Abstract
Background: Ventilator-induced lung injury (VILI) via respiratory mechanics is deeply interwoven with hemodynamic, kidney and fluid/electrolyte changes. We aimed to assess the role of positive fluid balance in the framework of ventilation-induced lung injury.Methods:Post-hoc analysis of seventy-eight pigs invasively ventilated for 48 h with mechanical power ranging from 18 to 137 J/min and divided into two groups: high vs. low pleural pressure (10.0 ± 2.8 vs. 4.4 ± 1.5 cmH2O; p < 0.01). Respiratory mechanics, hemodynamics, fluid, sodium and osmotic balances, were assessed at 0, 6, 12, 24, 48 h. Sodium distribution between intracellular, extracellular and non-osmotic sodium storage compartments was estimated assuming osmotic equilibrium. Lung weight, wet-to-dry ratios of lung, kidney, liver, bowel and muscle were measured at the end of the experiment.Results: High pleural pressure group had significant higher cardiac output (2.96 ± 0.92 vs. 3.41 ± 1.68 L/min; p < 0.01), use of norepinephrine/epinephrine (1.76 ± 3.31 vs. 5.79 ± 9.69 mcg/kg; p < 0.01) and total fluid infusions (3.06 ± 2.32 vs. 4.04 ± 3.04 L; p < 0.01). This hemodynamic status was associated with significantly increased sodium and fluid retention (at 48 h, respectively, 601.3 ± 334.7 vs. 1073.2 ± 525.9 mmol, p < 0.01; and 2.99 ± 2.54 vs. 6.66 ± 3.87 L, p < 0.01). Ten percent of the infused sodium was stored in an osmotically inactive compartment. Increasing fluid and sodium retention was positively associated with lung-weight (R2 = 0.43, p < 0.01; R2 = 0.48, p < 0.01) and with wet-to-dry ratio of the lungs (R2 = 0.14, p < 0.01; R2 = 0.18, p < 0.01) and kidneys (R2 = 0.11, p = 0.02; R2 = 0.12, p = 0.01).Conclusion: Increased mechanical power and pleural pressures dictated an increase in hemodynamic support resulting in proportionally increased sodium and fluid retention and pulmonary edema.
Highlights
It is well known that positive pressure mechanical ventilation is associated with hemodynamic impairment and sodium and water retention (Drury et al, 1947)
Increased mechanical power and pleural pressures dictated an increase in hemodynamic support resulting in proportionally increased sodium and fluid retention and pulmonary edema
In the late 70 s, Hemmer and Suter suggested the use of vasoactive drugs rather than fluid infusions to achieve adequate perfusion while preventing fluid overload (Hemmer and Suter, 1979). Both fluids and cardiovascular drugs are commonly used to compensate for the detrimental hemodynamic effects of mechanical ventilation, despite the common notion that positive fluid balance is associated with worse outcomes (Mendes et al, 2020)
Summary
It is well known that positive pressure mechanical ventilation is associated with hemodynamic impairment and sodium and water retention (Drury et al, 1947). In a series of animal experiments aimed to elucidate some of the mechanisms of ventilator-induced lung injury (VILI), the animals often required large amounts of fluids and catecholamines to prevent hemodynamic collapse (Collino et al, 2019; Vassalli et al, 2020). This approach is similar to what it is routinely done in clinical practice: to maintain adequate hemodynamics the fluid infused into the patient can amount to several liters (Boyd et al, 2011). We aimed to assess the role of positive fluid balance in the framework of ventilation-induced lung injury
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