Brazilian Journal of Anesthesiology
https://bjan-sba.org/article/doi/10.1590/S0034-70942006000300006
Brazilian Journal of Anesthesiology
Clinical Information

Análise da celularidade do lavado bronco-alveolar em pacientes submetidos à revascularização do miocárdio com circulação extracorpórea: relato de três casos

Broncho-alveolar lavage cellularity in patients submitted to myocardial revascularization with cardiopulmonary bypass: three case reports

Luciano Brandão Machado; Luciana Moraes dos Santos; Elnara Márcia Negri; Luiz Marcelo Sá Malbouisson; José Otávio Costa Auler Júnior; Maria José Carvalho Carmona

Downloads: 0
Views: 1204

Resumo

JUSTIFICATIVA E OBJETIVOS: A circulação extracorpórea (CEC) é um dos principais determinantes da resposta inflamatória sistêmica (SIRS) em cirurgia cardíaca. Demonstrou-se em modelo experimental que a CEC pode levar a aumento na produção das citocinas. No intuito de avaliar a ativação celular no pulmão após CEC, foi estudada a celularidade no lavado bronco-alveolar (LBA) em pacientes submetidos à cirurgia de revascularização do miocárdio (RM) com CEC. RELATO DOS CASOS: Foram estudados, prospectivamente, três pacientes adultos submetidos à RM com CEC. Após indução de anestesia geral e intubação traqueal, a ventilação mecânica foi realizada com sistema circular valvular; exceto durante a CEC, o volume corrente foi mantido entre 8 e 10 mL.kg-1 com O2 e ar, numa proporção de 50%. Antes do despinçamento da aorta, foram realizadas insuflações pulmonares com pressão de 40 cmH2O e coletadas duas amostras de LBA de cada paciente, no início da intervenção cirúrgica e ao final do procedimento, após a reversão da anticoagulação. Após a infusão de 60 mL de solução fisiológica a 0,9% pelo canal do broncofibroscópio, foi aspirado o LBA, sendo o material encaminhado para processamento laboratorial. A análise evidenciou aumento do número total de células, em média, de 0,6.10(6) cél.dL-1 para 6,8.10(6) cél.dL-1 com aumento de neutrófilos de 0,8% para 4,7%; 0,6% para 6,2% e 0,5% para 5,3% em cada paciente, respectivamente. Observou-se na lâmina o aumento de celularidade no fluido pulmonar após a CEC. CONCLUSÕES: O influxo leucocitário é descrito em diversas condições clínicas pulmonares inflamatórias, como na síndrome da angústia respiratória do adulto. Sabe-se que a CEC está relacionada com a inflamação sistêmica e pulmonar, demonstrando aumento do número de células após a CEC com o predomínio de macrófagos.

Palavras-chave

CIRURGIA, Cardíaca, CIRURGIA, Cardíaca, COMPLICAÇÕES

Abstract

BACKGROUND AND OBJECTIVES: Cardiopulmonary bypass (CPB) is a primary determinant of systemic inflammatory response (SIRS) during cardiac procedures. It has been shown in an experimental model that CPB may increase cytokine production. This study aimed at evaluating post-CPB lung cell activation by investigating broncho-alveolar lavage (BAL) cellularity in patients submitted to myocardial revascularization (MR) with CPB. CASE REPORTS: Participated in this prospective study 3 adult patients submitted to MR with CPB. After general anesthesia induction and tracheal intubation, mechanical ventilation was installed with valve circle system; except during CPB, tidal volume was maintained between 8 and 10 mL.kg-1 with 50% O2 and air. Before aortic unclamping, 40 cmH2O pulmonary inflations were performed. Two BAL samples were collected from all patients at beginning and end of procedure, after anticoagulation reversion. BAL was aspired after 60 mL infusion of 0.9% saline through the bronchofibroscope tube. Material was then referred to laboratorial processing. Analysis has evidenced mean increase in total number of cells from 0.6 × 10(6)cel.dL-1 to 6.8 × 10(6) cel.dL-1 with increased neutrophils from 0.8% to 4.7%; 0.6% to 6.2% and 0.5% to 5.3% for each patient, respectively. There has been increased pulmonary fluid cellularity after CPB. CONCLUSIONS: Leukocyte inflow is described in different clinical pulmonary inflammatory conditions, such as adult respiratory distress syndrome. It is known that CPB is related to systemic and pulmonary inflammation with increased number of cells after CPB and predominance of macrophages.

Keywords

COMPLICATIONS, SURGERY, Cardiac, SURGERY, Cardiac

References

Bennett-Guerrero E. Systemic Inflammation. Cardiac Anesthesia. 2000:297-320.

Brix-Christensen V, Petersen TK, Ravn HB. Cardiopulmonary bypass elicits a pro- and anti-inflammatory cytokine response and impaired neutrophil chemotaxis in neonatal pigs. Acta Anaesthesiol Scand. 2001;45:407-413.

Harlan JM. Neutrophil-mediated vascular injury. Acta Med Scand. 1987;715:123-129.

Cain BS, Shannon-Cain J. Cardiopulmonary bypass: homemade sepsis?. Crit Care Med. 2003;31:1281-1282.

Grace PA. Ischaemia-reperfusion injury. Br J Surg. 1994;81:637-647.

Hall RI, Smith MS, Rocker G. The systemic inflammatory response to cardiopulmonary bypass: pathophysiological, therapeutic, and pharmacological considerations. Anesth Analg. 1997;85:766-782.

Kollef MH, Wragge T, Pasque C. Determinants of mortality and multiorgan dysfunction in cardiac surgery patients requiring prolonged mechanical ventilation. Chest. 1995;107:1395-1401.

Kotani N, Hashimoto H, Sessler DI. Neutrophil number and interleukin-8 and elastase concentrations in bronchoalveolar lavage fluid correlate with decreased arterial oxygenation after cardiopulmonary bypass. Anesth Analg. 2000;90:1046-1051.

Higgins TL, Estafanous FG, Loop FD. Stratification of morbidity and mortality outcome by preoperative risk factors in coronary artery bypass patients. A clinical severity score. JAMA. 1992;267:2344-2348.

Cotran RS. Inflammation and Repair. Robbins Pathologic Basis of Disease. 1994;51.

Laffey JG, Boylan JF, Cheng DC. The systemic inflammatory response to cardiac surgery: implications for the anesthesiologist. Anesthesiology. 2002;97:215-252.

Wynne R, Botti M. Postoperative pulmonary dysfunction in adults after cardiac surgery with cardiopulmonary bypass: clinical significance and implications for practice. Am J Crit Care. 2004;13:384-393.

Macnaughton PD. Changes in lung function and pulmonary capillary permeability after cardiopulmonary bypass. Crit Care Med. 1992;20:1289-1294.

Asimakopoulos G. Lung injury and acute respiratory distress syndrome after cardiopulmonary bypass. Ann Thorac Surg. 1999;68:1107-1115.

Taggart D. Respiratory dysfunction after uncomplicated cardiopulmonary bypass. Ann Thorac Surg. 1993;56:1123-1128.

Massoudy P, Zahler S, Becker BF. Evidence for inflammatory responses of the lungs during coronary artery bypass grafting with cardiopulmonary bypass. Chest. 2001;119:31-36.

Bernardes CES, Messias ERR, Carmona MJC. Considerações anestésico-cirúrgicas sobre a revascularização do miocárdio através de minitoracotomia. Rev Bras Anestesiol. 1999;49:196-200.

Rinder C, Fitch J. Amplification of the inflammatory response: adhesion molecules associated with platelet/white cell responses. J Cardiovasc Pharmacol. 1996;27(^s1):S6-S12.

Hill GE, Alonso A, Spurzem JR. Aprotinin and methylprednisolone equally blunt cardiopulmonary bypass-induced inflammation in humans. J Thorac Cardiovasc Surg. 1995;110:1658-1662.

Kotani N, Hashimoto H, Sessler DI. Cardiopulmonary bypass produces greater pulmonary than systemic proinflammatory cytokines. Anesth Analg. 2000;90:1039-1045.

Jorens PG, De Jongh R, De Backer W. Interleukin-8 production in patients undergoing cardiopulmonary bypass: The influence of pretreatment with methylprednisolone. Am Rev Respir Dis. 1993;148:890-895.

Tsuchida M, Watanabe H, Watanabe T. Effect of cardiopulmonary bypass on cytokine release and adhesion molecule expression in alveolar macrophages: Preliminary report in six cases. Am J Respir Crit Care Med. 1997;156:932-938.

Wan S, DeSmet JM, Barvais L. Myocardium is a major source of proinflammatory cytokines in patients undergoing cardiopulmonary bypass. J Thorac Cardiovasc Surg. 1996:806-811.

Wachtfogel YT, Kucich U, Greenplate J. Human neutrophil degranulation during extracorporeal circulation. Blood. 1987;69:324-330.

Riegel W, Spillner G, Schlosser V. Plasma levels of main granulocyte components during cardiopulmonary bypass. J Thorac Cardiovasc Surg. 1988;95:1014-1019.

Luce JM. Acute lung injury and the acute respiratory distress syndrome. Crit Care Med. 1998;26:369-376.

Gu YJ, van Oeveren W, Boonstra PW. Leukocyte activation with increased expression of CR3 receptors during cardiopulmonary bypass. Ann Thorac Surg. 1992;53:839-843.

Osborn L. Leukocyte adhesion to endothelium in inflammation. Cell. 1990;62:3-6.

Herskowitz A, Mangano DT. Inflammatory cascade. A final common pathway for perioperative injury?. Anesthesiology. 1996;85:957-960.

Kharazmi A, Andersen LW, Baek L. Endotoxemia and enhanced generation of oxygen radicals by neutrophils from patients undergoing cardiopulmonary bypass. J Thorac Cardiovasc Surg. 1989;98:381-385.

Royston D, Fleming JS, Desai JB. Increased production of peroxidation products associated with cardiac operations. Evidence for free radical generation. J Thorac Cardiovasc Surg. 1986;91:759-766.

Boutten A, Dehoux MS, Seta N. Compartmentalized IL-8 and elastase release within the human lung in unilateral pneumonia. Am J Respir Crit Care Med. 1996;153:336-342.

Friedman M, Sellke FW, Wang SY. Parameters of pulmonary injury after total or partial cardiopulmonary bypass. Circulation. 1994;90:II262-II268.

Maggart M, Stewart S. The mechanisms and management of noncardiogenic pulmonary edema following cardiopulmonary bypass. Ann Thorac Surg. 1987;43:231-236.

Zahler S, Massoudy P, Hartl H. Acute cardiac inflammatory responses to postischemic reperfusion during cardiopulmonary bypass. Cardiovasc Res. 1999;41:722-730.

Shafique T, Johnson RG, Dai HB. Altered pulmonary microvascular reactivity after total cardiopulmonary bypass. J Thorac Cardiovasc Surg. 1993;106:479-486.

Erez E, Erman A, Snir E. Thromboxane production in human lung during cardiopulmonary bypass: beneficial effect of aspirin?. Ann Thorac Surg. 1998;65:101-106.

Hachenberg T, Tenling A, Nystrom SO. Ventilation-perfusion inequality in patients undergoing cardiac surgery. Anesthesiology. 1994;80:509-519.

Magnusson L, Zemgulis V, Wicky S. Atelectasis is a major cause of hypoxemia and shunt after cardiopulmonary bypass: an experimental study. Anesthesiology. 1997;87:1153-1163.

Kisala JM, Ayala A, Stephan RN. A model of pulmonary atelectasis in rats: activation of alveolar macrophage and cykine release. Am J Physiol. 1993;264:R610-R614.

Ranucci M, Mazzucco A, Pessotto R. Heparin-coated circuits for high-risk patients: a multicenter, prospective, randomized trial. Ann Thorac Surg. 1999;67:994-1000.

Fromes Y, Gaillard D, Ponzio O. Reduction of the inflammatory response following coronary bypass grafting with total minimal extracorporeal circulation. Eur J Cardiothorac Surg. 2002;22:527-533.

Gunaydin S, Farsak B, Kocakulak M. Clinical performance and biocompatibility of poly(2-methoxyethylacrylate)-coated extracorporeal circuits. Ann Thorac Surg. 2002;74:819-824.

5dd42f890e8825a738c63493 rba Articles
Links & Downloads

Braz J Anesthesiol

Share this page
Page Sections