Vasopressin and epinephrine for cardiac arrest

Abstract

Ian Stiell and colleagues (July 14, p 105)1Stiell IG Hebert PC Wells GA et al.Vasopressin versus epinephrine for inhospital cardiac arrest: a randomised controlled trial.Lancet. 2001; 358: 105-109Summary Full Text Full Text PDF PubMed Scopus (275) Google Scholar report a similar outcome and no adverse effects for vasopressin and epinephrine in patients being resuscitated in hospital. They disagree with the recommendation of vasopressin as an alternative treatment for cardiac arrest. By contrast, we believe these observations are in agreement with laboratory and clinical investigations, and suggest that Stiell and colleagues' results apply only to the subgroup of in-hospital cardiac arrest patients they studied. In pigs, with short duration of cardiac arrest and moderate cardiac ischaemia, we have noted that vasopressin and epinephrine are similarly effective. During severe acidosis, however, vasopressin causes a striking pressor response in vitro, but catecholamines do not; vasopressin might, therefore, be beneficial when the duration of cardiac arrest and cardiopulmonary resuscitation is long.2Mayr VD Wenzel V Voelckel WG et al.Developing a vasopressor combination in a pig model of adult asphyxial cardiac arrest.Circulation. 2001; 104: 1651-1656Crossref PubMed Scopus (99) Google Scholar In a study of asphyxia in pigs, we noted that combined epinephrine and vasopressin, but not epinephrine or vasopressin alone, maintained raised coronary perfusion pressures during cardiopulmonary resuscitation, and significantly improved survival rates.2Mayr VD Wenzel V Voelckel WG et al.Developing a vasopressor combination in a pig model of adult asphyxial cardiac arrest.Circulation. 2001; 104: 1651-1656Crossref PubMed Scopus (99) Google Scholar Interactions between vasopressin and epinephrine depend on the presence of each other more than was previously thought. After 4 min ventricular fibrillation, endogenous epinephrine concentrations were extremely high, and when vasopressin was then given during cardiopulmonary resuscitation, coronary perfusion pressure rose strikingly from about 15 mm Hg to about 50 mm Hg.3Wenzel V Lindner KH Baubin MA et al.Vasopressin decreases endogenous catecholamine plasma levels during CPR in pigs.Crit Care Med. 2000; 28: 1096-1100Crossref PubMed Scopus (43) Google Scholar During the asphyxia experiment, in contrast, high concentrations of endogenous epinephrine were released immediately after clamping of the endotracheal tube to maintain cardiocirculatory homoeostasis until cardiac arrest finally occurred around 8 min after induction of asphyxia. Under these particular conditions, an effective response might only be achieved with vasopressin when the plasma concentration of epinephrine is high because of either endogenously released epinephrine, or exogenously administered epinephrine. Morris and colleagues4Morris DC Dereczyk BE Grzybowsky M et al.Vasopressin can increase coronary perfusion pressure during human cardiopulmonary resuscitation.Acad Emerg Med. 1997; 4: 878-883Crossref PubMed Scopus (108) Google Scholar reported that four of ten patients undergoing extended cardiopulmonary resuscitation efforts (about 45 min) with around 18 mg epinephrine had return of spontaneous circulation after subsequent administration of 1 U/kg vasopressin. A combination of epinephrine and vasopressin therefore seems particularly effective during extended cardiopulmonary resuscitation, severe global ischaemia, or both. The same mechanism might also explain the response of patients with vasodilatory shock, when a vasopressin infusion in addition to catecholamines can prevent haemo-dynamic collapse.5Landry DW Levin HR Gallant EM et al.Vasopressin pressor hypersensitivity in vasodilatory shock.Crit Care Med. 1997; 25: 1279-1282Crossref PubMed Scopus (346) Google Scholar We suspect that, because of the many different causes of cardiac arrest and the varied conditions under which rescue teams have to reach and treat their patients, the numerous features of cardiopulmonary resuscitation management must be carefully differentiated. Accordingly, Stiell and colleagues' approach to extrapolate their findings to the larger proportion of cardiac arrest patients in the emergency medical service might be overly cautious. We agree that new cardiopulmonary resuscitation strategies should be handled prudently. We are, therefore, currently coordinating a multicentre randomised clinical trial of vasopressin versus epinephrine given up to two times out of hospital, followed by epinephrine. Global ischaemia might generally be more severe in these than in Stiell and colleagues' patients, and vasopressin might be beneficial. Meanwhile, two instead of one vasopressor options are available for the management of cardiac arrest patients, and we must look at how best to use them. Vasopressin and epinephrine for cardiac arrestAuthors' reply Full-Text PDF