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

Alveolar hypoventilation due to the chronic obstruction of the airway such as pulmonary emphysema, or severe restrictive dysfunction due to sequela of pulmonary tuberculosis causes chronic hypercapnia (chronic respiratory acidosis). Ninety-five percentile of significance band of chronic and acute hypercapnia of both experimental and clinical setting is introduced in the graphic display of the acid-base balance. On acute exacerbation of these disorders, examination of arterial blood gas in series are usually plotted along the significance band of hypercapnia. With clinical improvement, the plot will gradually drop down to the chronic stable area of the band. Although cases with metabolic disorders complicate the interpretation, evaluation of the acid-base status using the graphic display will be of help at bedside assessment.
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PMID:[Graphic evaluation of the significance band for hypercapnia in pulmonary disorders]. 143 7

Thirty six patients previously treated for pulmonary tuberculosis by thoracoplasty were studied to determine the prevalence and effect of airflow obstruction. The mean (SD) FEV1 was 1.3 (0.65) 1 and the mean forced expiratory ratio (FER) 64% (12%). FEV1 was less than predicted in every patient whereas FER was less than predicted in 30, being below the lower 98th percentile in 15 (42%). In the 18 patients who complained of breathlessness the means of the standardised residuals (SR) for FEV1, peak expiratory flow (PEF), and FER were significantly lower and that for residual volume/total lung capacity (RV/TLC) significantly higher than those for the 18 patients who were not breathless (all p less than 0.0001). There was no difference in the smoking history of the two groups. Only three of the 23 patients in whom reversibility of airflow obstruction was assessed showed a greater than 25% increase in PEF. None showed an increase in FEV1 of greater than 15%. The 18 who were breathless had significantly lower values of arterial oxygen tension (PaO2) and higher values of arterial carbon dioxide tension (PaCO2) (p less than 0.0001). Thirteen of these patients were in chronic respiratory failure (PaO2 less than 8.0 kPa or PaCO2 greater than 5.9 kPa, or both) compared with only one of the 18 who were not breathless. The indices correlating best with PaO2 and PaCO2 were SR FEV1 and SR PEF respectively. SR FEV1 accounted for 34% of the variance in PaO2 and SR PEF for 29% of the variance in PaCO2. Airflow obstruction has been found to be common in patients with a thoracoplasty and to be associated with hypoxia and hypercapnia.
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PMID:Importance of airflow obstruction after thoracoplasty. 366 Feb 88

To assess clinical significance of breath-by-breath variation of tidal volume and its distribution pattern displayed as a histogram, continuous measurement of tidal volume was made with electrical impedance pneumography for about 60 minutes. Subjects were composed of 26 normal male and 46 patients including 17 patients with restrictive lung disease and 29 patients with obstructive lung disease. To evaluate variation of tidal volume quantitatively, coefficient of variance (C.V.) was used. In comparison to the normal pattern of distribution (C.V. = 26.0 +/- 7.5%, mean +/- S.D.), patients with restrictive lung disease showed extremely narrow pattern of the distribution and significantly smaller C.V. (17.5 +/- 4.6% in old pulmonary tuberculosis, P less than 0.005 and 18.9 +/- 9.3% in pneumonitis, P less than 0.025). Whereas, patients with obstructive lung disease showed widespread pattern of the distribution and significantly greater C.V. (43.2 +/- 13.0% in pulmonary emphysema with hypercapnia, 33.0 +/- 7.5% in normocapnia and 35.8 +/- 9.4% in asthmatic attack, P less than 0.005). In all the patients with bronchial asthma after the treatment, the extremely widespread pattern of histogram was returned toward the normal one and the C.V. was decreased (22.4 +/- 6.4%). It was suggested that the distribution pattern of tidal volume was affected by the change of clinical condition, and was well correlated to the pathophysiological process related to restrictive or obstructive lung disease. We conclude that analysis of tidal volume distribution by the histogram is one of the useful approach to manage patients with respiratory diseases.
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PMID:Variability of breath-by-breath tidal volume and its characteristics in normal and diseased subjects. Ventilatory monitoring with electrical impedance pneumography. 402 Dec 11

Patients with respiratory failure based on pulmonary tuberculosis sequelae are second in number among some fifty thousand patients receiving home oxygen therapy in Japan. Its 5 year survival rate is 47% in man and 56% in woman. The prognosis is better in woman than in man and may be dependent, at least partially, on younger age in woman. The influence of arterial blood gases on the prognosis is quite different between tuberculosis sequelae and chronic obstructive pulmonary disease: PaO2 scarcely influence the prognosis while higher PaCO2 is beneficial for tuberculosis sequelae. Patients with hypercapnia have better nutrition as estimated by serum albumin and this fact may cause the longer survival. Pulmonary hypertension is more frequently observed but is less strongly related to arterial blood gases and ventilatory function in tuberculosis sequelae than chronic obstructive pulmonary disease.
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PMID:[Respiratory failure in pulmonary tuberculosis sequelae]. 936 12

Hypercapnia observed in patients with chronic respiratory failure may not be an ominous sign for prognosis when they are receiving long-term oxygen therapy (LTOT). In this study, we selected 4,552 patients with chronic obstructive pulmonary disease (COPD) and 3,028 with sequelae of pulmonary tuberculosis (TBsq) receiving LTOT from 1985 to 1993 throughout Japan and prospectively analyzed their prognoses. The hypercapnic patients (PaCO2 >= 45 mm Hg) had a better prognosis than the normocapnic patients (35 <= PaCO2 < 45 mm Hg) for TBsq, but no difference was found between the two groups with COPD. Furthermore, Cox's proportional hazards model revealed that in TBsq hypercapnia was an independent factor for favorable prognosis, and that the relative risk for mortality was 0.76 in patients with 45 <= PaCO2 < 55 mm Hg, 0.64 for those with 55 <= PaCO2 < 65 mm Hg, and 0. 49 for patients with PaCO2 >= 65 mm Hg against normocapnic patients. This favorable effect of hypercapnia in TBsq was particularly apparent in the patients without severe airway obstruction. Even a rise of 5 mm Hg or more in PaCO2 over the initial 6- to 18-mo follow-up period was not associated with poor prognosis in TBsq, although it was in COPD. From these findings, we conclude that hypercapnia should not be generally considered an ominous sign for prognosis in those patients who receive LTOT.
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PMID:Prognostic value of hypercapnia in patients with chronic respiratory failure during long-term oxygen therapy. 965 28

According to the complexity of pathological change of pulmonary tuberculosis sequelae (TB seq), on which respiratory failure based shows the higher incidence of marked degree of hypoxemia and hypercapnia than that based on chronic pulmonary emphysema (CPE). In TB seq, pulmonary artery mean pressure is higher, nocturnal oxyhemoglobin desaturation is much lower than in CPE. Also hypoxemia on exercise is lower, and oxygen inhalation for this hypoxemia is more effective than in CPE. The most effective therapy is continuous oxygen therapy. Home oxygen therapy has improved the prognosis and quality of life (QOL) of patients with respiratory failure based on TB seq. Artificial positive pressure ventilation (TIPPV) with intubation or tracheotomy is carried out for patients with severe hypercapnia and respiratory acidosis. Recently, early application of nasal mask ventilation (NPPV) on patients with TB seq has prohibited acute exacerbation of chronic respiratory failure. And also for patients with severe hypercapnia, NPPV with BIPAP method is effective for their QOL. Comprehensive respiratory rehabilitation is also successfully applied for their management.
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PMID:[Respiratory failure based on pulmonary tuberculosis sequelae and its management]. 988 38

We investigated pulmonary hemodynamics and chest X-ray findings to explore pathophysiological significance of chronic hypercapnia in patients with pulmonary tuberculosis sequelae. One hundred and seven patients underwent examinations of blood gases and right cardiac catheterization. The patients were divided into two groups, according to arterial carbon dioxide tension under room air breathing (PaCO2). Group I (n = 35) was defined as 45 Torr or lower of PaCO2, and Group II (n = 72) was the hypercapnic group whose PaCO2 was over 45 Torr. In addition, spirometry was done in 34 patients of Group I and 68 of Group II. First, the values of blood gases, spirometry and pulmonary hemodynamics were compared between the two groups. Secondly, between 22 of Group I and 50 of Group II, the values of pulmonary arteriolar resistance (PAR) before and after 100% oxygen breathing for 10 minutes were compared. These comparisons were made by exploratory data analysis. Lastly, we described in all cases with five items of chest X-ray findings and the extent of each finding we had defined. The items were emphysematous change; fibrosis, bronchiectasis, and/or cavity (hereafter abbreviated as "fibrosis"); lung resection and/or atelectasis; pleural thickening; and thoracoplasty. We explored the items of X-ray findings which may relate to hypercapnia by ridit (abbreviation for "relative to an identified distribution") analysis. The results were as follows. (1) Hypercapnic patients tended to have severer restrictive ventilatory impairment and hypoxemia. Under an even level of arterial oxygen tension (PaO2), tissue oxygenation was not poorer in Group II than in Group I. (2) Hypercapnic patients tended to have more unfavorable pulmonary hemodynamics. More than half of them had pulmonary hypertension defined as 20 mmHg or higher of pulmonary artery mean pressure (PAm). Under an even level of PaO2, PAm was higher in Group II. Although 34 patients of Group II showed PaO2 over 60 Torr, 23 of them had pulmonary hypertension. (3) PAR after oxygen breathing was more likely to decrease in Group II than in Group I. (4) As any mean ridit was standardized and adjusted to 0.5 in Group I, the maximum was the mean ridit of "pleural thickening" (= 0.67), next "fibrosis" (= 0.65) in Group II. The above two items of X-ray findings, in which each mean ridit was higher than in any other item, were more influential on hypercapnia. We conclude as follows. (1) Pulmonary hypertension is severer in hypercapnic patients with pulmonary tuberculosis sequelae; it may be mainly attributable to hypoxic pulmonary vasoconstriction. (2) An important cause of chronic hypercapnia may be pathological changes such as "pleural thickening" and "fibrosis" seen on the radiogram.
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PMID:[Investigation of pulmonary hemodynamics and chest X-ray findings in hypercapnic patients with pulmonary tuberculosis sequelae]. 1048 27

The prognostic value of hypercapnia and/or pulmonary hypertension differs in patients with sequela of pulmonary tuberculosis (TBseq) and those with chronic obstructive pulmonary disease (COPD) who are receiving home oxygen therapy (HOT). In an attempt to identify the factors, if any, that might explain this difference, we first compared nutritional status, respiratory function test results, dyspnea indexes, and other data for hypercapnic patients (PaCO2 > or = 45 Torr) and normocapnic patients (PaCO2 < 45 Torr) receiving HOT. Second, we examined the relationship between the degree of pulmonary hypertension and several respiratory function parameters for patients in each disease category. In 44 patients with TBseq, nutritional status estimated by body mass index and serum albumin was significantly better in the hypercapnic patients than in the normocapnic patients. However, this difference was not observed in 37 patients with COPD. In 30 patients with TBseq, the degree of pulmonary hypertension correlated significantly only with PaO2; in 32 patients with COPD, however, significant correlations were observed not only with PaO2 but also with PaCO2, %VC, and FEV1. These differences distinguishing groups of patients with the 2 diseases may provide an explanatory basis for the difference in prognostic value of hypercapnia and/or pulmonary hypertension in patients receiving HOT.
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PMID:[An analysis of nutritional status and pulmonary hypertension in patients with sequela of pulmonary tuberculosis and chronic obstructive pulmonary disease]. 1058 88

We investigated nocturnal oxygen desaturation (NOD) in 36 patients with stable chronic respiratory disease who were receiving home oxygen, therapy (HOT). Study data included medical history, chest roentgenograms, measurement of daytime arterial blood gases while awake, and spirometry. Each subject underwent full overnight oximetry monitoring. Three patients were excluded from further investigation because of periodic desaturation suggestive of sleep apnea. The remaining 33 subjects were divided into two groups: 21 patients with sequelae of pulmonary tuberculosis (TB-sequela) and 12 patients with chronic obstructive pulmonary disease (COPD). The COPD group was divided into two subgroups according to the Burrows classification (Am Rev Resp Dis. 90: 14-27, 1964): 5 patients with type A (Type A) and 7 patients with type B (Type B) COPD. The percentages of total sleep time with SaO2 < or = 85% (DST 85) and SaO2 < or = 90% (DST 90) were calculated for each subject. NOD was defined as DST 85 > or = 1%. Arterial oxygen partial pressure (PaO2) while awake was > or = 60 Torr in all subjects. No difference was observed in mean awake PaO2 values between the TB-sequela and COPD groups. NOD was detected in 8 TB-sequela patients but in none of the COPD patients. Mean DST 85 and DST 90 values were significantly (p < 0.05) higher for the TB-sequela group than for the COPD group. Of 15 TB-sequela patients who were able to complete spirometry tests, 6 had NOD. All 6 of these patients had hypercapnia while awake (PaCO2 > or = 50 Torr) and reduced vital capacity (< or = 50% predicted). No difference was observed in mean DST 90 or DST 85 values between the TypeA and TypeB COPD subgroups. We conclude that NOD is common in patients with chronic stable respiratory disease treated with HOT despite daytime euoxia. TB-sequela patients with hypercapnia and restrictive ventilatory impairment are at high risk for NOD.
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PMID:[Nocturnal oxygen desaturation during home oxygen therapy in patients with chronic respiratory disease]. 1072 46

Home medical care for the aged has become important with the increasing population of elderly people in Japan. Home oxygen therapy (HOT) is a representative treatment for aged patients with chronic obstructive pulmonary diseases (COPD) or sequelae of pulmonary tuberculosis. In order to provide appropriate and safe home medical care, the pulmonary function tests need to be performed easily and simply at home. These tests include a pulse oximeter for arterial blood oxygen saturation monitoring in HOT, a peak flow meter or a handy-type spirometer for air way monitoring in asthmatic patients and a handy-type monitor for screening patients with sleep apnea syndrome (SAS). In using a pulse oximeter, the users need to keep in mind that the case is sometimes severe even though the oxygen saturation values are in the normal ranges, and also that, when oxygen saturation is low, high concentrated oxygen exposure sometimes deteriorates hypercapnia in patients with type II respiratory failure. A peak flow meter is not suitable for air way monitoring in patients with COPD or small air way diseases. The handy-type monitor for SAS needs to be improved not to interfere with the patient's natural sleep, and also to provide more simple analysis programs. Doctors should educate patients to go to hospital to see a doctor and to undergo close examinations whenever unexpected abnormal values are obtained. Equipment which can provide high quality test results with easier maneuver ability and analysis needs to be developed in the future.
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PMID:[Pulmonary function tests in home medical care]. 1672 56


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