Bicarbonate therapy for organic acidosis: the case for its continued use.
Critics of bicarbonate therapy for life-threatening lactic acidosis have argued that the treatment is not only ineffective but that it also worsens morbidity and mortality. We critically examine the six major arguments used to condemn alkali treatment. We highlight the shortcomings of frequently cited uncontrolled human studies, experiments in animals, and in-vitro chemical analyses not clearly related to the human condition. The damaging hemodynamic effects of acidemia, which centralizes blood volume while depressing myocardial contraction (thereby causing hemodynamic collapse), are discussed and offered in support of alkali therapy. We also emphasize the extreme sensitivity of patients with acidosis to further small decreases in serum bicarbonate concentration or increases in arterial PCO2. In short, we have found no basis by which to condemn the use of alkali and believe that those who have scorned its use have yet to demonstrate its danger clearly. Until that time, sodium bicarbonate should remain the standard of therapy for this life-threatening condition.
D000140:Acidosis, Lactic / Q000188:drug therapy* / Q000378:metabolism / Q000401:mortality; D000818:Animals; D001639:Bicarbonates / Q000097:blood / Q000627:therapeutic use*; D002245:Carbon Dioxide / Q000097:blood; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007773:Lactates / Q000096:biosynthesis; D019344:Lactic Acid; D010100:Oxygen / Q000097:blood
D001639:Bicarbonates; D007773:Lactates; D002245:Carbon Dioxide; D019344:Lactic Acid; D010100:Oxygen