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

With airway obstruction there is a decrease in inspiratory intrathoracic pressure. This could lead to increased venous return to the right ventricle (RV) and increased afterload imposed on the left ventricle (LV). Chronic upper airway obstruction, caused by either upper airway lesions or obstructive sleep apnea, is a cause of congestive heart failure because of a chronic resistive load imposed on the respiratory system. To determine the effects of chronic upper airway obstruction on RV and LV in adolescent rats, we chronically obstructed the trachea so as to considerably increased inspiratory esophageal pressure excursion (-3.7 +/- 2.2 to -29.4 +/- 10.1 cm H2O). Rats were studied at 7 wk (Group 1) and at 1 yr (Group 2) after tracheal banding. Sham-operated time-matched rats served as controls. In neither group was there evidence of arterial hypoxemia, but in both groups there was chronic hypercapnia (PCO2, approximately 51 mm Hg; bicarbonate, 27 to 28 mEq/ml). Hemoglobin was also normal in both groups, confirming the absence of chronic hypoxia. There were no significant differences between obstructed and control rats in lung, liver, and LV weight to body weight ratio. However, RV weight to body weight ratio was increased in obstructed rats compared with that in control rats in both groups by approximately 50% (p < 0.005). Thus, chronic normoxic airway obstruction leads to evidence of RV but not LV hypertrophy. We conclude that the mechanical effects of airway obstruction impose a chronically increased afterload on the RV, probably caused by venous return effects, but they have relatively little effect on the LV.
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PMID:Chronic upper airway obstruction produces right but not left ventricular hypertrophy in rats. 823 74

Although nasal continuous positive airway pressure (CPAP) is effective in the treatment of most patients with obstructive sleep apnea (OSA), there is a small group of such patients in whom rapid eye movement (REM) hypoventilation and CO2 retention persist despite the use of CPAP and supplemental oxygen. In this report we describe our experience with nocturnal nasal ventilation (nocturnal nasal positive pressure ventilation [NIPPV] in such patients and its effectiveness in reversing daytime hypercapnia. Thirteen patients, aged 28 to 69 years, with severe OSA confirmed on polysomnography, failed to respond to initial CPAP therapy. All were grossly obese (body mass index [BMI] > 35 kg.ml-1) and hypercapnic (mean PaCO2, 62 mm Hg). Nocturnal nasal ventilation was commenced using a volume-cycled ventilator, which was well tolerated in all patients. After 7 to 18 days of NIPPV, significant improvements in daytime arterial blood gas values were achieved, with a rise in arterial oxygen tension from 50 +/- 2.6 (SEM) to 66 +/- 3 mm Hg (p < 0.001) and a fall in CO2 from 62 +/- 2.5 to 46 +/- 1 mm Hg (p < 0.0001). Nine of the 13 patients were able to be established on a regimen of nasal CPAP after this period, while 3 patients required a longer period (up to 3 months) before adequate nocturnal ventilation could be maintained. In one patient, the improvements in ventilatory drive achieved with NIPPV could not be maintained on CPAP, and she was transferred on to NIPPV long term. These results indicate that effective nasal ventilation leads to an overall improvement in spontaneous ventilation and blood gas values both awake and asleep. We believe this improvement is the result of improved central ventilatory drive. Short-term NIPPV provides lasting benefits allowing the majority of such patients to resume CPAP therapy. Short-term intervention with this therapy should be considered as an interim measure in patients with severe hypercapnic OSA who fail to respond to initial CPAP therapy.
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PMID:Effects of short-term NIPPV in the treatment of patients with severe obstructive sleep apnea and hypercapnia. 771 May 19

We hypothesized that obese children with a history of breathing difficulty during sleep would demonstrate (1) evidence of complete and partial obstructive sleep apnea (OSA) with hypercarbia and/or hypoxemia; and (2) correlation between symptoms, degree of obesity, adenoid and tonsil size, and polysomnography (PSG) results. We evaluated 32 obese children [% ideal body weight (IBW), 196 +/- 45%] with a sleep history questionnaire, airway radiographs, electrocardiograms (ECG), and PSG. By history, we found snoring (100%), difficulty breathing (59%), sweating (44%), restlessness (53%), arousals (41%), apnea (50%), worsening with upper respiratory infection (URI) (81%), hypersomnolence (59%), and mouth breathing (59%). We found adenoid and/or tonsil enlargement on 75% of airway x-ray pictures. ECGs were abnormal in 5 patients. Among all patients, mean sleep study oxyhemoglobin saturation (SaO2) was 85 +/- 16% and mean end-tidal CO2 (PetCO2) was 51 +/- 7 torr; 84% had paradoxical inward movement of the chest on inspiration, 59% had OSA, and 66% had partial OSA. In those with > or = 200% IBW and adenotonsillar enlargement, elevated PetCO2 and the presence of hypoxemia (SaO2 < 90%) for > or = 5% of the total sleep time (TST) were correlated, unlike in patients of similar weight but without adenotonsillar enlargement. Individuals symptoms did not correlate with the severity of PSG abnormalities. By discriminant analysis, using three variables (IBW, presence of adenotonsillar tissue, and presence of > or = 5 symptoms), we could predict PSG abnormalities with up to 81% reliability. Our findings indicate that in obese children, particularly those with %IBW > or = 200 and adenotonsillar hypertrophy, with sleep-disordered breathing evaluation by polysomnography should be considered.
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PMID:Polysomnography in obese children with a history of sleep-associated breathing disorders. 836 18

Obstructive sleep apnea (OSA), daytime hypoxemia, and hypercapnia complicate obesity and are alleviated by weight loss. The flow-volume curve is a sensitive screening tool for most patients; the curve can monitor therapeutic efficacy of weight reduction.
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PMID:Weight loss and OSA and pulmonary function in obesity. 841 57

Upper airway dilating muscle activity increases during apneic episodes in patients with obstructive sleep apnea (OSA). To elucidate the relative contribution of chemical and nonchemical stimuli to augmentation of the upper airway dilating muscle, we measured the response of genioglossus muscle (GG) and inspiratory intercostal muscle (IIM) activities to obstructive apnea during non-REM sleep and compared them with the response to progressive hypoxia and hypercapnia during awake periods in seven male patients with OSA. GG EMG was measured with a wire electrode inserted percutaneously, and IIM EMG was measured with surface electrodes placed in the second intercostal space parasternally. Responses to hypoxia and to hypercapnia were assessed by rebreathing methods in the supine position while awake. Following these measurements, a sleep study was conducted with the EMG electrodes placed in the same locations. The relationship between GG and IIM activities during the cycle of apnea and postapneic ventilation in non-REM sleep was quasi-linear, and the slope of the regression line was significantly greater than those during progressive hypoxia and progressive hypercapnia. The amplitude of GG activity at 70% of maximum IIM activities in the hypoxic test was 140 +/- 20% (mean +/- SEM) during non-REM sleep, which was also significantly greater than that during hypoxia (51 +/- 10%) and that during hypercapnia (59 +/- 15%). These results suggest that nonchemical factors contribute considerably to augmentation of GG activity during obstructive apneic episodes. The nonchemical stimuli may arise from mechanoreceptors activated by upper airway obstruction and behavioral factors associated with change in sleep states.
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PMID:Role of chemical drive in recruiting upper airway and inspiratory intercostal muscles in patients with obstructive sleep apnea. 842 Apr 16

Patients with obstructive sleep apnea syndrome (OSAS) may have daytime pulmonary hypertension (PH). Transient and sometimes severe elevations of pulmonary arterial pressure during sleep as a result of intermittent upper airway obstruction may lead to daytime PH. We sought to study the factors involved in the development of daytime PH. Right-heart catheterization, pulmonary function tests, and arterial blood gas measurements were done in 25 patients in whom OSAS was diagnosed by whole-night polysomnography. Eight of the patients (32%) had PH, defined by a mean pulmonary arterial (PA) pressure > or = 20 mmHg. For the group as a whole, mean PA pressure was positively and significantly correlated with daytime PaCO2 (r = 0.79), percent of ideal body weight (r = 0.45), and Hb (r = 0.40). Mean PA pressure was negatively and significantly correlated with PaO2 (r = -0.54), FEV 1% (r = -0.52), and %FVC (r = -0.68). In contrast, mean PA pressure was not significantly correlated with apnea index or with sleep desaturation. These data indicate that daytime PH was not directly related to sleep-disordered breathing, but was related to daytime hypoxemia, daytime hypercapnia, obesity, obstructive and restrictive respiratory impairments, and secondary polycythemia.
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PMID:[Daytime pulmonary hypertension in the obstructive sleep apnea syndrome]. 854 78

In healthy adults, a ventilatory pattern characterized by progressively increased tidal volume (VT), and decreased respiratory rate (RR) accompany repeated short hypercapnic ventilatory challenges, while minute ventilation (VE) remains constant. We hypothesized that the peculiar ventilatory pattern seen in adults would be blunted in children with obstructive sleep apnea syndrome (OSAS) who undergo comparable intermittent or chronic alveolar PCO2 elevation. We measured ventilatory responses to five challenges of 2-min duration (C1-C5) with 5% CO2 in O2, separated by 5-min room-air breathing intervals (R1-R4), in nine children with OSAS and in eight age-, sex-, and body mass index-matched controls. In all children, CO2 significantly increased VE when compared with baseline conditions (22.3 +/- 2.2 vs. 9.5 +/- 0.9 (SE) l/min; P < 0.001). In control subjects, progressive VT increases from 0.67 +/- 0.10 liter in C1 to 0.92 +/- 0.13 liter in C5 occurred (P < 0.01), whereas RR decreased from 33.9 +/- 5.1 breaths/min in C1 to 27.8 +/- 3.7 breaths/min in C5 (P < 0.02), resulting in VE increases across CO2 challenges (22.3 +/- 4.9 l/min in C1 vs. 25.1 +/- 5.0 l/min in C5; P < 0.005). The RR decrease was primarily related to progressive prolongation of expiratory time (TE) (1.1 +/- 0.1 s in C1 to 1.5 +/- 0.2 s in C5; P < 0.002). In contrast, VT, RR, and TE did not change in a consistent fashion in OSAS patients with repeated CO2 challenges (OSAS vs. control: P < 0.0001). Furthermore, in OSAS, VE was similar with repeated challenges (22.4 +/- 2.2 1/min in C1 vs. 23.9 +/- 1.9 l/min; P = not significant), such that changes in VE over time significantly differed in OSAS and controls (P < 0.001). We conclude that healthy children modify their ventilatory strategy to repeated hypercapnia. We speculate that in OSAS these mechanisms are already fully implemented because of recurrent alveolar hypoventilation accompanying increased upper airway resistance, leading to blunted temporal trends of ventilatory response.
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PMID:Ventilatory response to consecutive short hypercapnic challenges in children with obstructive sleep apnea. 859 21

We have investigated pulmonary hemodynamics in a large series of consecutive, unselected patients with obstructive sleep apnea syndrome (OSAS). The aims of this study were to evaluate the frequency of pulmonary artery hypertension (PH) in OSAS and to analyze, as far as possible, its mechanisms. Two hundred twenty patients were included on the basis of a polysomnographic diagnosis of OSAS (apnea+hypopnea index > 20). PH, defined by a resting mean pulmonary artery mean pressure (PAP) of at least 20 mm Hg, was observed in 37 of 220 patients (17%). Patients with PH differed from the others with regard to pulmonary volumes (vital capacity [VC], FEV1) and the FEV1/VC ratio that were significantly lower (p < 0.001); PaO2 (64.4 +/- 9.3 vs 74.7 +/- 10.1 mm Hg; p < 0.001); PaCO2 (43.8 +/- 5.4 vs 37.6 +/- 3.9 mm Hg; p < 0.001), apnea+hypopnea index (100 +/- 33 vs 74 +/- 32; p < 0.001), and mean nocturnal arterial oxygen saturation (SaO2) (88 +/- 6% vs 94 +/- 2%; p < 0.001). Patients with PH were also more overweight (p < 0.001). Multiple regression analysis showed that 50% of the variance of PAP could be predicted by an equation including PaCO2 (accounting for 32% of the variance), FEV1 (12%), airway resistance (4%), and mean nocturnal SaO2 (2%). In conclusion, PH is observed, in agreement with previous studies, in less than 20% of OSAS patients. PH is strongly linked to the presence of an obstructive (rather than restrictive) ventilatory pattern, hypoxemia, and hypercapnia, and is generally accounted for by an associated obstructive airways disease. In this regard, the severity of OSAS plays only a minor role.
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PMID:Pulmonary hemodynamics in the obstructive sleep apnea syndrome. Results in 220 consecutive patients. 899 33

We studied the relationship of sudden unexpected infant death/apparent life-threatening events (ALTE) to obstructive sleep apnea (OSA) in 74 index probands who had either sleep-laboratory-confirmed OSA or a clinical diagnosis of OSA requiring treatment, 62 matched control probands, and their spouses and first- and second-degree relatives. Sleep was monitored in the home overnight, and OSA was defined by respiratory disturbance indices (number of apneas/hypopneas per hour of sleep) corrected for normal increases with age. Information on sudden unexpected infant death/ALTE was obtained by questionnaire and was corroborated. For living relatives, data were obtained by questionnaire, examination, or study (cephalometric radiographs, ventilatory responsiveness to hypercapnia and hypoxia). Eight index families had 10 infants with sudden unexpected infant death/ALTE; two control families had three infants with sudden death (p = 0.11). All told, 91 of the 136 families (index plus control) included members with OSA, and all 10 infant death/ALTE families were among these (versus zero of 45 families with no OSA; p = 0.03). The sudden infant death/ALTE families had a greater frequency of two or more members with OSA (p = 0.06), reported more respiratory disease or allergy, were more frequently brachycephalic (p = 0.05), and had a smaller mean posterior nasal spine-basion distance (p = 0.0001) and ratio of anterior mandibular/anterior maxillary dental height (p < 0.05). Ventilatory responses to hypoxia were reduced in members of families with OSA (p = 0.008), with a trend toward the greatest blunting in subjects from families with OSA plus sudden unexpected infant death/ALTE. Thus, OSA in adults and sudden unexpected infant death/ALTE in their biologic relatives appear to be related. Familial factors influencing this association may include the degree of the predilection for OSA, liability for respiratory illness or allergy, dimensions of the oral-pharyngeal airway, and ventilatory response to hypoxia.
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PMID:The association of sudden unexpected infant death with obstructive sleep apnea. 866 46

Data concerning the occurrence of chronic-obstructive pulmonary disease (COPD) in patients with obstructive sleep apnea syndrome (OSAS) vary between 11 and 20% due to the underlying definition of COPD. We investigated the frequency of COPD in 202 patients with OSAS. The obstructive pattern was defined by bodyplethysmography (Rt > 0.35 kPa x 1(-1) x s(-1)), flow-volume-curve (MEF50 < 50% pred.), Tiffeneau-index (FEV1/IVC < 70% pred.) and anamnesis (cough and/or sputum). Prevalence of COPD in our 202 patients with OSAS was 16.3%. Patients with OSAS and COPD had a higher body-mass-index (BMI), lower PaO2 and spent more time in an oxygen saturation < or = 90% in relation to total recording time (t90). Polysomnographically there was no difference between the two groups with regard to the ventilatory parameters apnea-index (AI) and apnea-hypopnea-index (AHI). As there is a high risk of developing hypercapnia, pulmonary arterial hypertension and cor pulmonale in patients with OSAS and COPD there is need for early diagnosis of the combination of both diseases.
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PMID:[Incidence of chronic obstructive respiratory tract disease in patients with obstructive sleep apnea]. 868 3


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