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)

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

Occlusion pressure at 0.1 s (P0.1) and its evolution during progressive hyperoxic hypercapnia (CO2 chemosensitivity) were measured in 40 patients. Most of them (26) were affected by asthma and /or chronic bronchitis and had mild obstruction and hypoxemia. Measurements were made after 2 days of oral prazepam, diazepam or a placebo (single-blind study). Diazepam induced a significant decrease in P0.1 without affecting CO2 chemosensitivity. In contrast, prazepam did not significantly modify P0.1 or CO2 chemosensitivity. However, P0.1 decreased in 5/18 individual cases. 1 week of treatment by prazepam has advantages over diazepam by not depressing respiratory center output.
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PMID:Influence of anxiolytic drugs (Prazepam and Diazepam) on respiratory center output and CO2 chemosensitivity in patients with lung diseases. 680 3

Fourteen male patients with chronic bronchitis and hypoxia had a lateral radiograph of the pituitary fossa. Nine of the 14 had definite or probable abnormalities, a significantly higher frequency (p less than or equal to 0.01) than is represented by the two out of 14 age-matched men from a control group with head injuries. The most common change was thinning or erosion of the lamina dura. Patients with hypercapnia were no more prone to such abnormalities than were those with normocapnia, a finding that conflicts with a previous paper. We confirm that radiological pituitary fossa changes do occur in chronic bronchitis, that they are unrelated to steroid treatment, and that they are probably not solely due to the chronically raised intracranial pressure associated with hypercapnia. Other possible mechanisms are discussed--in particular hypoxia, which might produce changes on account of the increased cerebral blood flow and engorged intracranial blood vessels.
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PMID:Radiological pituitary fossa changes in chronic bronchitis. 713 92

To investigate the role of endorphins in central respiratory control, the effect of naloxone, a specific opiate antagonist, on resting ventilation and ventilatory control was investigated in a randomised double-blind, placebo-controlled study of normal subjects and patients with chronic airways obstruction and mild hypercapnia due to longstanding chronic bronchitis. In 13 normal subjects the ventilatory response to hypercapnia increased after an intravenous injection of naloxone (0.1 mg/kg), ventilation (VE) at a PCO2 of 8.5 kPa increasing from 55.6 +/- SEM 6.2 to 75.9 +/- 8.21 min-1 (p less than 0.001) and the delta VE/delta PCO2 slope increasing from 28.6 +/- 4.4 to 34.2 +/- 4.21 min-1 kPa-1 (p less than 0.05). There was no significant change after placebo (saline) injection. Naloxone had no effect on resting ventilation or on the ventilatory response to hypoxia in normal subjects. In all six patients naloxone significantly (p less than 0.02) increased mouth occlusion pressure (P 0.1) responses to hypercapnia. Although there was no change in resting respiratory frequency or tidal volume patients showed a significant (p less than 0.01) decrease in inspiratory timing (Ti/Ttot) and increase in mean inspiratory flow (VT/Ti) after naloxone. These results indicate that endorphins have a modulatory role in the central respiratory response to hypercapnia in both normal subjects and patients with airways obstruction. In addition, they have an inhibitory effect on the control of tidal breathing in patients with chronic bronchitis.
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PMID:Endogenous opiates and the control of breathing in normal subjects and patients with chronic airflow obstruction. 716 1

With a sensitive enzyme-linked immunoadsorbent assay that can detect as little as 0.5ng/ml of myelin basic protein (MBP), we studied serum specimens from 34 patients with chronic cor pulmonale (CP) and 33 patients with chronic bronchitis (CB) during acute attack in hospital and 30 control subjects. The results showed that the serum mean MBP level of CP patients was markedly higher than those of CB patients and controls (P < 0.01), but no statistically significant differences were found between CB patients and controls (P > 0.05). There was a positive correlation between elevated levels of serum MBP and carbon dioxide partial pressure (PaCO2). This suggested that elevated serum MBP levels may be associated with brain destruction by hypercapnia and hypoxia of CP patients.
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PMID:[Myelin basic protein level in serum of patients with chronic cor pulmonale in acute phase]. 749 17

In obese subjects with chronic bronchitis hypercapnia by limitation of tidal volume regresses if a slow ventilatory frequency is imposed by lengthening of expiration time. But hypoxemia due to shunt effect can either be corrected by global improvement of alveolar ventilation VA or persist and become worse by low pulmonary volume ventilation which lowers VA/Q. The effect of bradypnoea on 11 elderly patients with moderate obesity has been evaluated by simultaneous measurements of blood gases, ventilatory output coefficients, gas flow rate and steady state transfer for CO. Although hypo-VA disappeared in bradypnoea, hypoxemia persisted in 5 cases, the increase of P(Aa)O2 was accentuated in 7 cases, VCO always remained in deficit compared with VCO2 (in healthy subjects at rest, VCO and VCO2 are interrelated by a proportionally constant whatever the respiratory regimen: VCO/VCO2 = specific VCO, or VCO Sp). The VCO/VA variation correlated negatively with the P(Aa)O2 variation. This study: 1) confirms the link between PaCO2 and VT and the persistence of shunt effect bradypnoea compatible with the deficit of VCO versus VCO2; 2) distinguishes the efficiency of bradypnoea in ventilation and in alveolo-capillary exchange; 3) compares the variations of VCO Sp with those of PaO2 in relation to VT; 4) defines the characteristics of respiratory insufficiency in the obese and bronchitic subjects examined, and 5) specifies the value of VCO Sp measurement in testing the controlled ventilation technique used.
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PMID:[Gas exchange during spontaneous and controlled ventilation in obese subjects with chronic bronchitis. Value of normalized CO intake]. 804 79

We describe the clinical, radiologic, functional, and pulmonary hemodynamic characteristics of a group of 30 nonsmoking patients with a lung disease that may be related to intense, long-standing indoor wood-smoke exposure. The endoscopic and some of the pathologic findings are also presented. Intense and prolonged wood-smoke inhalation may produce a chronic pulmonary disease that is similar in many aspects to other forms of inorganic dust-exposure interstitial lung disease. It affects mostly country women in their 60s, and severe dyspnea and cough are the outstanding complaints. The chest roentgenograms show a diffuse, bilateral, reticulonodular pattern, combined with normalized or hyperinflated lungs, as well as indirect signs of pulmonary arterial hypertension (PAH). On the pulmonary function test the patients show a mixed restrictive-obstructive pattern with severe hypoxemia and variable degrees of hypercapnia. Endoscopic findings are those of acute and chronic bronchitis and intense anthracotic staining of the airways appears to be quite characteristic. Fibrous and inflammatory focal thickening of the alveolar septa as well as diffuse parenchymal anthracotic deposits are the most prominent pathologic findings, although inflammatory changes of the bronchial epithelium are also present. The patients had severe PAH in which, as in other chronic lung diseases, chronic alveolar hypoxia may play the main pathogenetic role. However, PAH in wood-smoke inhalation-associated lung disease (WSIALD) appears to be more severe than in other forms of interstitial lung disease and tobacco-related COPD. The patients we studied are a selected group and they may represent one end of the spectrum of the WSIALD.
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PMID:Pulmonary arterial hypertension and cor pulmonale associated with chronic domestic woodsmoke inhalation. 841 64

5 cases with obesity-hypoventilaion syndrome were reported. The clinical manifestations were obesity, palpitation, dyspnea, lethargy, cyanosis, distention of cervical vein, edema, enlargement of liver and hypertension. All of them were initially diagnosed as chronic bronchitis or heart diseases. Pulmonary function test showed restrictive ventilative defect and hypercapnia with hypoxemia. Mouth oclusion pressure at 0.1 second was higher than the normal value. The response to CO2 was decreased. Hypertrophy of right heart was shown in ECG and X-ray film improvement in symptoms and blood gases analyses were found to be associated with body weight decrease in a follow up period of one year.
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PMID:[Obesity-hypoventilation syndrome]. 927 46

Acute exacerbations of chronic bronchitis (AECB) can be classified into three levels according to severity: (1) home treatment sufficient; (2) hospitalisation required; (3) hospitalisation in the presence of respiratory failure. This evidence-based classification is useful in ranking the clinical relevance of the episode and its outcome, and makes it possible to define the clinical history, clinical evaluation and diagnostic procedures of an exacerbation. Treatment guidelines vary according to severity, but they are essentially based on appropriate bronchodilator therapy (beta(2) agonists and/or anticholinergics, corticosteroids and antibiotics selected according to the local bacterial resistance pattern). It is important that cases requiring management in an intermediate/special respiratory care unit or intensive care unit (ICU) be identified. This is the stage where oxygen therapy and ventilatory support become particularly important. As first choice, they should be non-invasive, saving intubation and invasive ventilatory support for most severe cases characterised by severe acidemia and hypercapnia. We identify the optimal criteria for hospital discharge and follow-up of patients with AECB. In view of the chronic nature of the underlying disease, a correct follow-up is essential to avoid frequent and repeated relapses.
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PMID:Acute exacerbation of chronic bronchitis: need for an evidence-based approach. 1634 61


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