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Am. J. Respir. Crit. Care Med., Volume 162, Number 6, December 2000, 2194-2200

Peripheral and Central Ventilatory Responses in Central Sleep Apnea with and without Congestive Heart Failure

PETER SOLIN, TEANAU ROEBUCK, DAVID P. JOHNS, E. HAYDN WALTERS, and MATTHEW T. NAUGHTON

Department of Respiratory Medicine, The Alfred Hospital and Monash University Medical School, Melbourne, Victoria, Australia

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 CO2 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 CO2 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/PETCO2 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/PETCO2 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 PaCO2 (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 CO2 ventilatory response predisposes to CSA promoting background hypocapnia and exposing the apnea threshold to fluctuations in ventilation, whereas raised and faster-acting peripheral CO2 ventilatory response determines the periodicity and severity of CSA.




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