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

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

Sleep apnea and snoring are widely discussed as risk factors for internal and neurological diseases. The prevalence of snoring in an Austrian population survey is about 27.2% (males 36.5%, females 18.9%), and that of apnea (respectively irregularity and/or cessation of breathing) about 8.5% (31% of all snorers). Clinical symptoms like naps, daytime sleepiness, unquiet sleep, hypertonia, headache in the morning and psychological symptoms may be characteristics of sleep apnea. They should lead to further diagnosis and removal of this risk factor for ischemic heart disease and stroke.
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PMID:[Sleep apnea as a risk factor]. 883 23

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

Although sleep apnea (SA) appears to be a cardiovascular risk factor, little is known about its frequency in patients with transient ischemic attack (TIA) and stroke. We prospectively studied 59 subjects (26 women and 33 men; mean age, 62 years) with stroke (n = 36) or TIA (n = 23) with the use of a standard protocol that included assessment of snoring and daytime sleepiness (Epworth Sleepiness Score [ESS]), a validated SA score (Sleep Disorders Questionnaire [SDQ-SA]), and a severity of stroke score (Scandinavian Stroke Scale [SSS]). SA was considered clinically probable (P-SA) when habitual snoring was associated with an ESS of > 10 or when SDQ-SA score was > or = 32 in women and > or = 36 in men. Polysomnography (PSG) was obtained in 36 subjects (group 1) a mean of 12 days after TIA or stroke. In 23 subjects (group 2), PSG was not available (n = 11), refused (n = 10), or inadequate (n = 2). Clinical and PSG data were compared with those obtained in 19 age- and gender-matched control subjects. Groups 1 and 2 were similar in mean age (61 versus 64 years), type of event (36% versus 44% TIA), reported habitual snoring (58% versus 52%), and P-SA (58% versus 50%). PSG showed SA (Apnea-Hypopnea Index [AHI], > or = 10) in 25 of 36 subjects (69%). The proportion of subjects with SA was similar in the TIA and stroke groups (69% versus 70%) and was well above the frequency found in our control group (15%). An AHI of > or = 20 and a minimal oxygen saturation of < 85% were each found in 20 of 36 subjects (55%). Gender and age did not correlate with severity of SA. Subjects with habitual snoring, P-SA, or severe stroke (SSS of < 30) had a significantly higher AHI (p < 0.05). The sensitivity of P-SA for SA was 64%, and the specificity was 67%. We conclude that SA has a high frequency in patients in the acute phase of TIA and stroke and SA cannot be predicted reliably on clinical grounds alone but is more likely in patients with habitual snoring, abnormal SDQ-SA, or severe stroke.
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PMID:Sleep apnea in patients with transient ischemic attack and stroke: a prospective study of 59 patients. 890 24

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

Sleep-related breathing disorders (SRBD) include several disorders gradually developing from simple and loud snoring through upper airway resistance syndrome and sleep apnoea up to the Pickwickian syndrome. They are manifestant as a respiratory distress and apnoeic episodes, desaturation of oxygen in the blood and interruption of sleep. These symptoms are demonstrated in a case of a patient with the Pickwickian syndrome. SRBD may result in severe secondary life-threatening cardiovascular complications (nocturnal arrhythmias, sudden cardiac death, stroke and pulmonary oedema). They may contribute also to the development of important disorders of public health such as hypertension, obesity, and traffic accidents resulting from hypersomnolence and fatigue. (Tab. 1, Fig. 3, Ref. 46.)
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PMID:[Sleep-related breathing disorders--an interdisciplinary topic in undergraduate and postgraduate medical education]. 926 12

Obstructive sleep apnoea (OSA) produces immediate effects on pulmonary haemodynamics during sleep in all subjects. In addition, in some subjects, OSA is accompanied by chronic abnormalities of the pulmonary circulation. During sleep, pressure in the main pulmonary artery oscillates within each apnoea, in synchrony with intrathoracic pressure changes; in addition, it may increase progressively as a consequence of prolonged severe hypoxaemia. Pulmonary capillary wedge pressure may increase during inspiratory efforts, possibly reflecting a mechanical limitation of left ventricular function. Cardiac output decreases at apnoea resolution as an effect of a decreased right ventricular stroke volume, despite increased cardiac frequency. During wakefulness, postcapillary pulmonary hypertension occurs on exercise in many OSA patients, whilst pulmonary hypertension at rest is precapillary and occurs in patients with an altered daytime respiratory function. Development of right ventricular hypertrophy and a decrease in right ventricular ejection fraction appear to be related to the severity of respiratory alterations during sleep, whilst an overt right heart failure requires an altered daytime respiratory function. Long-term treatment of the obstructive sleep apnoea syndrome is more effective in increasing right ventricular ejection fraction than in decreasing pulmonary artery pressure during wakefulness.
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PMID:Acute and chronic influences of obstructive sleep apnoea on the pulmonary circulation. 927 Feb 54

Sleep apnea is a surprisingly common disorder in end-stage renal disease (ESRD) and chronic renal failure. The symptoms of sleep apnea frequently go unreported or may be misdiagnosed as uremia, depression, chronic illness, or insomnia. A review of the literature was performed to define the prevalence, morbidity, and treatment of sleep apnea syndrome in the ESRD patient. Sleep apnea occurs in at least 60% of ESRD patients. The known complications of sleep apnea include arrhythmias, pulmonary hypertension, and systemic hypertension. In addition, sleep apnea has been implicated in coronary artery disease and strokes. The contribution of sleep apnea to the high mortality from cardiac disease and stroke in peritoneal dialysis and hemodialysis patients is unknown. The causes of the increased prevalence of sleep apnea in ESRD patients are unknown and likely differ from the general population, but the treatment is similar. The literature suggests that modality of renal replacement therapy does not matter; however, large nocturnal volume peritoneal dialysis may worsen sleep apnea. Renal transplantation may be curative. In conclusion, sleep apnea may be an under-diagnosed disease in patients on dialysis. There are significant reasons to suspect that sleep apnea may worsen the morbidity and mortality of ESRD, and there are potential successful therapies.
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PMID:Sleep apnea in renal failure. 936 Jun 57

An estimated 97 million adults in the United States are overweight or obese, a condition that substantially raises their risk of morbidity from hypertension, dyslipidemia, type 2 diabetes, coronary heart disease, stroke, gallbladder disease, osteoarthritis, sleep apnea and respiratory problems, and endometrial, breast, prostate, and colon cancers. Higher body weights are also associated with increases in all-cause mortality. Obese individuals may also suffer from social stigmatization and discrimination. As a major contributor to preventive death in the United States today, overweight and obesity pose a major public health challenge.
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PMID:Executive summary of the clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults. 975 81

Several studies have demonstrated a clear association between snoring, sleep apnoea and increased risk of stroke. However, the possible role of sleep apnoea in the pathophysiogenetic mechanisms of cerebrovascular disease is still unknown. Our aim in this study was to investigate cerebral haemodynamic changes during the waking state in eight patients with sleep apnoea syndrome (OSAS) by means of transcranial Doppler (TCD). In particular, we studied cerebral vascular reactivity (CVR) to hypercapnia calculated by means of the breath holding index (BHI). The investigation was performed in the early morning, soon after awakening, and in the late afternoon. Data were compared with those of eight healthy subjects matched for age and vascular risk factors. OSAS patients showed significantly lower BHI values with respect to controls both in the morning (0.56 vs. 1.36; P < 0.0001) and in the afternoon (1.12 vs. 1.53; P < 0.0001). In patients, BHI values in the afternoon were significantly higher than in the morning (P < 0.0001). These data demonstrate a diminished vasodilator reserve in OSAS patients, particularly evident in the morning. This reduction of the possibility of cerebral vessels to adapt functionally in response to stimulation could be linked to hyposensitivity of cerebrovascular chemoreceptors after the continuous stress caused by nocturnal hypercapnia.
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PMID:Impairment of daytime cerebrovascular reactivity in patients with obstructive sleep apnoea syndrome. 984 56


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