Cause Of Pulmonary Edema Research Articles

LUNG/HEART RATIO TC99m ALBUMIN STUDIES TO SEPARATE PULMONARY EDEHA DUE TO PRESSURE/VOLUME OVERLOAD FROM THAT DUE TO DAMAGED CAPILLARIES

The hypothesis tested was that edema resulting from pulmonary capillary damage is accompanied by an increased net leakage of molecules such as albumin from the vascular space into the lung, whereas edema resulting primarily from increased venous pressure is not. Tc99m albumin was injected intravenously in three groups of patients: normal, cardiac failure, and adult respiratory distress syndrome (ARDS). One minute of data from an anterior view of the chest was obtained at 20 minutes and 3 hours following injection of 20mCi. A lung heart ratio (L/H) was calculated placing a box region of interest over the right mid lung field and the middle of the cardiac silhouette. In absolute increase of less than 10% between L/H1 (20 min) and L/H2 13 hrs) included all normal patients. All but 2 of the 18 patients with heart failure or volume overload edema had a L/H ratio which increased less 10%. Patients with ARDS showed a spectrum of L/H ratio changes from less than 10% in all 6 with narcotic overdose to an increased ratio in 3/10 with pneumonia, 2 of 2 with seizures, one each with blood transfusion reaction, sickle cell disease, eclampsia and 1 of 2 with tuberculosis. Using a ratio change corrects for geometric factors, chest wall uptake, variable blood clearance rates and label loss. This simple procedure, adaptable to the bedside, clearly distinguishes a volume or pressure overload group showing no L/H change over time, from those with other causes of pulmonary edema. It suggests that ARDS contains a wide spectrum of capillary changes.

Abnormal pulmonary artery hemodynamics as a cause of pulmonary edema during resuscitation : Joseph P. Ornato, Jan L. Bredthauer. University of Nebraska, Omaha, NE 68105

Abnormal pulmonary artery hemodynamics as a cause of pulmonary edema during resuscitation : Joseph P. Ornato, Jan L. Bredthauer. University of Nebraska, Omaha, NE 68105

Postoperative Pulmonary Edema in Postcoronary Artery Bypass Graft Patients: Relationship of Total Serum Protein and Colloid Oncotic Pressures

A blinded, prospective study of 52 consecutive male patients undergoing coronary artery bypass grafting was designed to determine which factors were associated with pulmonary edema (PE) in the postoperative period. PE was demonstrated in 18 patients, but not in the remaining 34 patients. PE correlated with the maximum left atrial pressure (p <.001), but not with the degree of preoperative left ventricular dysfunction as manifested by ejection fraction. PE developed in nine of 18 patients at pulmonary capillary hydrostatic pressures (PCHP) ≤15 mm Hg, defining a population with noncardiogenic PE. Postoperative PE was associated with the degree of intraoperative dilutional hypoproteinemia which occurred to a varying degree in every patient. When the immediate postoperative total serum protein (TSP) was ≤4.0 g/dl, PE developed in 72 percent (13 of 18 patients), but occurred in only 15 percent (five of 34 patients) with levels above 4.0 g/dl. The calculated filtration gradient, reflecting the difference between the colloid oncotic pressure and the PCHP was The best univariate predictor of PE. When this fell to ≤2,100 percent (eight of eight patients) developed PE as compared to 12.5 percent (three of 24) above this value (p <.001). The magnitude of pump-induced, hemodilutional hypoproteinemia is the major cause of PE in patients with normal PCHP.

Ritodrine hydrochloride infusion in pregnant baboons: I. Biophysical effects

Pulmonary edema is a potentially fatal complication of β-sympathomimetic therapy for premature labor. Isolated case reports have supported either primary pulmonary capillary membrane injury or left ventricular failure as the cause of pulmonary edema. By simultaneously monitoring cardiac function and extravascular lung water in six control and six ritodrine hydrochloride-treated pregnant baboons, we attempted to define this pathophysiology. The pulmonary capillary wedge pressure increased in treated animals, reaching significance at 16 hours of ritodrine treatment (p < 0.0001) concurrent with the maximum increase in cardiac index (p = 0.02). Treated animals also retained 61% of intravenously administered fluids compared with 23% in untreated control animals (p < 0.002). There were, however, no significant differences between groups in extravascular lung water, central venous pressure, or pulmonary artery pressure. Chest radiographs and arterial blood gas analysis were also comparable between ritodrine-treated and control animals. Fluid retention and elevated hydrostatic pressure are postulated as the etiology of β-sympathomimetic-induced pulmonary edema. There was no evidence to support a primary pulmonary capillary membrane injury by ritodrine.

The spectrum of pulmonary edema: differentiation of cardiogenic, intermediate, and noncardiogenic forms of pulmonary edema.

Pulmonary edema fluid and serum samples were obtained from 20 patients with cardiac and noncardiac pulmonary edema, and total protein, albumin, and globulin concentrations were measured. The mean edema fluid to serum protein ratio in patients with pure cardiogenic pulmonary edema was 0.37 +/- 0.09. In contrast, the patients with pure noncardiogenic pulmonary edema had protein ratios of 0.84 +/- 0.12 (p less than 0.001). Another group of patients with both cardiac and noncardiac causes for edema demonstrated edema fluid to serum protein ratios that were significantly higher than those found in the cardiogenic patients and lower than the protein ratios in the noncardiogenic patients (0.60 +/- 0.07) (p less than 0.01) A cardiac or noncardiac causes of pulmonary edema could be determined in all patients, using edema fluid to serum total protein ratios in conjunction with globulin ratios. Cardiogenic and noncardiogenic pulmonary edema represent the extremes in the spectrum of pulmonary edema. A combination of increased permeability and hydrostatic pressure may account for an intermediate form of pulmonary edema.

Pulmonary oedema: a review.

Pulmonary oedema results from derangement of a normal physiological process which is continuously producing and removing extravascular lung water according to principles stated by Starling’s equation of fluid flow across semipermeable membranes. The parameters in Starling’s equation cannot all be measured. However, experiments have suggested that increased pulmonary capillary hydrostatic pressure forces fluid extravascularly, diluting the colloid osmotic pressure of tissue fluids and increasing the hydrostatic pressure of lung tissue fluids. Once these reserves and the ability of pulmonary lymphatics to remove lung water are overcome, pulmonary oedema results. This oedema can also result from reduced colloid osmotic pressure in the pulmonary capillaries and increased capillary permeability, even at low pulmonary capillary hydrostatic pressure. Perhaps because of the reserve created by colloid osmotic pressure of tissue fluids, hydrostatic pressure of lung tissue fluids and lymphatic drainage, pulmonary oedema accumulates at a slow rate initially, and at a much more rapid rate in later stages of oedema development. The rate of oedema formation may also relate to damage to the lung created by interstitial oedema, which opens the barrier to a later stage of alveolar oedema. While lung compliance is reduced with each successive increase in oedema formation, increased shunting and hypoxaemia do not result until alveolar oedema is present, in normal lung. The diagnosis of pulmonary oedema is best made by searching for causes of oedema and by chest radiographs. The management of pulmonary oedema must begin with maintenance of oxygenation of blood. This can best be achieved by applying continuous positive pressure ventilation (CPPV). CPPV does not remove lung water (in fact it may slightly increase it), but it does improve oxygenation by ventilating alveoli that were previously filled with fluid. The improved oxygenation buys time, so that therapy directed at the cause of pulmonary oedema (Starling’s law) can be applied. Since current knowledge is inadequate we do not know how to reverse an increased capillary permeability, other than by removing its cause; or how to reduce tissue colloid osmotic pressure, or to increase the hydrostatic pressure of lung tissue fluids or the intracapillary colloid osmotic pressure or the lymphatic flow of fluid. This leaves only increasing intracapillary colloid osmotic pressure or decreasing pulmonary capillary hydrostatic pressure as the means available to reduce pulmonary oedema. In the face of a non-compliant left ventricle colloid infusions may be dangerous, as the attendant increase in blood volume may increase pulmonary capillary hydrostatic pressure and worsen pulmonary oedema. If increased capillary permeability is the cause of pulmonary oedema, colloids might leak extravascularly and draw fluid with them. Therefore the most important therapy in pulmonary oedema, regardless of cause, is to reduce pulmonary capillary hydrostatic pressure. Depending on the cause of pulmonary oedema and the associated cardiac output, pul monary capillary hydrostatic pressure may be decreased by reducing left ventricular preload, increasing myocardial contractility, reducing left ventricular after-load or some combination of these. The anaesthetic implications are that Starling reserves are large and pulmonary oedema should not occur in the normal patient. In the patient with pulmonary oedema or reduced cardio-pulmonary reserve preoperatively, every effort must be made to optimize Starling’s forces before undertaking an anaesthetic in these life threatening situations.

The effect of sepsis and reduced colloid osmotic pressure on pulmonary edema

The interrelationship of hydrostatic pressure and osmotic forces across the capillary membrane are described by the Starling equation [lo]. Increasing pulmonary capillary hydrostatic pressure is a cause of pulmonary edema 131. Pulmonary edema develops at a lower hydrostatic pressure when plasma colloid oncotic pressure is lowered suggesting that the gradient between colloid oncotic pressure (COP) and pulmonary artery wedge pressure (PAW) is an important factor in the development of pulmonary edema [3]. Decrease in plasma oncotic pressure (COP) can also result in a reduction in the COP-PAW gradient. Pulmonary edema has been attributed to the reduction of the COP alone [7,8]. We have previously shown that reduction of the COP without elevation of the pulmonary artery wedge pressure does not result in pulmonary edema [14, 163. Sepsis is a common denominator in patients with respiratory failure [2] and it has been suggested that altered pulmonary capillary permeability is a possible cause for the development of pulmonary edema [ 11. The purpose of this investigation is to determine the effect of both reduced COP and sepsis on the development of pulmonary edema and pulmonary dysfunction in baboons.

Pulmonary Edema following Intracranial Hemorrhage

Hemodynamic changes and samples of fluid from pulmonary edema were studied in a 50-year-old woman who developed florid pulmonary edema following intracranial hemorrhage. Marked systemic and pulmonary arterial hypertension were associated with the rapid production of edema fluid that contained red blood cells, but had a lower protein content than plasma. After restoration of pulmonary vascular pressures to a normal range, the production of fluid ceased, and clinical signs of edema resolved. These findings point to the sudden increase in pulmonary microvascular pressure as the cause of pulmonary edema in this patient. Our findings contrast with those of previous reports and with speculations on the extent of a defect in permeability accounting for pulmonary edema following injury to the brain.

Current views on the mechanisms of pulmonary oedema

Understanding of the causes of pulmonary oedema must be based on knowledge of the mechanism responsible for fluid exchange between the several compartments of the normal lung. Recent physiological studies have clarified the main features of these mechanisms. However in three areas knowledge is still incomplete--the magnitude of the hydrostatic and oncotic forces responsible for fluid movement within the lung, the means by which protein leaks across the wall of small pulmonary vessels and the routes by which fluid and protein pass between the interstitial tissues of the lung and the alveolar space. Further work is needed in these areas. On the basis of this physiological knowledge the mode of development of hydrostatic oedema, the role of lymphatics in pulmonary oedema, and the several stages of pulmonary oedema development that may culminate in alveolar flooding are now clearly understood. Knowledge is less complete about oedema due to increased vascular permeability. In some experimental models, such as alloxan, leakage is due to irreversible injury to the alveolar wall; in other models, including ANTU, oedema formation has been shown to depend upon minor and reversible changes in pulmonary vascular endothelium similar to those that cause exudate formation in areas of acute inflammation. In no instance is detailed information available of both the rate and magnitude of protein leakage and of the morphological basis of increased vascular permeability. Further work is required in this area. Present knowledge allows an adequate explanation of the changes that occur in many clinically important types of pulmonary oedema, including cardiac failure and neurogenic pulmonary oedema. Other types of oedema, notably that which may complicate traumatic shock or extrapulmonary sepsis and high altitude pulmonary oedema, are more complex and the details of their pathogenesis are still obscure.

Diagnostic value of the portable chest x-ray technic in pulmonary edema

The ability of the portable chest x-ray film to define the amount of physiologic shunting and the severity of noncardiogenic pulmonary edema was evaluated in thirty-seven observations of eleven patients. Ten of the eleven patients were suffering from acute respiratory failure. The radiologic assessment of the amount of pulmonary edema and the severity of left ventricular failure were compared with the physiologic shunt fraction, tracer-measured lung water, and pulmonary arterial wedge pressure. The radiologic scores for edema did not predict the shunt fraction or tracer measurements of lung water. The radiologic score for congestive failure correlated with the wedge pressure but not well enough to be clinically useful. Five per cent of the x-ray results were false-positive and 11 per cent false-negative. Results indicate that the portable chest x-ray technic does not provide quantitative information regarding cardiopulmonary function. It is especially hazardous to accept an x-ray diagnosis of congestive failure as the cause of pulmonary edema.

Acute Airway Obstruction and Pulmonary Edema

To the Editor.— I read with interest the article, Pulmonary Edema as a Complication of Acute Airway Obstruction by Oswalt, Gates, and Holmstrom (238:1833, 1977). I was somewhat surprised to see the authors' statement that to their knowledge this condition has not been previously reported in the English literature. Airway obstruction leading to decreased intrathoracic pressure has been taught for many years by anesthesiologists as a common cause of pulmonary edema. It has been discussed in the English literature by Comroe et al, 1 Cherniack et al, 2 and Redding. 3 Comroe et al 1 considered this cause of decreased intrathoracic pressure as one of the four basic causes of pulmonary edema. I recommend these texts to the authors and interested readers as a review of this well-known and accepted basic cause of pulmonary edema. Decreased intrathoracic pressure caused by various forms of airway obstruction is being taught to the

Pulmonary Edema in Man and Animals.

This small volume attempts to present a comprehensive review of the experimental and clinical aspects of pulmonary edema. To me, its chief strengths were its recitation of the names of the various scientists who have studied the problem, (with brief mention of their specific contributions) and summaries of experimental approaches to mechanisms and management. It is well for the physician to be reminded of the diverse laboratory and clinical situations in which pulmonary edema may be encountered. The chief weaknesses are the incomplete description or lack of documentation of certain clinical states mentioned as causes of pulmonary edema, ie, uremia, bronchial asthma, pleurisy. The references are adequate in some sections and almost totally lacking in others. Certain of the material presented in earlier chapters is repeated later. The recommended measures for home, emergency room, and hospital treatment would not find universal acceptance and the dose of lanatoside C (Cedilanid) is

Paroxysmal pulmonary edema and the acute cardiac lung ∗

Paroxysmal pulmonary edema is defined, both in its pathologic and its clinical aspects. The various causes of pulmonary edema are listed, including medical, pediatric, surgical, neurologic, toxic and accidental conditions. The clinical episode and the possible variants of the attack are described. Various methods for inducing pulmonary edema in animals are mentioned. The mechanism of pulmonary edema is discussed. Osmotic changes and possible direct permeability changes are mentioned, but it is concluded that high pressure in the pulmonary capillaries is the most important factor. The various causes of increased left atrial and pulmonary venous pressure are discussed. The possible vascular and cardiac mechanisms of such increases are listed, and it is concluded that a “cardiovascular storm” involving both the peripheral vasculature and the left ventricle under the action of sympatho-adrenal stimulation is the most common occurrence. This may or may not be associated with left ventricular failure. Therapy of pulmonary edema is briefly discussed.

Pulmonary Edema Caused by Nitrofurantoin.

s1 May 1967Pulmonary Edema Caused by Nitrofurantoin.Robert H. Frankenfeld, M.D., F.A.C.P.Robert H. Frankenfeld, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-66-5-1055_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptPulmonary edema is a derangement of fluid balance in the pulmonary vasculature with causes and mechanisms more complex than mere failure of the left ventricle. Indeed, many instances occur in the presence of a normal heart. One of the unusual causes of pulmonary edema is sensitivity to nitrofurantoin. This is a specific response to this drug and is not related to other pulmonary reactions to drugs, such as asthma or pulmonary infiltration with eosinophilia.Five patients with this reaction are described, two of whom underwent hemodynamic study. The typical reaction consists of fever and pulmonary edema and is frequently confused... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Long Beach, California PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byDrug-Induced Respiratory Disease in Connective Tissue DiseasesChronic Nitrofurantoin (Furadantin) Pulmonary ReactionPleuropneumonic Reactions to NitrofurantoinPULMONARY REACTION TO NITROFURANTOINAllergic Pulmonary Complications During Treatment with NitrofurantoinChronic Nitrofurantoin Pulmonary Reaction 1 May 1967Volume 66, Issue 5Page: 1055-1055KeywordsAsthmaDrugsEdemaEosinophiliaFeversHeartHemodynamicsLeft ventricle Issue Published: 1 May 1967 PDF downloadLoading ...

Pulmonary edema

Pulmonary edema may be interstitial or alveolar or both; the roentgen appearance will vary according to the etiology and severity. Interstitial edema manifests itself by loss of sharpness around the hilus, haziness of the vascular markings and thickening of the interlobular and segmental septa. The most prominent and easily discoverable evidence of septal edema are the so-called B lines of Kerley. The edema often involves the interlobar pleurae. Free fluid in the pleural cavity may also be present. Early alveolar edema may have a miliary appearance, followed by coarse mottling, and finally by a rather homogeneous density. The characteristic picture is the so-called “butterfly” effect in which there is relative radiolucency of the periphery of the lungs demonstrable in all projections. In the more extreme cases, the density may extend to the periphery. In occasional cases, the edema may be confined to one segment, one lobe or one lung. Left heart failure is the most common cause of pulmonary edema and the typical roentgen findings generally make the diagnosis evident. When the patient presents with little or no cardiomegaly or atypical clinical findings, other etiologies must be sought. Some clues may be obtained from the roentgenogram, but clinical data are essential in determining the etiology. Pulmonary edema may be detected roentgenographically before it is clinically apparent.

Experimental Studies on Pulmonary Edema. : Part II: Seasonal influence on the production of pulmonary edema

Pulmonary edema has been studied extensively whereas the seasonal influence on the production of pulmonary edema has been barely investigated. The author carried out the experiments of pulmonary edema on the presumption of the season being influential on the cause of pulmonary edema.

Pulmonary edema of high altitude

Twenty-seven cases of pulmonary edema of high altitude are reported. The disease occurred at an altitude of 3,000 meters (9,900 feet) or higher. Pulmonary edema of high altitude was observed in persons with normal hearts and often in young subjects. It occurred during the first trip, or in one or more of the several trips, made to the higher altitude. Several patients were symptom free in previous and subsequent trips to the same altitude. The disease was often observed in normal subjects adapted to the altitude going back to the highlands after spending a variable length of time at sea level. Respiratory infections were an aggravating or precipitating factor. Pulmonary edema of high altitude was usually preceded by symptoms which, as a rule, appeared shortly after arrival at the high elevation. The knowledge of the premonitory symptoms is important to prevent death. The treatment of choice is oxygen or, when possible, descent to lower altitudes or sea level. The cause of pulmonary edema of high altitude is obscure. The various possible mechanisms are briefly discussed.

Therapy of experimental pulmonary edema in the dog: with special reference to burns of the respiratory tract.

The results of analysis of edema fluid and excised lungs show that there is leakage of protein-rich fluid into the lung tissue and ultimately into the respiratory passages. This leakage cannot be explained by the reduction in oxygen uptake as observed in lung tissue slices. The ultimate cause of pulmonary edema is not known. The survival time of anesthetized dogs suffering from thermal edema, can be prolonged by inhalation of oxygen and by administration of antihistaminic drugs and pulmonary vasodilators.

Pulmonary edema in acute heroin poisoning: Report of four cases

1. 1. Four cases of pulmonary edema secondary to acute heroin poisoning are reported. The characteristic features of this rare cause of pulmonary edema are mentioned. 2. 2. The pathogenesis of heroin-induced pulmonary edema is not clear. It is a manifestation of acute opium alkaloid toxicity.

The Roentgenological Manifestations of Pulmonary Edema

Considering the relative frequency of pulmonary edema, the paucity of references in the literature concerning its roentgen findings is astonishing. Standard texts on roentgen diagnosis contain only brief references to this condition; the descriptions in the literature deal largely with clinical cases, and few reports of cases verified by necropsy have been presented. Furthermore, the greatest emphasis has been placed upon a classical roentgen picture. In our experience there have been numerous variations from this typical appearance which we feel should be more fully described. Many of these variations simulate other pulmonary lesions to such a degree that frequent errors in diagnosis must result. For purposes of orientation, a brief review of the pathology and of the theories of the etiology of pulmonary edema must be undertaken. The pathology of pulmonary edema, consisting essentially of heavy, sodden lungs, with a microscopic picture of alveoli distended with serous fluid, is sufficiently well known to merit no further discussion. A distinction between pulmonary congestion and simple edema must be made. In the former there is dilatation of the blood vessels with venous stasis, but it is not necessarily accompanied by fluid in the alveoli. Eventually an accumulation of serum in the alveoli may occur as a result of congestion, in which case both will be present. Edema, however, when it is the result of other causes than circulatory failure, frequently occurs without a corresponding congestion of the blood vessels. It should also be pointed out that serum commonly accumulates in the alveoli as a result of atelectasis of the bronchial obstruction type, but in such instances the alveoli are collapsed rather than distended. The pathology of pulmonary edema and atelectasis may thus be confused, but a reasonable consideration of both the gross and microscopic characteristics of the two diseases should make the distinction possible. Likewise, the distinction between simple edema and that occurring with inflammatory processes is clearly obvious from the macroscopic and microscopic examination of lung tissue. Etiology The most common cause of pulmonary edema is generally considered to be left ventricular failure accompanied by a competent right ventricle which continues to pump blood into the pulmonary vascular bed. The increased pressure in the pulmonary system causes filtration into the alveoli resulting in edema of the lungs. There are, however, other causes as well, some of which have been best classified by Coelho and Ribeiro (3). 1. Claudication of the left ventricle such as occurs with renal sclerosis aortic insufficiency, and similar conditions. 2. Increased pulmonary venous pressure due to mitral stenosis. 3. Toxic substances such as neosalvarsan, iodides, and barbiturates.