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

Abstract

Given that the apnea-ventilation cycle length during central sleep apnea (CSA) with congestive heart failure (CHF) is approximately 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(CO(2)) 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(CO(2)) 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(CO(2)) (r = -0.61, p < 0.001), but not with central AHI or percentage 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.

Influence of arterial O2 on the susceptibility to posthyperventilation apnea during sleep

“…The ability of the carotid body to respond to the abrupt disturbance of blood gases has been tested with a transient increase in alveolar CO 2 . The maximum increase in V E after CO 2 administration was observed during the second or third breath with a latency of 10 -12 s (28,46,49). In patients with CSA, good agreement between the time from lowest PET CO 2 to the onset of apnea and LECD has also been observed (35).…”

Sleep Apnea and Heart Failure

“…4,5 When patients lie flat, increased venous return from the extremities causes central fluid accumulation and pulmonary congestion that stimulates vagal irritant receptors in the lungs to elicit reflex hyperventilation. Central apnea is usually initiated during sleep by a further acute increase in ventilation and reduction in PaCO 2 that is triggered by a spontaneous arousal.…”

Central periodic breathing during sleep in 74 patients with acute ischemic stroke – Neurogenic and cardiogenic factors

“…In both patients with and without stroke, CPBS has been linked to increased respiratory CO2 sensitivity [13,14] and left ventricular dysfunction [15,16]. CPBS has also been reported in patients with unilateral lesions of variable topography without disturbed level of consciousness or overt heart failure [4,10,17].…”