EPINEPHRINE-MEDIATED CHANGES IN CARBON-DIOXIDE TENSION DURING REPERFUSION OF VENTRICULAR-FIBRILLATION IN A CANINE MODEL

Citation
Mg. Angelos et Dj. Debehnke, EPINEPHRINE-MEDIATED CHANGES IN CARBON-DIOXIDE TENSION DURING REPERFUSION OF VENTRICULAR-FIBRILLATION IN A CANINE MODEL, Critical care medicine, 23(5), 1995, pp. 925-930
Citations number
21
Categorie Soggetti
Emergency Medicine & Critical Care
Journal title
ISSN journal
00903493
Volume
23
Issue
5
Year of publication
1995
Pages
925 - 930
Database
ISI
SICI code
0090-3493(1995)23:5<925:ECICTD>2.0.ZU;2-E
Abstract
Objective: Previous studies suggest that epinephrine may alter the cor relation of perfusion with measures of Pco(2) during cardiopulmonary r esuscitation. This study investigated the effects of epinephrine on Pa ce, and mixed venous Pco, in a high-flow reperfusion model of cardiac arrest. Design: Prospective, block randomized, blinded, placebo contro lled, laboratory study. Subjects: Thirty mixed breed canines. Interven tions: After a 12-min ventricular fibrillation cardiac arrest, 30 mixe d breed ca. nines were reperfused with standardized (3200 revolutions/ min) cardiopulmonary bypass and were given placebo (n = 10), standard dose epinephrine (0.02 mg/kg; n = 10), or high-dose epinephrine (0.2 m g/kg; n = 10). Arterial and mixed venous blood gases, coronary perfusi on pressure, pump flow and peripheral vascular resistance were compare d between groups during the early reperfusion period using analysis of variance with a post hoc Tukey's multiple comparison test. Measuremen ts and Main Results: Baseline variables were similar between groups. W ith reperfusion, the high-dose epinephrine group had higher coronary p erfusion pressures (p < .002), lower systemic pump flow (p < .01), and higher peripheral vascular resistance (p < .001). In the high-dose ep inephrine group, both Paco(2) (high-dose epinephrine, 40 +/- 6 torr [5 .3 +/- 0.8 kPa]; standard dose epinephrine, 45 +/- 7 torr [6.0 +/- 0.9 kPa]; placebo, 54 +/- 4 torr [7.2 +/- 0.5 kPa];p < .01) and mixed ven ous Pco(2) (high-dose epinephrine, 55 +/- 10 torr [7.3 +/- 1.3 kPa]; s tandard dose epinephrine, 57 +/- 9 torr [7.6 +/- 1.2 kPa]; placebo, 67 +/- 4 torr [8.9 +/- 0.5 kPa]; p < .05) were significantly decreased, and arterial pH, Pao(2), and mixed venous Po-2 were significantly incr eased compared with the placebo group. Conclusion: In this model, when ventilation and CO2 production are constant, the decrease in Paco(2) with epinephrine is due to decreased pulmonary blood flow (flow to mem brane oxygenator) and peripheral shunting.