Respiration; international review of thoracic diseases
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Patients with neuromuscular disease may suffer from nocturnal respiratory failure despite normal daytime respiratory function. The physiological reduction in muscle tone during sleep may be life-threatening in a patient with impaired muscle strength. Nocturnal respiratory failure may occur in patients with the postpolio syndrome, amyotrophic lateral sclerosis, myasthenia gravis, myotonic dystrophy, and muscular dystrophy. ⋯ Daytime symptoms may include morning drowsiness, headaches and excessive daytime sleepiness. Polycythemia, hypertension, and signs of heart failure may also be seen. Effective treatment is available, and may improve the quality of life, and possibly increase survival.
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Worsening of hypoxaemia during sleep in patients with chronic obstructive pulmonary disease has been extensively investigated in the past 20 years owing to the development of polysomnography and to the advent of reliable transcutaneous oximeters. Sleep-related hypoxaemia is characteristic of rapid-eye-movement (REM) sleep but may be present during other sleep stages. There is a strong relationship between nocturnal O2 saturation and the level of daytime PaO2: the more pronounced daytime hypoxaemia, the more severe nocturnal hypoxaemia. ⋯ The deleterious effects of sleep-related hypoxaemia include cardiac arrhythmias, 'hypoxaemic stress' on the coronary circulation and especially, peaks of pulmonary hypertension. The treatment of nocturnal hypoxaemia is conventional O2 therapy (both nighttime and daytime) in patients who exhibit marked daytime hypoxaemia (PaO2 < 55-60 mm Hg). At present data are not sufficient for justifying the use of isolated nocturnal O2 therapy in patients with nocturnal desaturation who do not qualify for conventional O2 therapy.
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Randomized Controlled Trial Clinical Trial
Breathing pattern and respiratory mechanics in chronically tracheostomized patients with chronic obstructive pulmonary disease breathing spontaneously through a hygroscopic condenser humidifier.
Hygroscopic condenser humidifiers (HCHs) have been proposed to artificially condition gases breathed by intubated and mechanically ventilated patients. These devices may improve viscosity and coloring of secretions, preventing further bacterial colonization, and heat inspiratory flow in chronically tracheostomized (CT) patients during spontaneous breathing. The aim of this study was to evaluate the effects of HCH on respiratory mechanics and breathing pattern in CT patients with chronic obstructive pulmonary disease (COPD) breathing spontaneously during quiet breathing and maximal voluntary ventilation (MVV). ⋯ These changes were not significantly different without the application of HCH. In CT COPD patients spontaneously breathing. HCHs have no significant effects on the breathing pattern and respiratory mechanics both during quiet breathing and MVV.
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Comparative Study Clinical Trial
Changes in arterial and transcutaneous oxygen and carbon dioxide tensions during and after voluntary hyperventilation.
The purposes of our study were (1) to investigate whether a 3-min short-term hyperventilation leads to posthyperventilatory hypoxemia and (2) to assess the role of transcutaneous blood gas measurements for monitoring oxygen and carbon dioxide changes during the after the test. In 10 male volunteers arterial and transcutaneous blood gases were measured simultaneously before, during and after a 3-min voluntary hyperventilation maneuver. Baseline arterial PO2 increased from 13.7 +/- 0.4 kPa (103 +/- 3 mm Hg) to 18.6 +/- 0.3 kPa (139 +/- 2.3 mm Hg; p < 0.005 compared to baseline) during hyperventilation. ⋯ A short-term over-breathing of 3 min causes a significant posthyperventilatory hypoxemia. We hypothesize that posthyperventilatory hypoxemia is caused by hypopnea as a result of depleted CO2 body stores. Noninvasive transcutaneous blood gas measurements are not reliable for monitoring blood gas changes during and after hyperventilation, most probably because of the slow response time of the electrodes and the reflex vasoconstriction of the skin vessels.