Reply to Tobin et al.: Respiratory Drive Measurements Do Not Signify Conjectural Patient Self-inflicted Lung Injury

From the Authors:

We read with some perplexity the comments by Tobin and colleagues to our editorial (1). Indeed, many of their questions or concerns should be more properly addressed to Esnault and colleagues, the authors of the original paper (2).

We believe that an important role of an editorial is first to bring fresh ideas to the fore and place them against an engaging conceptual background. Regarding the specific concerns of Tobin and colleagues, we find it fruitless to argue whether 4 cm H₂O of occlusion pressure at 100 milliseconds is tolerable or not in coronavirus disease (COVID-19) pneumonia. The real concern is that, at the time of our writing, the pandemic has caused about 1 million deaths initiated by pneumonia and respiratory failure. Because intensive care mortality has been reported to range from 10–20% to 80–90% of patients needing respiratory assistance, it is appropriate to ask ourselves to what extent different treatment choices may have contributed to such high differences in mortality. Indeed, it is conceivable that ill-timed decisions or inappropriate ventilatory settings may worsen the natural course of the disease. In this framework, the well-documented observations of heightened drive and sudden deterioration in patients with COVID-19 imply the genuine possibility of patient self-inflicted lung injury (P-SILI). It is also to be remembered that there exists a body of literature produced by other experts that expresses similar concerns and documents the reproducible nature of P-SILI (3–9). No one is entitled to pontificate on issues to which neither we nor Tobin and colleagues have found the answers. (We certainly are not “claiming” to know specifics, contrary to what the repeated mantra “Gattinoni and colleagues claim…” suggests.) However, in the context of the pressing clinical need to formulate a logical approach, an informed editorial hypothesis should be welcomed. Our intent was to underline that the assessment of abnormal drive is a step forward toward better understanding (and treatment) of COVID-19 pneumonia. Indeed, although the interplay between respiratory drive, muscular work, and applied energy is complex and far from completely understood, the possibility of excessive self-induced stress, strain, and edema (P-SILI) in these inflamed lungs must be taken into account. The work from Esnault and colleagues calls attention to this potential problem and is a first step toward its better understanding. Every measurement has its own biases and limitations, but measuring the strength of the respiratory drive and monitoring its changes must be better than not doing so and basing key decisions regarding respiratory support on mere guesswork.