From the CHU Nancy, Service de Réanimation Médicale Brabois, Pole Cardiovasculaire et Réanimation Médicale, Hôpital Brabois, Vandoeuvre les Nancy, France; Institut National de la Santé Et de la Recherche Médicale (INSERM) U1116, Equipe 2, Faculté de Médecine, Vandoeuvre les Nancy, France; Université de Lorraine, Nancy, France (A.K., N.D., and B.L.); INSERM U1116, Equipe 2, Faculté de Médecine, Vandoeuvre les Nancy, France; Université de Lorraine, Nancy, France (N.S., K.I., and C.S.); and Critallographie, Résonnance Magnétique et Modélisation (CRM2), Unité Médicale de Recherche (UMR), Centre National de la Recherche Scientifique (CNRS), Institut Jean Barriol, Faculté des Sciences et Technologies, Vandoeuvre les Nancy, France; Université de Lorraine, Nancy, France (J.-M.E. and S.L.).
Anesthesiology. 2014 Apr;120(4):926-34. doi: 10.1097/ALN.0000000000000077.
Lactic acidosis is associated with cardiovascular failure. Buffering with sodium bicarbonate is proposed in severe lactic acidosis. Bicarbonate induces carbon dioxide generation and hypocalcemia, both cardiovascular depressant factors. The authors thus investigated the cardiovascular and metabolic effects of an adapted sodium bicarbonate therapy, including prevention of carbon dioxide increase with hyperventilation and ionized calcium decrease with calcium administration.
Lactic acidosis was induced by hemorrhagic shock. Twenty animals were randomized into five groups: (1) standard resuscitation with blood retransfusion and norepinephrine (2) adapted sodium bicarbonate therapy (3) nonadapted sodium bicarbonate therapy (4) standard resuscitation plus calcium administration (5) hyperventilation. Evaluation was focused in vivo on extracellular pH, on intracellular pH estimated by P nuclear magnetic resonance and on myocardial contractility by conductance catheter. Aortic rings and mesenteric arteries were isolated and mounted in a myograph, after which arterial contractility was measured.
All animals in the hyperventilation group died prematurely and were not included in the statistical analysis. When compared with sham rats, shock induced extracellular (median, 7.13; interquartile range, [0.10] vs. 7.30 [0.01]; P = 0.0007) and intracellular acidosis (7.26 [0.18] vs. 7.05 [0.13]; P = 0.0001), hyperlactatemia (7.30 [0.01] vs. 7.13 [0.10]; P = 0.0008), depressed myocardial elastance (2.87 [1.31] vs. 0.5 [0.53] mmHg/μl; P = 0.0001), and vascular hyporesponsiveness to vasoconstrictors. Compared with nonadapted therapy, adapted bicarbonate therapy normalized extracellular pH (7.03 [0.12] vs. 7.36 [0.04]; P < 0.05), increased intracellular pH to supraphysiological values, improved myocardial elastance (1.68 [0.41] vs. 0.72 [0.44] mmHg/μl; P < 0.05), and improved aortic and mesenteric vasoreactivity.
A therapeutic strategy based on alkalinization with sodium bicarbonate along with hyperventilation and calcium administration increases pH and improves cardiovascular function.
乳酸酸中毒与心血管衰竭有关。在严重的乳酸酸中毒中,建议使用碳酸氢钠缓冲。碳酸氢盐会引起二氧化碳生成和低钙血症,这两种因素都会抑制心血管功能。因此,作者研究了一种改良的碳酸氢钠治疗方法的心血管和代谢效应,包括通过过度通气预防二氧化碳增加和通过钙给药预防离子钙降低。
通过失血性休克诱导乳酸酸中毒。将 20 只动物随机分为五组:(1)标准复苏加血液回输和去甲肾上腺素(2)改良碳酸氢钠治疗(3)非改良碳酸氢钠治疗(4)标准复苏加钙给药(5)过度通气。评估重点是细胞外 pH、通过 P 核磁共振估计的细胞内 pH 和通过电导导管测量的心肌收缩力。主动脉环和肠系膜动脉被分离并安装在肌动描记器中,然后测量动脉收缩性。
与假手术大鼠相比,过度通气组所有动物均过早死亡,未纳入统计分析。与假手术大鼠相比,休克引起细胞外(中位数,7.13;四分位距,[0.10] 与 7.30 [0.01];P = 0.0007)和细胞内酸中毒(7.26 [0.18] 与 7.05 [0.13];P = 0.0001)、高乳酸血症(7.30 [0.01] 与 7.13 [0.10];P = 0.0008)、心肌弹性降低(2.87 [1.31] 与 0.5 [0.53] mmHg/μl;P = 0.0001)和血管对血管收缩剂的低反应性。与非改良治疗相比,改良碳酸氢钠治疗使细胞外 pH 正常化(7.03 [0.12] 与 7.36 [0.04];P < 0.05),使细胞内 pH 升高至超生理水平,改善心肌弹性(1.68 [0.41] 与 0.72 [0.44] mmHg/μl;P < 0.05),并改善主动脉和肠系膜血管反应性。
基于碳酸氢钠碱化加过度通气和钙给药的治疗策略可提高 pH 值并改善心血管功能。