EDITORIAL
The Role of Continuous Jugular Venous Saturation Monitoring During Cardiac Surgery With Cardiopulmonary Bypass Randall M. Schell, MD, Frank H. Kern,
MD,
and J. G. Reves,
MD
Division of Cardiac Anesthesiology, Department of Anesthesiology, Duke University Medical Center, Durham, North Carolina
I
n this issue of Anesthesia & Analgesia, Nakajima et al. (1) demonstrate a practical method of confinuously monitoring cerebral oxygenation during cardiac surgery. They used an oximetry catheter to monitor the blood oxygen saturation in the jugular bulb (Sjo,) of 12 patients throughout cardiac surgery with cardio ulmonary bypass (systemic flows of 2.03.0 L.min-Pm-’, a-stat blood gas management, nonpulsatile flow, and moderate hypothermia). Of potential importance is the demonstration of jugular venous “desaturation,” which we believe should more properly be referred to as “reduced saturation” during rewarming. The reduced saturation was inversely and linearly correlated with nasopharyngeal temperature despite an average systemic flow >2.5 L.rnin-l.m-, and stable hemoglobin level. This abrupt decrease in saturation indicates a major alteration in the balance of cerebral oxygen supply and demand. This study emphasizes the importance of cerebral oxygen balance rather than absolute measurements of cerebral blood flow and cerebral metabolic rate for oxygen during cardiopulmonary bypass (CPB). It identifies the rewarming period following moderate hypothermic CPB as a potential period of increased neurologic risk. In the paradigm of neurologic injury after CPB, the relative importance of incomplete global ischemia is unclear. We recently found, using intermittent sampling from the jugular venous bulb during rewarming on CPB, a 23% incidence of desaturation to an Sjo, 5 50% partial pressure of jugular venous blood (2). In the patients who did not demonstrate jugular venous desaturation, cerebral blood flow was higher and the cerebral metabolic rate for Funded in part by a grant from the National Institutes of Health (R01 AG 9663-01). Accepted for publication March 12, 1992. Address correspondence to Dr. Reves, Division of Cardiac Anesthesiology, Department of Anesthesiology, Duke University Medical Center, Durham, NC 27710. 01992 by the International Anesthesia Research Society 0003-2999192155.00
oxygen was lower. The patients who had desaturation did not have impairment in postoperative neuropsychologic test performance compared with those patients who did not have desaturation. Our study suggests that these levels of reduced saturation as well as those reported by Nakajima et al. may be well tolerated although additional investigation is required to be certain of this. Neither study reached critical values of hemoglobin desaturation (vide infra). Much recent attention has been focused on cerebral blood flow and cerebral metabolism during hypothermic CPB, and the new knowledge has been recently reviewed (3). Hypothermia reduces the cerebral metabolic rate for oxygen to a greater extent than cerebral blood flow, resulting in luxuriant flow during moderate hypothermic CPB (4,5). Luxuriant flow means an increase in oxygen supply to the brain. As oxygen supply increases, the need for increased extraction across the brain diminishes. The measured Sjo, would therefore increase with temperature reduction during CPB (4-6). With rewarming, oxygen utilization increases while oxygen supply remains relatively fixed. Therefore, extraction across the brain increases. This is reflected in a reduction of Sjo, in the cerebral venous effluent. In the study by Nakajima et al., the measured Sjo, during rewarming was less than the measured Sjo, just after initiation of CPB. This implies a greater imbalance in the supply/ demand ratio of the brain with rewarming. We can theorize that with rewarming, oxygen demand may be dramatically increased at a time of relatively fixed delivery. On the supply side, hemodilution (reduced oxygen content) and a fixed pump flow rate may decrease oxygen delivery. Cerebral blood flow, although independent of pump flow rate during moderate hypothermic CPB (7,8), may be more dependent on pump flow rate during rapid rewarming and when regional areas of the brain are hyperthermic. The decrease in systemic vascular resistance Anesth Analg 1992;74:627-9
627
628
ANESTH ANALG 1992;74:627-9
EDITORIAL
with rewarming and the administration of systemic vasodilators, e.g., nitroprusside or chlorpromazine (a-blocker used in the reviewed study), coupled with increased whole body metabolism and nonpulsatile delivery of flow, may also affect cerebral oxygen supply. On the demand side, cerebral oxygen requirements may be increased secondary to excessive rewarming of the brain, e.g., high inflow temperatures, regional cerebral hyperthermia (9,lo), or lightened levels of anesthesia. These studies suggest that reduced levels of the oxygen supply/demand ratio for the brain exist during rewarming from hypothermic CPB. The pivotal question that remains is whether detection of a global reduction in hemoglobin saturation measured by jugular bulb oxygenation can explain, predict, or prevent brain injury. Unfortunately, the critical level of Sjo, as a predictor of neurologic injury in mildly hypothermic or normothermic patients on CPB is not known. There is some information regarding critical values in other settings. Although studies attempting to define the Sjo, thresholds for cerebral dysfunction have been described (11-21), the absolute Sjo, below which brain ischemia occurs is unknown. In 1935, measurements of jugular venous desaturation during nitrogen breathing demonstrated that if the Sjo, fell below =33%, patients became confused, and at an Sjo, of ~ 2 6 7 0 ,lost consciousness (11). Electroencephalographic slowing occurred in volunteer patients when the partial pressure of jugular venous blood oxygen fell below -19 mm Hg (Sjo, < 40%) during nitrogen breathing (15). Not only the absolute saturation level, but the length of time during which the brain is at a reduced supply/demand ratio is important. Continuous monitoring of Sjo, in the lateral sinus of patients undergoing carotid endarterectomy with local anesthesia revealed that transient neurologic dysfunction occurred when the saturation dropped below 50% for extended periods. Neurologic dysfunction, however, was not observed when the saturation was maintained above 60% (13). The article by Nakajima et al. raises the concern that Sjo, desaturation during rewarming from CPB may increase the risk of brain injury after CPB. Although the preponderance of evidence suggests embolic events as the primary mechanism for injury during adult CPB (3), specific periods such as rewarming are potential high-risk times for neurologic injury. Therefore, these periods deserve careful scrutiny, extensive evaluation, and possibly newer management strategies that may improve cerebral oxygen balance. Therapeutic approaches for Sjo, desaturation include slower rewarming, increasing cerebral blood flow (increasing arterial carbon dioxide ten-
sion), decreasing the cerebral metabolic rate for oxygen (anesthetics), increasing oxygen content (red cell transfusion), and increasing perfusion flow rate. Although the use of jugular venous oximeter catheters during cardiac surgery is unlikely to become as routine as pulmonary artery mixed venous saturation monitoring, continuous monitoring of cerebral oxygen balance is potentially important and intuitively satisfying. Monitoring oxygen balance may detect global hypoperfusion and then allow therapeutic interventions to prevent it. Unfortunately, it is unlikely to detect small areas of cerebral hypoperfusion caused by emboli. Newer technologies, e.g., optical spectroscopy (22), may allow continuous noninvasive monitoring of cerebral oxygen saturation. Clearly, further research in this area is needed so the clinician can predict whether a patient is at risk for sustaining injury from incomplete global cerebral ischemia during CPB.
References 1. Nakajima T, Masakazu K, Hayashi Y, l t a g u c h i K, Uchida 0, Takaki 0. Clinical evaluation of cerebral oxygen balance during cardiopulmonary bypass: on-line continuous monitoring of jugular venous oxvhemoglobin saturation. Anesth Analg 1992; 74:63@5. 2. Croughwell ND, Frasco P, Blumenthal JA, Leone BJ, White WD, Reves JG. Warming during cardiopulmonary bypass is associated with jugular bulb desaturation. Ann Thorac Surg 1992;53:827-32. 3. Newman M, Frasco P, Kern F, Greeley W, Blumenthal J, Reves JG. Central nervous system dysfunction after cardiac surgery. Adv Cardiovasc Surg 1992;3:243-73. 4. Greeley WJ, Kern FH, Ungerleider RM, et al. The effect of hypothermic cardiopulmonary bypass and total circulatory arrest on cerebral metabolism in neonates, infants and children. J Thorac Cardiovasc Surg 1991;101:78>94. 5. Croughwell N, Smith LR, Quill T, et al. The effect of temyerature on cerebral metabolism and blood flow in adults during cardiopulmonary bypass. J Thorac Cardiovasc Surg (in press). 6 . Kuwabara M, Nakajima N, Yamamoto F, et al. Continuous monitoring of blood oxygen saturation of internal jugular vein as a useful indicator for selective cerebral perfusion during aortic arch replacement. J Thorac Cardiovasc Surg 1992;103: 35562. 7. Govier AV, Reves JG, McKay RD, et a!. Factors and their influence on regional cerebral blood flow during nonpulsatile cardiopulmonary bypass. Ann Thorac Surg 1984;38:592400. 8. Rogers A, Prough D, Roy R, et al. Cerebrovascular and cerebral metabolic effects of alterations in perfusion flow rate during hypothermic cardiopulmonary bypass in man. J Thorac Cardiovasc Surg 1992;103:363-8. 9. Whitbv J, Dunkin L. Cerebral, oesophageal and nasopharyngeal temperatures. 6 r J Anaesth 1971;43:673-6. 10. Kern F, Jonas R, Mayer J, Hanley F, Castaneda A, Hickey P. Temperature monitoring during infant cardiopulmonary bypass: Does it predict efficient brain cooling? Ann Thorac Surg (in press). 11. Lennox WG, Gibbs FA, Gibbs EL. Relationship of unconsciousness to cerebral blood flow and to anoxemia. Arch Neurol Psvchiat 1935;34:1001-13. 12. Ferris E, Engel G, Stevens C, Logan M. The validity of internal
ANESTH ANALG 1992;74:627-9
13. 14. 15. 16. 17. 18.
jugular venous blood in studies of cerebral metabolism and blood flow in man. Am J Physiol 1946;147:517-21. Lyons C, Clark L, McDowell H, McArthur K. Cerebral venous oxygen content during carotid thrombintimectomy. Ann Surg 1964;160:561-7. Viancos J, Sechzer P, Keatts A, DeBakey M. Internal jugular venous oxygen tension as an index of cerebral blood flow during carotid endarterectomy. Circulation 1966;34:875-82. Meyer J, Gotoh F, Ebihara S, Tomita M. Effects of anoxia on cerebral metabolism and electrolytes in man. Neurology 1965; 151892-901, Salem M, Kim Y, Shaker M. The effect of alteration of inspired oxygen concentration on jugular-bulb oxygen tension during deliberate hypotension. Anesthesiology 1970;33:35&61. Meyer J, Gotoh F, Tazaki Y, et al. Regional cerebral blood flow and metabolism in vivo. Arch Neurol 1962;7:560-81. Meyer J, Gotoh F. Continuous recording of cerebral metabo-
EDITORIAL
19. 20.
21.
22.
629
lism, internal jugular flow and EEG in man. Trans Am Neurol Assoc 1964;89:151-6. Clauss R, Hass W, Ransohoff J. Simplified method for monitoring adequacy of brain oxygenation during carotid-artery surgery. N Engl J Med 1965;273:1127-31. Waltz A, Sundt T, Michenfelder J. Cerebral blood flow, jugular venous PO, and lactate concentration, and arterial-venous oxygen content during carotid endarterectomy. Eur Neurol 1971172;6:346-9, Garlick R, Bihari D. The use of intermittent and continuous recordings of jugular venous bulb oxygen saturation in the unconscious patient. Scand J Clin Lab Invest 1987;47(Suppl 188):47-52. McCormick P, Stewart M, Goetting M, Dujovny M, Lewis G, Ausman J. Noninvasive cerebral optical spectroscopy for monitoring cerebral oxygen delivery and hemodynami& Crit Care Med 1991;19:89-97.
The Role of Continuous Jugular Venous Saturation Monitoring During Cardiac Surgery With Cardiopulmonary Bypass Randall M. Schell, MD, Frank H. Kern,
MD,
and J. G. Reves,
MD
Division of Cardiac Anesthesiology, Department of Anesthesiology, Duke University Medical Center, Durham, North Carolina
I
n this issue of Anesthesia & Analgesia, Nakajima et al. (1) demonstrate a practical method of confinuously monitoring cerebral oxygenation during cardiac surgery. They used an oximetry catheter to monitor the blood oxygen saturation in the jugular bulb (Sjo,) of 12 patients throughout cardiac surgery with cardio ulmonary bypass (systemic flows of 2.03.0 L.min-Pm-’, a-stat blood gas management, nonpulsatile flow, and moderate hypothermia). Of potential importance is the demonstration of jugular venous “desaturation,” which we believe should more properly be referred to as “reduced saturation” during rewarming. The reduced saturation was inversely and linearly correlated with nasopharyngeal temperature despite an average systemic flow >2.5 L.rnin-l.m-, and stable hemoglobin level. This abrupt decrease in saturation indicates a major alteration in the balance of cerebral oxygen supply and demand. This study emphasizes the importance of cerebral oxygen balance rather than absolute measurements of cerebral blood flow and cerebral metabolic rate for oxygen during cardiopulmonary bypass (CPB). It identifies the rewarming period following moderate hypothermic CPB as a potential period of increased neurologic risk. In the paradigm of neurologic injury after CPB, the relative importance of incomplete global ischemia is unclear. We recently found, using intermittent sampling from the jugular venous bulb during rewarming on CPB, a 23% incidence of desaturation to an Sjo, 5 50% partial pressure of jugular venous blood (2). In the patients who did not demonstrate jugular venous desaturation, cerebral blood flow was higher and the cerebral metabolic rate for Funded in part by a grant from the National Institutes of Health (R01 AG 9663-01). Accepted for publication March 12, 1992. Address correspondence to Dr. Reves, Division of Cardiac Anesthesiology, Department of Anesthesiology, Duke University Medical Center, Durham, NC 27710. 01992 by the International Anesthesia Research Society 0003-2999192155.00
oxygen was lower. The patients who had desaturation did not have impairment in postoperative neuropsychologic test performance compared with those patients who did not have desaturation. Our study suggests that these levels of reduced saturation as well as those reported by Nakajima et al. may be well tolerated although additional investigation is required to be certain of this. Neither study reached critical values of hemoglobin desaturation (vide infra). Much recent attention has been focused on cerebral blood flow and cerebral metabolism during hypothermic CPB, and the new knowledge has been recently reviewed (3). Hypothermia reduces the cerebral metabolic rate for oxygen to a greater extent than cerebral blood flow, resulting in luxuriant flow during moderate hypothermic CPB (4,5). Luxuriant flow means an increase in oxygen supply to the brain. As oxygen supply increases, the need for increased extraction across the brain diminishes. The measured Sjo, would therefore increase with temperature reduction during CPB (4-6). With rewarming, oxygen utilization increases while oxygen supply remains relatively fixed. Therefore, extraction across the brain increases. This is reflected in a reduction of Sjo, in the cerebral venous effluent. In the study by Nakajima et al., the measured Sjo, during rewarming was less than the measured Sjo, just after initiation of CPB. This implies a greater imbalance in the supply/ demand ratio of the brain with rewarming. We can theorize that with rewarming, oxygen demand may be dramatically increased at a time of relatively fixed delivery. On the supply side, hemodilution (reduced oxygen content) and a fixed pump flow rate may decrease oxygen delivery. Cerebral blood flow, although independent of pump flow rate during moderate hypothermic CPB (7,8), may be more dependent on pump flow rate during rapid rewarming and when regional areas of the brain are hyperthermic. The decrease in systemic vascular resistance Anesth Analg 1992;74:627-9
627
628
ANESTH ANALG 1992;74:627-9
EDITORIAL
with rewarming and the administration of systemic vasodilators, e.g., nitroprusside or chlorpromazine (a-blocker used in the reviewed study), coupled with increased whole body metabolism and nonpulsatile delivery of flow, may also affect cerebral oxygen supply. On the demand side, cerebral oxygen requirements may be increased secondary to excessive rewarming of the brain, e.g., high inflow temperatures, regional cerebral hyperthermia (9,lo), or lightened levels of anesthesia. These studies suggest that reduced levels of the oxygen supply/demand ratio for the brain exist during rewarming from hypothermic CPB. The pivotal question that remains is whether detection of a global reduction in hemoglobin saturation measured by jugular bulb oxygenation can explain, predict, or prevent brain injury. Unfortunately, the critical level of Sjo, as a predictor of neurologic injury in mildly hypothermic or normothermic patients on CPB is not known. There is some information regarding critical values in other settings. Although studies attempting to define the Sjo, thresholds for cerebral dysfunction have been described (11-21), the absolute Sjo, below which brain ischemia occurs is unknown. In 1935, measurements of jugular venous desaturation during nitrogen breathing demonstrated that if the Sjo, fell below =33%, patients became confused, and at an Sjo, of ~ 2 6 7 0 ,lost consciousness (11). Electroencephalographic slowing occurred in volunteer patients when the partial pressure of jugular venous blood oxygen fell below -19 mm Hg (Sjo, < 40%) during nitrogen breathing (15). Not only the absolute saturation level, but the length of time during which the brain is at a reduced supply/demand ratio is important. Continuous monitoring of Sjo, in the lateral sinus of patients undergoing carotid endarterectomy with local anesthesia revealed that transient neurologic dysfunction occurred when the saturation dropped below 50% for extended periods. Neurologic dysfunction, however, was not observed when the saturation was maintained above 60% (13). The article by Nakajima et al. raises the concern that Sjo, desaturation during rewarming from CPB may increase the risk of brain injury after CPB. Although the preponderance of evidence suggests embolic events as the primary mechanism for injury during adult CPB (3), specific periods such as rewarming are potential high-risk times for neurologic injury. Therefore, these periods deserve careful scrutiny, extensive evaluation, and possibly newer management strategies that may improve cerebral oxygen balance. Therapeutic approaches for Sjo, desaturation include slower rewarming, increasing cerebral blood flow (increasing arterial carbon dioxide ten-
sion), decreasing the cerebral metabolic rate for oxygen (anesthetics), increasing oxygen content (red cell transfusion), and increasing perfusion flow rate. Although the use of jugular venous oximeter catheters during cardiac surgery is unlikely to become as routine as pulmonary artery mixed venous saturation monitoring, continuous monitoring of cerebral oxygen balance is potentially important and intuitively satisfying. Monitoring oxygen balance may detect global hypoperfusion and then allow therapeutic interventions to prevent it. Unfortunately, it is unlikely to detect small areas of cerebral hypoperfusion caused by emboli. Newer technologies, e.g., optical spectroscopy (22), may allow continuous noninvasive monitoring of cerebral oxygen saturation. Clearly, further research in this area is needed so the clinician can predict whether a patient is at risk for sustaining injury from incomplete global cerebral ischemia during CPB.
References 1. Nakajima T, Masakazu K, Hayashi Y, l t a g u c h i K, Uchida 0, Takaki 0. Clinical evaluation of cerebral oxygen balance during cardiopulmonary bypass: on-line continuous monitoring of jugular venous oxvhemoglobin saturation. Anesth Analg 1992; 74:63@5. 2. Croughwell ND, Frasco P, Blumenthal JA, Leone BJ, White WD, Reves JG. Warming during cardiopulmonary bypass is associated with jugular bulb desaturation. Ann Thorac Surg 1992;53:827-32. 3. Newman M, Frasco P, Kern F, Greeley W, Blumenthal J, Reves JG. Central nervous system dysfunction after cardiac surgery. Adv Cardiovasc Surg 1992;3:243-73. 4. Greeley WJ, Kern FH, Ungerleider RM, et al. The effect of hypothermic cardiopulmonary bypass and total circulatory arrest on cerebral metabolism in neonates, infants and children. J Thorac Cardiovasc Surg 1991;101:78>94. 5. Croughwell N, Smith LR, Quill T, et al. The effect of temyerature on cerebral metabolism and blood flow in adults during cardiopulmonary bypass. J Thorac Cardiovasc Surg (in press). 6 . Kuwabara M, Nakajima N, Yamamoto F, et al. Continuous monitoring of blood oxygen saturation of internal jugular vein as a useful indicator for selective cerebral perfusion during aortic arch replacement. J Thorac Cardiovasc Surg 1992;103: 35562. 7. Govier AV, Reves JG, McKay RD, et a!. Factors and their influence on regional cerebral blood flow during nonpulsatile cardiopulmonary bypass. Ann Thorac Surg 1984;38:592400. 8. Rogers A, Prough D, Roy R, et al. Cerebrovascular and cerebral metabolic effects of alterations in perfusion flow rate during hypothermic cardiopulmonary bypass in man. J Thorac Cardiovasc Surg 1992;103:363-8. 9. Whitbv J, Dunkin L. Cerebral, oesophageal and nasopharyngeal temperatures. 6 r J Anaesth 1971;43:673-6. 10. Kern F, Jonas R, Mayer J, Hanley F, Castaneda A, Hickey P. Temperature monitoring during infant cardiopulmonary bypass: Does it predict efficient brain cooling? Ann Thorac Surg (in press). 11. Lennox WG, Gibbs FA, Gibbs EL. Relationship of unconsciousness to cerebral blood flow and to anoxemia. Arch Neurol Psvchiat 1935;34:1001-13. 12. Ferris E, Engel G, Stevens C, Logan M. The validity of internal
ANESTH ANALG 1992;74:627-9
13. 14. 15. 16. 17. 18.
jugular venous blood in studies of cerebral metabolism and blood flow in man. Am J Physiol 1946;147:517-21. Lyons C, Clark L, McDowell H, McArthur K. Cerebral venous oxygen content during carotid thrombintimectomy. Ann Surg 1964;160:561-7. Viancos J, Sechzer P, Keatts A, DeBakey M. Internal jugular venous oxygen tension as an index of cerebral blood flow during carotid endarterectomy. Circulation 1966;34:875-82. Meyer J, Gotoh F, Ebihara S, Tomita M. Effects of anoxia on cerebral metabolism and electrolytes in man. Neurology 1965; 151892-901, Salem M, Kim Y, Shaker M. The effect of alteration of inspired oxygen concentration on jugular-bulb oxygen tension during deliberate hypotension. Anesthesiology 1970;33:35&61. Meyer J, Gotoh F, Tazaki Y, et al. Regional cerebral blood flow and metabolism in vivo. Arch Neurol 1962;7:560-81. Meyer J, Gotoh F. Continuous recording of cerebral metabo-
EDITORIAL
19. 20.
21.
22.
629
lism, internal jugular flow and EEG in man. Trans Am Neurol Assoc 1964;89:151-6. Clauss R, Hass W, Ransohoff J. Simplified method for monitoring adequacy of brain oxygenation during carotid-artery surgery. N Engl J Med 1965;273:1127-31. Waltz A, Sundt T, Michenfelder J. Cerebral blood flow, jugular venous PO, and lactate concentration, and arterial-venous oxygen content during carotid endarterectomy. Eur Neurol 1971172;6:346-9, Garlick R, Bihari D. The use of intermittent and continuous recordings of jugular venous bulb oxygen saturation in the unconscious patient. Scand J Clin Lab Invest 1987;47(Suppl 188):47-52. McCormick P, Stewart M, Goetting M, Dujovny M, Lewis G, Ausman J. Noninvasive cerebral optical spectroscopy for monitoring cerebral oxygen delivery and hemodynami& Crit Care Med 1991;19:89-97.
