C105-01 Biventricular Effects of Prolonged Lung Collapse: A 24-hour Pressure-volume Study in Pigs

Abstract Rationale A hallmark of acute respiratory distress syndrome (ARDS) is loss of lung volume which can be exacerbated by lung-rest ventilation strategies. ARDS models show higher mortality when a large proportion of lung is collapsed. Emphasis has focused on how sustained collapse, parenchymal injury, and driving pressure raise right ventricular (RV) afterload and promote dysfunction, with less attention to RV contractility. We hypothesized that sustained regional lung collapse increases RV afterload and alters myocardial contractile function, leading to impaired RV-pulmonary arterial mechanical coupling and secondarily affecting LV function. Methods Five pigs underwent 24-hour unilateral-lung collapse (IACUC #2023-0185). Ventilator settings: lowest FiO2 maintaining PaO2 80 mmHg, tidal volume (VT) 6-8 mL/kg, driving pressure 15 cmH2O, PEEP 5 cmH2O, respiratory rate maintaining PaCO2 50 mmHg. Biventricular pressure-volume data were acquired with conductance catheters at baseline (pre-collapse) and then 6, 12, and 24h post-collapse. Using single-beat analysis, the following metrics were derived: end-systolic elastance (Ees, contractility); effective arterial elastance (Ea, total afterload); ventriculoarterial coupling (VAC, Ees/Ea ratio); and stroke work (SW). A time-matched control group (n = 5) underwent identical instrumentation without lung collapse (same ventilation settings except for tidal volume (fixed at 8 mL/kg), PEEP 5-8 cmH2O to keep respiratory system compliance 1 mL/cmH2O/kg). Data were analyzed with a 2-way ANOVA. P 0.05 was considered significant. Results There were no time-related changes in any LV metric within either the control or lung collapse group, nor were there differences between groups (Fig. 1). In contrast, while the control group showed no change in RV volume or measures of RV function over time, for the lung collapse group there was an increase in RV end-systolic and end-diastolic volumes (EDV and ESV, respectively) (Fig. 1A) while Ea increased from baseline at all time points and Ees (Fig. 1B) trended upward but was statistically unchanged leading to a fall in VAC and EF (Fig. 1C). RV SV remained unchanged while SW increased at T24 (Fig. 1D). Conclusion In this 24-h model of unilateral lung collapse, loss of aeration alone markedly increased Ea with minimal change in Ees leading to reduced VAC and EF. However, despite RV dilation there was no evidence of failure as SV was maintained, consistent with preservation of heterometric autoregulation. LV performance remained unaffected. Study results suggest this platform supports future studies on interactions between collapse and other ARDS drivers (e.g., VILI, coagulopathy, or endotoxemia). This abstract is funded by: None