Glucocorticoids as an emerging pharmacologic agent for cardiopulmonary resuscitation

Giolanda Varvarousi, Antonia Stefaniotou, Dimitrios Varvaroussis, Theodoros Xanthos, Giolanda Varvarousi, Antonia Stefaniotou, Dimitrios Varvaroussis, Theodoros Xanthos

Abstract

Although cardiac arrest (CA) constitutes a major health problem with dismal prognosis, no specific drug therapy has been shown to improve survival to hospital discharge. CA causes adrenal insufficiency which is associated with poor outcome and increased mortality. Adrenal insufficiency may manifest as an inability to increase cortisol secretion during and after cardiopulmonary resuscitation (CPR). Several studies suggest that glucocorticoids during and after CPR seem to confer benefits with respect to return of spontaneous circulation (ROSC) rates and long term survival. They have beneficial hemodynamic effects that may favor their use during CPR and in the early post-resuscitation period. Moreover, they have anti-inflammatory and anti-apoptotic properties that improve organ function by reducing ischemia/reperfusion (I/R) injury. However, glucocorticoid supplementation has shown conflicting results with regard to survival to hospital discharge and neurological outcome. The purpose of this article is to review the pathophysiology of hypothalamic-pituitary-adrenal (HPA) axis during CPR. Furthermore, this article reviews the effects of glucocorticoids use during CRP and the post-resuscitation phase.

Conflict of interest statement

The authors declare that they have no conflict of interest.

Figures

Fig. 1
Fig. 1
Main mechanism of action of glucocorticoids. Glucocorticoids bind to GR within the cytoplasm of the cell. Upon glucocorticoid binding, the activated GR translocates into the nucleus. GR binds to GRE and affects protein synthesis at the transcription step GR glucocorticoid receptor, GRE glucocorticoid response element, a stretch of DNA that binds the GR and activates gene transcription
Fig. 2
Fig. 2
The hypothalamic-pituitary-adrenal axis during cardiac arrest CRH corticotropin-releasing hormone, ACTH adrenocorticotropin

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