Chest
Volume 117, Issue 1, January 2000, Pages 260-267
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Clinical Investigations in Critical Care
Sodium Bicarbonate for the Treatment of Lactic Acidosis

https://doi.org/10.1378/chest.117.1.260Get rights and content

Lactic acidosis often challenges the intensivist and is associatedwith a strikingly high mortality. Treatment involves discerning andcorrecting its underlying cause, ensuring adequate oxygen delivery totissues, reducing oxygen demand through sedation and mechanicalventilation, and (most controversially) attempting to alkalinize theblood with IV sodium bicarbonate. Here we review the literature toanswer the following questions: Is a low pH bad? Can sodium bicarbonateraise the pH in vivo? Does increasing the blood pH withsodium bicarbonate have any salutary effects? Does sodium bicarbonatehave negative side effects? We find that the oft-cited rationale forbicarbonate use, that it might ameliorate the hemodynamic depression ofmetabolic acidemia, has been disproved convincingly. Further, given thelack of evidence supporting its use, we cannot condone bicarbonateadministration for patients with lactic acidosis, regardless of thedegree of acidemia.

Section snippets

Is a Low pH Bad?

Proteins, which underlie the function and structure of human cells, contain areas of both positive and negative charge and are thereby sensitive to the pH of the surrounding milieu. One can conceive of innumerable ways in which excess acid could impair protein function and, by extension, the function of the whole body. Yet it is overly simplistic to assume that the clinician's window on acid-base state, the arterial blood pH, reflects accurately the pH at a (likely more important) cellular

Can Sodium Bicarbonate Raise the pH In Vivo?

It seems straightforward that adding a base to acidic blood will raise the pH–the reality is more complex. First, bicarbonate is not one of the independent determinants of the blood pH. Rather, these include the difference between the total concentrations of strong cations and anions (the strong ion difference, [SID]); the total concentration of weak acids; and the Paco2.44 Administration of exogenous sodium bicarbonate increases the SID (which tends to raise the pH) because sodium is a strong

Does Increasing the Blood pH With Sodium Bicarbonate Have any Salutary Effects?

The most direct question to pose regarding sodium bicarbonate therapy is whether it improves the problems that prompt its use. Namely, does it correct hemodynamics, “buy time” for other interventions, or improve outcome?

In isolated rat or rabbit hearts perfused with acidic solutions, bicarbonate fails to augment ventricular contractility.11, 71 In whole animals (including various models of metabolic acidosis), the effects of bicarbonate on ventricular function are more difficult to tease out

Does Sodium Bicarbonate Have Negative Side Effects?

The most obvious side effects of sodium bicarbonate are the fluid and sodium load. This can cause hypervolemia, hyperosmolarity, and hypernatremia.82 Sodium bicarbonate given as a rapid IV bolus can cause a transient fall in mean arterial pressure and a transient rise in intracranial pressure83 that is probably related to its hypertonicity, and this is alleviated when given as a slow IV infusion. Sodium bicarbonate has been shown in three studies to lower Pao2 from 5 to 15 mm Hg in both

Other Alkalinizing Therapies: Carbicarb, Dichloroacetate, Tris-Hydroxymethyl Aminomethane, and Dialysis

Carbicarb is an equimolar mixture of sodium carbonate and sodium bicarbonate. Compared with sodium bicarbonate, Carbicarb raises the SID (thereby the pH) far more45, 4849, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62 and boosts the Pco2 far less48, 49, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62, 63, 64 when given IV to animals with metabolic acidosis. To the extent that the failure of sodium bicarbonate to effect hemodynamic improvement is caused by the generation of carbon

Conclusion

Sodium bicarbonate is clearly effective in raising the arterial pH in critically ill patients with lactic acidosis. The impact on intracellular pH is unknown in such patients, but extrapolation from extensive animal studies suggests that it is negative. Despite the correction of arterial acidemia, sodium bicarbonate, like DCA, has no favorable cardiovascular effects, even for patients with severe acidemia and receiving continuous infusions of catecholamines. Although hemodynamic improvement is

References (91)

  • JM Ritter et al.

    Paradoxical effect of bicarbonate on cytoplasmic pH

    Lancet

    (1990)
  • J Levraut et al.

    Effect of sodium bicarbonate on intracellular pH under different buffering conditions

    Kidney Int

    (1996)
  • M Tanaka et al.

    Normovolemic hemodilution attenuates cardiac depression induced by sodium bicarbonate in canine metabolic acidosis

    Br J Anaesth

    (1996)
  • E Lever et al.

    Sodium bicarbonate therapy in severe diabetic ketoacidosis

    Am J Med

    (1983)
  • D Roberts et al.

    Early predictors of mortality for hospitalized patients suffering cardiopulmonary arrest

    Chest

    (1990)
  • JA Máttar et al.

    Cardiac arrest in the critically ill: II. Hyperosmolal states following cardiac arrest

    Am J Med

    (1974)
  • JS Huseby et al.

    Hemodynamic effects of rapid bolus hypertonic sodium bicarbonate

    Chest

    (1981)
  • RM Bersin et al.

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

    Am J Med

    (1989)
  • PW Stacpoole

    The pharmacology of dichloroacetate

    Metabolism

    (1989)
  • ND Vaziri et al.

    Bicarbonate-buffered peritoneal dialysis: an effective adjunct in the treatment of lactic acidosis

    Am J Med

    (1979)
  • MH Weil et al.

    Experimental and clinical studies on lactate and pyruvate as indicators of the severity of acute circulatory failure (shock)

    Circulation

    (1970)
  • DJ Cooper et al.

    Bicarbonate does not improve hemodynamics in critically ill patients who have lactic acidosis: a prospective, controlled clinical study

    Ann Intern Med

    (1990)
  • PW Stacpoole et al.

    A controlled clinical trial of dichloroacetate for treatment of lactic acidosis in adults

    N Engl J Med

    (1992)
  • AS Minot et al.

    The acidosis of guanidine intoxication

    J Clin Invest

    (1934)
  • HJ Adrogué et al.

    Management of life-threatening acid-base disorders: second of two parts

    N Engl J Med

    (1998)
  • A Warner et al.

    Treatment of lactic acidosis

    South Med J

    (1981)
  • JV Bonventre et al.

    Effects of metabolic acidosis on viability of cells exposed to anoxia

    Am J Physiol

    (1985)
  • PA Poole-Wilson et al.

    Effect of pH on ionic exchange and function in rat and rabbit myocardium

    Am J Physiol

    (1975)
  • JI Shapiro

    Functional and metabolic responses of isolated hearts to acidosis: effects of sodium bicarbonate and Carbicarb

    Am J Physiol

    (1990)
  • HE Cingolani et al.

    Depression of human myocardial contractility with “respiratory” and “metabolic” acidosis

    Surgery

    (1975)
  • T Nakanishi et al.

    Influence of acidosis on inotropic effect of catecholamines in newborn rabbit hearts

    Am J Physiol

    (1987)
  • CH Orchard et al.

    Effects of pH change on the contractile function of cardiac muscle

    Am J Physiol

    (1990)
  • SE Downing et al.

    Cardiovascular responses to metabolic acidosis

    Am J Physiol

    (1965)
  • DJ Cooper et al.

    Bicarbonate does not increase left ventricular contractility duringl-lactic acidemia in pigs

    Am Rev Respir Dis

    (1993)
  • K Wildenthal et al.

    Effects of acute lactic acidosis on left ventricular performance

    Am J Physiol

    (1968)
  • J-B Thorens et al.

    Effects of rapid permissive hypercapnia on hemodynamics, gas exchange, and oxygen transport and consumption during mechanical ventilation for the acute respiratory distress syndrome

    Intensive Care Med

    (1996)
  • F Feihl et al.

    Permissive hypercapnia: how permissive should we be?

    Am J Respir Crit Care Med

    (1994)
  • DV Tuxen et al.

    Use of a measurement of pulmonary hyperinflation to control the level of mechanical ventilation in patients with acute severe asthma

    Am Rev Respir Dis

    (1992)
  • KG Hickling et al.

    Low mortality rate in adult respiratory distress syndrome using low-volume, pressure-limited ventilation with permissive hypercapnia: a prospective study

    Crit Care Med

    (1994)
  • A Bidani et al.

    Permissive hypercapnia in acute respiratory failure

    JAMA

    (1994)
  • E Roupie et al.

    Titration of tidal volume and induced hypercapnia in acute respiratory distress syndrome

    Am J Respir Crit Care Med

    (1995)
  • G Gamba et al.

    Bicarbonate therapy in severe diabetic ketoacidosis: a double-blind, randomized, placebo controlled trial

    Rev Invest Clin

    (1991)
  • B Goldstein et al.

    Supercarbia in children: clinical course and outcome

    Crit Care Med

    (1990)
  • BS Meldrum et al.

    Physiology of status epilepticus in primates

    Arch Neurol

    (1973)
  • HR Beresford et al.

    Changes in brain lactate during induced cerebral seizures

    Arch Neurol

    (1969)
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