Peripheral and central ventilatory responses in central sleep apnea with and without congestive heart failure

Given that the apnea-ventilation cycle length during central sleep apnea (CSA) with congestive heart failure (CHF) is ∼ 70 s, we hypothesized that rapidly responsive peripheral CO 2 ventilatory responses would be raised in CHF-CSA and would correlate with the severity of CSA. Sleep studies and single breath and rebreathe hypercapnic ventilatory responses (HCVR) were measured as markers of peripheral and central CO 2 ventilatory responses, respectively, in 51 subjects: 12 CHF with no apnea (CHF-N), 8 CHF with obstructive sleep apnea (CHF-OSA), 12 CHF-CSA, 11 CSA without CHF ("idiopathic" CSA; ICSA), and 8 normal subjects. Single breath HCVR was equally elevated in CHF-CSA and ICSA groups compared with CHF-N, CHF-OSA, and normal groups (0.58 ± 0.09 [mean ± SE] and 0.58 ± 0.07 versus 0.23 ± 0.06, 0.25 ± 0.04, and 0.27 ± 0.02 L/min/PET CO2 mm Hg, respectively, p < 0.001). Similarly, rebreathe HCVR was elevated in both CHF-CSA and ICSA groups compared with CHF-N, CHF-OSA, and normal groups (5.80 ± 1.12 and 3.53 ± 0.29 versus 2.00 ± 0.25, 1.44 ± 0.16, and 2.14 ± 0.22 L/min/PET CO2 mm Hg, respectively, p < 0.001). Furthermore, in the entire CHF group, single breath HCVR correlated with central apnea-hypopnea index (AHI) (r = 0.63, p < 0.001) and percentage central/total apneas (r = 0.52, p = 0.022). Rebreathe HCVR correlated with awake Pa CO2 (r = -0.61, p < 0.001), but not with central AHI or percantage central/total apneas independent of its relationship with single breath HCVR. In conclusion, in subjects with CHF, raised central CO 2 ventilatory response predisposes to CSA promoting background hypocapnia and exposing the apnea threshold to fluctuations in ventilation, whereas raised and faster-acting peripheral CO 2 ventilatory response determines the periodicity and severity of CSA.