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last updated: November 30, 2016

Orlando Debesa

Effects of Bicarbonate

therapy on hemodynamics

and tissue oxygenation in

patients with lactic acidosis

Sodium Bicarbonate

for the treatment of

lactic acidosis

Sodium Bicarbonate

for Correction of

Metabolic Acidosis in

Open-Heart Surgery

Bicarbonate does not

improve hemodynamics

in Critically Ill patients 

who have lactic acidosis

Lactic acidosis on

LV performance

Lactic acidosis is a common finding in the post-operative cardiac surgery patient. There are many causes of lactic acidosis which can be divided into Type A and Type B. Mild lactic acidosis is common but severe or persistent lactic acidosis is a nonspecific sign of tissue hypoperfusion associated with an unfavorable prognosis and monitoring the blood lactate level during and after cardiac surgery is a valuable tool in identifying the patients who have the potential to deteriorate (1). Acquired lactic acidosis during cardiac surgery is almost always caused by excessive acid production that overwhelms the buffering capacity of the body and exceeds the ability of the kidneys and lung to eliminate the excess acid. The detection of lactic acidosis should prompt a search for sites of tissue ischemia and initiation of medical interventions to improve tissue perfusion. Despite the frequency of this problem, considerable controversy exists regarding the physiologic consequences of acute lactic acidosis and the role of sodium bicarbonate for the treatment of this problem.

Lactic Acidosis Physiology

Lactic acidosis causes a decrease in the pH (increase in protons) activating the following compensatory mechanism:

  • increase in respiratory rate causes an increase in minute ventilation and concomitant decrease in arterial PaCO2. There is only so much compensation that can be achieved this way. To figure out what the appropriate compensation should be, one can calculate Winter's formula (PaCO2 (mm Hg) = 1.5 [HCO3 - ]±2) 

  • right shift of the oxygen-hemoglobin dissociation curve favors the unloading of oxygen at the tissue level

  • release of endogenous catecholamines

Lactic acidosis also has the following deleterious effects:​

  • direct myocardial depression

  • decrease response of the myocardium to catecholamines (receptor regulation??)

  • arterial vasodilation

  • bradycardia 


Cardiovascular deterioration in the clinical setting is more difficult to establish because it is not possible to separate the independent cardiovascular actions of acidosis from the cardiovascular effects of the underlying conditions that produce acidosis.


It has been demonstrated that lactic acidosis has a negative inotropic effect on the left ventricle with a decrease responsiveness to exogenous catecholamines. In addition, laboratory investigations suggest that severe metabolic acidosis with pH values less than 7.2 cause the release of endogenous catecholamines, direct myocardial depression, a decreased responsiveness of the myocardium to catecholamines, arterial vasodilation, and even bradycardia at extremely low pH values (2). Based on these laboratory findings, a pH value of 7.2 is commonly considered the clinical threshold for treatment with alkalinizing agents such as sodium bicarbonate. 


(1) Toraman F, Evrenkaya S, Yuce M, Aksoy N, Karabulut H, Bozkulak Y, Alhan C. Lactic acidosis after cardiac surgery is associated with adverse outcome. Heart Surg Forum. 2004 Apr 1;7(2):E155-9.

(2) Wildenthal K, Mierzwiak DS, Myers RW, Mitchell JH. Effects of acute lactic acidosis on left ventricular performance. Am J Physiol. 1968 Jun;214(6):1352-9.

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