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

Previous studies have suggested that the hypoxia and/or hypercapnia associated with chronic lung diseases may lead to pituitary and gonadal dysfunction, with destruction of the sella turcica. It is unclear, however, whether these abnormalities were due to lung disease or to confounding factors. We studied the relationships between hormonal levels (triiodothyronine, thyroxine, T3 resin uptake, thyrotropin, prolactin, cortisol, and testosterone) and PaO2, PaCO2, pH, and alveolar-arterial gradient in 25 patients with chronic lung disease. These patients were highly homogeneous for diagnosis, age, sex, ambulatory status, lack of other illnesses, and minimal use of medications unrelated to lung disease, but did have various degrees of hypoxia and hypercarbia at the time of study. We found no relationship between hormonal levels and lung function, or evidence of major pituitary involvement on lateral roentgenograms of the skull, CT of the sella turcica, or stimulation of the pituitary. An inverse correlation did occur between serum levels of thyroxine and the daily dose of oral prednisone. We conclude that most of the endocrine dysfunction ascribed to chronic lung diseases is probably due to factors other than hypoxia or hypercarbia.
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PMID:Hypoxia and hypercarbia of chronic lung disease: minimal effects on anterior pituitary function. 210 79

Cor pulmonale is right ventricular enlargement secondary to pulmonary hypertension. Although most often caused by parenchymal lung disease, derangements of the ventilatory drive, the respiratory pumping mechanism, or the pulmonary vascular bed may also result in right ventricular hypertrophy and dilatation. Arterial hypoxemia (and resultant polycythemia), hypercapnia, and respiratory acidosis all contribute to the increased afterload on the right ventricle. Diagnosis is often difficult, since pulmonary vascular disease, pulmonary hypertension, and cor pulmonale have few specific manifestations, especially early in their evolution. Treatment is primarily directed at the underlying pulmonary or ventilatory disorder, rather than at the right ventricular failure per se. Supplemental oxygen is essential to avoid hypoxia; corticosteroids, anticoagulants, vasodilators, and other specific therapies are used as indicated to treat the underlying pulmonary disorders. When medical therapies fail, lung or heart-lung transplantation has become a possibility for selected patients.
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PMID:Chronic cor pulmonale. Etiology and management. 239 36

The inability to increase alveolar ventilation can lead to CO2 retention and acute respiratory acidosis in patients with ventilatory limitation. In this case, a young woman receiving maximum ventilatory support was unable to excrete excess CO2, associated with increasing dianeal concentrations of peritoneal dialysis. Since the patient's lung disease had necessitated a large amount of ventilatory support, the patient was unable to increase VE appropriately to handle excess CO2. Peritoneal dialysate was an additional source of carbohydrates. Peritoneal dialysate is an additional carbohydrate source that may result in hypercapnia and respiratory acidosis in patients with respiratory compromise. To our knowledge, this is the first case report in an adult which demonstrates that peritoneal dialysis with high glucose loads produced an acute respiratory acidosis that was reversed by decreasing the glucose concentrations in the dialysate. Excess CO2 production should be considered with respiratory disorders associated with dialysis.
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PMID:Dialysis-induced respiratory acidosis. 222 84

Urinary citrate prevents nephrocalcinosis in adults. Premature infants have a high incidence of nephrocalcinosis. We measured urinary citrate (Ucit) and creatinine (Ucre) concentrations in infants with and without lung disease. Ucit was lower in the infants requiring mechanical ventilation than in the controls (mean = 9.7 vs. 15, p = 0.05). Ucit/Ucre ratios were lower in hypercarbic (mean = 0.95 vs. 1.47 in normocarbic, p less than 0.05) and acidotic (mean = 0.57 vs. 1.44 in nonacidotic, p less than 0.004) premature infants. The lowered Ucit of premature infants with lung disease (and acidosis or hypercarbia) may predispose to nephrocalcinosis by increased urinary lithogenesis.
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PMID:Decreased urinary citrate in premature infants with lung disease. 225 55

The effects of oxygen administration were studied in 10 patients with severe obstructive lung disease. Sleep variable and gas exchanges were measured during two nights: one when they were breathing environmental air, the other when they were receiving oxygen. Carbon dioxide saturation and partial pressure measured by the transcutaneous method were continuously recorded. Sleep was perturbed in all patients, but despite wide interindividual variations its amount and quality were improved by oxygen. None of the patients had sleep apnoea syndrome. Oxygen administration was accompanied by a nocturnal increase in carbon dioxide pressure that was about twice as high as that observed under environmental air. Thus, in patients with chronic obstructive lung disease without concomitant infection suppression of the hypoxic stimulus by oxygen therapy seems to result in an increase in carbon dioxide partial pressure identical with the increase produced by sleep alone. Correlations between diurnal and nocturnal oxygen saturation and carbon dioxide partial pressure indicate that patients with the highest degree of hypoxia and hypercapnia in daytime have the most severe nocturnal blood gas disorders.
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PMID:[Chronic obstructive bronchopneumopathies. Changes in carbon dioxide pressure during sleep in environmental air and with oxygen]. 252 37

Noninvasive face mask ventilation has been used successfully in patients with paralytic respiratory failure. This study evaluated whether noninvasive face mask ventilation can be used for patients with acute respiratory failure due to intrinsic lung disease. Six patients with hypercapnia and four with hypoxemic acute respiratory failure met clinical and objective criteria for mechanical ventilation, which was delivered with pressure control and pressure support via a tightly strapped, clear face mask. No patient terminated the study because of inability to deliver adequate ventilation or to improve oxygen exchange; three eventually required endotracheal intubation. The mask was generally well tolerated. All patients had a nasogastric tube placed on suction, and none vomited or aspirated. The mean duration of treatment was 33 h (range, 3 to 88). The physiologic response was considered similar to that which would have been achieved with conventionally delivered ventilation. Noninvasive face mask ventilation may have a role in managing respiratory failure.
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PMID:Noninvasive face mask ventilation in patients with acute respiratory failure. 292 16

Factors related to risk of perioperative pulmonary complications include site of incision, obstructive lung disease, prolonged anesthesia time, smoking history with productive cough, and obesity. Hypercapnia is a consistent indicator of high risk. There is no difference between spinal and general anesthesia with regard to risk of pulmonary complications. In patients being evaluated for lung resection, high-risk indicators include predicted postoperative forced expiratory volume in one second of less than 1000 mL, hypercapnia, severe dyspnea on exertion, or advanced age when it is associated with advanced cardiopulmonary disease. Newer methods of assessing cardiopulmonary reserve may prove useful in identifying which patients with one or more of these risk factors are suitable operative candidates. Prevention of postoperative complications in chronic obstructive pulmonary disease patients should begin in the preoperative period with discontinuation of smoking at least eight weeks before surgery and vigorous pulmonary toilet in the 48 to 72 hours before surgery. Prophylactic lung expansion maneuvers can be effective in decreasing the incidence of postoperative atelectasis in high-risk patients undergoing high-risk operations.
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PMID:Preoperative pulmonary evaluation. 233 Nov 91

The main cause of secondary pulmonary hypertension in the view of a pulmonologist is alveolar hypoventilation - eventually potentiated by acidosis and hypercapnia - which leads to reflectory hypoxemic vasoconstriction of the small pulmonary arteries. Anatomic changes in the pulmonary vessels may be absent or may be limited to medial hypertrophy of the arterioles. If the underlying cause of the hypoxia can be corrected, this reflectory pulmonary hypertension is reversible. In diffuse progressive lung disease, interstitial fibrosis with destruction of the alveolar wall and capillaries may occur, leading to restriction of the pulmonary vascular bed. In such cases pulmonary hypertension may not be completely reversible. The most frequent causes of pulmonary hypertension in childhood are obstructive (e.g. Cystic Fibrosis) or restrictive lung diseases (e.g. interstitial fibrosis). Rare but important in the differential diagnosis are upper airway obstruction, thoracic cage deformity, neuromuscular disorders, high altitude and respiratory center dysfunction. The therapy is elimination of the underlying disease or optimal treatment. In addition prophylactic or therapeutic longterm application of oxygen is more efficient than treatment with pulmonary vasodilators or modern substances like Almitrine. Right heart decompensation should be treated by diuretics. The longterm prognosis is dependent of the underlying disease and is poor in a chronic progressive lung disease like cystic fibrosis and certain types of lung fibrosis.
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PMID:[Pulmonary hypertension from the viewpoint of the pediatric pulmonologist]. 310 Dec 91

A radiographic pattern associated with respiratory distress, distinct from hyaline membrane disease and transient tachypnea of the newborn, is described in eight infants of diabetic mothers. The radiographic findings demonstrate a regional distribution of reticulogranular densities accompanied by increased lung volumes. Clinical features were gestationally mature infants in moderate respiratory distress with tachypnea, hypercapnia, and hypoxemia requiring supplemental oxygen, with steady improvement and uneventful recovery within 2 weeks. There was no bacteriologic evidence of infection or radiographic evidence of delayed lung fluid absorption. The mothers had mild diabetes. These features characterize a newly recognized entity in diabetes-related idiopathic lung disease of the newborn. Possible causative factors are discussed.
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PMID:A newly recognized profile in neonatal lung disease with maternal diabetes. 387 61

Excess carbohydrate calories in total parenteral nutrition (TPN) solutions can precipitate acute hypercapnic respiratory failure in patients with chronic lung disease secondary to increased carbon dioxide (CO2) production. Two young patients recovering from the adult respiratory distress syndrome experienced hypercapnia during weaning as a result of nutritionally related increased CO2 production. As carbohydrate calories were decreased, CO2 production diminished and hypercapnia resolved. Hypercapnia as a complication of nutritional support during weaning can occur in patients without chronic lung disease and is corrected by decreasing carbohydrate calories.
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PMID:Hypercapnia during weaning. A complication of nutritional support. 392 89


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