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

Fourteen children with disordered breathing during sleep (obstructive apnea, obstructive hypopnea, or snoring) and anatomic obstruction of the upper airway were studied. Twelve children had hypertrophied tonsils and adenoids, and two had a deviated nasal septum. No child had sequelae of severe sleep apnea--that is, cor pulmonale, pulmonary hypertension, or alveolar hypoventilation. Results of polysomnographic studies were abnormal in all and revealed that obstructive hypopnea (increased respiratory effort with decreased airflow) was more common than obstructive apnea (increased respiratory effort without airflow). Surgical removal or correction of the upper airway obstructive lesion in 12 children resulted in normal nocturnal respiration. Surgical intervention was declined in two patients, and their symptoms persist. We conclude that surgical removal of upper airway obstructive lesions in children with disturbed nocturnal sleep should not be reserved only for those with serious sequelae of obstructive sleep apnea; considerable benefit is gained in selected patients with mild obstructive sleep apnea or hypopnea.
 ...
PMID:Upper airway obstruction and disordered nocturnal breathing in children. 685 72

Sleep is the period of greatest physiologic disturbance in chronic airflow obstruction and so is likely the time of greatest danger to these patients. Sleep in these patients aggravates gas exchange abnormalities resulting in secondary pulmonary hypertension and cardiac arrhythmias. The mechanism of these disturbances is not fully explained, but patients with chronic airflow obstruction do not characteristically have the sleep apnea syndrome. Patients with chronic airflow obstruction sleep badly, with less rapid eye movement sleep and increased sleep stage changes. Nocturnal oxygen therapy helps relieve pulmonary hypertension and may decrease cardiac arrhythmia, but has no effect on sleep profile.
 ...
PMID:Sleep disorders in chronic airflow obstruction. 701 3

The sleep apnea syndromes have been recognized clinically in the United States only within the past ten years. The true extent of the problem is not known, but it seems certain that these syndromes are much more common than was generally assumed five years ago. Every clinician should be aware of the signs and symptoms of sleep apnea because of the rapid and prompt response to therapeutic measures. Sleep apnea syndromes, whether obstructive or central, can result in systemic or pulmonary hypertension, arterial blood gas abnormalities, life-threatening cardiac arrhythmias, chronic respiratory failure, sleep disturbances, narcolepsy, excessive daytime somnolence, sexual dysfunction, and the suspicion of mental retardation. The immediate and dramatic improvement produced by tracheostomy in the obstructive type of sleep apnea, or nocturnal ventilatory support in the central type, can not only enhance the quality of life for these patients, but return them to functional and productive lives.
 ...
PMID:Sleep apnea syndromes. 703 20

A 17-year-old man presented with daytime sleepiness, episodic attacks of sleep and probable cataplexy. His EEG showed rapid eye movements and central sawtooth waves at sleep onset, and supported the clinical impression of narcolepsy. He improved with methylphenidate but died suddenly, and had cardiomegaly, right ventricular enlargement, and pulmonary hypertension at autopsy. These findings suggested concomitant features of sleep apnea which were not evident by history or examination.Central apneas have been frequently described in the sleep of narcoleptic patients. Few patients have had indications of obstructive or mixed apneas. This patient's course suggests that ventilation during sleep should be included in the polygraphic assessment of patients with suspected narcolepsy, as the agents used for treatment of narcolepsy may aggravate the cardiac complications of sleep apnea.
 ...
PMID:Narcolepsy with concomitant features of obstructive sleep apnea. 712 May 1

Certain patients with chronic obstructive pulmonary disease may be classified as blue bloaters or pink puffers. Recent studies suggest that physiologic changes during sleep contribute to the clinical expression of these syndromes. To investigate this, we monitored four blue bloaters and six pink puffers during one night's sleep to determine the incidence of sleep disordered breathing (SDB) and of arterial oxygen desaturation. There were no significant differences between the two groups for sleep period time, awake oxygen saturation, or the number of episodes of SDB. Blue bloaters had lower baseline oxygen saturations, more episodes of arterial oxygen desaturation, and larger falls in oxygen saturation and spent more time at low levels of oxygen saturation while asleep. We propose that the degree and the duration of sleep hypoxemia of blue bloaters but not of pink puffers may contribute to early pulmonary hypertension and cor pulmonale.
 ...
PMID:Oxygen desaturation during sleep as a determinant of the "Blue and Bloated" syndrome. 722 51

Excessive daytime sleepiness (EDS) in certain patients with sleep apnea syndrome may be the result of intermittent upper airway obstruction during sleep. The possible occurrence of daytime hypertension and pulmonary hypertension (PH) in these patients has been emphasized. Transient and sometimes severe elevations of systemic and pulmonary arterial pressures during sleep as a result of intermittent upper airway obstruction may lead to EDS, daytime hypertension, and PH. The aim of the present study was to investigate whether daytime hypoxemia and hypoxemia during sleep contribute to EDS, daytime hypertension, and PH. The results indicate that: (1) sleep disturbance and blood gas changes while awake and asleep may play a role for EDS, although these abnormalities were not present in some cases, (2) hypoxemia while awake and asleep is probably not involved in daytime hypertension, and (3) mean resting pulmonary arterial pressure is correlated with daytime PO2, PCO2, %IBW, %FVC, and FEV1.0%, Cardiopulmonary hemodynamic function may return to normal in some patients who receive appropriate treatment.
 ...
PMID:[Sleep apnea syndrome]. 760 17

In COPD patients hypoxaemia does worsen during sleep and particularly during REM sleep. However, severe sleep-related O2 desaturation is only observed in patients who exhibit a marked daytime hypoxaemia. Nocturnal desaturation is due to the combination of alveolar hypoventilation and ventilation-perfusion mismatch; alveolar hypoventilation is the predominant mechanism, at least during REM sleep. Sleep-related hypoxaemia leads to peaks of pulmonary hypertension but also to cardiac arrhythmias. Hypoxaemia can be particularly severe when COPD is associated with a sleep apnoea syndrome (this association is rather frequent). A severe nocturnal desaturation needs a treatment with prolonged oxygen therapy, especially if daytime hypoxaemia (PaO2 < 55-60 mmHg) is present. The real benefit from oxygen therapy limited to sleep time in nocturnal desaturators who have not a significant daytime hypoxaemia, has not been yet demonstrated.
 ...
PMID:[Sleep and COPD]. 765 71

To determine the frequency and correlates of pulmonary hypertension in sleep-disordered breathing, pulmonary artery pressure, lung function and arterial blood gases were measured in 100 consecutive patients with obstructive sleep apnoea (OSA) (respiratory disturbance index (RDI) of > 20 episodes.h-1). Twenty six of the patients had significant chronic airflow limitation (CAL). Overall, 42% of patients had awake pulmonary artery pressure > 20 mmHg. Patients with pulmonary hypertension were older, had higher arterial carbon dioxide tension (PaCO2), lower arterial oxygen tension (PaO2) and lower forced expiratory volume in one second (FEV1) values compared with normotensive patients. Pao2, PaCO2 and FEV1 were correlated with the levels of pulmonary artery pressure (correlation coefficient (r2) 0.50, 0.46 and 0.49, respectively). These three factors combined could explain 33% of the variability in pulmonary artery pressure. Six patients had pulmonary hypertension despite a PaO2 in excess of 10.7 kPa (80 mmHg). We conclude that pulmonary hypertension is common in patients with moderate and severe sleep apnoea, especially those with coexisting chronic airflow limitation. The presence of daytime hypoxaemia is not a prerequisite in the development of pulmonary hypertension in these patients.
 ...
PMID:Pulmonary hypertension in obstructive sleep apnoea. 766 50

The high prevalence of obstructive sleep apnea (OSA) has only recently been appreciated, in part because the symptoms and signs of chronic sleep disruption are often overlooked in spite of their debilitating consequences. They typically develop insidiously during a period of years. We now know that the lives of millions of people each year are significantly impaired by the sequelae of OSA. Many of these patients go unrecognized, with tremendous medical and economic consequences for individual patients and for society. Evidence indicates that chronic, heavy snoring may be associated with increased long-term cardiovascular and neurophysiologic morbidity. Therefore considerable interest lies in the study of the epidemiology and the natural history of these related disorders. The fundamental problem in OSA is the periodic collapse of the pharyngeal airway during sleep. The pathophysiology of this phenomenon is reviewed in some detail. During apneas caused by obstruction, airflow is impeded by the collapsed pharynx in spite of continued effort to breathe. This causes progressive asphyxia, which increasingly stimulates breathing efforts against the collapsed airway, typically until the person is awakened. Hypopneas predominate in some patients and are caused by partial pharyngeal collapse. The clinical sequelae of OSA relate to the cumulative effects of exposure to periodic asphyxia and to sleep fragmentation caused by apneas and hypopneas. Some patients with frequent, brief apneas and hypopneas and normal underlying cardiopulmonary function may have considerable sleep disruption without much exposure to nocturnal hypoxia. Patients with sleep apnea often have excessive daytime sleepiness. As the disorder progresses, sleepiness becomes increasingly irresistible and dangerous, and patients develop cognitive dysfunction, inability to concentrate, memory and judgment impairment, irritability, and depression. These problems may lead to family and social problems and job loss. Cardiac and vascular morbidity in OSA may include systemic hypertension, cardiac arrhythmias, pulmonary hypertension, cor pulmonale, left ventricular dysfunction, stroke, and sudden death. The challenge for the clinician is to routinely consider the diagnosis and to incorporate several basic questions in the historical review of systems regarding daytime or inappropriate sleepiness. The diagnosis of OSA is made with polysomnography, and the decision to treat is based on an overall assessment of the severity of sleep-disordered breathing, sleep fragmentation, and associated clinical sequelae. The therapeutic options for the management of OSA are reviewed. Recognition and appropriate treatment of OSA and related disorders will often significantly enhance the patient's quality of life, overall health, productivity, and safety on the highways.
 ...
PMID:Obstructive sleep apnea. 814 53

To determine whether pulmonary hypertension (PH) can occur in obstructive sleep apnea syndrome (OSAS) in the absence of lung or primary cardiac disease, we studied 27 patients (26 males, mean age 49 +/- 10 yr) with OSAS (respiratory disturbance index [RDI] > 10 events/h) in whom clinically significant lung or cardiac diseases were excluded. Pulsed Doppler measurements of pulmonary hemodynamics, pulmonary function tests, arterial blood gas analysis, and polysomnography were performed. A total of 11 OSAS patients (41%) were found to have pulmonary hypertension. The levels of PH were relatively mild (Ppa < or = 26 mm Hg). There were no differences between PH and non-PH patients in body mass index (BMI), smoking history, or lung function. PH patients were more hypoxemic when awake than non-PH patients (PaO2 = 72.2 +/- 7.6 versus 77.6 +/- 7.3 mm Hg, respectively; p < 0.05) but did not differ in severity of sleep apnea (RDI = 51.9 +/- 25.1 versus 56.8 +/- 26.2 events/h, respectively; p = NS) or indices of sleep desaturation. The hypoxemia in PH patients could not be explained by impairment of lung function, greater body mass, or a higher prevalence of smoking, and PaO2 in the study population was significantly correlated with Ppa (r = -0.46, p < 0.02) but not with FEV1 or BMI. We conclude that lung disease is not a prerequisite for PH in OSAS.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Pulmonary hypertension and hypoxemia in obstructive sleep apnea syndrome. 830 39


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>