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

The pathogenesis of obesity hypoventilation is incompletely understood. We investigated 505 patients with sleep apnoea in respect of determinants that correlate with chronic hypercapnia. 14 patients (2.8 per cent) exhibited daytime hypercapnia (PCO2 greater than or equal to 45 mmHg). Compared with the entire group of patients, these patients showed heavier overweight (p less than 0.001) and their nightly respiratory dysregulation defined by the apnoea index was more severe (p less than 0.001). If these patients were compared with 14 normocapnic controls matched for apnoea index, weight and age, there was no difference in respect of lung function data. We conclude that overweight and the severity of sleep apnoea are determinants that predispose to chronic alveolar hypoventilation.
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PMID:[Which factors promote chronic alveolar hypoventilation in patients with obstructive sleep apnea?]. 186 1

Here we have the case of a right nephrectomy ureterectomy for urothelial neoformations in the upper urinary apparatus, in the position of a left flexed lateral decubitus (nephrectomy) practised to a patient, in which a small right pleural aperture was unnoticed until the end of the operation when the closing was being carried out. In the immediate postoperative, the patient developed hypoxia and hypercapnia, as well as an atelectasis of the lower lobus in the left lung, that appeared in the radiological test. We comment now the causes that could have originated this picture, such as overweight, the position of the patient during the operation, its length and the pleural aperture throughout the surgical act, focusing the study in this latter point.
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PMID:[Pulmonary atelectasis in bent lateral decubital position (nephrectomy). Apropos of a case]. 278 Oct 85

There is a wide clinical spectrum in chronic obstructive pulmonary disease (COPD). The extremes of this spectrum, the "pink puffer" (PP) and "blue bloater" (BB) stereotypes differ in their degree of sleep hypoxemia and pulmonary hypertension. Most patients cannot be characterized as either PP or BB. The data amassed in the recent nocturnal oxygen therapy trial provide an opportunity to see to what extent differences in sleep oxygenation and hemodynamics in a large hypoxemic COPD population are related to awake hypoxemia and hypercapnia. From a large hypoxemic COPD population sleep SaO2 was examined in those with (PaCO2 greater than 44 mm Hg) and without (PaCO2 less than or equal to 44 mm Hg) hypercapnia. Hypercapnic patients (mean PaCO2 49.8 mm Hg) had the same PaO2 and degree of airflow obstruction as normocapnic patients (PaCO2 37.4 mm Hg) but had far greater sleep hypoxemia (measured by mean sleep SaO2, low sleep SaO2, and awake-low sleep SaO2, p less than 0.05). In addition, arterial blood gases of the large sleep O2 desaturaters were compared with those of the small desaturaters; PaO2 was similar in both groups, whereas PaCO2 was different (p less than 0.01). Two common subsets of hypoxemic patients were also compared; one was hypercapnic and overweight, the other normocapnic and hyperinflated. We found that patients in the hypercapnic group had far worse sleep hypoxemia, although they had better lung function. We conclude that hypercapnia is a marker for sleep O2 desaturation in hypoxemic COPD.
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PMID:Hypercapnia and sleep O2 desaturation in chronic obstructive pulmonary disease. 362 83

The relationship between low-awake chemosensitivity, exogenous respiratory load (obesity) and respiratory/oxygenation patterns during sleep was evaluated in a family with overall low ventilatory responses to hypoxia and hypercapnia. Six family members were of normal weight, in good health and had normal pulmonary function tests. Only one of these subjects had totally normal responses to the chemical control of breathing. A seventh family member had loaded breathing because of severe obesity. His ventilatory and mouth occlusion pressure responses to hypoxia or hypercapnia were severely blunted. After weight loss (200 percent of ideal body weight to 133 percent) the ventilatory responses were improved but still abnormally low. Significant nocturnal respiratory abnormalities and oxygen desaturation were only seen in the overweight member and improved following weight loss (load reduction).
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PMID:The effects of weight and chemosensitivity on respiratory sleep abnormalities: a family study. 377 Oct 93

The slope of ventilatory response to hypercapnia at rest was determined in 77 healthy male students by means of the CO2 rebreathing method. It was found that the hypercapnic ventilatory response slope (S) was significantly lower in the lean group with BMI (body mass index) below 19 than that in the normal group, while there were no significant correlation between S and body weight or height. These results indicate that sensitivity of hypercapnia in the lean subjects differed from that of normal and overweight subjects.
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PMID:The influence of body size on the ventilatory response to hypercapnia. 402 Dec 21

81 patients living at La Paz (3,600-4,000 m altitude) and suffering from chronic polycythaemia, with an haematocrit greater than 57% were studied. They were selected on clinical and spirometric criteria to exclude from the study patients with associated pulmonary diseases. 45% of them were overweight (group O). The group of patients having a normal weight was divided into two equal groups: "young" patients (less than 35 years, J) and "old" patients (greater than 35 years, V). The important findings of this study were: 1) the existence of hypoxaemia in all groups: compared to the control group, the mean differences are -2 kPa for O and V groups and -1.3 kPa for J group; 2) the presence of slight hypercapnia (+0.3 kPa in J and V groups; +0.5 kPa in O group), excluding diurnal hypoventilation as the major source of hypoxaemia; 3) a significant linear correlation between the increase in PaCO2 and haematocrit in O and (J + V) groups; 4) a significant linear correlation between hypoxaemia and the increase in haematocrit, particularly in group J, but also in O and (J + V) groups; hypoxaemia is also well correlated with age in (J + V) group: PaO2 (kPa) = 11.42 -0.025 Age (yr) -0.061 Hct (%) The classical assumption of a chronic hypoventilation syndrome producing a progressive increase in haematocrit is discussed. Haematocrit is suspected as a causative factor of hypoxaemia, itself a well known factor producing polycythaemia. This mechanism could be the source of a vicious circle.
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PMID:[Hypoxemia and the hematocrit in pathologic polycythemia due to altitude]. 647 87

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

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 evaluated the effect of non-invasive nocturnal ventilation with the bi-level positive airway pressure (BiPAP) ventilator in 12 overweight patients with verified obstructive sleep apnoea syndrome (OSAS) and nocturnal hypercapnia. All patients exhibited subsequently less overnight CO2 accumulation (p < 0.0001), the desaturation event frequency was reduced (p < 0.002), daytime O2 tension rose (p < 0.001), daytime CO2 tension was reduced (p < 0.01), and apnoeas were eliminated. All symptoms characterising the syndrome, when present at the beginning of the therapy, were eliminated during the treatment. Patient compliance was high. This study showed that OSAS patients with hypercapnia can be effectively treated by BiPAP ventilation during sleep.
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PMID:Bi-level positive airway pressure treatment of obstructive sleep apnoea syndrome. 958 Sep 22

We retrospectively evaluated data from 213 consecutive patients; 152 were affected by obstructive sleep apnea (OSA), 29 had OSA associated with chronic obstructive pulmonary disease (COPD), also known as overlap syndrome, and 32 had COPD. Patients with obesity-hypoventilation syndrome were not included. The aims of the study were to evaluate the anthropometric, pulmonary, and polysomnographic characteristics of patients affected by overlap syndrome compared to "simple" OSA and to COPD subjects and to analyze the determinants of hypercapnia in overlap syndrome. In the comparison between overlap and OSA patients, the overlap group had a significantly higher PaCO2 (44.59 vs. 39.22 mm Hg; p < 0.01), in the presence of a similar AHI (40.46 vs. 41.59/h). Comparing overlap to COPD patients, overlap showed a significantly higher PaCO2 value (44.59 vs. 39.63 mm Hg; p < 0.005) and had significantly less severe obstructive impairment (FEV 162.93 vs. 47.31%; FEV1/FVC ratio 66.71 vs. 59.25%; p < 0.005). Anthropometric, pulmonary function, and polysomnographic data did not differ between normo- and hypercapnic overlap patients. The best model (stepwise multiple regression analysis) for predicting PaCO2 in overlap patients showed r2 value 0.65: PaO2 contributed to 38%, FEV1 to 15%, and weight to 12%. In conclusion, the occurrence of hypercapnia in overlap patients is only partially explained by the combination of overweight and reduced respiratory function, supporting the hypothesis of a multifactorial genesis.
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PMID:Hypercapnia in overlap syndrome: possible determinant factors. 1191 59


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