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 decision to institute MV in patients with COPD and ARF is difficult because the risk of complications is high and the long-term prognosis is poor. We reviewed our experience with 95 COPD patients with ARF requiring MV. Fifty-five patients required MV for more than two weeks, 72 were weaned successfully, and 59 died within one year of follow-up. Survival was associated with premorbid level of activity (p less than .001), FEV1 (p less than .01), serum albumin level (p less than .05), and severity of dyspnea (p less than .01). Cor pulmonale on ECG, premorbid hypercarbia, and history of left ventricular failure were also more common among those who died. Weaning from MV was associated with premorbid level of activity (p less than .001), FEV1 (p less than .001), albumin level (p less than .05), and negative inspiratory pressure (p less than .001) and respiratory rate during T-piece trial (p less than .01). The duration of intubation was associated only with premorbid level of activity (p less than .01). Predictive models for the weaning success and the one-year survival were developed.
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PMID:Determinants of weaning and survival among patients with COPD who require mechanical ventilation for acute respiratory failure. 291 93

Exercise programs are a mainstay of pulmonary rehabilitation for COPD. COPD patients with elevated PCO2 are severely impaired and might benefit from rehabilitation more than other patients. However, there is no systematic data to indicate that hypercapnic COPD patients benefit from intensive rehabilitation. Indeed, in patients with hypercapnia, increased exercise might overtax respiratory muscles, which are weak relative to those of eucapnic patients. To investigate this issue, we reviewed all COPD patients admitted to our pulmonary inpatient program from 1983 to 1986 (n = 317). The program includes multiple daily sessions of upper and lower extremity exercise to tolerance. We assessed admission and discharge pulmonary function tests, arterial blood gases (room air), and functional status. Ambulation distance on a 6-min walk test was used as an objective measure of functional status. Patients were grouped according to the results of their admission room air PCO2. We found that eucapnic patients (n = 197) significantly increased ambulation (admission to discharge) from 409 to 816 feet (p less than 0.001). Hypercapnic patients improved as well. Patients with moderate hypercapnia (PCO2, 45 to 54 mm Hg; n = 86) increased their ambulation from 330 to 663 feet (p less than 0.0001). Patients with severe hypercapnia (PCO2 greater than 54 mm Hg; n = 34) increased their ambulation from 336 to 597 feet (p less than 0.0001). We found a small but significant improvement in discharge pulmonary function and arterial blood gas results. We conclude that COPD patients with hypercapnia, despite severe ventilatory impairment and weak respiratory muscles, tolerate exercise well and benefit significantly from intensive inpatient pulmonary rehabilitation.
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PMID:Pulmonary rehabilitation in COPD patients with elevated PCO2. 314 19

Quadriceps femoris muscle needle biopsies were performed in ten patients with chronic obstructive pulmonary disease and acute respiratory failure and in ten age- and sex-matched healthy control subjects. The main indices of skeletal muscle cell energy metabolism, intracellular acid-base equilibrium and lactate metabolism were evaluated. Reduced ATP and phosphocreatine content, intracellular acidosis related to hypercapnia, increased muscle lactate without alterations of the muscle lactate concentration gradient were observed in the skeletal muscle of the hypercapnic-hypoxemic COPD patients studied, in which group no correlation was found between hypoxia and energy or lactate metabolism parameters. These results suggest that an overall derangement of cell energy metabolism and acid-base equilibrium is present in severely hypercapnic-hypoxemic chronic obstructive pulmonary disease and that in this condition skeletal muscle seems to metabolize anaerobically-even though, in addition to hypoxia, other factors interfering with both cell energy and lactate metabolism are likely to be present.
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PMID:Skeletal muscle energetics, acid-base equilibrium and lactate metabolism in patients with severe hypercapnia and hypoxemia. 366 4

Almitrine bismesylate (A) is a peripheral chemoreceptor agonist that increases ventilation, improves V/Q matching, increases PaO2 and decreases PaCO2 in patients with COPD. We have used a placebo-controlled double-blind cross-over study to compare the effect of 1.5 mg.kg-1 A and placebo (P) (given orally twice a day for 14 days with a 2 wk wash-out period between) on sleep quality, blood oxygenation during sleep and the ventilatory response to hypoxia and hypercapnia when awake. We have measured ear oxygen saturation (SaO2) and EEG sleep stages during nocturnal sleep in 13 patients with COPD (FEV1 0.94 +/- 0.31 1). When awake and during P period PaO2 was 51.4 +/- 10.7 mmHg (SD), PaCO2 53.1 +/- 7.1 mmHg and SaO2: 83.1 +/- 8.0%: during A treatment PaO2 increased to 55.8 +/- 7.8 mmHg (p less than 0.01 paired Wilcoxon test), PaCO2 decreased to 48.5 +/- 6.4 mmHg (p less than 0.05) and SaO2 increased to 86.9 +/- 2.6 (p less than 0.01). A reduced nocturnal hypoxaemia: 1) during P treatment mean stage I SaO2 was 73.2 +/- 13.2%, stage II 70.5 +/- 15.7%, stage III 66.5 +/- 18.5%, stage IV 73.3 +/- 12.7% and rapid eye movement (REM) sleep 59.2 +/- 14.8%; the corresponding SaO2 values during A treatment were higher: stage I SaO2 80.6 +/- 5.2% (p less than 0.05), II 78.6 +/- 6.2% (p less than 0.01), III 77.3 +/- 7.4% (p less than 0.01), IV 80.4 +/- 3.8% (p less than 0.05), REM 69.9 +/- 7.9% (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Almitrine effect on nocturnal hypoxaemia in patients with chronic obstructive pulmonary disease (COPD). 369 30

When oxygen therapy is warranted, the minimum effective dose generally should be given. Hypoxemic patients who have normal baseline ABG may be treated initially with an intermediate to high FiO2 in the range of 35% to 100%, depending on the severity of the respiratory distress. The majority of patients with exacerbations of COPD who are not in extremis may be given an initial FiO2 of 28%, especially if their previous response to oxygen is known. When treating patients who have chronic severe hypercapnia (eg, those requiring chronic home oxygen), the initial FiO2 should be 24% even though renal compensation of the respiratory acidosis has occurred. Further mild elevation of the PaCO2, due mainly to the V/Q mismatch that oxygen therapy induces, may be sufficient to precipitate unacceptable hypercapnia. Patients with exacerbations of COPD who are obviously in extremis, with severe hypoxemia and acidosis, should start with an FiO2 of 24% unless they are being mechanically ventilated. The severity of the hypoxemia and acidosis is more predictive for the development of CO2 narcosis and respiratory failure than is the degree of hypercapnia in these patients. The FiO2 can be increased to 28% and incrementally higher if low FiO2 is tolerated. The use of a high FiO2 is subject to the following guidelines for prevention of clinically significant oxygen toxicity: 100% oxygen at atmospheric pressure is safe if given for less than six hours; 70% oxygen is probably safe for 24 hours; and after this time, 45% should be the approximate upper limit to the FiO2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oxygen therapy and oxygen toxicity. 641 43

In order to assess the role of hypoxemia in the sleep disruption of patients with COPD, we studied patients breathing air and oxygen during sleep. In 24 patients with COPD, we determined the 95% confidence bands for arterial O2 saturation (SaO2) in the various sleep stages. The lowest mean SaO2 was during REM sleep. Patients spent 22.4% of the night desaturated (SaO2 more than 5% below awake SaO2). Apneic episodes were uncommon and occurred in only 2 patients. When compared with established age-matched normal subjects from another center, poor sleep quality was indicated by reduced sleep time, increased sleep stage changes, and increased arousal frequency. Oxygen therapy had no apparent effect on sleep quality. Arousal frequency was independent of measurements of awake pulmonary function or chemical control of breathing. During room air breathing, arousals were strongly associated with periods of arterial oxygen desaturation. However, relief of the hypoxemia with supplemental oxygen had no effect on arousal frequency. This suggests that it is not hypoxemia per se, but an associated phenomenon such as hypercapnia that causes the arousals.
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PMID:Sleep, arousals, and oxygen desaturation in chronic obstructive pulmonary disease. The effect of oxygen therapy. 712 32

In 41 patients with hypoxemic COPD, nocturnal changes in arterial O2 saturation were compared with measurements of hypoxic and hypercapnic ventilatory control, which were carried out during wakefulness. In 24 patients, sleep was judged visually, whereas in 17, sleep was staged by electroencephalogram (EEG). There were no differences between the 2 groups in terms of lung function, blood gases, or sleep desaturation. All patients desaturated during sleep, with maximal desaturation occurring during rapid eye movement (REM) sleep. The maximal nocturnal change in O2 saturation observed in each patient was negatively correlated with the patient's ventilatory sensitivity to hypercapnia; this relationship was independent of sleep stage. Both maximal and mean nocturnal changes in O2 saturation were negatively correlated with O2 saturation during wakefulness. Hypoxic ventilatory response was not related to nocturnal desaturation. Patients who are sensitive to hypercapnia are unlikely to show major sleep desaturation, whereas those who are insensitive to CO2 may do so, particularly if they have low O2 saturations while awake.
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PMID:Chemical control of ventilation and sleep arterial oxygen desaturation in patients with COPD. 743 24

Respiratory failure is a severe impairment of pulmonary gas exchange, consequence of lung failure leading to hypoxaemia and/or pump failure causing hypercapnia. Acute respiratory failure (acute lung injury and asthma) or acute on chronic respiratory failure (COPD and chest wall disorders) are the two terms proposed to characterize different onset and development. Mechanical ventilation, is often a necessary life-saving treatment in many critically ill patients, it is associated with complications such as infection or barotrauma. Other innovative techniques are mask ventilation and proportional assist ventilation (PAV). The major aim of mask ventilation is to prevent complications related to tracheal intubation, particularly respiratory tract infections and barotrauma.
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PMID:Acute respiratory failure. 771 99

Prognostic factors in COPD patients receiving long-term oxygen (LTO) therapy were recently analyzed, but very few studies considered the prognostic value of pulmonary artery pressure (PAP) in these patients. We investigated 84 patients who had undergone a right heart catheterization just before the onset of LTO. There were 75 men and 9 women, with a mean age of 63.0 +/- 9.9 (SD) years, at the onset of LTO. When PaO2 was persistently less than 55 mm Hg, LTO was initiated. This therapy was started in some patients with PaO2 in the range of 55 to 60 mm Hg if they had signs of cor pulmonale or a resting PAP of 25 mm Hg or greater at right heart catheterization. The daily duration of LTO was 16 h/d or more. Oxygen flow was adapted to achieve a PaO2 of 65 mm Hg or more. The patients were subdivided into subgroups according to the median value of age (cutoff value = 63 years); vital capacity (2,250 mL); FEV1 (800 mL); residual volume-total lung capacity ratio (58%); PaO2 value (52 mm Hg), PaCO2 level (45 mm Hg); and PAP (25 mm Hg). The cumulative 5-year survival rate was 48% for the group as a whole. Actuarial survival curves were plotted for the two subgroups of patients subdivided according to the initial median value of the variables just listed. There was no significant difference in survival rate between subgroups except when taking into account the level of PAP and age. In patients with an initial PAP of 25 mm Hg or less (n = 44), the 5-year survival was of 62.2 vs 36.3% in the remainder (n = 40) [p < 0.001]. We performed a multivariate analysis of survival using Cox's model of the proportional hazards regression including sex and the variables with the same categorization in the stepwise procedure: PAP and age were the only variables included in the final model. We conclude that the best prognostic factor in COPD patients receiving LTO is not the FEV1, nor the degree of hypoxemia or hypercapnia, but the level of PAP.
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PMID:Prognostic factors in COPD patients receiving long-term oxygen therapy. Importance of pulmonary artery pressure. 775 Mar 5

Disturbances in hormonal systems involved in sodium and water homeostasis are common during respiratory insufficiency. To investigate the role of hypercapnia, we designed a study to examine the hormonal response to acute hypercapnia induced at constant cardiac filling pressures and without hypoxemia. Seven sedated patients with COPD receiving mechanical ventilation were studied during five successive periods. Hemodynamics, arterial blood gases, and plasma hormone levels (atrial natriuretic peptide, renin, angiotensin II, aldosterone, vasopressin) were measured three times during 60 min of acute hypercapnia (52 +/- 5 mm Hg) and at control periods, before (36 +/- 4 mm Hg) and after (42 +/- 3 mm Hg) acute hypercapnia. During acute hypercapnia, mean pulmonary arterial pressure and cardiac output were increased without variation of other measured cardiorespiratory data and hormonal levels when compared with control values. After acute hypercapnia, cardiorespiratory variables returned to control values without variations of hormonal levels. Our results show that moderate acute hypercapnia does not significantly influence the hormonal levels when cardiac filling pressures and sympathetic tone remain stable. We suggest that changes in those plasma hormones involved in salt and water homeostasis during acute hypercapnia are secondary to hemodynamic changes induced by acute respiratory failure and not to acute hypercapnia per se.
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PMID:Effect of acute hypercapnia on alpha atrial natriuretic peptide, renin, angiotensin II, aldosterone, and vasopressin plasma levels in patients with COPD. 787 53


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