Myocardial acidosis associated with CO2 production during cardiac arrest and resuscitation.

Previous studies from our institution demonstrated significant hypercarbic acidosis in the mixed venous (pulmonary artery) blood in animals and human patients during cardiac arrest and cardiopulmonary resuscitation (CPR). In the present study, the acid-base state of the myocardium during cardiac arrest was investigated. Cardiac arrest was electrically induced in 11 pentobarbital-anesthetized and mechanically ventilated domestic pigs. Precordial compression was begun 3 minutes after onset of ventricular fibrillation and continued for 8 minutes. During CPR, there was rapid onset of profound myocardial acidosis with an increase in intramyocardial [H+] from 54 +/- 5 to 146 +/- 20 nmol/l (7.27 +/- 0.04 to 6.88 +/- 0.20 pH units). Great cardiac vein PCO2 increased from 57 +/- 2 to 158 +/- 12 mm Hg. Profound hypercarbic acidosis in great cardiac vein blood was associated with myocardial lactate production to levels of 8.1 +/- 0.7 mmol/l. Only moderate decreases in cardiac vein bicarbonate concentrations from 31 +/- 1 to 23 +/- 1 mmol/l were observed. These acid-base changes were almost completely reversed over an interval of 60 minutes after the animals were successfully resuscitated by DC countershock. The PCO2 in cardiac vein blood was significantly greater than that of mixed venous blood, demonstrating disproportionate myocardial production of CO2 during CPR. Accordingly, it is CO2 production during ischemia that is implicated as the predominant mechanism accounting for myocardial [H+] increases during cardiac arrest. Important clinical implications for buffer therapy during CPR and, in particular, treatment with bicarbonate emerge from these observations.