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

Persons residing at high altitude who develop excessive polycythemia are more hypoxemic than normal high-altitude residents. We investigated the causes of hypoxemia in 20 patients with excessive polycythemia residing at an altitude of 3,100 m. Lung disease evidenced by abnormal spirometric features and results of a respiratory questionnaire was present in 10 of 20 patients and resulted in increased alveolar-arterial difference for PO2 [(A-a)PO2]. The excessive hypoxemia in the patients with normal lungs was not due to increased (A-a)PO2. We measured ventilatory responses to hypoxia and to hypercapnia to determine whether blunting of these responses was a cause of this excessive hypoxemia. We found, however, that chemical drives to breathe, although blunted, were the same in patients with polycythemia as in high-altitude control subjects. However, an abnormal breathing pattern was observed; the polycythemic patients had a smaller tidal volume and a greater ratio of dead space to tidal volume than did the normal subjects. In addition, the polycythemic patients had increased minute ventilation on breathing 100 percent O2, whereas the normal subjects did not. Thus, hypoxic depression of ventilation may have been present. Our findings suggested that blunted chemical drives are not causative in this disease, and that some other cause of hypoxemia must be present.
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PMID:Excessive polycythemia of high altitude: role of ventilatory drive and lung disease. 70 89

During sleep some patients with airways obstruction and hypoxaemia developed tachypnoea. This could not be explained by the severity of their abnormality of lung function, their CO2 responsiveness, the nature of their lung disease or their personality. This nocturnal tachypnoea correlated best with a raised resting arterial blood PCO2, and was not seen hypoxaemic patients with a normal PCO2 who showed the usual fall in respiratory rate when asleep. We suggest that in patients with both hypoxaemia and hypercapnia sleep removes a cortical inhibitory mechanism which slows breathing durigng waking hours, and is linked to the arterial blood PCO2.
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PMID:Sleeping ventilatory patterns in patients with severe chronic airflow obstruction causing respiratory failure. 95 25

For over 15 years, upper respiratory tract obstruction due to adenotonsillar hypertrophy has been known to cause hypoxia, hypercapnia, increased pulmonary vascular resistance and thereby cor pulmonale and congestive heart failure. This is now an uncommon but not rare entity and three recent cases prompted this report. The typical patient is dyspneic with retractions, cyanosis, occasional periods of apnea and somnolence. Edema and hepatomegaly and at times splenomegaly are common. X-rays show cardiomegaly, which on electrocardiogram is found to involved mainly the right ventricle. The strict definition of cor pulmonale is right ventricular hypertrophy secondary to lung disease or abnormal pulmonary function, a definition that may logically be stretched to include abnormal respiratory function secondary to upper airway pathology. The mechanisms by which this occurs are generally agreed upon. Hypoxia has been demonstrated to cause pulmonary vasoconstriction. Acidosis and hypercapnia are thought by some to have the same effect. Pressure across the pulmonary vascular bed is also increased, as predicted by Poiseuille's law, by the high rate of blood flow required to maintain tissue oxygenation with poorly oxygenated blood. Conditions producing hypoxia of hypercapnia or both lead to hypertrophy and eventually to dilatation of the right ventricle. Three cases of children who underwent cardiac catheterization while suffering from cor pulmonale due to adenotonsillar hypertrophy are reported. Right ventricular pressure averaged 44/5, PAO2 72, pH 7.32, and PACO2 52. All were clinically improved following adenotonsillectomy. Cardiac catheterization was repeated in one case, with right ventricular pressure dropping from 44/5 to 21/2, pulmonary vascular resistance from eight units to three, and PACO2 from 62 to 44.
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PMID:Cardiac and pulmonary failure secondary to adenotonsillar hypertrophy. 95 48

Six black infants and young children with high titers of milk precipitins were identified by screening the sera of 160 children with idiopathic chronic lung disease. None of the six had immunoglobulin deficiency, elevation of sweat chlorides, SS hemoglobin, or recurrent aspiration. All six children had typical manifestations of milk-induced pulmonary hemosiderosis: recurrent pulmonary infiltrates (6/6), hemosiderin-laden pulmonary macrophages (5/6), intermittent wheezing (5/6), eosinophilia (4/6), anemia (4/6), iron deficiency (4/4), failure to thrive (4/6), and elevated levels of serum IgE (4/4). Three children also had chronic rhinitis and eventually developed large adenoids, hypercapnia and acidosis during sleep, and right heart failure. Elimination of cow milk from the diet, symptomatic therapy, and adenoidectomy when indicated resulted in improvement of all six patients. Pulmonary hemosiderosis and some cases of upper airway obstruction with pulmonary hypertension appear to be two stages, early and delayed, of the same immunophysiologic process. Early dietary intervention may prevent the cardiovascular complications of this process.
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PMID:Hyperreactivity to cow milk in young children with pulmonary hemosiderosis and cor pulmonale secondary to nasopharyngeal obstruction. 117 19

Since February 1990, five children, aged 10 days to 6.5 years, were treated with extracorporeal lung support at our hospital for acute, unrelenting pulmonary failure. Two had viral pneumonia: one with respiratory syncytial virus (RSV) bronchiolitis, and one with herpes simplex virus pneumonia, encephalitis, and disseminated intravascular coagulation. One presented with a febrile illness followed by a pulmonary hemorrhage. Two patients had adult respiratory distress syndrome (ARDS) complicating severe systemic illnesses, toxic epidermal necrolysis in one and cat scratch disease with encephalitis in the other. All children had diffuse parenchymal lung disease by chest x-ray. On maximum medical management all patients were developing carbon dioxide retention and progressive hypoxemia, exceeding previously established NIH study criteria for extracorporeal treatment. Three children (10 days, 2 months, 13 months) were placed on venoarterial support and two children (20 months and 6.5 years) were placed on venovenous extracorporeal support (ECCO2R). Three of the five had open lung biopsies performed, which showed findings consistent with a moderate to severe cellular phase of ARDS. No viral inclusions were found in the patient with RSV infection. One hundred percent immediate survival was achieved in this patient population. Average duration of support was 330 hours (range, 89 to 840). Following completion of extracorporeal support, all children were successfully weaned from the ventilator with an average time to extubation of 23.2 days (range, 2 to 58 days). One child died of congestive heart failure following palliative surgery for a complex noncyanotic congenital cardiac lesion 35 days after successfully weaning from extracorporeal support for an acute febrile illness and pulmonary hemorrhage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment of acute pulmonary failure with extracorporeal support: 100% survival in a pediatric population. 132 87

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

According to conventional wisdom the difference between alveolar and arterial O2 tensions, the AaPO2, should distinguish between hypoxemia caused by alveolar hypoventilation and hypoxemia caused by alveolar hypoventilation complicated by other abnormalities of gas exchange. To test this concept we have calculated the AaPO2 from arterial blood gas measurements, breathing air, in 23 patients with hypercapnia, hypoxemia, and advanced obstructive lung disease (mean FEV1 = 0.88 L). We found that AaPO2 varied inversely with PaCO2 (r = -0.83, p less than 0.001). In five of these patients with the most severely elevated PaCO2 (range, 59 to 81 mm Hg) the AaPO2 was within normal limits. We also calculated the difference between the O2 contents of "ideal" pulmonary capillary blood and arterial blood and expressed this as the venous admixture (QVA/QT) based on an assumed arteriovenous content difference of 4.5 ml/dl. In contrast to the AaPO2, the QVA/QT, was abnormal in all patients (mean = 41 +/- 8%). We conclude that the AaPO2 may be an unreliable indicator of abnormal gas exchange in the presence of alveolar hypoventilation. This finding can be explained by substantial changes in the position of the alveolar and arterial points on the oxygen dissociation curve for hemoglobin in the presence of alveolar hypoxia secondary to hypoventilation.
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PMID:Interpretation of the alveolar-arterial oxygen difference in patients with hypercapnia. 189 45

Exercise training has been considered suitable only in cystic fibrosis (CF) patients with mild to moderate pulmonary dysfunction without progressive hypoxaemia during exercise. We trained 16 CF patients, all with advanced lung disease (mean standardized forced expiratory volume in 1 s (FEV1), 30% pred.), with a ventilatory limitation to exercise and a progressive hypoxaemia and hypercapnia at low maximal exercise capacity, Wmax (mean Wmax, 50% pred). Exercise training was performed on a cycle ergometer twice a day for 20 min at approximately 75% of the maximal predicted heart rate for at least 3 weeks. Supplemental oxygen was administered to reach a haemoglobin oxygen saturation of 90% during training. Patients considered malnourished because of a Quetelet Index of less than 20 kg m-2 received hyperalimentation orally or by duodenal tube (total 3500-4000 kcal day-1). Evaluation directly after the training period showed a statistically significant improvement in Wmax, maximal oxygen consumption, maximal minute ventilation, pulse, PaCO2 at rest, FEV1 and body weight. None of the pretraining variables was able to predict the outcome of the training programme in the individual patient. We detected no adverse effects of the programme. This study shows that oxygen-assisted exercise training in combination with correction of the nutritional status is safe and beneficial in CF patients with severe lung disease.
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PMID:Oxygen-assisted exercise training in adult cystic fibrosis patients with pulmonary limitation to exercise. 193 21

Infants, children, and adolescents with chronic respiratory failure are surviving in increasing numbers and, thereby, producing a significant population of ventilator-dependent pediatric patients. Chronic respiratory failure can occur as a complication of a wide variety of disease states; in pathophysiologic terms, it generally results from either decreased central nervous system output or inadequate force generated by the respiratory pump. Its laboratory hallmark is hypercapnia with or without hypoxemia. Stabilization of the patient with mechanical ventilatory support may permit long-term survival. Management of the ventilator-dependent pediatric patient is a complex task that must begin with an accurate prognostication of each patient's survival and quality of life. Once a decision is made concerning the practicality and appropriateness of long-term ventilatory support, informed choices must be made with respect to need for an artificial airway, mode of ventilation, and location of care. Many younger patients, especially those with intrinsic lung disease (like bronchopulmonary dysplasia), may require a hospital setting for long-term care, whereas others with neuromuscular or central disorders may benefit from being discharged to home. The patient's family must be thoroughly educated in the child's care, and they must be involved in decision-making. A multidisciplinary team of physicians, therapists, nurses, and other professionals is required to deliver optimal care. Outcome is good for most patients who are carefully selected.
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PMID:The ventilator-dependent child: issues in diagnosis and management. 198 23

The value of mechanical ventilation using intermittent positive pressure ventilation delivered non-invasively by nasal mask was assessed in six patients with life threatening exacerbations of chronic respiratory disease. Median (range) arterial oxygen and carbon dioxide tensions were 4.4 (3.5-7.2) kPa and 8.7 (5.5-10.9) kPa respectively, with four patients breathing air and two controlled concentrations of oxygen. The arterial oxygen tension increased with mechanical ventilation to a median (range) of 8.7 (8.0-12.6) kPa and the carbon dioxide tension fell to 8.2 (6.5-9.2) kPa. Four patients discharged after a median of 10 (8-17) days in hospital were well five to 22 months later. One died at four days of worsening sputum retention and another after five weeks using the ventilator for 12-16 hours each day while awaiting heart-lung transplantation. This technique of mechanical ventilation avoids endotracheal intubation and can be used intermittently. Hypercapnic respiratory failure can be relieved in patients with either restrictive or obstructive lung disease in whom controlled oxygen treatment results in unacceptable hypercapnia. Respiratory assistance can be tailored to individual need and undertaken without conventional intensive care facilities.
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PMID:Non-invasive mechanical ventilation for acute respiratory failure. 233 29


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