Respiratory physiology & neurobiology
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Respir Physiol Neurobiol · Feb 2006
Comparative StudyNocturnal non-invasive positive pressure ventilation: physiological effects on spontaneous breathing.
The dynamic process of how non-invasive positive pressure ventilation (NPPV) improves spontaneous ventilation is unclear. Therefore, daytime trends of blood gases and breathing pattern were assessed by measurements 0, 0.5, 1, 3, 7, 11 and 15 h after cessation of nocturnal controlled NPPV in patients with chronic hypercapnic respiratory failure. Twelve patients (six COPD/six restrictive) who were established on NPPV and 12 controls (six COPD/six restrictive) completed. ⋯ Lung function parameters and inspiratory impedance remained unchanged. Improvements in health-related quality of life were evident and were correlated to the decline of elevated bicarbonate levels (r = 0.72, P < 0.01). In conclusion, there is a stepwise adaptation process lasting 3h when switching from nocturnal controlled NPPV to daytime spontaneous breathing in which tidal volume increases and PaCO2 drops after an initial PaCO2 decrease while on NPPV.
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Respir Physiol Neurobiol · Feb 2006
Comparative Study Clinical TrialThe ventilatory response to carbon dioxide and sustained hypoxia is enhanced after episodic hypoxia in OSA patients.
Our primary hypothesis was that the acute ventilatory response to carbon dioxide in the presence of sustained hypoxia {VRCO2 (hypoxia)} or hyperoxia {VRCO2 (hyperoxia)} would increase in subjects with obstructive sleep apnea (OSA) after exposure to episodic hypoxia. Secondarily, we hypothesized that chronic (i.e. years) exposure to episodic hypoxia, a hallmark of OSA, would facilitate persistent augmentation of respiratory activity (i.e. long-term facilitation) after acute (i.e. minutes) exposure to episodic hypoxia. Nine healthy males with OSA that were healthy otherwise completed a series of rebreathing trials before and after exposure to eight 4 min episodes of hypoxia. ⋯ However, only the increase in the VRCO2 (hypoxia) after episodic hypoxia was greater than the increase measured after exposure to sham episodic hypoxia. Long-term facilitation of ventilation, tidal volume and breathing frequency was not evident after episodic hypoxia. We conclude that the VRCO2 (hypoxia) is enhanced after exposure to acute episodic hypoxia and that enhancement of the VRCO2 (hypoxia) occurs even though long-term facilitation is not evident.