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

Some 55% of American adults exceed the criteria for over-weight or obesity. Obesity contributes to numerous other illnesses including hypertension, type 2 diabetes, stroke, osteoarthritis, sleep apnea, and some cancers. Although several prescription medications have been developed to treat obesity, these medications have serious adverse effects. The two broad categories of causes for obesity are psychologic factors and physiologic factors. The first line of therapy is prevention, but to successfully help patients with long-term weight loss, the clinician must consider proper diet, adequate exercise, a positive mental attitude, and using nutrients and dietary supplements that are safe and effective.
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PMID:Individualizing the approach to treating obesity. 1004 77

Obstructive sleep apnoea (OSA) is described by some authors as a potentially lethal disease and by others as an almost harmless condition. Excessive daytime sleepiness, neuropsychological dysfunction, altered quality of life, cardiovascular disease (systemic and pulmonary hypertension, cardiac arrhythmias, stroke and ischaemic heart disease) and increased mortality have been described as OSA complications. There is little argument that OSA may determine sleepiness, alter cognitive functions, and worsen quality of life, although with great interindividual variability: this should induce OSA to be considered an important illness per se, since sleepiness in OSA was shown to lead to important consequences, like road traffic accidents. Besides, OSA may interact with coexisting cardiac and respiratory disease and favour the appearance of heart and respiratory failure. Therefore, OSA is certainly also worth careful consideration as an important aggravating factor of other diseases. The evidence that obstructive sleep apnoea is an independent risk factor for cardiovascular complications other than owing to the recurrent transient blood pressure surges associated with apnoeas during sleep, and for an increased mortality is more conflicting. More studies are necessary to identify which characteristics of obstructive sleep apnoea may be considered important markers of its severity and as risk factors for different possible complications.
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PMID:What is the evidence that obstructive sleep apnoea is an important illness? 1006 35

Although obstructive sleep apnea (OSA) appears to be a cardiovascular risk factor, its frequency in patients with transient ischemic attack (TIA) and stroke remains poorly known. We prospectively studied 128 patients (mean +/- SD age = 59 +/- 15 years) with stroke (n = 75) or TIA (n = 53). Assessment included body mass index (BMI); history of snoring and daytime sleepiness; cardiovascular risk factors and diseases; and severity of stroke (Scandinavian Stroke Scale = SSS). Polysomnography (PSG) was obtained in 80 subjects (group 1), a mean of 9 days (range, 1-71 days) after TIA or stroke. In 48 subjects (group 2), PSG was not available, refused, or inadequate. Groups 1 and 2 were similar with the exception of gender distribution. Clinical and PSG data were compared to those of 25 healthy controls matched for age, gender, and BMI. An apnea-hypopnea index (AHI) > 10 was found in 62.5% of subjects and 12.5% of controls. Between patients and controls there was a significant difference in AHI (mean [range]: 28 (0-140) vs 5 (0-24), p < 0.001), maximal apnea duration (mean + SD: 37 +/- 23 vs 23 +/- 13 seconds, p = 0.009), and minimal oxygen saturation (mean + SD: 82 +/- 10% vs 90 +/- 5%, p < 0.001). Conversely, frequency and severity of OSA were similar in stroke and TIA subjects. Multiple regression analysis identified age, BMI, diabetes, and SSS as independent predictors of AHI. Sleep apnea has a high frequency in patients with TIA and stroke, particularly in older patients with high BMI, diabetes, and severe stroke. These results may have implications for prevention, acute treatment, and rehabilitation of patients with acute cerebrovascular diseases.
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PMID:Sleep apnea in acute cerebrovascular diseases: final report on 128 patients. 1020 Oct 66

This self-directed learning module highlights new advances in the understanding of co-morbid conditions and medical complications of stroke. It is part of the chapter on stroke rehabilitation in the Self-Directed Physiatric Education Program for practitioners and trainees in physical medicine and rehabilitation. This article covers co-morbid conditions of stroke patients, including cardiovascular disease, diabetes, and sleep apnea. It reviews recent information on complications of stroke, including deep venous thrombosis, dysphagia and aspiration, hospital-acquired infections, depression, falls, spasticity, shoulder pain, and seizures. Treatment advances in diabetes, depression, and spasticity are highlighted. Recent information is presented regarding exercise guidelines for the stroke patient with cardiovascular disease, the relationship between stroke and sleep apnea, prophylaxis of deep venous thrombosis, the changing spectrum of hospital-acquired infections, malnutrition in stroke patients, the problem of falls during rehabilitation, the evaluation and management of poststroke shoulder pain, and the risk of seizures after stroke.
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PMID:Stroke rehabilitation. 2. Co-morbidities and complications. 1032 98

The repetitive respiratory events that characterize obstructive sleep apnea (OSA) are each followed by abrupt increases in heart rate and in pulmonary and systemic artery pressure and by sudden decreases in right and left ventricular stroke volume. The changes in systemic pressure may be profound, with patients who are normotensive while awake having systolic pressures approaching 300 mm Hg after apnea termination. Because of these dramatic hemodynamic oscillations during sleep, many clinicians and investigators have postulated a connection between sleep-disordered breathing and cardiovascular morbidity and even mortality. This review critically examines the evidence for such a causal relationship. We begin, however, by reviewing the normal hemodynamic changes that occur during sleep. We then describe the acute hemodynamic events associated with OSA. Finally, we summarize the evidence for and against a causal connection between sleep apnea and cardiovascular morbidity.
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PMID:Cardiovascular morbidity in obstructive sleep apnea. 1040 30

Impaired vasomotor reactivity of the cerebral vessels on morning awakening has been suggested as one of the mechanisms underlying the predisposition to stroke in the morning. This study investigated cerebrovascular reactivity to hypercapnia on morning awakening and its association with specific sleep-related parameters, including sleep-disordered breathing. Thirty patients undergoing nocturnal diagnostic polysomnography for sleep apnea underwent transcranial Doppler ultrasonography of the middle cerebral artery immediately before going to bed and immediately on morning awakening. Results indicated a morning reduction in cerebral blood flow velocity (CBFV) relative to values from the preceding evening both while breathing room air and 5% CO(2). Hypercapnia was associated with the expected increase in CBFV in both evening and morning. The evening-to-morning difference in CBFV during CO(2) inhalation was independently associated with both overnight CO(2) retention and number of movements with arousal per hour of sleep. Results indicated that more fragmented sleep and greater CO(2) retention during sleep predicted a diminished hypercapnic vasomotor response in the morning. Sleep fragmentation predicted approximately twice the variance in morning hypercapnic vasomotor reactivity relative to overnight CO(2) retention (24 versus 13%). No other polysomnographic measures predicted evening-to-morning differences in vasomotor reactivity. These results are consistent with a body of literature suggesting that sleep loss and sleep fragmentation are associated with blunted hypercapnic ventilatory response.
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PMID:Sleep fragmentation and morning cerebrovasomotor reactivity to hypercapnia. 1050 14

The time course of right ventricular output (RVO) and transmural pulmonary artery pressure (PAP) changes, detected beat-by-beat, were analysed in a sample of obstructive sleep apnoea (OSA) episodes recorded in six patients with OSA syndrome. RVO showed a trend to a decrease during apnoeas, due to a decrease in heart rate, and decreased further in the immediate post-apnoeic period, due to a decrease in right ventricular stroke volume [post-apnoeic RVO = 82.6 +/- 9.3 (SD) % of the value in the immediate pre-apnoeic period; P < 0.01]. Both systolic and diastolic transmural PAP showed a progressive increase throughout apnoeas (from 23.7 +/- 7.3 to 29 +/- 6.9 and from 9.1 +/- 4.4 to 14.3 +/- 3.3 mmHg, respectively, from early to late apnoeic period; P < 0.01), and similarly high values in the late apnoeic and in the immediate post-apnoeic period. Therefore, cardiac output and arterial pressure in the pulmonary circulation undergo simultaneous inverse changes in OSA, similar to what was previously shown in the systemic circulation. Although these data cannot define accurately the behaviour of pulmonary vascular resistance, they suggest that pulmonary vascular resistance could also undergo continuous oscillations in OSA, with recurring peaks detectable between apnoea termination and the immediate post-apnoeic period.
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PMID:Pulmonary haemodynamics in obstructive sleep apnoea. 1060 76

Sleep apnoeas are accompanied by large variations in heart rate (HR) and blood pressure (BP). This nocturnal variability in BP may be involved in the increased cardiovascular morbidity of these patients. Due to the complex interaction between asphyxia, intrathoracic pressure, cardiac function and autonomic activation, the exact haemodynamic mechanisms are unclear. To evaluate the components of the BP surges at resumption of breathing (RB) a non-invasive beat-to-beat measurement was taken of cardiac output (CO) by the pulse contour analysis of the Finapres signal. Six male normotensive patients, free of medication (37-60 y, BMI 26.5-43.0 kg m-2) were studied during polysomnography (apnoea index: 22-69 h-1). Systolic blood pressure rose from 126.5 +/- 1.3 mmHg at beginning apnoea (P1) to 140.4 +/- 1.3 at RB (P < 0.01, ANOVA). During sleep Stages 2 and 3, stroke volume decreased during RB to 96% of P1 value (NS). Due to an opposite change in HR, CO tended to rise at RB to 106% of P1. Computed total peripheral resistance rose during RB to 105% of P1 value (P < 0.011. Therefore, it is concluded that the surge in BP at RB after apnoea is due to concomitant increases in CO and in TPR. Both rises are presumably a consequence of sympathetic nervous activation by the arterial chemoreceptors.
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PMID:Non-invasive measurement of haemodynamics during sleep apnoea. 1060 79

Snoring, a leading symptom of the sleep apnoea syndrome (SAS), has been reported to be one of the risk factors for sleep-related cerebral strokes. Episodes of apnoea are accompanied by hypoxaemia as well as hypercapnia. As CO2 constitute a major regulatory factor controlling cerebral blood flow, it is likely that changes in cerebral perfusion are to be found in patients with SAS, which may be related to nocturnal stroke. A computer-assisted pulsed (2 mHz) Doppler ultrasonography system has been modified for continuous long-term and on-line recording of cerebral haemodynamics together with simultaneous polysomnography, continuous blood pressure recordings, and measurement of the end-expiratory CO2. The dynamics of cerebral blood flow velocity (CBFV) during sleep were measured in the right middle cerebral artery in 10 SAS patients. CBFV showed a characteristic nocturnal pattern with decreases during non-rapid eye movement (NREM) sleep and increases during REM sleep. Changes in sleep stage patterns as well as awakenings from NREM sleep were not regularly accompanied by corresponding changes in CBFV. Dramatic increases in CBFV could be observed during apnoeic episodes, with maximum increases during REM sleep. CO2 reactivity and changes in CBFV related to apnoea duration were markedly increased during sleep compared with the waking state in SAS patients. The dynamic feature of CBFV in relation to sleep patterns reflects quantitative uncoupling between cerebral electrical activity and cerebral perfusion during sleep in SAS patients as has been previously reported for normal subjects (Hajak et al. 1994). It supports a dissociation in the activity of central regulatory mechanisms during human sleep which might cause abnormal cerebral perfusion under certain circumstances. The increased CO2 reactivity during sleep in SAS suggests a 'hypersensitivity' of intracranial vasoactive receptors and/or disturbances in the central autonomic control of cerebrovascular functions. It may be concluded that, under certain conditions, the interaction of decreased cerebral perfusion in SAS patients with sleep-related cerebral perfusion patterns and haemodynamic changes during apnoeic episodes might lead to a critical reduction in cerebral perfusion.
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PMID:Cerebral perfusion during sleep-disordered breathing. 1060 90

Ischaemic stroke occurs most often during the morning hours before noon. In recent studies the peak time of onset has been between 10.00 and 12.00 hours. Snoring every night or almost every night (habitual snoring) is in relation with ischaemic stroke. Snoring occasionally, on the contrary, is not significantly related with stroke. Habitual snoring is the most typical sign of obstructive sleep apnoea syndrome and it is strongly associated with being overweight. Other possible pathophysiological factors that are in relation with habitual snoring, obstructive sleep apnoea and stroke include arterial hypertension, changes in fibrinolytic activity, adult onset diabetes and smoking. It remains to be seen whether nightly occurring partial upper airway obstruction (habitual snoring) with intrathoracic pressure changes is an independent risk factor of ischaemic stroke, There is recent evidence that everything cannot be explained by other known risk factors.
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PMID:Ischaemic stroke, snoring and obstructive sleep apnoea. 1060 93


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