MYOCARDIAL ACID-BASE CHANGES DURING CPR

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The aims of the research are to study changes in myocardial PCO2 and, more specifically, to measure the changes in myocardial pH and great cardiac vein PCO2 during conventional cardiopulmonary resuscitation (CPR) and the extent to which they determine resuscitability after cardiac arrest. During cardiac arrest, we have observed a critical reduction of pulmonary blood flow with critically decreased pulmonary clearance of CO2. We further observed that mixed venous and coronary sinus PCO2 are markedly increased. The CO2 diffuses into tissues. Myocardial (tissue) pH is decreased. In addition, decreases in myocardial blood flow account for anaerobically generated lactic acid with lactate increases in cardiac venous blood. Lactic acid is buffered by bicarbonate which increases CO2 generation and further reduces pH. Since increases in PCO2 (decreases in pH) are well known to decrease myocardial contractility, we hypothesize that nonresuscitability is related to large increases in PCO2. As yet, no rapid response intramyocardial PCO2 electrode has been perfected. We therefore will measure changes relating to PCO2, namely pH and PCO2, in a well established porcine model of cardiac arrest developed in our laboratory pending development and availability of a PCO2 electrode to fulfill this need. If our hypothesis that it is "CO2 narcosis" of the heart which accounts for nonresuscitability is correct, we will demonstrate a close relationship between nonresuscitability and minimal pH of the myocardium and maximal PCO2. We initially investigate the effects of hypercapnia induced by ventilation with FiCO2 0.1 and 0.3 with the anticipation that decreases in pH induced by increases in PCO2 will decrease myocardial function and resuscitibility. We then compare the effects of NaHCO3 and Na2CO3 with the anticipation that NaHCO3 as a "CO2 producing" buffer reduces pH, and Na2CO3 as a "CO2 consuming" producing buffer will reduce "CO2 narcosis" of the myocardium. We then examine the effects of these alkalinizing agents on myocardial pH and resuscitability during open chest CPR in which more effective blood flow is generated with internal cardiac compression. The model is then adapted for nondestructive, closed chest CPR to investigate 48 hour survival and neurological responsiveness in response to therapy and more specifically to evaluate the effects of potentially beneficial buffering agents.