Buckberg G, Towers B, Paglia D, Mulder D, Maloney J: Subendocardial ischemia after cardio ... Ghidoni J, Liotta D, Thomas H: Massive subendocardial damage ...
MYOCARDIAL PROTECTION DURING CARDIOPULMONARY BYPASS Domingo Liotta, M.D.
INTRODUCTION Myocardial protection during periods of obligatory anoxia remains a controversial area in cardiac surgery. Left ventricular subendocardial necrosis is the single major cause of death on the operating table, and warm anoxic arrest after cross-clamping of the aorta is responsible for the majority of these cases." 2'3 Depressed postoperative cardiac performance because of left ventricular subendocardial ischemia is associated with an extremely large number of deaths (approximately 90%) .4 The likelihood of these complications sharply increases in the hypertrophied left ventricle. Direct coronary arterial perfusion is widely recommended.5-8 However, fatal complications related directly to the procedure continue to be reported.9"10 Furthermore, it has become evident that perfusion of the subendocardium in the fibrillating heart during direct coronary perfusion is frequently inadequate.""2 Subendocardial necrosis has been demonstrated in the fibrillating heart with an unclamped aorta.13 Aortic cross-clamping provides the surgeon with a bloodless field so that the coronary anastomoses of aorta coronary bypass grafts can be performed with greater precision. Aortic cross-clamping coupled with profound local hypothermia can permit a safe cardiac arrest of at least 60 minutes. Surface cooling is a satisfactory method for myocardial preservation.14 However, unless the heart is almost completely submerged in cold saline, the intramyocardial temperature decreases only 3-5O C from the systemic temperature, and the posterior wall of the le;ft ventricle is cooler than the rest of the myocardium. A flooded operative field is troublesome. In addition, when only topical epicardial hypothermia is used, a 100 C gradient may be present between the epicardium and endocardium.'51"6 This report presents a simplified technique for performing profound, local hypothermia in -which a 10-15° C gradient between myocardial and systemic temperatures is obtained. The procedure provides a rapid and uniform cooling of the heart with emphasis on the subendocardial layers of the left ventricle. The flaccidity of the heart permits a better exposure of the intracardiac structure. The procedure entails the following principles: 1. Hypothermia of the myocardial mass by means of coronary circulation through perfusion of the ascending aorta. 2. Hypothermia of the inner myocardial layers by direct irrigation of the left ventricular cavity. 3. Hypothermia of the outer myocardial layers by intermittent irrigation of the pericardial sac. From the Division of Thoracic and Cardiovascular Surgery, Italian Hospital, Buenos Aires, Argentina, South America. 30
Cardiovascular Diseases, Bulletin of the Texas Heart Institute, Vol. 4, Number 1
METHOD With the patient undergoing partial cardiopulmonary bypass, the systemic temperature is lowered to 300 C. Topical heart hypothermia is reached during this period by filling the pericardial sac with 2-.4' C saline. Simultaneously, the epicardial temperature decreases 6-.8' C and the outer layers of the myocardium decrease 4-60 C (Fig. 1). When severe aortic insufficiency is present, clamping the aorta at 32-331 C is preferable. However, the systemic temperature is still lowered to 30' C.
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1. Period of Ventricular Anoxia Hypothermia of the myocardial mass is produced by direct coronary perfusion via the ascending aorta, employing 250 to 300 cc of 40 C Ringer's lactated solution started immediately after cross-clamping the aorta (Fig. 2). Approximately two minutes are required for the myocardial temperature to decrease to 1822' C.
RINGER'S LACTATED SOLUTION , 2 -4! C
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Fig. 2. Diagram of the profound local hypothermia system utilized during total cardiopulmonary bypass. Code P.S.: pericardial sac Inside diameter of plastic tubing: 4 mm, 1.5 mm Aortic needle: 17 gauge 32
Endocardial hypothermia is achieved by inserting a catheter through the left ventricular apex and infusing 259 to 399 cc's of Ringer's lactated solution at 2-4° C for approximately 30 minutes. Endocardial temperature decreases to 14-20° C. This fluid, including the 250 to 300 cc of coronary perfusion, is incorporated into the extracorporeal circulation. Cold blood, instead of Ringer's solution, may be infused into the left ventriculalr cavity when blood is required to expand the extracorporeal volume. In valvular replacement, a higher volume of Ringer's solution, 150 to 200 cc every 10 minutes, is necessary. This volume needs to be partially aspirated, either through the aortotomy or the mitral area. Intermittent topical cooling of the heart with 40 C saline and concomitant aspiration maintains epicardial hypothermia. 2. Post Anoxic Period
Digital partial compression of the ascending aorta distally from the aortic cannula for 2 to 4 seconds increases the aortic pressure to 100 to 120 mm Hg. The coronary flow is augmented, and occasionally air bubbles are expelled from the coronary arteries. In aortocoronary bypass grafts a lower coronary pressure, 80 to 90 mm Hg, is indicated (Fig. 3).
3. Two-staged Hypothermia When performing a double valve replacement, the mitral valve is replaced first. Systemic temperature is lowered to 300 C utilizing a heat exchanger in the cardiopulmonary bypass circuit. Following mitral valve replacement, coronary circulation and cardiac function is resumed for 6 to 8 minutes at 33-35° C. During the aortic valve replacement, profound local hypothermia is repeated. Left ventricular endocardial cooling is done by intermittent irrigation through the aortotomy with concomitant suction of the Ringer's solution. In combined mitral or aortic valve replacement with multiple coronary artery bypass grafts, the valve is replaced first. Prior to bypassing the coronary arteries, cardiac function is restored for 6 to 8 minutes. Profound local hypotherTnia is repeated during the coronary anastomoses. The aortic anastomosis is completed with partial aortic occlusion and a functioning heart.
DISCUSSION Extensive experimental and clinical data report the effects of hypothermia in protecting the myocardium.17-22 Direct rapid endocardial cooling compared with topical epicardial cooling after cross-clamping the aorta resulted in improved left ventricular function curves, greater ventricular contractility and increased regional blood flow to the subendocardium in dogs.23 Furthermore, isolated perfusion of the coronary arteries with 40 C Ringer's lactated solution by direct perfusion into the ascending aorta 33
demonstrated minimal changes in left ventricular function after one hour of aortic cross-clamping in dogs.24 The clinical application of profound local hypothermia, as described in this report, does not complicate the surgical procedure. Selective cooling, either of the endocardium or the myocardium, may be directed by the simple occlusion of one catheter. Also, direct cooling of the right ventricular cavity simultaneously with the cavity of the left ventricle may be considered in biventricular hypertrophy. Recently, it was applied in one extremely ill patient in our institution with excellent clinical results. Severe aortic insufficiency requires continuous massage of the heart during the 1 to 2 minutes of the ascending aorta perfusion period. During the coronary anastomosis of aortocoronary grafts with a competent mitral valve, mild dilatation of the left ventricle with Ringer's solution may occur, necessitating interruption of the endocardial perfusion for a few minutes. Profound local hypothermia has been employed from January 1974 to 120
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Fig. 3. Surgeon's view of the coronary flow augmentation technique. 34
March 1976 in 584 patients. Clinical observations have revealed that this technique is effective in reducing myocardial injury during aortic crossclamping.25 Coronary flow augmentation in the immediate post anoxic period has been used routinely since 1972.26
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REFERENCES Reuben C, Singh H, Tector A, Kampine J, Flemma R, Lepley D: The dynamics of subendocardial flow during cardiopulmonary bypass. J Thorac Cardiovasc Surg 70:989, 1975 Cooley D, Reul G, Wukasch D: Ischemic contracture of the heart: "Stone Heart." Am J Cardiol 29:575, 1972 Buckberg G, Towers B, Paglia D, Mulder D, Maloney J: Subendocardial ischemia after cardiopulmonary bypass. J Thorac Cardiovasc Surg 64:669, 1972 Buckberg G, Olinger G, Mulder D, Maloney J: Depressed postoperative cardiac performance. J Thorac Cardiovasc Surg 70:974, 1975 Dubost C, Piwinca A, Blondeau P, Carpentier A, Rioux C: L'angor des valvulopathies aortiques operees et son interpretation. Presse Med '1:1203, 1972 Mikaeloff P, Dupont J, Loire R, Delaye J, Age C, Amiel C: La perfusion des coronaries dans la chirurgie de remplacement valvulaire aortique et polyvalvulaire: Incidence sur la mortalite et la morbidite postoperatoire. Arch Mal Coeur 9:1023-1037, 1974 McGoon D: Coronary perfusion. J Thorac Cardiovasc Surg 70:1025, 1975 Spencer F: Coronary perfusion. J Thorac Cardiovasc Surg 70:1029, 1975 Osborn J, Cohn K, Hait M, Russi M, Salei A, Harkins G, Gerbode F: Hemolysis during perfusion. Sources and means of reduction. J Thorac Cardiovasc Surg 43:459, 1962 Fishmann N, Yanker J, Roe B: Mechanical injury to the coronary arteries during operative cannulation. Am Heart J 75:26, 1968 Hottenrott C, Towers B. Kurjki H, Malonez J, Buckberg G: The hazard of ventricular fibrillation in hypertrophied ventricles during cardiopulmonary bypass. J Thorac Cardiovasc Surg 66(5) :742-753, 1973 Hottenrott C, Buckberg G, Maloney J: Effects of ventricular fibrillation on distribution and adequacy of coronary blood flow. Surg Forum, Vol XXrII, 58th Annual Congress, 1972 Ghidoni J, Liotta D, Thomas H: Massive subendocardial damage accompanying prolonged ventricular fibrillation. Am J Pathol 15:56, 1969 Griepp R, Stinson E, Shumway N: Profound local hypothermia for myocardial protection during open heart surgery. J Thorac Cardiovasc Surg 66:731, 1973 Lundsgaard-Hansen P: Surgical aspects of cardiac metabolism. Collective review. Surg Gynecol Obstet 122:1095-1108, 1966 Kones R: Metabolism of the acutely ischemic and hypoxic heart. Critical Care Medicine 1:321330, 1973 Fuhrman G, Furman F, Field J: Metabolism of rat heart slices with special references to effects of temperature and anoxia. Am J Physiol 163:642, 1950 Rheinlander F, Wallace W, Robeles A: The effects of hypothermia on the metabolism of the post-arrested canine heart. J Cardiovasc Surg 6:126-133, 1965 Lower R, Stofer R, Hurley E: Successful homotransplantation of the canine heart after anoxic preservation for seven hours. Am J Surg 104:302, 1962 Cross F, Jones R, Berne R: Localized cardiac hypothermia as an adjunct to elective cardiac arrest. Surg Forum: Clinical Congress, 8:355, 1957 Ebert P, Greenfield I, Austen W, Morrow A: Experimental comparison of methods for protecting the heart during aortic occlusion. Ann Surg 155:25, 1962 Sapsford R, Blackestone E, Kirklin J, Karp R, Kouchoukos N, Pacifico A, Roe C, Bradley E: Coronary perfusion versus cold ischemic arrest during aortic valve surgery. Circulation, 49:11901199, 1974 Singh H, Tector A, Flemma R, Lepley D Jr: Topical myocardial cooling: An intensive laboratory investigation. The International Cardiovascular Society, 23rd Scientific Meeting. 1976 35
24. Tyers G, Hughes H, Todd G, Williams D, Andrews E, Prophet G, Waldhausen J: Protection from ischemic cardiac arrest by coronary perfusion with cold Ringer's lactate solution. J Thorac Cardiovasc Surg 67:411-418, 1974 25. Liotta D, Pisanu A, Vazquez J, D'Angelo N, Estala J, Ferrari H, Scandroglio A, Bracco D, Bertolozzi E, Cermesoni R, Donato F: Myocardial protection by local deep hypothermia during aortic cross-clamping. Pren Med Argent 62:303, 1975 26. Liotta D: Selective coronary hypertension. Chest 67(4) :502, 1975 ACKNOWLEDGMENT We are grateful to Miss Olga Canals for the excellent illustrations and to Miss Dora Lia Herrera and Miss Maria Graciela Liotta for their secretarial assistance.
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