BUFFER AGENTS DO NOT REVERSE INTRAMYOCARDIAL ACIDOSIS DURING CARDIAC RESUSCITATION
BUFFER AGENTS DO NOT REVERSE INTRAMYOCARDIAL ACIDOSIS DURING CARDIAC RESUSCITATION
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DOI：
10.1161/01.cir.81.5.1660
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发表时间：
1990-05-01
期刊：
影响因子：
37.8
通讯作者：
RACKOW, EC
中科院分区：
文献类型：
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作者：
KETTE, F;WEIL, MH;RACKOW, EC
我们研究了二氧化碳产生和二氧化碳消耗缓冲液对心肌内pH值和心脏复苏能力的影响。在29只猪中，用玻璃电极通过血管窗进入左心室后壁的中层心肌连续测量心肌内pH。通过向左心室的心外膜施加交流电来电诱发心室颤动（VF）。VF 3分钟后，开始心前区按压并持续8分钟。在心脏复苏期间，将碳酸氢钠（一种二氧化碳产生缓冲液）、碳酸氢钠（一种二氧化碳消耗缓冲液）和高渗氯化钠（对照溶液）输注到右心房。在VF 11分钟后，通过经胸直流电电击尝试除颤。心肌内pH值从VF前的平均值7.26逐渐下降到输注缓冲液前的6.87。两种缓冲剂给药后，体循环和心大静脉pH值显著升高。然而，心室颤动11分钟后，心肌内pH值继续下降至平均6.62，缓冲液或生理盐水对照组均未改变这种下降。在以前的研究中，复苏是密切相关的冠状动脉灌注压在直流电抗休克的时间，但没有pH值。因此，逆转酸中毒的理由，通过这些缓冲剂的管理是不支持的。更重要的是，在心脏骤停的受控实验条件下，消耗二氧化碳或产生二氧化碳的缓冲液都不能改变心肌酸中毒或改善心肌复苏能力。
We investigated the effects of carbon dioxide-producing and carbon dioxide-consuming buffers on intramyocardial pH and on cardiac resuscitability. In 29 pigs, intramyocardial pH was continuously measured with a glass electrode advanced into the midmyocardium of the posterior left ventricle through a diaphragmatic window. Ventricular fibrillation (VF) was electrically induced by alternating current applied to the epicardium of the left ventricle. After 3 minutes of VF, precordial compression was begun and continued for an interval of 8 minutes. Sodium bicarbonate (a carbon dioxide-generating buffer), Carbicarb (a carbon dioxide-consuming buffer), and hypertonic sodium chloride (control solution) were infused into the right atrium during cardiac resuscitation. Defibrillation was attempted by transthoracic direct-current shock after 11 minutes of VF. Intramyocardial pH progressively decreased from an average value of 7.26 before VF to 6.87 before infusion of buffers. Systemic circulation and great cardiac vein pH significantly increased after administration of the two buffer agents. However, intramyocardial pH continued to decline to an average of 6.62 after 11 minutes of VF, and this decline was not altered by either buffer solution or by the saline controls. As in previous studies, resuscitability was closely related to coronary perfusion pressure at the time of direct-current countershock but not to pH. Accordingly, the rationale of reversing acidosis by the administration of these buffer agents is not supported. Even more important, neither carbon dioxide-consuming nor carbon dioxide-producing buffers altered myocardial acidosis or improved myocardial resuscitability under controlled experimental conditions of cardiac arrest.