BACKGROUND: A previous study has demonstrated a decrease in the hypoxic ventilatory response in volunteers partially paralyzed with vecuronium. However, in this study, hypocapnia was allowed to occur. Because hypocapnia counteracts the ventilatory response to hypoxia during partial vecuronium-induced neuromuscular block and isocapnia, the hypoxic ventilatory response (HVR) was tested in 10 awake volunteers. METHODS: To avoid hypocapnia, the resting hyperoxic control end-tidal PCO2 was increased to 43.3 +/- 2.4 mmHg, raising inspiratory minute ventilation (VI) to 140 ml.kg-1.min-1. Hypoxic ventilatory response (delta VI/delta SpO2, L.min-1.%-1) was measured during a 5-min isocapnic step reduction to a mean arterial hemoglobin oxygen saturation (SpO2) of 84.8 +/- 1.4%. Immediately thereafter, hypercapnic ventilatory response (HCVR; delta VI/delta PETCO2, L.min-1.mmHg-1) was determined at the end of a 6-min step increase of PETCO2 to 50.5 +/- 2.7 mmHg. During a subsequent 30-40-min pause, an intravenous infusion of vecuronium was adjusted to reduce the adductor pollicis train-of-four ratio to 0.70, as monitored using mechanomyography. Ventilatory parameters, HVR and HCVR, were then redetermined. RESULTS: Resting VI, PETCO2, and SpO2 were unchanged by drug infusion. Hypoxic ventilatory response decreased from control (a) of 0.97 +/- 0.43 to 0.74 +/- 0.41 L.min-1.%-1 (P < 0.02) during drug infusion (b), while HCVR was unchanged (a = 1.91 +/- 0.82, b = 1.62 +/- 0.46 L.min-1.mmHg-1; NS). To correct HVR for possible vecuronium-induced respiratory muscle weakness or otherwise altered central nervous system reactivity, the drug/control ratio (HVRb/a) was divided by the associated HCVRb/a ratio. This HVR index, FHVR, was 0.84 +/- 0.12 (P < 0.01). CONCLUSIONS: We conclude that a vecuronium-induced partial neuromuscular block impairs HVR more than it does HCVR in humans, suggesting an effect of vecuronium on carotid body hypoxic chemosensitivity.
BACKGROUND: A previous study has demonstrated a decrease in the hypoxic ventilatory response in volunteers partially paralyzed with vecuronium. However, in this study, hypocapnia was allowed to occur. Because hypocapnia counteracts the ventilatory response to hypoxia during partial vecuronium-induced neuromuscular block and isocapnia, the hypoxic ventilatory response (HVR) was tested in 10 awake volunteers. METHODS: To avoid hypocapnia, the resting hyperoxic control end-tidal PCO2 was increased to 43.3 +/- 2.4 mmHg, raising inspiratory minute ventilation (VI) to 140 ml.kg-1.min-1. Hypoxic ventilatory response (delta VI/delta SpO2, L.min-1.%-1) was measured during a 5-min isocapnic step reduction to a mean arterial hemoglobin oxygen saturation (SpO2) of 84.8 +/- 1.4%. Immediately thereafter, hypercapnic ventilatory response (HCVR; delta VI/delta PETCO2, L.min-1.mmHg-1) was determined at the end of a 6-min step increase of PETCO2 to 50.5 +/- 2.7 mmHg. During a subsequent 30-40-min pause, an intravenous infusion of vecuronium was adjusted to reduce the adductor pollicis train-of-four ratio to 0.70, as monitored using mechanomyography. Ventilatory parameters, HVR and HCVR, were then redetermined. RESULTS: Resting VI, PETCO2, and SpO2 were unchanged by drug infusion. Hypoxic ventilatory response decreased from control (a) of 0.97 +/- 0.43 to 0.74 +/- 0.41 L.min-1.%-1 (P < 0.02) during drug infusion (b), while HCVR was unchanged (a = 1.91 +/- 0.82, b = 1.62 +/- 0.46 L.min-1.mmHg-1; NS). To correct HVR for possible vecuronium-induced respiratory muscle weakness or otherwise altered central nervous system reactivity, the drug/control ratio (HVRb/a) was divided by the associated HCVRb/a ratio. This HVR index, FHVR, was 0.84 +/- 0.12 (P < 0.01). CONCLUSIONS: We conclude that a vecuronium-induced partial neuromuscular block impairs HVR more than it does HCVR in humans, suggesting an effect of vecuronium on carotid body hypoxic chemosensitivity.