Seminar in Respiratory Medicine最新文献

{"title":"Future Directions for Clinical Medicine","authors":"K. Brigham","doi":"10.1055/s-2008-1070987","DOIUrl":"https://doi.org/10.1055/s-2008-1070987","url":null,"abstract":"As summarized in the several other articles in this volume, understanding of the pathogenesis of pulmonary edema is rapidly increasing. Many lines of current research promise to provide dramatic new insights which will undoubtedly revolutionize the clinical therapy of edema resulting from acute lung injury. Such progress is based on an understanding of how injury and edema come about and how lung function is affected. The areas of basic research that appear most promising should be obvious from the preceeding articles. But what are the important implications for clinical medicine in the near future? There are several. New approaches to measuring critical pathophysiologic variables are being tested in humans or soon will be. Groups are collaborating to critically evaluate proposed therapies. Functional abnormalities of the lungs, critical to survival, are being measured and related to clinical course in humans.","PeriodicalId":311434,"journal":{"name":"Seminar in Respiratory Medicine","volume":"5 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1983-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"115408954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pulmonary Vascular Reactivity in Primary Pulmonary Edema","authors":"J. Newman","doi":"10.1055/s-2008-1070983","DOIUrl":"https://doi.org/10.1055/s-2008-1070983","url":null,"abstract":"The entire cardiac output traverses only one organ, the lung; thus, pulmonary blood flow equals cardiac output. Changes in blood flow through the lung can have profound effects on left ventricular filling (preload), systemic pressures, cardiac output, and tissue perfusion. Within the lung, the distribution of blood flow, in relation to the distribution of ventilation, determines oxygenation of the blood and elimination of carbon dioxide. Normal arterial oxygenation requires that pulmonary blood flow in its entirety must be matched to ventilation; this requirement is easily met in health, but requires compensatory mechanisms in disease. The distribution of blood flow is partly determined by pulmonary vascular responses (reflexes), and derangement of these regulatory responses can lead to hypoxemia, especially if there are concurrent airway abnormalities. The purpose of this section is to review the characteristics of normal pulmonary pressures and blood flow, describe mechanisms and effects of abnormal vascular responses in primary pulmonary edema, and suggest strategies for management of patients who demonstrate these abnormalities.","PeriodicalId":311434,"journal":{"name":"Seminar in Respiratory Medicine","volume":"4 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1983-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"123891844","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Roles of Arachidonic Acid Metabolites in Endotoxin-Induced Pulmonary Edema","authors":"M. Ogletree","doi":"10.1055/s-2008-1070984","DOIUrl":"https://doi.org/10.1055/s-2008-1070984","url":null,"abstract":"Pulmonary edema develops after insults that increase lung vascular permeability (primary pulmonary edema) and/or increase lung vascular pressures (secondary pulmonary edema). Secondary pulmonary edema often results from high vascular pressures during left heart failure. The causes of primary pulmonary edema are less well understood. For example, abrupt, severe pulmonary hypertension may injure lung capillaries causing focal increases in capillary permeability. Other possible sources of increased lung vascular permeability include complement activation, release of histamine or lysosomal enzymes, and synthesis of leukotrienes (formerly slow reacting substances) or toxic oxygen radicals, such as superoxide and hydroxyl radicals. At Vanderbilt's Pulmonary Circulation Center, we are studying the pathogenesis of primary pulmonary edema in chronically instrumented, unanesthetized sheep prepared for continuous measurement of vascular pressures and collection of lung lymph. We can elicit primary pulmonary edema by infusing small amounts of E. coli endotoxin, which consistently causes a reaction characterized by an early period of severe pulmonary hypertension lasting less than one hour (phase I), followed by a period of increased lung vascular permeability from three to five hours after endotoxemia. We and others have measured concentrations of various potential mediators and metabolites in lung lymph and blood plasma\" during the pulmonary vascular response to endotoxin. Several metabolites of arachidonic acid have endured as potential mediators of both pulmonary hypertension (such as thromboxane [Tx] A2) and increased lung vascular permeability (such as SRSA or leukotrienes). Since several aspects of the pulmonary vascular response to endotoxemia are reproducible in the same animal, we have also investigated the influences of numerous pharmacologic interventions on the endotoxin reaction. This article will summarize our current understanding of the involvement of metabolites of arachidonic acid in the pathogenesis of pulmonary edema after endotoxemia.","PeriodicalId":311434,"journal":{"name":"Seminar in Respiratory Medicine","volume":"27 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1983-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"131836489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Primary (High Permeability) Pulmonary Edema","authors":"K. Brigham","doi":"10.1055/s-2008-1070980","DOIUrl":"https://doi.org/10.1055/s-2008-1070980","url":null,"abstract":"Although edema, that is, accumulation of excess fluid in the lungs, occurs when filtration pressures are increased in the lung microcirculation and in response to lung injury, pathogenetically the two forms of edema are different. The previous two articles provide the basis for examining the differences. The diagnosis of high permeability pulmonary edema is made clinically by inference. If pulmonary edema is evident on chest radiograph and pulmonary arterial wedge pressure is normal or low, it is inferred that the edema must be a result of increased permeability of exchange vessels in the lung. Additional criteria usually required for diagnosis of the adult respiratory distress syndrome (ARDS) include severe hypoxemia and decreased lung compliance. Other data collected from patients who meet these criteria support the inference of increased vascular permeability: protein concentrations in edema fluid are high; equilibration of intravascular proteins with edema fluid is rapid. Normally, the lungs are protected against accumulation of fluid by increasing lung lymph flow (draining away excess filtered fluid) and decreasing interstitial oncotic pressure (counteracting the effects of increased vascular hydrostatic pressure). When permeability of lung microvessels is increased, these protective mechanisms are compromised.","PeriodicalId":311434,"journal":{"name":"Seminar in Respiratory Medicine","volume":"517 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1983-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"123104886","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Basics of Lung Fluid Balance","authors":"T. Harris","doi":"10.1055/s-2008-1070978","DOIUrl":"https://doi.org/10.1055/s-2008-1070978","url":null,"abstract":"Precise physiologic investigations of circulatory fluid balance date from the pioneering work of Starling.' More recently, attention has been focused on the properties of the lung microvascularinterstitial barrier, using concepts from membrane exchange developed by Kedem and Katcha)sky.2 The purpose of this article is to discuss the physiology of lung fluid balance using the physics of semipermeable membranes as a conceptual base.","PeriodicalId":311434,"journal":{"name":"Seminar in Respiratory Medicine","volume":"19 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1983-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"127118970","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editor's Perspective","authors":"T. Petty","doi":"10.1055/s-2008-1070988","DOIUrl":"https://doi.org/10.1055/s-2008-1070988","url":null,"abstract":"Acute pulmonary edema is a common medical emergency encountered frequently in all hospitals that deal with seriously ill patients. Acute pulmonary edema may occur on any ward in the hospital, in the intensive care unit, or present to the emergency room. It is clear that acute pulmonary edema is the final common pathway of a variety of processes well described by Dr. Brigham's group in this issue of Seminars. Common denominators include increased hydrostatic forces and alterations in permeability of the so-called alveolar capillary membrane. The final result is lung leak and at least some degree of flooding of gas exchange units of the lung. The presence of acute pulmonary edema is not difficult to recognize. Understanding the basic mechanisms underlying the development of the acute pulmonary edema is fundamental to organizing specific, physiologically oriented therapy. if the primary problem is hemodynamic, that is, a problem incident to events of the left side of the heartsuch as in ischemic heart disease with impaired cardiac output or valvular diseasea specific diagnosis can usually be made on the basis of history, physical examination, and both noninvasive and invasive assessments of cardiac function. if the problem encountered at the bedside is one of fluid overload, acting either alone or in combination with a degree of cardiac dysfunction, this fact can usually be established by a careful review of antecedent events, including the details of fluid administration. Thus, when the problem is primarily hydrostatic pulmonary edema, therapeutic approaches focus on correction of the underlying problem, employing diuretics, afterload reduction of the left ventricle, use of mo tropic agents, appropriate fluid restriction and supportive care with oxygen. In desperate situations, aortic balloon assist Editor's Perspective","PeriodicalId":311434,"journal":{"name":"Seminar in Respiratory Medicine","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1983-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"125853359","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Pulmonary Edema on Lung Mechanics","authors":"J. Snapper, J. Sheller","doi":"10.1055/s-2008-1070981","DOIUrl":"https://doi.org/10.1055/s-2008-1070981","url":null,"abstract":"It is useful to distinguish between cardiogenic and noncardiogenic pulmonary edema when considering the effects of pulmonary edema on lung mechanics. Pulmonary edema can be caused by an increase in the hydrostatic and oncotic pressures favoring fluid transudation from the capillaries to the pulmonary interstitium and airspaces, or by increased permeability of the pulmonary capillary endothelium. In some patients, a combination of altered driving pressures and permeability may contribute to the development of pulmonary edema. Since left heart failure and increased left atrial pressure are by far the most common causes of increased driving pressures favoring fluid transudation, this type of pulmonary edema is often labelled cardiogenic. In the adult respiratory distress syndrome (ARDS), or noncardiogenic pulmonary edema, pulmonary edema develops in the setting of normal driving pressures. Considerable clinical and experimental evidence supports the concept that the development of pulmonary edema in ARDS is causally related to increased permeability of the pulmonary capillary endothelium.' Since the alterations in lung mechanics associated with cardiogenic pulmonary edema and ARDS differ, the two types of pulmonary edema will be considered separately. These differences may have clinical implications in the therapy of both cardiogenic pulmonary edema and ARDS.","PeriodicalId":311434,"journal":{"name":"Seminar in Respiratory Medicine","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1983-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"130297176","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Secondary Pulmonary Edema","authors":"R. Parker","doi":"10.1055/s-2008-1070979","DOIUrl":"https://doi.org/10.1055/s-2008-1070979","url":null,"abstract":"Secondary pulmonary edema may result from mitral stenosis, mitral regurgitation, or left heart failure. Each of these pathologic conditions elevate left atrial pressure and thereby increase pulmonary microvascular pressure. However, the degree to which left atrial pressure is elevated will determine if intraalveolar edema will occur. The rate at which fluid will traverse the pulmonary microvascular membrane is dependent upon the balance of intravascular and extravascular hydrostatic pressures, the intravascular to extravascular oncotic pressure gradient, hydraulic conductivity of the pulmonary microvascular membrane, and the permeability of the pulmonary microvascular membrane to plasma proteins. The relationship of these pressures and characteristics of the pulmonary microvascular membrane can be described by the Starling Equation:","PeriodicalId":311434,"journal":{"name":"Seminar in Respiratory Medicine","volume":"6 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1983-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"130927209","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pathology of Pulmonary Edema","authors":"B. Meyrick","doi":"10.1055/s-2008-1070977","DOIUrl":"https://doi.org/10.1055/s-2008-1070977","url":null,"abstract":"Pulmonary edema is a common finding in many clinical conditions and is the result of increased fluid leakage from the pulmonary microcirculation. The increased leakage may occur at the level of the pulmonary capillaries or from the small intraacinar arteries and veins (these are sometimes referred to as extraalveolar or corner vessels). The protein concentration of th fluid varies with the type of edema. When fluid leakage is the result of increased pressure, it is protein-poor; when it is the result of increased permeability of the pulmonary vascular endothelium, it is protein-rich. In the lung, some fluid normally escapes from the microcirculation into the interstitial space. This fluid provides nutrients to the cells and to structures within the interstitium. Excess fluid drains through the interstitium to the lymphatics in the loose connective tissue sheaths surrounding the airways and larger arteries and veins (the penbronchovascular sheaths) and in the interlobular septae. This process also occurs in the pleura, the excess fluid here draining to the hilar lymph nodes by way of the interlobular septae. It is only when these pathways are overwhelmed that pulmonary edema develops. Initially, fluid accumu]ation is in the peribronchovascular sheaths; then, if fluid accumulation continues, edema of the alveolar wall is seen. Jntraalveolar edema occurs only when there is damage to the alveolar epithelial layer. Thus, Unless there is direct damage to the epithelial cell layer, intraalveolar edema represents a late, and often end-stage, finding. This review starts with a brief description of the structure and ultrastructural appearance of the cells that are involved or damaged when pulmonary edema develops. The second part deals with experimental studies that give insights into the mechanisms that contribute to or cause the various types of pulmonary edema.","PeriodicalId":311434,"journal":{"name":"Seminar in Respiratory Medicine","volume":"7 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1983-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126855296","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Granulocytes as Mediators in Pulmonary Edema","authors":"G. Bernard","doi":"10.1055/s-2008-1070985","DOIUrl":"https://doi.org/10.1055/s-2008-1070985","url":null,"abstract":"The precise role of white blood cells (WBC) in lung injury has long been a matter of great interest. Granulocytes were first suspected of involvement when microscopic tissue sections from patients dying with \"shock lung\" revealed inordinate numbers of granulocytes. These cells were found to be plugging capillaries and occasionally passing transmurally into lung interstitium. However, no cause and effect realtionship could be established; that is, it was not clear whether the granulocytes were responsible for the lung damage or whether there were chemataxins produced by the injured lung causing granulocyte sequestration. In 1968, Kaplow and Goffinet discovered the phenomenon of sudden but transient neutropenia which occurs with cellophane membrane hemodialysis. Further investigation of this process has demonstrated neutrophils deposited in the pulmonary microvasculature during the neutropenia. Complement activation is thought to be involved, and indeed fragments of the C5a portion of complement cause in vitro aggregation of granulocytes. Infusion of Gram-negative bacteria, complement, endotoxin, glass beads, fat emulsion, and many other materials into sheep prepared with chronic lung lymph fistulas has produced hypoxemia, pulmonary hypertension, increases in protein-rich lung lymph, leukopenia, and pulmonary leukostasis. Hydroxyurea-induced depletion of WBCs, especially granulocytes, markedly attenuates the pulmonary lymph flow response without affecting the early pulmonary hypertension. From this data, it has been concluded that activated granulocytes are required for the increase in microvascular permeability induced by endotoxin. The mechanisms by which activated granulocytes produce lung injury has recently been the subject of intensive investigation. The phenomenon of leukocyte activation in the presence of bacteria was discovered in 1933 by Baldri( [<je and Gerard. Neutrophils were found to increase their uptake of oxygen when exposed to the microorganism Sarcina lutea. The increase in oxygen uptake was later found to represent activation of a metabolic pathway by which oxidizing agents (free radicals of oxygen) are produced. The whole process by which this phenomenon occurs has come to be called respiratory burst. The discovery of superoxide dismutase (SOD) in 1968 began a flood of investigations into the biology of free radicals of oxygen. The relationship of SOD to anti-inflammatory activity was discovered in 1973 when Babior and others demonstrated that phagocytosing polymorphonuclear leukocytes (PMN) release large amounts of superoxide into the suspension medium. Further investigation established that the production of superoxide radicals was at least in part the bacteriocidal mechanism of leukocytes. Respiratory burst comprises many biologic reactions. Some of these have been demonstrated, others are suspected by indirect observations, and still others are conjectural. Respiratory burst is now known to be initiated not only by phagocyt","PeriodicalId":311434,"journal":{"name":"Seminar in Respiratory Medicine","volume":"13 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1983-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"129203759","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}