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Inhaled Nitric Oxide for the Prevention of Impaired Arterial Oxygenation during Myocardial Revascularization with Extracorporeal Circulation

https://doi.org/10.15360/1813-9779-2011-1-31

Abstract

Objective: to study the efficacy of inhaled nitric oxide used intraoperatively to prevent lung oxygenating dysfunction in patients with coronary heart disease after myocardial revascularization under extracorporeal circulation (EC). Subjects and methods. Thirty-two patients aged 55.0±2.0 years were examined. The inclusion criteria were the standard course of surgical intervention (the absence of hemorrhage, acute cardiovascular insufficiency, perioperative myocardial infarction, etc.), a pulmonary artery wedge pressure of less than 15 – mm Hg throughout the study, and the baseline arterial partial oxygen tension/inspired mixture oxygen fraction (PaO2/FiO2) ratio of at least 350 mm Hg. There was a control group (n=21; Group 1) that used no special measures to prevent and/or to correct lung oxygenating dysfunction and Group 2 (n=11) that received inhaled nitric oxide. Ihe administration of inhaled nitric oxide at a concentration of 10 ppm was initiated after water anesthesia, stopped during EC, and resumed in the postperfusion period. Results. At the end, PaO2/FiO2 and intrapulmonary shunt fraction did not differ between the groups (p>0.05). Before EC, the patients receiving inhaled nitric oxide had a lower intrapulmonary blood shunting (8.9±0.7 and 11.7±1.0%; p<0.05). There were no intergroup differences in the values of PaO2/FiO2 at this stage. In the earliest postperfusion period, PaO2/FiO2 was higher in Group 2 than that in Group 1. At the end of operations, Groups 1 and 2 had a PaO2/FiO2 of 336.0±16.8 and 409.0±24.3 mm Hg, respectively (p<0.05) and an intrapulmonary shunt fraction of 14.5±1.0 and 10.4±1.0% (p<0.05). At the end of surgery, the rate of a reduction in PaO2/FiO2 to the level below 350 mm Hg was 52.4±11.1% in Group 1 and 18.2±11.6% in Group 2 (p<0.05). Six hours after surgery, PaO2/FiO2 values less than 300 mm Hg were diagnosed in 61.9±10.5% of Group 1 patients and in 27.3±13.4% of Group 2 ones (p<0.05). Conclusion. The prescription of inhaled nitric oxide at a concentration of 10 ppm to patients with the baseline normal level of PaO2/FiO2 ensured the prevention of lung oxygenating dysfunction in the postperfusion and early postoperative period. The preventive effect of inhaled nitric oxide was steady-state: 6 hours following myocardial revascularization under EC, the patients intraoperatively receiving inhaled nitric oxide showed a 2.3-fold lower rate of lung oxygenating dysfunction (PaO2/FiO2 less than 300 mm Hg) than the controls. Key words: lung oxygenating function, inhaled nitric oxide, operations under extracorporeal circulation, lung ischemia-reperfusion.

References

1. Козлов И. А, Дзыбинская Е. В., Романов А. А., Баландюк А. Е.

2. Дзыбинская Е. В., Воронина И. В, Козлов И. А.Ранняя активизация больных после реваскуляризации миокарда в условиях длительного искусственного кровообращения. Анестезиология и реаниматология 2008; 5: 22—26.

3. Козлов И. А., Романов А. А.Биомеханика дыхания, внутрилегочная вода и оксигенирующая функция лёгких во время неосложнённых операций с искусственным кровообращением. Общая реаниматология 2007; III (3): 17—22.

4. Романов А. А.Предикторы состояния оксигенирующей функции лёгких при неосложнённых операциях с искусственным кровообращением. Общая реаниматология 2007; III (5—6): 199—203.

5. Weiss Y. G., Merin G., Koganov E. et al.Postcardiopulmonary bypass hypoxemia: a prospective study on incidence, risk factors and clinical significance. J. Cardiothorac. Vasc. Anesth. 2000; 14 (5): 506—513.

6. Chai P. J., Williamson J. A., Lodge A. J. et al.Effects of ischemia on pulmonary dysfunction after cardiopulmonary bypass. Ann. Thorac. Surg. 1999; 67 (3): 731—735.

7. Dodd-o J. M., Welsh L. E., Salazar J. D. et al.Effect of bronchial artery blood flow on cardiopulmonary bypass-induced lung injury. Am. J. Physiol. Heart Circ. Physiol. 2004; 286 (2): H693—H700.

8. Schlensak C., Doenst T., Beyersdorf F.Lung ischemia during cardiopul-monary bypass. Ann. Thorac. Surg. 2000; 70 (1): 337—33

9. Козлов И. А., Романов А. А.Особенности транспорта кислорода при нарушении оксигенирующей функции легких в ранние сроки после искусственного кровообращения. Общая реаниматология 2009; V (6): 13—20.

10. Appel P .L., Shoemaker W. C.Relationship of oxygen consumption and oxygen delivery in surgical patients with ARDS. Chest 1992; 102 (3): 906—911.

11. Leach R. M., Treacher D. F.Clinical aspects of hypoxic pulmonary vasoconstriction. Exp. Physiol. 1995; 80 (5): 865—875.

12. Suematsu Y., Sato H., Ohtsuka T. et al.Predictive risk factors for pulmonary oxygen transfer in patients undergoing coronary artery bypass grafting. Jpn. Heart J. 2001; 42 (2): 143—153.

13. Chatila W. M., Furukawa S., Gaughan J. P., Criner G. J.Respiratory failure after lung transplantation. Chest 2003; 123 (1): 165—173.

14. de Perrot M., Liu M., Waddell T. K., Keshavjee S.Ischemia-reperfusion-induced lung injury. Am. J. Respir. Crit. Care Med. 2003; 167 (4): 490—511.

15. Баландюк А. Е., Вершута Д. В., Козлов И. А.Оксид азота для профилактики и лечения артериальной гипоксемии при операциях на восходящей аорте (предварительное сообщение). Общая реаниматология 2006; II (5—6): 133—135.

16. Meade M. O., Granton J. T., Matte-Martyn A. et al.A randomized trial of inhaled nitric oxide to prevent ischemia-reperfusion injury after lung transplantation. Am. J. Respir. Crit. Care Med. 2003; 167 (11): 1483—1489.

17. КозловИ. А., ПопцовВ. H.Ингаляционная окись азота ^и тpанс-плантации сеpдца. Анестезиология и pеаниматология 1999; 5: 9—12.

18. Зильбер А. П.Патологическая физиология для анестезиологов. М.: Медицина; 1977.

19. Козлов И. А., Выжигина М. А., Бархи М. Л.Метаболические функции легких. Анестезиология и pеаниматология 1983; 1: 67—76.

20. Дворецкий Д. П., Ткаченко Б. И.Гемодинамика в легких. М.: Медицина; 1987.

21. Shoemaker W. C., Patil R., Appel P. L., Kram H. B.Hemodynamic and oxygen transport patterns for outcome prediction, therapeutic goals, and clinical algorithm to improve outcome. Chest 1992; 102 (5 Suppl 2): 617S—625S.

22. Козлов И. А., Попцов В. Н., Алфёров А. В.Коррекция нарушений метаболизма оксида азота — новое патогенетическое направление интенсивной терапии в трансплантационной и сердечной хирургии. Вестн. трансплантологии и искусств. органов 2002; 3: 28—39.

23. Oemar B. S., Tschudi M. R., Godoy N. et al.Reduced endothelial nitric oxide synthase expression and production in human atherosclerosis. Circulation 1998; 97 (25): 2494—2498.

24. Le Cras T. D., McMurtry I. F.Nitric oxide production in the hypoxic lung. Am. J. Physiol. Lung Cell Mol. Physiol. 2001; 280 (4): L575—L582.

25. Frostell C. G., Blomqvist H., Hedenstierna G. et al.Inhaled nitric oxide reverses hypoxic pulmonary vasoconstriction without causing systemic vasodilation. Anesthesiology 1993; 78 (3): 427—435.

26. Bender K. A., Alexander J. A., Enos J. M., Skimming J. W.Effects of inhaled nitric oxide in patients with hypoxemia and pulmonary hypertension after cardiac surgery. Am. Crit. Care 1997; 6 (2): 127—131.

27. Rich G. F., Murphy G. D., Roos C. M., Johns R. A.Inhaled nitric oxide. Selective pulmonary vasodilatation in cardiac surgical patients. Anesthesiology 1993; 78 (6): 1028—1035.


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Kozlov I.A., Romanov A.A., Dzybinskaya E.V., Balandyuk A.E. Inhaled Nitric Oxide for the Prevention of Impaired Arterial Oxygenation during Myocardial Revascularization with Extracorporeal Circulation . General Reanimatology. 2011;7(1):31. (In Russ.) https://doi.org/10.15360/1813-9779-2011-1-31

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ISSN 1813-9779 (Print)
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