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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The most common causes of hypoxic cor pulmonale are chronic bronchitis and emphysema. Although the clinical situation in some patients is characterized early by hypoxemia, oedema is rare in patients with an arterial pO2 above 60 mm Hg. The presence of oedema can be regarded as an unfavorable prognostic indicator. For many years, peripheral oedema had been considered an expression of congestive cardiac failure; it may be assumed, however, that neither right nor left ventricular failure is prerequisite to the development of oedema. Oedema formation can be attributed to excessive retention of salt and water or a redistribution of body water into the extracellular compartment. Hypercapnia and acidosis affect direct stimulation of renal hydrogen ion secretion. The resulting electrochemical imbalance is compensated by reabsorption of sodium. Hypercapnia and, in acute phases possibly, hypoxia lead to a fall in renal blood flow mediated by alpha-adrenergic stimulation through activation of the renin-angiotensin-aldosterone system. An increase in plasma ADH may also contribute to development of oedema. The development of cor pulmonale or respiratory insufficiency can be enhanced by nocturnal hypoventilation and hypoxia during sleep as well as by sleep apnoea. Nocturnal hypoxia, smoking and reduced oxygen tension in the relevant kidney cells responsible for erythropoietin release promote the occurrence of secondary polycythaemia. For treatment of acute exacerbations in cor pulmonale associated with infections bronchitis antibiotics such as amoxycillin and cotrimoxacol are drugs of first choice. While the use of digoxin is of doubtful value, the cautious administration of diuretics may bring symptomatic relief. In addition to physiotherapy, beta-2-selective bronchodilators and nebulized bronchodilator therapy can be useful; theophyllines dilate airways and increase cardiac output but they can cause arrhythmias and a deterioration of arterial blood gases in hypoxic patients. If the patient has been treated chronically with corticosteroids, the dosage will have to be incremented; if asthma is suspected, corticosteroid treatment is essential. Controlled oxygen therapy is the most important single therapy aimed at relief of severe arterial hypoxaemia. Oxygen should be titrated initially (for the first one or two days) to achieve an arterial tension of at least 48 mm Hg. Thereafter, the oxygen flow should be increased to yield an arterial tension in excess of 60 mm Hg during continued treatment for two to three weeks.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hypoxic cor pulmonale: a review. 294 54

Hypoxaemia during the rapid eye movement phase of sleep is common in older healthy normal subjects over 55 years of age; the sleep apnoea syndromes--such as obstructive sleep apnoea, where oro-nasal airflow ceases for more than 10 seconds on many separate occasions throughout the night, due to failure of contraction of the genio-glossus muscle; "blue and bloated" patients with chronic bronchitis and emphysema, where profound nocturnal hypoxaemia is common in REM sleep, and is associated with further elevation of pulmonary arterial pressure; the overlap syndrome--where "blue and bloated" chronic bronchitis is associated with an obstructive sleep apnoea syndrome; and bronchial asthma, where hypoxaemia is associated with irregular breathing and possibly nocturnal bronchoconstriction. Although absolute recognition depends upon all night sleep studies, monitoring of ear oxygen saturation, breathing patterns, and EEG, the clinical features when awake can lead to suspicion of sleep hypoxaemia--as, for example, obesity and obstructive sleep apnoea with loud snoring and restlessness in sleep, hypoxaemia during wakefulness in the overlap syndrome, and nocturnal awakening with wheeze in bronchial asthma. Treatment depends on the cause, and may vary from weight loss and nasal continuous positive airway pressure in obstructive sleep apnoea, to nocturnal oxygen in "blue bloaters", a combination of these two in the overlap syndrome, and long acting bronchodilators such as slow release theophyllines in nocturnal asthma. Recognition and appropriate treatment of nocturnal hypoxaemia is an important new development in respiratory medicine.
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PMID:Breathing during sleep. 390 86

In five patients with hypoxic chronic bronchitis and emphysema we measured ear O2 saturation (SaO2), chest movement, oronasal airflow, arterial and mixed venous gas tensions, and cardiac output during nine hypoxemic episodes (HE; SaO2 falls greater than 10%) in rapid-eye-movement (REM) sleep and during preceding periods of stable oxygenation in non-REM sleep. All nine HE occurred with recurrent short episodes of reduced chest movement, none with sleep apnea. The arterial PO2 (PaO2) fell by 6.0 +/- 1.9 (SD) Torr during the HE (P less than 0.01), but mean arterial PCO2 (PaCO2) rose by only 1.4 +/- 2.4 Torr (P greater than 0.4). The arteriovenous O2 content difference fell by 0.64 +/- 0.43 ml/100 ml of blood during the HE (P less than 0.05), but there was no significant change in cardiac output. Changes observed in PaO2 and PaCO2 during HE were similar to those in four normal subjects during 90 s of voluntary hypoventilation, when PaO2 fell by 12.3 +/- 5.6 Torr (P less than 0.05), but mean PaCO2 rose by only 2.8 +/- 2.1 Torr (P greater than 0.4). We suggest that the transient hypoxemia which occurs during REM sleep in patients with chronic bronchitis and emphysema could be explained by hypoventilation during REM sleep but that the importance of changes in distribution of ventilation-perfusion ratios cannot be assessed by presently available techniques.
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PMID:Mechanism of transient nocturnal hypoxemia in hypoxic chronic bronchitis and emphysema. 407 77

The possibility of nocturnal oxygen desaturation (NOD) in patients with chronic bronchitis and emphysema (CBE) even with basal hypoxemia greater that 55 mmHg is well recognised. Nocturnal hypoventilation is admitted as the main cause for this NOD. In this study we evaluate how the presence of left ventricular dysfunction (LVD) could aggravate NOD. Thirty-six patients with CBE and basal stabilised PaO2 55-70 mmHg underwent right heart catheterisation and polysomnographic study. NOD was defined as more than 30% of total sleep time with SaO2 less than 90%; LVD was defined as capillary pressure greater than 15 mmHg. Six patients were excluded from analysis because of sleep apnoea syndrome. In the remaining 30 patients (20 men, 10 women; mean age = 65.88.6 years; mean FEV1 = 0.970.31 litres; 43.316.6% predicted; mean basal PaO2 = 61.83.6 mmHg) 8 had LVD and 18 and NOD. Patients with NOD had a greater diurnal level of hypoventilation (basal PaCO2 = 44.63.8 vs. 414.1 mmHg; p = 0.025). Patients with LVD, despite identical diurnal pulmonary function, showed a significantly p < 0.05) greater degree of NOD (mean nocturnal SaO2 = 84.56.4 vs 89.52.5; minimal nocturnal SaO2= 68.517.3 vs. 79.47.8; Time spent with SaO2 < 90% = 78.833.7 vs. 43.138.7). We conclude that the presence of LVD in patients with CBE and PaO2 55-70 mmHg aggravates the intensity and the time spent with NOD, probably because of aggravation of hypoventilation or ventilation/perfusion mismatching.
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PMID:[The effect of left ventricular dysfunction on nocturnal desaturation in patients with chronic emphysematous bronchitis and PaO2 55-70 mmHg]. 934 Oct 31

Sleep alters breathing pattern and respiratory responses to many external stimuli. These changes permit the development of sleep-related hypoxemia in patients with respiratory diseases and may contribute to the pathogenesis of apneas in patients with sleep apnea syndrome. Many respiratory problems during sleep are related to an abnormal control of ventilation. The impaired ventilatory responses permit the development of hypoventilation during sleep and of sleep-related hypoxemia in patients with hypoxic chronic emphysema post TB sequela and kyphoscoliosis. In all these conditions, the hypoxia is most marked in REM sleep, when the ventilatory responses are at their lowest. The impaired ventilatory responses during sleep may accompanied by a decrease in the response of the upper airway opening muscles to chemostimulation during sleep and both factors may be important in the initiation and continuation of apneas.
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PMID:[Breathing during sleep]. 950 31

We investigated the clinical usefulness of continuous nocturnal oxygen saturation monitoring in patients undergoing home oxygen therapy (HOT). The subjects were 11 patients with chronic respiratory disease in the process of healing from acute exacerbation. None were mechanically ventilated. Each subject underwent full overnight oximetry. One patient was excluded from further investigation because of periodic desaturation suggestive of sleep apnea. The remaining 10 subjects included 5 patients with sequelae of pulmonary tuberculosis, 2 with diffuse panbronchiolitis, 1 with chronic pulmonary emphysema, 1 with chronic bronchitis, and 1 with kyphoscoliosis. All underwent full overnight and 30 min daytime oximetry monitoring for 23.7 +/- 7.4 (mean +/- SD) consecutive days. Daytime oximetry was performed when subjects were awake and resting in supine position. Mean nocturnal oxygen saturation (NmSpO2) and mean daytime oxygen saturation (DmSpO2) were calculated from data obtained from 0:00 through 5:00 hrs and from data obtained during a stable 10 min daytime period, respectively. The difference between NmSpO2 and DmSpO2 (delta SpO2), the percentage of total sleep time with SpO2 < or = 90% (DST 90) and nocturnal lowest oxygen saturation (NLSpO2) were calculated once daily for each subject. There were significant (p < 0.05) correlations between NmSpO2 and NLSpO2, between NmSpO2 and DST 90, and between NLSpO2 and DST 90 in all subjects. However, significant (p < 0.05) correlations between NmSpO2 and DmSpO2 were observed in only 6. During acute exacerbation, NmSpO2 was lower than DmSpO2, and delta SpO2 increased. Conversely, with the amelioration of acute symptoms, delta SpO2 decreased and NmSpO2 was higher than DmSpO2. There was a significant (p < 0.05) reverse correlation between NmSpO2 and delta SpO2 in 9 subjects. We concluded that monitoring nocturnal oxygen saturation is clinically useful to assessments of oxygenation status in patients undergoing HOT, and that it may assist the early diagnosis of acute exacerbation of respiratory failure.
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PMID:[Continuous oximetry monitoring in patients undergoing home oxygen therapy for chronic respiratory failure]. 1054 Aug 34

The lungs are a delicate interface between the atmosphere and our bodies across which oxygen diffuses from the air we breathe to the blood which carries oxygen to the cells and mitochondria. In healthy lungs at sea level where there is a surfeit of oxygen, this process occurs easily, whereas, in lungs with disease it becomes a task which may not be fully successful and hypoxemia may ensue or worsen. At high altitude where the barometric pressure (Pb) and thus the supply of oxygen is lower, the job of getting oxygen to the blood, even in the healthy lung is more difficult, and in the diseased lung it may be impossible. This presentation will review the lungs' responses to high altitude, with emphasis on the abnormal. Both acute and chronic responses of patients with pre-existing lung disease will be reviewed. Pulmonary diseases encountered at high altitude in previously healthy people, such as high altitude pulmonary edema and chronic mountain sickness will be touched on only as they pertain to other patients. Pre-existing lung disease (with and without hypoxemia at sea level) such as obstructive lung diseases (asthma, COPD, emphysema), and restrictive lung diseases (sarcoid, asbestosis, interstitial pulmonary fibrosis) will be discussed in terms of gas exchange, lung mechanics, and treatment at high altitude. Disorders of ventilatory control; e.g., obesity-hypoventilation syndrome and sleep apnea, may present formidable problems, and guidelines for their treatment will be discussed. Infectious lung diseases; e.g., pneumonia, cystic fibrosis, and pulmonary vascular disorders such as chronic mountain sickness, primary pulmonary hypertension, and congenital absence of the pulmonary artery are important disorders that require special attention because of the accentuated hypoxic pulmonary vascular response encountered at high altitude. The purpose therefore, is to provide the medical practitioner with the insight into prevention, recognition, and treatment of pulmonary problems encountered specifically at high altitude, as well as guidance on how best to advise patients with lung disease who want to fly in airplanes and/or ascend to high altitude for work or pleasure.
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PMID:Lung disease at high altitude. 1063 92

Permanent tracheotomy was the first surgical procedure proposed for the treatment of severe obstructive sleep apnoea syndrome and is still the only surgical option that ensures, even in very severe cases, complete elimination of apnoea and, in turn, clinical remission. Improved knowledge of the causes of obstructive sleep apnoea syndromes and the increasing therapeutic options (instrumental, medical and surgical) have resulted in cases requiring tracheotomy as the only indispensable therapeutic option becoming more rare. At present, the only indications are in very occasional conditions of life-threatening obstructive sleep apnoea syndromes and in patients on whom continuous positive airway pressure is not tolerated or is not effective (severe deoxygenation or hypercapnia, severe respiratory disorder index, severe obstructive sleep apnoea syndrome-related arrhythmias, severe excessive daytime sleepiness, heart diseases or ischaemic encephalopathy exacerbated by obstructive sleep apnoea syndromes, obstructive pneumopathy exacerbated by obstructive sleep apnoea syndromes, severe obstructive sleep apnoea syndromes with few chances of resolution with other surgical procedures or failure of the latter). Moreover, it is the only therapeutic solution in rare nocturnal laryngeal stridor due to multisystemic atrophy (in which obstructive sleep apnoea syndrome is due to nocturnal laryngospasm of neurologic origin). Therapeutic tracheotomy must be permanent (tracheostomy) and, therefore, preferably carried out with a specific technique (skin-lined tracheotomy), able to guarantee greater stability, less risk of granulation tissue, wider opening of the tracheostomy, sufficient reversibility. In our experience, very few patients (10 cases) withsleep disorder breathing have been submitted to skin-lined tracheotomy. Of these, the majority were submitted to surgery for severe apnoea due to nocturnal laryngospasm on account of multisystemic atrophy (n = 7), while only 3 cases of obstructive sleep apnoea syndromes were submitted to skin-lined tracheotomy, i.e., 0.7% of the 424 patients operated on for obstructive sleep apnoea syndrome and 1.7% of the 175 operated on for severe, or very severe, obstructive sleep apnoea syndromes (RDI > 40). Skin-lined tracheotomy was not followed by important complications and expected results were achieved with immediate disappearance of daytime symptoms and considerable improvement in nocturnal apnoea. Besides sleep-related disorders, numerous clinical situations with indications for a permanent tracheotomy may benefit from the skinlined technique, such as severe laryngeal or tracheal stenoses, laryngeal diplegias, miasthenia gravis, lateral amyotrophic sclerosis, intractable aspiration, severe emphysema.
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PMID:Role of skin-lined tracheotomy in obstructive sleep apnoea syndrome: personal experience. 1546 94

Pulmonary artery hypertension secondary to chronic lung diseases is a clinical entity with no specific symptoms that can develop as a result of parenchymal lung disorders (COPD-emphysema, sleep apnea syndrome, diffuse parenchymal lung diseases, etc.) and pulmonary vascular disorders (vasculitis, sarcoidosis, etc.). In the clinical history of these chronic and invalidating diseases, pulmonary vasculature goes through various degenerative and/or proliferative changes, responsible of the pulmonary arterial hypertension appearance. The rise in pulmonary artery pressure can be subtle and the progression from an asymptomatic disease to a more severe syndrome is often common in all forms of secondary pulmonary arterial hypertension. Etiopathology of pulmonary artery hypertension secondary to chronic lung diseases is based on one or more of the following mechanisms: hypoxic vasoconstriction, decreased area of pulmonary vascular bed, volume/pressure overload. In these forms, the above three mechanisms show common mediators, all responsible of disease progression but singularly potential reversible. Therapies for secondary pulmonary artery hypertension consist primarily on the treatment of the underlying disease. Therapy is most effective when initiated prior to the onset of irreversible pulmonary vascular damage. In the last two decades, new medical treatments (prostacyclins, endothelin receptor antagonists, phosphodiesterase inhibitors) for pulmonary arterial hypertension have been available for the sporadic and the secondary to systemic sclerosis forms. The role of these drugs in the other forms of pulmonary arterial hypertension has not been well studied yet. This review will go through the pathogenesis and the several therapeutic approaches for pulmonary artery hypertension secondary to chronic pulmonary diseases or pulmonary vasculature disorders.
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PMID:Pulmonary arterial hypertension secondary to chronic lung diseases: pathogenesis and medical treatment. 1803 16

Wind instrument performance is a notable feature in pneumology under aspects of ventilatory physiology and respiratory diseases. It requires an adequate ventilatory function combined with precise control of air flow and the ability to generate sufficient mouth pressures. Depending on the type of wind instrument, the required rates of airway pressure and air flow differ significantly. The cause of respiratory disease in wind instrument players may be related to these increased airway pressures in terms of a barotrauma. Wind instrumentalists may suffer from hemoptysis, laryngoceles, velopharyngeal insufficiency and pneumoparotitis due to their musical performance. Even the development of lung cancer has been assumed to be related to wind instrument playing. Controversy exists about implicating wind instrument use as the cause of pulmonary emphysema or in changes of pulmonary function, which is, however, unlikely under physiological aspects. Furthermore, professional wind instrumentalists may be impaired in their work by the side effects of anti-obstructive medication and respiratory infection. On the other hand, the potential therapeutic effects of wind instrument performance have to be considered. For asthmatic teenagers a significant improvement of pulmonary function and of physical and emotional activities could be related to wind instrument playing. Last but not least, didgeridoo playing was shown to be a promising alternative treatment for obstructive sleep apnoea syndrome.
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PMID:[Pneumological aspects of wind instrument performance--physiological, pathophysiological and therapeutic considerations]. 1807 66


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