Ventilatory response to CO₂ in patients with snoring, obstructivehypopnoea and obstructive apnoea

Abstract

Obstructive sleep apnoea (OSA) is caused by an obstruction of the upper airway. Sufficient sensitivity to CO2 in the respiratory centre is known to be a critical factor for adequate tone in the upper airway muscles. The hypothesis of this study is, therefore, that the ventilatory response to CO2 is reduced in patients with OSA. Twenty-six patients who suffered from snoring, 19 snoring patients with obstructive hypopnoea (OH) and 33 snoring patients with obstructive apnoea (OA), were studied. The control group consisted of 25 subjects from a random sample with no history of snoring or daytime sleepiness. Tests of the hyperoxic and hypoxic ventilatory response to CO2 were performed, as well as static and dynamic spirometry. Subjects in the OA group displayed a higher hyperoxic (VE/FetCO2hy = 12.6 l min-1/%) and hypoxic (VE/FetCO2ho = 15.7 l min-1/%) ventilatory response to CO2 than patients with obstructive hypopnoea (VE/FetCO2hy = 8.6 l min-1/%; VE/FetCO2ho = 15.2 l min-1/%), snorers (VE/FetCO2hy = 8.4 l min-1/%; VE/FetCO2ho = 12.7 l min-1/%) and non-snorers (VE/FetCO2hy = 7.6 l min-1/%; VE/FetCOho = 9.6 l min-1/%). Multiple regression analysis reveals that neck circumference, apnoea index, oxygen desaturation index, PCO2 and sex (male gender) are correlated with VE/FetCO2hy (R2 = 0.43). Multiple regression analysis also reveals that ERV (expiratory reserve volume) and sex (male gender) are correlated with VE/FetCO2ho (R2 = 0.21). Arguing against the hypothesis, patients with OSA displayed an increased hyperoxic and hypoxic ventilatory response to CO2. Nocturnal apnoea frequency and the obesity factor in OSA may have contributed to these results.

Association between ventilatory response to hypercapnia and obstructive sleep apnea–hypopnea index in asymptomatic subjects

“…However, the severity of sleep disorder in that study was measured by in-home respiratory monitoring only [34]. In addition, the HCVR value was calculated as the slope of V E /FetCO 2 , which is different from established methods of HCVR measurement [21,34]. Another study has found both increased HCVR in 14 non-hypercapnic OSAHS and decreased HCVR in 11 chronic hypercapnic OSAHS patients compared with control subjects [32].…”

“…However, the severity of sleep disorder in that study was measured by in-home respiratory monitoring only [34]. In addition, the HCVR value was calculated as the slope of V E /FetCO 2 , which is different from established methods of HCVR measurement [21,34].…”

“…In the limited number of studies showing increased central chemosensitivity in OSAHS patients, only one study has found a direct association between HCVR and OSAHI [34]. However, the severity of sleep disorder in that study was measured by in-home respiratory monitoring only [34].…”

Delayed chemoreceptor responses in infants with apnoea

“…A response that is either too weak or too strong could contribute to respiratory control instability resulting, for example, in upper airway obstruction. [4][5][6] A response that is too fast or too slow could also destabilise respiration. An inability to promptly correct blood gas-that is, a delay in response time in certain infants, could contribute to the onset of bouts of periodic breathing.…”

“…[4][5][6] Very preterm infants with apnoea and periodic breathing exhibit diminished chemoreceptor responsiveness, [7][8][9] while full term infants with OSA can exhibit either subtle changes, 10 11 or normal responses to hypercapnia. 12 It can be difficult to make a clear and unequivocal distinction between different types of apnoeas.…”