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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Snoring usually is trivial and unimportant, but it can turn into a social or medical problem. Obesity, hypertension and heart disease are more frequent among snorers than among nonsnorers, and especially snorers with hypersomnia during the day are at risk. Hypersomnia in association with snoring usually signifies obstructive sleep apnea. Increased resistance in the upper airways, together with negative inspiratory pharyngeal pressure and muscular hypotonia during deep non-REM and REM sleep, lead to collapse of the pharynx, hypoxia and hypercapnia. Only after arousal from sleep does muscle tone return, pharyngeal obstruction reopen and airflow resume. Since this process can occur 300 or 400 times a night, repetitive alveolar hypoventilation leads to pulmonary-arterial hypertension and cor pulmonale, and the repetitive sympathetic activations can cause systemic hypertension or serious cardiac arrhythmias. The countless arousals deprive the sufferer of deep non-REM and REM sleep and their consequence is sleep fragmentation. The symptoms are excessive daytime sleepiness, intellectual deterioration and personality and behavioral changes. Oronasomaxillofacial, endocrine and neuromuscular anomalies and diseases predispose to sleep apnea, and alcohol or CNS-depressant drugs can favour its occurrence. Diagnosis is made by nighttime oxymetry, and if this is abnormal, by polysomnography. After polysomnography it is possible to distinguish between obstructive and nonobstructive sleep apnea, and the decisions for an adequate treatment can be made.
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PMID:[Dangerous snoring. Sleep-apnea syndrome]. 331 92

A woman aged 17 years presented with symptoms of somnolence. A bilateral diaphragmatic paralysis and an Arnold-Chiari malformation were diagnosed. Lung function tests revealed a marked restrictive defect and a blunted ventilatory response to hypercapnia and hypoxia. A sleep study also showed central apneas, an irregular pattern of breathing and marked hypoventilation.
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PMID:Arnold-Chiari malformation and paralysis of the diaphragm. 339 37

The authors describe the occurrence of a sleep-induced apnea syndrome with daytime hypersomnolence in a patient suffering from Thomsen's disease. Polysomnography showed, during the whole sleep, repetitive obstructive, and rarely mixed, apneas. The patient also had daytime alveolar hypoventilation, primarily obstructive, and waking chronic hypercapnia. Long-term diphenylhydantoin therapy relieved not only myotonia, but sleep-induced apneas, daytime sleepiness and waking breathing as well. This result, together with some EMG features recorded during sleep and with daytime obstructive hypoventilation, suggests that myotonia could be one of the pathogenic factors involved in nocturnal upper airway stenosis.
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PMID:Sleep apnea syndrome in Thomsen's disease. A case report. 619 46

The development of important respiratory disorders and significant hypertension in association with increasing body weight is not widely recognized. Altered respiratory function results from a combination of mechanical impedance to breathing exerted by thoracic and abdominal fat and a ventilation-perfusion mismatch. Sleep-disordered breathing with periods of hypoventilation, with or without apnoeic episodes, may commonly occur in patients with extreme obesity. Nocturnal hypercapnia and hypoxia in such patients may lead to a decrease in ventilatory drive, abnormal central respiratory control and possibly, in time, the development of the obese-hypoventilation syndrome. Respiratory abnormalities should be suspected in obese patients with a history of restlessness at night, loud snoring and daytime somnolence. Treatment is substantial weight reduction, but short-term measures include the use of compressed air via nasal cannulae for obstructive apnoea, and drugs which alter sleep pattern or stimulate respiration. The alterations in endocrine function, which accompany weight gain, may contribute to an increase in blood pressure and there appears to be a relationship between plasma insulin and catecholamine concentrations, fat cell size and the development of hypertension. The confirmation of a raised blood pressure requires that readings be taken with an adequately sized arm-cuff. In many instances endocrine function becomes normal with weight loss, and there is a corresponding decrease in blood pressure. The ideal management for an obese hypertensive patient is the combination of a suitable calorie-restricted diet with a programme of physical exercise.
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PMID:Clinical complications of obesity. 639 58

Fifteen out of 18 "pink and puffing" patients completed a double-blind, placebo-controlled cross-over trial of diazepam and promethazine for breathlessness and reduced exercise tolerance. Dosages were 25 mg and 125 mg daily, respectively, and each course lasted two weeks. Patients with psychiatric or other major medical histories were excluded. Of the three patients who did not complete the trial, one died during an exacerbation of breathlessness while taking diazepam, one was withdrawn because of mild hypercapnia while taking placebo, and one suffered intolerable drowsiness while taking diazepam. Of the remaining 15 patients, six needed a reduction in dosage because of drowsiness: one of these was taking promethazine and five diazepam. Diazepam had no effect on breathlessness and noticeably reduced exercise tolerance. Promethazine reduced breathlessness and improved exercise tolerance without altering lung function. From these results diazepam is contraindicated for breathlessness and reduced exercise tolerance in fixed airways obstruction, but promethazine may be beneficial.
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PMID:Drug treatment of breathlessness: contrasting effects of diazepam and promethazine in pink puffers. 678 19

Four morbidly obese men who had been found to have significant sleep-disordered breathing and oxygen desaturation were restudied after an average weight loss of 108 kg (range 53-155 kg). In all subjects, weight loss was accompanied by a significant reduction in the number of episodes per hour of sleep-disordered breathing events. In three of the four subjects, there was improvment in the severity of desaturation accompanying abnormal breathing. The two subjects with daytime somnolence and hypercapnia prior to weight loss showed the most dramatic improvement in desaturation. This suggests that obesity is a cause, rather than an effect, of the sleep apnea syndrome.
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PMID:The effect of weight loss on sleep-disordered breathing and oxygen desaturation in morbidly obese men. 710 55

The sleep apnea syndrome is a relatively unappreciated but by no means rare cause of nocturnal hypercapnia and hypoxemia that sometimes persist into the waking hours. The authors describe their experience in diagnosing and treating this disease in seven patients who were characteristically overweight, tended to snore, and had daytime somnolence, intellectual deterioration and elevated hematocrits.
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PMID:Sleep apnea syndrome: clinical features and treatment. 739 15

Detection of nocturnal hypoxaemia, defined as a mean arterial oxygen saturation below 90%, in normoxic or mildly hypoxic chronic obstructive pulmonary disease (COPD) patients seems clinically relevant, since this feature may precede pulmonary hypertension. Nocturnal studies are expensive and time-consuming procedures. The current study investigates to what extent it is possible to predict nocturnal hypoxaemia from daytime parameters. Forty two COPD patients with a daytime arterial oxygen tension (PaO2) above 8 kPa participated. Nocturnal oxygenation, daytime blood gas values, and ventilatory responses to hypercapnia were measured. In 10 patients, enough desaturations occurred to qualify as nocturnal hypoxaemia. They had a significantly lower daytime PaO2 value, and a lower steady-state hypercapnic ventilatory response. They also smoked more often, and complained about daytime sleepiness. Multiple linear regression analysis demonstrated that daytime PaO2 (32%) was the best independent predictor. Sleepiness (12%), and number of cigarettes smoked (5%) also contributed independently, but in a minor way. Patients with a high daytime PaO2 (> 11 kPa) did not develop nocturnal hypoxaemia. The hypercapnic ventilatory response was used to distinguish nocturnal hypoxaemic from normoxaemic patients. Only patients with a low response (< 3.5 l.min-1.kPa-1) appeared to run a risk of developing nocturnal hypoxaemia. The sensitivity of this test was 80%, and the specificity 70%. It is concluded that daytime PaO2, hypercapnic ventilatory response and sleepiness are helpful in predicting nocturnal hypoxaemia.
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PMID:Predictors for nocturnal hypoxaemia (mean SaO2 < 90%) in normoxic and mildly hypoxic patients with COPD. 774 97

In early phases of neuromuscular disease, patients are either free of respiratory symptoms or have exertional dyspnea not explained by obvious obstructive or restrictive lung disease. Physical examination may be negative because generalized muscle weakness does not correlate with the degree of respiratory muscle involvement. When the diaphragm is involved, one may detect the absence of outward excursion during inspiration or even paradoxic inward inspiratory movement of the abdomen on one side. A substantial loss of respiratory muscle strength is typically accompanied by little or no change in spirometry or arterial blood gas composition. Other characteristics are moderate loss of maximal voluntary ventilation and an increase in residual volume, yet PImax and PEmax may be as low as 50% of the predicted value. In more advanced neuromuscular disease, patients may have severe symptoms if the onset is acute or subacute; however, patients with chronic advanced generalized muscle weakness do not exercise and, therefore, may not be breathless. Many patients with advanced neuromuscular disease present with daytime somnolence as a manifestation of a sleep-related breathing disorder. Physical examination may reveal generalized muscle weakness and difficulty with speech or swallowing. Signs specific to respiratory involvement include tachypnea, use of neck inspiratory muscles and abdominal expiratory muscles, and loss of chest-abdomen synchrony. Sometimes paradoxic bilateral inward movement of the abdomen with inspiration is overt. Patients may be unable to cough effectively, have scoliosis, and lack a gag reflex. At this advanced stage, PImax and PEmax are lower than 50% of the predicted value, and the vital capacity is reduced. Maximal voluntary ventilation increases, and residual volume increases further. Patients may not yet exhibit CO2 retention during the day and may even have a low PaCO3. A sleep study may reveal significant hypopneas with severe desaturation and hypercapnia, especially during REM sleep. It is important to be aware that overt ventilatory failure can occur abruptly and that measurement of arterial blood gas composition is not a reliable indicator of this danger. Therefore, it is critically important to heed clinical phenomena, such as increasing dyspnea and tachypnea, and symptoms of sleep disturbance, such as morning headache and daytime somnolence. Physicians should make serial measurements of VC and respiratory muscle strength in patients considered to be at risk for further deterioration.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Assessment of ventilatory function in patients with neuromuscular disease. 786 89

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


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