Effects of hydroxyethyl starch resuscitation on extravascular lung water and pulmonary permeability in sepsis-related acute respiratory distress syndrome.Crit Care Med. 2009 Jun; 37(6):1948-55.CC
Hydroxyethyl starch (HES) has greater volume expansion effect and longer intravascular persistence than crystalloids. HES also decreases microvascular permeability and capillary leakage by biophysically plugging endothelial leaks, exerting an anti-inflammatory effect, and decreasing activation of endothelial cells. The aim of our study was to determine whether medium molecular weight HES (pentastarch) resuscitation in the early stage of acute respiratory distress syndrome (ARDS) simultaneously increases cardiac output without worsening pulmonary edema and whether it attenuates pulmonary vascular permeability.
Prospective observational study.
Twenty-bed medical intensive care unit of a tertiary medical center.
Twenty patients with early-stage ARDS.
Volume expansion with a 500-mL infusion of 10% pentastarch (HES 200/0.5) at a rate of 10 mL/kg/hr.
MEASUREMENTS AND MAIN RESULTS
Baseline hemodynamics including systemic and pulmonary artery blood pressures, central venous pressure, pulmonary artery occlusion pressure, and cardiac output were obtained from an online HP Component Monitoring System and a pulmonary artery catheter. Intrathoracic blood volume (ITBV), global end-diastolic volume, extravascular lung water (EVLW), and pulmonary vascular permeability (EVLW/ITBV) were measured with a PiCCOplus monitor. Hemodynamic measurements were repeated immediately and 2, 4, and 6 hours after volume expansion. Pentastarch loading significantly increased central venous pressure, pulmonary artery occlusion pressure, pulmonary arterial pressures, and cardiac output. Pulmonary mechanics, venous admixtures, and EVLW values remained unchanged throughout the study. EVLW/ITBV significantly decreased immediately after the pentastarch infusion.
In patients with early ARDS, pentastarch resuscitation significantly improved their hemodynamics and cardiac output without worsening pulmonary edema and pulmonary mechanics. It even attenuated pulmonary vascular permeability.