Hostname: page-component-586b7cd67f-dsjbd Total loading time: 0 Render date: 2024-11-26T15:06:22.706Z Has data issue: false hasContentIssue false

Effects of cardiopulmonary bypass on the coagulation system

Published online by Cambridge University Press:  19 August 2008

L. Henry Edmunds Jr*
Affiliation:
From the Department of Cardiac Surgery, The Hospital of the University of Pennsylvania, Philadelphia
*
Dr. L. Henry Edmunds, Jr., Department of Gardiac Surgery, The Hospital of the University of Pennsylvania, 4 Silverstein, 3400 Spruce Street, Philadelphia, PA 19104, USA. Tel. 215-662-2091.

Extract

Cardiopulmonary bypass makes a mess of homeostasis. Extracorporeal perfusion produces pulseless flow without physiologic controls, showers microemboli throughout the body, and brings blood diluted with additives to an enzymatic boil. Much of the morbidity associated with open heart surgery is due to contact of blood with the synthetic surfaces of the extracorporeal perfusion circuit. Bypass temporarily impairs function of every organ, alters concentrations of over 25 vasoactive substances within the plasma, and causes massive retention of fluid. In short, cardiopulmonary bypass makes patients sick.

Type
World Forum for Pediatric Cardiology Symposium on Cardiopulmonary Bypass (Part 1)
Copyright
Copyright © Cambridge University Press 1993

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

1.Edmunds, LH Jr. Pulseless cardiopulmonary bypass. J Thorac Cardiovasc Surg 1982; 84: 800804.Google Scholar
2.Blauth, CI, Smith, PL, Arnold, JV, Jagoe, JR, Wootton, R, Taylor, KM. Influence of oxygenator type on the prevalence and extent of microemboli retinal ischemia during cardiopulmonary bypass. J Thorac Cardiovasc Surg 1990; 99: 6169.CrossRefGoogle Scholar
3.Downing, SW, Edmunds, LH Jr. Release of vasoactive sub stances during cardioplumonary bypass. Ann Thorac Surg 1992; 54: 12361243.Google Scholar
4.Blackstone, EH, Kirklin, JW, Stewart, RW, Chenoweth, DE. The damaging effects ofcardiopulmonary bypass. In: Wu, KK, Roxy, EC (eds). Prostaglandins in Clinical Medicine: Cardio vascular and Thrombotic Disorders. Yearbook Medical Publishers Inc., Chicago, 1982, pp 355369.Google Scholar
5.Davies, GC, Salzman, EW, Sobel, M. Elevated fibrinopeptide A and thromboxane A2 levels during cardiopulmonary bypass. Circulation 1980; 61: 808814.Google Scholar
6.Hunt, BJ, Segal, HC, Yacoub, M. Guidelines for monitoring heparin by the activated clotting time when aprotinin is used during cardiopulmonary bypass. J Thorac Cardiovasc Surg 1992; 104: 211212.CrossRefGoogle ScholarPubMed
7.Colman, RW. Surface-mediated defense reactions. J Clin Invest 1984; 73: 12491252.Google Scholar
8.Wachtfogel, YT, Harpel, PC, Edmunds, LH Jr, Colmari, RW. Formation of Cis-Clinhibitor, kallikrein-C 1-inhibitor and plasmin-alpha 2-plasmin inhibitor complexes during cardiop ulmonary bypass. Blood 1989; 73: 468471.Google Scholar
9.Kappelmayer, J, Bernabei, A, Edmunds, LH Jr, Edgington, TS, Colman, RW. Tissue factor is expressed on monocytes during simulated extracorporeal circulation. Circ Res 1993. [In press]CrossRefGoogle ScholarPubMed
10.Tabuchi, N, de Haan, J, Boonstra, PW, van Overen, W. Activa tion of fibrinolysis in the pericardial cavity during cardiopul monary bypass. J Thorac Cardiovas Surg 1993. [In press]Google Scholar
11.Uniyal, S, Brash, JL. Patterns of adsorption of proteins from human plasma onto foreign surfaces. Thromb Haemost 1982; 47: 285290.Google Scholar
12.Brash, JL, Scott, CF, ten Hove, P, Wojciechowski, P, Colman, RW. Mechanism of transient adsorption of fibrinogen from plasma to solid surfaces: role of the contact and fibrinolytic systems. Blood 1988; 71: 932939.Google Scholar
13.Gluszko, P, Rucinski, B, Musial, J, Wenger, RK, Schmaier, AH, Colman, RW, Edmunds, LH Jr, Niewiarowski, S. Fibrinogen receptors in platelet adhesion to surfaces of extracorporeal circuit. Am J Physiol 1987; 252: H615H621.Google Scholar
14.Sheppeck, RA, Bentz, M, Dickson, C, Hribar, S, White, J, Janosky, J, Berceli, SA, Borovetz, HS, Johnson, PC. Examination of the roles of glycoprotein Ib and glycoprotein IIb/IIIa in platelet deposition on an artificial surface using clinical antiplatelet agents and monoclonal antibody blockade. Blood 1991; 78: 673680.Google Scholar
15.Wenger, RK, Lukasiewicz, H, Mikuta, BS, Niewiarowski, S, Edmunds, LH Jr. Loss of platelet fibrinogen receptors during clinical cardiopulmonary bypass. J Thorac Cardiovasc Surg 1989; 97: 235239.Google Scholar
16.George, JN, Thoi, LL, McManus, LM, Reimann, TA. Isolation of human platelet membrane microparticles from plasma and serum. Blood 1982; 60: 834840.Google Scholar
17.Salzman, EW, Landon, J, Brier, D. Surface-induced platelet adhesion, aggregation and release. In: Vroman, L, Leonard, E (eds). The Behavior of Blood and its Components in Interfaces. NY Acad Sci, 1977, pp 114127.Google Scholar
18.Laufer, N, Merin, G, Grover, NB, Pessachowicz, B, Borman, JB. The influence ofcardiopulmonaiy bypass on the size of human platelets. J Thorac Cardiovasc Surg 1975; 70: 727731.Google Scholar
19.Edmunds, LH JrEllison, N, Colman, RW, Niewiarowski, S, Rao, AK, Addonizio, VP Jr, Stephenson, LW, Edie, RN. Platelet function during open heart surgery: comparison of the membrane and bubble oxygenators. J Thorac Cardiovasc Surg 1982; 83: 805812.Google Scholar
20.Woodman, RC, Harker, LA. Bleeding complications associated with cardiopulmonary bypass. Blood 1990; 76: 16801697.Google Scholar
21.Stibbe, J, Kluft, C, Brommer, EJP, Gomes, M, de Jong, DS, Nauta, J. Enhanced fibrinoytic activity during cardiopulmo nary bypass in open-heart surgery in man is caused by extrinsic (tissue-type) plasminogen activator. Eur J Clin Invest 1984; 14: 375382.Google Scholar
22.Edmunds, LH Jr. The Sangreal. J Thorac Cardiovasc Surg 1985; 90: 16.Google Scholar
23.Bidistrup, BP, Royston, D, Sapsford, RN, Taylor, KM. Reduction in blood loss and blood use after cardiopulmonary bypass with high dose aprotinin (Trasylol). J Thorac Cardiovasc Surg 1989; 97: 364372.CrossRefGoogle Scholar
24.Dietrich, W, Barankay, A, Diltahey, G, Henze, R, Niekau, E, Sebening, F, Richter, JA. Reduction of homologous blood requirement in cardiac surgery by intraoperative aprotinin application-clinical experience in 152 cardiac surgical patients. Thorac Cardiovasc Surgeon 1989; 37: 9298.Google Scholar
25.Blauhut, B, Gross, C, Necek, S, Doran, JE, Spath, P, Lundsgaard-Hansen, P. Effects of high-dose aprotinin on blood loss, platelet function, fibrinolysis, complement, and renal function after cardiopulmonary bypass. J Thorac Cardiovasc Surg. 1991; 101: 958967.CrossRefGoogle ScholarPubMed
26.Edmunds, LH Jr. J Thorac Cardiovasc Surg 1993. [Invited letter] [In press]Google Scholar
27.FitzGerald, GA. Dipyridamole. N EngI J Med 1987; 316: 12471257.Google Scholar
28.Teoh, KH, Christakis, GT, Weisel, RD, Wong, PY, Mee, AV, Ivanov, J, Madonik, M, Levitt, DS, Reilly, PA, Rosenfeld, JM, Glynn, MFX. Dipyridamole preserved platelets and reduced blood loss after cardiopulmonary bypass. J Thorac Cardiovasc Surg 1988; 96: 332341.Google Scholar
29.Pedersen, AK, Fitzgerald, GA. The human pharmacology of platelet inhibition: pharmacokinetics relevant to drug action. Circulation 1985; 72: 11641176.CrossRefGoogle ScholarPubMed
30.Kappa, JRFisher, CA, Bell, P, Campbell, FW, Ellison, N, Addonizio, VP. Inrraoperarive management of patients with heparin-induced thrombocytopenia. Ann Thorac Surg 1990; 49: 713723.CrossRefGoogle ScholarPubMed
31.Musial, J, Niewiarowski, S, Rucinski, B, Stewart, GJ, Cook, JJ, Williams, JA, Edmunds, LH Jr. Inhibition of platelet adhesion to surfaces of extracorporeal circuits by disinregrins. Circulation 1990; 82: 261273.Google Scholar