Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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)
 ...
PMID:Indications for long-term oxygen therapy. 151 74

Neonates with congenital diaphragmatic hernia (CDH) are known to be susceptible to stress-induced persistent pulmonary hypertension (PPHN). Congenital cystic adenomatoid malformations (CCAMs) may also present as respiratory distress in the newborn. Intubation and mechanical ventilation cause clinical deterioration because of air trapping within cystic spaces; these patients require prompt lobectomy. PPHN has not been commonly associated with CCAM. Three patients with CCAM were encountered who developed PPHN postlobectomy. Three newborns, 36 to 38 weeks' gestation, presented with respiratory distress. Two had diagnosis of thoracic tumors on fetal ultrasound (22 and 33 weeks). Chest x-ray at birth confirmed cystic intrathoracic tumors in all and they underwent immediate thoracotomy and lobectomy (1 right upper, 1 left lower, 1 left upper). The patients were stable for 4 hours to 5 days postoperatively and then developed findings consistent with PPHN by cardiac echocardiography and required extracorporeal membrane oxygen (ECMO) support. ECMO was required for 66.5 to 120 hours. Each patient was successfully weaned to conventional ventilatory support. The clinical course of these patients was similar to those with CDH who undergo immediate surgery. The stress of surgical intervention combined with hypoxia and hypercarbia stimulates a hyperactive pulmonary vasculature and the development of PPHN. ECMO provides an effective adjunct to support patients with PPHN on the basis of congenital cystic adenomatoid malformations.
 ...
PMID:Persistent pulmonary hypertension complicating cystic adenomatoid malformation in neonates. 155 45

Hilltop (H) and Madison (M) strains of Sprague-Dawley rats exhibit strikingly different susceptibilities to the effects of chronic altitude exposure. The H rats develop greater polycythemia, hypoxemia, and pulmonary hypertension. We studied ventilation, pulmonary gas exchange, tissue oxygenation, and hematologic adaptations in the two rat strains during a 50-day exposure to a simulated altitude (HA) of 5,500 m (18,000 ft). There were no strain differences among the variables we studied under sea level (SL) conditions. Within the first 14 days of hypoxic exposure, the only significant strain differences were that erythropoietin (EPO) rose much higher and erythroid activity was greater in the H rats, even though arterial Po2 and PCo2 (Pao2 and PaCo2, respectively), renal venous PO2 (Prvo2), and ventilation (VE) were equivalent in the two strains during this time. By day 14 at HA, the H rats had significantly higher erythroid activity, hematocrit (Hct), and EPO levels, significantly lower PaO2 and PrvO2, but equivalent VE and PaCO2. These changes persisted for the remainder of the exposure, except that the Hct continued to rise and the increase was greater in H rats. Despite the greater O2-carrying capacity of H rats in the later stages of hypoxic exposure, PaO2 and PrvO2 were significantly lower in H rats. There were no strain differences at either SL or HA in ventilatory responses to hypercapnia or hypoxia, in blood O2 affinity or 2,3-diphosphoglycerate, in extrarenal production of EPO, or in EPO clearance. We conclude that early in the hypoxic exposure the H rats produce more EPO at apparently equivalent levels of hypoxia, and this is the first step in the pathogenesis of the maladaptation to HA manifest by H rats. We find no consistent evidence that differences in VE contribute to the variable susceptibility to hypoxia in the two rat strains.
 ...
PMID:Ventilatory and hematopoietic responses to chronic hypoxia in two rat strains. 162 91

Single lung transplantation was performed in several steps: laparotomy to prepare an omentopexy, followed by pneumonectomy and implantation of a pulmonary graft, both by postero-lateral thoracotomy. The patients suffered from lymphangiomyomatosis (1), panacinar emphysema (2) and idiopathic pulmonary fibrosis (1). Immunosuppressive treatment was started before surgery. Anaesthesia was induced and maintained with alfentanil, midazolam and vecuronium. The patients were intubated with a Carlens endotracheal tube. Ventilation was carried out using an oxygen-air mixture, without any nitrous oxide or halogenated anaesthetic agent. Besides the usual parameters, expired CO2 concentrations, and oxygen saturation in the pulmonary artery were monitored. Partial femoro-femoral cardiopulmonary bypass was not required. Three major problems were encountered: hypoxia, hypercapnia, and pulmonary arterial hypertension. Hypoxia first occurred during the period of one-lung ventilation, during pneumonectomy, and again after unclamping of the graft vessels before the bronchus had been anastomosed. It was treated either by increasing the FiO2, inflating the lungs with pure oxygen, or partial clamping of the homolateral pulmonary artery. Hypercapnia occurred in three of the four patients until the graft was ventilated again. Except in one patient with preoperative pulmonary hypertension, the increase in pulmonary vascular resistances remained moderate after clamping of the pulmonary artery. Sufficient oxygen delivery, with more than 50% venous oxygen saturation, was maintained at this time by the infusion of dopamine and dobutamine. Two other specific problems were encountered in the emphysematous patients: severe hypotension following the start of artificial ventilation and after placing the patient in lateral position; thoracic asymetry with overdistension of the emphysematous lung, and mediastinal shift.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Anesthesia in unilateral pulmonary transplantation]. 185 49

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.
 ...
PMID:Chronic cor pulmonale. Etiology and management. 239 36

Arterial oxyhemoglobin saturation (SaO2) falls to a variable extent during sleep in patients with COPD. These nocturnal falls in SaO2 may contribute to the development of pulmonary hypertension, nocturnal cardiac arrhythmias, and death during sleep. In order to determine which physiologic factors measured during wakefulness might contribute to the development of nocturnal hypoxemia, we performed multiple stepwise linear regression analyses in 48 patients with stable COPD with mean and lowest nocturnal SaO2 as dependent variables. It was concluded that the two chief variables, measured while awake, which are associated with alterations in nocturnal oxygenation in patients with COPD are baseline awake SaO2 and PaCO2. Hypercapnia appears to be a risk factor for the development of nocturnal hypoxemia in patients who are normoxic while awake.
 ...
PMID:Daytime hypercapnia in the development of nocturnal hypoxemia in COPD. 229 55

Pulmonary neuroendocrine cells (PNEC) are granulated epithelial cells distributed throughout conducting airways. Among the bioactive products identified within the secretory granules of these cells are potent mitogens and bronchoactive and vasoactive agents. The secretory status of these cells, which are in greatest number in the fetus and newborn, is modulated by neural reflexes and by changes in airway gas composition. The aggregate data suggest roles for PNEC in airway "chemoception" and/or regulation of airway epithelial differentiation. Marked increases in PNEC are observed in bronchopulmonary dysplasia, where airway and alveolar fibrosis, epithelial metaplasia, and airway and vascular smooth muscle hypertrophy contribute to marked pathophysiologic changes in lung function. Considering the biologic effects of PNEC secretory products, particularly gastrin-releasing peptide on airway epithelial cell and fibroblast proliferation, we propose that an increase in PNEC secretory products in the regenerating airway epithelium may contribute to the development of the pathologic alterations in lung structure seen in bronchopulmonary dysplasia. In this proposed scheme, secretion of abnormally large amounts of bronchoactive and vasoactive agents from PNEC (e.g., serotonin, gastrin-releasing peptide) in response to airway hypoxia and hypercapnia may be partially responsible in the genesis of reactive airway disease and pulmonary hypertension seen in this disease.
 ...
PMID:Pulmonary neuroendocrine cells. Their secretory products and their potential roles in health and chronic lung disease in infancy. 257 71

To define the parameters of respiratory insufficiency in OSA, 114 consecutive patients (108 men, six women) were prospectively studied. In addition to standard polysomnography, they underwent pulmonary function tests, right heart catheterization, and ventilatory response tests to hypercapnia. Nineteen patients (19 percent) had a resting PAP greater than or equal to 20 mm Hg. Multiple regression analysis showed that FEV1 and PaO2 (both with a negative coefficient) and PaCO2 (with a positive coefficient) significantly contributed to PAP. Thirteen patients (12 percent) had a PaCO2 greater than or equal to 45 mm Hg. A multiple regression analysis showed that FEV1 and the minute ventilation at PETCO2 = 60 mm Hg (both with a negative coefficient) and the cumulative apnea duration (with a positive coefficient) significantly contributed to PaCO2. Thirty-seven patients (33 percent) had a PaO2 less than or equal to 65 mm Hg. A multiple regression analysis showed that FEV1 (with a positive coefficient) and the hypopnea + apnea index (with a negative coefficient) significantly contributed to PaO2. These data confirm that impaired daytime pulmonary function (diffuse airway obstruction) contributes to the development of daytime pulmonary hypertension, hypoxemia, and hypercapnia in OSA patients. They show that the amount of sleep-related breathing disorders also plays a significant role.
 ...
PMID:Pulmonary hypertension, hypoxemia, and hypercapnia in obstructive sleep apnea patients. 279 65

Sleep related disorders of respiratory regulation can result, through various mechanisms, in impairment of the hemodynamics of the heart and the systemic and pulmonary circulations. The group of patients with sleep apnea has been most thoroughly investigated thus far. The patients frequently develop essential and/or pulmonary hypertension. In sleep all forms of cardiac arrhythmia may occur, and thus the patients are at high risk for nocturnal sudden cardiac death. Responsibility for most hemodynamic alterations is attributed to apnea-induced hypoxia and hypercapnia and the intrathoracic pressure fluctuations observed in obstructive apnea. However, we are still short of detailed knowledge regarding the individual pathologic mechanisms. The hemodynamic changes observed in patients with sleep related disorders of respiratory regulation lead in the long run to cardiac failure. Early diagnosis and care of these patients is therefore urgently necessary to render timely therapeutic action possible.
 ...
PMID:[Cardiovascular diseases in nocturnal disorders of respiratory regulation]. 305 70

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.
 ...
PMID:[Pulmonary hypertension from the viewpoint of the pediatric pulmonologist]. 310 Dec 91


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>