Lung-Protective Mechanical Ventilation in Patients with Severe Acute Brain Injury

with his point regarding pulmonary artery occlusion pressure.The small reduction from 13 mm Hg to 12 mm Hg passing from lower to higher flow actually suggests that neither an increase in left ventricular afterload nor a reduction in ventricular contractility occurred.On the contrary, this change likely reflects the reduction in sympathetic tone, which resulted in decreased cardiac workload and decreased volume centralization.Jha's letter gives a sense of the intricate overlapping of several cardiocirculatory effects, which could result in unexpected changes in hemodynamic variables.Indeed, mean arterial pressure (MAP) was slightly but not significantly higher at lower blood flow rates and SV. O 2 (MAP: 83 mm Hg [range = 79-96 mm Hg] vs. 85 mm Hg [range = 79-90 mm Hg] vs. 79 mm Hg [range = 74-86 mm Hg]; P = 0.217), whereas systemic vascular resistance was not different (689 dynes/s/cm 25 [range = 601-871 dynes/s/cm 25 ] vs. 730 dynes/s/ cm 25 [range = 625-914 dynes/s/cm 25 ] vs. 684 dynes/s/cm 25[range = 619-894 dynes/s/cm 25 ]; P = 0.717).We disagree with the statement that "MAP drives venous return."Rather, venous return depends on venous resistance and the difference between right atrial pressure and the mean systemic filling pressure, the latter being determined by the distribution of vascular compliance and overall blood volume.The suggestion to assess ventricular systolic function by means of echocardiography is well received.As pulmonary hemodynamics and right ventricular workload may be significantly affected by ECMO blood flow, a more comprehensive evaluation of biventricular function could enhance the physiological understanding of ECMO's effects, especially in patients with right ventricular dysfunction or failure.We also disagree with Jha's comment regarding the ratio between oxygen delivery (DO 2 ) and _ VO 2 falling below the critical threshold of 2. Across the different study steps, the DO 2 remained consistently above 1,000 ml/min, whereas the estimated _ VO 2 likely ranged between 200 and 300 ml/min.As blood flow rates increased, the patient's _ VO 2 decreased from approximately 200 ml/min to 100 ml/min, with an estimated ECMO _ VO 2 contribution changing from 75 to 175 ml/min (approximately 50 ml/L of blood flow).Therefore, given the "clinically safe" steps of the study design, the DO 2 / _ VO 2 ratio was consistently above 3 (2), well above the critical threshold.Far from believing that we have provided a definitive description of the complex interaction between ECMO and cardiocirculatory function, we stick to the study results, which did not show that the decrease in cardiac output at higher ECMO blood flow affected the adequacy of DO 2 in relation to total _ VO 2 .Once again, we appreciate Dr. Jha's thoughtful feedback and believe that this exchange will contribute to further optimizing ECMO support in patients with severe acute respiratory distress syndrome.