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

We studied the effects of medroxyprogesterone acetate, a respiratory stimulant, on the incidence and duration of episodes of apnea and disordered breathing in 13 nonhypercapnic men with obstructive sleep apnea. Nocturnal polysomnography was done before and after four weeks of treatment with medroxyprogesterone acetate (60 mg/day) and one week after cessation of treatment. There were no significant (p less than 0.05) differences in the mean frequency of apneic episodes per hour of sleep before (31.3 +/- 5.7 [+/- SE]), during (26.8 +/- 6.6), or after (23.6 +/- 7.0) treatment, or in the mean number of disordered breathing episodes per hour of sleep before (19.4 +/- 5.6), during (21.4 +/- 5.8), or after (23.1 +/- 6.3) the period of treatment. Medroxyprogesterone did not alter significantly the total time of apnea or the total time for disordered breathing, expressed as percentages of total sleep time. Arterial oxygen desaturation during apnea and disordered breathing did not change with treatment. Medroxyprogesterone increased the minute ventilation and occlusion pressure responses to hypercapnia measured in the awake state; however, the results of this study demonstrate that medroxyprogesterone does not improve the breathing disorders during sleep in the nonhypercapnic patient with obstructive sleep apnea.
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PMID:Effects of medroxyprogesterone acetate in obstructive sleep apnea. 294 59

Administration of nocturnal oxygen for 1 night to patients with obstructive sleep apnea (OSA) causes a moderate reduction in apnea frequency without improving hypersomnolence. Therefore, we administered oxygen chronically to patients with OSA to determine: whether apnea frequency would be further reduced, whether the effect of oxygen upon apnea frequency is correlated with an increased ventilatory response to hypoxia and hypercapnia, and whether hypersomnolence improves with more prolonged oxygen administration. In a single-blinded, nonrandomized trial, we compared the effects of 1 month of oxygen (4 L/min by nasal cannula) with room air (4 L/min by nasal cannula) placebo during sleep in 7 men and 1 woman with obstructive sleep apnea. During non-REM sleep, acute oxygen administration elevated the average low oxy-hemoglobin saturation during apneic events and decreased apnea frequency. These acute effects persisted during chronic oxygen administration but reverted to the preoxygen effects immediately upon discontinuing oxygen. One month of oxygen did not affect the waking ventilatory response to hypoxia or hypercapnia; however, waking PaCO2 increased from 40 +/- 1 mm Hg (mean +/- SE) after placebo to 43 +/- 1 mm Hg after oxygen (p less than 0.01). Neither subjective nor objective hypersomnolence consistently improved after 1 month of oxygen administration. We conclude that: first, oxygen has no effect upon apnea frequency beyond the period of administration, and the reduction of apnea frequency is not correlated with an increased sensitivity to chemical ventilatory stimuli. The reduced apnea frequency may be related to an increased PaCO2 stimulating ventilation during sleep.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of chronic nocturnal oxygen administration upon sleep apnea. 309 78

In patients with obstructive apnea, it was hypothesized that stimulation of the ventilatory system by hypercapnia during sleep would increase pharyngeal inspiratory muscle activity and thereby increase upper airway caliber. We predicted that this increase in caliber would decrease the number of apneas and sleep time spent apneic. In contrast, suppression of the ventilatory system activity with hyperoxia was predicted to decrease both inspiratory muscle activity and pharyngeal caliber and thereby increase the number of apneas and apnea time. In all 7 patients with symptomatic obstructive sleep apnea studied, 3 with upper airway narrowing obvious during wakefulness, inhalation of 3 to 6% CO2 preferentially stimulated upper airway inspiratory muscle tonic electrical activity relative to the activity of chest wall inspiratory muscles and diminished periodic breathing. Apnea time decreased from 60 +/- 2% (mean +/- SEM) of sleep time during ambient air inhalation to 12 +/- 3% during CO2 inhalation; 50% O2 had the reverse effect on inspiratory muscle tonic electrical activity and increased apnea time to 75 +/- 5% of sleep time. We conclude that manipulation of inspiratory muscle tonic activity and alteration of the pattern of breathing by CO2 and O2 inhalation lead to significant changes in the pattern of upper airway inspiratory collapse during sleep. We speculate that physiologic variables related to the control of upper airway inspiratory muscle function are instrumental in the pathophysiology of obstructive sleep apnea.
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PMID:Alteration in obstructive apnea pattern induced by changes in oxygen- and carbon-dioxide-inspired concentrations. 314 3

Snoring (inspiratory noise related to narrowing of the upper airways) and obstructive sleep apnea (OSA) are two aspects of the same basic disorder: sleep-related narrowing of the upper airways. Patients with OSA have been heavy snorers for years and even decades. Lying supine induces snoring and mild OSA in heavy snorers due to hypotonia of pharyngeal dilator muscles, decreasing waking neural drive and recumbent position, which contribute to functional narrowing of the upper airways. Functional factors in obstruction during sleep include (a) respiratory instability prevalent in the male sex, (b) increased extensibility of the lax tissues surrounding the oro-pharynx and (c) deficient contraction of the pharyngeal dilator muscles during inspiration. These effects are worsened by sleep deprivation and fragmentation, alcohol intake and sedatives. Anatomical factors favoring narrowing of the upper airways in snorers and OSA patients are (a) abnormally narrow airways as well as (b) increased thickness and length of the velum palatinum in snorers and OSA patients, (c) tonsillar and adenoid hypertrophy, micro- and retrognathia, and nasal insufficiency, (d) obesity with fat infiltration of the soft tissues and in particular of the oropharynx, (e) relatively open mandibular angle, hypertrophy and thickness of the tongue, and lowered hyoid bone (as shown by MRI imaging). It is possible that many anatomical abnormalities may be the consequence of snoring and obstructive apnea. During NREM sleep the ineffective inspiratory efforts progressively increase with worsening hypoxia and hypercapnia. The upper airways become patent again when arousal induces phasic activation of the dilator pharyngeal muscles.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathogenic aspects of snoring and obstructive apnea syndrome. 318 70

Persons with alveolar hypoventilation have abnormal daytime arterial blood gases and abnormal responses to hypercapnia and hypoxia in the absence of any identifiable lung or neuromuscular disease. The underlying defect in the control of breathing has not, however, been confirmed. We studied a 6-yr-old girl who was admitted in respiratory failure after a long history of disturbed breathing awake and asleep, which had been diagnosed as primary alveolar hypoventilation, (PaCO2 = 120). After several days of endotracheal intubation and assisted ventilation, her condition improved and she was extubated. At this time her ventilatory response to hypoxia was absent (VE/SaO2:0.1 l/min/% at a CO2 of 45) and there was a right-shifted response to hypercapnia (VE/PaCO2:2.6 l/min/mmHg). As obstructive sleep apnea was suspected, nocturnal nasal continuous positive airway pressure (CPAP) was tried; however, it was not effective in maintaining arterial oxyhemoglobin saturation. Definite central apneas were observed during sleep both with and without nasal CPAP, and there was an absence of snoring. Her condition deteriorated, and there was a progressive increase in her awake arterial CO2 levels for a period of 4 wk. The IPPV with 5 cm H2O of PEEP was administered through a nose mask during sleep and this maintained both oxygen saturation and transcutaneous CO2 levels within the normal range. After 10 days of nocturnal assisted ventilation, the hypercapnic response returned to the normal position (VE/CO2:2.1 l/min/mmHg).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment of alveolar hypoventilation in a six-year-old girl with intermittent positive pressure ventilation through a nose mask. 330 Apr 41

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

The mechanisms of hypercapnia in eight patients with the "Pickwickian" syndrome and obstructive sleep apnea (OSAS) were evaluated pretherapy and posttherapy (tracheostomy in seven patients and chronic nocturnal use of nasal CPAP in one). Four patients (correctors) became eucapnic within two weeks of therapy. Four others (noncorrectors) remained hypercapnic. Neither residual apneas, changes in pulmonary function, change in anatomic dead space, nor changes in ventilatory chemoresponsiveness differentiated the two groups, nor did the last three factors account for return to eucapnia in the correctors. The results indicated two separate mechanisms exist for chronic hypercapnia in OSAS: a critical balance between the ventilation during the time spent awake and hypoventilation due to apneas, a mechanism removed by treatment for obstructive apnea; and sustained hypoventilation independent of the apnea phenomenon and therefore not correctible. The subset of patients with the second mechanism appears to represent the true "Pickwickian" syndrome and can be identified before therapy by measuring a low level of ventilation in the sustained awake state.
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PMID:Hypercapnia in the obstructive sleep apnea syndrome. A reevaluation of the "Pickwickian syndrome". 351 86

Because obstructive sleep apnea (OSA) is unusual in premenopausal women, we describe ten women with this syndrome and compare them to 13 postmenopausal women and with 32 men with OSA. Two premenopausal women had structural abnormalities of their pharynx, and the remaining eight were significantly more obese than men with OSA. In these eight patients, there was no relationship between pulse flow resistance and the degree of OSA in contrast to significant relationships in postmenopausal women, and men. Hypercapnia occurred in three premenopausal women, no postmenopausal women and in two men. We conclude that premenopausal women with OSA are more likely than men and postmenopausal women to have structural abnormalities of their upper airway, to be extremely obese, and to be hypercapneic, and that OSA occurs in them independent of their upper airway dimensions.
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PMID:Obstructive sleep apnea in premenopausal women. A comparison with men and with postmenopausal women. 356 69

Uvulopalatopharyngoplasty (UPPP) has been acclaimed in the treatment of obstructive sleep apnea (OSA). Evaluation of the effect of UPPP has usually been done 6 to 8 weeks postoperatively. Recently, a patient died suddenly at home of unknown causes 48 hours following UPPP. Autopsy evaluation demonstrated no evidence of hemorrhage, aspiration, or airway edema; however, it caused us to reassess our postoperative program. Three obese patients (192%, 162% and 157% of ideal body weight) with OSA underwent polysomnography on the second postoperative night. The mean duration of the postoperative apneas was not significantly different; however, the nadir SaO2 during apnea in one patient was significantly lower postoperatively. Those individuals with awake hypercapnia nad hypoxemia who had significant sleep associated hemoglobin unsaturation preoperatively may be at greatest risk. These observations indicate that careful postoperative monitoring is warranted in this group of patients.
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PMID:Breathing during sleep immediately after uvulopalatopharyngoplasty. 377 23

The mechanisms responsible for the development of chronic hypercapnia in patients with obstructive sleep apnea (OSA) are not well defined. Therefore, we tested the hypothesis that diffuse airway obstruction may be involved by studying 50 patients with a well-documented OSA syndrome. Seven patients had daytime hypercapnia with a mean PaCO2 of 51 +/- 2 (SEM) mm Hg, compared to a PaCO2 of 35 +/- 1 in the other 43 patients. There were no differences between the 2 groups in the number or duration of nocturnal obstructive events. In contrast, the hypercapnic patients were significantly heavier than the normocapnic patients (body weight, 189 +/- 11 versus 148 +/- 6% of ideal; p less than 0.005) and had evidence of diffuse airway obstruction, as indicated by an increased residual volume and a reduction in all expiratory flow rates. When the hypercapnic patients were compared with a weight-matched group of 9 normocapnic patients (body weight, 196 +/- 8% of ideal), there were still no differences in nocturnal obstructive events, but the differences in tests of airway mechanics persisted. Multiple regression analysis of PaCO2 against several anthropometric, respiratory physiologic, and polysomnographic variables revealed that only 2 variables (expiratory reserve volume and FEV1/FVC), both of which are influenced by airway mechanics, were significantly correlated with PaCO2 (multiple r = 0.78; p = 0.0001). The findings suggest that OSA alone does not produce daytime hypercapnia even in obese patients, and that the presence of diffuse airway obstruction is an important predisposing factor to the development of chronic CO2 retention in such patients.
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PMID:Role of diffuse airway obstruction in the hypercapnia of obstructive sleep apnea. 377 88


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