Predictors of pulmonary edema formation during fluid loading in the critically ill with presumed hypovolemia*.

OBJECTIVE

It is largely unknown why extravascular lung water may increase during fluid loading in the critically ill with presumed hypovolemia. In this study we evaluated the hemodynamic predictors of such an increase.

METHODS

A prospective observational study.

METHODS

Sixty-three presumed hypovolemic mechanically ventilated patients (22 septic and 41 nonseptic patients).

METHODS

Fluid loading with saline or colloid fluids guided by (changes in) cardiac filling pressures.

RESULTS

Before and after fluid-loading, hemodynamic and respiratory variables were recorded, including variables obtained by transpulmonary dilution such as cardiac index, pulmonary blood volume index, and extravascular lung water. Baseline parameters and change in parameters were compared between patients with a change in extravascular lung water <10% and patients with a change in extravascular lung water ≥ 10%. Predictive values for change in extravascular lung water ≥ 10% were evaluated. Baseline cardiac index and pulmonary blood volume index were higher, whereas change in cardiac index, change in pulmonary blood volume index, and change in PaO2/FIO2 ratio were lower in patients with a change in extravascular lung water ≥ 10% than in patients with a change in extravascular lung water <10%. The change in extravascular lung water correlated to baseline cardiac index (r = 0.17; p = .001), baseline pulmonary blood volume index (r = 0.15; p = .001), change in pulmonary blood volume index (r = 0.16; p < .001), and change in PaO2/FIO2 ratio (r = 0.13; p = .004). In multiple logistic regression analysis baseline cardiac index, baseline pulmonary blood volume index, the change in cardiac index, change in pulmonary blood volume index, and change in PaO2/FIO2 ratio individually contributed to prediction of a change in extravascular lung water ≥ 10%, independent of the presence of sepsis, pulmonary vascular permeability, and cardiac filling pressures. A change in extravascular lung water ≥ 10% was predicted by baseline cardiac index (77% sensitivity, 98% specificity) and pulmonary blood volume index (92% sensitivity, 68% specificity), and by change in cardiac index (69% sensitivity, 59% specificity), change in pulmonary blood volume index (77% sensitivity, 82% specificity), and change in PaO2/FIO2 ratio (77% sensitivity, 66% specificity).

CONCLUSIONS

Extravascular lung water increase during fluid loading in the critically ill is predicted by a plateau of cardiac function and pulmonary vascular filling at baseline, rather than by pulmonary vascular permeability and filling pressures. Increasing extravascular lung water is further reflected by a decrease of PaO2/FIO2 ratio. These observations may help preventing pulmonary fluid overloading.