Mark N H, Leung J M, Arieff A I, Mangano D T
Department of Anesthesia, Department of Veterans Affairs Medical Center, San Francisco, CA 94121.
Crit Care Med. 1993 May;21(5):659-65.
Recent recommendations suggest that sodium bicarbonate may not be useful for the treatment of metabolic acidosis. However, these recommendations are based primarily on both clinical studies and animal models of metabolic acidosis with arterial hypoxemia (PaO2 of < 80 torr [< 10.7 kPa]). This study was designed to determine the safety and physiologic effects of low-dose sodium bicarbonate in humans who developed intraoperative metabolic acidosis in the absence of hypoxemia.
Prospective, double-blind, randomized trial.
Veterans Affairs Medical Center (a teaching hospital of the University of California, San Francisco).
We prospectively studied 40 patients with coronary artery disease who underwent major surgery and developed mild intraoperative metabolic acidosis (decrease of plasma bicarbonate by > 3 mM).
Patients were randomly assigned to receive either sodium bicarbonate (n = 20) or sodium chloride (n = 20) by intravenous bolus, up to a maximum dose of 88 mmol of sodium.
Bicarbonate treatment significantly increased the mean arterial pH from 7.36 to 7.39; the mean serum bicarbonate concentration from 21 to 25 mmol/L; and PCO2 from 41 to 44 torr (5.5 to 5.9 kPa). Total body oxygen consumption and lactate production did not change. Similarly, no adverse changes occurred in systemic or pulmonary arterial pressures or in cardiac ejection fraction. After bicarbonate administration, both the cardiac output and systemic oxygen consumption decreased by 8% to 11%, while both variables increased by 13% after sodium chloride administration; but, none of the changes was significant. One patient in the bicarbonate group developed myocardial ischemia, compared with three patients in the saline group.
Administration of sodium bicarbonate to well-oxygenated patients with mild metabolic acidosis resulted in a correction of the acidosis, without significant changes in cardiac output, total body oxygen use, or PaO2 (oxygen tension). These effects remain to be validated in patients with hypoxemia, more severe acidosis, or less stable circulation.
近期的建议表明，碳酸氢钠可能对代谢性酸中毒的治疗并无作用。然而，这些建议主要基于代谢性酸中毒合并动脉血氧不足（动脉血氧分压[PaO2]<80托[<10.7千帕]）的临床研究和动物模型。本研究旨在确定低剂量碳酸氢钠对术中发生代谢性酸中毒且无低氧血症患者的安全性及生理效应。
前瞻性、双盲、随机试验。
退伍军人事务医疗中心（加利福尼亚大学旧金山分校的一家教学医院）。
我们前瞻性地研究了40例接受大手术且术中发生轻度代谢性酸中毒（血浆碳酸氢盐降低>3毫摩尔/升）的冠心病患者。
患者被随机分配通过静脉推注接受碳酸氢钠（n = 20）或氯化钠（n = 20），最大钠剂量为88毫摩尔。
碳酸氢盐治疗使平均动脉pH值从7.36显著升至7.39；平均血清碳酸氢盐浓度从21毫摩尔/升升至25毫摩尔/升；二氧化碳分压从41托（5.5千帕）升至44托（5.9千帕）。全身氧耗量和乳酸生成量未改变。同样，体循环或肺动脉压以及心脏射血分数未出现不良变化。给予碳酸氢盐后，心输出量和全身氧耗量均下降8%至11%，而给予氯化钠后这两个变量均增加13%；但所有变化均无统计学意义。碳酸氢盐组有1例患者发生心肌缺血，而生理盐水组有三例。
对轻度代谢性酸中毒且氧合良好的患者给予碳酸氢钠可纠正酸中毒，心输出量、全身氧利用或动脉血氧分压（氧张力）无显著变化。这些效应仍有待在合并低氧血症、更严重酸中毒或循环更不稳定的患者中得到验证。
