Role of Hypoxic Drive in Regulation of Postapneic Ventilation during Sleep in Patients with Obstructive Sleep Apnea

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Abstract
To elucidate the role of chemoresponsiveness in determining postapneic ventilation in sleep-disordered periodic breathing, we measured ventilatory response associated with apnea-induced arterial oxygen desaturation during sleep and compared it with the awake hypoxic ventilatory response (HVR) in 12 male patients with obstructive sleep apnea (OSA). Awake HVR was measured at a slight hypocapnic level (end-tidal PCO2 = 37 ± 1 mm Hg, mean ± SEM), and separately at a PCO2 of 45 mm Hg. During non-REM sleep both the ventilatory rate ( e) and the average respiratory frequency (f) in the ventilatory phase between apneic episodes were inversely correlated with the nadir of arterial oxygen saturation (nSaO2) produced by the preceding apneic phase in all patients ( e versus nSaO2; r = −0.74 ± 0.03, mean ± SEM; f versus nSaO2> r = −0.56 ± 0.04). The average tidal volume (Vt) also was correlated with nSaO2 in 10 of the patients (r = −0.56 ± 0.05). During REM sleep e was correlated with nSaO2 in 11 patients (r = −0.75 ± 0.03, p < 0.02). The response of e to nSaO2 (Δ e/ΔnSaO2) varied widely among the patients (non-REM, 0.52 to 2.16; REM, 0.29 to 1.44 L/min/%) and was significantly lower during REM than non-REM sleep (p < 0.01). The value of Δ e/ΔnSaO2 during both non-REM and REM sleep was correlated with awake HVR at an end-tidal PCO2 of 45 mm Hg (non-REM, r = 0.83, p < 0.02; REM, r = 0.76, p < 0.05) but not with that at the hypocapnic level. These results suggest that hypoxic drive is an important factor that determines postapneic ventilation in patients with OSA. Mild increases in PCO2 produced by apneas may affect ventilation partly by modulating the hypoxic response during sleep.