Least Injurious Mechanical Ventilation in Pulmonary Resection Surgery

To the Editor In a prospective observational cohort study, Amar et al1 examined the relationship between intraoperative “protective lung ventilation” (defined as mean tidal volume per case <8 mL/kg predicted body weight) and development of postoperative pulmonary complications in patients undergoing lung resection surgery. There are certain points of interest to be discussed: Driving pressure: Theoretically, any positive pressure mechanical ventilation could be “injurious” leading to ventilator-induced lung injury and therefore the terms “low tidal volume” and “lung protective” cannot be synonymous. In patients receiving 1-lung ventilation (OLV), a tidal volume of 6–8 mL/kg predicted body weight may still be “injurious” because it is applied to one lung only and one might argue that those patients receive twice the desired tidal volume. Using parameters such as driving pressure (ΔP) (difference between plateau pressure and total positive end expiratory pressure [PEEP]) as a surrogate for “lung strain” may be more appropriate than using peak airway or plateau pressure alone to guide a “least injurious” ventilatory model as it has been recently shown that ΔP predicts mortality in acute respiratory distress syndrome patients.2 It would stand to reason that a ventilatory bundle that includes higher PEEP would reduce ΔP and “strain” and thus be “less injurious.” However, this hypothesis should be tested in large-scale randomized controlled trials and the “optimal—lung protective” level of PEEP and ΔP to prevent subclinical ventilator-induced lung injury in OLV is unknown.2 Right ventricular (RV) dysfunction: It has been shown that patients undergoing lung resection surgery are at risk of RV dysfunction as evidenced by cardiac magnetic resonance (gold standard noninvasive imaging modality).3 In particular, there is a significant reduction in RV ejection fraction which can remain depressed for up to 2 months postoperatively. Therefore a “least injurious” “low-ΔP” (<18 cm H2O) ventilatory strategy during OLV could potentially be “RV-protective” by reducing RV afterload.3,4 RV dysfunction can lead to RV failure and potentially biventricular failure. It would therefore be important to know the pre- and postoperative cardiac function. If postoperative pulmonary edema is suspected, echocardiography to differentiate cardiogenic from noncardiogenic volume overload would be paramount. Understanding of lung heterogeneity, “RV–lung interactions” and pathophysiology of “atelectrauma” and recruitment/derecruitment is key to the development of a “least damaging” intraoperative ventilation bundle (low tidal volume, optimal PEEP, alveolar recruitment maneuvers, “safe” ΔP) that may improve pulmonary morbidity in this high-risk patient population. Vasileios Zochios, MDUniversity Hospitals Birmingham NHS Foundation TrustDepartment of Critical Care MedicineQueen Elizabeth Hospital BirminghamEdgbaston, Birmingham, United KingdomPerioperative Critical Care and Trauma Trials GroupInstitute of Inflammation and Ageing Centre of Translational Inflammation ResearchUniversity of BirminghamBirmingham, United Kingdom[email protected]