CARDIAC ARREST Arteriovenous carbon dioxide and pH gradients during cardiac arrest

In a porcine preparation of cardiac arrest, we demonstrated that there is a marked paradox of venous acidemia and arterial alkalemia. This paradox is related to decreased clearance of CO2 from the lungs when pulmonary blood flow is critically reduced. Accordingly, increased venous Pco2 rather than metabolic acidosis due to lactic acidosis predominates during the initial 8 min of cardiopulmonary resuscitation. Arterial blood gases fail as indicators of systemic acid-base status and therefore as indicators of tissue acidosis. Circulation 74, No. 5, 1071-1074, 1986. THE ACIDEMIA and consequent cellular acidosis that result from cardiopulmonary resuscitaton (CPR) have been attributed to critical reduction of oxygen transport function with consequent anaerobic metabolism and metabolic lactic acidosis due to increases in the concentration of blood lactic acid. However, Fillmore et al.' and subsequently Bishop et al.2 observed alkalemia in arteral blood during the initial 10 min of CPR. This was due to hypocapnea and therefore respiratory alkalosis. During this initial period, only minor increases in blood lactate concentrations were observed.1 This is of importance because sodium bicarbonate is routinely administered in the clinical setting of cardiac arrest and this intervention both augments alkalosis and carries the added risk of fatal hyperosmolality.3 These observations prompted the clinical recommendation of the American Heart Association that the decision of whether to administer bicarbonate therapy be based on measurements of arterial blood gases.4 During CPR in a porcine preparation of cardiac arrest, we observed a remarkable paradox between the pH and Pco2 conditions in arterial and central venous blood. Decreased arterial Pco2 and elevated arterial pH were accompanied by an elevated venous Pco2 and depressed venous pH. This paradox was reversed after From the University of Health Sciences/The Chicago Medical School, North Chicago. Supported by UHS/The Chicago Medical School, Biomedical Research support grant No. 2-595-739; The Institute of Critical Care Medicine, Rancho Mirage, CA; Critical Care Foundation, Beverly Hills, CA; and The Laerdal Foundation for Acute Medicine, Stavanger, Norway. Address for correspondence: Max Harry Weil, M.D., Ph.D., Professor and Chairnan, Department of Medicine, UHS/The Chicago Medical School, 3333 Green Bay Rd., North Chicago, IL 60064. Received Feb. 3, 1986; revision accepted July 31, 1986. restoration of spontaneous circulation. These observations indicate that earlier concepts relating to acid-base changes during CPR and the presumed benefits of bicarbonate treatment are invalid.