Inspiratory neural drive response to hypoxia adequately estimates peripheral chemosensitivity in OSAHS patients

Abstract

The aim of the present study was to examine the relationships between the responses to progressive isocapnic hypoxia and hypoxic withdrawal test in patients with obstructive sleep apnoea-hypopnoea syndrome (OSAHS) and to analyse the determinants of carotid body sensitivity in OSAHS.Nineteen consecutive OSAHS patients and 13 healthy subjects were selected. Ventilatory (DV9I/Sa,O 2 /BSA) and inspiratory neural drive (DP0.1/Sa,O 2 ) responses to progressive isocapnic hypoxia were determined. Peripheral chemosensitivity was evaluated by the hypoxic withdrawal test, which measures the decrease in ventilation caused by two breaths of 100% oxygen (%DV9I).Withdrawal response and ventilatory and inspiratory neural drive responses to hypoxia were lower in OSAHS patients than in control subjects. In patients with OSAHS, %DV9I correlated significantly with DV9I/Sa,O 2 /BSA and with DP0.1/Sa,O 2 . On stepwise multiple linear regression analysis, a strong correlation between %DV9I and DP0.1/Sa,O 2 was found. Moreover, %DV9I, DV9I/Sa,O 2 /BSA and DP0.1/Sa,O 2 were significantly correlated with minimum arterial oxygen saturation and with arousal index.Obstructive sleep apnoea-hypopnoea syndrome patients have a strong relationship between peripheral chemosensitivity and respiratory response to hypoxia, suggesting that hypoxic stimulation of central chemoreceptors is minimally relevant in obstructive sleep apnoea-hypopnoea syndrome. Moreover, sensitivity of the carotid body in patients with obstructive sleep apnoea-hypopnoea syndrome is related to sleep disruption and to nocturnal hypoxia. Eur Respir J 2002; 20: 724-732 The study of peripheral chemosensitivity in patients with obstructive sleep apnoea-hypopnea syndrome (OSAHS) has been of considerable interest over several years [1][2][3][4][5][6][7]. The peripheral chemoreflexes are an important mechanism for regulation of both breathing and autonomic cardiovascular function [8]. In fact, abnormalities in chemoreflex mechanisms have been implicated in the increased cardiovascular stress in patients with OSAHS. The relationship between peripheral chemosensitivity and blood pressure profile suggests that recurrent obstructive apnoeas may reset the peripheral chemoreceptor output to a higher level, causing a chronic increase in sympathetic tone and initiating hypertension [9,10]. Intersubject variation of heart rate changes during sleep apnoea could also be due to variations in response to hypoxia [11].In spite of these pathophysiological implications, the role of peripheral chemoreception in OSAHS has not been adequately evaluated. The nature of the respiratory response to chemical stimuli in awake patients with OSAHS is still unclear. In these patients, depression of peripheral chemosensitivity has been reported [7]. In contrast, other investigators have concluded that response to hypoxia in OSAHS patients is normal [2][3][4][5][6] These discrepancies in findings concerning chemical sensitivity in OSAHS could be due in part to confounding factors, such as obesity, age, ...

Ventilatory drive and the apnea-hypopnea index in six-to-twelve year old children

“…Although the relationship was not particularly strong (explaining about 9–10% of the variability), it was nonetheless statistically significant. Our findings are consistent with observations showing reduced hypoxic sensitivity in adults [36,37], which may be the result of altered dopaminergic neurotransmission at the carotid body [38]. In contrast, the data in children are equivocal.…”

The human diving response, its function, and its control

“…Reduced chemosensitivity is also described in sleep apnea patients. Both a reduced hypoxic ventilatory response and a hypercapnic ventilatory response have been described in sleep apnea patients (Garcia-Rio et al, 2002). A reduced hypoxic ventilatory response has been observed in the Japanese Ama (Masuda et al, 1981) and synchronized swimmers (Bjurstrom & Schoene, 1987) while the hypercapnic ventilatory response was not different from that of the controls.…”

Carotid body oxygen sensing

“…Intermittent hypoxia in rats induces plastic changes in the CB, thus increasing its sensitivity and tonic sympathetic activation without obvious morphological alterations [62,98]. Similarly, OSAS patients have enhanced peripheral chemoreflex sensitivity and in those who experience repetitive hypoxaemia this increase might contribute to high levels of sympathetic activity even during normoxic daytime wakefulness [99,100].…”