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WHEN IS CARDIOPULMONARY BYPASS TOTAL?
WHEN IS CARDIOPULMONARY BYPASS TOTAL? Albert H. Pemberton, M.D., Mortimer M. Bertin, M.D" and Benjamin G. Narodick, M.D., Milwaukee, Wis.
T
cardiopulmonary bypass is generally considered to have its onset at the time the snares are tightened about the caval vessels and their contained venous cannulas. At this time active ventilation of the lungs by the anesthesiologist is usually stopped and the lungs are held partially inflated by a mixture of helium and oxygen or allowed to collapse completely. A variable period of time then elapses before cardiotomy is carried out while flows are stabilized, cannulas re-adjusted, and stay sutures placed. A similar interval of time also occurs after cardiorrhaphy before releasing the caval snares and instituting partial bypass. During these periods an unoxygenated cardiopulmonary flow exists, as demonstrated by Julian and associates.' This has also been recognized by others but its significance has not, perhaps, been sufficiently stresSed. Coronary sinus blood is not diverted to the oxygenator and passes through the right heart to the pulmonary artery. It is not oxygenated in its passage through the lungs and is ejected by the left ventricle into the ascending aorta. There it mixes with the arterial perfusate from the pump oxygenator. Some of this mixed blood then enters the coronary arteries, thereby perfusing the myocardium with blood of lower than normal oxygen saturation. The myocardial hypoxia elicits prompt coronary vasodilatation with great augmentation of the coronary sinus blood flow." The mixed blood in the aorta, available for myocardial perfusion, becomes increasingly made up of markedly unsaturated coronary sinus blood, thus creating a vicious cycle. That cerebral hypoxia might also develop during these intervals of nonoxygenation of coronary sinus blood seemed 'possible if the zone of mixing in the ascending aorta extended distally to involve the carotid arteries. To investigate this possibility, a study was carried out in the laboratory. OTAL
METHOD
Adult mongrel dogs of either sex, weighing from 1G to 20 kilograms, were lightly anesthetized with sodium Pentothal, intubated. and automatically rospired with a .Tefferson ventilator. Arterial and central veuous PI'{'SSlll'('S "'C\'(' From the Cardiovascular Research Laboratory, Evangelical Deaconess Hospital, and the Departments of Medicine and Surgery, Marquette University School of Medicine, Milwaukee, Wis. Supported by a research grant from the John A. Hartford Foundation, New York City. Received for publication May 10, 1961.
685
686
PEMBERTON, BORTIN, NARODICK
J. Thoracic and Cardiovas. Surg.
continuously recorded on a Sanborn Poly-Viso by means of Sanborn transducers. A right thoracotomy was routinely performed and, after heparinization, large cannulas were placed in the superior and inferior venae cavae through the right atrial appendage for venous inflow to the pump oxygenator. Arterial return was by means of a cannula inserted into the left femoral artery. Bypass was begun and shortly followed by tightening the snares about the caval cannulas diverting returning venous blood to the oxygenator. A rotating disc oxygenator with gravity drainage of the venae cavae was employed in all experiments at normothermic temperatures. During bypass, venous inflow to the pump oxygenator was the determinant of flow rate. The blood volume was expanded, if necessary, to maintain flow rates averaging 2.1 L./min./M2. In all experiments, the arterial oxygen saturations averaged 95 per cent and the venous saturations 61 per cent. Venous pressure averaged 7 mm. Hg. Blood for priming the oxygenator was collected from healthy donor dogs from 1 to 4 days before bypass in Edglugate anticoagulant preservative solution." This blood was heparinized and reconstituted by the addition of calcium just prior to priming. Simultaneous blood samples were obtained anaerobically at various times during bypass from the venous and arterial ends of the oxygenator, from the proximal ascending aorta just above the valve by direct puncture, and from the right carotid artery in the neck by means of a Cournand needle previously inserted. Th~ oxygen saturation of the blood obtained from each of these sites was immediately determined by means of a cuvette oximeter and read on a double scale galvanometer.t The animals were divided into two groups.
Controls (Group [).-A. Four dogs: Active ventilation of the lungs was continued during bypass. Cardiotomy was not performed. Oxygen saturations were determined on blood drawn simultaneously from the arterial end of the oxygenator and the ascending aorta at intervals during the bypass period. B. Two dogs: After establishing bypass, right ventriculotomy was performed and the coronary sinus blood was aspirated from the open heart and returned to the oxygenator. Ventilation of the lungs was discontinued at the time of ventriculotomy and resumed following closure of the ventricle. Simultaneous oxygen saturations were recorded from the arterial end of the oxygenator and the ascending aorta at intervals after ventriculotomy. Experimental Cases (Group II).-Five dogs: Ventilation of the lungs was discontinued on initiation of bypass and the lungs were allowed to collapse. Anectine was given in sufficient dosage to prevent spontaneous respiratory movements. Cardiotomy was not performed. Simultaneous oxygen saturations were determined at regular intervals from the arterial end of the oxygenator, the ascending aorta, and the right carotid artery. After 35 minutes of bypass, ventilation of the lungs was resumed for 5 minutes following which simultaneous oxygen saturation determinations from the t.hree sites were again obtained. 'Supplied by Cutter Laboratories, Berkeley, California. tWaters Corporation, Rochester, Minnesota. (One standard deviation equals 0.289 per cent). Oximetric method repeatedly standardized against gasometric' and spectrophotometric' analyses.
Vol. 43, No.5 May, 1962
687
WHEN IS CARDIOPULMONARY BYPASS TOTAL'
RESULTS
Table I shows the results in the control group of animals. Simultaneously obtained samples reveal similar oxygen saturations in the blood from the arterial perfusate and the ascending aorta, TABLE
CONTROLS GROUP I
A
1.
CONTROLS (GROUP
CASE NO.
SITE
1
Arterial perfusate Ascending aorta
2
Arterial perfusate Ascending aorta
3
Arterial perfusate Ascending aorta
4
Arterial perfusate Ascending aorta Arterial perfusate Ascending aorta
1 B
I, A
AND
I
B) * OXYGEN SATURATION (%) TIME ON BYPASS (MIN.)
I
15
20 93 93
I
30
I
40 96 96
I
92 95 96 96
75
96 96
97 98
94 94
94 95 98 98
93 95
Arterial perfusate 93 95 Ascending aorta 92 96 *Slmultaneous oxygen saturations from arterial perfusate and ascending aorta during cardiopulmonary bypass. Group I, A.-no cardiotomy, active ventilation of lungs. Group I, B.-cardiotomy, no pulmonary ventilation. 2
Table II demonstrates the results obtained in the experimental animals in which ventilation of the lungs was discontinued on initiation of bypass and cardiotomy not performed. While the oxygen saturation of the arterial perfusate remained relatively constant, there was a prompt fall in the oxygen saturation of the blood in the ascending aorta which was manifested in all cases within 15 minutes after the onset of bypass. In 3 animals this had developed TABLE
II.
EXPERIMENTAL CASES* OXYGEN SA'!'URATION
(%)
TIME ON BYPASS (MIN.) CASE NO.
5 SITE
15 I 25
I
35
NO VENTILATION
40 VENTILATION
1
Arterial perfusate Ascending aorta R. carotid artery
97 89 87
93 85 91
92 69 84
92 52 83
96 96 97
2
Arterial perfusate Ascending aorta R. carotid artery
93 66 95
90 70 64
94 74 70
97 56 64
97 96 95
3
Arterial perfusate Ascending aorta R. carotid artery
96 96 96
96 74 89
94 56 82
94 50 83
94 96 96
4
Arterial perfusate Ascending aorta R. carotid artery
96 79 96
96 55 84
95 48 88
95 48 71
95 96 97
Arterial perfusate 96 97 96 96 96 Ascending aorta 96 70 54 77 96 R. carotid artery 96 91 91 96 97 *Oxygen saturations from arterial perfusate, ascendin!'l aorta. and right carotid artery in 5 animals undergoing cardiopulmonary bypass. No ca.rdlotomy. no pulmonary ventilation during first 35 minutes, ventilation resumed after 35 'minutes. 5
688
PEMBERTON, BORTIN, NARODICK
J. Thoracic and Cardiovas. Surg.
within 5 minutes after tho start of bypass. In all cases there was a significant difference in carotid arterial oxygen saturation when compared with that of the arterial perfusate. This, however, did not develop as rapidly as the desaturation seen in the ascending aorta. Fig. 1 graphically demonstrates the changes in oxygen saturation in the aorta and carotid artery, when compared with that of the arterial perfusate, and represents the average values obtained in the 5 experimental cases at regular intervals after bypass. There is a prompt and progressive fall in the oxygen saturation of the ascending aorta and a delayed but significant fall in carotid arterial oxygen saturation. It is to be noted from Table II and Fig. 1 that, 5 minutes after active ventilation of the lungs was resumed, the oxygen saturations at the three sites (arterial perfusate, ascending aorta, carotid artery) were similar and within the normal range for arterial blood. 100
90
%
02
80
SATURATION
70
60
WITHOUT VENTILATION OF LUNG 0510.15202530
3540
TIME ON BYPASS (Minutes) Fig. 1.
DISCUSSION
The results of this study confirm the work of Julian and his co-workers and, in addition, demonstrate a consistent arterial oxygen unsaturation of carotid blood under the condition of cardiopulmonary bypass here described. Upon resuming active pulmonary ventilation, full arterialization of aortic and carotid blood was obtained. It thus seems apparent that coronary sinus blood must be oxygenated during bypass by the lungs while it remains within a closed circuit if myocardial and cerebral hypoxia are to be avoided. On establishing cardiotomy with aspiration of the open heart, active ventilation of the lungs is no longer necessary since the pump oxygenator takes over the function of oxygenating the coronary sinus blood. Continued ventilation of the lungs at this time may, in fact, be deleterious since air may be sucked into the pulmonary arterial tree or a postoperative tracheobronchitis may ensue secondary to the exposure of bloodless alveoli to high oxygen tensions."
Vol. 43, No.5 May, 1962
WHEN IS CARDIOPULMONARY BYPASS 'l'O'l'ALf
689
CONCLUSIONS
1. Total cardiopulmonary bypass begins with cardiotomy or decompression of the right atrium and is concluded after cardiorrhaphy. Cessation and resumption of active pulmonary ventilation by the anesthesiologist should coincide with cardiotomy and cardiorrhaphy and not with the institution and discontinuance of caval bypass if aortic and carotid hypoxemia are to be avoided. 2. Survival studies in the laboratory to test new equipment and develop the techniques of bypass should include continued ventilation of the lungs if cardiotomy or right atrial decompression are not performed. 3. If active ventilation of the lungs is discontinued at the onset of caval bypass, the aortic and resultant coronary hypoxemia which rapidly develops may so augment the coronary sinus flow that intracardiac visualization is obscured when cardiotomy is performed. SUMMARY
Pulmonary ventilation is necessary during cardiopulmonary bypass prior to cardiotomy and after cardiorrhaphy in order to avoid aortic and carotid arterial oxygen unsaturation which presumably leads to myocardial and cerebral hypoxia. REFERENCES
1. Julian, 0., Lopez-Belio, M., and Hung, H. S.: The Effect of a Nonoxygenated Coronaropulmonary Flow in Certain Phases of Cardiac Bypass, S. Forum 8: 424, 1957. 2. Green, H. D., and Wegira, J.: The Effects of Asphyxia, Anoxia, and Myocardial Ischemia on Coronary Blood Flow. Am. J. PhysioI. 135: 271, 1942. 3. Van Slyke and Neill: J. BioI. Chem. 61: 523,1924. 4. Gordy, E., and Drabkin, D. L.: Spectrophotometric Studies, J. Biol, Chern. 227: 285, 1957. 5. Patrick, R. S.: Problems to Be Solved in Anesthesia for Cardiae Surgery in Collected Papers of Mayo Clinic and Mayo Foundation, Philadelphia, 1959, W. B. Saunders Company, vol. 51, p. 739.
T
cardiopulmonary bypass is generally considered to have its onset at the time the snares are tightened about the caval vessels and their contained venous cannulas. At this time active ventilation of the lungs by the anesthesiologist is usually stopped and the lungs are held partially inflated by a mixture of helium and oxygen or allowed to collapse completely. A variable period of time then elapses before cardiotomy is carried out while flows are stabilized, cannulas re-adjusted, and stay sutures placed. A similar interval of time also occurs after cardiorrhaphy before releasing the caval snares and instituting partial bypass. During these periods an unoxygenated cardiopulmonary flow exists, as demonstrated by Julian and associates.' This has also been recognized by others but its significance has not, perhaps, been sufficiently stresSed. Coronary sinus blood is not diverted to the oxygenator and passes through the right heart to the pulmonary artery. It is not oxygenated in its passage through the lungs and is ejected by the left ventricle into the ascending aorta. There it mixes with the arterial perfusate from the pump oxygenator. Some of this mixed blood then enters the coronary arteries, thereby perfusing the myocardium with blood of lower than normal oxygen saturation. The myocardial hypoxia elicits prompt coronary vasodilatation with great augmentation of the coronary sinus blood flow." The mixed blood in the aorta, available for myocardial perfusion, becomes increasingly made up of markedly unsaturated coronary sinus blood, thus creating a vicious cycle. That cerebral hypoxia might also develop during these intervals of nonoxygenation of coronary sinus blood seemed 'possible if the zone of mixing in the ascending aorta extended distally to involve the carotid arteries. To investigate this possibility, a study was carried out in the laboratory. OTAL
METHOD
Adult mongrel dogs of either sex, weighing from 1G to 20 kilograms, were lightly anesthetized with sodium Pentothal, intubated. and automatically rospired with a .Tefferson ventilator. Arterial and central veuous PI'{'SSlll'('S "'C\'(' From the Cardiovascular Research Laboratory, Evangelical Deaconess Hospital, and the Departments of Medicine and Surgery, Marquette University School of Medicine, Milwaukee, Wis. Supported by a research grant from the John A. Hartford Foundation, New York City. Received for publication May 10, 1961.
685
686
PEMBERTON, BORTIN, NARODICK
J. Thoracic and Cardiovas. Surg.
continuously recorded on a Sanborn Poly-Viso by means of Sanborn transducers. A right thoracotomy was routinely performed and, after heparinization, large cannulas were placed in the superior and inferior venae cavae through the right atrial appendage for venous inflow to the pump oxygenator. Arterial return was by means of a cannula inserted into the left femoral artery. Bypass was begun and shortly followed by tightening the snares about the caval cannulas diverting returning venous blood to the oxygenator. A rotating disc oxygenator with gravity drainage of the venae cavae was employed in all experiments at normothermic temperatures. During bypass, venous inflow to the pump oxygenator was the determinant of flow rate. The blood volume was expanded, if necessary, to maintain flow rates averaging 2.1 L./min./M2. In all experiments, the arterial oxygen saturations averaged 95 per cent and the venous saturations 61 per cent. Venous pressure averaged 7 mm. Hg. Blood for priming the oxygenator was collected from healthy donor dogs from 1 to 4 days before bypass in Edglugate anticoagulant preservative solution." This blood was heparinized and reconstituted by the addition of calcium just prior to priming. Simultaneous blood samples were obtained anaerobically at various times during bypass from the venous and arterial ends of the oxygenator, from the proximal ascending aorta just above the valve by direct puncture, and from the right carotid artery in the neck by means of a Cournand needle previously inserted. Th~ oxygen saturation of the blood obtained from each of these sites was immediately determined by means of a cuvette oximeter and read on a double scale galvanometer.t The animals were divided into two groups.
Controls (Group [).-A. Four dogs: Active ventilation of the lungs was continued during bypass. Cardiotomy was not performed. Oxygen saturations were determined on blood drawn simultaneously from the arterial end of the oxygenator and the ascending aorta at intervals during the bypass period. B. Two dogs: After establishing bypass, right ventriculotomy was performed and the coronary sinus blood was aspirated from the open heart and returned to the oxygenator. Ventilation of the lungs was discontinued at the time of ventriculotomy and resumed following closure of the ventricle. Simultaneous oxygen saturations were recorded from the arterial end of the oxygenator and the ascending aorta at intervals after ventriculotomy. Experimental Cases (Group II).-Five dogs: Ventilation of the lungs was discontinued on initiation of bypass and the lungs were allowed to collapse. Anectine was given in sufficient dosage to prevent spontaneous respiratory movements. Cardiotomy was not performed. Simultaneous oxygen saturations were determined at regular intervals from the arterial end of the oxygenator, the ascending aorta, and the right carotid artery. After 35 minutes of bypass, ventilation of the lungs was resumed for 5 minutes following which simultaneous oxygen saturation determinations from the t.hree sites were again obtained. 'Supplied by Cutter Laboratories, Berkeley, California. tWaters Corporation, Rochester, Minnesota. (One standard deviation equals 0.289 per cent). Oximetric method repeatedly standardized against gasometric' and spectrophotometric' analyses.
Vol. 43, No.5 May, 1962
687
WHEN IS CARDIOPULMONARY BYPASS TOTAL'
RESULTS
Table I shows the results in the control group of animals. Simultaneously obtained samples reveal similar oxygen saturations in the blood from the arterial perfusate and the ascending aorta, TABLE
CONTROLS GROUP I
A
1.
CONTROLS (GROUP
CASE NO.
SITE
1
Arterial perfusate Ascending aorta
2
Arterial perfusate Ascending aorta
3
Arterial perfusate Ascending aorta
4
Arterial perfusate Ascending aorta Arterial perfusate Ascending aorta
1 B
I, A
AND
I
B) * OXYGEN SATURATION (%) TIME ON BYPASS (MIN.)
I
15
20 93 93
I
30
I
40 96 96
I
92 95 96 96
75
96 96
97 98
94 94
94 95 98 98
93 95
Arterial perfusate 93 95 Ascending aorta 92 96 *Slmultaneous oxygen saturations from arterial perfusate and ascending aorta during cardiopulmonary bypass. Group I, A.-no cardiotomy, active ventilation of lungs. Group I, B.-cardiotomy, no pulmonary ventilation. 2
Table II demonstrates the results obtained in the experimental animals in which ventilation of the lungs was discontinued on initiation of bypass and cardiotomy not performed. While the oxygen saturation of the arterial perfusate remained relatively constant, there was a prompt fall in the oxygen saturation of the blood in the ascending aorta which was manifested in all cases within 15 minutes after the onset of bypass. In 3 animals this had developed TABLE
II.
EXPERIMENTAL CASES* OXYGEN SA'!'URATION
(%)
TIME ON BYPASS (MIN.) CASE NO.
5 SITE
15 I 25
I
35
NO VENTILATION
40 VENTILATION
1
Arterial perfusate Ascending aorta R. carotid artery
97 89 87
93 85 91
92 69 84
92 52 83
96 96 97
2
Arterial perfusate Ascending aorta R. carotid artery
93 66 95
90 70 64
94 74 70
97 56 64
97 96 95
3
Arterial perfusate Ascending aorta R. carotid artery
96 96 96
96 74 89
94 56 82
94 50 83
94 96 96
4
Arterial perfusate Ascending aorta R. carotid artery
96 79 96
96 55 84
95 48 88
95 48 71
95 96 97
Arterial perfusate 96 97 96 96 96 Ascending aorta 96 70 54 77 96 R. carotid artery 96 91 91 96 97 *Oxygen saturations from arterial perfusate, ascendin!'l aorta. and right carotid artery in 5 animals undergoing cardiopulmonary bypass. No ca.rdlotomy. no pulmonary ventilation during first 35 minutes, ventilation resumed after 35 'minutes. 5
688
PEMBERTON, BORTIN, NARODICK
J. Thoracic and Cardiovas. Surg.
within 5 minutes after tho start of bypass. In all cases there was a significant difference in carotid arterial oxygen saturation when compared with that of the arterial perfusate. This, however, did not develop as rapidly as the desaturation seen in the ascending aorta. Fig. 1 graphically demonstrates the changes in oxygen saturation in the aorta and carotid artery, when compared with that of the arterial perfusate, and represents the average values obtained in the 5 experimental cases at regular intervals after bypass. There is a prompt and progressive fall in the oxygen saturation of the ascending aorta and a delayed but significant fall in carotid arterial oxygen saturation. It is to be noted from Table II and Fig. 1 that, 5 minutes after active ventilation of the lungs was resumed, the oxygen saturations at the three sites (arterial perfusate, ascending aorta, carotid artery) were similar and within the normal range for arterial blood. 100
90
%
02
80
SATURATION
70
60
WITHOUT VENTILATION OF LUNG 0510.15202530
3540
TIME ON BYPASS (Minutes) Fig. 1.
DISCUSSION
The results of this study confirm the work of Julian and his co-workers and, in addition, demonstrate a consistent arterial oxygen unsaturation of carotid blood under the condition of cardiopulmonary bypass here described. Upon resuming active pulmonary ventilation, full arterialization of aortic and carotid blood was obtained. It thus seems apparent that coronary sinus blood must be oxygenated during bypass by the lungs while it remains within a closed circuit if myocardial and cerebral hypoxia are to be avoided. On establishing cardiotomy with aspiration of the open heart, active ventilation of the lungs is no longer necessary since the pump oxygenator takes over the function of oxygenating the coronary sinus blood. Continued ventilation of the lungs at this time may, in fact, be deleterious since air may be sucked into the pulmonary arterial tree or a postoperative tracheobronchitis may ensue secondary to the exposure of bloodless alveoli to high oxygen tensions."
Vol. 43, No.5 May, 1962
WHEN IS CARDIOPULMONARY BYPASS 'l'O'l'ALf
689
CONCLUSIONS
1. Total cardiopulmonary bypass begins with cardiotomy or decompression of the right atrium and is concluded after cardiorrhaphy. Cessation and resumption of active pulmonary ventilation by the anesthesiologist should coincide with cardiotomy and cardiorrhaphy and not with the institution and discontinuance of caval bypass if aortic and carotid hypoxemia are to be avoided. 2. Survival studies in the laboratory to test new equipment and develop the techniques of bypass should include continued ventilation of the lungs if cardiotomy or right atrial decompression are not performed. 3. If active ventilation of the lungs is discontinued at the onset of caval bypass, the aortic and resultant coronary hypoxemia which rapidly develops may so augment the coronary sinus flow that intracardiac visualization is obscured when cardiotomy is performed. SUMMARY
Pulmonary ventilation is necessary during cardiopulmonary bypass prior to cardiotomy and after cardiorrhaphy in order to avoid aortic and carotid arterial oxygen unsaturation which presumably leads to myocardial and cerebral hypoxia. REFERENCES
1. Julian, 0., Lopez-Belio, M., and Hung, H. S.: The Effect of a Nonoxygenated Coronaropulmonary Flow in Certain Phases of Cardiac Bypass, S. Forum 8: 424, 1957. 2. Green, H. D., and Wegira, J.: The Effects of Asphyxia, Anoxia, and Myocardial Ischemia on Coronary Blood Flow. Am. J. PhysioI. 135: 271, 1942. 3. Van Slyke and Neill: J. BioI. Chem. 61: 523,1924. 4. Gordy, E., and Drabkin, D. L.: Spectrophotometric Studies, J. Biol, Chern. 227: 285, 1957. 5. Patrick, R. S.: Problems to Be Solved in Anesthesia for Cardiae Surgery in Collected Papers of Mayo Clinic and Mayo Foundation, Philadelphia, 1959, W. B. Saunders Company, vol. 51, p. 739.