Intraoperative Mechanical Ventilation and Postoperative Pulmonary Complications After Cardiac Surgery

Michael R. Mathis, M.D.; Neal M. Duggal, M.D.; Donald S. Likosky, Ph.D.; Jonathan W. Haft, M.D.; Nicholas J. Douville, M.D., Ph.D.; Michelle T. Vaughn, M.P.H.; Michael D. Maile, M.D., M.S.; Randal S. Blank, M.D., Ph.D.; Douglas A. Colquhoun, M.B., Ch.B., M.Sc., M.P.H.; Raymond J. Strobel, M.D., M.S.; Allison M. Janda, M.D.; Min Zhang, Ph.D.; Sachin Kheterpal, M.D., M.B.A.; Milo C. Engoren, M.D.

Disclosures

Anesthesiology. 2019;131(5):1046-1062. 

In This Article

Discussion

Using robust, validated observational databases, we report an overall pulmonary complication incidence of 10.9% after cardiac surgery, and identify an intraoperative lung-protective ventilation bundle as independently associated with a clinically and statistically significant reduction in pulmonary complications. Our study builds on existing literature by providing an analysis of the impact of intraoperative ventilation strategies on postoperative outcomes among a generalizable cardiac surgery population. Although unaccounted for in current risk scoring systems, we report that an intraoperative lung-protective ventilation strategy is independently associated with development of postoperative pulmonary complications. Through a sensitivity analysis evaluating components of the lung-protective ventilation bundle, we importantly note that driving pressure, but not VT or PEEP, is independently associated with postoperative pulmonary complications.

Compared with previous literature, our findings demonstrate the importance of considering multiple components of lung-protective ventilation when evaluating the impact of mechanical ventilation on outcomes. Notably, we observed that not all components of lung-protective ventilation were independently associated with decreased postoperative pulmonary complications; however, a lung-protective ventilation bundled approach was independently associated with decreased postoperative pulmonary complications. Furthermore, within the lung-protective ventilation bundle studied, we observed driving pressure as the component primarily driving the association with reduced postoperative pulmonary complications, rather than VT or PEEP. These findings offer insight toward sustaining a trend of expedited recovery from cardiac surgery, a process in which postoperative care teams are increasingly reliant on intraoperative practices—such as lung-protective ventilation—to target reduced postoperative complications and to safely enable rapid de-escalation of care on arrival to the ICU.[46,47]

Our study highlights the importance of driving pressure, and conversely the limitations of VT and PEEP, as independently associated with postoperative pulmonary complications and secondary outcomes. We offer two hypotheses to explain these findings: (1) increased driving pressure is a marker for noncompliant lungs, assuming such patients are at increased risk of postoperative pulmonary complications and remain unidentified by model covariates; or (2) increased driving pressure reflects direct pulmonary injury via barotrauma as a postoperative pulmonary complication mechanism. Countervailing to a hypothesis that driving pressure serves as a marker for noncompliance, however, was our observation that lower VT was not independently associated with increased postoperative pulmonary complications, as would be the case for increasingly noncompliant lungs at a given constant driving pressure exposure (controlled covariate). This finding was similarly observed in an analysis performed among 3,562 patients with acute respiratory distress syndrome enrolled across nine randomized trials.[17] Within a surgical population, a recent randomized, controlled trial demonstrated a driving pressure-guided ventilation strategy during one-lung ventilation to be similarly associated with a lower incidence of postoperative pulmonary complications compared with conventional ventilation strategies, during thoracic surgery.[48]

Additionally of note, in a sensitivity analysis analyzing pre-CPB driving pressure and post-CPB driving pressure separately, our observations that (1) pre-CPB and post-CPB variables were not collinear and (2) post-CPB driving pressure but not pre-CPB driving pressure below 16 cm H2O was independently associated with postoperative pulmonary complications, suggests our driving pressure findings cannot solely be explained as a marker for poor baseline lung function. However, whether this independent association between post-CPB driving pressure below 16 cm H2O and postoperative pulmonary complications can be explained by a direct lung injury hypothesis, versus a marker for varying degrees of CPB-induced pulmonary dysfunction, remains unanswerable based on our data. Other explanations for a lack of collinearity between pre-CPB and post-CPB driving pressure may include nuanced surgery stage-specific ventilation strategies, such as low VT and low driving pressure during internal mammary artery surgical dissection and/or cannulation before CPB. Finally, although a driving pressure threshold below 16 cm H2O enabled class balance between cases adherent versus nonadherent to an overall lung-protective ventilation bundle, an optimal driving pressure threshold defining lung-protective ventilation remains unclear, and likely varies by clinical context.

Our findings that lower intraoperative driving pressure was associated with improved outcomes suggest an opportunity for improved care through the implementation of an lung-protective ventilation protocol favoring lower driving pressure. Additionally, our observation that intraoperative driving pressure, but not VT or PEEP, was independently associated with postoperative pulmonary complications, reflects a potential benefit of individualized ventilation strategies among patients with varying respiratory compliance (ignored with VT-targeted ventilator management) or varying volume of aerated functional lung (ignored with uniform application of PEEP). However, given the observational nature of this study, our findings require prospective interventional evaluation and validation before large-scale adoption of the technique.

Our 10.9% observed incidence of postoperative pulmonary complications is consistent with previous studies.[1,6] However, this comparison is challenged by varied definitions of a postoperative pulmonary complication, which remain subject to debate. Our postoperative pulmonary complication definition is consistent with international consensus guidelines[35,36] and was derived from clinician-adjudicated data available within the Society of Thoracic Surgeons database or our electronic health record. Nonetheless, other recognized components of postoperative pulmonary complications include (1) atelectasis defined by radiographic evidence, (2) pulmonary aspiration defined by clinical history and radiographic evidence,[35] (3) pleural effusion defined by radiographic evidence,[36] (4) pneumothorax,[35] (5) bronchospasm defined by expiratory wheezing treated with bronchodilators,[36] or (6) aspiration pneumonitis.[36] We determined a priori to exclude these additional postoperative pulmonary complication components in our composite outcome on the basis of either unclear clinical significance in a cardiac surgical population, underlying mechanisms likely not amenable to treatment via lung-protective ventilation, or lack of access to component-specific high-fidelity data across all patients in the study cohort.

Study Limitations

Our study has several limitations. First, we were unable to account for all potential mechanisms leading to a composite postoperative pulmonary complication. Mechanisms for pulmonary injury after cardiac surgery are multifactorial.[7] In our study, we investigated lung-protective ventilation as a means to reduce ventilator-induced lung injury, leading to postoperative pulmonary complications through mechanisms including volutrauma, barotrauma, and atelectasis, and respectively mitigated by lower VT, lower driving pressure, and application of PEEP.[8] However, additional postoperative pulmonary complication mechanisms to be targeted by anesthesiologists include (1) pulmonary edema, mitigated by fluid and transfusion management,[49] (2) inadequate respiratory effort, mitigated by monitoring/reversal of neuromuscular blockade[50,51] or rapid-acting, opioid-limiting anesthetic agents,[52] and (3) respiratory infection, mitigated by ventilator associated pneumonia prevention bundles.[53,54] In our study, we successfully accounted for several of these targets as covariates. However, the relative importance of each technique, and the impact of lung-protective ventilation on the association between such techniques and postoperative pulmonary complications, remains beyond the scope of this study.

In our study, precise times for sternotomy and chest closure were unavailable; however, cases excluded redo-sternotomies with protracted closed chest times. As such, driving pressures were assessed during open-chest conditions for a majority of intraoperative ventilation. Our study adds new data to studies of protective ventilation, previously performed during closed-chest conditions. As this relates to the driving pressures observed, our study may demonstrate comparatively less bias introduced by variable chest wall compliance. Thus, airway driving pressure in this study is likely to more closely reflect actual transpulmonary driving pressure, a determinant of dynamic lung strain.[55] Despite this strength, we caution generalizing our findings to more commonly studied patient populations ventilated under closed-chest conditions. We additionally caution generalizing our driving pressure threshold below 16 cm H2O as lung-protective ventilation without consideration of clinical context. In previous studies of cardiac surgical populations,[16,37] thresholds for lung-protective ventilation defined by driving pressure (plateau pressure – PEEP) ranged from 8 to 19 cm H2O. Such variation may be explained by (1) time of measurement (e.g., intraoperative versus postoperative), (2) surgical conditions (e.g., closed-chest versus open-chest), (3) patient populations and practice patterns varying by year and institution, and (4) covariates used for multivariable adjustment. However, it should be noted that despite such sources of variation influencing driving pressure-based lung-protective ventilation thresholds, independent associations between increased ventilator driving pressures and increased postoperative complications have been consistently observed.

Additional limitations to our study include those inherent to our single-center, observational study design: our conclusions require prospective multicenter validation. Patients receiving a lung-protective ventilation bundle were nonrandom; although multiple covariates associated with the lung-protective ventilation exposure were accounted for via multivariable analyses, unmeasured confounders influencing receiving a lung-protective ventilation bundle and impacting our postoperative pulmonary complication primary outcome was a source of potential bias. As pertaining to our lung-protective ventilation exposure variable, limitations included a lack of formal Pplat ventilator data for more accurate characterization of driving pressure. Although differences between ventilator peak inspiratory pressure and Pplat may be approximated in specified circumstances, the availability of all data necessary for calculations—and the degree to which confounding factors may bias such calculations (e.g., patient differences in airway resistance, endotracheal tube obstructions from kinking/secretions, and the use of end-inspiratory pressure to approximate inspiratory pause pressure for calculating true Pplat)—remain beyond the scope of our study.

Consistent with existing literature,[1,28] we represented the intraoperative period using lung-protective ventilation exposure median values—potentially failing to account for brief periods of profoundly injurious ventilation. Finally, although our study goal was to specifically examine relationships between intraoperative ventilation and postoperative pulmonary complications, relationships between postoperative ventilation and postoperative pulmonary complications were not studied.

Conclusions

Despite limitations, our study advances understanding of the relationship between intraoperative lung-protective ventilation and impact on costly, life-threatening postoperative pulmonary complication outcomes. In summary, we describe a 10.9% incidence of postoperative pulmonary complications among adults undergoing cardiac surgery. Importantly, we observed that a bundled lung-protective ventilation strategy was independently associated with a lower likelihood of postoperative pulmonary complications and that this was mostly associated with lower driving pressure. Through robust capture of variables describing intraoperative anesthesia management for cardiac surgery patients, our study provides data which may better inform postoperative pulmonary complication multivariable models in this population. Additionally, our findings offer targets for future prospective trials investigating the impact of specific lung-protective ventilation strategies for improving cardiac surgery outcomes.

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