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

Fourteen patients with acute exacerbations of chronic bronchitis and hypercapnia received two treatment periods with Intermittent Positive Pressure Breathing, the ventilator being driven by gas containing about 24% or about 45% oxygen. Arterial PO2 and PCO2 were measured before, during and after each treatment. The results demonstrated that increasing hypercapnia did not, as a rule, occur when 45% oxygen was used as the driving gas. When hypercapnia did occur it appeared to be independent of the inspired oxygen concentration. The importance of short treatment periods, correct ventilator settings and supervision of the patient during and after treatment is emphasised.
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PMID:IPPB and hypercapnia in respiratory failure: the effect of different concentrations of inspired oxygen on arterial blood gas tensions. 37 21

A homogeneous sample of 14 patients with advanced chronic bronchitis and emphysema complicated by secondary polycythaemia and pulmonary hypertension was examined. Eight patients who were receiving long-term oxygen therapy (LTO2) for 15-20 h in the 24 h day showed a significantly faster, that is more normal, frequency of the dominant EEG activity and a higher level of arterial oxygenation when breathing air than six similar patients not receiving LTO2. Acute administration of oxygen (2 1/min) for 15 min did not change the EEG pattern in either group of patients. The frequency of the dominant EEG activity in all 14 patients showed a significant positive correlation with the arterial oxygen saturation and negative correlation with the level of polycythaemia. Occurrence of intermixed EEG show activity theta and delta was positively correlated both with hypoxaemia and hypercapnia. The results suggest that the LTO2 in patients with chronic ventilatory failure has a beneficial effect on cerebral function as measured by EEG.
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PMID:The effects of long-term oxygen therapy on the EEG in patients with chronic stable ventilatory failure. 49 89

Hemodynamic values obtained during right heart catheterization in about 35 patients with chronic bronchitis were compared with the same variables 3.3 years later (range, 2 to 5 years). In the group of 13 patients with mean pulmonary arterial pressure less than 20 mm Hg at the first catheterization, the average value was 15.8 mm Hg at rest and 25.2 mm Hg during moderate exercise at the first investigation, and 16.9 and 26.3 mm Hg, respectively at the second catherization; the changes were not significant. In the group of pulmonary hypertensive patients, the mean pulmonary arterial pressure was 27.0 mm Hg at rest and 44.1 mm Hg during moderate exercise at the first catheterization, and 26.8 and 38.9 mm Hg, respectively, at the second catheterization. Thus, even in this group, there was no deterioration in pulmonary hemodynamics, because there was no significant change in right or left filling pressure, or in cardiac output. There was, however, a marked decrease in systemic arterial pressure, which was significant in the group with pulmonary hypertension. This decrease in left ventricular afterload could be partly responsible for the stabilization of pulmonary hemodynamics, and it could be due to the peripheral vasodilating effect of hypoxia and hypercapnia.
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PMID:Pulmonary and systemic hemodynamic evolution in chronic bronchitis. 61 21

In a group of patients with chronic bronchitis, repeated night sedation with 10 mg nitrazepam produced a fall in central respiratory drive and a steady rise in arterial carbon dioxide tension. The changes produced over a five-day period were not clinically important, except in two patients who were already hypercapnic before receiving nitrazepam. The use of this drug in patients with carbon dioxide retention should be avoided.
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PMID:Depression of central respiratory drive by nitrazepam. 64 47

Respiratory drive (deltaP 0.1/deltaPCO2) and ventilatory response (deltaVE/deltaPCO2) to CO2 has been estimated in 20 normal subjects and 28 patients with chronic obstructive pulmonary disease (COPD). In patients with COPD, drive and ventilatory response to CO2 were diminished, but no statistical correlation with FEV1, MBC, TLC, FRC, RV/TLC was found. A statistically negative correlation was found between blood bicarbonate and drive or ventilatory response to CO2. Patients with emphysema and normal PaCO2 demonstrated normal deltaP 0.1/deltaPCO2. In contrast, patients with chronic bronchitis with the same pulmonary function abnormalities and hypercapnia had significant diminution of the deltaP 0.1/deltaPCO2. Therefore, we feel that pulmonary function abnormalities alone cannot explain the deltaP 0.1/deltaPCO2 decrease; in most cases there sould coexist a diminished respiratory sensitivity.
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PMID:Respiratory drive in patients with chronic obstructive pulmonary disease. 67 65

A consecutive series of ten patients with chronic bronchitis and hypercapnia were studied. All seven patients with chronic hypercapnia and one patient with intermittent hypercapnia showed evidence on skull radiographs of raised intracranial pressure. In five male and three female chronic bronchitics matched for age and ventilatory impairment, but without hypercapnia, no such radiological abnormalities were shown. The clinical significance and pathophysiology of this hitherto unreported finding is discussed. It would appear that in some cases the chronicity of hypercapnia may be diagnosed from a radiograph of the pituitary fossa.
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PMID:Chronic hypercapnia and radiological changes in the pituitary fossa. 74 95

The Medical Research Council and the Nocturnal Oxygen Therapy Trial studies clearly demonstrated that long-term oxygen therapy (LTOT) for more than 15 h/day improved mortality and morbidity in a well-defined group of patients with chronic obstructive pulmonary disease. There are no similar randomised control studies in patients with other hypoxaemic lung diseases such as pulmonary fibrosis and pneumoconiosis. The prescription of oxygen for other restrictive lung disorders is complicated by hypoventilation requiring mechanical support as well as oxygen and should be restricted to special centres. The clearest indications for LTOT are for patients with cor pulmonale, hypoxic chronic bronchitis and emphysema, and in terminally ill patients who require palliation. Before LTOT is considered, the patient must be clinically stable and on appropriate optimum therapy such as antibiotics, bronchodilators, physiotherapy and having stopped smoking tobacco. Many patients first present for LTOT with profound hypoxaemia and hypercapnia during an infective, often oedematous exacerbation of their lung disease. Assessments should occur during convalescence when the patient is clinically stable. They should be shown to have a PaO2 less than 7.3 kPa and/or a PaCO2 greater than 6 kPa on two occasions at least 3 weeks apart. FEV1 should be less than 1.5 litres, and there should be a less than 15% improvement in FEV1 after bronchodilators. All patients should be assessed by an experienced chest physician. Patients with a PaO2 between 7.3 and 8 kPa who have polycythaemia, right heart failure or pulmonary hypertension may gain benefit from LTOT but this is still to be clearly proven.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Indications for long-term oxygen therapy. 151 74

A decrease in the arterial blood saturation by oxygen in patients with POChP is a frequent phenomenon. It is more serious in patients type blue boaters and less frequent among patients type pink puffers. The aim of the paper was to compare the arterial blood saturation by oxygen in the groups examined during two nights: during the first night the patients breathed atmospheric air whereas during the second night they were given oxygen. The author also studied the influence of oxygenation of an organism on the frequency of cardiac rhythm disorders (ZRS). The author examined a group of 20 patients with the predominance of chronic bronchitis--blue boaters (average VC was 1.95 l, FEV1--0.81 l, PaO2 while breathing atmospheric air 52 mm Hg and 68 mm Hg after giving oxygen, PaCO2 47 and 51 mm Hg respectively) and 20 patients with the predominance of emphysema--pink puffers (average VC--2.30 l, FEV1--0.86 l, PaO2 while breathing atmospheric air 60 mm Hg and 70 mm Hg after giving oxygen, PaCO2 39 and 40 mm respectively). It was found that the patients with heavy hypoxaemia and hypercapnia had worse arterial blood saturation by oxygen during the two nights of investigation in comparison with the other group. The author also found more frequent cardiac rhythm disorders in this group of patients. Giving oxygen improved blood oxygenation in the two groups and lowered the frequency of cardiac rhythm disorders. The results obtained indicate to the need of oxygen therapy in patients with advanced POChP, especially during the night so as to avoid nocturnal hypoxaemia of an organism.
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PMID:[Nocturnal hypoxemia and arrhythmia in patients with chronic obstructive lung diseases (COLD)]. 262 58

The most common causes of hypoxic cor pulmonale are chronic bronchitis and emphysema. Although the clinical situation in some patients is characterized early by hypoxemia, oedema is rare in patients with an arterial pO2 above 60 mm Hg. The presence of oedema can be regarded as an unfavorable prognostic indicator. For many years, peripheral oedema had been considered an expression of congestive cardiac failure; it may be assumed, however, that neither right nor left ventricular failure is prerequisite to the development of oedema. Oedema formation can be attributed to excessive retention of salt and water or a redistribution of body water into the extracellular compartment. Hypercapnia and acidosis affect direct stimulation of renal hydrogen ion secretion. The resulting electrochemical imbalance is compensated by reabsorption of sodium. Hypercapnia and, in acute phases possibly, hypoxia lead to a fall in renal blood flow mediated by alpha-adrenergic stimulation through activation of the renin-angiotensin-aldosterone system. An increase in plasma ADH may also contribute to development of oedema. The development of cor pulmonale or respiratory insufficiency can be enhanced by nocturnal hypoventilation and hypoxia during sleep as well as by sleep apnoea. Nocturnal hypoxia, smoking and reduced oxygen tension in the relevant kidney cells responsible for erythropoietin release promote the occurrence of secondary polycythaemia. For treatment of acute exacerbations in cor pulmonale associated with infections bronchitis antibiotics such as amoxycillin and cotrimoxacol are drugs of first choice. While the use of digoxin is of doubtful value, the cautious administration of diuretics may bring symptomatic relief. In addition to physiotherapy, beta-2-selective bronchodilators and nebulized bronchodilator therapy can be useful; theophyllines dilate airways and increase cardiac output but they can cause arrhythmias and a deterioration of arterial blood gases in hypoxic patients. If the patient has been treated chronically with corticosteroids, the dosage will have to be incremented; if asthma is suspected, corticosteroid treatment is essential. Controlled oxygen therapy is the most important single therapy aimed at relief of severe arterial hypoxaemia. Oxygen should be titrated initially (for the first one or two days) to achieve an arterial tension of at least 48 mm Hg. Thereafter, the oxygen flow should be increased to yield an arterial tension in excess of 60 mm Hg during continued treatment for two to three weeks.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hypoxic cor pulmonale: a review. 294 54

A thirty-three-year-old man with diffuse pulmonary ossification associated with chronic bronchitis is described. Chest roentgenograms of the patient showed diffuse reticulo-nodular shadows partially super-imposed by calcified reticular opacities. Marked declines in forced vital capacity and air-flow limitation were associated with decreased diffusing capacity of the lung for CO, hypoxemia, and hypercapnia. In the postmortem examination, diffuse dendriform ossification was found mainly in the alveolar space. Neither interstitial fibrosis nor capillary congestion was found histopathologically in the lung.
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PMID:Diffuse pulmonary ossification associated with chronic bronchitis. 312 98


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