Rapid fluid loading is standard treatment for hypovolemia. Because volume expansion does not always improve hemodynamic status, predictive parameters of fluid responsiveness are needed. Passive leg raising is a reversible maneuver that mimics rapid volume expansion. Passive leg raising-induced changes in stroke volume and its surrogates are reliable predictive indices of volume expansion responsiveness for mechanically ventilated patients. We hypothesized that the hemodynamic response to passive leg raising indicates fluid responsiveness in nonintubated patients without mechanical ventilation.
Intensive care unit of a general hospital.
We investigated consecutive nonintubated patients, without mechanical ventilation, considered for volume expansion.
We assessed hemodynamic status at baseline, after passive leg raising, and after volume expansion (500 mL 6% hydroxyethyl starch infusion over 30 mins).
Measurements and Main Results:
We measured stroke volume using transthoracic echocardiography, radial pulse pressure using an arterial catheter, and peak velocity of femoral artery flow using continuous Doppler. We calculated changes in stroke volume, pulse pressure, and velocity of femoral artery flow induced by passive leg raising (respectively, Δstroke volume, Δpulse pressure, and Δvelocity of femoral artery flow). Among 34 patients included in this study, 14 had a stroke volume increase of ≥15% after volume expansion (responders). All patients included in the study had severe sepsis (n = 28; 82%) or acute pancreatitis (n = 6; 18%). The Δstroke volume ≥10% predicted fluid responsiveness with sensitivity of 86% and specificity of 90%. The Δpulse pressure ≥9% predicted fluid responsiveness with sensitivity of 79% and specificity of 85%. The Δvelocity of femoral artery flow ≥8% predicted fluid responsiveness with sensitivity of 86% and specificity of 80%.
Changes in stroke volume, radial pulse pressure, and peak velocity of femoral artery flow induced by passive leg raising are accurate and interchangeable indices for predicting fluid responsiveness in nonintubated patients with severe sepsis or acute pancreatitis.