Background: Limited data exist regarding ventilation in patients with class III obesity [body mass index (BMI) > 40 kg/m 2 ] and acute respiratory distress syndrome (ARDS). The aim of the present study was to determine whether an individualized titration of mechanical ventilation according to cardiopulmonary physiology reduces the mortality in patients with class III obesity and ARDS. Methods: In this retrospective study, we enrolled adults admitted to the ICU from 2012 to 2017 who had class III obesity and ARDS and received mechanical ventilation for > 48 h. Enrolled patients were divided in two cohorts: one cohort (2012-2014) had ventilator settings determined by the ARDSnet table for lower positive end-expiratory pressure/higher inspiratory fraction of oxygen (standard protocol-based cohort); the other cohort (2015-2017) had ventilator settings determined by an individualized protocol established by a lung rescue team (lung rescue team cohort). The lung rescue team used lung recruitment maneuvers, esophageal manometry, and hemodynamic monitoring. Results: The standard protocol-based cohort included 70 patients (BMI = 49 ± 9 kg/m 2 ), and the lung rescue team cohort included 50 patients (BMI = 54 ± 13 kg/m 2 ). Patients in the standard protocol-based cohort compared to lung rescue team cohort had almost double the risk of dying at 28 days [31% versus 16%, P = 0.012; hazard ratio (HR) 0.32; 95% confidence interval (CI95%) 0.13-0.78] and 3 months (41% versus 22%, P = 0.006; HR 0.35; CI95% 0.16-0.74), and this effect persisted at 6 months and 1 year (incidence of death unchanged 41% versus 22%, P = 0.006; HR 0.35; CI95% 0.16-0.74). Conclusion: Individualized titration of mechanical ventilation by a lung rescue team was associated with decreased mortality compared to use of an ARDSnet table.

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Right ventricular (RV) afterload is a key determinant of RV function and is increased in many cardiopulmonary pathologies. Pulmonary circulation input impedance has been used to quantify afterload previously but due to its complexity has not been widely applied. This study examines the effect of a subset of the impedance spectrum, the zeroth and first harmonic impedance moduli (Z (0), Z (1)), on RV performance in large animals. An artificial circuit with adjustable resistance and compliance (C) was implanted into the pulmonary circulation of five sheep. Resistance was varied to increase Z (0) in increments of 2 mmHg/(L/min) until Z (0) was 8 mmHg/(L/min) above baseline. At each Z (0), C was adjusted between 0, 0.5 and 2 mL/mmHg or 0, 1, and 5 mL/mmHg. Fourier transforms of the pulmonary artery pressure and flow in each situation were used to calculate the pulmonary impedance. Results show that the percent change in cardiac output (%DeltaCO) is linearly related to the change in Z (0) (DeltaZ (0)). Increases in Z (1) (DeltaZ (1)) decreased %DeltaCO but to a much smaller degree, with the effect of DeltaZ (1) increasing with DeltaZ (0). Regression of these results produce the equation: %DeltaCO = (-0.0829DeltaZ (1) - 3.65)DeltaZ (0) - 9.02 (R (2) = 0.69). Blood flow and pressure moduli are small at harmonics higher than the first and are unlikely to affect RV function. Therefore, during acute, high afterload states, Z (0) is the primary determinant of CO, while the effect of Z (1) is minor.