Post cardiac arrest syndrome

Last revised by Dr Daniel J Bell on 03 Jul 2021

The post cardiac arrest syndrome (PCAS) describes the clinicopathological state that manifests following most cardiac arrests. Clinically, it is manifested by a combination of neurological disturbance, multiorgan dysfunction and a systemic inflammatory response syndrome-like state.

The pathogenesis of post-cardiac arrest syndrome (PCAS) is clearly complex and remains poorly understood. In essence, during the arrest phase, organ dysfunction occurs due to ischemic injury. Following the re-establishment of normal circulation, the ischemic damage is compounded by "reperfusion injury".

As the body tissues are replenished with oxygenated blood, a mélange of activation of systemic inflammatory, clotting, endocrine and immunological cascades occurs, resulting in a state resembling the systemic inflammatory response syndrome, as seen in sepsis and with other severe systemic insults.

Clinically, this phase might be manifested by fever, elevated infection risk, deranged hemodynamics and/or potential multiorgan failure.

Moreover, contributing to this complex mix, will be the patient's original pathology which caused the arrest in the first place as well as any other co-morbidities that they might (and often) have.

The imaging features of the post cardiac arrest syndrome are myriad and non-specific, representing a medley of:

A favorable prognosis following a cardiac arrest correlates positively with careful focused attention to the blood pressure, oxygen saturation, partial pressure of carbon dioxide, blood glucose and core temperature. When these parameters are allowed to shift markedly from their normal ranges, then neurological prognosis and long term survival tend to be significantly negatively impacted. Indeed, despite optimal management, the number of post-cardiac arrest patients achieving discharge from medical care with an optimal neurological recovery remains small 1-3

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