Ultraprotective Ventilation during CPB Protects the Alveolar-Capillary Barrier in Pulmonary Normotensive Congenital Heart Patients

Authors

  • Ugur Gocen Department of Cardiovascular Surgery, Cukurova University Medical Faculty, Adana,
  • Atakan Atalay Department of Cardiovascular Surgery, Cukurova University Medical Faculty, Adana,

DOI:

https://doi.org/10.1532/hsf.1766

Abstract

Background: Alveolar-capillary membrane damage develops as a result of the inflammatory effect of cardiopulmonary bypass (CPB). In the presence of a healthy alveolar-capillary barrier, there is little or no surfactant in the blood. The aim of this study was to evaluate the protective effects of ultraprotective ventilation during CPB by measuring serum and bronchoalveolar lavage (BAL) surfactant protein B (SPB) values in congenital heart surgery.

Methods: This prospective study was designed for
46 patients with congenital heart defects. Patients were classified into two groups: group 1 comprising pulmonary normotensive patients and group 2 consisting of pulmonary hypertensive (PH) patients. Each group was divided into two sub-groups: (a) those who received ultraprotective ventilation during CPB and (b) those who did not receive ultraprotective ventilation during CPB. Serum SPB (S-SPB) values were measured preoperatively (ST1); at the fourth hour postop (ST2); and at the 24th hour postop (ST3). BAL SPB values were measured preoperatively (BT1); and at the fourth hour postop (BT2). 

Results: ST1, ST2, and ST3 values of group 1a (pulmonary normotensive ventilated patients) and group 1b (pulmonary normotensive non-ventilated patients) were much lower than those of group 2a (pulmonary hypertensive ventilated patients) and group 2b (pulmonary hypertensive non-ventilated patients) (P < .05). The evaluation of ST1, ST2, and ST3 values between groups 1a and 1b did not show statistically significant differences. When comparing ST1 to ST3, a decrease in value was observed in group 1a (32.28 ± 13.27 ng/mL to 19.38 ± 7.6 ng/mL) (P = .006). In Group 1b, values increased between ST1 and ST2 before decreasing from ST2 to ST3; however, the ST3 values were still higher than their ST1 counterparts. It was recorded that there was no statistically significant difference between the ST1, ST2, and ST3 values of group 2a and group 2b. A comparison of the BT1 and BT2 values in groups also yielded no statistically significant differences. 

Conclusion: Although pulmonary hypertension is known to result in lung injury, this study is important as it shows that ultraprotective ventilation protects the alveolar-capillary barrier in pulmonary normotensive congenital heart patients. 

References

Serrano AG, Perez-Gil J. Protein-lipid interactions and surface activity in the pulmonary surfactant system. Chem Phys Lipids 2006; 141: 105–18.

F. R. Poulain, L. Allen, M. C. Williams, R. L. Hamilton, S. Hawgood.Effects of surfactant apolipoproteins on liposome structure: implications for tubular myelin formation. Am J Physiol 1992; 262: 730–9.

P. Agostoni, C. Banfi, M. Brioschi, D. Magrì, S. Sciomer, G. Berna, C. Brambillasca, G. Marenzi, E. Sisillo.Surfactant protein B and RAGE increases in the plasma during cardiopulmonary bypass: a pilot study. European Respiratory Journal 2011; 37: 841–7.

Gerwin E Engels, Y John Gu, Willem van Oeveren, Gerhard Rakhorst , Massimo A Mariani and Michiel E Erasmus. The utility of lung epithelium specific biomarkers in cardiac surgery: a comparison of biomarker profiles in on- and off-pump coronary bypass surgery. Journal of Cardiothoracic Surgery 2013; 8: 4.

Gerwin E. Engels, Jan van Klarenbosch , Y. John Gu , Willem van Oeveren and Adrianus J. de Vries. Intraoperative cell salvage during cardiac surgery is associated with reduced postoperative lung injury. Interactive CardioVascular and Thoracic Surgery 2016; 22: 298–304.

The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000; 342: 1301–8.

Futier E, Constantin JM, Paugam-Burtz C, Pascal J, Eurin M, Neuschwander A, Marret E, Beaussier M, Gutton C, Lefrant JY, Allaouchiche B, Verzilli D, Leone M, De Jong A, Bazin JE, Pereira B, Jaber S.A trial of intraoperative low-tidal-volume ventilation in abdominal surgery. N Engl J Med 2013; 369: 428–37.

Sundar S, Novack V, Jervis K, et al. Influence of low tidal volume ventilation on time to extubation in cardiac surgical patients. Anesthesiology 2011; 114: 1102–10.

Schreiber JU, Lancé MD, de Korte M, Artmann T, Aleksic I, Kranke P.The effect of different lung-protective strategies in patients during cardiopulmonary bypass: a meta-analysis and semiquantitative review of randomized trials. J Cardiothorac Vasc Anesth 2012; 26: 448–54.

Pasquina P, Tramer MR, Walder B. Prophylactic respiratory physiotherapy after cardiac surgery: systematic review. BMJ 2003; 327: 1379.

Magnusson L, Zemgulis V,Tenlig A, Wernlund J, Tyden H, Thelin S, Hedenstierna G. Use of a vital capacity maneuver to prevent atelectasis after cardiopulmonary bypass: An experimental study. Anesthesiology 1998; 88: 134-42.

Berry CB, Butler PJ, Myles PS: Lung management during cardiopulmonary bypass: Is continuous positive airway pressure beneficial? Br J Anaesth 1993; 71: 864-8.

Royston D: The inflammatory response and extracorporeal circulation. J Cardiothorac Vasc Anesth 1997; 11: 341-54.

Westaby S, Fleming J, Royston D: Acute lung injury during cardiopulmonary bypass, the role of neutrophil sequestration and lipid peroxidation. TransAm Soc Artif Intern Organs 1985; 31: 604-9.

Hachenberg T, Tenling A, Nyström SO, Tyden H, Hedenstierna G.: Ventilationperfusion inequality in patients undergoing cardiac surgery. Anesthesiology 1994; 80: 509-19.

De Pasquale CG, Arnolda LF, Doyle IR, Grant RL, Aylward PE, Bersten AD.Prolonged alveolocapillary barrier damage after acute cardiogenic pulmonary edema. Crit Care Med 2003; 31: 1060–7.

Dobbs LG. Pulmonary surfactant. Ann Rev Med 1989; 40: 431-46.

Hamm H, Fabel H, Bartsch W. The surfactant system of the adult lung: Physiology and clinical perspectives. Clin Invest 1992; 70: 637-57.

Ng CS, Wan S, Yim AP, Arifi AA: Pulmonary dysfunction after cardiac surgery. Chest 2002; 121: 1269-77

Berry CB, Butler PJ, Myles PS: Lung management during cardiopulmonary bypass: is continuous positive airways pressure beneficial?. Br J Anaesth 1993; 71: 864-8.

Keavey PM, Hasan A, Au J, Dark JH: The use of 99Tcm-DTPA aerosol and caesium iodide mini-scintillation detectors in the assessment of lung injury during cardiopulmonary bypass surgery. Nucl Med Commun 1997; 18: 38-43.

De Haan J, Boonstra PW, Monnink SH, Ebels T, van Oeveren W. Retransfusion of suctioned blood during cardiopulmonary bypass impairs hemostasis. Ann Thorac Surg 1995; 4: 901–7.

Greene KE1, Wright JR, Steinberg KP, Ruzinski JT, Caldwell E, Wong WB, Hull W, Whitsett JA, Akino T, Kuroki Y, Nagae H, Hudson LD, Martin TR.Serial changes in surfactant-associated proteins in lung and serum before and after onset of ARDS. Am J Respir Crit Care Med 1999; 160: 1843–50.

Chang AC. Inflammatory mediators in children undergoing cardiopulmonary bypass: is there a unified field theory amidst this biomolecular chaos? Pediatr Crit Care Med 2003; 4: 386–7.

Gott JP1, Cooper WA, Schmidt FE Jr, Brown WM 3rd, Wright CE, Merlino JD, Fortenberry JD, Clark WS, Guyton RA.Modifying risk for extracorporeal circulation: trial of four antiinflammatory strategies. Ann Thorac Surg 1998; 66: 747–53.

Published

2017-05-01

How to Cite

Gocen, U., & Atalay, A. (2017). Ultraprotective Ventilation during CPB Protects the Alveolar-Capillary Barrier in Pulmonary Normotensive Congenital Heart Patients. The Heart Surgery Forum, 20(2), E045-E051. https://doi.org/10.1532/hsf.1766

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