title: Buffer agents do not reverse intramyocardial acidosis during cardiac resuscitation.
abstract: We investigated the effects of carbon dioxide-producing and carbon dioxide-consuming buffers on intramyocardial pH and on cardiac resuscitability. In 29 pigs, intramyocardial pH was continuously measured with a glass electrode advanced into the midmyocardium of the posterior left ventricle through a diaphragmatic window. Ventricular fibrillation (VF) was electrically induced by alternating current applied to the epicardium of the left ventricle. After 3 minutes of VF, precordial compression was begun and continued for an interval of 8 minutes. Sodium bicarbonate (a carbon dioxide-generating buffer), Carbicarb (a carbon dioxide-consuming buffer), and hypertonic sodium chloride (control solution) were infused into the right atrium during cardiac resuscitation. Defibrillation was attempted by transthoracic direct-current shock after 11 minutes of VF. Intramyocardial pH progressively decreased from an average value of 7.26 before VF to 6.87 before infusion of buffers. Systemic circulation and great cardiac vein pH significantly increased after administration of the two buffer agents. However, intramyocardial pH continued to decline to an average of 6.62 after 11 minutes of VF, and this decline was not altered by either buffer solution or by the saline control. As in previous studies, resuscitability was closely related to coronary perfusion pressure at the time of direct-current countershock but not to pH. Accordingly, the rationale of reversing acidosis by the administration of these buffer agents is not supported. Even more important, neither carbon dioxide-consuming nor carbon dioxide-producing buffers altered myocardial acidosis or improved myocardial resuscitability under controlled experimental conditions of cardiac arrest.
authors.affiliation: Department of Medicine, University of Health Sciences/The Chicago Medical School, North Chicago, IL 60064.
authors.forename: F
authors.initials: F
authors.lastname: Kette
authors.forename: M H
authors.initials: MH
authors.lastname: Weil
authors.forename: M
authors.initials: M
authors.lastname: von Planta
authors.forename: R J
authors.initials: RJ
authors.lastname: Gazmuri
authors.forename: E C
authors.initials: EC
authors.lastname: Rackow
mesh_terms: D000138:Acidosis / Q000188:drug therapy* / Q000209:etiology; D000818:Animals; D001639:Bicarbonates / Q000627:therapeutic use; D001769:Blood; D002021:Buffers; D002245:Carbon Dioxide / Q000097:blood; D002254:Carbonates / Q000627:therapeutic use; D004195:Disease Models, Animal; D004338:Drug Combinations / Q000627:therapeutic use; D006323:Heart Arrest / Q000150:complications / Q000503:physiopathology / Q000628:therapy*; D006863:Hydrogen-Ion Concentration; D007773:Lactates / Q000097:blood; D019344:Lactic Acid; D009206:Myocardium / Q000378:metabolism*; D012151:Resuscitation / Q000379:methods*; D012462:Saline Solution, Hypertonic; D012964:Sodium / Q000627:therapeutic use; D017693:Sodium Bicarbonate; D013552:Swine
chemical_list: D001639:Bicarbonates; D002021:Buffers; D002254:Carbonates; D004338:Drug Combinations; D007773:Lactates; D012462:Saline Solution, Hypertonic; C046283:sodium bicarbonate, sodium carbonate drug combination; D002245:Carbon Dioxide; D019344:Lactic Acid; D017693:Sodium Bicarbonate; D012964:Sodium