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

A total of 34 severely obese men with a history of heavy snoring and excessive daytime sleepiness indicative of obstructive sleep apnoea syndrome (OSAS) were studied prospectively. Their mean age was 46 years, and mean body mass index was 41.6 kg m-2. During a 4-year follow-up, 15% (5/34) of these subjects died (three cases of acute myocardial infarction and two cases of pulmonary oedema), all of them suddenly and unexpectedly, outside hospital. On autopsy the degree of atherosclerosis was found to be moderate in all cases. In 68% (15/22) of the men a pathological apnoea index (mean value 46 +/- 20) confirmed the OSAS diagnosis. Exercise tests and neurological examinations did not reveal any other causes of daytime sleepiness. Mean blood pressure at rest and during exercise was normal, and mean serum lipid and blood glucose levels were normal. Spirometry revealed intrapulmonary restrictive changes that could not be attributed to the heavy thoracic wall. Compliance was reduced to about 50% of reference values, and the mean pCO2 level (5.8 kPa) was close to the upper reference limit. Blood tests suggested that high alcohol consumption may be an important factor contributing to OSAS. These results demonstrate that morbidly obese men with a history of OSAS have a high risk of sudden cardiovascular death, despite the absence of other conventional risk factors.
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PMID:The sleep apnoea syndrome in obesity: risk of sudden death. 186 65

Five patients with congestive heart failure (CHF) and 1 with left ventricular dysfunction but without CHF were found to have sleep apnea. Central sleep apnea (CSA) related to Cheyne-Stokes respiration was seen in 4 cases while obstructive sleep apnea (OSA) was seen in 2. All patients had symptoms of sleep apnea. Nasal continuous positive airway pressure (NCPAP) was effective in reversing CSA and OSA in all patients with improvement in sleep structure and alleviation of symptoms of sleep apnea. In addition, all experienced a reduction in cardiac dyspnea. This was associated with a 5% or greater increase in left ventricular ejection fraction while on NCPAP, compared to baseline value off NCPAP in 5 patients and resolution of chronic pleural effusion and pulmonary edema in the sixth. We conclude that Cheyne-Stokes respiration during sleep may give rise to a CSA syndrome that is reversible by NCPAP. In addition, NCPAP therapy may lead to a reduction in cardiac dyspnea and improvement in left ventricular function in patients with left ventricular dysfunction and sleep apnea.
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PMID:Sleep apnea in patients with left ventricular dysfunction: beneficial effects of nasal CPAP. 219 97

Pulmonary edema due to upper airway obstruction can be observed in a variety of clinical situations. The predominant mechanism is increased negative intrathoracic pressure, although hypoxia and cardiac and neurologic factors may contribute. Laryngospasm associated with intubation and general anesthesia is a common cause of pulmonary edema in children. However, only seven cases of pulmonary edema presumably due to laryngospasm have been reported in adolescents and adults. Five of the seven had other risk factors for upper airway obstruction, and in four, the diagnosis of "laryngospasm" could be explained by other factors. Patients with underlying risk factors for upper airway obstruction, such as a forme fruste of sleep apnea or nasopharyngeal abnormalities, appear to be at increased risk for the development of pulmonary edema in the setting of intubation and anesthesia. This form of pulmonary edema usually resolves rapidly without the need for aggressive therapy or invasive monitoring.
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PMID:Post-extubation pulmonary edema following anesthesia induced by upper airway obstruction. Are certain patients at increased risk? 378 Mar 26

Many cardiorespiratory problems have been identified in patients with sleep apnea syndrome. Acute pulmonary edema as the primary feature of obstructive sleep apnea has recently been reported, and is thought to be caused by the effects of severe hypoxemia and/or extreme negative intrathoracic pressure. We have described another patient with sleep apnea syndrome who had pulmonary edema on at least three different occasions. Extremely high pulmonary artery pressure, paradoxic motion of the interventricular septum, and very low right heart ejection fraction were found. The paradoxic septal motion disappeared and the right heart ejection fraction increased after tracheostomy.
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PMID:Pulmonary edema due to obstructive sleep apnea. 671 Feb 6

Patients with sleep apnea syndrome may present with many types of cardiopulmonary abnormalities. Acute pulmonary edema, however, either as a part, or as the presenting feature, of the sleep apnea syndrome has not been reported to our knowledge. A 20-year-old obese woman with no history of cardiopulmonary disease presented twice to the emergency room because of sudden onset of shortness of breath. Each time her chest roentgenogram showed bilateral pulmonary edema. On nocturnal polysomnographic recording, the patient had obstructive apneic episodes; the longest apneic episode lasted 132 seconds. Complete resolution to her symptoms occurred following tracheostomy.
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PMID:Pulmonary edema as a presenting feature of sleep apnea syndrome. 708 22

A patient had recurrent acute nocturnal pulmonary oedema following an anterior myocardial infarction despite a normal maximal stress electrocardiogram. He had a history of chronic heavy snoring and other symptoms to suggest a diagnosis of obstructive sleep apnoea (OSA) which was supported by an overnight sleep study. The recurrent acute pulmonary oedema was most likely due to a combination of poor left ventricular function and obstructive sleep apnoea.
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PMID:Recurrent acute pulmonary oedema associated with obstructive sleep apnoea. 789 6

The central autonomic network (CAN) is an integral component of an internal regulation system through which the brain controls visceromotor, neuroendocrine, pain, and behavioral responses essential for survival. It includes the insular cortex, amygdala, hypothalamus, periaqueductal gray matter, parabrachial complex, nucleus of the tractus solitarius, and ventrolateral medulla. Inputs to the CAN are multiple, including viscerosensory inputs relayed on the nucleus of the tractus solitarius and humoral inputs relayed through the circumventricular organs. The CAN controls preganglionic sympathetic and parasympathetic, neuroendocrine, respiratory, and sphincter motoneurons. The CAN is characterized by reciprocal interconnections, parallel organization, state-dependent activity, and neurochemical complexity. The insular cortex and amygdala mediate high-order autonomic control, and their involvement in seizures or stroke may produce severe cardiac arrhythmias and other autonomic manifestations. The paraventricular and other hypothalamic nuclei contain mixed neuronal populations that control specific subsets of preganglionic sympathetic and parasympathetic neurons. Hypothalamic autonomic disorders commonly produce hypothermia or hyperthermia. Hyperthermia and autonomic hyperactivity occur in patients with head trauma, hydrocephalus, neuroleptic malignant syndrome, and fatal familial insomnia. In the medulla, the nucleus of the tractus solitarius and ventrolateral medulla contain a network of respiratory, cardiovagal, and vasomotor neurons. Medullary autonomic disorders may cause orthostatic hypotension, paroxysmal hypertension, and sleep apnea. Neurologic catastrophes, such as subarachnoid hemorrhage, may produce cardiac arrhythmias, myocardial injury, hypertension, and pulmonary edema. Multiple system atrophy affects preganglionic autonomic, respiratory, and neuroendocrine outputs. The CAN may be critically involved in panic disorders, essential hypertension, obesity, and other medical conditions.
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PMID:The central autonomic network: functional organization, dysfunction, and perspective. 841 66

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

A 33-year-old male was scheduled for tonsillectomy and pharyngoplasty due to sleep apnea syndrome. The intubation was uneventful following induction with thiamylal and vecuronium. Anesthesia was maintained with O2-N2O-sevoflurane. No complications were observed during the 90 min operation. After the termination of the anesthesia, a hyperadrenergic state was observed: arterial pressure and heart rate rose to 230/135 mmHg and 135 bpm, respectively. Immediately after extubation, he developed dyspnea with tracheal tag and stridor, and became cyanotic despite the use of a simple oxygen mask and assisted ventilation. Laryngospasm was suspected. The patient was reintubated and suctioned; pink, frothy sputum was not obtained. Arterial blood gases 5 minutes after reintubation revealed a pH of 7.24, Pao2 86 mmHg (FIo2 1.0), and Paco2 54 mmHg. Chest X-ray 30 minutes after reintubation revealed bilateral diffuse alveolar infiltration. The diagnosis was interstitial pulmonary edema. The patient was ventilated mechanically by applying a positive end-expiratory pressure of 5cm H2O, and furosemide and dopamine were administered intravenously. The patient was extubated the next day, and discharged from hospital ten days later. We considered that the lung edema was induced by the severe negative pressure generated by inspirating against a closed upper airway, as well as by the hyperadrenergic state and severe hypoxemia observed during and after extubation.
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PMID:[Pulmonary edema due to acute airway obstruction immediately after tracheal extubation]. 985 97

The lungs are a delicate interface between the atmosphere and our bodies across which oxygen diffuses from the air we breathe to the blood which carries oxygen to the cells and mitochondria. In healthy lungs at sea level where there is a surfeit of oxygen, this process occurs easily, whereas, in lungs with disease it becomes a task which may not be fully successful and hypoxemia may ensue or worsen. At high altitude where the barometric pressure (Pb) and thus the supply of oxygen is lower, the job of getting oxygen to the blood, even in the healthy lung is more difficult, and in the diseased lung it may be impossible. This presentation will review the lungs' responses to high altitude, with emphasis on the abnormal. Both acute and chronic responses of patients with pre-existing lung disease will be reviewed. Pulmonary diseases encountered at high altitude in previously healthy people, such as high altitude pulmonary edema and chronic mountain sickness will be touched on only as they pertain to other patients. Pre-existing lung disease (with and without hypoxemia at sea level) such as obstructive lung diseases (asthma, COPD, emphysema), and restrictive lung diseases (sarcoid, asbestosis, interstitial pulmonary fibrosis) will be discussed in terms of gas exchange, lung mechanics, and treatment at high altitude. Disorders of ventilatory control; e.g., obesity-hypoventilation syndrome and sleep apnea, may present formidable problems, and guidelines for their treatment will be discussed. Infectious lung diseases; e.g., pneumonia, cystic fibrosis, and pulmonary vascular disorders such as chronic mountain sickness, primary pulmonary hypertension, and congenital absence of the pulmonary artery are important disorders that require special attention because of the accentuated hypoxic pulmonary vascular response encountered at high altitude. The purpose therefore, is to provide the medical practitioner with the insight into prevention, recognition, and treatment of pulmonary problems encountered specifically at high altitude, as well as guidance on how best to advise patients with lung disease who want to fly in airplanes and/or ascend to high altitude for work or pleasure.
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PMID:Lung disease at high altitude. 1063 92


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