[Physiopathology of edemas. 8. Pulmonary edema. Pulmonary edema without pressure changes].
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Humans↗
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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↗
[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↗
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↗
[Hemodynamic data in lesional pulmonary edemas].
Pulmonary edema due to disorders in alveolo-capillary permeability (or lesional) are differentiated from hemodynamic pulmonary edema by the fact that they arise in spite of normal pulmonary capillary pressure (PCP). A hemodynamic study was carried out in 42 cases of lesional P.E. The PCP was normal whatever the date of the examination and the gravity of the P.E. Pulmonary arterial hypertension was only found in the presence of frank hypoxemia and disappeared with the correction of the latter. If there was no hemodynamic profile due to P.E. itself, its etiology sometimes induced a hyperkinetic or hypovolemic syndrome. Finally it was apparent that PCP was significantly higher- although normal- at the initial stage than after 6 hours of P.E.; that an elevation in PCP of only a few mm Hg by the perfusion of colloids aggravated the P.E., that despite the normal value for the PCP dehydration evidently improved hematosis. Thus this study confirms that numerous cases of P.E. can occur while the PCP remains normal. It also confirms the noxious nature of too abundant perfusions in these cases and the effectiveness of dehydration.
Hemodynamics↗
Postpneumonectomy pulmonary edema.
Pulmonary edema is an uncommon but serious complication associated with major resection of the lung, usually after pneumonectomy. The pathophysiology of this condition is not completely understood, but recent experimental and clinical data suggest that this condition results from a combination of increased filtration gradient across the pulmonary microcirculation together with hyperpermeability. Overzealous perioperative infusions of fluid have been implicated in clinical cases. We present the reports of 2 patients with postpneumonectomy pulmonary edema we recently encountered and a review of the literature to provide diagnostic and therapeutic guidelines in dealing with this serious complication.
Aged↗
Negative pressure pulmonary edema.
Pulmonary Edema associated with negative airway pressure caused by upper airway obstruction is a most serious complications in anaesthetic practice (Tami et al, 1986). Laryngospasm associated with intubation and general anaesthesia is the most common cause of upper airway obstruction leading to negative pressure pulmonary edema (NPPE) in the anaesthetic adult (Tami et al, 1986). Other risk factors for the development of upper airway obstruction are identified, and individuals at risk should be observed closely while they remain at risk during the post anaesthetic period. NPPE appears to be related to markedly negative intrathoracic pressure due to forced inspiration against a closed upper airway resulting in transudation of fluid from pulmonary capillaries to the interstitium. The following is a presentation of a case of a healthy young male who developed NPPE secondary to airway obstruction caused by biting down on the endotracheal tube while awakening from general anaesthesia.
Adult↗
Pulmonary tissue volume in dogs during pulmonary edema.
Pulmonary tissue volume (Vt) and pulmonary capillary blood flow (Qc) were measured in anesthetized dogs by analyzing end-expiratory concentrations of dimethyl ether (DME), acetylene (C2H2), and sulfur hexafluoride during a 30-s rebreathing maneuver. Vt was compared to the postmortem lung weight of control dogs and dogs with hemodynamic and nonhemodynamic (alloxan) pulmonary edema. Qc was compared to the cardiac output measured by dye dilution. A 100-ml increase in alveolar volume (VA) in the range of 1-2 liters resulted in a 9 +/- 3 ml increase in Vt. Vt measured at a VA of 1.9 liters measures 114 +/- 18% of the postmortem lung weight in 20 control dogs and in 6 dogs with moderate edema (lung weight < 250% of predicted). Vt measured only 53 +/- 14% of the lung weight in 11 dogs with more severe edema. DME and C2H2 gave the smae mean values of Vt, but the reproducibility of a series of 3-7 measurements was greater with DME (coefficient of variation was 5% with DME and 8% C2H2). Qc measured 96 +/ 15% of the cardiac output during the rebreathing maneuver, but the maneuver caused a 4-40% fall in the cardiac output. These data show that Vt determined by rebreathing DME is between 86% and 135% of the lung weight in dogs with pulmonary edema until the lung weight is greater than 250% of the predicted value.
Animals↗
Postictal pulmonary edema requires pulmonary vascular pressure increases.
The pathogenesis of neurogenic pulmonary edema has been debated for many years. Whether cardiogenic mechanisms and increased pulmonary vascular pressures are primary or even necessary for the production of pulmonary edema has been argued. We used postictal pulmonary edema to study this problem in a sheep model of neurogenic pulmonary edema with bicucullin-induced status epilepticus. Seizure-induced increases in pulmonary vascular pressures were averted with a reservoir system to maintain left atrial pressure (LAP) and pulmonary artery pressure (PAP) at preseizure levels. No increase in lung lymph flow occurred during seizures, in contrast to the doubling of lung lymph flow that occurred during seizures when ictal pulmonary vascular hypertension was not blocked. These data support a primary role of pulmonary vascular pressure increases in the production of neurogenic pulmonary edema.
Animals↗
Decreasing hydrostatic pressure does not uniformly decrease high-pressure pulmonary edema.
Pulmonary artery wedge pressure (PAWP) of 30 mm Hg with left atrial balloon inflation for 1 1/2 hours produced pulmonary edema in eight dogs. PAWP was then decreased to 10 mm Hg for two hours, and shunt, lung water (extravascular thermal volume, or ETV, by thermal dye), and perfusion distribution (radiomicrosphere technique) were measured and compared with four other dogs (group 1) whose PAWP was maintained at 10 mm Hg. The eight dogs with PAWP of 30 mm Hg for 1 1/2 hours were retrospectively subdivided into two groups of four based on ETV (group 2, double baseline ETV; group 3, triple baseline ETV). Baseline ETV and shunt were similar for all groups and remained unchanged for group 1. At 1 1/2 hours, 2 hours (1/2 hour after decreasing PAWP), 2 1/2 hours, and 3 1/2 hours, respectively, ETV were: 13.9 +/- 1.9, 12.8 +/- 2.0, 9.3 +/- 1.5, and 8.5 +/- 1.0 ml/kg in group 2; and 21.9 +/- 2.1, 22.7 +/- 2.2, 22.5 +/- 2.0, and 22.2 +/- 2.0 ml/kg in group 3. A more variable rate of edema formation was detected in eight additional dogs, but failure to resolve higher levels of edema after decreasing PAWP was also demonstrated in this group. Edema was greatest in lower lobes and decreased lobar perfusion. Shunt was higher in group 3 than in group 2 at 1 1/2 hours and decreased in group 2 but not in group 3 at 3 1/2 hours. Changes in colloid osmotic pressure may account for the differences in edema formation and resolution, but our data suggest that, independent of the rate of edema formation, a decrease in vascular exchange surface area at higher levels of edema may inhibit edema resolution when PAWP is decreased.
Animals↗