{"title":"Pulmonary oedema","authors":"Samuel Oram","doi":"10.1016/S0366-0869(58)80079-9","DOIUrl":null,"url":null,"abstract":"<div><p>Acute pulmonary œdema is encountered in a great variety of patients, the commonest of which have cardiac disease, usually left ventricular failure or mitral stenosis. The severity may vary from fulminating to chronic. Two types of patient may be recognised, namely those with a high blood pressure and full pulse, and those with a low blood pressure, poor pulse and a tendency to shock.</p><p>The exact mechanism of the production of pulmonary œdema is still uncertain, but a high pulmonary capillary pressure, increased permeability of the pulmonary capillaries and a decrease in the osmotic pressure are the most important features. The level of the pulmonary capillary pressure in both left ventricular failure and mitral stenosis always exceeds the effective osmotic pressure of the plasma.</p><p>Emergency treatment is to prop the patient as upright as possible and if necessary insert a suction catheter down the trachea. Other useful agents in treatment are morphine, aminophylline, venesection, oxygen and mercurial diuretics. Digitalis should be used with caution. De-foaming agents are simple to use and seem worthy of further trial. Before using any particular method of treatment it should be determined whether a reduction in venous return is likely to prove beneficial, for example in patients with a raised blood pressure, or harmful, as in those with a low blood pressure and tendency to shock.</p></div>","PeriodicalId":100202,"journal":{"name":"British Journal of Tuberculosis and Diseases of the Chest","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1958-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0366-0869(58)80079-9","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"British Journal of Tuberculosis and Diseases of the Chest","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0366086958800799","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1
Abstract
Acute pulmonary œdema is encountered in a great variety of patients, the commonest of which have cardiac disease, usually left ventricular failure or mitral stenosis. The severity may vary from fulminating to chronic. Two types of patient may be recognised, namely those with a high blood pressure and full pulse, and those with a low blood pressure, poor pulse and a tendency to shock.
The exact mechanism of the production of pulmonary œdema is still uncertain, but a high pulmonary capillary pressure, increased permeability of the pulmonary capillaries and a decrease in the osmotic pressure are the most important features. The level of the pulmonary capillary pressure in both left ventricular failure and mitral stenosis always exceeds the effective osmotic pressure of the plasma.
Emergency treatment is to prop the patient as upright as possible and if necessary insert a suction catheter down the trachea. Other useful agents in treatment are morphine, aminophylline, venesection, oxygen and mercurial diuretics. Digitalis should be used with caution. De-foaming agents are simple to use and seem worthy of further trial. Before using any particular method of treatment it should be determined whether a reduction in venous return is likely to prove beneficial, for example in patients with a raised blood pressure, or harmful, as in those with a low blood pressure and tendency to shock.