心脏病患者使用碳酸氢钠的代谢和血流动力学后果。

Metabolic and hemodynamic consequences of sodium bicarbonate administration in patients with heart disease.

作者信息

Bersin R M, Chatterjee K, Arieff A I

机构信息

Cardiology Division, University of California Medical Center, San Francisco.

出版信息

Am J Med. 1989 Jul;87(1):7-14. doi: 10.1016/s0002-9343(89)80476-0.

DOI:10.1016/s0002-9343(89)80476-0

PMID:2741982

Abstract

PURPOSE

The use of sodium bicarbonate (NaHCO3) in cardiopulmonary arrest has been questioned, but the effects of NaHCO3 in patients with heart disease are not known. We therefore prospectively evaluated the effects of NaHCO3 in patients with congestive heart failure.

PATIENTS AND METHODS

Ten patients received NaHCO3 and control infusions of equimolar sodium chloride (NaCl). Measurements were made of blood gases, 2,3-diphosphoglyceric acid (2,3-DPG), glucose, lactate, cardiac hemodynamics, and oxygen consumption.

RESULTS

The arterial oxygen tension (pO2) fell an average of 10 mm Hg after NaHCO3 administration in patients with congestive heart failure, whereas it rose with NaCl (p less than 0.005). Myocardial oxygen consumption decreased by 17% (p less than 0.002) without an accompanying change in oxygen demand. Systemic oxygen consumption fell by 21%. Red blood cell 2,3-DPG levels were elevated at baseline, but did not change with NaHCO3 administration. The oxygen pressure at 50% hemoglobin saturation (P50) was correspondingly elevated at baseline in these patients and decreased significantly with NaHCO3 (Bohr effect) (p less than 0.003). The arterial and mixed venous carbon dioxide tensions increased with NaHCO3 but decreased with NaCl administration (p less than 0.05). Blood glucose concentrations fell by 1.7 mmol/L with NaHCO3 (p less than 0.003) and blood lactate concentrations increased uniformly (p less than 0.001). Three patients developed net myocardial lactate generation during NaHCO3 administration; two of these three developed symptoms of angina. Coronary blood flow did not change with NaHCO3 but increased with NaCl (p less than 0.04). Two patients developed transient pump failure.

CONCLUSION

These data demonstrate that NaHCO3 impairs arterial oxygenation and reduces systemic and myocardial oxygen consumption. The decrease in oxygen utilization is associated with anaerobic metabolism, enhanced glycolysis, and elevation of the blood lactate level, and may lead to transient myocardial ischemia in some patients. Thus, the use of NaHCO3 in such patients warrants re-evaluation.

摘要

目的

碳酸氢钠（NaHCO₃）在心肺复苏中的应用一直存在争议，但其对心脏病患者的影响尚不清楚。因此，我们前瞻性地评估了NaHCO₃对充血性心力衰竭患者的影响。

患者与方法

10例患者接受了NaHCO₃和等摩尔氯化钠（NaCl）的对照输注。对血气、2,3-二磷酸甘油酸（2,3-DPG）、葡萄糖、乳酸、心脏血流动力学和氧消耗进行了测量。

结果

充血性心力衰竭患者给予NaHCO₃后，动脉血氧分压（pO₂）平均下降10mmHg，而给予NaCl后则升高（p＜0.005）。心肌氧消耗下降了17%（p＜0.002），而氧需求无相应变化。全身氧消耗下降了21%。红细胞2,3-DPG水平在基线时升高，但给予NaHCO₃后未发生变化。这些患者在基线时血红蛋白饱和度为50%时的氧分压（P50）相应升高，而给予NaHCO₃后显著降低（玻尔效应）（p＜0.003）。动脉血和混合静脉血二氧化碳分压随NaHCO₃升高，但随NaCl输注降低（p＜0.05）。给予NaHCO₃后血糖浓度下降1.7mmol/L（p＜0.003），血乳酸浓度均升高（p＜0.001）。3例患者在给予NaHCO₃期间出现净心肌乳酸生成；这3例中的2例出现心绞痛症状。冠状动脉血流给予NaHCO₃后未改变，但给予NaCl后增加（p＜0.04）。2例患者出现短暂性泵衰竭。