Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe seven years' experience with the University of Cape Town lenticular mitral valve prosthesis in 122 patients. All the patients had severe mitral valve disease. In 98 severe mitral stenosis was present with or without incompetence and in 24 the dominant or sole lesion was mitral incompetence. Other valves, particularly the tricuspid, were also frequently affected. The disability was severe or total in almost every patient. One hundred and five patients were discharged from hospital, and in 90 per cent of these the clinical improvement was most gratifying, with the disappearance of pulmonary oedema, paroxysmal dyspnoea, angina pectoris, and congestive cardiac failure. Return to full normal activity including physical work was the rule. The hospital mortality was 14 per cent and a further 38 per cent died during the follow-up period. The major post-operative complication was systemic embolism which could occur at any time after operation. The most important factor influencing the frequency of this complication was the nature of the valve seat. A bare steel seat was associated with a 100 per cent embolism, and a significant reduction occurred when a cloth-covered seat of Dacron-velour was introduced. Anticoagulant therapy appeared to prevent large or fresh clots but had no effect on the deposition of fibrin or platelet thrombi. The only other factor of importance was the age of the patient: after the age of 50 life expectancy and trouble-free long-term survival was reduced.
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PMID:Immediate and long-term results of mitral valve replacement with University of Cape Town mitral valve prosthesis. 544 May 20

Four cases are presented of maternal pulmonary edema occurring in patients who had no primary cardiac disease but who were receiving terbutaline and glucocorticoids or terbutaline alone for treatment of premature labor. Fluid overload was the event that triggered this decompensation. The physiologic high-output cardiac state of pregnancy is described and the manner in which betamimetic drugs and corticosteroids exacerbate this situation and cause congestive heart failure is shown. Methods of management to avoid this complication of premature labor therapy are suggested.
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PMID:Maternal pulmonary edema resulting from betamimetic and glucocorticoid therapy. 610 17

184 cases of acute poststreptococcal glomerulonephritis were investigated and six of these were associated with a peculiar, uncommon pneumonia, and another one had a lethal course. The clinicoradiological and especially pathological data summarized in this study attempt to demonstrate the individuality of this type of pneumonia. Pneumonia associated with acute poststreptococcal glomerulonephritis is similar or identical to rheumatic pneumonia. In both entities, pneumonia and pulmonary edema may and do coexist, and the differentiation of pneumonia from congestive heart failure is difficult and often impossible without pathological evidence. The most attractive pathogenic interpretation is the hypothesis of an immune mechanism in the induction of pneumonia. Authors attributed the lung changes, consecutive to a vascular damage, to a hypersensitivity phenomenon, with accumulation of fibrinogen in alveoli where it is converted to fibrin. Then, the hyaline membrane lining the alveoli, an important feature of pneumonia associated with glomerulonephritis is built up. It is, however, plausible that the effect of the immune reaction is associated with those of hydrosaline retention, arterial hypertension and congestive heart failure. Analogous to rheumatic pneumonia, the "peculiar pneumonia" associated with acute poststreptococcal glomerulonephritis should be named nephritic pneumonia.
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PMID:Uncommon pneumonia associated with acute poststreptococcal glomerulonephritis. 621 50

Acute lymphoblastic leukemia (cytologically typical) was diagnosed in an 18-year-old man presenting with major eosinophilia. Prednisone therapy was initiated but sudden congestive heart failure occurred (left ventricular insufficiency with pulmonary edema). Concomitantly, blood counts became normal. Remission of the leukemic process was obtained while severe mitral regurgitation developed, due to bacterial endocarditis. Successful mitral valvuloplasty was achieved. Remission is still persisting one year after diagnosis.
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PMID:[Acute lymphoblastic leukemia with major eosinophilia. Inaugural cardiac insufficiency, endocarditis grafting and valve replacement]. 630 90

We describe continuous positive airway pressure (CPAP) by mask to reduce hypercarbia in two patients who had pulmonary edema due to congestive heart failure. In such patients, beside reducing venous return and filling pressures, CPAP improves compliance and decreases the work of breathing, thereby improving effective ventilation. Hence, CPAP may be useful to combat not only hypoxemia but also hypercarbia that is associated with pulmonary edema.
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PMID:Effectiveness of CPAP by mask for pulmonary edema associated with hypercarbia. 633 82

A 20-year-old woman presented with malignant hypertension, pulmonary edema, anemia, and azotemia. Blood pressure was adequately controlled only after progressively more intensive drug regimens, finally including minoxidil, nadolol, and furosemide. On these drugs, the patient developed progressive left and right heart failure, anasarca, and malnutrition. The control of hypertension, heart failure, and fluid retention, was accomplished by administration of captopril and furosemide. Captopril is a logical alternative to vasodilators in refractory hypertension complicated by congestive heart failure.
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PMID:Efficacy of captopril in relieving congestive heart failure developing during management of hypertension. Case report. 634 Dec 22

In a randomized, controlled trial, ten patients with pulmonary heart disease due to severe chronic airflow obstruction were stratified into two groups: group 1 had clinical features of congestive heart failure during respiratory failure and were regularly receiving diuretics; group 2 had no such clinical features and were not receiving diuretics. In group 1, when placebo was substituted for diuretics, pulmonary edema developed in three patients; exercise performance and ventricular function of the remaining two patients deteriorated. In group 2, there was no difference in exercise tolerance or ventricular function between placebo and diuretic therapy. The clinical deterioration in group 1 was related to abnormal left ventricular function. Thus, diuretics benefit only patients who have clinical features of congestive heart failure. In patients with isolated abnormal right ventricular function, diuretics may be harmful.
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PMID:Effect of diuretics on cardiopulmonary performance in severe chronic airflow obstruction. A controlled clinical trial. 638 21

Bumetanide is a potent 'loop' diuretic for the treatment of oedema associated with congestive heart failure, hepatic and renal diseases, acute pulmonary congestion and premenstrual syndrome and in forced diuresis during and after surgery. Bumetanide may be given orally, intravenously or intramuscularly and produces a rapid and marked diuresis, and increased urinary excretion of sodium, chloride and other electrolytes (within 30 minutes) which persists for 3 to 6 hours. Its principal site of action is on the ascending limb of the loop of Henle, with a secondary action on the proximal tubule. Pharmacologically, bumetanide is about 40-fold more potent than frusemide (furosemide), with the exception of its effects on urinary potassium excretion where its potency is lower. Studies in patients with oedema due to congestive heart failure, pulmonary oedema or hepatic disease show that oral or intravenous bumetanide 0.5 to 2 mg/day produces results comparable to those with frusemide 20 to 80 mg/day. In acute pulmonary oedema, intravenous bumetanide produces a very rapid diuresis. Higher doses of bumetanide may be required (up to 15 mg/day) in patients with chronic renal failure or nephrotic syndrome. In these patients muscle cramps are not uncommon with bumetanide, but glomerular filtration rates are unaffected. In most studies, diuretic effects were accompanied by decreased bodyweight, abdominal girth and improvements in a variety of haemodynamic parameters. Comparison of bumetanide with frusemide at a dose ratio of 1 : 40 reveals no significant differences in clinical response with the exception of renal disease, where patients with oedema appear to respond better to bumetanide. Combination with thiazide diuretics enhances the clinical response to bumetanide. Potassium supplements and spironolactone may be beneficial additions to bumetanide where patients at risk of hypokalaemia can be identified. Clinically important side effects are infrequent, with audiological impairment occurring to a lesser extent than with frusemide. Bumetanide thus offers an important alternative to frusemide when a 'loop' diuretic is indicated.
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PMID:Bumetanide. A review of its pharmacodynamic and pharmacokinetic properties and therapeutic use. 639 89

Fluid movement from the pulmonary capillaries into the interstitial space occurs continuously and is drained by the lymphatics. With increased leakage or decreased clearance, excessive extravascular lung water accumulates, initially as interstitial edema and subsequently as alveolar edema. The most common cause of pulmonary edema is an increase in microvascular hydrostatic pressure. An increased permeability of the capillaries is the other mechanism of production of pulmonary edema. An acute, critical reduction in colloid osmotic pressure may play a contributory role in pulmonary edema even at normal hydrostatic pressures. Dyspnea, diaphoresis, and anxiety characterize the clinical picture. A history of heart disease and congestive heart failure may be present in CPE, whereas evidence of an inciting event or disease process suggests NCPE. Hypoxia, decreased lung compliance, and increased shunt fraction are seen in both types of pulmonary edema, but the duration of pulmonary edema tends to be more severe and prolonged in NCPE. Evidence of increased permeability in NCPE distinguishes it from CPE. Clinically, this is assumed when pulmonary edema is demonstrated at normal PCWP and when edema fluid protein concentration and COP are close to those of plasma. The management of pulmonary edema consists of the improvement of gas exchange by methods that range from supplemental oxygen administration to mechanical ventilatory support with PEEP, depending on the severity of the disturbance in lung function. Improvement in myocardial function and a decrease in pulmonary congestion are accomplished with diuretics and morphine; in those patients who do not respond to this therapy, manipulation of preload, afterload, and myocardial contractility by vasodilators and inotropic agents may be required. In acute pulmonary edema, intravenously administered agents with a short half-life and rapid onset of action are preferred. The role of colloids in the treatment of pulmonary edema is controversial. The indications for the use of corticosteroids in ARDS are controversial, and an optimum dose has not been determined. Many clinicians tend to choose steroids to treat these patients, but the value of these agents in this setting awaits the results of controlled trials now under way.
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PMID:Acute pulmonary edema. 644 44

In a 21/2-year period, hypertrophic cardiomyopathy was found at necropsy of 23 cats that died (13 cats) or were euthanatized (10) because of problems associated with hyperthyroidism. Of these, 4 (17%) also had evidence of cardiac failure (pulmonary edema or pleural effusion). The mean body weight of the cats with hyperthyroidism and hypertrophic cardiomyopathy was significantly less (P less than 0.001) than that of clinically normal cats and cats with primary cardiomyopathy (congestive or restrictive) or excessive moderator band cardiomyopathy. In addition, the ratio of heart weight to body weight was significantly greater (P less than 0.001) in the 23 hyperthyroid cats than in the normal cats and cats with primary cardiomyopathy. Twenty (87%) of the cats had symmetric hypertrophy of the ventricular septum and left ventricular free wall, whereas the remaining 3 cats had disproportionate thickening of the ventricular septum, compared with the free wall, similar to what is found in cats with asymmetric hypertrophic cardiomyopathy. Histologic cardiac abnormalities included large, hyperchromatic nuclei, interstitial fibrosis, endocardial fibroplasia, fibrosis of the atrioventricular node, and marked disorganization of cardiac muscle cells. The study showed that hypertrophic cardiomyopathy develops in most hyperthyroid cats, some of which also develop congestive heart failure. Although the signs of heart disease in primary myocardial disease and thyrotoxic disease are similar, the characteristic signalment and clinical signs of hyperthyroidism should lead one to suspect the association of hypertrophic cardiomyopathy with the hyperthyroidism.
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PMID:Hypertropic cardiomyopathy and hyperthyroidism in the cat. 654 Feb 56


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