Increased Propensity for Central Apnea in Patients with Obstructive Sleep Apnea

Abstract

Rationale: There is increasing evidence of increased ventilatory instability in patients with obstructive sleep apnea (OSA), but previous investigations have not studied whether the hypocapnic apneic threshold is altered in this group. Objectives: To compare the apneic threshold, CO 2 reserve, and controller gain between subjects with and without OSA matched for age, sex, and body mass index. Methods: Hypocapnia was induced via nasal mechanical ventilation for 3 minutes. Cessation of mechanical ventilation resulted in hypocapnic central hypopnea or apnea depending upon the magnitude of the hypocapnia. The apnea threshold (PET CO 2 -AT) was defined as the measured PET CO 2 at which the apnea closest to the last hypopnea occurred. The CO 2 reserve was defined as the change in PET CO 2 between eupneic PET CO 2 and PET CO 2 -AT. Controller gain was defined as the ratio of change in VE between control and hypopnea or apnea to the DPET CO 2 . Measurements and Main Results: Eleven pairs of subjects were studied. There was no difference in the PET CO 2 -AT between the two groups. However, the CO 2 reserve was smaller in the subjects with OSA (2.2 6 0.6 mm Hg) compared with the control subjects (4.5 6 1.4 mm Hg; P , 0.001). The controller gain was increased in the subjects with OSA (3.7 6 1.3 L/min/mm Hg) compared with the control subjects (1.6 6 0.5 L/min/mm Hg; P , 0.001). Controller gain decreased and CO 2 reserve increased in seven subjects restudied after using continuous positive airway pressure for 1 month. Conclusions: Ventilatory instability is increased in subjects with OSA and is reversible with the use of continuous positive airway pressure.

Air Leak during CPAP Titration as a Risk Factor for Central Apnea

“…15 Second, CPAP serves to stabilize the upper airway, which would be predicted to increase controller gain in these patients. 15,16 Chemoresponsiveness, defi ned as the body's ventilatory response to CO 2 plus the ability to respond to chemical stimuli (an open airway), would increase with CPAP-induced patency of the upper airway. 17 Thus, central apnea may occur due to CPAP-induced hypocapnia.…”

Clinical Use of Loop Gain Measures to Determine Continuous Positive Airway Pressure Efficacy in Patients with Complex Sleep Apnea. A Pilot Study

“…However, we note that 1 month is considered sufficient to normalize the effects of sleep apnea on loop gain (13,14). Hence, available evidence suggests that at 1 month it is reasonable to reconsider the use of alternative strategies with a greater scope for resolving ventilatory instability (e.g., ASV) (18).…”

“…In patients with heart failure, CPAP reduces residual CSAs over time (12), indicating that loop gain is gradually reduced with ongoing treatment. In patients with OSA without heart failure, the ventilatory chemoreflex response to CO 2 (a key component of ventilatory stability) is normalized with approximately 4 weeks of CPAP treatment (13,14).…”

Central sleep apnea during continuous positive airway pressure therapy in obstructive sleep apnea patients: from the compliance to adaptation, maladaptation and reflexes

“…It remains unclear to what extent sleep impairment is the cause or the effect of CompSAS (24). It was suggested that an elevated nasal resistance might relate to frequent arousals, which could presumably contribute to an increase in central apneas (25).  All these pathophysiological issues may be clinically important, since they can potentially affect treatment approaches, keeping in mind that patients developing CSA after OSAS treatment seem to have a poorer prognosis as compared to those only affected by OSAS, eventually also because of low CPAP compliance.…”