513 2. Kossovsky N, Heggers JP, Robson MC. Experimental demonstration of the immunogenicity of silicone-protein complexes. J Biomed Mater Res
7. Varga J, Schumacher HR, Jimenez SA. Systemic sclerosis after augmentation mammoplasty with silicone implants. Ann Intern Med
1987; 21: 1125-33. 3. Bowman BH, Schneider L, Barnett DR, Kurosky A, Goldblum RM. Novel urinary fragments from human basement membrane collagen. J Biol Chem 1980; 255: 9484-89. 4 Fnsch EE. Technology of silicones in biomedical applications. In: Rubin LR, ed. Biomaterials in reconstructive surgery. New York: CV Mosby, 1983: 73-90. 5. Peimer CA, Medige J, Eckert BS, Wright JR, Howard CS. Reactive synovitis after silicone arthroplasty. J Hand Surg 1986; 11A: 624-38. 6. Kircher T. Silicone lymphadenopathy. Hum Pathol 1980; 11: 240-44.
1989; 111: 377-83. 8. Baldwin CM, Kaplan EN. Silicone-induced human adjuvant disease? Ann Plastic Surg 1983; 10: 270-73. 9. Gower DJ, Lewis JC, Kelly DL. Sterile shunt malfunction: a scanning electron microscopic perspective. J Neurosurg 1984; 61: 1079-84. 10. Snow RB, Kossovsky N. Hypersensitivity reaction associated with sterile ventriculoperitoneal shunt malfunction. Surg Neurol 1989; 31: 209-14. 11. Warren KS. A functional classification of granulomatous inflammation. Ann NY Acad Sci 1976; 278: 7-18.
SHORT REPORT Cardiac resuscitation with
percutaneous cardiopulmonary support
Percutaneous cardiopulmonary support (CPS) was initiated in 9 patients to provide haemodynamic stability after failure of conventional resuscitation. 4 patients were in cardiogenic shock and 4 remained in asystole, with 1 in resistant ventricular fibrillation, after cardiac arrest. During CPS for those in cardiogenic shock, the mean intra-arterial pressures ranged from 65 to 100 mm Hg (mean 84), at flow rates of between 3 to 5 l/min (mean 3·9). 2 patients underwent technically successful coronary angioplasty. No patient in this group survived. In the cardiac arrest group, acceptable mean intra-arterial blood pressures were achieved (mean 95, range 90-100 mm Hg) at flow rates of between 2 to 3 l/min (mean 2·6). All 5 subjects underwent technically successful coronary angioplasty whilst on CPS. 4 survived. 2 were alive and well at 12 months follow-up, 1 of whom had returned to work; the third is alive and well at 4 months.
The first report of cardiopulmonary support (CPS) by peripheral cannulation was described in dogs by Proctor and Kowalik 25 years ago.’ Litzie and Roberts successfully scaled down CPS machines and freed them from the constraints of being operating-theatre based.2 This advance has enabled their application as an adjunct to emergency resuscitation in the cardiac catheter laboratory and by the patient’s bedside. Prolonged cardiopulmonary resuscitation (CPR) and advanced life support cannot reliably restore blood pressure sufficiently well to perfuse both the coronary and cerebral circulation.3 CPS not only provides reliable tissue perfusion but is also capable of controlling flow, composition, and the temperature of blood. Results from prospective studies have described successful outcome after CPR in hospitals in below 10% to about 24% of cases,4 and mortality rates rise if the duration of resuscitation is long.s Treatment of
cardiogenic shock still has a mortality approaching 80%.’ Early surgical revascularisation and percutaneous transluminal coronary angioplasty (PTCA) have improved survival in this group of patients to around 50%.’ Once established, CPS provides haemodynamic stability enabling interventional procedures to be completed safely. By step-wise dilatation, size 18 French cannulae were inserted into femoral vessels after gaining vascular access according to a modified Seldinger technique. The tip of the arterial cannula was positioned in the common iliac artery and that of the venous cannula at the junction of the inferior vena cava and the right atrium. The extracorporeal circulation was connected to a heat exchanger, a membrane oxygenator, and a vortex pump, all of which were mounted on a portable cart that also contained the control console. Cardiopulmonary support was initiated at a flow rate of 50 ml/kg per min and then regulated according to the need of the individual
patient. 9 patients (8 male, 1 female; mean age 67 years; see table), 4 in the cardiogenic shock group and 5 in the arrest group, received emergency CPS. There were no excluding criteria and the decision to offer CPS was based on clinical grounds alone. In the arrest group, 4 patients were undergoing cardiac catheterisation at the time of the arrest; the remaining patient arrested on the ward 24 h after a technically successful coronary angioplasty. In all instances, cardiac arrest was probably caused by abrupt vessel closure, as was shown on coronary angiograms done subsequently once haemodynamic stability was achieved on CPS. Advanced life support was commenced immediately in all patients, but 4 remained in asystole and 1 in resistant ventricular fibrillation when the decision to commence CPS was made. CPS was established between 25 to 40 min into the arrest. Once the haemodynamic variables were stabilised, patients who were undergoing cardiac catheterisation at the time of the arrest went on to have successful revascularisation coronary technically procedures. In 3 patients, complete revascularisation was achieved-ie, all stenoses of 50% or more were successfully dilated-and all survived. In the other 2, only critical lesions were tackled with technically good results. 1 of these patients died after an uncontrolled haemorrhage into his right lung; necropsy revealed a ruptured aortic root, which probably resulted from external cardiac massage. In all patients, the electrocardiogram reverted to sinus rhythm after successful PTCA. The 4 survivors were successfully weaned off CPS within 2 h. 2 of the 4 who survived were alive and well at 12 months follow-up, and 1 had returned to work. The third patient is alive and well 4 months after his arrest. 1 survivor died of unrelated causes (bronchopneumonia) about 2 months after his arrest. The 4 patients with cardiogenic shock varied considerably in their duration of illness. All had electrocardiographic and biochemical evidence that supported a diagnosis of recent myocardial infarction. The interval between the acute
514 PATIENT CHARACTERISTICS
AVR, aortic valve replacement, RCA, nght coronary artery, MI, myocardial infarction, VSD, ventncular septal defect, LAD, left
insult and the commencement of CPS ranged 24 h. 3 patients underwent coronary angiography once they were haemodynamically stabilised on CPS. 2 patients had technically successful PTCAs to critical proximal lesions, but on weaning off support they were unable to maintain an adequate cardiac output and they died within 1 h of termination of CPS. 1 patient had a large ventricular septal defect complicating an extensive anterior myocardial infarction. The other patient, who underwent an aortic valvuloplasty 24 h earlier and subsequently had an extensive subendocardial myocardial infarction, had vessels unsuitable for angioplasty or coronary bypass surgery. The patient who underwent aortic valve replacement and coronary artery bypass grafting was hypertensive at the end of the operation despite maximum inotropic support. Electrocardiography suggested a diagnosis of perioperative myocardial infarction. Intra-aortic balloon pumping could only achieve a systolic blood pressure of 60 mm Hg. Percutaneous CPS was initiated to give adequate time for myocardial recovery. Once begun on CPS, his mean blood pressure was 80 mm Hg at a flow rate of 3 1/min. Several attempts were then made to wean him from CPS during the subsequent 30 h, but he eventually died. In the 4 survivors, one patient had a deep wound infection and another had a large haematoma that led to a 31 unit blood transfusion. Femoro-femoral cardiopulmonary support has been adopted as a method of resuscitation both experimentally and in cases of prolonged cardiac arrest.1-3 Resuscitation with CPS restores haemodynamic stability and ensures organ perfusion and flow in patent coronary vessels. This stability provides a controlled setting to intervene if indicated. Since the site of cannula insertion is remote from the thorax, cardiac massage and attempts at defibrillation can proceed and are vital to limit the effects of ischaemic cerebral damage. Although CPS provides haemodynamic stability, ischaemia in the distribution of the diseased vessel persists. Therefore improvement in patient survival will depend on prompt revascularisation either by PTCA or by vessel grafting. Our 4 survivors were still in asystole or ventricular fibrillation 25 min or more after the arrest; without revascularisation on CPS they would have died. In
myocardial from 5
to
anterior
descending artery, Cx, circumflex artery
the cardiogenic shock group, although all patients had restoration of blood pressure and improved tissue perfusion on CPS, none survived. Shawl’s group have reported good survival figures after CPS intervention for cardiogenic shock but after much shorter intervals (mean 106 min, maximum 180 min) than in our patients.8 Progressive myocellular injury occurs in patients with cardiogenic shock and, since there was considerable delay between the onset of shock and the establishment of CPS in our group (5-24 h), all of our patients would have had extensive myocardial damage that was already present before intervention; this was confirmed on 3 completed necropsies. From this small study we have been encouraged to continue to resuscitate patients with CPS who are in persistent asystole or in ventricular fibrillation. refractory Supported revascularisation can only improve survival in cardiogenic shock if completed at an early stage. This
study was supported by the National Heart Research Fund. REFERENCES
1. Proctor
2. 3.
E, Kowalik TA. Circulatory support by pump-oxygenator in experimental ventricular fibrillation and acute left heart failure induced by coronary artery ligation. Cardiovasc Resus 1967; 1: 189-93. Litzie AK, Roberts CP. Emergency femoro-femoral cardiopulmonary bypass. Proc Amer Acad CV Perfusion 1987; 8: 60-65. Safar P, Abramson N, Angelos M, et al. Emergency cardiopulmonary bypass for resuscitation from prolonged cardiac arrest. Am J Emerg Med 1990; 8: 55-67.
4. DeBard ML. Cardiopulmonary resuscitation: analysis of six years’ experience and review of the literature. Ann Emerg Med 1981; 10: 408. 5. Rozenbaum EA, Shenkman L. Predicting outcome of inhospital cardiopulmonary resuscitation. Crit Care Med 1988; 16: 583-86. 6. Afifi A, Chang PC, Liu VY, et al. Prognostic indexes in acute myocardial infarction complicated by shock. Am J Cardiol 1974; 33: 826-32. 7. O’Neill. Management of cardiogemc shock. In: Topol E, ed. Acute coronary intervention. New York: Alan R. Liss, 1988: 195-213. 8. Shawl F, Domanski MJ, Hernandez J, Punja S. Emergency percutaneous cardiopulmonary support in cardiogenic shock from acute myocardial infarction. Am J Cardiol 1989; 64: 967-70.
ADDRESS Cardiac Research Unit, Regional Cardiothoracic Centre, Killingbeck Hospital, York Road, Leeds LS14 6UQ, UK (M R. Rees, FRCR, T. Browne, FRCS, U M Sivananthan, FRCR, S Whittaker, ACP, D. Hick, L. B Tan, MRCP, G. A Davies, FRCS) Correspondence to Dr M R Rees
7. Varga J, Schumacher HR, Jimenez SA. Systemic sclerosis after augmentation mammoplasty with silicone implants. Ann Intern Med
1987; 21: 1125-33. 3. Bowman BH, Schneider L, Barnett DR, Kurosky A, Goldblum RM. Novel urinary fragments from human basement membrane collagen. J Biol Chem 1980; 255: 9484-89. 4 Fnsch EE. Technology of silicones in biomedical applications. In: Rubin LR, ed. Biomaterials in reconstructive surgery. New York: CV Mosby, 1983: 73-90. 5. Peimer CA, Medige J, Eckert BS, Wright JR, Howard CS. Reactive synovitis after silicone arthroplasty. J Hand Surg 1986; 11A: 624-38. 6. Kircher T. Silicone lymphadenopathy. Hum Pathol 1980; 11: 240-44.
1989; 111: 377-83. 8. Baldwin CM, Kaplan EN. Silicone-induced human adjuvant disease? Ann Plastic Surg 1983; 10: 270-73. 9. Gower DJ, Lewis JC, Kelly DL. Sterile shunt malfunction: a scanning electron microscopic perspective. J Neurosurg 1984; 61: 1079-84. 10. Snow RB, Kossovsky N. Hypersensitivity reaction associated with sterile ventriculoperitoneal shunt malfunction. Surg Neurol 1989; 31: 209-14. 11. Warren KS. A functional classification of granulomatous inflammation. Ann NY Acad Sci 1976; 278: 7-18.
SHORT REPORT Cardiac resuscitation with
percutaneous cardiopulmonary support
Percutaneous cardiopulmonary support (CPS) was initiated in 9 patients to provide haemodynamic stability after failure of conventional resuscitation. 4 patients were in cardiogenic shock and 4 remained in asystole, with 1 in resistant ventricular fibrillation, after cardiac arrest. During CPS for those in cardiogenic shock, the mean intra-arterial pressures ranged from 65 to 100 mm Hg (mean 84), at flow rates of between 3 to 5 l/min (mean 3·9). 2 patients underwent technically successful coronary angioplasty. No patient in this group survived. In the cardiac arrest group, acceptable mean intra-arterial blood pressures were achieved (mean 95, range 90-100 mm Hg) at flow rates of between 2 to 3 l/min (mean 2·6). All 5 subjects underwent technically successful coronary angioplasty whilst on CPS. 4 survived. 2 were alive and well at 12 months follow-up, 1 of whom had returned to work; the third is alive and well at 4 months.
The first report of cardiopulmonary support (CPS) by peripheral cannulation was described in dogs by Proctor and Kowalik 25 years ago.’ Litzie and Roberts successfully scaled down CPS machines and freed them from the constraints of being operating-theatre based.2 This advance has enabled their application as an adjunct to emergency resuscitation in the cardiac catheter laboratory and by the patient’s bedside. Prolonged cardiopulmonary resuscitation (CPR) and advanced life support cannot reliably restore blood pressure sufficiently well to perfuse both the coronary and cerebral circulation.3 CPS not only provides reliable tissue perfusion but is also capable of controlling flow, composition, and the temperature of blood. Results from prospective studies have described successful outcome after CPR in hospitals in below 10% to about 24% of cases,4 and mortality rates rise if the duration of resuscitation is long.s Treatment of
cardiogenic shock still has a mortality approaching 80%.’ Early surgical revascularisation and percutaneous transluminal coronary angioplasty (PTCA) have improved survival in this group of patients to around 50%.’ Once established, CPS provides haemodynamic stability enabling interventional procedures to be completed safely. By step-wise dilatation, size 18 French cannulae were inserted into femoral vessels after gaining vascular access according to a modified Seldinger technique. The tip of the arterial cannula was positioned in the common iliac artery and that of the venous cannula at the junction of the inferior vena cava and the right atrium. The extracorporeal circulation was connected to a heat exchanger, a membrane oxygenator, and a vortex pump, all of which were mounted on a portable cart that also contained the control console. Cardiopulmonary support was initiated at a flow rate of 50 ml/kg per min and then regulated according to the need of the individual
patient. 9 patients (8 male, 1 female; mean age 67 years; see table), 4 in the cardiogenic shock group and 5 in the arrest group, received emergency CPS. There were no excluding criteria and the decision to offer CPS was based on clinical grounds alone. In the arrest group, 4 patients were undergoing cardiac catheterisation at the time of the arrest; the remaining patient arrested on the ward 24 h after a technically successful coronary angioplasty. In all instances, cardiac arrest was probably caused by abrupt vessel closure, as was shown on coronary angiograms done subsequently once haemodynamic stability was achieved on CPS. Advanced life support was commenced immediately in all patients, but 4 remained in asystole and 1 in resistant ventricular fibrillation when the decision to commence CPS was made. CPS was established between 25 to 40 min into the arrest. Once the haemodynamic variables were stabilised, patients who were undergoing cardiac catheterisation at the time of the arrest went on to have successful revascularisation coronary technically procedures. In 3 patients, complete revascularisation was achieved-ie, all stenoses of 50% or more were successfully dilated-and all survived. In the other 2, only critical lesions were tackled with technically good results. 1 of these patients died after an uncontrolled haemorrhage into his right lung; necropsy revealed a ruptured aortic root, which probably resulted from external cardiac massage. In all patients, the electrocardiogram reverted to sinus rhythm after successful PTCA. The 4 survivors were successfully weaned off CPS within 2 h. 2 of the 4 who survived were alive and well at 12 months follow-up, and 1 had returned to work. The third patient is alive and well 4 months after his arrest. 1 survivor died of unrelated causes (bronchopneumonia) about 2 months after his arrest. The 4 patients with cardiogenic shock varied considerably in their duration of illness. All had electrocardiographic and biochemical evidence that supported a diagnosis of recent myocardial infarction. The interval between the acute
514 PATIENT CHARACTERISTICS
AVR, aortic valve replacement, RCA, nght coronary artery, MI, myocardial infarction, VSD, ventncular septal defect, LAD, left
insult and the commencement of CPS ranged 24 h. 3 patients underwent coronary angiography once they were haemodynamically stabilised on CPS. 2 patients had technically successful PTCAs to critical proximal lesions, but on weaning off support they were unable to maintain an adequate cardiac output and they died within 1 h of termination of CPS. 1 patient had a large ventricular septal defect complicating an extensive anterior myocardial infarction. The other patient, who underwent an aortic valvuloplasty 24 h earlier and subsequently had an extensive subendocardial myocardial infarction, had vessels unsuitable for angioplasty or coronary bypass surgery. The patient who underwent aortic valve replacement and coronary artery bypass grafting was hypertensive at the end of the operation despite maximum inotropic support. Electrocardiography suggested a diagnosis of perioperative myocardial infarction. Intra-aortic balloon pumping could only achieve a systolic blood pressure of 60 mm Hg. Percutaneous CPS was initiated to give adequate time for myocardial recovery. Once begun on CPS, his mean blood pressure was 80 mm Hg at a flow rate of 3 1/min. Several attempts were then made to wean him from CPS during the subsequent 30 h, but he eventually died. In the 4 survivors, one patient had a deep wound infection and another had a large haematoma that led to a 31 unit blood transfusion. Femoro-femoral cardiopulmonary support has been adopted as a method of resuscitation both experimentally and in cases of prolonged cardiac arrest.1-3 Resuscitation with CPS restores haemodynamic stability and ensures organ perfusion and flow in patent coronary vessels. This stability provides a controlled setting to intervene if indicated. Since the site of cannula insertion is remote from the thorax, cardiac massage and attempts at defibrillation can proceed and are vital to limit the effects of ischaemic cerebral damage. Although CPS provides haemodynamic stability, ischaemia in the distribution of the diseased vessel persists. Therefore improvement in patient survival will depend on prompt revascularisation either by PTCA or by vessel grafting. Our 4 survivors were still in asystole or ventricular fibrillation 25 min or more after the arrest; without revascularisation on CPS they would have died. In
myocardial from 5
to
anterior
descending artery, Cx, circumflex artery
the cardiogenic shock group, although all patients had restoration of blood pressure and improved tissue perfusion on CPS, none survived. Shawl’s group have reported good survival figures after CPS intervention for cardiogenic shock but after much shorter intervals (mean 106 min, maximum 180 min) than in our patients.8 Progressive myocellular injury occurs in patients with cardiogenic shock and, since there was considerable delay between the onset of shock and the establishment of CPS in our group (5-24 h), all of our patients would have had extensive myocardial damage that was already present before intervention; this was confirmed on 3 completed necropsies. From this small study we have been encouraged to continue to resuscitate patients with CPS who are in persistent asystole or in ventricular fibrillation. refractory Supported revascularisation can only improve survival in cardiogenic shock if completed at an early stage. This
study was supported by the National Heart Research Fund. REFERENCES
1. Proctor
2. 3.
E, Kowalik TA. Circulatory support by pump-oxygenator in experimental ventricular fibrillation and acute left heart failure induced by coronary artery ligation. Cardiovasc Resus 1967; 1: 189-93. Litzie AK, Roberts CP. Emergency femoro-femoral cardiopulmonary bypass. Proc Amer Acad CV Perfusion 1987; 8: 60-65. Safar P, Abramson N, Angelos M, et al. Emergency cardiopulmonary bypass for resuscitation from prolonged cardiac arrest. Am J Emerg Med 1990; 8: 55-67.
4. DeBard ML. Cardiopulmonary resuscitation: analysis of six years’ experience and review of the literature. Ann Emerg Med 1981; 10: 408. 5. Rozenbaum EA, Shenkman L. Predicting outcome of inhospital cardiopulmonary resuscitation. Crit Care Med 1988; 16: 583-86. 6. Afifi A, Chang PC, Liu VY, et al. Prognostic indexes in acute myocardial infarction complicated by shock. Am J Cardiol 1974; 33: 826-32. 7. O’Neill. Management of cardiogemc shock. In: Topol E, ed. Acute coronary intervention. New York: Alan R. Liss, 1988: 195-213. 8. Shawl F, Domanski MJ, Hernandez J, Punja S. Emergency percutaneous cardiopulmonary support in cardiogenic shock from acute myocardial infarction. Am J Cardiol 1989; 64: 967-70.
ADDRESS Cardiac Research Unit, Regional Cardiothoracic Centre, Killingbeck Hospital, York Road, Leeds LS14 6UQ, UK (M R. Rees, FRCR, T. Browne, FRCS, U M Sivananthan, FRCR, S Whittaker, ACP, D. Hick, L. B Tan, MRCP, G. A Davies, FRCS) Correspondence to Dr M R Rees
