythmias. Cardiogenic shock may occur in patients with end-stage cardiomyopathies (ischemic, valvular, hypertrophic, restrictive, or idiopathic in origin). Cardiogenic shock may also be the presenting manifestation of acute myocarditis (infectious, toxic, rheumatologic or idiopathic). A more recently recognized entity is stress cardiomyopathy (also known as apical ballooning syndrome or tako-tsubo ...

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