BACKGROUND: To quantify the effects of acute pain on ventilatory control in the awake and sedated human volunteer, the acute hypoxic ventilatory response was studied in the absence and presence of noxious stimulation before and during 0.1 minimum alveolar concentration sevoflurane inhalation. METHODS: Step decreases in end-tidal partial pressure of oxygen from normoxia into hypoxia (approximately 50 mmHg) were performed in 11 healthy volunteers. Four acute hypoxic ventilatory responses were obtained per subject: one in the absence of pain and sevoflurane (C), one in the absence of sevoflurane with noxious stimulation in the form of a 1-Hz electrical current applied to the skin over the tibial bone (C + P), one in the absence of pain during the inhalation of 0.1 minimum alveolar concentration sevoflurane (S), and one during 0.1 minimum alveolar concentration sevoflurane with noxious stimulation (S + P). The end-tidal partial pressure of carbon dioxide was held constant at a value slightly greater than baseline (44 mmHg). To assess the central nervous system arousal state, the bispectral index of the electroencephalogram was monitored. Values are mean +/- SE. RESULTS: Pain caused an increase in prehypoxic baseline ventilation before and during sevoflurane inhalation: C = 13.7 +/- 0.9 l.min-1, C + P = 16.0 +/- 1.0 l.min-1 (P < 0.05 vs. C and S), S = 12.7 +/- 1.2 l.min-1, and S + P = 15.9 +/- 1.1 l.min-1 (P < 0.05 vs. C and S). Sevoflurane decreased the acute hypoxic ventilatory response in the absence and presence of noxious stimulation: C = 0.69 +/- 0.20 l.min-1 (% change in arterial hemoglobin-oxygen saturation derived from pulse oximetry [SpO2])-1, C + P = 0.64 +/- 0.13 l.min-1.%SpO2(-1), S = 0.48 +/- 0.15 l.min-1.%SpO2(-1) (P < 0.05 vs. C and C + P) and S + P = 0.46 +/- 0.21 l.min-1.%SpO2(-1) (P < 0.05 vs. C and C + P). The bispectral indexes were C = 96.2 +/ 0.7, C + P = 97.1 +/- 0.4, S = 86.3 +/- 1.3 (P < 0.05), and S + P = 95.0 +/- 1.0. CONCLUSIONS: The observation that acute pain caused an increase in baseline ventilation with no effect on the acute hypoxic ventilatory response indicates that acute pain interacted with ventilatory control without modifying the effect of low-dose sevoflurane on the peripheral chemoreflex loop. Acute pain increased the level of arousal significantly during sevoflurane inhalation but did not restore the approximately 30% depression of the acute hypoxic ventilatory response by sevoflurane. The central nervous system arousal state per se did not contribute to the impairment of the acute hypoxic ventilatory response by sevoflurane.
BACKGROUND: To quantify the effects of acute pain on ventilatory control in the awake and sedated human volunteer, the acute hypoxic ventilatory response was studied in the absence and presence of noxious stimulation before and during 0.1 minimum alveolar concentration sevoflurane inhalation. METHODS: Step decreases in end-tidal partial pressure of oxygen from normoxia into hypoxia (approximately 50 mmHg) were performed in 11 healthy volunteers. Four acute hypoxic ventilatory responses were obtained per subject: one in the absence of pain and sevoflurane (C), one in the absence of sevoflurane with noxious stimulation in the form of a 1-Hz electrical current applied to the skin over the tibial bone (C + P), one in the absence of pain during the inhalation of 0.1 minimum alveolar concentration sevoflurane (S), and one during 0.1 minimum alveolar concentration sevoflurane with noxious stimulation (S + P). The end-tidal partial pressure of carbon dioxide was held constant at a value slightly greater than baseline (44 mmHg). To assess the central nervous system arousal state, the bispectral index of the electroencephalogram was monitored. Values are mean +/- SE. RESULTS:Pain caused an increase in prehypoxic baseline ventilation before and during sevoflurane inhalation: C = 13.7 +/- 0.9 l.min-1, C + P = 16.0 +/- 1.0 l.min-1 (P < 0.05 vs. C and S), S = 12.7 +/- 1.2 l.min-1, and S + P = 15.9 +/- 1.1 l.min-1 (P < 0.05 vs. C and S). Sevoflurane decreased the acute hypoxic ventilatory response in the absence and presence of noxious stimulation: C = 0.69 +/- 0.20 l.min-1 (% change in arterial hemoglobin-oxygen saturation derived from pulse oximetry [SpO2])-1, C + P = 0.64 +/- 0.13 l.min-1.%SpO2(-1), S = 0.48 +/- 0.15 l.min-1.%SpO2(-1) (P < 0.05 vs. C and C + P) and S + P = 0.46 +/- 0.21 l.min-1.%SpO2(-1) (P < 0.05 vs. C and C + P). The bispectral indexes were C = 96.2 +/ 0.7, C + P = 97.1 +/- 0.4, S = 86.3 +/- 1.3 (P < 0.05), and S + P = 95.0 +/- 1.0. CONCLUSIONS: The observation that acute pain caused an increase in baseline ventilation with no effect on the acute hypoxic ventilatory response indicates that acute pain interacted with ventilatory control without modifying the effect of low-dose sevoflurane on the peripheral chemoreflex loop. Acute pain increased the level of arousal significantly during sevoflurane inhalation but did not restore the approximately 30% depression of the acute hypoxic ventilatory response by sevoflurane. The central nervous system arousal state per se did not contribute to the impairment of the acute hypoxic ventilatory response by sevoflurane.