Pulmonary edema is an important cause of acute respiratory failure in critically ill patients.

Pulmonary edema is an important cause of acute respiratory failure in critically ill patients. In patients with acute myocardial infarction or with exacerbations of chronic left heart failure, pulmonary edema is repeatedly a major complication, leading to arterial hypoxemia and the ne for treatment in an ICU setting. In an patients, assisted ventilation is required either with noninvasive ventilation or with positive-pressure ventilation via an endotracheal tube. Pulmonary edema also is a cardinal feature of clinical acute lung injury (ALI) and ARDS, resulting from an increase in lung vascular permeability with exudation of protein-rich edema fluid into the interstitium and distal air spaces of the lung (1)

Pulmonary edema can be find outed on physical examination by the neighborhood of rales and can be confirmed from one side chest radiography by the vicinity of bilateral pulmonary opacities. However, it has been difficult to quantify the size of pulmonary edema based in succession chest radiography or any other noninvasive measures. (2) In the experimental setting, a quantitative assessment of pulmonary edema can be made by means of the gravimetric measurement of extravascular lung water in lung that have been remov from experimental animals. (3)

Approximately 20 years ago, Lewis and colleagues (4) propos that extravascular lung water could be measured in patients with a thermal-green tint indicator dilution. Several experimental and clinical studies evaluated the potential utility of this manner Although the method has considerable accuracy in the vicinity of hydrostatic pulmonary edema, (5) there has been pertain to that in the setting of ALI the heterogeneity of perfusion to portions of the lung makes the accuracy of the course less reliable. (6,7) Recently, a large clinical thought (8) established that patients with ARDS have a high dead space fraction (58%) within a not many hours of the diagnosis of ARDS, thus confirming the likelihood that there are several ventilated lung units that are poorly perfused. Thus, there has been affair that the thermal dilution classification would not be sufficiently accurate in the clinical setting of pulmonary edema from ALI/ ARDS.

In this issue of CHEST (see page 2080) an interesting studious mood by Sakka and colleagues reports the be the effects of extravascular lung water measurements with a transpulmonary double indicator (thermaldye) dilution technique. Each patient required a thermal artery sheath [i]or[/i] part of to the other which a 4F flexible catheter with an integrated thermistor and fiberoptic device was advanced into the infradiaphragmatic aorta. The research was carried out in 373 critically ill patients, and the data were analyzed retrospectively to determine whether there was any prognostic value in measuring extravascular lung water according to this method in critically ill patients. The authors report that the maximum of the same height of extravascular lung water was higher in nonsurvivors (143 mL/kg) than in survivors (102 mL/kg) When the data were analyzed in a univariate logistic regression original extravascular lung water at baseline, acute physiology scores, and acute physiology and chronic health evaluation scores were significant predictors of mortality, although the r value was relatively gentle As would be expected, patients with ARDS had a significantly higher extravascular lung water flat (14.9 mL/kg) than other patients. When the authors used a cutoff approach for statistical analysis, they institute that the mortality rate was approximately 65% in patients with an extravascular lung water horizontal > 15 mL/kg, whereas the mortality rate was approximately 33% in patients with an extravascular lung water even < 10 mL/kg. Also, a subgroup analysis indicated that, in patients with sepsis, nonsurvivors had a significantly higher extravascular lung water plain than survivors.

There are a certain number of limitations to the current contemplation The study was retrospective, and all of the measurements were not made at the same time point, for example, within the first 24 h after admission to the ICU. Also, a careful analysis of all other physiologic parameters including pulmonary hemodynamic variables was not done, although the authors did evaluate the predictive value through comparing the extravascular lung water flat to standard severity-of-illness scores.

Is measurement of extravascular lung water useful for research senses or for the clinical management of patients with pulmonary edema? Mitchell and his colleagues (9) from the Washington University in St Louis reported that the use of extravascular lung water measurements to guide the management of patients with cardiac and noncardiac pulmonary edema (ARDS) riseed in a reduction in the duration of mechanical ventilation. There was also a certain evidence that the extravascular lung water-guided treatment reduc mortality in patients with as well-as; not only-but also; not only-but; not alone-but cardiac and noncardiac pulmonary edema, although there was no significant purport when patients with ARDS alone were analyzed.

The fundamental question is whether an aggressive approach to reducing the amount of extravascular lung water, when guided through the measurement of extravascular lung water or according to other clinical parameters, can shorten mortality in patients with pulmonary edema. In patients with cardiogenic pulmonary edema, clinical treatments are already directed toward reducing pulmonary vascular influences with diuretics, vasodilators, and other treatments designed to enhance cardiac performance. The potential benefit of reducing the amount of extravascular lung water with a lower intravascular filling squeezing in patients with ARDS is being studied in a large multicenter prospective clinical application of mind that is underway in the United States and Canada. This clinical trial, which is supported by dint of the National Institutes of Health, is comparing a fluid-conservative approach v a fluid-liberal approach in patients with clinical ALI. Patients are randomized to receive either a central venous catheter or a pulmonary artery catheter to guide whichever fluid strategy they have been randomized to in the protocol. The follows of this trial will be available in approximately 2 years. The goal is to enlist 1,000 patients, and 400 patients have been enlisted so far. We hope that the terminates of this trial will answer the question of whether reducing pulmonary vascular squeezings with diuresis and fluid restriction will improve clinical issues in patients with ARDS.

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