Effects of alkaline buffer administration on survival and myocardial energy metabolism in pigs subjected to ventricular fibrillation and closed chest CPR.
Nineteen anaesthetized piglets were investigated. After characterization and a stabilization period, ventricular fibrillation was induced by a transthoracic DC shock, after which a 10-min period of cardiopulmonary resuscitation (CPR) took place. CPR included manual chest compression and mechanical ventilation with pure oxygen. After 1 min of CPR an infusion of alkaline buffer was begun and was completed within 5 min. A total of 50 mmol of one of two different buffer solutions was given, either sodium bicarbonate (n = 6) or tris buffer mixture (n = 7). These two groups were compared with a third control group (n = 6) receiving the same volume of normal saline. After 8 min of CPR all animals were given 0.5 mg adrenaline i.v., and after 10 min DC shocks were used to return the heart to normal sinus rhythm. If this procedure was successful, the heart was rapidly (within 15 s) stopped again by another DC shock. Myocardial biopsies were then taken immediately in all animals. Successful CPR was more frequent in the animals given normal saline or tris buffer mixture and no effect was seen in the group given sodium bicarbonate. Survival was statistically correlated to low myocardial content of creatine phosphate and low base excess values in blood. Such parameters as myocardial content of ATP or ACP (adenylate charge potential) had no direct correlation to survival. Sodium bicarbonate induced significantly higher base excess and PCO2 values, while the tris buffer mixture seemed to have a greater alkalizing effect intracellularly. We consider it probable that the poor results regarding survival after experimental CPR combined with a rapid infusion of sodium bicarbonate were a result of the excessive alkalosis created in combination with the higher resulting PCO2. Indirect evidence was given that a slightly alkaline pH also intracellularly supported critical reactions including ATPases essential for cellular survival.
Wiklund
L
L
Department of Anaesthesiology and Intensive Care, University Hospital, Uppsala, Sweden.
Ronquist
G
G
Stjernström
H
H
Waldenström
A
A
D000818:Animals; D001639:Bicarbonates / Q000008:administration & dosage*; D004734:Energy Metabolism / Q000187:drug effects*; D009206:Myocardium / Q000378:metabolism*; D012151:Resuscitation; D012964:Sodium / Q000008:administration & dosage*; D017693:Sodium Bicarbonate; D013552:Swine; D014325:Tromethamine / Q000008:administration & dosage*; D014693:Ventricular Fibrillation / Q000401:mortality / Q000628:therapy*
D001639:Bicarbonates; D014325:Tromethamine; D017693:Sodium Bicarbonate; D012964:Sodium