ESSENTIALS OF DIAGNOSIS
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.
Cardiogenic shock is an extremely morbid condition. Despite recent advances in treatment, nearly 50% of patients with cardiogenic shock still do not survive to hospital discharge. 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 cardiomyopathies can also lead to cardiogenic shock.
Cardiogenic shock is defined by both the clinical signs of a reduced cardiac output and associated hemodynamic findings. 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 are as follows: (1) a systolic blood pressure of < 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=""> 15 mm Hg (which excludes hypovolemia), and (3) a cardiac index < 2.2 L/min/m2.
Acute MI accounts for most cases of cardiogenic shock. Acute MI results in cardiogenic shock in 5–10% of patients presenting for emergency care; 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 a weakened heart from prior MIs. “Mechanical” complications of an acute MI can also cause shock, and these include ventricular septal defect (VSD), 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 takotsubo cardiomyopathy) in which severe heart failure and sometimes cardiogenic shock result from extreme emotional distress. Finally, certain endocrine abnormalities may cause severe cardiac dysfunction and cardiogenic shock (Table 9–1).
Table 9–1.Causes of Cardiogenic Shock