title: Use of base in the treatment of severe acidemic states.
abstract: Severe acidemia (blood pH < 7.1 to 7.2) suppresses myocardial contractility, predisposes to cardiac arrhythmias, causes venoconstriction, and can decrease total peripheral vascular resistance and blood pressure, reduce hepatic blood flow, and impair oxygen delivery. These alterations in organ function can contribute to increased morbidity and mortality. Although it seemed logical to administer sodium bicarbonate to attenuate acidemia and therefore lessen the impact on cardiac function, the routine use of bicarbonate in the treatment of the most common causes of severe acidemia, diabetic ketoacidosis, lactic acidosis, and cardiac arrest, has been an issue of great controversy. Studies of animals and patients with these disorders have reported conflicting data on the benefits of bicarbonate, showing both beneficial and detrimental effects. Alternative alkalinizing agents, tris-hydroxymethyl aminomethane and Carbicarb, have shown some promise in studies of animals and humans, and reevaluation of these buffers in the treatment of severe acidemic states seems warranted. The potential value of base therapy in the treatment of severe acidemia remains an important issue, and further studies are required to determine which patients should be administered base therapy and what base should be used.
authors.affiliation: Division of Nephrology, Veterans Administration Greater Los Angeles Health Care System, Los Angeles, CA 90073, USA. jkraut@ucla.edu
authors.forename: J A
authors.initials: JA
authors.lastname: Kraut
authors.forename: I
authors.initials: I
authors.lastname: Kurtz
mesh_terms: D000138:Acidosis / Q000097:blood / Q000150:complications / Q000628:therapy*; D000140:Acidosis, Lactic / Q000150:complications / Q000188:drug therapy / Q000209:etiology; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology; D001639:Bicarbonates / Q000378:metabolism*; D002021:Buffers; D002118:Calcium / Q000378:metabolism; D002254:Carbonates / Q000627:therapeutic use; D002302:Cardiac Output / Q000187:drug effects; D016883:Diabetic Ketoacidosis / Q000188:drug therapy; D004338:Drug Combinations; D006323:Heart Arrest / Q000150:complications / Q000188:drug therapy; D006801:Humans; D009200:Myocardial Contraction; D010100:Oxygen / Q000378:metabolism; D011188:Potassium / Q000378:metabolism; D017693:Sodium Bicarbonate / Q000009:adverse effects / Q000627:therapeutic use*; D014325:Tromethamine / Q000627:therapeutic use; D014655:Vascular Resistance; D014882:Water-Electrolyte Balance / Q000502:physiology
chemical_list: D001639:Bicarbonates; D002021:Buffers; D002254:Carbonates; D004338:Drug Combinations; C046283:sodium bicarbonate, sodium carbonate drug combination; D014325:Tromethamine; D017693:Sodium Bicarbonate; D011188:Potassium; D010100:Oxygen; D002118:Calcium