We have recently shown that breathing 50% O2 markedly stimulates ventilation in healthy subjects if end-tidal PCO2 (PETCO2) is maintained. The aim of this study was to investigate a possible dose-dependent stimulation of ventilation by O2 and to examine possible mechanisms of hyperoxic hyperventilation. In eight normal subjects ventilation was measured while they were breathing 30 and 75% O2 for 30 min, with PETCO2 being held constant. Acute hypercapnic ventilatory responses were also tested in these subjects. The 75% O2 experiment was repeated without controlling PETCO2 in 14 subjects, and in 6 subjects arterial blood gases were taken at baseline and at the end of the hyperoxia period. Minute ventilation (VI) increased by 21 and 115% with 30 and 75% isocapnic hyperoxia, respectively. The 75% O2 without any control on PETCO2 led to 16% increase in VI, but PETCO2 decreased by 3.6 Torr (9%). There was a linear correlation (r = 0.83) between the hypercapnic and the hyperoxic ventilatory response. In conclusion, isocapnic hyperoxia stimulates ventilation in a dose-dependent way, with VI more than doubling after 30 min of 75% O2. If isocapnia is not maintained, hyperventilation is attenuated by a decrease in arterial PCO2. There is a correlation between hyperoxic and hypercapnic ventilatory responses. On the basis of data from the literature, we concluded that the Haldane effect seems to be the major cause of hyperventilation during both isocapnic and poikilocapnic hyperoxia.

The mechanisms leading to hypoxemia during sleep in patients with respiratory failure remain poorly understood, with few studies providing a measure of minute ventilation (V I) during sleep. The aim of this study was to measure ventilation during sleep in patients with nocturnal desaturation secondary to different respiratory diseases. The 26 patients studied had diagnoses of chronic obstructive pulmonary disease (COPD) (n = 9), cystic fibrosis (CF) (n = 2), neuromusculoskeletal disease (n = 4), and obesity hypoventilation syndrome (OHS) (n = 11). Also reported are the results for seven normal subjects and seven patients with effectively treated obstructive sleep apnea (OSA) without desaturation during sleep. Ventilation was measured with a pneumotachograph attached to a nasal mask. In the treated patients with OSA and in the normal subjects, only minor alterations in V I were observed during sleep. In contrast, mean V I for the group with nocturnal desaturation decreased by 21% during non-rapid-eye-movement (NREM) sleep and by 39% during rapid-eye-movement (REM) sleep as compared with wakefulness. This reduction was due mainly to a decrease in tidal volume (V T). Hypoventilation was most pronounced during REM sleep, irrespective of the underlying disease. These data indicate that hypoventilation may be the major factor leading to hypoxia during sleep, and that reversal of hypoventilation during sleep should be a major therapeutic strategy for these patients.

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Breathing O2 for up to 1 h has been shown to either not influence or slightly increase (6-13%) minute ventilation. However, end-tidal PCO2 was not kept constant in these experiments. In nine healthy men, we studied the ventilatory, blood pressure, and heart rate responses to 30 min of normobaric hyperoxia (50% O2) at isocapnic conditions. Hyperoxia led to a 60% increase in mean minute ventilation (P = 0.002), largely due to an increase in mean tidal volume from 0.66 +/- 0.04 (SE) to 0.88 +/- 0.05 liter (P = 0.007). Fifteen minutes after the termination of hyperoxia, minute ventilation was still increased (P = 0.02) compared with baseline, although it was reduced compared with hyperoxia (P = 0.02). Arterial blood gas analyses in six subjects before and during hyperoxia showed an increase in arterial PO2 and O2 saturation but no change in arterial PCO2 or pH. Hyperoxia induced no changes in arterial blood pressure or heart rate. We conclude that 1) isocapnic hyperoxia stimulates respiration markedly, an effect that is approximately five times higher than previously measured; 2) the increase in ventilation induced by hyperoxia does not affect arterial blood pressure and heart rate; and 3) in experiments using hyperoxia, its effect on breathing and subsequently on PCO2 has to be taken into account.

Sleep apnoea is common in patients with heart failure. While most patients have central sleep apnoea (CSA), a minority have obstructive sleep apnoea (OSA). The pathophysiology of CSA is not well understood. We hypothesized that central chemosensitivity would be an important pathophysiological factor in patients with CSA, and not in OSA. The aim of this study was to compare ventilatory responses between patients with CSA and those with OSA.Acute ventilatory responses to eucapnic hypoxia and hyperoxic hypercapnia were measured during wakefulness in 34 patients (33 males and one female, aged 59±8 yrs (mean±sd)), with stable medically-treated left ventricular dysfunction (LVD) and sleep apnoea (18 OSA and 16 CSA).Patients with CSA had a decreased awake end-tidal carbon dioxide tension (4.1± 0.5 kPa), increased ventilatory response to carbon dioxide (0.65±0.43 L·min-1·kPaPCO2-1), and eucapnic hypoxic responses in the normal range (0.6±0.4 L·min-1/% fall in arterial oxygen saturation (Sa,O2)). In contrast, patients with OSA had normal endtidal carbon dioxide tension (4.9±0.5 kPa), and normal ventilatory responses to hypercapnia (0.29±0.16 L·min-1·kPaPCO2-1) and hypoxia (0.5±0.5 L·min-1/% fall inSa,O2).These findings suggest that augmented chemosensitivity to hypercapnia may be an important factor in the pathophysiology of central sleep apnoea in patients with heart failure.