MYOCARDIAL ACID-BASE CHANGES DURING CPR

研究的目的是研究心肌细胞的变化， PCO2，更具体地说，测量 心肌pH和心大静脉PCO2 心肺复苏术（CPR）及其程度 确定心脏骤停后的可复苏性。 在心脏骤停期间，我们观察到 肺血流量严重降低 清除CO2。 我们进一步观察到，混合静脉和 冠状窦PCO2明显升高。 二氧化碳扩散 变成组织。 心肌（组织）pH值降低。 此外，本发明还提供了一种方法， 心肌血流量的减少可以解释 产生的乳酸随着心脏静脉乳酸盐的增加而增加 血 乳酸被碳酸氢盐缓冲， 产生二氧化碳，进一步降低pH值。 由于众所周知PCO2的增加（pH值的降低） 降低心肌收缩力，我们假设， 不可复苏性与PCO2的大幅增加有关。 到目前为止， 没有快速反应的心肌内PCO2电极， 完美 因此，我们将测量与PCO2相关的变化， 即pH和PCO2，在一个良好建立的猪模型中， 心脏骤停在我们的实验室发展待定 以及PCO2电极的可用性来满足这一需求。 如果我们的 假设这是“二氧化碳麻醉”的心脏， 对于不可复苏是正确的，我们将展示一个关闭 不可复苏性和最低pH值之间的关系 心肌和最大PCO2。 我们初步研究了高碳酸血症的影响， FiCO2为0.1和0.3的通气，预计 由PCO2增加引起的pH值下降将减少 心肌功能和复苏能力。 然后我们比较 NaHCO3和Na2CO3的影响， NaHCO3作为“CO2产生”缓冲剂降低pH，Na2CO3作为 “消耗CO2”的缓冲液将减少“CO2麻醉”， 心肌 然后，我们研究这些影响 碱化剂对心肌pH值和复苏能力的影响 开胸心肺复苏术，其中产生更有效的血液流动 心脏内压 然后，该模型适用于 非破坏性、闭合式胸部CPR，以研究48小时存活率 以及对治疗的神经反应等 特别是为了评估潜在的有益的影响， 缓冲剂。

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.