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

Severe pulmonary edema occurred in a patient during the third trimester of two consecutive pregnancies, 17 months apart. Noncardiac origin of the pulmonary edema was demonstrated by normal pulmonary capillary wedge pressures, normal roentgenographic cardiac dimensions with absence of effusions, normal echocardiographic ejection fraction, and elevated thermodilution cardiac outputs; moderate reduction in serum albumin levels may have contributed. In the setting of pregnancy-induced hypertension, the development of ARDS on each occasion suggests a pathophysiologic link.
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PMID:Recurrent noncardiac pulmonary edema accompanying pregnancy-induced hypertension. 195 25

Perfusion scintigraphy of the lungs has shown that a reverse direction of postural reactions of the pulmonary blood flow is observed in patients with mitral valvular disease: perfusion of the upper lung rather than the lower lung increases. It is accounted for by the action of gravitation on capillary hydrostatic pressure resulting in the localization of interstitial edema in pulmonary venous hypertension mainly in the lower lung, its microcirculatory bed being compressed and the blood flow redistributed to the opposite upper lung. Therefore successive perfusion scintigraphy of the lungs in the vertical position and in the lateral position with a RP administered twice, can serve as a sensitive test for diagnosis of interstitial lung edema in various pathological conditions.
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PMID:[Radionuclide diagnosis of interstitial pulmonary edema]. 199 78

A spectrum of presentation of phaeochromocytoma in black South Africans is described. Ten patients were reviewed over a 9-year period. Sweating, headache, and palpitations were prominent symptoms in 9 patients; postural dizziness occurred in 5; gastro-intestinal symptoms in 7; diabetes in 3; and hypertension in all. One patient developed a phaeochromocytoma crisis, characterised by hypotension and pulmonary oedema, before operation. One woman presented in pregnancy. Urinary vanillylmandelic acid was elevated in 9 out of 10 subjects tested; plasma catecholamines were elevated in 6 out of 6 tested. Computed tomography detected 7 adrenal tumours and 3 paragangliomas. All patients were stabilised pre-operatively with alpha- and/or beta-receptor blockers. Intraoperative pressor crises were controlled with sodium nitroprusside, phentolamine, or magnesium sulphate infusions. At operation all tumours appeared benign, each was successfully removed, and the diagnosis confirmed on histological examination. There was no operative mortality. Two patients had residual hypertension. This study highlights the various challenges presented by this catecholamine-producing tumour.
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PMID:Phaeochromocytoma. A report of 10 patients. 199 41

Pulmonary edema is a common concomitant of valvular heart disease and ventricular dysfunction. In addition, left atrial dysfunction due to thrombus, myxoma, or cor triatriatum can produce the same clinical picture. We encountered a patient with intractable pulmonary edema secondary to obliteration of the left atrial cavity by an extrinsically compressing lung tumor. We believe extrinsic compression of the left atrium caused impaired left atrial filling, leading to pulmonary venous hypertension and pulmonary edema.
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PMID:Pulmonary edema due to extreme left atrial compression. 200 Jan 87

The importance of recognizing symptomatic heart failure with preserved left ventricular (LV) systolic function has only recently been appreciated. To determine its frequency and identify clinical features that make the bedside diagnosis likely, 82 patients admitted for decompensated heart failure were classified into 2 groups based on their LV systolic performance, as defined by fractional shortening (FS): group I (n = 59), with impaired systolic function (fractional shortening less than 24%), and group II (n = 23) with preserved systolic function (fractional shortening greater than or equal to 24%). Mean fractional shortening was 15 +/- 5% and 39 +/- 1% for groups I and II, respectively. Female gender (p less than 0.05), obesity (p less than 0.01) and diastolic blood pressure greater than or equal to 105 mm Hg (p less than 0.05) predominated in group II. Jugular venous distention was identified more frequently in group I (p less than 0.05). No statistically significant difference between the 2 groups was noted among various demographic variables (age, duration of symptoms, history of hypertension, ischemic heart disease and heavy alcohol drinking) or physical findings (S3 gallop, edema, cardiomegaly, pulmonary congestion and pulmonary edema). Echocardiographic mean left ventricular dimension measured 6.6 +/- 1 versus 5.0 +/- 1 cm (p less than 0.01) and mean posterior wall thickness 1.1 +/- 0.3 versus 1.4 +/- 0.4 cm (p less than 0.01) in group I and II, respectively. The combination of diastolic blood pressure greater than or equal to 105 mm Hg and an absence of jugular venous distention had a high specificity and positive predictive value (100%) for identifying group II patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bedside diagnosis of preserved versus impaired left ventricular systolic function in heart failure. 173 66

Endothelins are endothelial cell-derived peptides with potent vasoconstrictor properties. We investigated the actions of porcine/human endothelin-1 (ET-1) on the microvasculature of the guinea pig lung perfused at constant flow with Ringers-albumin. We measured the perfusion pressure, distribution of pulmonary vascular resistance (using the double occlusion method), lung weight change, and the pulmonary capillary filtration coefficient. At concentrations of greater than or equal to 10(-10) M, ET-1 produced dose-dependent increases in mean pulmonary artery pressure (EC50, approximately 10(-9.5) M), which were rapid in onset and biphasic (first phase peaking at 1-2 minutes; second phase peaking at 10-15 minutes) up to 60 minutes of the perfusion period. The vasoconstrictor response was sustained for the 60-minute perfusion period. The pulmonary vasoconstriction was inhibited by pretreatment with indomethacin (10(-5) M), the thromboxane A2 receptor antagonist SQ-29,548 (4 x 10(-6) M), or papaverine (10(-5) M). Nifedipine (10(-5) or 10(-7) M) had no effect on the first phase but prevented the second phase of the vasoconstriction. The vasoconstriction was primarily the result of a 10-fold increase in pulmonary venous resistance. Pulmonary edema developed after ET-1 challenge because of the venoconstriction and the resultant pulmonary capillary hypertension. However, the pulmonary capillary filtration coefficient was unchanged, indicating that pulmonary vascular permeability did not increase. ET-1 also had no effect on transendothelial 125I-albumin flux. The results indicate that ET-1 is a potent thromboxane-dependent venoconstrictor in the guinea pig lung.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanism of endothelin-1-induced pulmonary vasoconstriction. 205 31

Since Shumway carried out the first successful heart-lung transplant (HLT) in Stanford in 1981, HLT has become a new therapeutic means for patients with end-stage pulmonary disease or arterial hypertension. However, it is still rarely carried out because of a lack of donors and the complexity of the surgery and postoperative course. This review described the criteria for proper donor and recipient selection, as well as the anaesthetic and postoperative management of HLT patients at Marie Lannelongue Hospital. The lack of suitable organ grafts results, at least in part, from improper donor management. Pulmonary oedema by fluid overloading and excessive haemodilution should be carefully prevented. Low doses of catecholamines and vasopressin maintain circulatory stability and convenient organ function. The indications for HLT (primary pulmonary hypertension, Eisenmenger's complex, and end-stage bronchopulmonary disease) are all characterized by severe pulmonary hypertension, hypoxaemia and cardiac failure. Careful anaesthetic induction is required to avoid circulatory collapse. Cardiopulmonary bypass (CPB) should be started early, so that mediastinal dissection may be carried out in satisfactory haemodynamic conditions. After unclamping the aorta, circulatory support with fluid and catecholamine infusion is often required. High inspired oxygen fraction and end-expiratory positive pressure may be required because of reperfusion pulmonary oedema. Blood transfusion is often needed as there are major blood losses due to dissection of the posterior mediastinum during CPB. Postoperative catecholamine administration is prolonged over several days. Negative fluid balance is often necessary to reduce pulmonary oedema. Improvement in surgical technique, early extubation, and late prescription of steroids have reduced the incidence of tracheal complications. Acute renal failure often occurs as a result of prolonged CPB, hypovolaemia, drug nephrotoxicity and sepsis. Bacterial complications (pneumonia, mediastinitis) are the main causes of early death. After the 15th postoperative day, opportunistic infections and allograft rejection are the main complications. Since 1981, major advances in HLT recipient management resulted in improved survival rates (70-80% at 1 year, and 60-70% at 2 years for the best teams). Despite the complexity of management, and the longterm threat of obliterative bronchiolitis, HLT is, at present time, the only possibility for these young patients to recover a normal quality of life.
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PMID:[Anesthesia and intensive care for heart-lung transplantation]. 205 32

A good model of adult respiratory distress syndrome is lung injury induced by phorbol myristate acetate (PMA). In the present study we examined the effect of mepacrine, an inhibitor of phospholipase A2, on lung injury induced by PMA in isolated blood-perfused rat lungs. In the isolated lung, saline (1 ml) or mepacrine (75 microM) alone in the perfusion system did not discernibly change the pulmonary arterial pressure (PAP) and lung weight (LW). After administration of PMA (0.16 micrograms/ml), severe hypertension and lung edema developed (delta PAP = 40.1 +/- 6.0 mmHg, p less than 0.001; delta LW = 5.5 +/- 0.7 g, p less than 0.001). Whereas, the addition of mepacrine (75 microM) prevented PMA-induced lung edema and pulmonary hypertension (delta PAP = 4.7 +/- 2.2 mmHg, delta LW = 0.2 +/- 0.2 g). To further elucidate the protective mechanism of mepacrine on lung injury, a vasodilator (nitroprusside) was given to decrease PAP levels to +6 mmHg from baseline values in the PMA group, as well as in the mepacrine-pretreated PMA (MPMA) group. During a subsequent venous pressure challenge, severe lung injury developed in the PMA group (delta LW = 9.5 +/- 2.1 g, p less than 0.001). However, with the same venous pressure challenge in the MPMA the lung weight was markedly less than that of the PMA group (delta LW = 1.0 +/- 0.2 g). Histologic findings examined by light microscopy presented intraalveolar hemorrhage and fluid accumulation, disruption of vascular basements and alveolar septa, and aggregation of inflammatory cells within the parenchyma in the lungs of the PMA group. In the MPMA group there was no evidence of intraalveolar hemorrhage and alveolar fluid accumulation, however, the occasional presence of granulocytes in the parenchyma and slight interstitial edema were still observed. In addition, depressed the chemiluminescence release from PMA activated granulocytes which were in a dose-dependent manner in vitro. These observations suggest that mepacrine inhibits PMA-induced lung injury chiefly by protection of vascular permeability. The mechanism of the protection may be due to the inhibition of oxygen radicals released from activated neutrophils and the reduction of neutrophil chemotaxis.
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PMID:The protective effect of mepacrine on acute lung edema induced by phorbol myristate acetate in rats. 209

Edema of the lungs complicates the course of closed and concurrent trauma of the chest in 24.2% of cases. Depending on the system with the primary trauma, three types of lung edema may occur according to the clinical course and character of pathophysiological disorders: cardiogenic (28.3%)--in primary trauma or pathology of the heart with the cardiac insufficiency syndrome; noncardiogenic (34.3%)--in contusion or pathology of the lungs with development of the hypertension syndrome; edema of a mixed form (37.4%) induced by hypovolemia in blood loss and shock with the development of the "small cardiac output syndrome". It is just their pathogenetic essence which determines the character of intensive therapy. The lung edema mortality rate is 11.6%, maximum mortality rate (9.1%) occurs in edema of a mixed form.
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PMID:[Lung edema in closed injury of the chest and polytrauma]. 214 89

A prospective study of acute nephritis in children was conducted at the Universiti Sains Malaysia Hospital, Kubang Kerian between July 1987 and June 1988. One hundred and twenty four children were admitted with acute glomerulonephritis. The aim of the study was to determine the clinical pattern of the nephritis as well as its aetiology. The majority of our patients came from the lower socio-economic group and 54% of the families had incomes below the poverty line. Preceding skin infection was much more common than throat infection. The children showed a high incidence of complications: severe hypertension (43.6%), hypertensive encephalopathy (11.3%), clinical pulmonary oedema (36.3%), severe azotaemia (10.5%), and prolonged gross haematuria (13.7%). By using immunologic indices such as ASOT, anti-DNase B and complement 3, it was concluded that 121 of the 124 patients had post-streptococcal nephritis.
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PMID:Acute glomerulonephritis in Kelantan--a prospective study. 215 16


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