Correspondence  |   November 2016
In Reply
Author Notes
  • Department of Anesthesiology, Emergency and Intensive Care Medicine, University of Göttingen, Germany (L.G.).
  • (Accepted for publication July 14, 2016.)
    (Accepted for publication July 14, 2016.)×
Article Information
Correspondence   |   November 2016
In Reply
Anesthesiology 11 2016, Vol.125, 1071-1072. doi:10.1097/ALN.0000000000001298
Anesthesiology 11 2016, Vol.125, 1071-1072. doi:10.1097/ALN.0000000000001298
We thank Dr. Samary and her colleagues for their interest in our article and for the data they provide supporting our thesis. The primary aim of our study was to prove whether the ventilator-related cause of ventilator-induced lung injury (VILI) is mechanical power. In our study,1  we found a VILI-threshold of 12 J/min in a group of healthy animals in which the baseline lung conditions were similar. This threshold value, obviously, strictly refers to an experimental set up in which the lung size, the lung-specific elastance, and the lung homogeneity2  were equal at baseline (the lung size and homogeneity, of course, changed during the experiment3 ).
If we want to compare different animal species or patients with different lung alterations, the lung-related contributions to VILI (lung inhomogeneities, lung collapse and decollapse, size of the remaining inflated lung) play a substantial role for a given mechanical power. The authors are correct in stating that mechanical power should be normalized to the lung size and/or the grams of open ventilatable lung (i.e., joule/minute/gram or milliliter), but some problems remain. The first relates to the specific elastance, i.e., the transpulmonary pressure at which the lung doubles its size. While the total lung capacity is two to three times the functional residual capacity in humans, pigs, and rats, the specific elastance is ≈12, ≈6, and ≈4 cm H2O/L, respectively. It means that the pressure–volume product (energy) transferred to the lung parenchyma to reach the near-total lung capacity will vary proportionally in humans, pigs, and rats, respectively.
The second issue relates to the role of positive end-expiratory pressure (PEEP). PEEP was zero in our experiments. If the applied PEEP is not zero, as in the manuscript by Samary4 et al., the contribution of PEEP to mechanical power may be considered equal to zero if one computes the work as delta-transpulmonary pressure times delta-volume. In contrast, it may be relevant if the work is computed as transpulmonary pressure (absolute values) times delta-volume. The different ways of considering the problem do have an impact on the normalization of the mechanical power: normalize to functional residual capacity (PEEP out) or normalize to end-expiratory lung volume (PEEP in)?
Although we believe that mechanical power is the ventilator-related variable that contribute to VILI, further conceptual effort has to be made to fully understand its meaning and to prove it experimentally.
Competing Interests
The authors declare no competing interests.
Massimo Cressoni, M.D., Chiara Chiurazzi, M.D., Luciano Gattinoni, M.D., F.R.C.P. Department of Anesthesiology, Emergency and Intensive Care Medicine, University of Göttingen, Germany (L.G.).
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Samary, CS, Santos, RS, Santos, CL, Felix, NS, Bentes, M, Barboza, T, Capelozzi, VL, Morales, MM, Garcia, CS, Souza, SA, Marini, JJ, Gama de Abreu, M, Silva, PL, Pelosi, P, Rocco, PR Biological impact of transpulmonary driving pressure in experimental acute respiratory distress syndrome.. Anesthesiology. (2015). 123 423–33 [Article] [PubMed]