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Low tidal volume ventilation ameliorates left ventricular dysfunction in mechanically ventilated rats following LPS-induced lung injury.

Cherpanath TG, Smeding L, Hirsch A, Lagrand WK, Schultz MJ, Groeneveld AB - BMC Anesthesiol (2015)

Bottom Line: High tidal volume ventilation has shown to cause ventilator-induced lung injury (VILI), possibly contributing to concomitant extrapulmonary organ dysfunction.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.Our data advocates the use of low tidal volumes, not only to avoid VILI, but to avert ventilator-induced myocardial dysfunction as well.

View Article: PubMed Central - PubMed

Affiliation: Department of Intensive Care Medicine, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands. t.g.cherpanath@amc.uva.nl.

ABSTRACT

Background: 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.

Methods: Twenty 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.

Results: Ees/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.

Conclusions: Low 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.

No MeSH data available.


Related in: MedlinePlus

Pressure-volume loops obtained during three seconds showing left ventricular (LV) hemodynamics during steady state (a) and vena cava occlusion (b). a LV function is described during 4 phases of the cardiac cycle: 1) diastolic filling, 2) isovolumetric contraction, 3) ejection and 4) isovolumetric relaxation. EDP = end-diastolic pressure, ESP = end-systolic pressure, Ea = effective arterial elastance which slope is calculated by end-systolic pressure divided by stroke volume, dP/dtmax = maximum rate of pressure development during isovolumetric contraction, dP/dtmin = maximum rate of pressure decline during isovolumetric relaxation. b By decreasing preload through vena cava occlusion, the pressure-volume loops move to the left and become smaller, enabling the measurement of end-systolic elastance (Ees) by the pressure-volume relationship at end-systole. Simultaneously, end-diastolic elastance (Eed) can be measured by the pressure-volume relationship at end-diastole. A representative sample trace as displayed and analyzed by PVAN 3.6 is shown
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Fig1: Pressure-volume loops obtained during three seconds showing left ventricular (LV) hemodynamics during steady state (a) and vena cava occlusion (b). a LV function is described during 4 phases of the cardiac cycle: 1) diastolic filling, 2) isovolumetric contraction, 3) ejection and 4) isovolumetric relaxation. EDP = end-diastolic pressure, ESP = end-systolic pressure, Ea = effective arterial elastance which slope is calculated by end-systolic pressure divided by stroke volume, dP/dtmax = maximum rate of pressure development during isovolumetric contraction, dP/dtmin = maximum rate of pressure decline during isovolumetric relaxation. b By decreasing preload through vena cava occlusion, the pressure-volume loops move to the left and become smaller, enabling the measurement of end-systolic elastance (Ees) by the pressure-volume relationship at end-systole. Simultaneously, end-diastolic elastance (Eed) can be measured by the pressure-volume relationship at end-diastole. A representative sample trace as displayed and analyzed by PVAN 3.6 is shown

Mentions: LV systolic and diastolic parameters could successfully be derived from the pressure-volume loops in the rats during steady state (Fig. 1a) and during balloon inflation of the vena cava catheter (Fig. 1b). Ees/Ea decreased over time in rats receiving LPS compared to non-LPS treated rats (p = 0.045), as well as in rats subjected to high tidal volume ventilation vs. low tidal volume ventilation (p = 0.007) (Fig. 2a). Mean Ees/Ea was lower in the rats with high tidal volume ventilation plus LPS compared to the other groups (p < 0.001) (Table 2). Furthermore, mean dP/dtmax was lower in the rats with high tidal volume ventilation plus LPS compared to the rats with low tidal volume ventilation. Mean end-systolic pressure was higher in the rats receiving low tidal volume ventilation without LPS compared to LPS-treated rats.Fig. 1


Low tidal volume ventilation ameliorates left ventricular dysfunction in mechanically ventilated rats following LPS-induced lung injury.

Cherpanath TG, Smeding L, Hirsch A, Lagrand WK, Schultz MJ, Groeneveld AB - BMC Anesthesiol (2015)

Pressure-volume loops obtained during three seconds showing left ventricular (LV) hemodynamics during steady state (a) and vena cava occlusion (b). a LV function is described during 4 phases of the cardiac cycle: 1) diastolic filling, 2) isovolumetric contraction, 3) ejection and 4) isovolumetric relaxation. EDP = end-diastolic pressure, ESP = end-systolic pressure, Ea = effective arterial elastance which slope is calculated by end-systolic pressure divided by stroke volume, dP/dtmax = maximum rate of pressure development during isovolumetric contraction, dP/dtmin = maximum rate of pressure decline during isovolumetric relaxation. b By decreasing preload through vena cava occlusion, the pressure-volume loops move to the left and become smaller, enabling the measurement of end-systolic elastance (Ees) by the pressure-volume relationship at end-systole. Simultaneously, end-diastolic elastance (Eed) can be measured by the pressure-volume relationship at end-diastole. A representative sample trace as displayed and analyzed by PVAN 3.6 is shown
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4597388&req=5

Fig1: Pressure-volume loops obtained during three seconds showing left ventricular (LV) hemodynamics during steady state (a) and vena cava occlusion (b). a LV function is described during 4 phases of the cardiac cycle: 1) diastolic filling, 2) isovolumetric contraction, 3) ejection and 4) isovolumetric relaxation. EDP = end-diastolic pressure, ESP = end-systolic pressure, Ea = effective arterial elastance which slope is calculated by end-systolic pressure divided by stroke volume, dP/dtmax = maximum rate of pressure development during isovolumetric contraction, dP/dtmin = maximum rate of pressure decline during isovolumetric relaxation. b By decreasing preload through vena cava occlusion, the pressure-volume loops move to the left and become smaller, enabling the measurement of end-systolic elastance (Ees) by the pressure-volume relationship at end-systole. Simultaneously, end-diastolic elastance (Eed) can be measured by the pressure-volume relationship at end-diastole. A representative sample trace as displayed and analyzed by PVAN 3.6 is shown
Mentions: LV systolic and diastolic parameters could successfully be derived from the pressure-volume loops in the rats during steady state (Fig. 1a) and during balloon inflation of the vena cava catheter (Fig. 1b). Ees/Ea decreased over time in rats receiving LPS compared to non-LPS treated rats (p = 0.045), as well as in rats subjected to high tidal volume ventilation vs. low tidal volume ventilation (p = 0.007) (Fig. 2a). Mean Ees/Ea was lower in the rats with high tidal volume ventilation plus LPS compared to the other groups (p < 0.001) (Table 2). Furthermore, mean dP/dtmax was lower in the rats with high tidal volume ventilation plus LPS compared to the rats with low tidal volume ventilation. Mean end-systolic pressure was higher in the rats receiving low tidal volume ventilation without LPS compared to LPS-treated rats.Fig. 1

Bottom Line: High tidal volume ventilation has shown to cause ventilator-induced lung injury (VILI), possibly contributing to concomitant extrapulmonary organ dysfunction.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.Our data advocates the use of low tidal volumes, not only to avoid VILI, but to avert ventilator-induced myocardial dysfunction as well.

View Article: PubMed Central - PubMed

Affiliation: Department of Intensive Care Medicine, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands. t.g.cherpanath@amc.uva.nl.

ABSTRACT

Background: 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.

Methods: Twenty 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.

Results: Ees/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.

Conclusions: Low 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.

No MeSH data available.


Related in: MedlinePlus