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Spontaneous ventricular fibrillation occurring immediately after institution of cardiopulmonary bypass: Possible clinical implications
J
THoRAc CARDIOVASC SURG
86:306-313, 1983
Brief communications Spontaneous ventricular fibrillation occurring immediately after institution of cardiopulmonary bypass: Possible clinical implications Tomas A. Salerno, M.D., and Henry J. Stefaniszyn, M.D., Montreal, Quebec, Canada From the Departments of Surgery, Queen's University and McGill University, Montreal, Quebec, Canada.
Twenty-four patients developed spontaneous ventricular fibrillation (SVF)Jor no apparent reasons, immediately after the institution ofcardiopulmonary bypass (CPB)and prior to aortic cross-elamping and cardioplegic arrest. These were compared to 76 similar patients who remained in normal sinus rhythm (NSR). The following observations were made: (I) SVF occurred more frequently in patients undergoing urgent coronary bypass and having unstable or crescendo angina with severe triple coronary artery disease and/or left main coronary artery stenosis; (2) in nonvented hearts the mean left atrial pressure increasedto levels above 28 mm Hg during SVF and prior to cardioplegicarrest; (3) at the end of CPB, arrhythmias and episodes of ventricular fibrillation were common (48% SVF versus 8% NSR); (4) the overall myocardial infarction rate was 37% SVF versus 4% NSR; and (5) the mortality rates were 25% SVFversus 1.3% NSR. It is postulated that the occurrence ofSVF at the start ofCPB may be indicative of serious derangements in myocardial cellular metabolism and/or function and may have clinical and prognostic implications.
Since the introduction of the cardioplegic method of myocardial protection, we have noticed the occasional occurrence of spontaneous ventricular fibrillation (SVF) at the start of cardiopulmonary bypass (CPB), prior to aortic cross-clamping and cardioplegic arrest. To our knowledge the significance of this observation has not been clearly defined either clinically or in the laboratory.
Because of difficulties in simulating this situation in animals, we prospectively followed patients undergoing cardiac operations in whom SVF occurred immediately after the institution of CPB. We compared their clinical course with that of a similar group of patients in whom the heart remained in normal sinus rhythm (NSR) until cardioplegic arrest. . Patients and methods. Over the past 3 years, SVF has developed at the initiation of CPB and prior to aortic cross-clamping in 24 patients at our institution. Table I summarizes the profile of these patients. Most patients had severe triple coronary artery disease and/or left main stenosis, presenting as crescendo angina, and underwent urgent operations. In the urgent group, 10 patients had had a previous myocardial infarction and remained symptomatic despite maximum medical therapy. Five of these patients had had a recent myocardial infarction 10 ± 5 days before the operation. Coronary artery disease was present in all patients undergoing valvular operations. Aorta-coronary bypass was performed in three of these patients: aortic valve replacement plus one bypass graft in two patients and mitral valve replacement plus one bypass graft in one patient. The other three patients were thought to have insignificant coronary disease. This group of patients was compared to a consecutive series of 76 patients operated upon over a period of 5 months, whose hearts remained in NSR until cardiaplegic arrest (Table 11). The technique of CPB was identical in all patients. The disposable Shiley lQO-A bubble oxygenator and hemodilution techniques were used in all cases. Hypothermic CPB (25° C) was instituted and cardioplegic solution* was infused in a volume of 8 ± 3 ml/kg, The solution was reinfused at 20 minutes (4 ml/kg) in order to maintain the septal temperature at 8° to 12° C. In the SVF group the mean perfusion pressure (pulsatile flow measured by means of a modification of the pump head) was approximately 100/50 mm Hg. Mean cross-clamp time was 45 ± 16 minutes for the coronary bypass
Supported by a grant from the Medical Research Council. Address for reprints: Dr. T. Salerno, Division of Cardiovascular Surgery, St. Michael's Hospital, 38 Shuter St., Toronto, Ontario, Canada M5B IA6.
306
*Cardioplegic solution: 500 ml lactated Ringer's, 10 mEq KCI, 12.5 mEq NaHCO, 12 mI 2% lidocaine, 17 ml 50% dextrose, 125 mg Solu-Cortef, pH 7.7, temperature 4° C.
Volume 86 Number 2 August. 1983
Brief communications 3 0 7
Table I. Summary of the profiles of the patients having SVF
Procedures Coronary artery bypass Elective Urgent Valvular operation Aortic Mitral Coronary artery disease! Triple Triple and LMCA stenosis LMCA stenosis
Mean LVEDP (mm Hg)
No. of patients
Mean age (yr)
Mean LAP during SVF (mm Hg)
Previous MI
Course
3 15
53 61.5
II ± 3*
14 ± 4
32 ± 4 31 ± 2
2 10
8 MIs, 4 deaths
4 2
54.3 49.0
15 ± 6 17 ± 2
29 ± 1 28 ± 3
Well
1 MI, 2 deaths Well
14 6 1
Legend:SVF. Spontaneous ventricular fibrillation. LVEDP. Left ventricular end-diastolic pressure. LAP. Left atrial pressure. MI. Myocardial infarction. LMCA. Left main coronary artery. "Standard deviation of the mean. tEighteen of the patients had coronary artery bypass operations alone. three patients had both valvular and coronary artery bypass operations. and three patients had valvular operations alone.
Table II. Profiles of patients who remained in normal sinus rhythm at institution of bypass Procedure Coronary artery bypass Elective Urgent Valvular operation Aortic Mitral MVR+AVR Coronary artery disease! Triple Triple and LMCA stenosis LMCA stenosis
No. of patients
Mean age (yr)
LVEDP (mmHg)
Previous MI
53 15
54.3 57.9
13 ± 4* 14 ± 3
7 3
61 52 62
II ± 5
4 3 1
16 ± 2 19
Course 2 MIs. no deaths I MI. 1 death No deaths No deaths No deaths
48 15 5
Legend:LVEDP. Left ventricular end-diastolic pressure. MI. Myocardial infarction. MVR. Mitral valvereplacement. AYR. Aortic valve replacement. LMCA. Left main coronary artery. "Standard deviation of the mean. t All patient' in the valvular group had normal coronary arteries.
group and 38 ± 7 minutes for the valvular group. When necessary, the percutaneous 'intra-aortic balloon was used. It was inserted by cannulation of the femoral artery in six patients, the iliac artery in two, and the ascending aorta in two patients. Serial enzyme values (slays I to 3) were measured and electrocardiograms were recorded. In the NSR group, the mean cross-clamp period was 47 ± 15 minutes for coronary artery bypass and 51 ± 15 minutes for valvular operations. The intra-aortic balloon was used in two patients who had a transient episode of hypotension when CPB was discontinued (both recovered). Results. There were six deaths in the SVF group (25%) and one death (1.3%) in the NSR group.
Autopsy revealed acute evolving myocardial infarction of a few days' duration in three SVF patients and in the one NSR patient. One patient who had had a valvular operation (SVF group) had subendocardial and septal hemorrhage, possibly related to an acute infarction. Autopsy was not performed in the other patient having a valvular operation, who died of a low-output state. Among patients undergoing valvular procedures, two of the six (33%) with SVF died whereas none of the eight with NSR died. There were 15 patients in each group who underwent urgent aorta-coronary bypass for triple and/or left main coronary artery disease; the mortality for those with SVF was 27% (4/15), compared with 7% (1/15) for those who remained in NSR.
The Journal of Thoracic and Cardiovascular Surgery
3 0 8 Brief communications
Fifty-three percent (8/15) of the patients undergoing urgent aorta-coronary bypass and having pre-cardioplegia SVF had a perioperative myocardial infarction. By contrast, only one of the 15 patients (7%) in the NSR group had this complication, and this was the only patient in this group who died. At the end of CPB, premature ventricular contractions and episodes of ventricular fibrillation (VF) occurred more frequently in the SVF group (48%) than in the NSR group (8%). Discussion. VF, even for short periods, is detrimental to the myocardium." In normothermic hearts, subendocardial ischemia occurs during VF; it is accentuated in areas distal to coronary stenosis' and in hypertrophied hearts,"!' Ischemia is associated with an increase in lactate production" and decreases in myocardial highenergy stores," contractility," and total oxygen consumption,1,I2 despite increased myocardial blood flow." For these reasons cardioplegia has replaced VF as the primary means of myocardial preservation. A previous report concerning valvular operations" examined SVF occurring during coronary perfusion after aortic cross-clamping.* SVF was associated with a higher mortality (7.3% in SVF versus 1.5% in nonSVF). In our institution SVF has occurred in some patients prior to aortic cross-clamping and cardioplegic arrest, and the clinical impression that it might adversely affect the outcome in these patients was the reason for this prospective clinical study. Results indicate an increased overall mortality (25% SVF versus 1% NSR), especially in patients requiring valvular operations (33% SVF versus 0% NSR) and urgent coronary bypass (27% SVF versus 7% NSR), and a higher perioperative myocardial infarction rate (37% SVF versus 4% NSR). No common etiologic factor could be documented in this and other studies," apart from a high incidence of irreversible myocardial ischemia (i.e., 37% rate of perioperative myocardial infarction). It is conceivable that a significant proportion of the remaining SVF patients had reversible ischemia during the period before cardioplegic arrest, perhaps enough to induce SVF. This theory is supported by the fact that laboratory animals with normal coronary arteries seldom have SVF prior to CPB. It is impossible to determine whether this degree of perioperative myocardial infarction caused, was caused by, or was indirectly related to the development of SVF. We postulate that SVF prior to aortic cross-clamping *McGoon DC: Personal communication, 1982.
and cardioplegic arrest is the result of a serious derangement in myocardial cellular metabolism, possibly secondary to ischemia. VF may further aggravate the ischemic injury and cause a poorer outcome for this group of patients. REFERENCES Hottenrott C, Maloney JV Jr, Buckberg G: Studies of the effects of ventricular fibrillation in the adequacy of regional myocardial flow. I. Electrical vs. spontaneous fibrillation. J THORAC CARDIOVASC SURG 68:615-625, 1974 2 Hottenrott CE, Towers B, Kurkji HJ, Maloney JV, Buckberg GD: The hazard of ventricular fibrillation in hypertrophied ventricleSduring cardiopulmonary bypass. J THORAC CARDIOVASC SURG 66:742-753, 1973 3 Hottenrott C, Buckberg G: Studies of the effects of ventricular fibrillation on the adequacy of regional myocardial flow. II. Effects of ventricular distention. J THoRAc CARDIOVASC SURG 68:626-633, 1974 4 Hottenrott C, Maloney JV Jr, Buckberg G: Studies of the effects of ventricular fibrillation on the adequacy of regional myocardial flow. III. Mechanisms of ischemia. J THORAC CARDIOVASC SURG 68:634-645, 1974 5 Ciardullo RC, Schaff HV, Flaherty JT, Gott VL: Myocardial ischemia during cardiopulmonary bypass. The hazards of ventricular fibrillation in the presence of a critical coronary stenosis. J THORAC CARDIOVASC SURG 73:746-757, 1977 6 Becker RM, Shizgal HM, Dobell ARC: Distribution of coronary blood flow during cardiopulmonary bypass in pigs. Possible implications for left ventricular hemorrhagic necrosis. Ann Thorac Surg 16:228-238, 1973 7 Buckberg GD, Towers B, Paglia DE, Mulder DG, Maloney JV: Subendocardial ischemia after cardiopulmonary bypass. J THoRAc CARDIOVASC SURG 64:669-684, 1972 8 Cooley DA, Reul GJ, Wukasch DC: Ischemic contracture of the heart. "Stone heart." Am J Cardiol 29:575-577, 1972 9 Huang SN, Masse S: Pathogenesis of hemorrhagic myocardial necrosis following cardiac surgery. Circulation 41,42:Suppl 3:17, 1970 10 Najafi H, Henson D, Dye WS, Javid H, Hunter JA, Callaghan R, Eisenstein R, Julian OC: Left ventricular hemorrhagic necrosis. Ann Thorac Surg 7:550-561, 1969 11 Salerno TA, Shizgal HM, Dobell ARC: Pulsatile perfusion. Its effects on blood flow distribution in hypertrophied hearts. Ann Thorac Surg 27:559-563, 1979 12 Grover FL, Fewel JG, Ghidoni JJ, Norton JB, Arom KV, Trinkle JK: Effects of ventricular fibrillation on coronary blood flow and myocardial metabolism. J Thorac Cardiavase Surg 73:616-624, 1977 13 Salerno TA, Chiong MA: Should ventricular fibrillation be induced prior to the infusion of cardioplegic solution? Ann Thorac Surg 35:367-371, 1983
Volume 86 Number 2 August. t983
14 Spanos PK, Brown AL Jr, McGoon DC: The significance of intraoperative ventricular fibrillation during aortic valve replacement. J THORAC CARDIOVASC SURG 73:605-610 , 1977
Pulmonary artery partition: New method for correction of interrupted aortic arch Joe R. Utley, M.D., Julie A. Swain, M.D., Charles B. Higgins, M.D., and Iraj A. Kashani, M.D., San Diego. Calif. From the Division of Cardiothoracic Surgery, Department of Radiology, and Divisionof Pediatric Cardiology, University of California, San Diego, San Diego, Calif.
We have successfully corrected interrupted aortic arch with ventricularseptal defect by employing deep hypothermia and circulatory arrest. a median sternotomy incision, and a pulmonary arteriotomy. This simplified technique has the advantageofan abbreviated period ofcerebral ischemia, with a relatively simple partitioning of the pulmonary artery. Address for reprints : Joe R. Utley, M.D. , Division of Cardiothoracic Surgery (H-892), UC Medical Center, 225 Dickinson St. , San Diego, Cal if. 92103 .
Brief communications 3 0 9
Palliative procedures or total correction of interruption of the aortic arch has been accomplished by a variety of methods. We have employed a simple method of total correction accomplished through a median sternotomy and a pulmonary artery incision. Case description and surgical technique. The patient was a lO-year-old boy weighing 20 kg at operation . Preoperative cardiac catheterization showed equal systolic pressures in the right ventricle, left ventricle, pulmonary artery, ascending aorta, and descending aorta. The pulmonary-systemic blood flow ratio was 5: I. The pulmonary-systemic resistance ratio was 0.15: 1.0. Angiograms showed a type B interruption of the aortic arch with both subclavian arteries arising from the descending aorta. The operation was performed through a median sternotomy. The common trunk of the carotid arteries, pulmonary artery , and ascending aorta was mobilized. Cardiopulmonary bypass was begun with two venous cannulas. Arterial cannulation was with a Y connector to the right femoral artery and the ascending aorta . The patient was cooled to 17° C rectal temperature. The ascending aorta was clamped and 700 ml of cold blood cardioplegic solution was infused into the ascending aorta . The carotid arteries were clamped . The circulation was arrested and blood was drained into the oxygenator. A 1.5 em anastomosis was performed between the ascending aorta and pulmonary artery. A longitudinal incision was then made into the pulmonary artery (Fig. I). An elliptical piece of Teflon felt
Fig. 1. Stages of repair of the interruption of the aorta. a. The carotid arteries originated from the ascending aorta and the subclavian arteries from the descending aorta distal to the ductus. b, A side-to-side anastomosis (1.5 em) is performed between the pulmonary artery and ascending aorta . c, A longitudinal incision is placed in the pulmonary artery 1.0 em lateral to the aortopulmonary anastomosis. d. The orifices of the aortopulmonary anastomosis, ductus arteriosus, right pulmonary, and left pulmonary arteries are seen through the pulmonary arteriotomy. e. The suture of the patch of Teflon felt is begun at the base of the ductus arteriosus.j, The patch is sutured into place with the orifice of the ductus and aortopulmonary anastomosis beneath the patch. g, The completed suture of the patch is shown. Ao, Aorta. PA, Pulmonary artery .
THoRAc CARDIOVASC SURG
86:306-313, 1983
Brief communications Spontaneous ventricular fibrillation occurring immediately after institution of cardiopulmonary bypass: Possible clinical implications Tomas A. Salerno, M.D., and Henry J. Stefaniszyn, M.D., Montreal, Quebec, Canada From the Departments of Surgery, Queen's University and McGill University, Montreal, Quebec, Canada.
Twenty-four patients developed spontaneous ventricular fibrillation (SVF)Jor no apparent reasons, immediately after the institution ofcardiopulmonary bypass (CPB)and prior to aortic cross-elamping and cardioplegic arrest. These were compared to 76 similar patients who remained in normal sinus rhythm (NSR). The following observations were made: (I) SVF occurred more frequently in patients undergoing urgent coronary bypass and having unstable or crescendo angina with severe triple coronary artery disease and/or left main coronary artery stenosis; (2) in nonvented hearts the mean left atrial pressure increasedto levels above 28 mm Hg during SVF and prior to cardioplegicarrest; (3) at the end of CPB, arrhythmias and episodes of ventricular fibrillation were common (48% SVF versus 8% NSR); (4) the overall myocardial infarction rate was 37% SVF versus 4% NSR; and (5) the mortality rates were 25% SVFversus 1.3% NSR. It is postulated that the occurrence ofSVF at the start ofCPB may be indicative of serious derangements in myocardial cellular metabolism and/or function and may have clinical and prognostic implications.
Since the introduction of the cardioplegic method of myocardial protection, we have noticed the occasional occurrence of spontaneous ventricular fibrillation (SVF) at the start of cardiopulmonary bypass (CPB), prior to aortic cross-clamping and cardioplegic arrest. To our knowledge the significance of this observation has not been clearly defined either clinically or in the laboratory.
Because of difficulties in simulating this situation in animals, we prospectively followed patients undergoing cardiac operations in whom SVF occurred immediately after the institution of CPB. We compared their clinical course with that of a similar group of patients in whom the heart remained in normal sinus rhythm (NSR) until cardioplegic arrest. . Patients and methods. Over the past 3 years, SVF has developed at the initiation of CPB and prior to aortic cross-clamping in 24 patients at our institution. Table I summarizes the profile of these patients. Most patients had severe triple coronary artery disease and/or left main stenosis, presenting as crescendo angina, and underwent urgent operations. In the urgent group, 10 patients had had a previous myocardial infarction and remained symptomatic despite maximum medical therapy. Five of these patients had had a recent myocardial infarction 10 ± 5 days before the operation. Coronary artery disease was present in all patients undergoing valvular operations. Aorta-coronary bypass was performed in three of these patients: aortic valve replacement plus one bypass graft in two patients and mitral valve replacement plus one bypass graft in one patient. The other three patients were thought to have insignificant coronary disease. This group of patients was compared to a consecutive series of 76 patients operated upon over a period of 5 months, whose hearts remained in NSR until cardiaplegic arrest (Table 11). The technique of CPB was identical in all patients. The disposable Shiley lQO-A bubble oxygenator and hemodilution techniques were used in all cases. Hypothermic CPB (25° C) was instituted and cardioplegic solution* was infused in a volume of 8 ± 3 ml/kg, The solution was reinfused at 20 minutes (4 ml/kg) in order to maintain the septal temperature at 8° to 12° C. In the SVF group the mean perfusion pressure (pulsatile flow measured by means of a modification of the pump head) was approximately 100/50 mm Hg. Mean cross-clamp time was 45 ± 16 minutes for the coronary bypass
Supported by a grant from the Medical Research Council. Address for reprints: Dr. T. Salerno, Division of Cardiovascular Surgery, St. Michael's Hospital, 38 Shuter St., Toronto, Ontario, Canada M5B IA6.
306
*Cardioplegic solution: 500 ml lactated Ringer's, 10 mEq KCI, 12.5 mEq NaHCO, 12 mI 2% lidocaine, 17 ml 50% dextrose, 125 mg Solu-Cortef, pH 7.7, temperature 4° C.
Volume 86 Number 2 August. 1983
Brief communications 3 0 7
Table I. Summary of the profiles of the patients having SVF
Procedures Coronary artery bypass Elective Urgent Valvular operation Aortic Mitral Coronary artery disease! Triple Triple and LMCA stenosis LMCA stenosis
Mean LVEDP (mm Hg)
No. of patients
Mean age (yr)
Mean LAP during SVF (mm Hg)
Previous MI
Course
3 15
53 61.5
II ± 3*
14 ± 4
32 ± 4 31 ± 2
2 10
8 MIs, 4 deaths
4 2
54.3 49.0
15 ± 6 17 ± 2
29 ± 1 28 ± 3
Well
1 MI, 2 deaths Well
14 6 1
Legend:SVF. Spontaneous ventricular fibrillation. LVEDP. Left ventricular end-diastolic pressure. LAP. Left atrial pressure. MI. Myocardial infarction. LMCA. Left main coronary artery. "Standard deviation of the mean. tEighteen of the patients had coronary artery bypass operations alone. three patients had both valvular and coronary artery bypass operations. and three patients had valvular operations alone.
Table II. Profiles of patients who remained in normal sinus rhythm at institution of bypass Procedure Coronary artery bypass Elective Urgent Valvular operation Aortic Mitral MVR+AVR Coronary artery disease! Triple Triple and LMCA stenosis LMCA stenosis
No. of patients
Mean age (yr)
LVEDP (mmHg)
Previous MI
53 15
54.3 57.9
13 ± 4* 14 ± 3
7 3
61 52 62
II ± 5
4 3 1
16 ± 2 19
Course 2 MIs. no deaths I MI. 1 death No deaths No deaths No deaths
48 15 5
Legend:LVEDP. Left ventricular end-diastolic pressure. MI. Myocardial infarction. MVR. Mitral valvereplacement. AYR. Aortic valve replacement. LMCA. Left main coronary artery. "Standard deviation of the mean. t All patient' in the valvular group had normal coronary arteries.
group and 38 ± 7 minutes for the valvular group. When necessary, the percutaneous 'intra-aortic balloon was used. It was inserted by cannulation of the femoral artery in six patients, the iliac artery in two, and the ascending aorta in two patients. Serial enzyme values (slays I to 3) were measured and electrocardiograms were recorded. In the NSR group, the mean cross-clamp period was 47 ± 15 minutes for coronary artery bypass and 51 ± 15 minutes for valvular operations. The intra-aortic balloon was used in two patients who had a transient episode of hypotension when CPB was discontinued (both recovered). Results. There were six deaths in the SVF group (25%) and one death (1.3%) in the NSR group.
Autopsy revealed acute evolving myocardial infarction of a few days' duration in three SVF patients and in the one NSR patient. One patient who had had a valvular operation (SVF group) had subendocardial and septal hemorrhage, possibly related to an acute infarction. Autopsy was not performed in the other patient having a valvular operation, who died of a low-output state. Among patients undergoing valvular procedures, two of the six (33%) with SVF died whereas none of the eight with NSR died. There were 15 patients in each group who underwent urgent aorta-coronary bypass for triple and/or left main coronary artery disease; the mortality for those with SVF was 27% (4/15), compared with 7% (1/15) for those who remained in NSR.
The Journal of Thoracic and Cardiovascular Surgery
3 0 8 Brief communications
Fifty-three percent (8/15) of the patients undergoing urgent aorta-coronary bypass and having pre-cardioplegia SVF had a perioperative myocardial infarction. By contrast, only one of the 15 patients (7%) in the NSR group had this complication, and this was the only patient in this group who died. At the end of CPB, premature ventricular contractions and episodes of ventricular fibrillation (VF) occurred more frequently in the SVF group (48%) than in the NSR group (8%). Discussion. VF, even for short periods, is detrimental to the myocardium." In normothermic hearts, subendocardial ischemia occurs during VF; it is accentuated in areas distal to coronary stenosis' and in hypertrophied hearts,"!' Ischemia is associated with an increase in lactate production" and decreases in myocardial highenergy stores," contractility," and total oxygen consumption,1,I2 despite increased myocardial blood flow." For these reasons cardioplegia has replaced VF as the primary means of myocardial preservation. A previous report concerning valvular operations" examined SVF occurring during coronary perfusion after aortic cross-clamping.* SVF was associated with a higher mortality (7.3% in SVF versus 1.5% in nonSVF). In our institution SVF has occurred in some patients prior to aortic cross-clamping and cardioplegic arrest, and the clinical impression that it might adversely affect the outcome in these patients was the reason for this prospective clinical study. Results indicate an increased overall mortality (25% SVF versus 1% NSR), especially in patients requiring valvular operations (33% SVF versus 0% NSR) and urgent coronary bypass (27% SVF versus 7% NSR), and a higher perioperative myocardial infarction rate (37% SVF versus 4% NSR). No common etiologic factor could be documented in this and other studies," apart from a high incidence of irreversible myocardial ischemia (i.e., 37% rate of perioperative myocardial infarction). It is conceivable that a significant proportion of the remaining SVF patients had reversible ischemia during the period before cardioplegic arrest, perhaps enough to induce SVF. This theory is supported by the fact that laboratory animals with normal coronary arteries seldom have SVF prior to CPB. It is impossible to determine whether this degree of perioperative myocardial infarction caused, was caused by, or was indirectly related to the development of SVF. We postulate that SVF prior to aortic cross-clamping *McGoon DC: Personal communication, 1982.
and cardioplegic arrest is the result of a serious derangement in myocardial cellular metabolism, possibly secondary to ischemia. VF may further aggravate the ischemic injury and cause a poorer outcome for this group of patients. REFERENCES Hottenrott C, Maloney JV Jr, Buckberg G: Studies of the effects of ventricular fibrillation in the adequacy of regional myocardial flow. I. Electrical vs. spontaneous fibrillation. J THORAC CARDIOVASC SURG 68:615-625, 1974 2 Hottenrott CE, Towers B, Kurkji HJ, Maloney JV, Buckberg GD: The hazard of ventricular fibrillation in hypertrophied ventricleSduring cardiopulmonary bypass. J THORAC CARDIOVASC SURG 66:742-753, 1973 3 Hottenrott C, Buckberg G: Studies of the effects of ventricular fibrillation on the adequacy of regional myocardial flow. II. Effects of ventricular distention. J THoRAc CARDIOVASC SURG 68:626-633, 1974 4 Hottenrott C, Maloney JV Jr, Buckberg G: Studies of the effects of ventricular fibrillation on the adequacy of regional myocardial flow. III. Mechanisms of ischemia. J THORAC CARDIOVASC SURG 68:634-645, 1974 5 Ciardullo RC, Schaff HV, Flaherty JT, Gott VL: Myocardial ischemia during cardiopulmonary bypass. The hazards of ventricular fibrillation in the presence of a critical coronary stenosis. J THORAC CARDIOVASC SURG 73:746-757, 1977 6 Becker RM, Shizgal HM, Dobell ARC: Distribution of coronary blood flow during cardiopulmonary bypass in pigs. Possible implications for left ventricular hemorrhagic necrosis. Ann Thorac Surg 16:228-238, 1973 7 Buckberg GD, Towers B, Paglia DE, Mulder DG, Maloney JV: Subendocardial ischemia after cardiopulmonary bypass. J THoRAc CARDIOVASC SURG 64:669-684, 1972 8 Cooley DA, Reul GJ, Wukasch DC: Ischemic contracture of the heart. "Stone heart." Am J Cardiol 29:575-577, 1972 9 Huang SN, Masse S: Pathogenesis of hemorrhagic myocardial necrosis following cardiac surgery. Circulation 41,42:Suppl 3:17, 1970 10 Najafi H, Henson D, Dye WS, Javid H, Hunter JA, Callaghan R, Eisenstein R, Julian OC: Left ventricular hemorrhagic necrosis. Ann Thorac Surg 7:550-561, 1969 11 Salerno TA, Shizgal HM, Dobell ARC: Pulsatile perfusion. Its effects on blood flow distribution in hypertrophied hearts. Ann Thorac Surg 27:559-563, 1979 12 Grover FL, Fewel JG, Ghidoni JJ, Norton JB, Arom KV, Trinkle JK: Effects of ventricular fibrillation on coronary blood flow and myocardial metabolism. J Thorac Cardiavase Surg 73:616-624, 1977 13 Salerno TA, Chiong MA: Should ventricular fibrillation be induced prior to the infusion of cardioplegic solution? Ann Thorac Surg 35:367-371, 1983
Volume 86 Number 2 August. t983
14 Spanos PK, Brown AL Jr, McGoon DC: The significance of intraoperative ventricular fibrillation during aortic valve replacement. J THORAC CARDIOVASC SURG 73:605-610 , 1977
Pulmonary artery partition: New method for correction of interrupted aortic arch Joe R. Utley, M.D., Julie A. Swain, M.D., Charles B. Higgins, M.D., and Iraj A. Kashani, M.D., San Diego. Calif. From the Division of Cardiothoracic Surgery, Department of Radiology, and Divisionof Pediatric Cardiology, University of California, San Diego, San Diego, Calif.
We have successfully corrected interrupted aortic arch with ventricularseptal defect by employing deep hypothermia and circulatory arrest. a median sternotomy incision, and a pulmonary arteriotomy. This simplified technique has the advantageofan abbreviated period ofcerebral ischemia, with a relatively simple partitioning of the pulmonary artery. Address for reprints : Joe R. Utley, M.D. , Division of Cardiothoracic Surgery (H-892), UC Medical Center, 225 Dickinson St. , San Diego, Cal if. 92103 .
Brief communications 3 0 9
Palliative procedures or total correction of interruption of the aortic arch has been accomplished by a variety of methods. We have employed a simple method of total correction accomplished through a median sternotomy and a pulmonary artery incision. Case description and surgical technique. The patient was a lO-year-old boy weighing 20 kg at operation . Preoperative cardiac catheterization showed equal systolic pressures in the right ventricle, left ventricle, pulmonary artery, ascending aorta, and descending aorta. The pulmonary-systemic blood flow ratio was 5: I. The pulmonary-systemic resistance ratio was 0.15: 1.0. Angiograms showed a type B interruption of the aortic arch with both subclavian arteries arising from the descending aorta. The operation was performed through a median sternotomy. The common trunk of the carotid arteries, pulmonary artery , and ascending aorta was mobilized. Cardiopulmonary bypass was begun with two venous cannulas. Arterial cannulation was with a Y connector to the right femoral artery and the ascending aorta . The patient was cooled to 17° C rectal temperature. The ascending aorta was clamped and 700 ml of cold blood cardioplegic solution was infused into the ascending aorta . The carotid arteries were clamped . The circulation was arrested and blood was drained into the oxygenator. A 1.5 em anastomosis was performed between the ascending aorta and pulmonary artery. A longitudinal incision was then made into the pulmonary artery (Fig. I). An elliptical piece of Teflon felt
Fig. 1. Stages of repair of the interruption of the aorta. a. The carotid arteries originated from the ascending aorta and the subclavian arteries from the descending aorta distal to the ductus. b, A side-to-side anastomosis (1.5 em) is performed between the pulmonary artery and ascending aorta . c, A longitudinal incision is placed in the pulmonary artery 1.0 em lateral to the aortopulmonary anastomosis. d. The orifices of the aortopulmonary anastomosis, ductus arteriosus, right pulmonary, and left pulmonary arteries are seen through the pulmonary arteriotomy. e. The suture of the patch of Teflon felt is begun at the base of the ductus arteriosus.j, The patch is sutured into place with the orifice of the ductus and aortopulmonary anastomosis beneath the patch. g, The completed suture of the patch is shown. Ao, Aorta. PA, Pulmonary artery .