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

Plasma renin activity (PRA) and plasma angiotensin II (PAT II) level were determined with the method of radioimmunoassay in 55 patients with advanced chronic obstructive pulmonary disease (COPD) and chronic cor pulmonale (41 of them had respiratory failure) and 12 healthy aged persons. The results showed that PRA and PAT II levels were significantly elevated in the presence of such factors as severe hypoxia and hypercapnia (PaO2 less than or equal to 45 mmHg, mean 40 mmHg, PaCO2 greater than or equal to 65 mmHg), right heart failure, acidosis, hyponatremia and hypochloremia. It is shown that the prognosis would be poor when the patient's PRA level is significantly elevated.
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PMID:[Influence of acute respiratory failure on plasma renin activity and plasma angiotensin II level in advanced chronic obstructive pulmonary disease and chronic cor pulmonale]. 268 74

The pathogenesis of edema in COPD patients is poorly understood. In 50 COPD patients without cor pulmonale, we measured water sodium and potassium excretion in 24 hours, concentration of sodium and potassium in plasma as well as PRA, ATII and aldosterone levels. We found that PRA, ATII, and aldosterone levels in COPD patients with edema are much higher than those in patients without edema and sodium and water excretion decreased significantly in edematous COPD patients. Elevation of PRA, ATII, and aldosterone correlated with inability to excrete sodium and water. These data suggest that, in conjunction with hypercapnia-hypoxia-mediated disturbance in renal function, stimulation of RAAS, especially the resulting increase of aldosterone may contribute to edema formation in COPD patients.
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PMID:[Role of the renin-angiotensin-aldosterone system in the pathogenesis of edema formation in chronic obstructive pulmonary disease]. 280 68

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

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

The histories and the results of the postmortem examinations of 507 patients with chronic pulmonary heart disease were studied. In 62.6% of them left ventricular hypertrophy was found. As probable causes for this left ventricular hypertrophy are suggested: arterial hypertension, ischemic heart disease, hypoxemia, hypercapnia, heart failure, diabetes mellitus. The weight measurement correlations between the left and the right heart ventricles were studied in: "normal hearts", hearts with right ventricular, hypertrophy only, hypertrophy of both ventricles, left ventricular hypertrophy only. A correlation between the mass increase and the wall thickness of the ventricles was established. In the patients with chronic pulmonary heart disease and hypertrophy of both ventricles the mass and the wall thickness of the ventricles increase simultaneously. The possible pathogenetic mechanisms of the left ventricular involvement in patients with chronic pulmonary heart disease are discussed.
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PMID:[Left heart ventricle in chronic cor pulmonale patients. Etiological, pathomorphological and organ weight measurement studies]. 296 38

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

Eleven cases of cor pulmonale secondary to tonsil and adenoid hypertrophy and upper airway obstruction were reviewed. These patients presented with a spectrum disease ranging from mild, with only abnormal ECG or chest X-ray findings, to severe with hypercarbia, hypoxia, and right heart failure. One patient with severe disease suffered a postoperative respiratory arrest. We have successfully managed 4 patients with severe cor pulmonale with postoperative intubation and assisted ventilation. Hypoxia is the driving stimulus for respiration in patients with upper airway obstruction and hypercarbia. Relief of respiratory obstruction by tonsillectomy and adenoidectomy with postoperative oxygen administration may remove the hypoxic drive, resulting in respiratory arrest. Patients undergoing tonsillectomy and adenoidectomy for upper airway obstruction disease should be screened for cor pulmonale. Affected patients should be managed after surgery in an intensive care unit (ICU) environment with careful monitoring of the respiratory status. Patients with severe cor pulmonale can be successfully managed with planned postoperative intubation and mechanical ventilation to prevent respiratory arrest.
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PMID:Cor pulmonale secondary to tonsillar and adenoidal hypertrophy: management considerations. 306 49

The present study was undertaken to evaluate the short-term effects of nitroglycerin, nifedipine, and supplemental oxygen on hemodynamics and gas exchange in 11 patients in stable condition with chronic obstructive pulmonary disease and cor pulmonale. In general, both intravenous nitroglycerin and sublingual nifedipine significantly reduced the pulmonary vascular resistance index. For the group as a whole, nifedipine decreased the pulmonary vascular resistance index by significantly increasing the cardiac index, with minimal reductions in mean pulmonary arterial pressure. Conversely, nitroglycerin decreased the pulmonary vascular resistance index by markedly reducing the mean pulmonary arterial pressure but also decreased the cardiac index in some patients. Nitroglycerin also caused a significant decrease in mixed venous oxygen tension. Administration of oxygen did not cause any clinically significant improvement in resting hemodynamics following short-term administration. During the follow-up period, eight of 11 patients who were treated with pulmonary vasodilators in addition to long-term therapy with low-flow oxygen died within a mean of six months. This rate of survival was not significantly different than an age-matched and sex-matched control group with similar severity of disease who received only long-term therapy with low-flow oxygen. Based on these data, it seems unlikely that a substantial increase in survival will be obtained by combining pulmonary vasodilators with long-term oxygen therapy in patients with stable emphysema who have cor pulmonale and carbon dioxide retention.
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PMID:Pulmonary vasodilator therapy for chronic obstructive pulmonary disease and cor pulmonale. Treatment with nifedipine, nitroglycerin, and oxygen. 310 14

Snoring usually is trivial and unimportant, but it can turn into a social or medical problem. Obesity, hypertension and heart disease are more frequent among snorers than among nonsnorers, and especially snorers with hypersomnia during the day are at risk. Hypersomnia in association with snoring usually signifies obstructive sleep apnea. Increased resistance in the upper airways, together with negative inspiratory pharyngeal pressure and muscular hypotonia during deep non-REM and REM sleep, lead to collapse of the pharynx, hypoxia and hypercapnia. Only after arousal from sleep does muscle tone return, pharyngeal obstruction reopen and airflow resume. Since this process can occur 300 or 400 times a night, repetitive alveolar hypoventilation leads to pulmonary-arterial hypertension and cor pulmonale, and the repetitive sympathetic activations can cause systemic hypertension or serious cardiac arrhythmias. The countless arousals deprive the sufferer of deep non-REM and REM sleep and their consequence is sleep fragmentation. The symptoms are excessive daytime sleepiness, intellectual deterioration and personality and behavioral changes. Oronasomaxillofacial, endocrine and neuromuscular anomalies and diseases predispose to sleep apnea, and alcohol or CNS-depressant drugs can favour its occurrence. Diagnosis is made by nighttime oxymetry, and if this is abnormal, by polysomnography. After polysomnography it is possible to distinguish between obstructive and nonobstructive sleep apnea, and the decisions for an adequate treatment can be made.
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PMID:[Dangerous snoring. Sleep-apnea syndrome]. 331 92

Blood gas and haemodynamic changes caused by chronic respiratory insufficiency affect the right ventricle and produce chronic cor pulmonale. Equally important but less well known modifications affect the left ventricle and the general circulation and are the subject of the present report. Hypoxemia, hypercapnia and acidosis caused by severe hypoxia create functional disturbances in both ventricles that are manifested in a volume overload that added to other major malfunctions provoke congestive heart failure. The coronary circulation is affected by metabolic factors, perfusion alterations, right ventricular hypertrophy and concomitant coronary lesions. Advanced respiratory insufficiency caused by poorly compensated respiratory acidosis and metabolic acidosis reduces cardiac output and frequency so that tissue perfusion is compromised. Furthermore alterations in transmembrane electrolytic concentrations produce repeated multifocal ventricular arrhythmias that expose the patient to the risk of sudden death. Cardiac failure is reflected in other organs like the kidney and the central nervous system and also contributes to tissue and cerebral hypoxia. The later depresses the respiratory centres and develops into often irreversible coma. A better knowledge of these elements may contribute to the development of appropriate treatment.
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PMID:[General cardiocirculatory effects in chronic respiratory insufficiency]. 354 42


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