Sometimes called pump failure, cardiogenic shock is a condition of diminished cardiac output that severely impairs tissue perfusion. It reflects severe left-sided heart failure and occurs as a serious complication in nearly 15% of all patients hospitalized with an acute myocardial infarction (AMI).
Cardiogenic shock typically affects patients whose area of infarction exceeds 40% of muscle mass; in such patients, the fatality rate may exceed 85%. Most patients with cardiogenic shock die within 24 hours of onset. The prognosis for those who survive is extremely poor.
Cardiogenic shock can result from any condition that causes significant left ventricular dysfunction with reduced cardiac output, such as an MI (most common), myocardial ischemia, papillary muscle dysfunction, end-stage cardiomyopathy and other cardiomyopathies (viral, toxic), cardiac arrest, ventricular arrhythmias (fibrillation, tachycardia), cardial amyloidosis, and myocardial degeneration.
Regardless of the underlying cause, left ventricular dysfunction sets into motion a series of compensatory mechanisms that attempt to increase cardiac output and, in turn, maintain vital organ function.
As cardiac output falls in patients with left ventricular dysfunction, aortic and carotid baroreceptors initiate sympathetic nervous responses. These responses, in turn, increase heart rate, left ventricular filling pressure, and peripheral resistance to flow to enhance venous return to the heart.
These compensatory responses initially stabilize the patient’s condition but later cause deterioration with rising oxygen demands of the already compromised myocardium. The result? A vicious circle of low cardiac output, sympathetic compensation, myocardial ischemia, and even lower cardiac output.
Signs and symptoms
Cardiogenic shock produces signs and symptoms of poor tissue perfusion: cold, pale, clammy skin; a drop in systolic blood pressure to 30 mm Hg below baseline or a sustained reading below 80 mm Hg not attributable to medication; tachycardia; rapid, shallow respirations; oliguria (less than 20 ml of urine/hour); restlessness, mental confusion and obtundation; narrowing pulse pressure; and cyanosis.
Although many of these signs and symptoms also occur in patients with heart failure and other shock syndromes, they’re usually more profound in those with cardiogenic shock.
Auscultation detects gallop rhythm, faint heart sounds and, possibly, if the shock results from rupture of the ventricular septum or papillary muscles, a holosystolic murmur.
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