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

Postpolio syndrome is a group of related signs and symptoms occurring in people who had paralytic poliomyelitis years earlier. New weakness, fatigue, poor endurance, pain, reduced mobility, increased breathing difficulty, intolerance to cold, and sleep disturbance in various degrees and expressions make up the syndrome. The reported incidence is between 25% and 80%. The origins are multifactorial and can be associated with underexertion, overexertion, inactivity due to intercurrent illness or injury, hypo-oxygenation, sleep apnea, deconditioning, and the failure of sprouted, compensatory large motor units. The exercise question in postpolio syndrome is related to the experience of new weakness or loss of muscle function due to overuse, which is often associated with injudicious repeated challenges to weakened musculature. Carefully prescribed exercise can be used for increasing strength and endurance and improving cardiopulmonary conditioning.
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PMID:Postpolio syndrome and cardiopulmonary conditioning. 186 50

Adaptation of the heart to the disturbed gas exchange function in chronic diseases of the lung consists of hypertrophy of the right ventricle (cor pulmonale). Prognosis of the chronic cor pulmonale depends on the degree of the pulmonary hypertension. Chronic obstructive diseases of the lung (COLD) are, in accordance with their widespread occurrence, the most frequent contributing causes to the development of chronic cor pulmonale. Sleep apnoea can also lead to pulmonary hypertension, independent of COLD. The diagnostic value of measurement of pulmonary arterial pressure at rest and under stress, compared with noninvasive examination methods such as echocardiography or radionuclide venography, remains indubitable. Treating the underlying pulmonary disease is the therapy of choice. Long-term O2 therapy is the only safely established cardiac therapeutic principle in hypoxaemic patients that prolongs survival times.
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PMID:[The heart in lung diseases]. 236 56

Recreational diving is a popular sport, although human ability to stay in and under water is severely limited physiologically. An understanding of these limitations enhances safety and enjoyment of sports diving. Breath-hold diving involves head-out water immersion, apnoea and submersion, exercise, cold stress, and pressure exposure. Each of these components, by itself, elicits prominent and specific physiological effects. Combination of these factors produces a unique and interesting physiological response generally known as diving reflex. Humans display weak diving responses, but exhibit no oxygen conservation function. Nevertheless, application of diving-induced physiological changes is now finding its way into clinical practice. Apnoea, face immersion, and head-out water immersion all show promise of clinical application. There are several spin-offs from diving research worth noting. Diuresis, enhancement of cardiac performance, and redistribution of blood flow, all produced by head-out water immersion, have been shown to be clinically useful, besides providing physiological data useful to space travel. Results from investigations on apnoea have been shown to be relevant to the following: treating some forms of cardiac arrhythmias; understanding drowning, sudden infant death syndrome and sleep apnoea; and confirming hyperventilation as the major cause of drowning. In comparison to marine mammals, humans are poor divers because of severe physiological constraints which limit their breath-hold time, diving depth, and ability to conserve body heat. Although under special circumstances humans can achieve unusually long breath-hold time and reach exceptional depth with a single breath, the sustainable working time and depth are only about 1 minute and 5 metres, respectively. Hypothermia inevitably results in divers working in the ocean. Without thermal protection, the intolerable limit of 35 degrees C is reached within 30 minutes in winter (10 degrees C) water and within 60 to 90 minutes in summer. Nevertheless, effective harvest work can be performed by humans in the ocean, and recreational benefits enhanced when these physiological limitations are respected. An unusual circulatory state exists during head-out water immersion in that there is a sustained increase of stroke volume. This results in 30% increase in cardiac output when the subject is resting in thermal neutral water, indicating a substantial overperfusion for the oxygen requirement. Furthermore, animal experiments showed that the elevated blood flow is preferentially channeled to the liver, fat, and the organs in the splanchnic region.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Applied physiology of diving. 327 55

We studied ten men with olivopontocerebellar degeneration. Our findings of the autonomic deficits as manifested by orthostatic hypotension, impaired Valsalva's response, abnormal findings on cold pressor and mental arithmetic tests, and plasma renin and norepinephrine abnormalities in some patients with olivopontocerebellar degeneration suggested a defective central control of the sympathetic nervous system. Five patients had sleep apnea. Autonomic dysfunction and sleep apnea in olivopontocerebellar degeneration may result from degenerative lesions in the cerebellum and the brain stem.
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PMID:Autonomic dysfunction and sleep apnea in olivopontocerebellar degeneration. 638 99

Asthma is increasing in prevalence and morbidity worldwide. Worsening of asthma symptoms during sleep and following exercise is an important component of this morbidity. Better recognition and management of nocturnal asthma and exercise-induced broncho-constriction should lead to improved outcomes. Measures to alleviate nocturnal asthma include elimination of exposure to allergens, use of measures to control contributing factors (rhinitis, sinusitis, gastroesophageal reflux, sleep apnea), maximization of the dosage of daytime asthma medications, and appropriately timed use of medications such as a long-acting inhaled beta 2 agonist, a once-daily sustained-release theophylline product, and an oral corticosteroid. Bronchoconstriction after exercise can be decreased by physical conditioning, warm-up exercises, wearing of a face mask in cold weather, postponement of exercise until at least 2 hours after a meal, and pretreatment with an inhaled beta agonist. Pretreatment with inhaled cromolyn sodium (Intal), nedocromil sodium (Tilade), or ipratropium bromide (Atrovent) may be added if necessary.
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PMID:Nocturnal asthma and exercise-induced bronchospasm. Why they occur and how they can be managed. 777 48

Cardiovascular autonomic function in normotensive awake patients with obstructive sleep apnoea syndrome was studied in 21 normotensive (mean age 48 +/- 14 years), drug-free men with obstructive sleep apnoea syndrome. Cardiovascular reflex tests with continuous blood pressure monitoring and biochemical indices were performed the morning after a standard polygraphic sleep recording. A group of 20 age-matched (mean age 49 +/- 19 years) normal subjects was used as controls. The obstructive sleep apnoea syndrome patients showed higher heart rate and noradrenaline plasma levels (p < 0.05) at rest and a higher blood pressure response to head-up tilt (p < 0.01), suggesting sympathetic overactivity. Respiratory arrhythmia, baroreflex sensitivity index and Valsalva ratio were significantly lower in the obstructive sleep apnoea syndrome group (p < 0.01) whereas the decrease in heart rate induced by the cold face test was significantly higher (p < 0.05) showing a blunting of reflexes dependent on baroreceptor or pulmonary afferents with normal or increased cardiac vagal efferent activity. These abnormalities in autonomic regulation may predispose obstructive sleep apnoea syndrome patients to cardiovascular complications like hypertension and cardiac arrhythmias.
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PMID:Cardiovascular autonomic dysfunction in normotensive awake subjects with obstructive sleep apnoea syndrome. 805 38

The PPS is now a well-recognized entity encompassing the late manifestations that occur because of previous poliomyelitis. Common signs and symptoms include fatigue, cold intolerance, joint deteriorations with pain, and prominent neurologic problems that include new weakness, muscle pain, atrophy, respiratory insufficiency, dysphagia, and sleep apnea. It is estimated that there are 1.63 million polio survivors in the United States and that half of them will develop PPS. PPS and PPMA usually begin 30 to 40 years after the acute illness and are very slowly progressive. The etiology is unclear, although premature exhaustion of the new sprouts that develop after acute poliomyelitis and of their motor neurons appears most likely. Less likely is a persistent polio-virus infection or an immune-mediated problem. Treatment is primarily supportive, although nonfatiguing strengthening exercise may improve strength over the short term. The long-term effects of this type of exercise remain to be clarified.
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PMID:Post-polio syndrome: an update. 827

Weight loss reduces many of the health hazards associated with obesity including insulin resistance, diabetes mellitus, hypertension, dyslipidemia, sleep apnea, hypoxemia and hypercarbia, and osteoarthritis. Potential adverse effects of weight loss include a greater risk for gallstone formation and cholecystitis, excessive loss of lean body mass, water and electrolyte problems, mild liver dysfunction, and elevated uric acid levels. Less consequential problems such as diarrhea, constipation, hair loss, and cold intolerance may also occur. The short-term adverse effects are not severe enough to contraindicate weight loss, nor do they outweigh its short-term benefits.
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PMID:Short-term medical benefits and adverse effects of weight loss. 836 5

Our own investigations comprising 23,174 patients suffering from sleep apnoea showed that about 4 per cent of these patients suffer from a hyperreactive bronchial system. In some of these patients treatment with nCPAP causes coughing or mild dyspnoea even after having been previously asymptomatic. Loss of water and heat on the surface of bronchial mucosa may induce reversible bronchoconstriction. We examined in 60 patients suffering from obstructive sleep apnoea whether mechanical treatment with nCPAP would cause a change in bronchial reactivity. Cold air hyperventilation was used in provocation testing. Provocation tests were performed before and after a 3-day treatment with nCPAP in the early morning. In some patients with previously positive reaction, application of nCPAP alone decreased the lung function. Cold air hyperventilation challenge may be helpful to detect possible risks in patients using nCPAP, and to minimise such risks.
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PMID:[Effect of n-CPAP therapy on outcome of cold provocation]. 934 Jun 38

-Patients with obstructive sleep apnea are at increased risk for hypertension. The mechanisms underlying this increased risk are not known. We tested the hypothesis that obstructive sleep apnea, independent of factors such as hypertension, obesity, and age, is characterized by impairment of baroreflex sensitivity. We measured muscle sympathetic nerve activity (MSNA) and heart rate responses to activation and deactivation of baroreceptors in newly diagnosed, never treated, normotensive patients with obstructive sleep apnea. These responses were compared with those obtained in healthy control subjects closely matched for age, body mass index, and blood pressure. Heart rate and MSNA changes during infusion of phenylephrine (baroreceptor activation) were similar in the control subjects and patients with sleep apnea. Infusion of nitroprusside (baroreceptor deactivation) elicited similar decreases in mean arterial pressure (MAP) but lesser MSNA increases in patients with sleep apnea than in control subjects. Calculation of DeltaMSNA/DeltaMAP ratio revealed that baroreflex regulation of sympathetic activity for similar blood pressure changes was diminished in patients with sleep apnea in comparison to normal control subjects (P=0.01). However, increases in heart rate during nitroprusside infusion were comparable in both groups. Sympathetic, blood pressure and heart rate responses to the cold pressor test were also similar in the 2 groups. Our results indicate that normotensive patients with sleep apnea have a selective impairment of the sympathetic response to baroreceptor deactivation but not to baroreceptor activation or to the cold pressor test. The impairment of baroreflex sympathetic modulation in patients with sleep apnea is not accompanied by any impairment of baroreflex control of heart rate.
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PMID:Baroreflex control of sympathetic nerve activity and heart rate in obstructive sleep apnea. 985 70


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