The effects of epinephrine/norepinephrine on end-tidal carbon dioxide concentration, coronary perfusion pressure and pulmonary arterial blood flow during cardiopulmonary resuscitation

End-tidal CO2 concentration correlates with pulmonary blood flow during car diopulmonary resuscitation and has been claimed to be a useful tool to judg e the effectiveness of chest compression. A high concentration of end-tidal CO2 has been related to a better outcome. However, most authors have notic ed a decrease in end-tidal CO2 concentration after administration of epinep hrine, concomitant with an increase in coronary perfusion pressure and an i ncreased incidence of return of spontaneous circulation. This study was per formed to evaluate changes in end-tidal CO2 concentration after injection o f vasopressors during cardiopulmonary resuscitation and to investigate the time-course of the response and possible explanations for it. After 1 min o f electrically induced cardiac arrest and 5 min of chest compressions, 18 p igs were randomly assigned to receive 0.045 mg kg(-1) epinephrine, 0.045 mg kg(-1) norepinephrine or no drug. After another 4 min of chest compression s the pigs were defibrillated. End-tidal CO2 pulmonary blood flow and coron ary perfusion pressure decreased immediately after the induction of cardiac arrest, increased slightly during chest compressions and increased initial ly to supernormal levels after the return of spontaneous circulation. Injec tion of epinephrine or norepinephrine during chest compressions decreased e nd-tidal CO2 51 1 2%, (mean +/- S.E.M.), and 43 +/- 1%, respectively, and p ulmonary blood flow by 134 +/- 13 and 125 +/- 16%, respectively, within 1 m in, simultaneously increasing coronary perfusion pressure from 10 +/- 2 to 45 +/- 5 mm Hg and from 11 +/- 1 to 38 +/- 5 mm Hg, respectively. The coron ary perfusion pressure slowly fell, but the effects on end-tidal CO2 and pu lmonary blood flow were prolonged. In conclusion, vasopressors increased co ronary perfusion pressure and the likelihood of a return of spontaneous cir culation, but decreased end-tidal CO2 concentration and induced a critical deterioration in cardiac output and thus oxygen delivery in this model of c ardiopulmonary resuscitation. (C) 2000 Elsevier Science Ireland Ltd. All ri ghts reserved.