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)

A decreased metabolic rate has been associated with decreased ventilatory response to hypoxia and hypercapnia, and also with starvation. We fed a 500-calorie carbohydrate diet with supplemental electrolytes, designed to simulate alimentation by usual intravenous fluids, to seven normal subjects for 10 days to determine the effect of semi-starvation on metabolic rate and ventilatory responses. By the 10th day metabolic rate was significantly decreased, and hypoxic ventilatory response decreased to 42% of control (P less than 0.05). In two subjects, hypoxic ventilatory response was virtually abolished at day 10. These changes reversed toward normal with refeeding. The decrease in hypoxic ventilatory response response was significantly (P less than 0.01) related to the decrease in metabolic rate. Hypercapnic ventilatory response, measured as the slope of the ventilatory response to hypercapnia, decreased slightly but not significantly. The decrease in hypoxic ventilatory response seen during semi-starvation may contribute to the hypoxemia and respiratory failure subsequent to caloric restriction.
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PMID:Clinical semi-starvation: depression of hypoxic ventilatory response. 81 29

1. The concentration of metabolites in intercostal and quadriceps muscle, and pulmonary function, were studied in twelve patients with chronic obstructive lung disease and acute respiratory failure before, during and after standardized treatment at an intensive care unit. The findings were compared with those obtained in hospitalized patients of comparable age with non-pulmonary diseases. 2. On admission, when the patients had marked hypoxaemia, hypercapnia and acidosis, the concentrations of ATP and creatine phosphate were low in both intercostal and quadriceps muscle, particularly the latter. The lactate concentration was increased in relation to control values but glycogen did not differ significantly. 3. In response to therapy, the Pa,CO2 and the patient's acidosis decreased, the vital capacity increased and lung mechanics improved along with the clinical condition. At the same time there were significant increases in the concentrations of ATP, creatine phosphate and glycogen in intercostal and quadriceps muscles, to values similar to, and for glycogen in excess of, those found in control subjects. Lactate concentration fell significantly during treatment. 4. In view of the low initial muscle concentrations of ATP and creatine phosphate in the patients, it is suggested that dysfunction of the respiratory muscles may be an important component of respiratory failure. Moreover, the concentration of energy-rich compounds in muscle rose significantly as the patients responded to treatment, which emphasizes the importance of adequate nutritional therapy in this disorder.
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PMID:Muscle metabolism in patients with chronic obstructive lung disease and acute respiratory failure. 86 35

Respiratory failure has been associated with depressed ventilatory responses to hypoxia or hypercapnia or both. The possibility that familial factors are responsible for decreased chemosensitivity prompted this study of a child with unexplained respiratory failure and normal lung function. We found his ventilatory response to hypoxia and hypercapnia to be virtually absent. Studies of six healthy immediate family members (parents and siblings) showed that hypoxic response, as measured by an index of the relation between ventilation and hypoxia (index A), was consistently reduced: 45 +/- 8.7 S.E.M. (normal, 127 +/- 8.7) (P less than 0.005). Response to hypercapnia, measured as the slope of the ventilatory response to hypercapnia, was lower than normal, averaging 0.95 +/- 0.16 liters per minute per millimeter of mercury (normal, 1.76 +/- 0.13) (P less than 0.01). The patient's respiratory failure seemed related to deficient ventilatory responses to hypoxia and hypercapnia. It seems likely that this depressed hypoxic response is of familial origin.
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PMID:Respiratory failure associated with familial depression of ventilatory response to hypoxia and hypercapnia. 95 89

Acid-base parameters were studied in 10 adult patients with chronic respiratory failure during spontaneous acute exacerbations of chronic hypercapnia and after return and stabilization of PaCO2 values at previous levels with improvement of clinical conditions. All factors interfering with acid-base equilibrium were carefully avoided. The results of this investigation confirm qualitatively those obtained by GOLDSTEIN et al. [7] in dog studies and those of INGRAM et al. [9]in human studies: increasing degrees of chronic hypercapnia tend to minimize the pH reduction induced by acute PACO2 changes. From a quantitative standpoint INGRAM's data in humans are considerably different from GOLDSTEIN's data obtained in dogs. Our data, although numerically limited, confirm the acute deltaH+/deltaPaCO2 slope obtained from dogs by GOLDSTEIN et al. As data are not yet sufficient, definitive conclusions cannot be drawn. However the pattern of acid-base equilibrium changes in man in this situation seems to be similar to that observed by GOLDSTEIN et al. in the dog and could be described with reasonable accuracy by the theoretical model of LEUENBERGER et al.[13].
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PMID:Acid-base changes in acute exacerbation of chronic hypercapnia in man. 101 67

The bone is often considered as a slow exchanger and bone sampling from the iliac crest, by needle-biopsy, is a commonly used and atraumatic technique; therefore the significance of the evolution of CO2 stores has been investigated in iliac crest in respiratory failure. Samples are taken before ventilation and on the first, second, and in some cases third days after ventilation. The results show that ageing is to be considered, since the CO2/Ca ratio varies according to the age group (0.84 at 30 years and 1.35 at 60 years). Patients with respiratory failure may be distributed into two main categories: hypoxic patients without hypercapnia, and patients with predominant hypercapnia. Hypercapnic patients may be differentiated from the hypoxic ones, both before assisted ventilation and on account of the dynamic phenomena that come into play during respiratory support in this group of patients. If the equilibrium state (at least five days with rigorously steady gazometry), before assisted ventilation, remains unknown, it is not possible to distribute the patients in one of these two groups. The results' significance is discussed, as well as the possible therapeutic applications.
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PMID:[Iliac crest bone CO2 and CO2/Ca ratio in man during respiratory failure (author's transl)]. 101 76

The efficacy of a respiratory stimulant (doxapram) in antagonizing carbon dioxide retention associated with controlled oxygen therapy (28 per cent) in acute-on-chronic respiratory failure was assessed by a double-blind crossover trial in eight patients. PaCO2 rose in egery case during the placebo in the initial treatment period (mean increase 10 mm Hg). In those patients receiving doxapram initially PaCO2 fell in three and rose in one (mean decrease 4 mm Hg). All who has shown a rise in PaCO2 during the initial period on placebo showed a fall in the subsequent period on doxapram. In the six patients who completed the study, mean PaCO2 at the end of the doxapram period was significantly lower than the end of the placebo period (60 mm Hg against 67 mm M Hg). In three patients the rise in PaCO2 was accompanied by significant impairment in the level of consciousness which was reversed during the doxapram period. PaCO2 was not significantly different during either treatment period. No serious unwanted effects were encountered.
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PMID:A controlled trail of doxapram in acute respiratory failure. 109 46

Adrenocortical function and plasma growth hormone pattern were investigated in 15 patients with chronic obstructive lung disease, in a period of acute respiratory failure and again after recovery. During the acute period, secretion rate and plasma concentrations of cortisol were markedly enhanced; urinary excretion of cortisol metabolites was only slightly increased, suggesting an alteration of the catabolism of cortisol under these conditions; adrenocortical sensitivity to corticotropin and capacity of maximal adrenal secretion were normal. The increase of cortisol secretion was probably due to hypoxemia and/or hypercapnia acting through the hypothalamo-pituitary axis. During the chronic phase of respiratory insufficiency, adrenocortical secretion and responsiveness were within the normal range. Finally, respiratory failure did not stimulate the secretion of growth hormone.
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PMID:Adrenocortical and somatotrophic secretions in acute and chronic respiratory insufficiency. 114 86

Because of the previous finding of an attenuated hypoxic ventilatory drive in a teenager with severe asthma, the ventilatory responses to hypoxia and hypercapnia were examined during remission in 16 patients with the history of severe asthma. Spirometric and body plethysmographic pulmonary functions were normal or nearly normal just prior to ventilatory drive testing. The ventilatory responses to progressive isocapnic hypoxia and to hyperoxic hypercapnia were studied. Both hypoxic and hypercapnic drives were significantly depressed in the asthmatic patients. Factors known to blunt the ventilatory drives were not present in this group of patients. Hence, the etiology of these changes is unclear. In some patients, these depressed respiratory drives might contribute to hypoventilation, to severe hypoxemia, and to respiratory failure during severe asthma.
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PMID:Depression of hypoxic and hypercapnic ventilatory drives in severe asthma. 117 5

The degree of disability of a patient with chronic respiratory failure must be determined on a theoretical basis. Using a water filled spirometer, VC and FEV1 tracings are observed several times until the maximal values are clearly reproduced. The percentage deficit of the patients' ventilatory capacity is determined by the formula (see article) and represents the first approximation of the degree of disability (in %). The result must now be corrected by arterial blood gas data obtained during 5 mon exhaustive work on a bicycle or tread-mill ergometer. The percentage disability results from a correction depending on the arterial pO2 and the pCO2 found during exercise: deterioration of the arterial hypoxemia and/or hypercapnia leads to an increase and their normalization to a decrease in the disability quota found during spirometry. Patients with unstable chronic obstructive lung disease and respiratory failure should be evaluated only after adequate rehabilitation at home and at work, and after cessation of smoking. Patients under tuberculostatic treatment must also be excluded from disability evaluation. The degree of disability determined on the basis of lung function tests is a theoretical one; the tests must be performed by trained staff in a pulmonary function laboratory.
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PMID:[Proceedings: Home treatment of chronic respiratory insufficiency: criteria of disability]. 121 92

Digoxin-like immunoreactive factor (DLIF) is an endogenous substance with natriuretic and diuretic activity. Elevated plasma levels of DLIF are found in various clinical states characterized by water and sodium retention. Chronic respiratory failure, particularly of an advanced stage, also is frequently associated with water and sodium retention. In order to determine whether elevated plasma levels of DLIF are present in chronic respiratory failure, we measured plasma DLIF levels in seven patients (four with COPD [two of whom had associated sleep apnea disturbance] and three with kyphoscoliosis) suffering from advanced chronic respiratory failure with severe hypoxemia and hypercapnia. We found that in these patients plasma levels of DLIF were significantly higher than in healthy control subjects. We conclude that patients with advanced chronic respiratory failure respond with increased levels of DLIF. This may represent an attempt at homeostasis of water and sodium metabolism which is frequently deranged in this clinical condition.
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PMID:Endogenous digoxin-like immunoreactive factor is elevated in advanced chronic respiratory failure. 130 96


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