Cooper D J, Walley K R, Wiggs B R, Russell J A
St. Paul's Hospital, University of British Columbia, Vancouver, Canada.
Ann Intern Med. 1990 Apr 1;112(7):492-8. doi: 10.7326/0003-4819-112-7-492.
To determine whether correction of acidemia using bicarbonate improves hemodynamics in patients who have lactic acidosis.
Prospective, randomized, blinded, crossover study. Each patient sequentially received sodium bicarbonate and equimolar sodium chloride. The order of the infusions was randomized.
Intensive care unit of a tertiary care hospital.
Fourteen patients who had metabolic acidosis (bicarbonate less than 17 mmol/L and base excess less than -10) and increased arterial lactate (mean, 7.8 mmol/L). All had pulmonary artery catheters and 13 were receiving catecholamines.
Sodium bicarbonate (2 mmol/kg body weight over 15 minutes) increased arterial pH (7.22 to 7.36, P less than 0.001), serum bicarbonate (12 to 18 mmol/L, P less than 0.001), and partial pressure of CO2 in arterial blood (PaCO2) (35 to 40 mm Hg, P less than 0.001) and decreased plasma ionized calcium (0.95 to 0.87 mmol/L, P less than 0.001). Sodium bicarbonate and sodium chloride both transiently increased pulmonary capillary wedge pressure (15 to 17 mm Hg, and 14 to 17 mm Hg, P less than 0.001) and cardiac output (18% and 16%, P less than 0.01). The mean arterial pressure was unchanged. Hemodynamic responses to sodium bicarbonate and sodium chloride were the same. These data have more than 90% power of detecting a 0.5 L/min (7%) change in mean cardiac output after administration of sodium bicarbonate compared with that after sodium chloride. Even the 7 most acidemic patients (mean pH, 7.13; range, 6.90 to 7.20) had no significant hemodynamic changes after either infusion.
Correction of acidemia using sodium bicarbonate does not improve hemodynamics in critically ill patients who have metabolic acidosis and increased blood lactate or the cardiovascular response to infused catecholamines in these patients. Sodium bicarbonate decreases plasma ionized calcium and increases PaCO2.
确定使用碳酸氢盐纠正酸血症是否能改善乳酸酸中毒患者的血流动力学。
前瞻性、随机、双盲、交叉研究。每位患者依次接受碳酸氢钠和等摩尔的氯化钠。输注顺序随机。
一家三级医院的重症监护病房。
14例患有代谢性酸中毒(碳酸氢盐低于17 mmol/L且碱剩余低于-10)且动脉血乳酸升高(平均7.8 mmol/L)的患者。所有患者均有肺动脉导管,13例正在接受儿茶酚胺治疗。
碳酸氢钠(15分钟内2 mmol/kg体重)使动脉pH值升高(从7.22升至7.36,P<0.001)、血清碳酸氢盐升高(从12 mmol/L升至18 mmol/L,P<0.001)、动脉血二氧化碳分压(PaCO2)升高(从35 mmHg升至40 mmHg,P<0.001),并使血浆离子钙降低(从0.95 mmol/L降至0.87 mmol/L,P<0.001)。碳酸氢钠和氯化钠均使肺毛细血管楔压短暂升高(分别为15至17 mmHg和14至17 mmHg,P<0.001),心输出量增加(分别为18%和16%,P<0.01)。平均动脉压无变化。对碳酸氢钠和氯化钠的血流动力学反应相同。与输注氯化钠后相比,这些数据有超过90%的把握检测到输注碳酸氢钠后平均心输出量有0.5 L/min(7%)的变化。即使是7例最酸血症的患者(平均pH值7.13;范围6.90至7.20),在输注任何一种溶液后血流动力学均无显著变化。
使用碳酸氢钠纠正酸血症并不能改善患有代谢性酸中毒且血乳酸升高的重症患者的血流动力学,也不能改善这些患者对输注儿茶酚胺的心血管反应。碳酸氢钠会降低血浆离子钙并升高PaCO2。