• Antoine Kimmoun, Nicolas Ducrocq, Nacira Sennoun, Khodr Issa, Charlène Strub, Jean-Marie Escanyé, Sébastien Leclerc, and Bruno Levy.
• 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 1;120(4):926-34.

BackgroundLactic 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.MethodsLactic 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.ResultsAll 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.ConclusionsA therapeutic strategy based on alkalinization with sodium bicarbonate along with hyperventilation and calcium administration increases pH and improves cardiovascular function.

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