Recognizing and Managing Cardiogenic Shock

Abstract

Cardiogenic shock is an acute state of end-organ hypoperfusion following cardiac failure. This occurs mainly due to primary pump failure with or without contributions from inadequate preload and afterload. The consequence of cardiogenic shock is hypoxia at the cellular level resulting in loss of function.

The etiology of cardiogenic shock varies by age. Critical congenital heart diseases present in the neonatal period, whereas acquired heart diseases and dysfunction of palliated or repaired congenital heart diseases often present later in life. Arrhythmias, myocarditis, cardiomyopathy, sepsis, and electrolyte disturbances can cause cardiogenic shock at all ages.

Symptoms and signs of cardiogenic shock are often nonspecific and can easily be misdiagnosed for various common illnesses like bronchiolitis or gastritis. The diagnosis of cardiogenic shock is based on a high clinical index of suspicion. No single diagnostic laboratory test or imaging modality will confirm the diagnosis.

Treatment of cardiogenic shock is accomplished by optimizing oxygen delivery to meet tissue demands. Oxygen delivery can be improved by optimizing preload, increasing contractility, mild afterload reduction, and improving atrioventricular synchrony. Oxygen demand can be limited by decreasing the basal metabolic rate via treatment of pain, fever, and agitation.

Ductal-dependent congenital heart diseases develop cardiogenic shock in the newborn period and can be difficult to differentiate from hypovolemic or septic shock or inborn errors of metabolism. Newborn myocardium is less compliant and hence not preload responsive. Cardiac output is often rate-dependent since stroke volume is already at maximum. Treatment consists of prompt initiation of prostaglandins, urgent echocardiogram for accurate diagnosis, optimizing electrolytes and glucose, and judicious use of oxygen.

Cardiac tamponade is a medical emergency. The presence of pulsus paradoxus, muffled heart sounds, cardiomegaly on chest radiograph, and classic ECG changes should help clinch the diagnosis. Bedside cardiac ultrasound will help confirm the clinical suspicion and assist the ED physician in therapeutic pericardiocentesis.