Management of acidosis: the role of buffer agents
© Current Science Ltd 1997
Published: 26 November 1997
For more than 50 years, continuing up to about 1980, sodium bicarbonate was used for the treatment of metabolic acidosis. The rationale was that administration of an alkaline fluid would correct an acidotic state. However, the potential value of sodium bicarbonate was called into question when more recent studies demonstrated that it induced venous hypercarbia, and decreases in tissue and cerebrospinal fluid pH, as well as provoking tissue hypoxia, circulatory congestion, hypernatremia, and hyperosmolality, with consequent brain damage [1,2,3,4,5,6]. Bicarbonate buffers may intensify rather than ameliorate cellular acidosis because sodium bicarbonate generates CO2 and thereby increases intracellular (hypercarbic) acidosis .
Sodium bicarbonate administered to patients with diabetic ketoacidosis failed to favorably alter the clinical course or outcome. More specifically, the survival rate was similar in patients who did not receive bicarbonate . During hypoxic lactic acidosis, sodium bicarbonate produced a decline in both systemic arterial pressure and cardiac output without improvement in outcome . The declines in arterial pressure and cardiac output were associated with the hypertonicity of buffer agents which produced arterial vasodilation .
Several other agents have been investigated for the treatment of lactic acidosis. The intent was to increase blood pH during hypoxic states, without reducing oxygen delivery or increasing blood and tissue CO2. Among the most promising are the organic buffers, including TRIS (THAM), and a mixture of equimolar concentrations of sodium carbonate and bicarbonate named Carbicarb. Both of these agents are CO2-consuming, rather than CO2-generating, bicarbonate buffers. In animal studies, both THAM and Carbicarb appeared to have advantages over sodium bicarbonate in the treatment of lactic acidosis and diabetic ketoacidosis [5,11]. However, no well-controlled human trials are available at this time and neither agent is as yet regarded as appropriate for routine management.
Only in exceptional circumstances, particularly in cases of poisoning, drug intoxication, life threatening hyperkalemia or acute epinephrine-fast broncho-constriction, is there likely to be an indication for the reversal of acidosis by the administration of buffer agents.
In settings of cardiac arrest, there is currently no secure evidence of improved outcome after buffer administration. Moreover, measurements indicate that buffer agents including sodium bicarbonate, THAM and Carbicarb do not alter myocardial pH during cardiac resuscitation . Nevertheless, a minority of data, based on experimental cardiopulmonary resuscitation (CPR) studies in dogs, are cited to encourage continued use of sodium bicarbonate during CPR [13,14]. A very recent study in our laboratory may be of interest as it indicates that buffer agents, when administered during CPR, may reduce the severity of post-resuscitation myocardial dysfunction and prolong survival in animals  We must await confirmation from studies on patients before we see whether this will prove to be clinically applicable.
In conclusion, we cannot, at the time of writing, recommend routine bicarbonate or other buffer administration for the reversal of acidosis associated with low flow states.
- Bishop RL, Weisfeldt ML: Sodium bicarbonate administration during cardiac arrest. Effect on arterial pH, PCO 2 , and osmolality. JAMA 1976, 235: 506-509. 10.1001/jama.235.5.506View ArticlePubMedGoogle Scholar
- Arieff AI, Leach W, Park R, Lazarowitz VC: Systemic effects of NaHCO 3 in experimental lactic acidosis in dogs. Am J Physiol 1982, 242: F586-F591.PubMedGoogle Scholar
- Graf H, Leach W, Arieff AI: Evidence for a detrimental effect of bicarbonate therapy in hypoxic lactic acidosis. Science 1985, 227: 754-756.View ArticlePubMedGoogle Scholar
- Graf H, Leach W, Arieff AI: Metabolic effects of sodium bicarbonate in hypoxic lactic acidosis in dogs. Am J Physiol 1985, 249: F630-F635.PubMedGoogle Scholar
- Gazmuri RJ, von Planta M, Weil MH, Rackow EC: Cardiac effects of carbon dioxide-consuming and carbon dioxide-generating buffers during cardiopulmonary resuscitation. J Am Coll Cardiol 1990, 15: 482-490.View ArticlePubMedGoogle Scholar
- Weil MH, Rackow EC, Trevino R, Grundler W, Falk JC, Griffel MI: Difference in acid-base state between venous and arterial blood during cardiopulmonary resuscitation. N Engl J Med 1986, 315: 153-156.View ArticlePubMedGoogle Scholar
- von Planta M, Weil MH, Gazmuri RJ, Bisera J, Rackow EC: Myocardial acidosis associated with CO 2 production during cardiac arrest and resuscitation. Circulation 1989, 80: 684-692.View ArticlePubMedGoogle Scholar
- Morris LR, Murphy MB, Kitabachi AE: Bicarbonate therapy in severe diabetic ketoacidosis. Ann Intern Med 1986, 105: 836-840.View ArticlePubMedGoogle Scholar
- Cooper DJ, Walley KR, Wiggs BR, Russell JA: Bicarbonate does not improve hemodynamics in critically ill patients who have lactic acidosis. Ann Intern Med 1990, 112: 492-498.View ArticlePubMedGoogle Scholar
- Kette F, Weil MH, Gazmuri RJ: Buffer solutions may compromise cardiac resuscitation by reducing coronary perfusion pressure. JAMA 1991, 266: 2121-2126. 10.1001/jama.266.15.2121View ArticlePubMedGoogle Scholar
- von Planta M, Gudipati C, Weil MH, Kraus LJ, Rackow EC: Effects of tromethamine and sodium bicarbonate buffers during cardiac resuscitation. J Clin Pharmacol 1988, 28: 594-599.View ArticlePubMedGoogle Scholar
- Kette F, Weil MH, von Planta M, Gazmuri RJ, Rackow EC: Buffer agents do not reverse intramyocardial acidosis during cardiac resuscitation. Circulation 1990, 81: 1660-1666.View ArticlePubMedGoogle Scholar
- Neumar RW, Bircher NG, Sim KM, et al.: Epinephrine and sodium bicarbonate during CPR following asphyxial cardiac arrest in rats. Resuscitation 1995, 29: 249-263. 10.1016/0300-9572(94)00827-3View ArticlePubMedGoogle Scholar
- Vukmir RB, Bircher N, Radovsky A, Safar P: Sodium bicarbonate may improve outcome in dogs with brief or prolonged cardiac arrest. Crit Care Med 1995, 23: 515-522. 10.1097/00003246-199503000-00017View ArticlePubMedGoogle Scholar
- Sun S, Weil MH, Tang W, Fukui M: Effects of buffer agents on postresuscitation myocardial dysfunction. Crit Care Med 1996, 24: 2035-2041. 10.1097/00003246-199612000-00017View ArticlePubMedGoogle Scholar