- 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 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 6–1).
Table 6–1. Causes of Cardiogenic Shock.
| Save Table
Table 6–1. Causes of Cardiogenic Shock.
|I. Acute myocardial infarction (MI)|
|A. Pump failure|
|B. Mechanical complications of acute MI|
|1. Acute mitral regurgitation |
|2. Ventricular septal defect|
|3. Free wall rupture/tamponade|
|C. Right ventricular MI|
|II. End-stage, severe cardiomyopathies secondary to|
|A. Valvular disease|
|B. Chronic ischemic disease|
|C. Restrictive/infiltrative |
|III. Acute myocarditis: viral/infectious, toxic|
|IV. Stress cardiomyopathy|
|V. Endocrine disease (eg, hypothyroidism, pheochromocytoma)|
|VII. Secondary to medications|
Babaev A et al. Trends in management and outcomes of patients with acute myocardial infarction complicated by cardiogenic shock.
JAMA. 2005 Jul 27;294(4):448–54.
Hochman JS et al. Cardiogenic shock complicating acute myocardial infarction–etiologies, management and outcome: a report from
the SHOCK Trial Registry. SHould we emergently revascularize Occluded
Coronaries for cardiogenic shocK? J Am Coll Cardiol. 2000 Sep;36(3
Sharkey SW et al. Acute and reversible cardiomyopathy provoked by stress in women from the United States. Circulation. 2005 Feb 1;111(4):472–9.
The principle feature of shock is hypotension with evidence of end-organ hypoperfusion. In cardiogenic shock, this occurs as a consequence of inadequate cardiac function. The usual response to low cardiac
output is sympathetic stimulation to increase cardiac performance
and maintain vascular tone. This results in tachycardia and increased
myocardial contractility (Î²-adrenergic mediated effects) and peripheral
vasoconstriction (an α-adrenergic mediated effect).
The classic patient with cardiogenic shock has evidence of peripheral
vasoconstriction (cool, clammy skin) and tachycardia. Corresponding classic
hemodynamics are a reduced cardiac output and increased systemic
vascular resistance (SVR), defined as:
Recent evidence suggests that many patients with cardiogenic shock do not have these classic hemodynamics and instead have a
lower SVR much like patients in septic shock. In fact, it has been
postulated that a systemic inflammatory response-like syndrome with
a low SVR may be encountered in up to 25% of patients in
cardiogenic shock. Furthermore, patients with severe septic shock
often have depressed myocardial function, and patients with cardiogenic
shock can have a component of hypovolemia. Thus, there can be considerable
overlap in pathophysiologies.
Cardiogenic Shock after Acute MI
If at least 40% of the left ventricular myocardial muscle mass is lost, either acutely or as a result of prior damage, cardiogenic shock can result from pump failure (ie, there is not sufficient
left ventricular muscle mass to maintain forward cardiac output).
This usually occurs as a consequence of an MI. The initial event
in an acute MI is obstruction of a coronary artery, commonly termed
the “infarct-related artery.” The acute obstruction
decreases oxygen supply ...