Pulseless electrical activity pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Pathophysiology

There is often a downward spiral in the pathophysiology of PEA. A severe initial insult often reduces cardiac output which may in turn cause myocardial ischemia, left ventricular failure, hypoxia and metabolic acidosis. These pathophysiologic disturbances further reduce cardiac output further exacerbating the downward spiral. With loss of cardiac output; hypotension, loss of consciousness and apnea rapidly ensue.

Reduced Preload and Inadequate Filling of the Left Ventricle or

PEA may be due to inadequate filling of the left ventricle with blood to stretch the cardiac sarcomeres adequately to result in a cardiac contraction (i.e. there is inadequate preload). Examples include rapid fluid or blood loss as occurs in major trauma. Cardiac tamponade, pneumothorax, and pulmonary embolism are other examples.

Elevated Afterload

Elevated afterload is rarely a cause of PEA.

Electromechanical Dissociation

In some cases, PEA may be caused by electromechanical dissociation. The normal condition when electrical activation of muscle cells precedes mechanical contraction is known as electromechanical coupling. This coupling is lost in some forms of PEA, and this is known as electromechanical dissociation.

Reduced Contractility

Contraction of the myocardium depends upon the integrity of the troponin subunits.

Reduced Calcium Influx

Calcium binding to troponin is required for contractility. This binding can be reduced in calcium channel blocker overdoses.

Reduced Affinity of Troponin for Calcium

In the setting of hypoxia, calcium binds less avidly to troponin.