© 2000
<http://www.chestjournal.org/misc/terms.shtml>American
College of Chest Physicians
Sodium Bicarbonate for the Treatment of Lactic Acidosis*
Sean M. Forsythe, MD and Gregory A. Schmidt, MD, FCCP
* From the Department of Medicine (Dr. Forsythe)
and the Section of Pulmonary and Critical Care
(Dr. Schmidt), University of Chicago School of Medicine, Chicago, IL.
Correspondence to: Gregory A. Schmidt, MD, FCCP,
Section of Pulmonary and Critical Care: MC6026,
5841 S. Maryland Ave, Chicago, IL 60637; e-mail:
<mailto:gschmidt@medicine.bsd.uchicago.edu>gschmidt@medicine.bsd.uchicago.edu
Lactic acidosis often challenges the intensivist
and is associated with a strikingly high
mortality. Treatment involves discerning and
correcting its underlying cause, ensuring
adequate oxygen delivery to tissues, reducing
oxygen demand through sedation and mechanical
ventilation, and (most controversially)
attempting to alkalinize the blood with IV sodium
bicarbonate. Here we review the literature to
answer the following questions: Is a low pH bad?
Can sodium bicarbonate raise the pH in vivo? Does
increasing the blood pH with sodium bicarbonate
have any salutary effects? Does sodium
bicarbonate have negative side effects? We find
that the oft-cited rationale for bicarbonate use,
that it might ameliorate the hemodynamic
depression of metabolic acidemia, has been
disproved convincingly. Further, given the lack
of evidence supporting its use, we cannot condone
bicarbonate administration for patients with
lactic acidosis, regardless of the degree of acidemia.
Cooper, D. J., et al, "Bicarbonate does not
improve hemodynamics in critically ill patients
who have lactic acidosis," Annals Internal Med. 112: 492-498 (1990)
Ritter, J. M., et al, "Paradoxical effect of
bicarbonate on cytoplasmic pH," Lancet 335: 1243-1246 (1990)
Stacpoole, P. W., "Lactic acidosis: The case
against bicarbonate therapy," Annals Internal Med. 105: 276-279 (1986)
(Chest. 2001;119:1622-1623.)
© 2001
<http://www.chestjournal.org/misc/terms.shtml>American
College of Chest Physicians
Evaluating Sodium Bicarbonate Controversy
Viktor Rosival, PhD
Dérer's Hospital Bratislava, Slovakia
Correspondence to: Viktor Rosival, PhD, Dérer's
Hospital, Department of Clinical Biochemistry,
Limbová 5, SK-833 05 Bratislava, Slovakia
To the Editor:
The discussion of the article "Sodium Bicarbonate
Controversy in Lactic Acidosis" by Cuhaci et al
(September
2000)<http://www.chestjournal.org/cgi/content/full/119/5/1622#B1>1
is very interesting. Since the last sentence of
the article states "We hope that our article
generates discussion, causes critical evaluation
of the data, and provokes clinicians to rethink
the use of bicarbonate for patients with lactic
acidosis," I would like to point out some aspects
of the article that could help the "critical evaluation of the data."
According to
Kellum,<http://www.chestjournal.org/cgi/content/full/119/5/1622#B2>2
"lactate is more important as a marker of disease
than as an etiologic factor per se." In other
words, if lactic acidosis is dangerous, the
killer is the hydrogen cation H+ and not the
lactate anion. This also means that the dangerous
effects of H+ are independent of the name and
chemical structure of the accompanying anion (or anions).
In contrast to observations in experiments with
animals, reporting negative cardiovascular
effects of increased concentrations of H+
(usually expressed as its negative decadic
logarithm, decreased pH) in human patients is
most important because of its influence on the
level of consciousness of the
patient.<http://www.chestjournal.org/cgi/content/full/119/5/1622#B3>3
The glycolytic enzyme phosphofructokinase is pH
dependent, and decreasing pH (in the range
observed in humans) inhibits its activity,
resulting in the impaired utilization of glucose.
The main consequence of this is the decreased
activity of brain cells, a condition that
eventually ends in death because glucose is the
main energy source of brain cells.
When Cuhaci et
al<http://www.chestjournal.org/cgi/content/full/119/5/1622#B1>1
asked "How many humans have the authors seen who
could survive with a pH < 7.0," one can assume
that they had seen the majority of such patients
die. According to Lever and
Jaspan,<http://www.chestjournal.org/cgi/content/full/119/5/1622#B4>4
full alertness occurs very seldom in patients who
have a pH < 7.0. Therefore, I am sure that the
patients of Cuhaci et al who died with a pH < 7.0
were comatose during the last hours or days before their deaths.
It is very probable that in such comatose
patients who have very low blood pH levels, a
substantial increase in or normalization of their
blood pH could be lifesaving (if the coma was not
caused directly by the underlying disease, eg,
cerebral hemorrhage), no matter how this increase
would be achieved (eg, sodium bicarbonate,
carbicarb, hemodialysis, etc). It seems that the
administration of sodium bicarbonate is the
simplest method for increasing low blood pH. And,
according to Lever and
Jaspan,<http://www.chestjournal.org/cgi/content/full/119/5/1622#B4>4
this method is also effective and safe; all 27
comatose patients with blood pH levels < 7.10
recovered to full alertness simultaneously with
an increase or normalization of their blood pH
after IV sodium bicarbonate administration. No
deaths and no adverse reactions to sodium bicarbonate have been observed.
* Cuhaci, B, Lee, J, Ahmed, Z (2000) Sodium
bicarbonate controversy in lactic acidosis. Chest 118,882-883
* Posner, JB, Plum, F (1967) Spinal-fluid pH
and neurologic symptoms in systemic acidosis N Engl J Med 277,605-613
* Hoffman, EK, Simonsen, LO (1989) Membrane
mechanisms in volume and pH regulation in
vertebrate cells Physiol Rev
69,315-382<http://www.chestjournal.org/cgi/ijlink?linkType=PDF&journalCode=physrev&resid=69/2/315>[Free<http://www.chestjournal.org/cgi/ijlink?linkType=PDF&journalCode=physrev&resid=69/2/315>
Full Text]
* Lidofsky, SD, Fitz, JG, Scharschmidt, BF
(1993) Mechanisms and functional role of
intracellular pH regulation in hepatocytes Prog
Liver Dis
11,69-83<http://www.chestjournal.org/cgi/external_ref?access_num=8272517&link_type=MED>[Medline]
* Potkin, RT, Swenson, ER (1992)
Resuscitation from severe acute hypercapnia:
determinants of tolerance and survival Chest
102,1742-1745<http://www.chestjournal.org/cgi/ijlink?linkType=ABST&journalCode=chest&resid=102/6/1742>[Abstract/Free<http://www.chestjournal.org/cgi/ijlink?linkType=ABST&journalCode=chest&resid=102/6/1742>
Full Text]
* Siggaard-Andersen O. Chapter II: normal
values and extreme values in acid base status of
blood. Scand J Clin Lab Invest 1963; 15:S70:26–29
* Adrogue', HJ, Madias, NE (1998) Management
of life-threatening acid-base disorders: second
of two parts N Engl J Med
338,107-111<http://www.chestjournal.org/cgi/ijlink?linkType=FULL&journalCode=nejm&resid=338/2/107>[Free<http://www.chestjournal.org/cgi/ijlink?linkType=FULL&journalCode=nejm&resid=338/2/107>
Full Text]
* Lever, E, Jaspan, JB (1983) Sodium
bicarbonate therapy in severe diabetic ketoacidosis. Am J Med 75,263-268
Journal of Intensive Care Medicine, Vol. 2, No. 2, 76-84 (1987)
DOI: 10.1177/088506668700200204
© 1987 SAGE Publications
Lactic Acidosis: An Update
Robert A. Kreisberg
University of South Alabama College of Medicine,
2451 Fillingim St, Mobile, AL 36617
Lactic acidosis is an etiologically and
biochemically heterogeneous disorder that is due
to the overproduction of lactic acid or the
underutilization of lactate. It occurs with
disorders in which tissue oxygenation is impaired
(Type A) and with disorders in which it is not
(Type B). Lactic acidosis is an anion-gap
metabolic acidosis in which the lactate
concentration is greater than or equal to 5 mM
and the systemic pH is less than 7.30. Treatment
is largely empiric and generally unsatis factory.
The use of sodium bicarbonate in lactic acidosis
is currently controversial. The adverse effects
of bicarbonate and the beneficial effects of
dichloroacetate in experimental models of lactic acidosis are reviewed.
[Non-text portions of this message have been removed]
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