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  • Hypotension: systolic blood pressure less than 90 mm Hg.

  • Reduced cardiac output: cardiac index less than 2.2 L/min/m2 in the absence of hypovolemia.

  • Tissue hypoperfusion: depressed mental status, cool extremities, decreased urinary output.

  • Laboratory abnormalities: elevated lactate, elevated creatinine, elevated liver enzyme tests, elevated b-type natriuretic peptide, decreased bicarbonate.


Cardiogenic shock results when the heart fails in its function as a pump resulting in inadequate cardiac output, systemic hypotension, and resultant tissue hypoperfusion. The acute insult leading to cardiogenic shock is often caused by acute myocardial infarction from an occluded artery, or from exacerbation of ischemic heart disease. Mechanical complications of delayed-presentation myocardial infarction, valve lesions, and arrhythmias can further complicate the clinical presentation. Cardiogenic shock remains an extremely morbid condition and despite advances in device-based treatment nearly 50% of patients with cardiogenic shock still do not survive hospital discharge in randomized control trials. However, recent advances in cardiogenic shock pathways and multidisciplinary shock teams have been associated with improved outcomes in acute myocardial infarction cardiogenic shock (AMI-CS) and acute decompensated heart failure cardiogenic shock (ADHF-CS).


Cardiogenic shock is defined by clinical and biochemical signs of reduced cardiac output, systemic hypotension, and tissue hypoperfusion. Clinical signs of reduced cardiac output include cool extremities, weak distal pulses, altered mental status, and diminished urinary output (< 30 mL/h). Hemodynamic findings in cardiogenic shock include a reduced cardiac output without evidence of hypovolemia. One commonly used set of hemodynamic criteria is as follows: (1) a systolic blood pressure of less than 90 mm Hg for at least 30 minutes (or the need for medications or devices 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. A helpful hemodynamic measurement that summarizes some of the hemodynamic findings above is cardiac power output which is mean arterial pressure × cardiac output divided by 451, with cardiac power output less than 0.6 consistent with cardiogenic shock in the right clinical scenario. Supportive laboratory studies include elevated lactate, elevated b-type natriuretic peptide, increasing creatinine, elevated liver enzymes, and metabolic acidosis.


Acute myocardial infarction accounts for many cases of cardiogenic shock and can occur due to an acutely occluded coronary artery, or due to active ischemia from increased demand in patients with a weakened heart from prior MIs. In patients with an acutely occluded coronary artery who present in a delayed fashion, cardiogenic shock can occur from mechanical complications including ventricular septal defect (VSD), acute mitral regurgitation as a result of papillary muscle rupture or dysfunction, 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 ...

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