Abstract
BackgroundHigh tidal volume ventilation has shown to cause ventilator-induced lung injury (VILI), possibly contributing to concomitant extrapulmonary organ dysfunction. The present study examined whether left ventricular (LV) function is dependent on tidal volume size and whether this effect is augmented during lipopolysaccharide(LPS)-induced lung injury.MethodsTwenty male Wistar rats were sedated, paralyzed and then randomized in four groups receiving mechanical ventilation with tidal volumes of 6 ml/kg or 19 ml/kg with or without intrapulmonary administration of LPS. A conductance catheter was placed in the left ventricle to generate pressure-volume loops, which were also obtained within a few seconds of vena cava occlusion to obtain relatively load-independent LV systolic and diastolic function parameters. The end-systolic elastance / effective arterial elastance (Ees/Ea) ratio was used as the primary parameter of LV systolic function with the end-diastolic elastance (Eed) as primary LV diastolic function.ResultsEes/Ea decreased over time in rats receiving LPS (p = 0.045) and high tidal volume ventilation (p = 0.007), with a lower Ees/Ea in the rats with high tidal volume ventilation plus LPS compared to the other groups (p < 0.001). Eed increased over time in all groups except for the rats receiving low tidal volume ventilation without LPS (p = 0.223). A significant interaction (p < 0.001) was found between tidal ventilation and LPS for Ees/Ea and Eed, and all rats receiving high tidal volume ventilation plus LPS died before the end of the experiment.ConclusionsLow tidal volume ventilation ameliorated LV systolic and diastolic dysfunction while preventing death following LPS-induced lung injury in mechanically ventilated rats. Our data advocates the use of low tidal volumes, not only to avoid VILI, but to avert ventilator-induced myocardial dysfunction as well.
Highlights
High tidal volume ventilation has shown to cause ventilator-induced lung injury (VILI), possibly contributing to concomitant extrapulmonary organ dysfunction
We investigated whether tidal volume size affects left ventricular (LV) function in a two-hit animal model of high tidal volumes and lung injury induced by intrapulmonary administered LPS
We observed a progressive decrease in end-systolic elastance (Ees)/Effective arterial elastance (Ea) with a ratio < 1.0 in the rats subjected to high tidal volume ventilation plus LPS, with a lower dP/dtmax compared to rats receiving low tidal volume ventilation
Summary
High tidal volume ventilation has shown to cause ventilator-induced lung injury (VILI), possibly contributing to concomitant extrapulmonary organ dysfunction. The present study examined whether left ventricular (LV) function is dependent on tidal volume size and whether this effect is augmented during lipopolysaccharide(LPS)-induced lung injury. The effect of changes in tidal volume size on stroke volume are in part dependent on right ventricular (RV) preload, contractility and afterload which in turn are affected by lung volume, lung compliance and chest wall compliance among others [2]. These complex interactions make an accurate prediction of the change in RV stroke volume upon increased tidal volume size challenging. LV afterload can be assessed and used for the determination of the relationship between LV contractility and afterload which has been used in various experimental and clinical conditions as the primary parameter for LV function [7,8,9,10,11]
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