Sodium Bicarbonate during CPR: Does It Help or Hinder?

Abstract

It has been well established that acidemia prior to onset of cardiopulmonary arrest prognosticates unsuccessful resuscitation.1Camarata J. Weil M.H. Hanashiro P.K. Shubin H. Cardiac arrest in the critically ill. I. A study of pre-disposing causes in 32 patients.Circulation. 1971; 44: 688-695Crossref PubMed Scopus (113) Google Scholar The assumption that correction of acidemia by infusion of sodium bicarbonate improves the outcome is not documented. To the contrary, there is increasing evidence that this may be counterproductive.2Lever E. Jaspon J.B. Sodium bicarbonate therapy in severe diabetic ketoacidosis.Am J Med. 1983; 75: 263-268Abstract Full Text PDF PubMed Scopus (117) Google Scholar, 3Arreff N.I. Leach W. Park R. Lazarowitz V.C. Systemic effects of NaHCO3 in experimental lactic acidosis in dogs.Am J Physiol. 1982; 242: F586-91Google Scholar, 4Ostrea E.M. Odell G.B. The influence of bicarbonate administration on blood pH in a “closed system”: Clinical implications.J Pediatrics. 1972; 80: 671-680Abstract Full Text PDF PubMed Scopus (88) Google Scholar However, this may not necessarily apply to patients in whom acidemia follows the onset of arrest with cessation of ventilation and systemic perfusion. In this setting of catastrophic cardiac arrest, rapid onset of acidemia may be related to hypoventilation with hypercapnia and the accumulation of lactic acid due to critical reduction in oxygen delivery to tissues. However, during cardiopulmonary resuscitation, increases in arterial Pco2 are uncommonly observed during the initial 30 minutes when the patient is externally ventilated. To the contrary, arterial blood gas analysis usually discloses respiratory alkalosis. Under experimental conditions in the mechanically ventilated dog and pig, there is no significant acidemia during the initial ten minutes of CPR.5Vincent J.L. Thijs L. Weil M.H. Michaels S. Silverberg R.A. Clinical and experimental studies on electromechanical dissociation.Circulation. 1981; 64: 18-27Crossref PubMed Scopus (71) Google Scholar, 6Bishop R.L. Weisfeldt M.L. Sodium bicarbonate administration during cardiac arrest.JAMA. 1976; 235: 506-509Crossref PubMed Scopus (151) Google Scholar, 7Grundler W. Weil M.H. Yamaguchi M. Michaels S. Rackow E.C. The paradox of venous acidosis and arterial alkalosis during CPR.Chest. 1984; 86: 282Google Scholar Comparable observations have been made in human patients after witnessed cardiac arrest.8Weil M.H. Grundler W. Rackow E.C. Bisera J. Miller J.M. Michaels S. Blood gas measurements in human patients during CPR.Chest. 1984; 86: 282Google Scholar Nevertheless, current practices support the routine administration of 1 mEq/kg of sodium bicarbonate as part of the initial life-support intervention and half of the initial dose at intervals of ten minutes.9Standards and Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiac Care.JAMA. 1980; 244 (Suppl): 453-509Crossref PubMed Scopus (383) Google Scholar This intervention accounts for iatrogenic increases in plasma levels of sodium, hyperosmolality of plasma, and metabolic alkalosis. Both iatrogenic alkalosis and the hyperosmolal state following cardiopulmonary resuscitation have been associated with high mortality.10Mattar J.H. Weil M.H. Shubin H. Stein L. Cardiac arrest in the critically ill. II. Hyperosmolal states following cardiac arrest.Am J Med. 1974; 56: 162-168Abstract Full Text PDF PubMed Scopus (158) Google Scholar, 11Ruiz C.P. Weil M.H. Carlson R. Iatrogenic alkalosis and hyperosmolality following CPR.Circulation. 1979; 60: 127Google Scholar More recently, the demonstration of marked hypercapnia in mixed venous blood and the paradox of arterial respiratory alkalosis and venous respiratory acidosis during the initial minutes of cardiopulmonary arrest and CPR have been confirmed in both experimental animal and human subjects.7Grundler W. Weil M.H. Yamaguchi M. Michaels S. Rackow E.C. The paradox of venous acidosis and arterial alkalosis during CPR.Chest. 1984; 86: 282Google Scholar, 8Weil M.H. Grundler W. Rackow E.C. Bisera J. Miller J.M. Michaels S. Blood gas measurements in human patients during CPR.Chest. 1984; 86: 282Google Scholar The administration of bicarbonate to experimental animal subjects further augments the severity of respiratory acidosis in mixed venous blood and, therefore, in tissue acidosis.12Lindner K.H. Ahnefeld F.W. Dick W. Lotz P. Natriumbikar-bonatgabe Während der kardiopulmonalen Reanimation.Anaesthetist. 1985; (in press)Google Scholar In contrast, after the administration of the non-carbon dioxide generating organic buffer tromethamine, increases in the pH of both mixed venous and arterial blood are observed with a decrease rather than an increase in carbon dioxide tension in venous blood. Finally, current studies indicate that the rationale of alkalinization during cardiac arrest must be critically examined in terms of ultimate benefit. Bicarbonate-induced alkalosis, hypernatremia, hyperosmolality, and mixed venous hypercapnia are more likely to compromise rather than improve ultimate survival.10Mattar J.H. Weil M.H. Shubin H. Stein L. Cardiac arrest in the critically ill. II. Hyperosmolal states following cardiac arrest.Am J Med. 1974; 56: 162-168Abstract Full Text PDF PubMed Scopus (158) Google Scholar, 11Ruiz C.P. Weil M.H. Carlson R. Iatrogenic alkalosis and hyperosmolality following CPR.Circulation. 1979; 60: 127Google Scholar Objective evidence fails to securely establish that beneficial effects of alkali, especially sodium bicarbonate, outweigh these risks.