To summarize my arguments, I contend that established biophysical injury mechanisms, a huge body of experimental literature, and observations from clinical practice have identified Vt as a determinant of lung injury risk. I suspect that in a normal lung, in the absence of other stressors, the clinical manifestations of high-Vt ventilation are generally subtle and inconsequential. But even if that was true, why would I want to expose my patient to an intervention that I fear will amplify the pulmonary stress response to other insults? Of course, my reasoning is only valid if so-called low-Vt mechanical ventilation proves safe. This warrants a comment about the meaning of low. In the absence of lung disease, PBW is strongly correlated with lung size. It turns out that a Vt between 6 and 8 mL/kg PBW, which is the standard of care in patients with ALI who are mechanically ventilated, corresponds to a volume of ≈6% to 8% of TLC.18,19 With minor rate adjustments, an otherwise normal lung, whose function is impaired by the effects of anesthesia and neuromuscular blockade, should be able to provide sufficient gas exchange at Vt settings in that range. The same holds true for most patients with hypercapnic respiratory failure, regardless of specific cause. As a result, the average Vt setting in patients with all-cause respiratory failure in my institution is nowadays 7 mL/kg PBW. I have already pointed out that, to date, none of the clinical ventilator management trials in surgical patients has favored the high-Vt arm,16 and I have provided a reference, which suggests that a low-Vt strategy is associated with a lower incidence of ventilator-associated pneumonia.15 I have offered post hoc evidence that ventilating patients with large Vts increases their risk of hospital-acquired ALI,1 which has been confirmed recently in a prospective clinical trial.20 So please, Dr Gattinoni, sigh your patients ever so often; just don’t do it on every breath!