INFLUENCE OF EPINEPHRINE ON SYSTEMIC, MYOCARDIAL, AND CEREBRAL ACID-BASE STATUS DURING CARDIOPULMONARY-RESUSCITATION

During cardiopulmonary resuscitation (CPR), arterial pH and carbon dioxide tension (P(co2)) do not reflect the marked acidosis and hypercapnia seen in venous blood samples during CPR. Epinephrine causes an increase in myocardial and cerebral blood flow during CPR, but the influence on regional venous P(co2) and pH is as yet unknown. Fourteen pigs were allocated to receive either 0.9% saline (n = 7), or 45-mu-g/kg epinephrine (n = 7) after 5 min of ventricular fibrillation and 3 min of open-chest CPR. Blood samples were obtained during CPR from the aorta, pulmonary artery, great cardiac vein, and sagittal sinus before and 90 s and 5 min after drug ministration. Regional blood flow was measured with tracer microspheres. Plasma catecholamines were quantified by high-performance liquid chromatography in arterial blood. P(co2) 90 s after drug administration arterial, mixed venous, myocardial venous, and cerebral venous blood were (means +/- SD) 36 +/- 8, 67 +/- 9, 74 +/- 14, and 79 +/- 19 mmHg in the control group and 35 +/- 11, 62 +/- 12, 73 +/- 10, and 71 +/- 14 mmHg in the epinephrine group. pH values 90 s after drug administration in the same blood samples were 7.29 +/- 0.11, 7.11 +/- 0.09, 7.04 +/- 0.09, and 7.07 +/- 0.10 in the control group and 7.31 +/- 0.13, 7.17 +/- 0.07, 7.08 +/- 0.08, and 7.07 +/- 0.12 in the epinephrine group. Despite a significant increase in myocardial and cerebral blood flow after epinephrine, P(co2) and pH in all blood samples were not different from those of the control group. During CPR and prior to epinephrine, plasma epinephrine concentrations in arterial blood increased from a prearrest value of 1.23 +/- 1.90 to 72.1 +/- 56.4 ng/ml, and plasma norepinephrine concentrations increased from 0.32 +/- 0.38 to 106.8 +/- 53.0 ng/ml. After exogenous epinephrine, there was an additional increase to 265.7 +/- 82.2 at 90 s in arterial plasma epinephrine but no significant alteration in arterial plasma norepinephrine. No significant correlation between arterial catecholamine concentrations and myocardial or cerebral blood flow was found. We conclude that the effectiveness of vasopressor treatment in improving myocardial and cerebral blood flow during CPR cannot be evaluated by determining the P(co2) and pH in regional venous blood. We hypothesize that after epinephrine, more anaerobically produced hydrogen ions are neutralized by the endogenous bicarbonate system, which in turn generates more carbon dioxide.