To determine the effects of hypercarbia and hypocarbia on a pancuronium or vecuronium neuromuscular blockade, 54 patients were anesthetized with halothane and 60% nitrousoxide in oxygen. In 30 patients, end-tidal Pcos was maintained at either 25 mmHg (3.5 kPa, N = 10), 41 mmHg (5.5 kPa, N = 10), or 56 mmHg (7.5 kPa, N = 10). Five patients in each group then were given pancuronium or vecuronium 0.022 mg/kg iv. Neither maximal depressions of twitch tension nor recovery indexes (time for spontaneous recovery of twitch tension from 25 to 75% of control) were altered by hypercarbia or hypocarbia. The remaining 24 patients were divided into three equal groups. Either pancuronium (N = 8) or vecuronium (N = 8) was administered iv as continuous infusion at a rate sufficient to produce a 50% depression of twitch tension. In the remaining eight patients, no muscle relaxant was given. After twitch tension was stable, half of the patients in each group had hypercarbia induced, which depressed twitch tension in all three groups. The patients who received vecuronium had a significantly larger decrease in twitch tension than those who received pancuronium or no muscle relaxant. Conversely, in the remaining patients, hypocarbia produced a significant increase in twitch tension. There was no difference in the magnitude of the increases in twitch tension among the three groups. The authors conclude that pre-muscle relaxant administration-induced hypercarbia or hypocarbia has no effect on a subsequent neuromuscular blockade from pancuronium or vecuronium. Conversely, hypercarbia decreases and hypocarbia increases twitch tension when no muscle relaxant is given and during a partial pancuronium or vecuronium neuromuscular blockade. Vecuronium was affected by hypercarbia more than the other two groups. The authors propose that when larger doses of vecuronium are given, hypercarbia may increase the danger of residual neuromuscular blockade