Background: The increase in peripheral chemoreflex sensitivity in patients with obstructive sleep apnea (OSA) is associated with activation of autonomic nervous system and hemodynamic responses. Nasal CPAP (nCPAP) is an effective treatment for OSA, but little is known on its effect on chemoreflex sensitivity.
Objectives: To assess the effect of nCPAP treatment or placebo (sham nCPAP) on ventilatory control in patients with OSA.
Setting: Sleep laboratory of Azienda Ospedaliera Garibaldi.
Patients: Twenty-five patients with moderate-to-severe OSA.
Design and measurements: Patients were randomly assigned to either therapeutic nCPAP (use of optimal pressure, n = 15) or sham nCPAP (suboptimal pressure of 1 to 2 cm H2O, n = 10) in a double-blind fashion and treated for 1 month. A rebreathing test to assess ventilatory response to normocapnic hypoxia and normoxic hypercapnia was performed at basal condition and after 1 month of treatment.
Results: The use of therapeutic nCPAP or sham nCPAP did not affect daytime percentage of arterial oxygen saturation (Sao2%) or end-tidal Pco2. The normocapnic hypoxic ventilatory response was reduced after 1 month of treatment with nCPAP (the slope was 1.08 ± 0.02 L/min/Sao2% at basal condition and 0.53 ± 0.07 L/min/Sao2% after 1 month of treatment, p = 0.008) [mean ± SD], but not in patients treated with sham nCPAP (slope, 0.83 ± 0.09 L/min/Sao2% and 0.85 ± 0.19 L/min/Sao2% at basal condition and after 1 month, respectively). The normoxic hypercapnic ventilatory response remained unchanged after 1 month in both groups. No changes in ventilatory response to either hypoxia or hypercapnia were observed after a single night of nCPAP treatment.
Conclusion: The ventilatory response to hypoxia is reduced during regular treatment, but not after short-term treatment, with nCPAP. Readjusted peripheral oxygen chemosensitivity during nCPAP treatment may be a side effect of both reduced sympathetic activity and increased baroreflex activity, or a possible continuous positive airway pressure-related mechanism leading to a reduced activation of autonomic nervous system per se.