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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)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,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.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 al1 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,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,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.
References
Medical College of Pennsylvania/Hahnemann University Philadelphia, PA
Correspondence to: Bulent Cuhaci, MD, FCCP, Medical College of Pennsylvania/Hahnemann University, 3300 Henry Ave, Fourth Floor, Division of Nephrology, Philadelphia, PA 19129; e-mail: bulentcuhaci@yahoo.com
To the Editor:
We appreciate Dr. Rosival’s comments on our letter that was published in CHEST (September 2000).1 Unfortunately, a patient with severe lactic acidosis has a poor prognosis and generally does not live long. It is hard to claim that such patients die of acidosis per se, but it is also hard to argue that the presence of severe acidosis is not detrimental. We agree that most of these patients become comatose, or at least unresponsive, as their disease progresses. However, there are many conditions that contribute to this decreased level of consciousness, which include the effects of sedative or paralytic agents that are used while patients are receiving mechanical ventilation, metabolic derangements including hypoxia, hypoperfusion, and possible concomitant hepatic and/or renal failure in addition to the likely effects of severe acidosis itself. So, very often it is difficult to separate out the role of severe acidosis.
Some investigators2 have noted a better correlation between the spinal fluid pH and encephalopathy rather than the arterial pH. One of the explanations for why patients with severe respiratory acidosis become more encephalopathic compared to patients with metabolic acidosis with similar pH values is the more rapid diffusion of CO2 into the cerebrospinal fluid (CSF).2 There is probably a time lag between the changes in the arterial pH and those in spinal fluid pH, and if the severe acidosis persists, it is very likely that CSF will become more acidotic as well. This delay in the acidification of the CSF or cerebral cells (and many other cells) is also due to the tremendous ability of the cells to regulate their intracellular pH by various pump mechanisms.3 4 These mechanisms are energy consuming and require that the cells remain well oxygenated and perfused. It is likely that these mechanisms will be exhausted if the severe acidosis lasts long enough.3 5 This is one argument to support the judicious use of bicarbonate therapy in patients with severe acidosis, since it is the simplest and cheapest substance available with which to treat acidosis, as Dr. Rosival also points out.
The optimum ways and methods of delivery (ie, the dose, the rate of application, the use of renal replacement therapies, etc) are beyond the scope of this discussion. Even though there are rare case reports5 of very low pH values (as low as 6.6 for a brief period of time) compatible with life, most authors5 accept the "limits of pH compatible with life" to be between 7.0 and 7.8. Some authors6 extend these limits to 6.8 to 7.8. Along with other investigators,7 we continue to believe that it is reasonable to maintain, if possible, arterial pH at > 7.0 (cautiously in so doing) in patients with severe lactic acidosis.
In all fairness, we should also note that our interpretation of the study by Lever and Jaspan8 that was cited by Dr. Rosival is different from his. These authors do not seem to support the idea of giving sodium bicarbonate to patients with diabetic ketoacidosis. In their retrospective analysis of 95 episodes of severe diabetic ketoacidosis, they concluded that sodium bicarbonate might not confer any special benefits in the treatment of diabetic ketoacidosis. It is difficult to extrapolate these results to lactic acidosis since diabetic ketoacidosis is a different disease that has an established treatment aimed at the etiology, and because this retrospective study has its own limitations.
References
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