Introduction

Although there is persuasive evidence that the administration of adrenaline during CPR favors the success of electrical defibrillation as well as the return of pulsatile rhythm, its more ultimate benefit on survival is unproven. To the contrary, the more recent discovery of reversible myocardial dysfunction after successful resuscitation from cardiac arrest initially in experimental models and subsequently in human patients led to a re-examination of its role. Although there is only indirect evidence that impaired myocardial function accounts for early death, the high correlation between the severity of myocardial impairment and decreased survival supports this assumption. Accordingly, postresuscitation myocardial dysfunction may therefore explain, at least in part, the high fatality rate within the initial 72 hours after successful resuscitation from cardiac arrest such that fewer than 5% of victims recover to be discharged from the hospital without major impairment.

The immediate effort during CPR is to restore blood flows to sustain the functions of vital organs, and most especially, to the heart and the brain prior to successful restoration of spontaneous circulation. Blood flow to the vital organs during CPR is contingent primarily on the cardiac output generated by precordial or direct cardiac compression and by the resistance in the systemic arterial bed. Yet the cardiac output that is generated by precordial compression represents only approximately 25% to 30% of normal values. Vasopressor drugs increase arterial and arteriolar vasoconstriction, and thereby produce increases in aortic diastolic pressure.