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

The Pickwickian Syndrome stimulated new pathophysiological concepts in regard to control of ventilation. With the advent of sleep laboratories, the peculiar sleep apnea occurring in some of these patients has been explained on the basis of intermittent upper airway obstruction. Two patients with different manifestations of the Pickwickian Syndrome are presented. The suggestion is made that these two subsyndromes should have unique designations. The Auchincloss Syndrome is manifested by right heart failure and respiratory acidosis in obese patients who are alert and have no major abnormality of breathing pattern. The fundamental cause of this abnormality is the increased work of breathing caused by the obesity. The cost of breathing is so high that the ventilatory regulation is compromised and respiratory acidosis results. The Gastaut Syndrome is characterized principally by hypersomnia and sleep apnea. The fundamental defect is upper airway obstruction during sleep, resulting in increased work of breathing, which together with the increased work caused by obesity leads to respiratory acidosis and right ventricular failure. Hypersomnia, rather than heart failure or respiratory acidosis, is the major manifestation of this syndrome, and is the result of sleep loss.
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PMID:Pickwickian syndrome, 20 years later. 117 87

An awakening has taken place over the last 25 years to the science of sleep disorders. Foremost amongst these, both in the medical world and the public eye, has been Sleep Apnoea Syndrome (SAS). The prevalence is thought to be the order of 1-2%. Males are eight times more commonly affected than females, although after the menopause the gap narrows considerably. Sleep apnoea occurs in children, usually in relation to large tonsils and adenoids, but in adult life patients usually present between the age of 40 and 60 and the prevalence increases with age. Numerous apnoeas or hypopnoeas during the night's sleep result in disordered sleep architecture and unrefreshing sleep. This is usually accompanied by night-long snoring which may lead to marital discord and even complaints from neighbours. Symptoms on waking may be a headache and a feeling of not being refreshed by sleep. Sleepiness during the day can interfere with work and social activities and may produce risks to the patient and others if it occurs while operating dangerous machinery or driving. Over a longer time scale SAS results in intellectual and memory deterioration, a higher incidence of ischaemic heart disease, hypertension, polycythemia and pulmonary hypertension. Right heart failure is particularly likely if there is chronic airflow obstruction contributing to a low arterial oxygen level. Asystolic periods and tachyarrhythmias may occur during apnoeic periods. The increased mortality of SAS relates to coronary and cerebrovascular disease and arrhythmias. Sudden death occurs with greater frequency in patients with SAS, mainly at night.
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PMID:Sleep apnoea: causes, consequences and treatment. 141 52

Obstructive sleep apnea may contribute to the development of pulmonary hypertension and RVF primarily through pulmonary vasoconstriction secondary to hypoxia. Several recent studies indicate, however, that intermittent apnea-related hypoxia is not sufficient to cause sustained pulmonary hypertension. These studies have been consistent in showing that pulmonary hypertension and RVF are almost invariably seen in the presence of diurnal hypoxia. Sustained pulmonary hypertension, therefore, appears to be associated with sustained hypoxia as is the case in COPD. Patients with OSA who have hypoxia while awake are, as a rule, obese and have mild-to-moderate diffuse obstructive airways disease. Thus, most cases of pulmonary hypertension in association with OSA result from a combination of OSA, obesity, and diffuse obstructive airways disease, a so-called overlap syndrome. However, from the therapeutic viewpoint, it is apparent that treatment of OSA by NCPAP or tracheostomy, in such cases, is usually sufficient to reverse pulmonary hypertension and RVF. More recent work has provided strong evidence that OSA can play a role in the pathogenesis of LV heart failure in patients with CHF of otherwise unknown etiology. It is likely that this occurs through a combination of increased LV afterload related to exaggerated negative Pit swings during obstructive apneas, to intermittent hypoxia, and to chronically elevated sympathoadrenal activity. Reversal of OSA by NCPAP in these patients may relieve LV heart failure. These findings add a new dimension to our understanding of the pathophysiologic effects of OSA on the cardiovascular system by demonstrating that the LV is a structure that may suffer functional impairment secondary to the stresses imposed by OSA. Finally, it has now become apparent that CSR in patients with CHF can cause symptoms of a sleep apnea syndrome when associated with intermittent hypoxia and arousals from sleep. Reversal of CSR during sleep by NCPAP can lead to alleviation of these symptoms and possibly to reduced cardiac dyspnea and LV systolic function as well. Taken together, this suggests that much more extensive use of polysomnography may be warranted in the investigation of cardiovascular disease. The reasons are compelling: sleep apnea disorders are common and eminently treatable conditions whose reversal can result in improved right and left heart function and symptomatic improvement in patients with impaired myocardial function.
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PMID:Right and left ventricular functional impairment and sleep apnea. 152 13

The factors that contribute to the development of chronic cor pulmonale (CCP) in sleep apnea syndrome (SAS) are being continuously reviewed, as well as the role played by the coexistence of chronic obstructive pulmonary disease (COPD). Right ventricular function was evaluated in 20 SAS patients, 10 of whom presented associated (COPD). In all of them the following tests were performed while fasting: blood gasometry, spirometry, body mass index and isotopic ventriculography which included the determination of righ ventricular ejection fraction (RVEF). The RVEF of the group presenting COPD (mean +/- DS) (0.43 +/- 0.07) was not significantly different from the group without COPD (0.46 +/- 0.09). When the patients were regrouped according to the presence of hypoxemia during the day (paO2 less than 70 mmHg) a significant difference was evidenced between the mean value of the RVEF group with hypoxemia (n = 10) (0.40 +/- 0.02) and that of the group with normoxemia (n = 10) (0.50 +/- 0.09) (p less than 0.05). There were no statistically significant differences between the degree of obstruction and the BMI in either group. These results suggest that the worsening of RVF is more frequent in SAS patients who present daytime hypoxemia.
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PMID:[Right ventricular function in sleep apnea syndrome and chronic obstructive pulmonary disease]. 178 98

To clarify the roles of lung function, nocturnal hypoxemia and obesity in the development of peripheral edema in patients with the sleep apnea/hypopnea syndrome (SAHS), 65 consecutive SAHS patients had diagnostic sleep studies and respiratory function testing. Eighteen patients (27%) had peripheral edema without other explanation. Their sleep apnea/hypopnea index was similar to those without edema, but they were more obese (p less than 0.01) and had worse lung function (p less than 0.01) and lower oxygen saturation (SaO2) awake (p less than 0.01). These 18 became more hypoxemic during sleep than predicted from their awake SaO2 (p less than 0.005). Eleven patients with edema had evidence of pulmonary hypertension on cardiac catheterization, chest radiograph, or electrocardiograph and could be weight matched to 11 SAHS patients without edema. Those with right heart failure were more hypoxic (p less than 0.01) when awake, desaturated more frequently during sleep (p less than 0.01), and had lower FEV1% predicted (p less than 0.01). Thus, extent of both daytime and nighttime hypoxemia are important in the development of right heart failure in patients with SAHS.
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PMID:Peripheral edema in the sleep apnea/hypopnea syndrome. 194

Several well controlled epidemiologic and hemodynamic studies suggest that about 20% of sleep apnea syndrome (SAS) patients will have chronic obstructive pulmonary disease (COPD), and the majority of these patients (with combined diseases) will have pulmonary hypertension. Indeed it has been suggested that only patients with underlying hypoxemia, such as that from COPD, will develop right heart failure in the OSA setting. Experience shows that apnea/COPD patients will have severe hypersomnolence associated with the OSA, cough and dyspnea with the airways disease, and edema and plethora related to chronic hypoxemia. Many patients present with respiratory failure and are diagnosed at the time of initial intubation and mechanical ventilation. Episodic nocturnal hypoxemia may be worsened by a steeper rate of desaturation due to lower alveolar and blood oxygen stores, and longer apneas perhaps contributed to by depressed chemosensitivity. Daytime hypoxemia may also add to the severe hemodynamic disturbances. Since COPD cannot be cured, aggressive treatment of SAS is critical. Past studies have shown that tracheostomy or nasal CPAP in this setting not only leads to resolution of episodic nocturnal desaturation but may lead to rapid improvement in daytime oxygenation in many patients. Pulmonary hypertension and other measures of cardiopulmonary function improve when apnea is cured. Elimination of the SAS may disclose nonapneic REM related desaturation that could require supplemental oxygen therapy in addition to tracheostomy or nasal CPAP. Pulmonary function testing in SAS patients with smoking histories, followed by aggressive treatment of SAS, is recommended.
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PMID:Chronic lung disease in the sleep apnea syndrome. 211 88

Holter recordings of subjects apparently free from cardiovascular disease have demonstrated a moderate sinusal and nodal depression during sleep. This depression does not seem to be sufficient to create overt cardiovascular disorders in apparently healthy subjects, but it may aggravate or even reveal an underlying disorder of rhythm or conduction in elderly people or in patients taking drugs that potentiate its effects. In sleep apnea syndrome prolonged episodes of apnea may produce a paroxysmal, then permanent increase in pulmonary arterial pressure, which may lead to right heart failure. These episodes also increase the pre- and after-load and decrease myocardial contractility, thus facilitating the occurrence of left ventricular failure, potentiated by systemic arterial hypertension, overweight or even coronary disease, all conditions that are often present in these subjects. Arterial hypertension is so frequent in sleep apnea syndrome that some authors advocate a systematic search for the syndrome by Holter recordings before the hypertension is pronounced "essential". All studies confirm the existence of rhythm and conduction disorders directly related to apneic episodes. These disorders decrease or regress after a well-conducted treatment of the sleep apnea syndrome. They are mainly of the "hypokinetic" type, created by depression of sinus activity and conduction pathways. Their frequency, their severity and, in particular, the risk of sudden death they carry seem to have been overestimated, especially since no evidence has ever been produced of a potentially lethal rhythm disorder occurring during sleep apnea. Nevertheless, there is no certainty that these patients are not at risk of sudden death related to their sleep apnea syndrome.
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PMID:[Cardiovascular disorders during sleep]. 214 78

Sleep apnea syndromes have been identified only relatively recently. Their most frequent form is characterized by a sleep-related upper airway obstruction resulting in apneas which may repeat themselves up to several hundred times during a night's sleep. Their mean duration is about 30 to 40 seconds, but some apneas last over one minute. Breathing resumption requires an arousal, which may be clearly identified on the EEG but usually goes unnoticed by the patient. The most immediate consequence are hypoxemia and sleep fragmentation. There may be associated arrhythmias and hemodynamic changes, especially in the pulmonary circulation. The predominant clinical signs are snoring (during the breathing resumption between the apneas) and daytime somnolence due to sleep fragmentation. In addition to the risks of work and traffic accidents, these patients run a long-term risk of cardiovascular accidents. About 20% develop pulmonary hypertension, a contributing factor to right heart failure. About 50% are hypertensive, which combined with a frequently observed polycythemia, makes them vulnerable to ischemic accidents. The treatment is based upon the use of continuous positive airway pressure (CPAP) during sleep. In case of failure, surgical alternatives may be considered.
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PMID:[Sleep apnea syndromes]. 253 41

A case of the obstructive sleep apnea syndrome revealed reversible leftward displacement of the interventricular septum by echocardiography during sleep. A 46-year-old housewife with congenital micrognathia was admitted to our hospital complaining of severe dyspnea and general edema. On admission, she had severe hypoxemia (PaO2 = 35.2 mmHg), pulmonary hypertension (mean pulmonary artery pressure = 70 mmHg) and right heart failure. Her echocardiograms revealed enlargement of the right ventricle with a flattened left ventricle. A sleep study performed after partial resolution of her right heart failure disclosed that severe hypoxemia and pulmonary hypertension (mean pulmonary artery pressure = 70 mmHg) occurred after relatively long periods of apnea. With vigorous inspiratory efforts during sleep apnea, transient enlargement of the right ventricle and leftward displacement of the septum causing the flattened left ventricle were observed echocardiographically. A concomitant decrease in left ventricular inflow velocities was also observed by the pulsed Doppler method. However, these findings immediately returned to normal with the resumption of ventilation. We concluded that these repetitive apneic events due to obstruction of the airway during sleep might accelerate complete eventual pulmonary hypertension and right heart failure.
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PMID:[Obstructive sleep apnea syndrome with reversible interventricular septal displacement during sleep: a case report]. 322 14

Enlarged tonsils and adenoids can cause chronic upper airway obstruction that may result in a spectrum of clinical findings ranging from sleep apnea to cor pulmonale and right heart failure. The clinical findings associated with this entity are reversible if the condition is identified early and removal of the obstructing tissue is performed before life-threatening changes occur.
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PMID:Upper airway obstruction and the pharyngeal lymphoid tissue. 329 7


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