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

Marked variability in resting steady-state arterial PCO2 (PaCO2) values are observed among patients with chronic obstructive pulmonary disease (COPD), independent of severity of their obstructive airways defect. The reasons for the development of hypercapnia in some but not in the others remain unclear. One hypothesis states that the level of morbid resting PaCO2 may be related to the premorbid hypercapnic ventilatory response (HCVR); accordingly, subjects who were relatively insensitive to CO2 breathing (low responders) develop CO2 retention in the face of lung disease. The present study investigated this hypothesis in the hamster model of elastase-induced emphysema. After obtaining steady-state HCVR in 19 unanesthetized unrestrained hamsters, emphysema was induced by intratracheal instillation of pancreatic elastase. Forty-five days later, minute ventilation and PaCO2 measurements were done, and lung function tests were obtained. The slopes of HCVR and morbid PaCO2 values varied from -0.09 to 2.36 ml/min/mmHg inspired PCO2 and 48.7 to 63.1 mmHg, respectively. There were no significant correlations between morbid PaCO2 values and premorbid HCVR or lung function test abnormalities caused by emphysema. These animal model studies do not support the hypothesis that the level of PaCO2 in patients with COPD is related to their premorbid HCVR.
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PMID:Premorbid ventilatory response to hypercapnia is not related to resting arterial carbon dioxide tension in hamsters with elastase-induced emphysema. 393 90

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

Forty-five newborn infants in respiratory failure with respiratory distress syndrome were treated with intermittent negative pressure ventilation (INPV). There was a survival rate of 38% (17/45).All infants were initially treated without nasotracheal intubation. However, 24 of these developed a Paco(2) greater than 70 mm. Hg and were subsequently intubated. Intubation was followed by a decrease in the degree of hypercarbia in each instance and simultaneous increase in Pao(2).COMPLICATIONS ENCOUNTERED DURING VENTILATION WERE: emphysema (one patient), aspiration pneumonia (two patients), septicemia (two patients), misplaced nasotracheal tube (one patient).Follow-up of the 17 surviving patients for periods of four to 36 months disclosed two patients with post-intubation hoarseness. One infant initially had spastic quadriplegia with EEG abnormalities, both of which cleared by 5 months of age. In the remaining 14 infants, the results of physical, neurological and psychological examinations have remained within normal limits.
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PMID:Negative pressure artificial respiration: use in treatment of respiratory distress syndrome of the newborn. 526 98

Factors determining survival have been analysed retrospectively in 157 admissions of 135 patients with an acute exacerbation of chronic bronchitis and emphysema causing hypoxaemia and carbon dioxide retention. All were treated with controlled oxygen therapy. The death-rate increased with the age of the patient, but was not correlated with the age of the patient, but was not correlated with the severity of hypoxaemia on admission, when the patient was breathing air. The death-rate was significantly higher in those patients in whom arterial [H+] rose above 55 nmol/1 (pH = 7.26) during controlled oxygen therapy. The absence of a rise in the arterial PCO2 during controlled oxygen therapy was not necessarily indicative of a good prognosis, since 5 out of 18 patients showing this response subsequently died in that admission. Only 28% of the 111 patients who left hospital alive survived for five years.
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PMID:Respiratory failure revisited: acute exacerbations of chronic bronchitis between 1961-68 and 1970-76. 610 93

A controlled trial of long term domiciliary oxygen therapy has been carried out in three centres in the U.K. The 87 patients, all under 70 years of age, who took part had chronic bronchitis or emphysema with irreversible airways obstruction, severe arterial hypoxaemia, carbon dioxide retention, and a history of congestive heart failure. The patients were randomised to oxygen therapy (treated) or no oxygen (controls). Oxygen was given by nasal prongs for at least 15 h daily, usually at 2 1/min. The two groups were well matched, both clinically and in terms of lung function and other laboratory findings. 19 of the 42 oxygen treated patients died in the five years of survival follow-up compared with 30 out of 45 controls: in the 66 men in this trial the survival advantage of oxygen did not emerge until 500 days had elapsed. Survival for the 12 female controls was surprisingly poor, 8 of them being dead at 3 years. Mortality was not easy to predict, though a summation of arterial carbon dioxide tension and red cell mass was helpful. Neither time spent in hospital because of exacerbations of respiratory failure nor work attendance were affected by oxygen therapy, but these patients were very ill at the start of the trial and many had already retired on grounds of age or ill-health. Physiological measurements suggested that oxygen did not slow the progress of respiratory failure in those who died early. However, in longer term survivors on oxygen, arterial oxygenation did seem to stop deterioration.
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PMID:Long term domiciliary oxygen therapy in chronic hypoxic cor pulmonale complicating chronic bronchitis and emphysema. Report of the Medical Research Council Working Party. 611 Sep 12

From 1967 to 1972 12 patients were operated on for emphysematous bullae in the Liverpool regional cardiothoracic centre. The patient with the poorest lung function died in the immediate postoperative period but the remainder survived for more than five years. All but one of the survivors showed evidence of benefit three to six months after surgery and all those not retired returned to full-time employment for at least five years. Nine patients were reviewed 5-10 years after surgery. These all reported a gradual return of dyspnoea, which was matched by a falling one-second forced expiratory volume (FEV1) (mean fall 82 ml a year); but five were still maintaining some of their postoperative improvement. When mean preoperative lung function values were compared with the values obtained 5-10 years later there was still a significant improvement in forced vital capacity; but FEV1, residual volume, transfer coefficient, and arterial oxygen and carbon dioxide tensions were unchanged. Chest radiographs showed no new bullae or (except in one case) any increase in size of pre-existing bullae. We conclude that the removal of large emphysematous bullae did not hasten the progress of the underlying emphysema and that in most patients some benefit lasted for more than five years after the operation. Patients treated by lobectomy fared at least as well as those treated by bullectomy alone. It may be relevant to the relatively good progress of patients in this series that only three had suffered from chronic bronchitis before operation or smoked after operation, all but two had bullae occupying half or more of one hemithorax, and none had hypercapnia.
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PMID:Surgical treatment of emphysematous bullae: late outcome. 640 36

Changes in blood gas tensions occurring when 100% oxygen or air was used as the driving gas for nebulised salbutamol were studied in 23 patients with severe airways obstruction. The patients fell into three groups: nine had chronic bronchitis and emphysema with carbon dioxide retention, seven had emphysema and chronic bronchitis without carbon dioxide retention, and seven had severe asthma (no carbon dioxide retention). When oxygen was used as the driving gas patients who retained carbon dioxide showed a mean rise of 1.03 kPa (7.7 mm Hg) in their pressure of carbon dioxide (Pco2) after 15 minutes (p less than 0.001) but the Pco2 returned to baseline values within 20 minutes of stopping the nebuliser. The other two groups showed no rise in Pco2 with oxygen. When air was used as the driving gas none of the groups became significantly more hypoxic. Although it is safe to use oxygen as the driving gas for nebulisers in patients with obstructive airways disease with normal Pco2, caution should be exercised in those who already have carbon dioxide retention.
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PMID:Oxygen as a driving gas for nebulisers: safe or dangerous? 641 92

The development of right ventricular failure due to pulmonary hypertension is a common complication of severe chronic bronchitis and emphysema (Renzetti et al. 1976) but is rare in bronchial asthma (Clark 1977). We report a 20-year-old extrinsic asthmatic with persistent hypoxaemia and carbon dioxide retention, secondary polycythaemia and cor pulmonale and describe his further investigation.
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PMID:Cor pulmonale in asthma. 661 6

Emphysema is known to progress in severity during the year after its induction by pancreatic elastase. A barometric chamber and indwelling aortic cannulas were used to evaluate the effects of worsening emphysema on pulmonary ventilation and arterial blood gases. Unanesthetized, unrestrained hamsters were studied 1, 5, and 13 months after panlobular emphysema was induced by intratracheal injection of porcine pancreatic elastase (0.2 mg in 0.5 ml of 0.15 M NaCl solution/100 g body weight). Lung volumes were subsequently measured in the anesthetized animals and the lungs were examined histologically and stereologically. The pattern of breathing in the 1-month emphysematous hamsters (n = 12) wsa the same as that of untreated control animals (n = 28) but the 5-month (n = 7) and 13-month (n = 6) animals breathed more deeply and slowly; there were no changes in mean inspiratory flow rate of proportion of time per breath occupied by inspiration. The PaO2 for all elastase-treated groups was significantly lower than the control but hypoxemia did not progress significantly with advancing age of the animals. The hematocrit was elevated for the 1-month and 5-month treated animals but not for the 13-month emphysematous animals. The arterial pH and PaCO2 values were not significantly different from control values in any of the three groups of emphysematous animals. We conclude that as hamsters with emphysema age their breathing becomes slower and deeper, that hypoxemia is present from 1 month onwards and does not progress and that hypercapnia is not found at any time.
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PMID:Pulmonary ventilation and blood gas values in emphysematous hamsters. 680 49

A 31-year-old woman sustained multiple injuries, including severe contusion of the right lung with massive subcutaneous emphysema. Four weeks later she was transferred to our institution with post-traumatic adult respiratory distress syndrome and carbon dioxide retention, resulting from a postlaceration stenosis of the left main-stem bronchus. Bronchoplasty was contraindicated because of the serious condition of the patient. Repeated bronchial dilatations produced initial improvement in oxygenation and minute ventilation requirements. However, because of the nature of the stenosis and the lack of recovery of right lung function, the patient's encouraging clinical course reached a plateau and attempts at weaning from the respirator were unsuccessful. Bronchoplasty was performed on postadmission day 50 and resulted in gradual recovery of pulmonary function. Six months following discharge, the patient continues a steady improvement. Management of the patient's injuries represented a unique challenge previously unencountered.
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PMID:Post-traumatic bronchial stenosis and acute respiratory insufficiency. 737 4


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