The influence of induced hypocapnia and sleep on the endogenous respiratory rhythm in humans.

Datta, Avijit; Shea, Steven A.; Horner, Richard L.; Guz, A.

doi:10.1113/jphysiol.1991.sp018693

Cited by 103 publications

(64 citation statements)

References 20 publications

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“…In humans, apnoeas or unstable breathing patterns can be induced by small reductions in Pa,CO 2 below the resting level both in sleep [29,30] and sometimes in the awake state [26,[31][32][33]. Venous carbon dioxide unloading by haemodialysis [16,27] and the ventilatory response to transient carbon dioxide pulses during recovery from voluntary overbreathing [34] suggested that the apnoeic threshold for Pa,CO 2 may be up to 1.3 kPa below the resting level, but with wide individual variation.…”

Section: Discussionmentioning

confidence: 99%

Effect of oxygen on breathing irregularities during haemodialysis in patients with chronic uraemia

Yap¹,

Wang²,

Poh³

1998

Eur Respir J

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Hypoxaemia and breathing irregularities have been shown to occur during haemodialysis in patients with chronic renal failure. This study examined the role of hypoxia in the genesis of the irregular breathing during haemodialysis. The ventilatory patterns using respiratory inductance plethysmography and arterial blood gases were studied in seven males with chronic renal failure on long-term haemodialysis. The study was carried out before and during dialysis on one day without (D1) and another day with intranasal oxygen at 4 L x min(-1) (D2). On D1, mean (SD) arterial oxygen tension (Pa,O2) fell 1.9 (0.9) kPa (p<0.001) and mean minute ventilation (V'E) fell 1.9 (1.1) L x min(-1) (p<0.01) during dialysis. The arterial carbon dioxide tension (Pa,CO2) did not show a significant decrease (4.7 (0.2) kPa before and 4.6 (0.2) kPa during dialysis). Cumulative number of apnoeas was 64 and the coefficients of variation (COV) of respiratory frequency (fR) and tidal volume (VT) were 29.6 (11.9) and 38.2 (11.9)%, respectively. On D2, mean Pa,O2 remained stable (20.4 (4.1) kPa before, 21.3 (4.1) kPa during dialysis). There was no significant change in mean V'E (6.4 (0.9) L x min(-1) before, 5.5 (0.5) L x min(-1) during dialysis). Pa,CO2 decrease was not significant but the fall was greater (4.8 (0.1) kPa before, 45 (0.5) kPa during dialysis). Cumulative number of apnoeas was 94 and the COVs offR and VT were 35.8 (5.1) and 40.5 (11.3)%, respectively. Oxygen administration did not significantly affect the haemodialysis-induced changes in ventilation and breathing pattern, despite a significant protective effect from the fall in arterial oxygen tension. It was concluded that the fall in arterial oxygen tension is not the main determinant of breathing irregularities during haemodialysis.

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Section: Discussionmentioning

confidence: 99%

Effect of oxygen on breathing irregularities during haemodialysis in patients with chronic uraemia

Yap¹,

Wang²,

Poh³

1998

Eur Respir J

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“…These findings are consistent in general with ours in demonstrating an apnoeic threshold well below the resting level of PET,Co2 This threshold can be decreased by hypoxia (Honda, Natsui, Hasumura & Nakamura, 1963;Lahiri et al 1978) and by after-discharge, which also tends to prevent periodic breathing, whereas anaesthesia, sleep, altitude and metabolic alkalosis favour instability and periodicity (Cherniack, Euler, Homma & Kao, 1979). Passive HV in hyperoxia in non-rapid eye movement (REM) sleep in subjects who did not show awake post-hyperventilation apnoea resulted in apnoea when PCo2 fell 3-6 mmHg below the sleeping rest value and 1-2 mmHg below the awake rest value, with increase in incidence of apnoea both with increasing depth of sleep and in hyperoxia (Datta et al 1991). Similar results were obtained in hypoxia (Skatrud & Dempsey, 1983).…”

Section: Discussionmentioning

confidence: 99%

“…Moser et al (1965) showed more apnoea in hyperoxia, but normal breathing following both active and passive HV has also been described (Ashbridge, Jennett & North, 1972;Jennett, Ashbridge & North, 1974;Skatrud & Dempsey, 1983;Datta et al 1991), as has hyperpnoea, at least in the minute or so following the end of HV (Mills, 1946;Fink, 1961;Tawadrous & Eldridge, 1974;Swanson, Ward & Bellville, 1976;Folgering & Durlinger, 1983;Cummin, Sidhu, Telford & Saunders, 1992). Most of these studies were performed in normoxia.…”

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confidence: 99%

“…The occurrence of apnoea in humans following hyperventilation is more controversial. Apneoa has been reported to occur following voluntary or active hyperventilation (VHV) in sleep (Fink, 1961;Skatrud, Henke & Dempsey, 1990;Datta, Shea, Horner & Guz, 1991), in anaesthesia (Fink, Hanks, Holaday & Ngai, 1960), following sedation (Moser, Rhodes & Kwaan, 1965) and during venous C02 unloading by haemodialysis (De Backer, Heyrman, Wittesaele, Waeleghem, Vermeire & Broe, 1987), but the relationship of this apnoeato Pa°2 was less certain than in animals.…”

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confidence: 99%

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Post‐hyperventilation apnoea in conscious humans.

Meah

Gardner

1994

The Journal of Physiology

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1. In nine normal subjects, analysis was performed of the number, length and location of apnoeic pauses during 20 min of recovery following voluntary overbreathing (VHV). Based on a definition of apnoea as expiratory time greater than 6 s, apnoeas occurred between mean times of 0-8 and 5-6 min after the end of VHV, the end of this period being associated with a mean PET,cO, value of 36-4 mmHg, which was below the initial mean resting value of 39-8 mmHg. 3. Within this apnoeic period, 80 % of experiments produced apnoeas of less than 10 s duration, 61 % of between 10 and 20 s duration and 42 % of between 20 and 30 s duration. Only one out of nine subjects consistently failed to show apnoeas.4. The range of lengths of individual apnoeas and the number per minute were independent of the length and level of VHV and were not significantly different between the four protocols. 5. The number and length of apnoeas did not change in repeated runs in each subject. We were not able to confirm previous reports that apnoeas occurred more frequently in subjects familiar with the experiment. 6. These results reconciled previous studies showing either apnoea or hyperpnoea following voluntary overbreathing in conscious humans. They showed an initial period of heightened breathing lasting about a minute with few apnoeas, consistent with 'afterdischarge'. Beyond that, apnoeas occurred as an 'all-or-nothing' phenomenon as long as PET,C02 was on average less than 3-4 mmHg below resting PET,co0, The occurrence and length of apnoeas was consistent in individual subjects with no evidence of a learning effect.

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“…The picture is completely different during sleep or under anaesthesia. Several studies have shown that, under these circumstances, the maintenance of respiratory rhythm is critically dependent on chemical feedback [41,[48][49][50]. Reducing Pa,CO 2 by only a few mmHg causes apnoea.…”

Section: Chemical Feedbackmentioning

confidence: 99%

Control of breathing in mechanically ventilated patients

Georgopoulos¹,

Roussos²

1996

Eur Respir J

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Thus, the response of ventilator to patient effort, and that of patient effort to ventilator-delivered breath are inevitably the two components of control of breathing during mechanical ventilation; the ventilatory output is the final expression of the interaction between these two components. As a result of this interaction, the various aspects of control of breathing of the respiratory system may be masked or modulated by mechanical ventilation, depending on several factors related both to patient and ventilator. This should be taken into consideration in the management of mechanically ventilated patients.

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The influence of induced hypocapnia and sleep on the endogenous respiratory rhythm in humans.

Cited by 103 publications

References 20 publications

Effect of oxygen on breathing irregularities during haemodialysis in patients with chronic uraemia

Effect of oxygen on breathing irregularities during haemodialysis in patients with chronic uraemia

Post‐hyperventilation apnoea in conscious humans.

Control of breathing in mechanically ventilated patients

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