Interaction of arousal states and low dose halothane on the acute hypercapnic ventilatory response in humans.

The purpose of this study was to examine the effect of low dose halothane on the acute ventilatory response to hypercapnia, and to assess whether arousal (due to audiovisual (AV) stimulation or pain) modulates the response to halothane. Single step increases in end-tidal Pco(2) using dynamic end-tidal forcing were performed from eucapnia (end-tidal Pco(2) held 1 mmHg (0.13 kPa) above ambient) to hypercapnia (end-tidal Pco(2) 6 mmHg (0.79 kPa) above ambient) in eight healthy volunteers, with end-tidal PO(2) held at 100 mmHg (13.2 kPa), in six protocols: 1) control conditions (darkened, quiet room, eyes closed) without halothane; 2) control conditions with 0.1 MAC halothane; 3) AV stimulation (bright room, loud television) without halothane; 4) AV stimulation with 0.1 MAC halothane; 5) pain (electrical stimulation of skin over tibia to produce visual analogue pain score 5-6/10) without halothane; 6) pain with 0.1 MAC halothane. Both AV stimulation (p = 0.014) and pain (p = 0.0003) significantly increased the baseline eucapnic minute ventilation modestly (by approximately 1.5-4 l.min(-1)). Halothane did not influence the baseline minute ventilation in any arousal state (p = 0.572), nor did it affect the hypercapnic ventilatory response in any arousal state (p = 0.208). Arousal (either AV stimulation or pain) did not affect the ventilatory response to CO(2), regardless of the presence or absence of halothane (p = 0.585). We conclude that halothane affects neither baseline minute ventilation nor the response to CO(2). Arousal can increase baseline ventilation but has no influence on the ventilatory response to CO(2)