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

The syndrome of obstructive sleep apnoea is associated with an increased morbidity (the consequence of diurnal hypersomnolence and cardiovascular complications). The contraction of the dilator muscles of the upper airways (nose and pharynx) allows their patency at the time of inspiration. The obstruction of the airways resulted in a disequilibrium between the forces which tend to their collapse (negative inspiratory transpharyngeal pressure gradient) and those which contribute to their opening (muscle contraction). The mechanisms which underlie the triggering of obstructive apnoea are multiple including a reduction in the calibre of the superior airways, an increase in their compliance, and a reduction in the activity of the muscle dilators. This latter is intimately linked to the respiratory muscles and these muscles respond in a similar manner to a stimulation or a depression of the respiratory centre. The ventilatory fluctuations observed during sleep (alternately hyper and hypo ventilation of periodic respiration) thus favours an instability of the superior airways and the occurrence of oropharyngeal obstruction. The depth of post-apnoeic desaturation depends on the value of the arterial oxygen saturation at the beginning of apnoea, the duration of the period of apnoea and the pulmonary volume as the period of apnoea passes off. The cardiovascular consequences of apnoea include disorders of rhythm (bradycardia, auriculoventricular block, ventricular extrasystoles) and haemodynamic (pulmonary and systemic hypertension). This results in a stimulatory metabolic and mechanical effect on the autonomic nervous system. The electroencephalographic awakening which precedes the easing of obstruction of the upper airways is responsible for the fragmentation of sleep. The factors implicated in the cessation of the apnoea include hypoxia and hypercapnia but one also invokes a role for the negative pressure generated during the course of the apnoea.
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PMID:[Physiopathology of obstructive sleep apneas]. 269 Feb 8

The ventilatory response to hypoxia (VRH) in relation to daytime arterial blood pressure was studied in 37 patients with the sleep apnea syndrome (SAS). The patients were divided into hypertensives (n = 16) and normotensives (n = 21). The hypertensive group had a significantly higher VRH (ventilatory increase 1.48 1/min BTPS per percent decrease in arterial oxygen saturation) than the normotensive group (0.69 1/min/%, P less than 0.01). The observed difference raises the question whether a high chemoreceptor sensitivity to hypoxaemia can contribute in causing arterial hypertension among cases with SAS.
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PMID:High ventilatory response to hypoxia in hypertensive patients with sleep apnea. 271 41

Obstructive sleep apnea is frequently found in middle-aged men. Usually, these patients are obese and therefore predisposed to hypertension. This study aimed to elucidate the relationships between hypertension, obesity and obstructive sleep apnea in 48 men suffering from sleep apnea. Hypertension was found in 39 of them (= 81%), 27 patients (= 56%) were morbidly obese (Broca index above 125%), 17 patients (= 36%) were moderately obese (Broca index between 100 and 125%) and 4 patients (= 8%) showed normal weight (Broca index below 100%). Severity of sleep apnea did not correlate with obesity or hypertension. Patients with sleep apnea who were hypertensive were significantly (p less than 0.025) more obese than those with normal blood pressure. Compared with an unselected population showing a similar degree of obesity, patients with obstructive sleep apnea showed a higher prevalence of hypertension and this is independent of age. These findings establish sleep apnea as a risk factor for hypertension.
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PMID:[Obstructive sleep apnea--a risk factor for arterial hypertension]. 271 93

Sleep-related respiratory pattern was evaluated in 175 hypertensive and 110 normotensive men, none of whom reported difficulties in initiating or maintaining sleep. Patients were grouped according to sexual status (complaint of erectile problems), hypertension treatment status (treated or untreated), and blood pressure (diastolic less than 90 or greater than or equal to 90). The prevalence of sleep apnea, apnea index, duration of the longest episode of apnea, and penile rigidity were tabulated. The group with elevated blood pressure, persistent even with antihypertensive drug therapy, had the most sleep apnea. The treated hypertensive men with controlled blood pressure had significantly less apnea than those whose blood pressure remained high. Untreated hypertensive groups, however, did not differ from normotensive groups with respect to apnea. Evidence of abnormal sleep-related respiratory activity was found in both hypertensive and normotensive groups with erectile problems. Interestingly, penile rigidity was significantly lower for hypertensive men with erectile complaints than for normotensive men with erectile complaints. There was also a small, but significant, negative correlation between apnea index and penile rigidity among men with erectile complaints. These results indicate that sexual status is an important consideration in the diagnosis of hypertension and sleep apnea. Moreover, these data suggest an interrelationship among hypertension, erectile dysfunction, and sleep apnea.
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PMID:Hypertension, erectile dysfunction, and occult sleep apnea. 274 Jun 93

To examine the hypothesis that the tendency to raised blood pressure in snorers is associated with nocturnal hypoxaemia and snoring, blood pressure was measured and snoring, oxyhaemoglobin saturation (SaO2), and thoraco-abdominal movements were monitored overnight in 372 snorers. Snoring was quantified as number of snores per hour of sleep (snoring index). The data were analysed by multiple linear regression of diastolic blood pressure against age, body mass index (BMI), apnoea-hypopnoea index (AHI, number of episodes per hour), snoring index, and SaO2. Diastolic blood pressure correlated significantly with BMI, AHI, and mean nocturnal oxygen saturation, but not with the snoring index. However, snoring index correlated with BMI, AHI, and mean nocturnal oxygen saturation. Snoring is thus not a direct risk factor for hypertension, but may influence blood pressure via its association with obesity, obstructive sleep apnoea, and nocturnal hypoxaemia.
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PMID:Determinants of blood pressure in snorers. 290 95

The present study reports on polysomnographic findings of sleep apnea syndrome in a representative sample of otherwise healthy middle-aged blue collar workers (age 45.7 +/- 8.5) with normal to borderline blood pressure (systolic 135.5 +/- 16.1; diastolic: 88.3 +/- 10.2), mild overweight (Broca 114.9 +/- 14.7) and with reported nocturnal sleep disturbances. The prevalence of sleep apnea in this sample (N = 20 out of a total of 78 workers with reported sleep disturbances) is 40%. Mean frequency of apnoeic episodes during night was 97.6 +/- 42.7 in the apnea-positive group as compared to 27.1 +/- 19.9 in the apnea-negative group (T = 5.0; p less than 0.0001), with an apnea index of 13.3 +/- 6.2 as compared to 3.5 +/- 2.3 (T = 7.2, p less than 0.0001). Left ventricular hypertrophy (mean diameter of end diastolic left ventricle: 64.0 +/- 9.5 mm) was found in individuals with apnea although manifest hypertension was absent in most individuals.
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PMID:Prevalence of sleep apnea in healthy industrial workers. 293 98

In normal humans, both hypoxia and hypercapnia result in sympathetic nerve activation, and when combined, i.e. hypoxic hypercapnia, synergistically increase sympathetic activity. Apnea during the hypoxic and hypercapnic stress results in further increases in sympathetic activity. Borderline hypertensive humans have exaggerated sympathetic nerve responses to hypoxia. Hypertensives are also prone to sleep apnea. We suggest that sleep apnea may result in very high levels of sympathetic activity which may contribute to daytime hypertension and/or precipitate cardiovascular catastrophe in hypertensive people during sleep.
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PMID:Sympathetic activation by hypoxia and hypercapnia--implications for sleep apnea. 307 27

Snoring has only recently come under wide study. Recent research has established the close relationship of severe snoring to sleep apnea in terms of the obstructive pathophysiology. Snoring tends to increase in severity over time and may progress to sleep apnea. Severe snoring may be associated with pulmonary and systemic hypertension, secondary polycythemia, and cardiac arrhythmias.
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PMID:Snoring: clinical implications and treatment. 310 90

A syndrome of sleep apnoea may appear 15 to 29 years after acute anterior poliomyelitis (PAA). It is generally a mixed syndrome with an association of central type and obstructive apnoea in variable proportions. We report such a case occurring in a patient who had presented 30 years before with PAA, and presenting on this occasion with resting pulmonary artery hypertension, polycythaemia but without disturbance of blood gases. Treatment with positive pressure ventilation was given by the nasal route at 10 cm of water leading to an improvement with a significant decrease in the number and duration of apnoeic episodes and a disappearance of desaturation. The sleep apnoea syndrome (SAS) should be considered as a possible late sequel of PAA.
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PMID:[Sleep apnea syndrome: late sequela of poliomyelitis]. 318 71

Muscle nerve sympathetic activity was recorded in six patients with the sleep apnoea syndrome (SAS). Compared with age- and sex-matched control patients, an increased activity during wakefulness was found. Sleep apnoic events were associated with sequencies of progressively increasing sympathetic activity followed by a sudden reduction of activity. The high sympathetic activity associated with SAS may be important in the development of the systemic hypertension commonly seen in these patients.
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PMID:Is high and fluctuating muscle nerve sympathetic activity in the sleep apnoea syndrome of pathogenetic importance for the development of hypertension? 324 Dec 51


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