MYOCARDIAL ACID-BASE CHANGES DURING CPR

这项研究的目的是研究心肌细胞的变化。 二氧化碳，更具体地说，来测量 心内直视手术期间心肌pH和大静脉二氧化碳分压 心肺复苏(CPR)及其程度 确定心脏骤停后的可复苏性。 在心脏骤停期间，我们观察到严重的减少 肺血流量严重减少 清除二氧化碳。我们进一步观察到混合静脉和 冠状静脉窦二氧化碳分压明显升高。二氧化碳扩散 变成了组织。心肌(组织)pH值降低。此外, 心肌血流量的减少是厌氧性疾病的原因 心脏静脉中产生的乳酸随着乳酸的增加而增加 血。乳酸被重碳酸盐缓冲，重碳酸盐增加了 二氧化碳的产生，并进一步降低pH值。 由于二氧化碳的增加(pH的降低)是众所周知的 降低心肌收缩能力，我们假设 不可复苏性与二氧化碳分压的大幅增加有关。目前为止， 无快速反应的心肌内二氧化碳电极 完美无瑕。因此，我们将测量与PCO2相关的变化， 即pH和二氧化碳，在一个公认的猪的模型中 我们实验室发现的心脏骤停尚待开发 以及PCO2电极的可用性来满足这一需求。如果我们的 假设是心脏的“二氧化碳麻醉”导致的 对于不可复活是正确的，我们将展示一个结束 心脏不可复苏性与最低pH的关系 心肌和最大二氧化碳分压。 我们初步调查了高碳酸血症的影响。 使用FiCO2 0.1和0.3进行通风，并预期 二氧化碳浓度升高引起的酸碱度下降将会减少 心肌功能和复苏性。然后，我们比较 NaHCO3和Na2CO3的影响，预计 NaHCO3作为产生二氧化碳的缓冲液降低pH，Na2CO3作为 “二氧化碳消耗”生产缓冲液将减少“二氧化碳麻醉”。 心肌。然后我们研究这些因素的影响 碱性药物对心肌pH和复苏力的影响 开胸心肺复苏，可产生更有效的血液流动 心脏内受压。然后，对该模型进行修改以适应 无损、闭合胸腔心肺复苏术观察48小时存活率 以及对治疗的神经反应和更多 具体地说，评估潜在有益的 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.