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)

Ventilatory responses to carbon dioxide (Sco2) were measured in 15 asymptomatic asthmatic patients in whom CO2 retention had been documented during a previous attack of acute asthma. At the time when Sco2 was measured, the patients had normal or only mildly impaired ventilatory function (vital capacity (VC) 3,5 +/- 0,19 I, 98,7 +/- 4% of predicted (mean +/- SE); forced expiratory volume in 1 second (FEV1) 2,37 +/- 0,161, 83,8 +/- 5,2% of predicted; and FEV1/VC 68 +/- 2,5%). Fifteen control subjects without lung disease were also studied (VC 4,38 +/- 0,28 I, 103 +/- 2,6% of predicted; FEV1 3,76 +/- 0,23 I, 112 +/- 4,4% of predicted; FEV1/VC 86 +/- 7,8%). Sco2 in the patients (1,21 +/- 0,14 l/min/mmHg, range 0,62 - 2,81) was significantly different (P less than 0,001) from that in controls (2,13 +/- 0,17 l/min/mmHg, range 1,13 - 3,17). Sco2 in a subgroup of 5 patients with normal pulmonary function was also significantly different from that in controls. Correction for lung size (Sco2/VC) did not detract from the significance of the difference between patients and controls, suggesting that inherently low respiratory centre sensitivities to CO2 may have played a role in the development of hypercapnia during severe asthma in these patients.
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PMID:Ventilatory responses to carbon dioxide in asthmatics with previous carbon dioxide retention during severe asthma. 640 23

Forty children with severe asthma were admitted to an intensive care unit from 1970 to 1981. Criteria of severity were alteration of consciousness, circulatory failure, hypercarbia greater than 7 KPa and paradoxical pulse greater than 35 mmHg persisting in spite of correct treatment. Some therapeutic measures (oxygen, corticosteroids, antibiotics, hydratation) were not modified during this period. On the contrary, bronchodilators, used at a higher dose since June 1980, were very effective on bronchospasm without side effects, making controlled ventilation unnecessary. These results seem to be very encouraging but have to be confirmed.
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PMID:[Therapy of severe asthma crisis in children. Therapeutic course. A propos of 40 cases]. 641 34

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

Two female patients revived from fulminant attacks of asthma are described. Ventilatory responses to asphyxia in these patients were 0.70 +/- 0.10 l min-1 % SaO2-1 and 0.64 +/- 0.21 l min-1 % SaO2-1 (mean +/- SEM), respectively. These values were significantly less than the responses of seven normal female subjects (1.54 +/- 0.11 l min-1 % SaO2-1 mean +/- SEM; p less than 0.01). Ventilatory responses to hypercapnia of the two patients were in the low normal range. Dopamine-receptor blockade with prochlorperazine significantly increased the ventilatory response to asphyxia in normal subjects (p less than 0.05 or less for each subject) but did not alter the depressed responses in the asthmatic patients. In one patient, naloxone in a dose of 400 micrograms reversed the decreased ventilatory responsiveness; the response to asphyxia was increased from 0.72 l min-1 % SaO-1 to 1.80 l min-1 % SaO2-1 (p less than 0.01) and the response to hypercapnia was increased from 0.90 l min-1 mmHg-1 to 4.80 l min-1 mmHg-1 (p less than 0.01). Naloxone had no effect in the second asthmatic patient nor in five normal subjects. Defective chemoreceptor responses to chemical stimuli may play a role in sudden death from asthma; endogenous opioids may mediate this disorder of ventilatory control.
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PMID:Ventilatory control in two asthmatics resuscitated from respiratory arrest. 659 13

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

We measured the ventilation and inspiratory muscle activity responses to hypoxia and hypercapnia in 18 children with asthma. Ventilation was less efficient in the asthmatic children in that more inspiratory muscle activity per liter of ventilation was required than in normal children. Asthmatic and healthy children had similar ventilation responses to hypercapnia; at all levels of end-tidal Pco2, the inspiratory muscle activity was greater in those with asthma. However, during progressive isocapnic hypoxia, asthmatic patients did not increase their inspiratory muscle activity at a rate greater than normal. Thus, because of inefficient ventilation, they had significantly decreased ventilatory responses to hypoxia. Neither ventilation nor inspiratory muscle activity response to hypoxia was correlated with duration of illness or with the degree of airways obstruction present. These results demonstrate that children with chronic asthma have decreased hypoxic responsiveness and suggest that neither long-term airways obstruction nor intermittent hypoxia associated with asthma is necessary to diminish hypoxic response in asthmatic patients. An asthmatic child with depressed hypoxic responsiveness may be at increased risk of hypoxic complications or respiratory failure during acute asthma.
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PMID:Decreased ventilation response to hypoxia in children with asthma. 677 53

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

Arterial blood gas (ABG) measurements are used frequently in acute asthma. Because ABGs are expensive and may have significant side effects, a method is needed to identify those patients at risk for a significantly abnormal ABG. We studied the use of peak expiratory flow rates (PEFR) to identify those patients at such risk. Data from 89 emergency visits by 51 asthmatic patients were analyzed. A small but significant correlation between ABG parameters and PEFR was observed (P less than 0.05). No patient with a PEFR greater than or equal to 25% predicted has a PaCO2 greater than 45 mm Hg or pH less than 7.35. This suggests that only those patients with a PEFR less than 25% predicted are at risk for significant hypercarbia or acidosis. We concluded that PEFR may be used as a simple screening tool to safely eliminate ABGs in at least 40% of acute asthmatic patients.
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PMID:Use of peak expiratory flow rates to eliminate unnecessary arterial blood gases in acute asthma. 681 15

The drive and performance of breathing during hypercapnia, isocapnic hypoxia, and transient hyperoxia were studied in 20 normal children (mean age 12.3 years), in ten children with asthma, and in ten children with cystic fibrosis (CF) matched by sex and age. These latter two groups of patients had had obstructive respiratory symptoms since infancy and their pulmonary disease was of moderate severity as documented by their pulmonary function studies. During hypercapnia, normal children had a linear increase in minute ventilation (delta VE), in tidal volume (delta VT) and in the inspiratory drive (VT/Ti). The drive of breathing was evaluated by the occlusion pressure (P0.1) at functional residual capacity. The P0.1 response to PaCO2 was linear. Patients with asthma and CF showed a blunted ventilatory response (delta VE, delta VT, VT/Ti) to Co2 but a normal response in P0.1. In normal subjects, the test of isocarbic hypoxia demonstrated an exponential type of increase in delta VE, delta VT, and P0.1 as PAO2 decreased from 110 to 40 torr. With severe hypoxia (PAO2 less than 50 torr), children with CF (but not asthmatic patients) experienced a paradoxical decrease in delta VE while the drive (P0.1) remained above normal in both groups of patients. Finally, the transient O2 inhalation test caused a decrease in VE of 26%, 21%, an 34%, respectively, in normal subjects, in asthmatic children, and in children with CF. It is concluded that the CO2 and O2 drive of normal children resembles that described for adults and that the CO2 and O2 command of breathing is normal in children with asthma and CF. However, the ventilatory response in children with chronic obstructive pulmonary disease is subnormal probably due to the impairment of the respiratory mechanics. Finally the respiratory depression induced by severe hypoxia in children with CF is unexplained, but it may reflect the high dependency of their respiratory muscle on oxygen supply.
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PMID:Neural drive and ventilatory strategy of breathing in normal children, and in patients with cystic fibrosis and asthma. 726 24

Three children and two young adults with severe asthma who had frequent episodes of respiratory failure were studied. Isocapnic hypoxia and hyperoxic hypercapnia were produced separately using a rebreathing apparatus. Alveolar carbon dioxide tension and oxygen tension were estimated by continuously sampling expired gases. The three young children had a diminished response to hypoxia but a normal response to hypercapnia when compared to control asthmatic children (p less than 0.05) or healthy children (p less than 0.05). The two young adult patients had a normal response to hypoxia but one had a low response to hypercapnia. Studies of parents of these patients suggested that the chance combination of a possibly familial, inappropriate response to hypoxia with severe asthma would lead to a risk of respiratory failure.
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PMID:Hypoxic and hypercapnic response in asthmatic subjects with previous respiratory failure. 733 Jul 94


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