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Perioperative lung protective ventilation.

ABSTRACT: Perioperative lung injury is a major source of postoperative morbidity, excess healthcare use, and avoidable mortality. Many potential inciting factors can lead to this condition, including intraoperative ventilator induced lung injury. Questions exist as to whether protective ventilation strategies used in the intensive care unit for patients with acute respiratory distress syndrome are equally beneficial for surgical patients, most of whom do not present with any pre-existing lung pathology. Studied both individually and in combination as a package of intraoperative lung protective ventilation, the use of low tidal volumes, moderate positive end expiratory pressure, and recruitment maneuvers have been shown to improve oxygenation and pulmonary physiology and to reduce postoperative pulmonary complications in at risk patient groups. Further work is needed to define the potential contributions of alternative ventilator strategies, limiting excessive intraoperative oxygen supplementation, use of non-invasive techniques in the postoperative period, and personalized mechanical ventilation. Although the weight of evidence strongly suggests a role for lung protective ventilation in moderate risk patient groups, definitive evidence of its benefit for the general surgical population does not exist. However, given the shift in understanding of what is needed for adequate oxygenation and ventilation under anesthesia, the largely historical arguments against the use of intraoperative lung protective ventilation may soon be outdated, on the basis of its expanding track record of safety and efficacy in multiple settings.

SUBMITTER: O'Gara B

PROVIDER: S-EPMC6889848 | biostudies-literature | 2018 Sep

REPOSITORIES: biostudies-literature

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Perioperative lung protective ventilation.

O'Gara Brian B Talmor Daniel D

BMJ (Clinical research ed.) 20180910

Perioperative lung injury is a major source of postoperative morbidity, excess healthcare use, and avoidable mortality. Many potential inciting factors can lead to this condition, including intraoperative ventilator induced lung injury. Questions exist as to whether protective ventilation strategies used in the intensive care unit for patients with acute respiratory distress syndrome are equally beneficial for surgical patients, most of whom do not present with any pre-existing lung pathology. S ...[more]

PMID: 30201797

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Project description:BackgroundIn the Protective Ventilation in Cardiac Surgery (PROVECS) randomized, controlled trial, an open-lung ventilation strategy did not improve postoperative respiratory outcomes after on-pump cardiac surgery. In this prespecified subanalysis, the authors aimed to assess the regional distribution of ventilation and plasma biomarkers of lung epithelial and endothelial injury produced by that strategy.MethodsPerioperative open-lung ventilation consisted of recruitment maneuvers, positive end-expiratory pressure (PEEP) = 8 cm H2O, and low-tidal volume ventilation including during cardiopulmonary bypass. Control ventilation strategy was a low-PEEP (2 cm H2O) low-tidal volume approach. Electrical impedance tomography was used serially throughout the perioperative period (n = 56) to compute the dorsal fraction of ventilation (defined as the ratio of dorsal tidal impedance variation to global tidal impedance variation). Lung injury was assessed serially using biomarkers of epithelial (soluble form of the receptor for advanced glycation end-products, sRAGE) and endothelial (angiopoietin-2) lung injury (n = 30).ResultsEighty-six patients (age = 64 ± 12 yr; EuroSCORE II = 1.65 ± 1.57%) undergoing elective on-pump cardiac surgery were studied. Induction of general anesthesia was associated with ventral redistribution of tidal volumes and higher dorsal fraction of ventilation in the open-lung than the control strategy (0.38 ± 0.07 vs. 0.30 ± 0.10; P = 0.004). No effect of the open-lung strategy on the dorsal fraction of ventilation was noted at the end of surgery after median sternotomy closure (open-lung = 0.37 ± 0.09 vs. control = 0.34 ± 0.11; P = 0.743) or in extubated patients at postoperative day 2 (open-lung = 0.63 ± 0.18 vs. control = 0.59 ± 0.11; P > 0.999). Open-lung ventilation was associated with increased intraoperative plasma sRAGE (7,677 ± 3,097 pg/ml vs. 6,125 ± 1,400 pg/ml; P = 0.037) and had no effect on angiopoietin-2 (P > 0.999).ConclusionsIn cardiac surgery patients, open-lung ventilation provided larger dorsal lung ventilation early during surgery without a maintained benefit as compared with controls at the end of surgery and postoperative day 2 and was associated with higher intraoperative plasma concentration of sRAGE suggesting lung overdistension.Editor’s perspective

Project description:BACKGROUND:Lung-protective ventilation (LPV) has been found to minimize the risk of ventilator-induced lung injury (VILI). However, whether LPV is able to diminish ventilator-induced diaphragm dysfunction (VIDD) remains unknown. This study was designed to test the hypothesis that LPV protects the diaphragm against VIDD. METHODS:Adult male Wistar rats received either conventional mechanical (tidal volume [VT]: 10 ml/kg, positive end-expiratory pressure [PEEP]: 2 cm H2O; CV group) or lung-protective (VT: 5 ml/kg, PEEP: 10 cm H2O; LPV group) ventilation for 12 h. Then, diaphragms and lungs were collected for biochemical and histological analyses. Transcriptome sequencing (RNA-seq) was performed to determine the differentially expressed genes in the diaphragms between groups. RESULTS:Our results suggested that LPV was associated with diminished pulmonary injuries and reduced oxidative stress compared with the effects of the CV strategy in rats. However, animals that received LPV showed increased protein degradation, decreased cross-sectional areas (CSAs) of myofibers, and reduced forces of the diaphragm compared with the same parameters in animals receiving CV (p < 0.05). In addition, the LPV group showed a higher level of oxidative stress in the diaphragm than the CV group (p < 0.05). Moreover, RNA-seq and western blots revealed that the peroxisome proliferator-activated receptor γ coactivator-1alpha (PGC-1α), a powerful reactive oxygen species (ROS) inhibitor, was significantly downregulated in the LPV group compared with its expression in the CV group (p < 0.05). CONCLUSIONS:Compared with the CV strategy, the LPV strategy did not protect the diaphragm against VIDD in rats. In contrast, the LPV strategy worsened VIDD by inducing oxidative stress together with the downregulation of PGC-1α in the diaphragm. However, further studies are required to determine the roles of PGC-1α in ventilator-induced diaphragmatic oxidative stress.

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Perioperative lung protective ventilation.

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Perioperative lung protective ventilation.

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