von Planta M, Bar-Joseph G, Wiklund L, Bircher N G, Falk J L, Abramson N S
IRRC, University of Pittsburgh, Pennsylvania 15260.
Ann Emerg Med. 1993 Feb;22(2 Pt 2):404-10. doi: 10.1016/s0196-0644(05)80471-8.
Acid-base changes occurring during cardiac arrest and subsequent CPR are related to a complex low-perfusion state characterized clinically by venous and tissue hypercarbic and metabolic (lactic) acidosis. This low-flow state is a dynamic process dependent on the time intervals between onset of arrest, initiation of CPR, and restoration of adequate spontaneous circulation. Increased release of CO2 from ischemic tissues and reduced CO2 transport from the tissues to the lungs result in profound tissue acidosis. However, recent experimental data suggest that even very low pH is compatible with neurologically intact survival. Thus, the clinical use of buffer agents, and especially of sodium bicarbonate, is currently controversial. Because results of controlled clinical studies are not available, a careful review of well-performed experimental studies is necessary. So far, the use of either CO2-generating or CO2-consuming buffers has not been proved conclusively to increase neurologically intact long-term survival after CPR. More importantly, adequate ventilation and effective chest compressions must be quickly established after cardiac arrest. This will counterbalance the hypercarbic and metabolic acidemia of cardiac arrest by creating concurrent hypocarbic arterial alkalemia during at least the early phase of CPR. Thus, the treatment of the complex acid-base changes associated with CPR is based primarily on the classical maneuvers of A and B (airway and breathing = adequate oxygenation and ventilation), C (chest compressions), and D (early defibrillation for rapid restoration of spontaneous circulation). In cases of prolonged cardiac arrest or preexisting metabolic acidemia, buffer therapy may be indicated.
心脏骤停及后续心肺复苏期间发生的酸碱变化与一种复杂的低灌注状态有关，临床上其特征为静脉血和组织高碳酸血症以及代谢性（乳酸）酸中毒。这种低血流状态是一个动态过程，取决于心脏骤停发作、开始心肺复苏以及恢复充分自主循环之间的时间间隔。缺血组织中二氧化碳释放增加以及二氧化碳从组织向肺部的转运减少导致严重的组织酸中毒。然而，最近的实验数据表明，即使是非常低的pH值也与神经功能完好的存活情况相符。因此，缓冲剂尤其是碳酸氢钠在临床上的应用目前存在争议。由于缺乏对照临床研究的结果，有必要仔细回顾精心开展的实验研究。到目前为止，使用产生二氧化碳或消耗二氧化碳的缓冲剂尚未被确凿证明能增加心肺复苏后神经功能完好的长期存活率。更重要的是，心脏骤停后必须迅速建立充分的通气和有效的胸外按压。这将通过在至少心肺复苏的早期阶段产生并发的低碳酸血症性动脉碱血症来抵消心脏骤停的高碳酸血症和代谢性酸血症。因此，与心肺复苏相关的复杂酸碱变化的治疗主要基于A和B（气道和呼吸 = 充分的氧合和通气）、C（胸外按压）以及D（早期除颤以快速恢复自主循环）这些经典操作。在长时间心脏骤停或既往存在代谢性酸血症的情况下，可能需要进行缓冲治疗。
