Pressor with promise: using vasopressin in cardiopulmonary arrest.

Despite their widespread use, current methods of cardiopulmonary resuscitation and advanced cardiac life support continue to yield poor results. In the United States, the national average for long-term survival after cardiac arrest in patients with an out-of-hospital arrest remains <5%. Surprisingly, the use of epinephrine, the mainstay of pharmacological therapy in cardiac arrest, is supported only by animal studies and anecdotal case reports. We would like to present evidence that vasopressin, alone or in combination with epinephrine, is more effective than epinephrine in the treatment of cardiopulmonary arrest. Its use during advanced cardiac life support may improve the chances of survival after cardiopulmonary arrest. All forms of stress elicit an endocrine response. Cardiopulmonary arrest, the ultimate stress,1 results in the release of endogenous epinephrine and norepinephrine in animals and humans. Systemic vascular resistance increases, with preferential redistribution of blood flow to myocardial and cerebral vessels.2 The discovery of this pressor response prompted trials of catecholamines in animal models of cardiac arrest, ultimately leading to the use of epinephrine in human subjects. For more than three decades, epinephrine has been the drug of choice and the major pharmacological intervention in cardiac arrest. A recent randomized, controlled trial comparing epinephrine with placebo showed that neither high-dose nor standard-dose epinephrine altered survival in cardiac …