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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sleep disordered breathing has increasingly been recognised as a frequent cause of ill-health in the community. Moderate or severe forms of the most common condition, obstructive sleep apnea (OSA), occur in up to 12% of the adult male population. A substantial body of literature has been published on the potential relationship between OSA and cardiovascular disease. In particular, OSA has been associated with cardiac failure, stroke, myocardial infarction and hypertension. Part of this association may be explained by other confounders, mainly obesity, which is common in OSA patients. The present review was prepared following a workshop aimed to critically review available scientific evidence suggesting that hypertension is a direct consequence of OSA. In addition, pathophysiologic mechanisms that may be involved in the relationship between OSA and cardiovascular disease, particularly brief intermittent elevation of blood pressure and sustained systemic hypertension, are discussed.
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PMID:Obstructive sleep apnea and blood pressure elevation: what is the relationship? Working Group on OSA and Hypertension. 820 10

Cerebral vascular ischemic strokes are known to precipitate Cheyne-Stokes periodic breathing. Interestingly, Cheyne-Stokes-like breathing during sleep may be associated with obstructive sleep apnea (OSA) in some individuals. Therefore, it was reasoned that stroke patients with periodic breathing in sleep would be susceptible to OSA. Because oscillations in upper airway resistance can occur as a component of sleep-induced periodic breathing, we hypothesized that stroke patients with sleep-induced periodic breathing would have oscillations in upper airway resistance. These oscillations in resistance would be expected to contribute to OSA. We studied stroke patients with sleep-induced periodic breathing and control subjects to evaluate the relationship between upper airway resistance and ventilation in periodic breathing in sleep. Ventilation and upper airway resistance were measured in presleep wakefulness and in stage 2 NREM sleep. Mean tidal volume, minute ventilation, respiratory cycle timing variables, and upper airway resistance were not different between stroke and control subjects, either awake or asleep. Upper airway resistance increased and ventilation volume decreased from wakefulness to sleep in both groups. In an equivalent number of subjects from each group, reciprocal patterned oscillations in tidal volume and upper airway resistance were present at a 5 to 12.5 breath frequency during sleep. As upper airway resistance increased, tidal volume decreased. Stroke patients had wider fluctuations in upper airway resistance than control subjects, likely contributing to the higher number of sleep-disordered breathing events observed in the stroke patients.
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PMID:Mechanism of sleep-induced periodic breathing in convalescing stroke patients and healthy elderly subjects. 822 15

Obstructive sleep apnea syndrome (OSAS) is the most important form of sleep-related breathing disorders due to its high prevalence and its potential for developing cardiovascular diseases. The increased morbidity of these patients is explained by the coincidence with cardiovascular diseases, and the increased mortality of untreated patients is due to cardiovascular complications, which depend on the degree of the breathing disorder. Heavy snoring, as a partial obstruction of the upper airways, and OSAS are independent risk factors for the development of cardiovascular diseases and stroke. Causal associations exist between acute hemodynamic changes, pressure and volume load, changes in the humoral and the central nervous system, and blood gas alterations during the obstructive apnea and the long-term condition due to OSAS. Obstructive apnea can be divided into an early phase, a late phase, and a phase of the postapneic hyperventilation with respect to hemodynamic changes, blood gas alterations, and the autonomic nervous system. The most striking changes in these parameters are seen at the end of apnea and in the first resumption of breathing, with an increase in systemic and pulmonary blood pressure, decrease in stroke volume, and a distinct change in heart rate. Manifestation of systemic hypertension even in the awake state is promoted by changes in the volume system, with activation of neurohumoral changes and by a resetting of baro- and chemoreceptors. Similar mechanisms are discussed in the development of pulmonary hypertension. In this circumstance the role of hypoxemia as a causal factor for pulmonary hypertension or as a consequence due to structural changes of the pulmonary vessels is controversial. OSAS is frequent in patients with coronary heart disease and these patients must be classified as a particular risk group because of apnea-associated silent myocardial ischemia and electric instability of the myocardium. The occurrence of arrhythmia in patients with OSAS is closely related to the apnea and hyperventilation events and depends on the sympathovagal balance. Early diagnosis and suitable therapy of patients at risk not only abolishes the sleep-related breathing disorder but also improves long-term outcome.
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PMID:[Sleep apnea and cardiovascular risk]. 857 38

Obstructive sleep apnea (OSA) is a common disorder associated with systemic hypertension, myocardial infarction, stroke, and premature death. Elevated sympathetic tone has been documented previously in OSA and may contribute to the cardiovascular risk. As OSA therapy appears to reduce mortality, we wondered if decreased apnea activity would attenuate the sympathetic hyperactivity of untreated patients. Muscle sympathetic nerve activity (MSNA) was measured during wakefulness via peroneal microneurography in seven patients with documented OSA before and at least 1 mo after compliance-monitored nasal continuous positive airway pressure (CPAP) therapy. Before institution of CPAP therapy, MSNA was high in all patients and decreased after CPAP therapy (baseline versus CPAP: 69.4 +/- 15.3 versus 53.9 +/- 10.5 bursts/min, mean +/- SD; p<0.01). However, the decrease in MSNA was limited to the four patients with the greatest nightly use of CPAP (> or = 4.5 h/night), whereas it remained unchanged in the three patients who were less compliant. There was a direct linear correlation between the decrease in MSNA (bursts/min) and the average hours of CPAP use per night (r = 0.87, p = 0.01). We conclude that in patients with OSA effective reduction in apnea activity with CPAP therapy diminishes the high sympathetic tone present during resting wakefulness.
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PMID:Influence of treatment on muscle sympathetic nerve activity in sleep apnea. 861 63

Obstructive sleep apnea (OSA) is a common condition with serious health and social consequences for millions of people. If untreated, it has significant effects on mortality, particularly by contributing to the rate of hypertension, stroke, and cardiac pathology. Standard therapy involves the use of a nasal continuous positive airway pressure device during sleep. This keeps the upper airway from collapsing, avoiding the cause of apneas and hypopneas. The inconvenience and side effects of the device make compliance with its use less than ideal. There are several surgical techniques that have been developed to correct OSA. These techniques have had variable success rates and are accompanied by some morbidity and mortality. Intraoral devices that position the mandible forward show promise for increasing the hypopharyngeal airway. A technique for physiologically determining an effective jaw relationship is described, as is a design for a device that maximizes nighttime retention. Radiographic analyses in the upright and supine positions are used to determine adequate airway improvement. The intraoral device can be used as a diagnostic tool to select patients who will most likely benefit from surgery.
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PMID:Obstructive sleep apnea: a mandibular positioning device for treatment and diagnosis of an obstruction site. 862 Mar 90

Sleep apnea, defined as the cessation of breathing for at least 10 seconds during sleep, can have detrimental effects on the critically ill. Three types of sleep apnea exist, the most common being obstructive sleep apnea. Though its prevalence is only 1% to 3% in adults, it is very important to diagnose it and treat it early in the critically ill because it causes respiratory failure and difficult weaning from mechanical ventilation. Its most characteristic manifestations are repetitive apneic episodes during sleep, snoring, and diurnal hypersomnolence. Complications of sleep apnea include dysrhythmias, systemic and pulmonary hypertension, hypoxia, hypoventilation, left ventricular dysfunction, and stroke. Treatment methods depend on the cause and include medications, surgery, and nasal continuous positive airway pressure. The main nursing role is astute assessment and early detection, proper respiratory management, provision of psychologic support, and patient and family teaching.
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PMID:Sleep apnea: a challenge in critical care. 877 69

Patients with obstructive sleep apnea demonstrate both acute and chronic hemodynamic changes attributable to their disease. Acutely, these patients experience repetitive nocturnal hemodynamic oscillations. Sudden increases in heart rate and arterial pressure occur in association with decreases in left ventricular stroke volume immediately following apnea termination. These hemodynamic changes are likely attributable primarily to the effects of oxygen desaturation and arousal, an abrupt change in state. These acute changes occur against a background of altered cardiovascular control. Patients with sleep apnea, even when sleeping without obstructions, fail to display the normal nocturnal decline in arterial pressure of 10-15% from the waking value. The absence of a nocturnal decline may have chronic consequences, such as development of left ventricular hypertrophy. Another chronic hemodynamic consequence of sleep apnea may be sustained diurnal hypertension. Epidemiologic studies suggest individuals with sleep disordered breathing are at greater risk of daytime hypertension, even after controlling for other risk factors. Although sleep apnea may contribute to pulmonary, as well as systemic hypertension, sleep apnea alone does not appear to be a cause of decompensated right heart failure. Although knowledge of the hemodynamic consequences of sleep apnea has grown in recent years, much remains to be learned.
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PMID:Hemodynamic consequences of obstructive sleep apnea. 884 30

Obstructive sleep apnoea (OSA) has been implicated through epidemiologic studies as a co-morbid factor in cardiovascular disease. There is a greater incidence of hypertension and atherosclerosis related diseases such as stroke, angina, and acute myocardial infarction in patients with OSA. However, obesity is a common problem in OSA as well as cardiovascular disease and is argued by some to be the etiologic factor for both OSA and cardiovascular morbidity. Clearly, there is shortened longevity in patients with untreated or inadequately treated OSA. Other factors which could account for this early mortality in OSA are sudden death during sleep (arrhythmia) or even fatalities from sleep related automobile accidents. The reason that the association between OSA and cardiovascular disease remains unclear is that the relationship thus far is demonstrated only by epidemiological association, not by mechanisms showing a cause-effect relationship. Some of these possible mechanisms are discussed below. Regardless of the mechanisms, the evidence is that OSA needs to be treated aggressively if patient morbidity and mortality from cardiovascular disease is to be reduced.
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PMID:Obstructive sleep apnoea and cardiovascular morbidity. 890 28

Several health hazards and social disabilities are associated with obesity. Increased mortality is associated with increased body weight. A high rate of mortality results from heart disease, diabetes mellitus, gallbladder disease, high blood pressure, and cancer. Physiologic cardiovascular changes occur, leading to left ventricular hypertrophy and lipid abnormalities. Hypertension, stroke, and venous stasis are increased. Pulmonary abnormalities include obstructive sleep apnea, which can be associated with secondary polycythemia and right ventricular hypertrophy. Gallstones, gallbladder disease, and accumulation of fat on the liver are significantly increased. Gout and reproductive abnormalities in women are common. Osteoarthritis of the knees and spine occur, although osteoporosis is rare. Risk for endometrial and breast cancer is increased, particularly in the presence of increased central fat. Changes in the skin include stretch marks, acanthosis negricans, hirsutism, intertrigo, and multiple papillomas. Impaired psychosocial function is manifested as social isolation, loss of job mobility, increased employee absenteeism, and economic and social discrimination.
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PMID:Health hazards of obesity. 897 52

Patients with obstructive sleep apnea syndrome (OSAS) present upper airway obstruction during sleep which can be documented by electromyography. The cause of weakness in oropharyngeal muscles is still unknown. Lesions of pons and medulla oblongata have to be expected. Brainstem auditory evoked potentials (BAEP) may indicate pathological changes in these regions. Several studies described normal BAEP in OSAS-patients. Moderate forms of OSAS as well as central sleep apnea syndromes were investigated, however. In our study 20 patients (17 men, 3 women, mean age 53.9 +/- 2.1 ys) with severe OSAS (apnea/hypopnea-index: 34.2 +/- 14.1/h, part of O2-saturation < or = 90% during sleep (SaO2 < or = 90%): 13.5 +/- 4.2%, minimal nocturnal O2-saturation: 78.0 +/- 2.5%) before starting nCPAP-therapy were investigated. BAEP were elicited after applying clicks 70 dB above threshold to each ear. Means of single wave latencies as well as interpeak latencies (I-V, I-III, III-V) were delayed significantly compared to normal controls. Main prolongations were seen regarding wave latency I (p < or = 0.001) and-interpeak latency I-V (p < or = 0.001). Prolongation of interpeak latencies (mean +/- 2.5 SD) of one or two sides could be demonstrated in 12 out of 20 patients. Pontomesencephal lesions (9 patients) dominated. There was no connection with respiratory parameters. As against pathological BAEP changes correlated with the duration of the disease. In conclusion pathological BAEP indicating brainstem lesions were seen in 60% of the examined OSAS-patients. Mesencephal lesions dominated, number of lesions increased with duration of disease. Therefore pathological findings have not to be considered as cause but as a result of hypoxemia in OSAS. Pathological BAEP may reveal a higher risk for cerebrovascular stroke. Therefore these patients should be leaded to further cerebrovascular investigation.
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PMID:[Acoustic evoked potentials (AEP) in obstructive sleep apnea syndrome]. 909 89


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