Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-two infants and children were found to have clinically significant obstructive sleep apnea. A history suggesting complete or partial airway obstruction during sleep was obtained on all patients, and physical examination of the sleeping patient revealed snoring, retractions, or OSA in 21 patients. Nevertheless, the mean delay in referral for 20 patients first seen after the neonatal period was 23 +15 (+ SD) months. Sixteen of 22 patients (73%) developed serious sequelae: cor pulmonale in 12 (55%), failure to thrive in six (27%), permanent neurologic damage in two (9%), and behavioral disturbances, hypersomnolence, or developmental delays in five (23%). Clinical and radiologic evaluations revealed anatomic abnormalities which narrowed the upper airway in 21 patients; enlarged tonsils and/or adenoids in 14, micrognathia in three,generalized facial abnormalities in three, and cleft palate repair/tonsillar hypertrophy in one. In five patients, upper airway fluoroscopy was performed and was helpful in establishing the site and mechanism of obstruction. Polygraphic monitoring was utilized to quantify the frequency and duration of OSA. Prolonged partial airway obstruction during sleep resulted in significant hypercarbia in 11 patients and hypoxemia in five. Twenty patients improved after surgery which relieved or bypassed the pharyngeal airway obstruction; two cases are pending. Increased awareness of OSA and examination of the sleeping patient should result in earlier treatment and less morbidity for infants and children with OSA.
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PMID:Obstructive sleep apnea in infants and children. 705 14

The prevalence of reported sleep disturbances in a general population is high. Many of the complaints are the result of sleep-related breathing disorders, due mainly to the occurrence of obstructive and central apnoeas. Obstructive sleep apnoea is a fully described and well-recognized entity. Central sleep apnoea (CSA) however, has been poorly studied. There is accumulating evidence that central sleep apnoea should be considered as the end of a spectrum. Instability in the breathing pattern is the main underlying mechanism and is due to the interaction of many factors. Breathing during sleep is dependent on metabolic control and the activity of the respiratory muscles. Decreased chemical drive and/or failing respiratory muscle function are associated with CSA and usually also with ongoing hypoventilation during wakefulness, characterized by chronic daytime hypercapnia. Central respiratory drive can also be inhibited by upper airway reflexes. Mostly, however, CSA occurs as the hallmark of unstable breathing during sleep brought about by an overall increase in loop gain (especially in light sleep stages) and the unmasking of a CO2 threshold. Arousal following central apnoeas acts as an amplification of the instability. Micro electroencephographic (EEG) arousals are often observed as a consequence of CSA. They are responsible for sleep fragmentation and hypersomnolence during the day. The daytime hypersomnolence and complaints of awakenings during sleep in patients with CSA can be striking. CSA can occur in specific pathologies, such as chronic heart failure and (post-traumatic) brain lesions, that are associated with irregular breathing. Treatment strategies are remarkably few in number. Use of nasal ventilation and the inhalation of CO2 are mainly of theoretical interest, since patients do not often tolerate these more invasive therapies. Drug treatment, especially with acetazolamide, is easier to perform. Stimulation of upper airway reflexes, by less invasive methods, seems to be promising for the near future.
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PMID:Central sleep apnoea, pathogenesis and treatment: an overview and perspective. 748 5

Important pathophysiological mechanisms in obstructive sleep apnea at night are increasing pleural pressure swings, hypoxia and hypercapnia, as well as central nervous arousals with consecutive fragmentation of regular sleep structure. They influence the cardiovascular system, at first only at night and at a later stage also during the day. This might result in cardiac structural changes: dilation and hypertrophy of the right ventricle, hypertrophy of the left ventricle, (especially of the muscular ventricular septum), dilation of right and left atrium. It is suggested that these cardiac structural changes are characteristic for obstructive sleep apnea and therefore define the "sleep apnea heart".
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PMID:[Structural cardiac changes in patients with obstructive sleep apnea]. 762 97

Sedation elicited by some centrally acting antihypertensive agents may interfere with respiratory control, and by selectively inhibiting upper airway dilating muscle activity it may facilitate obstructive sleep apnea. Autoradiographic studies with [125I]p-iodoclonidine in the presence of 10 microM epinephrine to block alpha 2-adrenergic sites or 100 nM moxonidine to mask I1-imidazoline sites show that both I1- as well as alpha 2-sites are localized in putative chemosensory areas of the rostral ventrolateral medulla in the cat. We sought to determine the effect of activating I1 and alpha 2-receptors on central chemosensitivity by using moxonidine as a selective I1 agonist, clonidine as a mixed I1/alpha 2 agonist, SK&F-86466 as a specific alpha 2-antagonist, and efaroxan as a mixed I1/alpha 2 antagonist. We recorded responses of phrenic, hypoglossal, and cervical sympathetic nerve activities to progressive hypercapnia after hyperventilation to apnea. Moxonidine (3-100 micrograms/kg i.v.) caused dose-dependent decreases in tonic cervical sympathetic nerve activity and blood pressure, but had no effect on the CO2 threshold (after 30 or 100 micrograms/kg moxonidine, phrenic nerve activity reappeared at 5.8 +/- 0.2% CO2 versus 5.6 +/- 0.3% CO2 in control). Following moxonidine, the slope of the steep portion of the CO2 response tended to increase (10.3 +/- 1.8 versus 7.3 +/- 0.9). Peak phrenic nerve activity was comparable to control at 7.5% CO2 (20 +/- 2 U in control) and at 9.5% CO2 (30 +/- 3 versus 27. +/- 2 U). Similarly, the response of hypoglossal and inspiratory phasic cervical sympathetic nerve activity to a progressive CO2 rise was not affected by moxonidine. By contrast, clonidine in the same doses decreased CO2 sensitivity, because the CO2 threshold was elevated from 5.3 +/- 0.5% to 6.7 +/- 0.4% (p < 0.001). The slope of the CO2 response was decreased from 9.7 +/- 1.9 to 7.4 +/- 1.3 (p = 0.05). Peak phrenic nerve activity was reduced at 7.5% CO2 (11 +/- 5 versus 25 +/- 2 U; p < 0.05) and at 9.5% CO2 (21 +/- 4 versus 33 +/- 2 U; p = 0.06). Clonidine selectively inhibited the response of hypoglossal nerve activity to CO2. The depressive effects of clonidine were reversed by alpha 2-blockade with SK&F-86466 (0.5 or 1 mg/kg). Inspiratory phasic cervical sympathetic nerve activity increased after SK&F-86466 in parallel with phrenic and hypoglossal nerve activity, but the tonic component of cervical sympathetic nerve activity and blood pressure increased only transiently.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effect of I1-imidazoline receptor activation on responses of hypoglossal and phrenic nerve to chemical stimulation. 767 59

A 46-year-old extremely obese black woman presented with headaches, blurred vision, and visual obscurations. Her exam was notable for bilateral severe papilledema, retinal hemorrhages, and lethargy. Her CAT scan was normal, and a spinal tap revealed a very high opening pressure. Although this patient's presentation mimicked pseudotumor cerebri, the lethargy and retinal hemorrhages were atypical. Her hospital evaluation was notable for elevation of the serum bicarbonate level, and she was subsequently found to have hypoxia and hypercapnia on a blood gas. The patient was diagnosed as Pickwickian syndrome, with obstructive sleep apnea. Treatment of the pulmonary problem resulted in dramatic improvement in her eye findings and her lethargy, and optic nerve sheath fenestration was not necessary.
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PMID:Disk edema in an overweight woman. 854 13

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

The depression of EMG activity in upper airway muscles during sleep is known to be a predisposing factor causing upper airway obstruction in patients with obstructive sleep apnea syndrome (OSAS). To clarify whether or not the selective depression of upper airway muscles could be associated with the hypoxic ventilatory depression, we performed sustained hypercapnic hypoxia tests during wakefulness in 11 control subjects and 10 patients with OSAS. Isocapnic sustained hypoxia around SaO2 80% with mild hypercapnia [PETO2: 45.8 +/- 1.6 (SD) and 46.7 +/- 2.8 mm Hg and PETCO2: 44.2 +/- 4.7 and 43.1 +/- 5.0 mm Hg in control and OSAS groups, respectively] was applied for 20 min. Electromyogram activities were recorded from the genioglossal muscle (EMGGG) and diaphragm (EMGDIA) with ventilatory variables. The magnitudes of hypoxic depression in terms of minute ventilation (VI) and minute EMGDIA (EMGDIA/min) were compared in percentage between peak value and the value at the late period. These values were not significantly different between two groups (VI: 79.2 +/- 10.7 and 66.9 +/- 12.8% and EMGDIA/min: 63.2 +/- 17.1 and 60.4 +/- 24.0% in control and OSAS, respectively). On the contrary, the depression in EMGGG was not consistently observed in control (86.1 +/- 38.6% of the peak value) whereas EMGGG was markedly depressed in OSAS (38.6 +/- 15.7% of the peak value; p < 0.01). It is concluded that sustained hypoxia attenuates the activity in genioglossal muscle in patients with OSAS, but not in control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differences in the response of genioglossal muscle activity to sustained hypoxia between healthy subjects and patients with obstructive sleep apnea. 804 19

Although obstructive sleep apnea (OSA) occurs commonly in acromegaly, we have recently reported an unexpectedly high prevalence of central sleep apnea (CSA) in these patients. Acromegalic patients with CSA have increased growth hormone (GH) and insulin-like growth factor-1 (IGF-1) levels compared with their counterparts with OSA. Studies in animals, normal humans, and patients with sleep apnea have suggested that CSA is associated with increased gain of the respiratory control system. To examine the relationship between sleep apnea, respiratory control, and hormonal activity in acromegaly, we performed sleep studies and examined ventilatory responses to hypoxia at resting CO2 (HVR) and 8 mm Hg above resting CO2 (HHVR) and hypercapnia (HCVR) in 54 patients with acromegaly who also underwent detailed endocrine evaluation. Patients with CSA (n = 11) had higher HCVR (3.47 +/- 0.57 L/min/mm Hg) than did patients with obstructive sleep apnea (OSA) (1.86 +/- 0.19, n = 33) and patients without sleep apnea (1.77 +/- 0.21, n = 10). Measures of ventilatory control were all correlated with the mean of 12 hourly GH concentrations, but only HCVR was correlated with IGF-1 levels. Multiple linear regression analysis revealed that HCVR, HHVR, and IGF-1 could explain 39% of the variability in the degree of CSA in acromegalic patients with sleep apnea. We conclude that increased ventilatory responsiveness and elevated hormonal parameters of disease activity both contribute to the pathogenesis of central sleep apnea in acromegaly.
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PMID:Central sleep apnea is associated with increased ventilatory response to carbon dioxide and hypersecretion of growth hormone in patients with acromegaly. 804 36

Profound periodic sleep hypoxemia (as low as 9-10% saturation) was observed in 41 morbidly obese patients with obstructive sleep apnea (OSA). Group 1 consisted of 14 patients with awake hypercapnia (mean PaCO2 54 +/- 8 torr, s.d.) and group 2 were 27 with eucapnia (PaCO2 38.6 +/- 2.9). Group 1 OSA patients were more obese (BMI 48.7 +/- 8.5 vs 38.3 +/- 6.8 kg/m2, had lower FEV1 (61 +/- 17% vs 86 +/- 15% pred.) and lower FVC (62 +/- 16% vs 77 +/- 13% pred.), all the differences insufficient per se to account for hypercapnia. Group I remained apneic longer in REM (100 +/- 50 s vs 65 +/- 32 s), and tolerated lower mean SpO2 (pulse oximeter SaO2) in NREM (71 +/- 16% vs 81 +/- 7%) and lower minimum SpO2 values in NREM (54 +/- 12% vs 69 +/- 11%) (all the differences were significant, p < 0.05). We conclude that daytime hypercapnia predicts more severe sleep desaturation in NREM in obese patients with OSA. The combination of morbid obesity and hypercapnia with OSA is associated with the most profound and repeated hypoxemia ever reported as occurring without evident brain damage or death.
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PMID:Profound sleep hypoxia in morbidly obese hypercapnic patients with obstructive sleep apnea. 807 11

The pathophysiology of the obstructive sleep apnea syndrome (OSAS) is not fully understood. In children, airway obstruction secondary to tonsilloadenoidal hypertrophy is the leading cause of OSAS. However, not all children with tonsilloadenoidal hypertrophy develop OSAS. Thus, other factors, including abnormalities in ventilatory control, may contribute to the etiology of OSAS. To test this, we performed polysomnography and hypercapnic and hypoxic ventilatory response testing in 20 children and adolescents with OSAS (mean age, 8 +/- 3 [SD] yr) and 19 control subjects. Only two children with OSAS were obese. Children with OSAS had an apnea index of 16 +/- 20, peak PETCO2 of 54 +/- 5 mm Hg, and SaO2 nadir of 84 +/- 13% during polysomnography. Ventilatory responses were performed by rebreathing techniques. The slope of the hypercapnic ventilatory responses, corrected for body surface area, was 1.74 +/- 0.79 L/min/m2/mm Hg PETCO2 in children with OSAS and 1.45 +/- 0.58 L/min/m2/mmHg PETCO2 in control subjects (NS). Hypoxic ventilatory responses, corrected for body surface area, were -0.94 +/- 0.49 L/min/m2/% SaO2 in children with OSAS and -0.95 +/- 0.45 L/min/m2/% SaO2 in control subjects (NS); however, the sample size was small. There was a weak inverse correlation between the slope of the hypercapnic ventilatory response and the duration of hypoventilation during polysomnography (r = -0.44, p < 0.05). We conclude that children with OSAS have normal ventilatory responses to hypercapnia, and they may have normal ventilatory responses to hypoxia. We speculate that abnormal central ventilatory drive plays little if any role in the pathogenesis of pediatric OSAS.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ventilatory responses during wakefulness in children with obstructive sleep apnea. 811 41


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