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how to minimise ventilator-induced lung injury in transplanted lungs

Sutherasan, Yuda; Soluri-Martins, Andre; Silva, Pedro L.; Pelosi, Paolo; Rocco, Patricia R.M.

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European Journal of Anaesthesiology: April 2016 - Volume 33 - Issue 4 - p 300-301
doi: 10.1097/EJA.0000000000000413
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We thank Dr Michael Eberlein and colleagues1 for their interest in our article and their insightful comments.2 Higher tidal volumes can precipitate lung injury, not only in acute respiratory distress syndrome but also in healthy lungs, with the main known mechanisms being barotrauma from high transpulmonary pressure (stress), volume trauma from alveolar overdistension (strain) and atelectrauma by transient opening and collapsed alveoli, as well as direct biotrauma or mechanotransduction. Recent meta-analyses have demonstrated that, in patients without preexisting lung injuries at the onset of mechanical ventilation and during surgery, lower tidal volume ventilation is associated with lower incidence of acute respiratory distress syndrome, mortality and pulmonary infections, as well as shorter duration of mechanical ventilation.3,4 Meta-analyses of individual patient data, in patients undergoing general surgery, examining the individual associations between tidal volume and positive end-expiratory pressure (PEEP) level and the occurrence of postoperative pulmonary complications, demonstrated a dose–response relationship of tidal volume, but not of PEEP level, with the occurrence of postoperative pulmonary complications.3–6 Thus, a tidal volume less than 8 ml kg−1 predicted body weight is currently recommended in the mechanically ventilated patients without a preexisting lung injury.

In a rat-transplanted lung model, during the early reperfusion period, animals ventilated with a tidal volume equal to 20% of the inspiratory capacity of the left lung and PEEP set according to the shape of the pressure–time curve (stress index), thus minimising pulmonary stress (protective ventilation group), demonstrated higher oxygenation, lower lung elastance and pro-inflammatory cytokine levels than a conventional ventilation group (tidal volume equal to the half of the inspiratory capacity of the left lung and low PEEP).4

Regarding donor–recipient lung size mismatch, size also does matter. An observational study by Dezube et al.7 demonstrated that, among patients with undersized [lowest predicted total lung capacity (pTLC) ratio = donor pTLC/recipient pTLC], matched and oversized (highest pTLC ratio) allografts, with the same levels of PEEP (8.6 versus 7.5 versus 8 cmH2O, respectively) and similar tidal volumes in ml kg−1 recipient-predicted body weight (8.8 versus 9.3 versus 9.8), there was a significant difference in tidal volumes in ml kg−1 donor-predicted body weight between undersized, matched and oversized subsets (11.4 versus 9.4 versus 8.1, respectively). The same group has shown that undersized allografts which receive relatively higher tidal volume in ml kg−1 donor-predicted body weight are associated with a significant increase in the risk of primary graft dysfunction, bronchiolitis obliterans syndrome and mortality after lung transplantation.8,9 From the current evidence, it is clearly very important to set the tidal volume according to donor-predicted body weight, and even more attention is needed regarding donor-to-recipient lung size mismatch, especially in undersized subsets. Nevertheless, there are no sufficient data on the optimal levels of tidal volume and PEEP to decrease lung injury and pulmonary complications in this subgroup. The low level of PEEP may be set by the measurement of lung compliance as well as that of stress index. To date, there are no guidelines on optimal ventilator strategies after lung transplantation. As this intervention becomes more common over time, there will be a growing need for guidance to prevent deleterious effects. One step in this direction could be the conduction of prospective multicentre studies.

Acknowledgements relating to this article

Assistance with the reply: we express our gratitude to Filippe Vasconcellos for his assistance in editing the manuscript.

Financial support and sponsorship: this work was funded by the Brazilian Council for Scientific and Technological Development (CNPq), Rio de Janeiro State Research Supporting Foundation (FAPERJ) and Coordination for the Improvement of Higher Level Personnel (CAPES).

Conflicts of interest: none.


1. Eberlein M, Barnes L, Pena T, Reed RM. How to minimise ventilator-induced lung injury in transplanted lungs. Eur J Anaesthesiol 2016; 33:300–301.
2. Soluri-Martins A, Sutherasan Y, Silva PL, et al. How to minimise ventilator-induced lung injury in transplanted lungs: the role of protective ventilation and other strategies. Eur J Anaesthesiol 2015; 32:828–836.
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9. Eberlein M, Reed RM, Bolukbas S, et al. Lung size mismatch and primary graft dysfunction after bilateral lung transplantation. J Heart Lung Transplant 2015; 34:233–240.
© 2016 European Society of Anaesthesiology