- Tissue hypoperfusion: Depressed mental status, cool extremities, decreased
- 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 ...