Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We reported a 39-year-old man with myotonic dystrophy. He suffered from morning headache. Respiratory function tests showed restrictive pattern and arterial gas analysis showed hypoxia and hypercapnia with respiratory acidosis (PaCO2 50.8 mmHg, PaO2 63.8mmHg, pH 7.317, SaO2 89.8%). Polysomnograph showed central apneas exclusively in light sleep (stage 1 and 2). O2 saturation fell at most to as low as 50% during the apneas. We conclude that sleep apnea should be consider in patients with myotonic dystrophy associated with morning headache.
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PMID:[A case of myotonic dystrophy with morning headache following sleep apnea syndrome]. 766 17

The hypercapnic ventilation response (HCVR) is positively correlated with forced expired volume in 1 s (FEV1). Therefore, subjects of small stature or patients with lung disease have low values for HCVR. However, indexing the HCVR for the subject's predicted maximal voluntary ventilation (MVV) results in a corrected HCVR (CHCVR) which is not dependent on FEV1 in normal subjects [Respiration 1993;60:197-202]. We hypothesized that the CHCVR would also be useful in assessing chemosensitivity in patients with poor lung function. To obtain the predicted MVV, we used the linear regression for FEV1 vs. measured MVV obtained from 411 patients with a wide range of FEV1 values (MVV = 31.2 x FEV1 + 11.8, r = 0.90, p < 0.001). We compared HCVR and CHCVR to the occlusion pressure response to hypercapnia (OPRH) in 34 patients with chronic obstructive pulmonary disease (COPD) and in 19 patients with low FEV1 due to small stature. All patients had been referred for assessment of possible sleep apnea. The results for the two groups of patients were similar. For the COPD patients, the HCVR had high values for sensitivity (86%) and negative predictive value (94%), but specificity, positive predictive value and accuracy were low (59, 35 and 65%, respectively). In contrast, CHCVR had high values for all the foregoing (86, 96, 100, 100 and 97%, respectively). Our results suggest that the CHCVR is useful in assessing chemosensitivity in patients who are ventilation-limited.
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PMID:Hypercapnic ventilation response in patients with lung disease: improved accuracy by correcting for ventilation ability. 778 12

The association of chronic obstructive pulmonary disease (COPD) and sleep apnea syndrome (SAS), which are both frequent diseases, is likely to occur in a number of patients. We have prospectively investigated a large series (n = 265) of patients who were selected solely on the basis of a confirmed diagnosis of SAS (apnea + hypopnea index > 20/hr). An obstructive spirographic pattern, defined by an FEV1/VC ratio < or = 60%, was observed in 30 of 265 patients (11%). These patients (subgroup "overlap") were older (58 +/- 9) versus 53 +/- 10 yr, p = 0.01) than the remainder of the study population, and all were male patients. Body mass index (BMI) was identical in overlap patients to that in the remainder. Vital capacity and FEV1 were lower, by definition, in the overlap group. PaO2 was lower (66 +/- 10 versus 74 +/- 10 mm Hg, p < 0.001) and PaCO2 higher (42 +/- 6 versus 38 +/- 4 mm Hg, p < 0.001) in the overlap group. Hypoxemia (Pao2, < or = 65 mm Hg) was observed in 17 of 30 overlap patients and in 54 of 235 of the remainder. Hypercapnia (Paco2 > or = 45 mm Hg) was observed in 8 of 30 overlap patients and in 19 of 235 of the remainder. The pulmonary artery mean pressure (PAP) was higher in overlap patients both at rest (20 +/- 6 versus 15 +/- 5 mm Hg, p < 0.01) and during steady-state exercise (37 +/- 12 versus 29 +/- 10 mm Hg, p = 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Association of chronic obstructive pulmonary disease and sleep apnea syndrome. 781 77

In order to determine the relationship between chronic hypercapnia and anthropomorphic data, pulmonary function tests and slopes of ventilatory responses to hypercapnia (HVCR) and hypoxia (HVR), we studied 55 patients with sleep apnea-hypopna syndrome (SAHS). Patients were divided into hypercapnic, PaCO2 > or = 45 mm Hg (Group I, n = 23, PaO2 = 61 +/- 10 and PaCO2 = 50 +/- 5 mm Hg, and [HCO3-] = 30 +/- 4 mEq/l [means +/- SD]) and normocapnic (or eucapnic), PaCO2 < 45 mm Hg (Group II, n = 32, PaO2 = 76 +/- 10 and PaCO2 = 39 +/- 4 mm Hg and [HCO3-] = 25 +/- 3 mEq/l [means +/- SD]) groups. When compared to the normocapnic group, hypercapnic patients were significantly heavier (with greater body surface area) and had significantly more severe restrictive and obstructive defects and impaired HVR and HCVR. The means (+/- SD) of some of the data follow (* indicates p < 0.05 when Group I is compared to Group II): [table: see text] When subgroups of hypercapnic and eucapnic patients with similar lung functions were compared, the subgroups differed significantly in their weights; conversely, in subgroups with comparable weights, lung function tests differed significantly. These data suggest that the mechanisms of chronic hypercapnia are multifactorial, and we hypothesize that, in the face of repetitive apneas and hypopneas, increased weight and abnormal lung function tests interact and contribute to the generation and maintenance of hypercapnia.
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PMID:Chronic hypercapnia in obstructive sleep apnea-hypopnea syndrome. 799 52

The two broad categories of sleep apnea syndrome are associated with obstructive or mixed events on the one hand, and central events on the other. The pathogenesis of both seems to involve periodic reduction in respiratory drive, although obstructive apneas may also involve an anatomic abnormality of the upper airway. Patients with obstructive sleep apnea syndrome most commonly exhibit resuscitative snoring and daytime sleepiness. Snoring is generally less prominent in the central sleep apnea syndromes; those with daytime hypercapnia generally complain of daytime sleepiness, whereas those without hypercapnia complain of disturbed sleep. The overnight polysomnogram is the preferred method of diagnosing both disorders.
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PMID:Sleep apnea syndromes: overview and diagnostic approach. 802 35

In postnatal infants, there is similarity between the time course of transient gonadal steroid secretion and the age-related incidence of sudden infant death syndrome (SIDS). The cause of death in SIDS is generally thought to be a ventilatory arrest, but the mechanism responsible for such an event remains unknown. Testosterone has been demonstrated to depress ventilatory drive and increase sleep apnea in adult men. We tested the hypothesis that the gonadal steroid testosterone depresses infant ventilatory drive during sleep. Three newborn male infant primates were gonadectomized after birth. Ventilation was observed and quantified for each animal during completely natural unencumbered sleep by plethysmography for an average of 16 wk. Ventilatory patterns were recorded, and ventilatory drive was challenged with hypercapnia and hypoxia during quiet sleep on the night before and the night after testosterone administration. Hypercapnic ventilatory drive during sleep was significantly depressed by an average of 33.6% on the night after compared with the night before testosterone administration. Depression of the response to hypercapnia after testosterone was not accompanied by any change in resting minute ventilation measured during quiet sleep. Hypoxic ventilatory drive, incidence of apneic events, and length of apnea were not different after testosterone. The effects of injecting a placebo on ventilatory patterns and drive were tested by giving the placebo to all animals on several test weeks. Placebo injections produced no significant change in any measured parameters. These results support the hypothesis that testosterone depresses hypercapnic ventilatory drive during sleep in the infant primate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Depression of hypercapnic ventilatory drive by testosterone in the sleeping infant primate. 804 60

Although obstructive sleep apnea (OSA) occurs commonly in acromegaly, we have recently reported an unexpectedly high prevalence of central sleep apnea (CSA) in these patients. Acromegalic patients with CSA have increased growth hormone (GH) and insulin-like growth factor-1 (IGF-1) levels compared with their counterparts with OSA. Studies in animals, normal humans, and patients with sleep apnea have suggested that CSA is associated with increased gain of the respiratory control system. To examine the relationship between sleep apnea, respiratory control, and hormonal activity in acromegaly, we performed sleep studies and examined ventilatory responses to hypoxia at resting CO2 (HVR) and 8 mm Hg above resting CO2 (HHVR) and hypercapnia (HCVR) in 54 patients with acromegaly who also underwent detailed endocrine evaluation. Patients with CSA (n = 11) had higher HCVR (3.47 +/- 0.57 L/min/mm Hg) than did patients with obstructive sleep apnea (OSA) (1.86 +/- 0.19, n = 33) and patients without sleep apnea (1.77 +/- 0.21, n = 10). Measures of ventilatory control were all correlated with the mean of 12 hourly GH concentrations, but only HCVR was correlated with IGF-1 levels. Multiple linear regression analysis revealed that HCVR, HHVR, and IGF-1 could explain 39% of the variability in the degree of CSA in acromegalic patients with sleep apnea. We conclude that increased ventilatory responsiveness and elevated hormonal parameters of disease activity both contribute to the pathogenesis of central sleep apnea in acromegaly.
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PMID:Central sleep apnea is associated with increased ventilatory response to carbon dioxide and hypersecretion of growth hormone in patients with acromegaly. 804 36

The cardio-respiratory complications of sleep apnea syndrome have been prospectively assessed in 60 patients with massive obesity and free of chronic obstructive lung disease while the associated cardiovascular diseases and the alterations of pulmonary function were taken into account. These cardio-respiratory complications were observed only in patients with a number of apneas per hour of sleep greater than 20. The sleep apneas induced nocturnal hypoxemia that is frequently severe and independently correlated to the apnea index, diurnal hypoxemia and hypercapnia that are usually moderate, and presumably left ventricular hypertrophy that is not related to the development of daytime hypertension. However the nocturnal apneas were not associated with the development of an impairment of right or left ventricular function, or with the occurrence of cardiac arrhythmias or conduction disturbances. The absence of severe cardiac complications in this study may be related to the fact that the patients were relatively young and that the sleep apnea syndrome was diagnosed at an early stage of evolution. The findings of this study could help to define a more rationale approach in several therapeutic indications of sleep apnea syndrome.
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PMID:[Cardio-respiratory complications of sleep apnea in obese patients]. 822 Nov 69

Massive obesity may be accompanied by severe and sometimes lethal respiratory complications. The restrictive ventilatory deficit which results from a decrease in thoracic wall compliance and perhaps also from diaphragmatic dysfunction is more severe in males and in subjects with abdominal obesity. Diurnal hypoxaemia results from 2 mechanisms: diminution of the ventilation/perfusion ratio at the base of the lung, and alveolar hypoventilation. Hypercapnia is a fairly frequent complication of massive obesity. Although usually moderate, hypercapnia is a major indicator as it is very often associated with sleep apnoea syndrome. The most severe respiratory complication of massive obesity is this syndrome which must be looked for systematically by questioning the patient and her husband or his wife before serious cardiopulmonary and neuropsychic disorders appear. The effects of weight loss of nocturnal apnoea are inconsistent and variable. Continuous positive pressure ventilation by means of a nasal mask is the choice treatment of sleep apnoea syndrome, especially since the results of rhino-laryngeal surgery are often disappointing.
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PMID:[Respiratory function in massive obesity]. 831 Feb 44

The medical hazards of obesity are discussed. Risks include insulin resistance, diabetes mellitus, hypertriglyceridemia, decreased levels of high-density lipoprotein cholesterol, and increased levels of low-density lipoprotein cholesterol. Obesity is also associated with gallbladder disease and some forms of cancer as well as sleep apnea, chronic hypoxia and hypercapnia, and degenerative joint disease. Obesity is an independent risk factor for death from coronary heart disease. A central distribution of body fat enhances the risk for most of these conditions.
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PMID:Medical hazards of obesity. 836 92


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