[Physiopathology of edemas. 8. Pulmonary edema. Pulmonary edema without pressure changes].
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Humans↗
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Results for “Pulmonary Edema”
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Clinical and radiologic features of pulmonary edema.
Pulmonary edema may be classified as increased hydrostatic pressure edema, permeability edema with diffuse alveolar damage (DAD), permeability edema without DAD, or mixed edema. Pulmonary edema has variable manifestations. Postobstructive pulmonary edema typically manifests radiologically as septal lines, peribronchial cuffing, and, in more severe cases, central alveolar edema. Pulmonary edema with chronic pulmonary embolism manifests as sharply demarcated areas of increased ground-glass attenuation. Pulmonary edema with veno-occlusive disease manifests as large pulmonary arteries, diffuse interstitial edema with numerous Kerley lines, peribronchial cuffing, and a dilated right ventricle. Stage 1 near drowning pulmonary edema manifests as Kerley lines, peribronchial cuffing, and patchy, perihilar alveolar areas of airspace consolidation; stage 2 and 3 lesions are radiologically nonspecific. Pulmonary edema following administration of cytokines demonstrates bilateral, symmetric interstitial edema with thickened septal lines. High-altitude pulmonary edema usually manifests as central interstitial edema associated with peribronchial cuffing, ill-defined vessels, and patchy airspace consolidation. Neurogenic pulmonary edema manifests as bilateral, rather homogeneous airspace consolidations that predominate at the apices in about 50% of cases. Reperfusion pulmonary edema usually demonstrates heterogeneous airspace consolidations that predominate in the areas distal to the recanalized vessels. Postreduction pulmonary edema manifests as mild airspace consolidation involving the ipsilateral lung, whereas pulmonary edema due to air embolism initially demonstrates interstitial edema followed by bilateral, peripheral alveolar areas of increased opacity that predominate at the lung bases. Familiarity with the spectrum of radiologic findings in pulmonary edema from various causes will often help narrow the differential diagnosis.
Altitude Sickness↗
Pathophysiology of pulmonary edema.
Pulmonary edema is a frequent and common cause of death in patients in critical care settings. It is seen as a complication of myocardial infarcts, hypertension, pneumonia, smoke inhalation, and high-altitude pulmonary edema. Pulmonary edema occurs when there are alterations in Starling forces and capillary permeability, opposition to lymphatic flow in the lungs, decreased plasma oncotic pressure, central nervous system lesions, and following some types of strenuous exercise. Pulmonary edema presents initially with crackles, wheezing, and dry cough and progresses to tachypnea, dyspnea, orthopnea, pink frothy sputum, and cyanosis. Treatment involves supportive therapy, reduction in blood volume, and oxygen therapy.
Critical Care↗
The role of pulmonary lymphatics in the clearance of hydrostatic pulmonary edema.
Pulmonary lymphatics are believed to play a major role in preventing the formation of pulmonary edema, but their role in clearance of established edema has not been defined. To measure the lymphatic contribution to the clearance of acute hydrostatic pulmonary edema, a lung lymph fistula was established in 16 anesthetized sheep. Pulmonary edema was induced by a rapid volume infusion of Ringer's lactate (six animals) or homologous plasma (six animals). Four control animals received no fluid. Simultaneous measurements of lymph flow and extravascular lung water (EVLW) were made. Data were analyzed for the resolution phase of pulmonary edema. The contribution of the pulmonary lymphatics to resolution was expressed as a percentage of total lung water resolved. Resolution rates for crystalloid and plasma infusion groups were 3.8 +/- 2.4 cc/kg/hr and 2.7 +/- 1.0 cc/kg/hr, respectively. There was no statistically significant difference between the groups in terms of EVLW increases or resolution rates. Net measured pulmonary lymph flow during the resolution phase of pulmonary edema was 0.33 +/- 0.18 cc/kg/hr and 0.39 +/- 0.20 and accounted for only 8.8 and 14.6% of resolved pulmonary edema in these respective groups. These data suggest the pulmonary lymphatic drainage plays a very minor role in the clearance of acute hydrostatic edema. The lungs appear to be capable of resolving as much as 40% per hour of increased extravascular lung water produced under these circumstances.
Animals↗
Noncardiogenic pulmonary edema.
Pulmonary edema is a consequence of high pressures in the pulmonary microcirculation (predominantly capillaries) or an increase in the permeability of the alveolar-capillary barrier (generally of its endothelial aspect) or a combination of both. It occurs when the rate of transudation from the capillaries exceeds the rate of lymphatic drainage from the interstitium. If the plasma oncotic pressure is low due to hypoproteinemia, transudation of fluid occurs at lower pressures. Permeability pulmonary edema is strongly influenced by fluctuations in pulmonary capillary pressures: an increase in pulmonary capillary pressure can add a large component of hemodynamic pulmonary edema to that originating in leaky vessels. Noncardiogenic forms of pulmonary edema are described.
Humans↗
Experimental pulmonary edema. IV. Pulmonary edema accompanying trauma to the brain.
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Brain↗
[Permeability pulmonary edema (neurogenic pulmonary edema) following isolated head and brain injury].
This paper reports on 3 patients with permeability pulmonary oedema accompanying an isolated head injury (neurogenic pulmonary oedema - NPE). The occurrence of a NPE in our patients with isolated head injury amounts to 0.62%. Comparing our case reports and results, respectively, with those published in the literature, the pathogenesis of NPE is discussed and delineated.
Adult↗
Swimming-induced pulmonary edema.
Pulmonary edema of water immersion, which is not associated with aspiration or a closed glottis, is infrequently described in the literature. Swimming-induced pulmonary edema is a syndrome whose pathophysiologic characteristics have not been fully elucidated. Immersion alone has marked effects on central vascular volume, redistribution of pulmonary blood flow, and lung volumes. These changes are more prominent in cold water. These changes, coupled with an elevated cardiac output, may expose regions of the capillary bed to high pressures that favor the extravasation of fluid by hydrostatic forces and potential stress failure of the capillaries. Patients with swimming-induced pulmonary edema present with dyspnea, cough, hypoxemia, and occasionally hemoptysis. Physical examination and chest radiographs usually reveal evidence of pulmonary edema. Treatment is symptomatic and conservative. Improvement and resolution of symptoms are usually rapid, with radiographic normalization in 24 to 48 hours. We describe here 3 cases of swimming-induced pulmonary edema.
Adult↗
[Pathogenesis of pulmonary edema. II. Pulmonary edema in dogs with vitium cordis and in vagotomized dogs with ligated lymphatic vessels].
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Animals↗
Uremic pulmonary edema.
Pulmonary edema fluid analyses and hemodynamic evaluations were performed in two uremic patients with acute pulmonary edema. The colloid osmotic pressure of the pulmonary edema fluid ranged from 57 per cent to 93 per cent that of the serum. Although cardiac function was normal in both patients, the serum colloid osmotic pressure--pulmonary artery wedge pressure gradients were markedly reduced. Uremic pulmonary edema is the result of alterations of pulmonary intravascular Starling forces and increases in pulmonary capillary membrane permeability, allowing for the efflux of protein-rich fluid from the capillaries into the lung.
Adult↗
Assessment of lung water by magnetic resonance in three types of pulmonary edema.
Pulmonary edema was produced in nine mongrel dogs by: (a) saline lavage; (b) intravenous injection of oleic acid; and (c) intravenous injection of propranolol followed by ureteral ligation. The resulting effect could be characterized by varying the protein concentration in the pulmonary edema fluid. After induction, all dogs were killed and 20 samples from each passively deflated lung were obtained. Proton T1 and T2 values were measured on a Praxis II NMR spectrometer operated at 10.7 MHz and 37 degrees C. The water content of all samples was determined gravimetrically. Correlation between T1 or T2 measured in vitro and the ratio of wet to dry weight was highly significant (r greater than 0.95, P less than 0.001) in each pathological state. Regression curves indicate that although all three types of pulmonary edema can be characterized by slightly different slopes, the differences are statistically insignificant. Moreover, the slopes of previous studies, when recast in the same format, are very similar to our findings despite the use of different magnetic field strengths and different animal models. This study indicates that quantitation of pulmonary edema is possible, but in vitro measurements do not give useful information for characterizing the etiology of pulmonary edema.
Animals↗
Lung mechanics in pulmonary edema.
Pulmonary edema can cause alterations in lung mechanics that directly contribute to clinical morbidity and mortality rates. Both the location of the edema fluid (interstitital versus alveolar pulmonary edema) and the etiology of the pulmonary edema contribute to the severity and type of abnormalities of lung mechanics observed. The alterations in lung mechanics associated with the adult respiratory distress syndrome may involve the direct effects of released mediators, alterations in pulmonary surfactant, and altered airway reactivity, as well as the direct effects of the edema fluid.
Animals↗
BW-755C diminishes smoke-induced pulmonary edema.
Pulmonary edema following smoke inhalation is due to the chemical toxins in smoke and not to the heat. We have shown that acrolein, a common component of smoke, induces pulmonary edema, perhaps via release of leukotrienes. We, therefore, hypothesized that acrolein, a component of smoke from burning cotton, might have a major role in producing pulmonary edema in sheep after cotton smoke inhalation and that BW-755C, a combined cyclo- and lipoxygenase inhibitor, would prevent the edema, whereas indomethacin, a cyclooxygenase inhibitor, would not. In control anesthetized sheep (n = 7), 128 breaths of cotton smoke induced no change in pulmonary arterial pressure but induced increases (P < 0.05) in pulmonary lymph flow from 4.4 +/- 0.8 (SE) to 15 +/- 2.7 ml/h, lymph protein flux from 0.25 +/- 0.08 to 0.80 +/- 0.16 g/h, and blood-corrected wet-to-dry weight ratios from a normal value of 3.8 +/- 0.07 (n = 9) to 4.5 +/- 0.18. Indomethacin (n = 6) did not significantly prevent these changes, whereas BW-755C decreased lung lymph flow change from 5 +/- 1 to 7 +/- 2 ml/h (P = NS), lymph protein flux from 0.25 +/- 0.08 to 0.35 +/- 0.1 g/h (P = NS), and weight-to-dry ratio from normal to 3.9 +/- 2.1 (P = NS). These data suggest leukotrienes may have a role in producing cotton smoke-induced noncardiogenic pulmonary edema.
4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
Laryngospasm-induced pulmonary edema.
Pulmonary edema after relief of airway obstruction due to laryngospasm is an uncommon but recognized entity. The authors report a case of a previously healthy young man who developed pulmonary edema after relief of laryngospasm following extubation of the trachea. Pulmonary edema after relief of acute airway obstruction should be included in the differential diagnosis of noncardiogenic pulmonary edema in the appropriate clinical setting.
Adolescent↗
Methods for detecting pulmonary edema.
Pulmonary edema appears to develop in three phases: after an initial injury to the lung, permeability of the air-blood barrier to water increases; a subsequent increase in movement of extra-vascular fluid; and finally, there is a significant increase in extravascular fluid volume (interstitial and alveolar). Ideally, early detection should monitor the initial phases of pulmonary edema, namely, the injury and the increased permeability. All established clinical and most of the research methods, however, monitor only the final or volume phase of the edema process. The chest radiograph is perhaps the most commonly used method for clinical detection of pulmonary edema, although it lacks the sensitivity for assessment of edema much before clinical signs are apparent. This paper reviews some of the clinical and research methods for detecting pulmonary edema with special emphasis on radiographic methods.
Acetylene↗
Acute postobstructive pulmonary edema.
Pulmonary edema developing after the relief of upper airway obstruction has been reported in association with a variety of factors including laryngospasm, foreign bodies, and tumors. However, as the phrase "negative pressure pulmonary edema" suggests, markedly negative intrapleural pressure is the dominant mechanism for the genesis of pulmonary edema associated with upper airway obstruction. A review for anesthesia providers of this poorly recognized and often perplexing syndrome may help to reduce the occurrence of this potential complication and facilitate its treatment.
Acute Disease↗
[Current concepts of pathophysiology, monitoring and resolution of pulmonary edema].
Pulmonary edema, both in its lesional as well as hydrostatic version, is a frequent cause of acute respiratory failure. From the pathophysiological point of view, the most important advance is undoubtedly the knowledge that the reabsorption process of pulmonary edema is an active process with energy consumption. This concept has revolutionized this field due to the possibility of finding substances or factors that stimulate or inhibit this reabsorption. Furthermore, in the monitoring field, significant advances have also been experimented due to the possibility of quantifying the edema in a simple and reliable way with transpulmonary thermodilution.
Acute Lung Injury↗
Noncardiogenic pulmonary edema.
Pulmonary edema is differentiated into two categories--cardiogenic and noncardiogenic. Noncardiogenic pulmonary edema is due to changes in permeability of the pulmonary capillary membrane as a result of either a direct or an indirect pathologic process. It is a spectrum of illness ranging from the less severe form of ALI to the severe ARDS. The mainstay of treatment is mechanical ventilation with maximization of ventilation and oxygenation through the judicious use of PEEP. Newer ventilation techniques, such as high-frequency oscillatory ventilation and partial fluid ventilation, are promising but are in the early stages of clinical testing. Mortality rates remain high despite increasing intensive care unit care.
Administration, Inhalation↗