Vasopressin and epinephrine for cardiac arrest

• Published in: The Lancet (British edition) Vol. 358; no. 9298; pp. 2080 - 2081
• Main Authors: Wenzel, Volker, Lindner, Karl H
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 15.12.2001; Elsevier Limited
• Subjects: Acidosis; Animals; Asphyxia - drug therapy; Cardiac arrest; Cardiopulmonary resuscitation; CPR; Defibrillators; Emergency medical services; Epinephrine; Epinephrine - therapeutic use; Heart Arrest - drug therapy; Hospitalization; Humans; Survival; Swine; Vasoconstrictor Agents - therapeutic use; Vasopressin; Vasopressins - therapeutic use
• ISSN: 0140-6736; 1474-547X
• DOI: 10.1016/S0140-6736(01)07112-4

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.2 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.2 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.3 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. [...]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.