Control of breathing in obstructive sleep apnoea patients: Role of CPAP therapy

Control of breathing in obstructive sleep apnoea patients: Role of CPAP therapy A. Re, F. Mormile, A. Di Marco Berardino, D. Visca, B. Iovene, S. Valente (Rome, Italy) Aim: Control of breathing during wakefulness in obstructive sleep apnoea (OSA) and the role of CPAP therapy is an ongoing controversy. We studied the ventilatory response of healthy controls and OSA patients before and after at least 1 year of CPAP therapy. Methods: 17 never treated OSA patients (16 M; 53\ub113.2yrs; BMI=34.5\ub18.1; AHI=45\ub114.7) underwent nocturnal cardiopulmonary monitoring, spirometry and blood gas analysis. Read's rebreathing test was used to evaluate hypercapnic ventilatory response (HVR CO2); hypoxic ventilator response (HVRO2) was studied by both progressive and transient methods, to explore both peripheral oxygen chemoceptors and the central modulation. The relationship between minute ventilation (VE) or mean inspiratory flow (VT/Ti) and PETCO2 or PETO2 was expressed in terms of slope of linear regression for HVRCO2 and of parameter A of hyperbolic relation for HVRO2. Results: OSA patients showed an increased responsiveness to transient, but not to progressive, hypoxemia, and a reduced response to hypercapnia when compared to controls. Transient HVRO2 showed a significant reduction during CPAP therapy (p<0.01), whereas HVRCO2 increased only slightly. Progressive HVRO2 was not modified by CPAP [Tab 1]. Conclusions: the daytime glomic reactivity to transient hypoxia is increased by repeated nocturnal hypoxic stimuli; CPAP significantly restores the ventilatory stability during sleep. Chemosensitivity in Controls and in OSAS pre e post CPAP Controls(a) OSAS Pre CPAP(b) p(a vs b) OSAS Post CPAP(c) p(b vs c) HVR CO2(l/min/mmHg) 2.7\ub11.2 2.0\ub10.9 <0.05 2.2\ub10.9 0.63 HPVRO2(l/min*mmHg) 355.3\ub1115.2 357.5\ub1117.9 0.46 336.9\ub1129.9 0.99 HTVRO2(l/min*mmHg) 119.2\ub162.7 217.7\ub1107.7 <0.01 97.5\ub124.1