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

The authors present two cases of unsuccessful hanging which hat lead to a very severe neurological picture and especially the very rapid appearance of acute pulmonary edema resulting in a vertiable flooding of the alveoli. The victims, aged respectively 21 and 15 years, were free from any pre-existing cardiopathy. These cases of pulmonary edema, resistant to depletive therapy (bleeding, diuretics) and cardiotonic agents (Cedilanid) should only be jugulated after a one hour session of oxygen at 3 ATA with a baro-assisted respirator. The following are discussed with reference to these two cases: 1- The mode of occurrence of this type of pulmonary edema: - implication of sub-acute anoxic cerebral damage; - high negative alveolar pressures owing to a gasp-type ventilation with a closed glottis. 2- The opportunity for the very early treatment of the oxygen deficit contracted by the brain and myocardium.
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PMID:[Pulmonary edema in hangings]. 0 73

A case of acute pulmonary edema after subarachnoid hemorrhage is presented. A supra and infratentorial arteriovenous malformation was revealed by serial cerebral angiography. Sequential chest films documented regression of both, pulmonary edema and cardiac enlargment. The literature is reviewed and a possible physiopathology is discussed.
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PMID:[Acute neurogenic pulmonary edema]. 16 44

Acute fulminating pulmonary edema developed in three patients after acute airway obstruction secondary to tumor, strangulation, and interrupted hanging (one case each). The common etiologic factor was vigorous inspiratory effort against a totally obstructed upper airway. Acute pulmonary edema followed the event in minutes to hours and required ventilatory assistance to maintain oxygenation. All patients eventually responded to fluid restriction, diuretics, and steroids. One case was complicated by aspiration of gastric contents following respiratory failure. To our knowledge, this condition is previously unreported in English literature. We presume that the pathogenesis is related to alveolar and capillary damage, induced by the severe negative pressure generated by attempting to inspire against the closed upper airway.
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PMID:Pulmonary edema as a complication of acute airway obstruction. 33 33

This report describes a patient who developed acute pulmonary edema as a complication of Plasmodium falciparum malaria. Hemodynamic evaluation revealed a pulmonary artery wedge pressure of 3 mm Hg and a cardiac index of 4.6 liter per min per m2. The patient exhibited an acute decrease in serum colloid osmotic pressure from 25.1 mm Hg to 16.8 mm Hg. These findings suggest that pulmonary edema in this patient was the result of altered capillary membrane permeability.
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PMID:Acute pulmonary edema in Plasmodium falciparum malaria. 35 80

We have presented a case of acute fulminating pulmonary oedema, not cardiogenic in origin, occurring at the end of anaesthesia. This precise diagnosis was made with the help of measurement of the capillary wedge pressure and cardiac output as well as analysis of the alevolar oedema fluid. The haemodynamic values and the gas exchange, as measured under various ventilatory patterns, confirms the usefulness of continuous positive pressure ventilation (CPPV). In the genesis of acute pulmonary oedema as described, the role of hypoxia and acute obstruction of the upper airways as presented by the patient is discussed in the light of the present proposed theories.
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PMID:[Non-cardiac acute fulminating pulmonary edema occurring at the end of anesthesia]. 36 39

Artificial ventilation with positive end-expiratory pressure (PEEP) reduces venous return by raising intrathoracic pressure. To determine whether PEEP decreases cardiac output further by depressing myocardial function, we constructed Starling curves, using rapid dextran infusion in 7 anesthetized dogs ventilated with zero (ZEEP) and 20 cm PEEP. The changes in stroke volume and in left ventricular stroke work (LVSW) when PEEP was added or removed were significantly greater than could be attributed to the corresponding change in transmural left ventricular end-diastolic pressure (LVEDPTM) on these Starling curves. To the extent that PEEP did not alter left ventricular diastolic volume-pressure characteristics, these data indicated PEEP depressed ventricular function. Identical changes with PEEP in cardiac output (-30%), esophageal pressure (+10 cmH2O), and left ventricular function were observed after pulmonary edema was induced with oleic acid. These results confirm and extend recent suggestions that high levels of PEEP depress left ventricular function in dogs, accounting for about half of the reduction in cardiac output before and during acute pulmonary edema.
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PMID:Effect of positive end-expiratory pressure on ventricular function in dogs. 37 68

Pulmonary edema is common cause of acute respiratory failure and can be seen in not only cardiac but also noncardiac diseases. The pathophysiologic mechanism for the development of acute pulmonary edema in any clinical situation can usually be explained alterations in the forces governing the transvascular flux of fluid in the pulmonary microvasculature, according to the Starling equation. "Cardiac" pulmonary edema is primarily due to an increase in the capillary hydrostatic pressure of sufficient magnitude to overcome the forces maintaining fluid within the vessel and the ability of the lymphatics to drain the transudated fluid. On the other hand, pulmonary edema occurring in association with noncardiac disease (e.g., sepsis, aspiration or shock) is secondary to an increase in the permeability of the pulmonary microvasculature and is referred to as noncardiogenic pulmonary edema or the adult respiratory distress syndrome. This article examines the mechanisms for the development of pulmonary edema and discusses the differences between the cardiac and noncardiac types.
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PMID:Pathogenesis of pulmonary edema associated with the adult respiratory distress syndrome. 37 80

Acute pulmonary edema developed in two young, previously healthy women immediately after the intravenous administration of contrast media. The pulmonary edema, rare in young persons, could not be explained by classical anaphylaxis, contrast media overdose, sodium and fluid overload, or acute myocardial infarction. A nonimmunologic osmotic mechanism causing reversible pulmonary capillary leak might explain the clinical events observed in both patients. Both responded to continuous positive airway pressure (CPAP), indicating the possible utility of CPAP in treating pulmonary capillary-leak contrast reactions.
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PMID:Acute pulmonary edema after the intravenous administration of contrast media. 38 41

Five patients are reported who developed evidence of acute lung damage after proved ingestion of paraquat. In two the lung changes resolved; in one an aspiration pneumonia occurred, which was successfully treated, while two developed fatal pulmonary oedema. These pulmonary complications after paraquat intoxication appear more common than the progressive pulmonary fibrosis previously described. It is suggested that acute pulmonary oedema is a response to large doses, usually of Gramoxone, that subclinical lung changes result from small doses, usually of Weedol, and that pulmonary fibrosis occurs after intermediate doses. Preliminary data on plasma paraquat concentrations suggest that these are of value in prognosis.
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PMID:Further clinical observations on the pulmonary effects of paraquat ingestion. 48 82

We describe a patient who presented with acute massive pulmonary edema, clinically and on chest roentgenogram. Two hours later the patient became hypotensive and was found to have a low pulmonary capillary wedge pressure (PCWP). The blood pressure returned to normal after administration of fluids. Acute pulmonary edema develops if PCWP rises higher than 25 to 30 mm Hg. In our patient, the elevated PCWP fell to low normal within two hours, when chest roentgenogram and clinical examination still suggested severe pulmonary edema. A phase lag existed between lowering of the pulmonary capillary wedge pressure and clearing of fluid from the alveolar and interstitial spaces in the lungs. At least three different pathogenetic mechanisms in patients with coronary artery disease can produce this phase lag. Transient global ischemia of the left ventricle was thought to be the responsible mechanism in our patient.
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PMID:Cardiac-pulmonary edema and low pulmonary capillary wedge pressure. 50 73


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