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Is Selective Pulmonary Perfusion Required to Mitigate Lung Injury Postcardiopulmonary Bypass?

Beer, Lucian MD, PhD; Ankersmit, Hendrik Jan MD, MBA; Dworschak, Martin MD, MBA

doi: 10.1213/ANE.0000000000001521
Letters to the Editor: Letter to the Editor
Free

Published ahead of print July 26, 2016.

Department of Biomedical Imaging and Image-Guided Therapy, Medical University of Vienna, Vienna, Austria

Department of Thoracic Surgery, Medical University of Vienna, Vienna, Austria

Department of Anesthesia, General Intensive Care, and Pain Management, Medical University of Vienna, Vienna, Austria, martin.dworschak@meduniwien.ac.at

Published ahead of print July 26, 2016.

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To the Editor

We read with interest the article by da Costa Freitas et al1 on the effect of pulmonary perfusion and ventilation during cardiopulmonary bypass (CPB) on lung injury in swine.

Pulmonary ischemia/reperfusion (I/R) is a complex phenomenon and a reason for poor oxygenation and lung compliance observed after CPB. However, pulmonary I/R in this setting is distinct from anoxic pulmonary I/R, in which all 3 sources of lung oxygenation (ventilation, pulmonary, and bronchial artery blood flow) temporarily ceased.

One approach to tackle pulmonary I/R damage is to maintain pulmonary perfusion and ventilation during CPB as the authors did. Their strategy attenuated lung injury and improved oxygenation and lung function postoperatively. However, the fast recovery probably reflects avoidance of myocardial ischemia in healthy young pigs. Unlike these animals, multimorbid patients frequently exhibit prolonged impairment after cardiac surgery on CPB. Interestingly, this investigation also revealed that interleukins (ILs)-6, -8, and -10 in plasma and bronchoalveolar lavage fluid were not different between the treatment and the control groups; this indicates equivalent chemokine release within the lung, probably attributable to high tidal volume ventilation, causing augmented release of inflammatory markers through alveolar strain.

Other perfusion models with a collapsed lung have already been used clinically. Nonpulsatile intermittent perfusion with deoxygenated blood during CPB has not yet shown any benefits. It not only failed to attenuate impairment of gas exchange, but it also yielded similar results to controls regarding serum chemokine levels and was associated with prolonged aortic cross-clamp and bypass time. In contrast, pulsatile perfusion with oxygenated blood reduced the inflammatory response and improved oxygenation.2 These data highlight that the mode of pulmonary perfusion with or without concomitant ventilation differentially impact postoperative lung function.

Furthermore, biventricular bypass with high tidal volume ventilation, as used in the current investigation, implicates greater invasiveness and complexity. It goes along with enlargement of the artificial contact surface and poses an additional workload for surgeons and perfusionists. Therefore, the benefits of this technique should clearly outweigh its undisputable disadvantages.

In patients undergoing coronary artery bypass grafting surgery, we could demonstrate that simple continued lung protective ventilation during CPB mitigated systemic pro-inflammatory and anti-inflammatory markers (eg, IL-6, IL-10, matrix metalloproteinases, and soluble suppression of tumorigenicity [sST2]).3 It also improved the oxygenation index up to 6 hours postoperatively.4 Ventilated ischemia in an isolated rat lung model further preserved lung adenosine triphosphate content when lungs were ventilated with a low oxygen gas mixture during ischemia, indicating satisfactory substrate availability for adenosine triphosphate synthesis and sufficient oxygen supply through alveolar diffusion.5

Therefore, continued low tidal volume ventilation during CPB with supplemental bronchial artery blood flow may just be as efficacious as its combination with pulmonary perfusion. It can be easily implemented with hardly any impact on the surgical procedure and duration, and it should ensure adequate oxygen delivery and mechanotransduction to the most vulnerable cells of the lung located close to the alveolus that also trigger cytokine release. Thereby, cannulation of the pulmonary artery and the added risks for hemolysis, complement activation, and surgical injury can be obviated. Why not keep it simple if the effect is comparable?

Lucian Beer, MD, PhDDepartment of Biomedical Imaging andImage-Guided TherapyMedical University of ViennaVienna, Austria

Hendrik Jan Ankersmit, MD, MBADepartment of Thoracic SurgeryMedical University of ViennaVienna, Austria

Martin Dworschak, MD, MBADepartment of Anesthesia, General Intensive Care,and Pain ManagementMedical University of ViennaVienna, Austriamartin.dworschak@meduniwien.ac.at

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REFERENCES

1. da Costa Freitas CR, Sa Malbouisson LM, Benicio A, et al. Lung perfusion and ventilation during cardiopulmonary bypass reduces early structural damage to pulmonary parenchyma. Anesth Analg. 2016;122:943952.
2. Santini F, Onorati F, Telesca M, et al. Pulsatile pulmonary perfusion with oxygenated blood ameliorates pulmonary hemodynamic and respiratory indices in low-risk coronary artery bypass patients. Eur J Cardiothorac Surg. 2011;40:794803.
3. Beer L, Szerafin T, Mitterbauer A, et al. Continued mechanical ventilation during coronary artery bypass graft operation attenuates the systemic immune response. Eur J Cardiothorac Surg. 2013;44:282287.
4. Beer L, Warszawska JM, Schenk P, et al. Intraoperative ventilation strategy during cardiopulmonary bypass attenuates the release of matrix metalloproteinases and improves oxygenation. J Surg Res. 2015;195:294302.
5. Fisher AB, Dodia C, Tan ZT, Ayene I, Eckenhoff RG. Oxygen-dependent lipid peroxidation during lung ischemia. J Clin Invest. 1991;88:674679.
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