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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

5 patients developed pulmonary oedema after retrograde femoral arteriography under general anesthesia. Because of the haemodynamic changes associated with radiographic contrast media, a good preoperative cardiological assessment is essential. The volume and nature of the contrast media injected and any other fluid administered should be carefully monitored. There is no apparent safe maximum dose of radiographic contrast media, but this work suggests that for 'Conray 420' (sodium iothalamate 70% w/v) a total dose should be less than 200 ml in a fit patient. The dose should be substantially smaller in patients with a history of evidence of myocardial infarction, myocardial insufficiency, myocardial ischaemia, or hypertension.
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PMID:Pulmonary oedema after radiological investigation of peripheral occlusive vascular disease. Adverse reaction to contrast media. 7 42

Left ventricular wall motion abnormalities, the extent and location of coronary artery stenoses, and the radiographic evidence of pulmonary venous hypertension were analyzed in a retrospective study of 40 patients who had surgically proven rupture of the interventricular septum after myocardial infarction. In 33 patients in whom chest films were available, interstitial or alveolar pulmonary edema was present in 78%, while left ventricular enlargement was present in 82%. Of 26 patients who had coronary angiography, complete occlusion of the right coronary artery, left anterior descending artery, or left circumflex artery was present in 92%, with few, if any, collateral vessels around the occlusion. The location of the rupture in the muscular septum was always in the region of akinesis or dyskinesis. Posterior defects were associated with posterobasal and diaphragmatic akinesis, and anterior defects with apical akinesis. Left ventricular aneurysms were adjacent to the septal rupture in 68%, and 74% had mitral regurgitation. The right ventricular diaphragmatic wall in posterior rupture was always akinetic, indicating right ventricular infarction. Thus ventricular septal defect after myocardial infarction (1) tends to occur with multiple coronary occlusions about which little collateral flow develops; (2) can accurately be localized anteriorly or posteriorly in the muscular septum by the location of the akinetic left ventricular wall segment; and (3) has an associated right ventricular infarct when rupture is posterior.
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PMID:Coronary, ventricular, and pulmonary abnormalities associated with rupture of the interventricular septum complicating myocardial infarction. 10 43

Complex study of blood platelet adhesion and aggregation, blood coagulation activity and oxidation-reduction processes was conducted in dynamics in 340 patients with myocardial infarction. in 53 of them before and after treatment with fibrinolysin and heparin. It is shown that in patients with myocardial infarction, particularly in the first days of the disease and with the development of cardiogenic shock and pulmonary edema, the adhesion and aggregation of blood platelets increase with parallel increase in the content of incompletely oxidized products in the blood. A definite parallelism was found between the changes in the kinetic properties of platelets and the oxidoreduction processes. A decrease in the platelet kinetic properties and improvement in the oxidation-reduction processes due to the effect of fibrinolysin and heparin were observed.
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PMID:[Effect of fibrinolysin and heparin on the kinetic properties of the thrombocytes and the oxidation-reduction processes in myocardial infarct]. 14 57

Clinical studies have long suggested the presence of a specific cardiomyopathy in sickle cell anemia secondary to intracoronary thrombosis and subsequent infarction. Fifty-two autopsy patients were studied (48 with SS hemoglobin, 4 with S-C or S-Thal hemoglobin) to ascertain the range of cardiac pathologic abnormalities associated with this disease. The average age was 17 years (range 1 month to 48 years). Renal failure and infection were the most common causes of death; the former was a more common cause in adults than in children. Right and left ventricular hypertrophy and dilatation were the most common abnormal pathologic findings. No evidence of recent or remote myocardial infarction, coronary thrombosis or arteritis was noted in any patient. Eight patients who were studied with postmortem coronary arteriograms exhibited markedly increased coronary arterial caliber with no evidence of atherosclerosis. Seventeen of the 52 patients studied had clinical evidence of congestive heart failure before death. Of these 17 patients, 7 had moderate to severe left ventricular hypertrophy associated with chronic renal failure and hypertension, 2 had right ventricular hypertrophy with organized pulmonary thrombosis, 2 had rheumatic mitral valve disease and 2 died during the second trimester of pregnancy. Two of the 17 patients thought to have pulmonary edema before death in fact had aspiration pneumonia and hemorrhagic pneumonitis, respectively. The data suggest that cardiac dysfunction in sickle cell anemia can usually be explained by the adverse effect of coexisting disease on the diminished cardiac reserve of chronic anemia. The data do not support the concept of a specific "sickle cell cardiomyopathy".
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PMID:Clinicopathologic analysis of cardiac dysfunction in 52 patients with sickle cell anemia. 15 Jul 86

Serial chest x-rays were used as a means of evaluating the hemodynamic status of 43 patients in acute left ventricular power failure (LVPF) complicating acute myocardial infarction who were assisted with balloon pumping. The following findings were reported: 1. In patients with acute myocardial infarction, prediction of the hemodynamic status on the basis of chest x-rays is less reliable when severe LVPF is present as a complication. 2. The incidence and severity of roentgenographic findings of congestive heart failure and pulmonary edema are increased in patients with severe LVPF compared to patients with uncomplicated myocardial infarction. 3. Improvement in the roentgenographic degree of heart failure with positive clinical and hemodynamic responses to 24 hr or less of balloon pumping is an indication that patients in severe acute LVPF may survive. Patients with deteriorating or unchanging chest x-ray findings have an extremely poor prognosis. These patients should be evaluated by cardiac catheterization and coronary arteriography to determine the appropriateness of emergency surgical correction.
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PMID:The chest x-ray in acute left ventricular power failure: an aid to determining prognosis of patients supported by intraaortic balloon pumping. 17 71

The clinical behaviour of 90 patients on beta-blocking drugs for established coronary heart disease who were admitted to a coronary care unit with prolonged ischaemic myocardial pain was compared with that of 90 similar patients not on this therapy. Transmural myocardial infarction was confirmed in 30 of the patients on beta-blockers and in 62 controls. A diagnosis of myocardial necrosis without infarction was made in 20 patients on beta-blockers and in 14 controls. Coronary insufficiency was diagnosed in 40 patients on beta-blockers and in 14 controls. The incidence of simus bradycardia, hypotension, syncope, and radiological pulmonary oedema was similar in the two groups. Established beta-blockade, therefore, has not been shown to prejudice the outcome of patients with coronary heart disease admitted to hospital with prolonged ischaemic myocardial pain. On the contrary, it may protect some patients from the development of a myocardial infarction.
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PMID:Long-term beta blockade: possible protection from myocardial infarction. 23 66

Forty-three patients (mean age 62 +/- 1 years) were treated for ventricular septal defect (VSD) secondary to myocardial infarction. Whenever possible, operation was postponed until six weeks post-onset chest pain. However, hemodynamic instability, evidenced by cardiogenic shock, refractory pulmonary edema, or a rising blood urea nitrogen (BUN) forced operation in 21 patients within 21 days post-infarct (Group I). In seven patients operation was performed three to six weeks post-infarct (Group II). In only eight patients could operation be delayed beyond six weeks post-infarct (Group III). Clinical deterioration, once begun, progressed rapidly, and could be reversed only temporarily by intra-aortic balloon pumping, used in 26 patients for safe conduct of cardiac catheterization and for peri-operative hemodynamic support. Hospital survival was achieved in 24 of the 36 operated patients (66%). In Group I patients, ten of 21 survived. In Group II, six of seven survived. In Group III, eight of eight patients survived. There have been five late deaths with a mean follow-up of 41 months in survivors. Improved survival has been achieved recently by the greater use of prosthetic material to replace necrotic muscle and by a transinfarct incision regardless of infarct location. Operative mortality before 1973 was 47%; mortality after 1973 was only 18%, with a concomitant reduction of mortality (30%) even in Group I patients.
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PMID:Surgery for post-myocardial infarct ventricular septal defect. 30 10

The first home dialysis was carried out from Guy's Hospital in London in 1968. Since then, 141 patients have been treated in this manner. The age of the patients ranged from 4 to 64 years. 24 patients have died (cerebrovascular accidents, myocardial infarction, pulmonary edema, sepsis, peritonitis, hyperkalemia etc.). Some of the deaths were due to a slackening of discipline on the part of the patients and nursing staff during the years of constant dialysis. Of 60 adults 52 were able to start work again; full rehabilitation still seems possible in 6 cases. Nevertheless, many patients cannot lead a normal life because their social and sexual activity is greatly restricted. The present economic crisis led to financial limitations in the National Health Service. In future, home dialysis may have to be reduced and more transplantations performed.
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PMID:[Guy's Hospital home dialysis program (author's transl)]. 41 3

Current evidence suggests that pulmonary edema accompanying human sepsis may result either from changes in the serum oncotic and hydrostatic pressures or an increase in the permeability of the pulmonary microvasculature. In this study, we compared the "clearance" of injected 131I-labeled human serum albumin from blood to bronchoalveolar secretions in intubated patients with pulmonary edema secondary to sepsis or myocardial infarction. A significantly increased mean +/- SE clearance of the radionuclide was seen in patients with sepsis (0.34 +/- 0.03 ml per hour) compared to those with myocardial infarction (0.043 +/- 0.008 ml per hour) (P less than 0.001), although both groups had similar degrees of edema on chest radiographs. Because the patients with sepsis had no severe decrease in serum oncotic pressure (18.4 +/- 5.0 mm Hg) or evidence of left heart failure, as determined by the pulmonary wedge pressure (11.0 +/- 6.8 mm Hg), we concluded that the genesis of the pulmonary edema in sepsis was due to an increase in pulmonary microvascular permeability, as measured by the increased clearance of 131I-labeled human serum albumin.
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PMID:Documentation of pulmonary capillary permeability in the adult respiratory distress syndrome accompanying human sepsis. 45 8

The authors examined 90 patients with myocardial infarction with a view to the lung changes developed and especially to the manifestations of pulmonary stasis. Series of face roentgenographies of the lungs were made of the patients in lying down position. In 76,7 per cent of the patients X-ray findings of pulmonary stasis were found. The dilated veins in the upper lung lobes are the earliest and most frequent manifestations, suggesting congestion. They are found in 23,3 per cent of the cases. Most important, among the X-ray findings, according to the authors, are those of perivascular edema--hilus images with widened and indistinct lines (24,4%). The X-ray findings of lung congestion and interstitial edema are early symptoms of pulmonary edema, in case the physical data from the lung examinations are negative. The therapeutic measures, at that stage, could prevent the development of a severe and very often fatal edema of the lungs.
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PMID:[Pulmonary changes in myocardial infarct]. 65 21


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