Effect of supramaximal vagal stimulation in combination with hypoxia, respiratory acidosis and deep halothane anaesthesia on cardiovascular function in dogs.

Vagal reflexes are generally recognized as a possible cause of cardiac arrest during anaesthesia. Studies were performed to determine whether hypoxia, respiratory acidosis or deep halothane anaesthesia modify the cardiovascular effect of vagal stimulation (VS) in dogs. The animals were anaesthetized with intravenous urethane and chloralose, and paralysed with metocurine. Normal temperature and arterial blood gas variables were maintained and supramaximal VS was applied to the distal end of both vagus nerves for 5 min. No differences were found in any of the variables measured among the time periods when VS was repeated five times in six control dogs receiving urethane-chloralose basal narcosis only to determine the effects of time. VS resulted in 15 +/- 3 s (mean +/- s.e. mean) of asystole. Heart rate, cardiac output (CO) and mean arterial pressure (MAP) were still significantly decreased (P less than 0.001) and central venous pressure, right atrial pressure, pulmonary capillary wedge pressure (PCW), systemic (SVR) and pulmonary vascular resistance significantly increased (P less than 0.01--P less than 0.001) at the end of stimulation when compared to values before VS in all 24 dogs. Neither hypoxia [PaO2 5.3 kPa (40 mmHg)] nor respiratory acidosis [pH 7.00, PaCO2 10.6 kPa (80 mmHg)] modified these effects of VS. VS during halothane anaesthesia (1.6% end-tidal concentration) resulted in further significant decreases (P less than 0.05--P less than 0.001) in CO, MAP, mean pulmonary arterial pressure, PCW and SVR when compared to VS under basal narcosis. VS under halothane anaesthesia combined with hypoxia or respiratory acidosis did not decrease the cardiovascular parameters as much as VS under halothane anaesthesia alone. VS alone, or in combination with hypoxia or respiratory acidosis, failed to cause persistent asystole.