• M H Weil and W Tang.
• Institute of Critical Care Medicine Palm Springs, California, USA.
• Dis Mon. 1997 Jul 1;43(7):429-501.

AbstractAfter failure of initial external defibrillation, restoration of spontaneous circulation is largely contingent on rapid and effective reversal of myocardial ischemia by both mechanical and pharmacologic means. Despite the introduction of modern cardiopulmonary resuscitation (CPR) more than 35 years ago, its universal acceptance, and its wide implementation, no improvements in outcome excepting early defibrillation have been documented over these many years. The science of CPR therefore is still in its infancy. It was incorrectly assumed that all that needs to be known is known and that the need for scientific research was therefore not apparent. Accordingly, serious resuscitation research was neither encouraged nor equitably supported. The ABCs of CPR currently provide for the establishment of a patent airway (A) and intermittent positive pressure ventilation, preferably with oxygen-enriched air (B). These are to be immediately followed with precordial compression (C). This ordering of priorities, however, is based on consensus rather than objective outcome measurements. The ABCs recently have been seriously challenged on the basis of results of both experimental and clinical studies. Conventional external precordial compression restores systemic blood flow. It may be used by both professional and nonprofessional CPR providers, especially bystanders, because of its apparent simplicity and noninvasiveness. However, manual or mechanical external precordial compression typically generates cardiac outputs that represent less than 30% of normal values. Coronary blood flow, which is critical for restoration of spontaneous circulation, is correspondingly reduced. Accordingly, several alternatives to conventional precordial compression have been proposed with the intent of increasing cardiac output and both coronary and cerebral blood flows. Among the large number of pharmaceutical agents initially recommended for cardiac resuscitation, only agents that produce peripheral vasoconstriction are of proved benefit. Epinephrine has been the preferred vasopressor agent for the management of cardiac arrest for more than 35 years because of its alpha-adrenergic effects. However, the potentially adverse effects of epinephrine are related to its beta-adrenergic inotropic actions. The beta-adrenergic actions account for disproportionate increases in myocardial oxygen consumption with increased severity of myocardial ischemic injury and provocation of ectopic ventricular tachycardia and ventricular fibrillation. Nevertheless, epinephrine remains the drug of choice, although adrenergic drugs with selective alpha-adrenergic actions or nonadrenergic vasoconstrictor drugs are likely to emerge as useful alternatives. Experimental and clinical observations have led to identification of continuous monitoring of both end-tidal carbon dioxide and ventricular fibrillation waveforms as practical noninvasive guides because they are highly correlated with both cardiac output and coronary blood flow. Both end-tidal carbon dioxide and ventricular fibrillation waveforms now serve as predictors of the likelihood of successful resuscitation. These two measurements may now be used to guide interventions and especially to assure optimal precordial compression. It is well established that sudden death among adults is predominantly due to malignant ventricular arrhythmias and ventricular fibrillation. Early defibrillation serves as an unequivocally effective immediate intervention. Minimally trained first responders and members of the general public are being enfranchised to use automated external defibrillators for very early defibrillation. Use of these devices by bystanders is the most promising new intervention since CPR was first proposed in the early 1960s. Postresuscitation ventricular dysrhythmias and heart failure are now called postresuscitation myocardial dysfunction. This complication has been recognized as a leading cause of the high postresuscitation mor

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