Cardiogenic shock can result from any condition that causes significant left ventricular dysfunction with reduced cardiac output, such as MI (most common), myocardial ischemia, papillary muscle dysfunction, and end stage cardiomyopathy.

Other causes include myocarditis and depression of myocardial contractility after cardiac arrest and prolonged cardiac surgery. Mechanical abnormalities of the ventricle, such as acute mitral or aortic insufficiency or an acutely acquired ventricular septal defect or ventricular aneurysm, may also result in cardiogenic shock.

Regardless of the cause, left ventricular dysfunction initiates a series of compensatory mechanisms that attempt to increase cardiac output and, in turn, maintain vital organ function. As cardiac output falls, aortic and carotid baroreceptors activate sympathetic nervous responses. These compensatory responses increase heart rate, left ventricular filling pressure, and peripheral resistance to flow in order to enhance venous return to the heart. The action initially stabilizes the patient but later causes deterioration with rising oxygen demands on the already compromised myocardium. These events constitute a vicious circle of low cardiac output, sympathetic compensation, myocardial ischemia, and even lower cardiac output.

Death usually ensues because the vital organs can’t overcome the deleterious effects of extended hypoperfusion. Despite advances in treatment, the mortality rate
from cardiogenic shock remains greater than 80%.

Typically, the patient’s history includes a disorder (such as MI or cardiomyopathy) that severely decreases left ventricular function. Patients with underlying cardiac disease may complain of anginal pain because of decreased myocardial perfusion and oxygenation. Urine output is usually less than 20 ml/hour.

Inspection usually reveals pale skin, decreased sensorium, and rapid, shallow respirations. Palpation of peripheral pulses may detect a rapid, thready pulse. The skin feels cold and clammy.

Auscultation of blood pressure usually discloses a mean arterial pressure of less than 60 mm Hg and a narrowing pulse pressure. In a patient with chronic hypotension, the mean pressure may fall below 50 mm Hg before he exhibits any signs of shock. Auscultation of the heart detects gallop rhythm, faint heart sounds and, possibly (if shock results from rupture of the ventricular septum or papillary muscles), a holosystolic murmur.

Although many of these clinical features also occur in heart failure and other shock syndromes, they are usually more profound in cardiogenic shock. Patients with pericardial tamponade may have distant heart sounds.