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Ann Thorac Surg 1998;65:653-657
© 1998 The Society of Thoracic Surgeons

Original Articles: Cardiovascular

Jugular Venous Bulb Oxygen Saturation Depends on Blood Pressure During Cardiopulmonary Bypass

Georg Grubhofer, MD, Andrea M. Lassnigg, MD, Barbara Schneider, PhD, Maria A. Rajek, MD, Thomas Pernerstorfer, MD, Michael J. Hiesmayr, MD

Department of Cardiothoracic and Vascular Anesthesia and Intensive Care, University Clinic, Vienna, Austria

Accepted for publication August 28, 1997.

Dr Grubhofer, University Clinic of Anesthesia, Waehringer Guertel 18-20, A-1090 Vienna, Austria (e-mail: georg.grubhofer@univie.ac.at).


   Abstract
Top
 Abstract
Introduction
 Material and Methods
 Results
 Comment
 Appendix 1
 References
 
Background. Central nervous system dysfunction after cardiopulmonary bypass is frequent and can be caused by inadequate cerebral perfusion and oxygenation.

Methods. To test the effectiveness of cerebral autoregulation during cardiopulmonary bypass, we induced changes in the cerebral perfusion pressure by administering phenylephrine during moderate (29°C) hypothermia. Using the Fick principle, we calculated relative changes in cerebral blood flow from changes in the jugular venous bulb oxygen saturation.

Results. Increasing the cerebral perfusion pressure (from 47 ± 8.2 to 93 ± 16 mm Hg) induced increases in the jugular venous bulb oxygen saturation by 4.9% and a calculated increase in the cerebral blood flow by 19.9%, strongly suggesting impaired cerebral autoregulation.

Conclusions. Because cerebral autoregulation is impaired during cardiopulmonary bypass, phenylephrine is effective in increasing the cerebral blood flow and may contribute to the prevention of postoperative neurologic dysfunction, especially in patients who have a low jugular venous bulb oxygen saturation.


   Introduction
Top
 Abstract
 Introduction
Material and Methods
 Results
 Comment
 Appendix 1
 References
 
Central nervous system dysfunction is a frequent complication after cardiopulmonary bypass (CPB) and often results in long-term neurologic sequelae. Early postoperative deficits in intellectual function have been noted in 64% to 79% of patients and permanent cerebral deficits have been reported in 2% to 10% [1]. Although the exact cause of this cerebral dysfunction is not known, it may be related to diminished cerebral oxygenation resulting from inadequate cerebral perfusion [2].

During low perfusion states, the brain can compensate for the fall in cerebral blood flow by increasing oxygen off-loading from arterial hemoglobin, which is reflected in a decrease in the jugular venous bulb oxygen saturation (SjvO2). This decrease in the SjvO2 indicates a mismatch between cerebral oxygen supply and demand. Decreased SjvO2 during CPB is associated with reduced cerebral perfusion pressure (CPP) [3] and postoperative cerebral dysfunction [2]. Thus, cerebral injury related to CPB may be due in part to cerebral hypoperfusion. Cerebral perfusion is maintained by autoregulation over a wide range (50 to 150 mm Hg) of CPP ( ) [4]. Although cerebral autoregulation is considered to be intact during hypothermic CPB, considerable controversy exists concerning the appropriate level of MAP [5][6][7].

The aim of our study was to determine the effectiveness of cerebral autoregulation during moderate hypothermic CPB. During changes in the MAP (range, 50 to 100 mm Hg) induced by phenylephrine, we recorded SjvO2 continuously. Using the Fick principle, we calculated relative changes in cerebral blood flow from the differences in oxygen content between the arterial and jugular venous blood.


   Material and Methods
Top
 Abstract
 Introduction
 Material and Methods
Results
 Comment
 Appendix 1
 References
 
Patients and Anesthetics
After institutional review board approval (granted April 11, 1994) and written informed consent, 20 patients scheduled for elective coronary artery bypass grafting were entered into the study. Patients who had a history of stroke or other neurologic disease, poorly controlled hypertension, or diabetes mellitus were excluded.

After sedation with 0.05 mg/kg of intravenous midazolam and infiltration with 2% lidocaine, an arterial cannula was inserted into the radial artery and a central venous catheter was placed through the right internal jugular vein. The electrocardiogram, heart rate, and systemic and central venous pressures were recorded continuously. A 4F oximetric catheter (Opticath; Oxymetrix, Mountain View, CA) was introduced retrogradely into the left internal jugular bulb. Placement of the jugular bulb catheter was confirmed by radiography before operation using the criteria described by Bankier and associates [8]. Catheter calibration (CO-oximeter 482; Instrumentation Laboratories, Lexington, MA) was performed before CPB and immediately before the start of the study protocol (ie, the first bolus of phenylephrine). Temperature readings were taken from nasopharyngeal and vesical probes.

Anesthesia was induced with 0.2 mg/kg of midazolam, 0.1 mg/kg of pancuronium, and 0.3 mg/kg of etomidate by intravenous bolus injection. Fentanyl, 0.02 mg/kg, was infused over a 5-minute period during mask ventilation with 100% oxygen. After oral endotracheal intubation, anesthesia was maintained with O2/air, an inspired oxygen fraction of approximately 50%, fentanyl (0.25-mg bolus), and midazolam (5-mg bolus) as necessary. No volatile anesthetic agents were administered before or during CPB.

Extracorporeal circulation during CPB was performed with a Stoeckert Shiley (Munich, Germany) multiflow roller pump that provided pulsatile flow, a membrane oxygenator (Stoeckert Shiley), and an arterial filter (Dideco, Mirandola, Italy) at pulsatile flow rates of 2 L · min-1 · m-2. The oxygenator was primed with Ringer’s lactate (2,000 mL), heparin (8,000 IU), aprotinin (1/106 IU), and mannitol (20 g). The pump flow and hemoglobin concentration were kept within a 5% range of variation during the study period.

Arterial blood gases were controlled to maintain the oxygen tension between 100 and 200 mm Hg and the carbon dioxide tension between 35 and 45 mm Hg using alpha-stat management (measured at 37°C, without temperature correction). Arterial and jugular venous hemoglobin and hemoglobin oxygen saturation were measured by the CO-oximeter (model 482; Instrumentation Laboratories). To achieve a nasopharyngeal temperature of 29°C, initially a minimal perfusion temperature of 26° to 27°C (10°C below rectal body temperature at the start of CPB) was used. As the rectal and nasopharyngeal temperatures were decreasing, the perfusion temperature was increased using a step-by-step approach that ended at 29°C.

Measurements and Calculations
After at least 5 minutes at a nasopharyngeal temperature of 29°C, the MAP was increased by the repeated administration of a 20-µg bolus of phenylephrine, until it reached 200% of baseline values, with an allowed maximum of 100 mm Hg. The study period was limited to 20 minutes in each patient. After the first bolus of phenylephrine, MAP, jugular venous pressure, SjvO2, CPB pump flow, and temperature values were recorded every minute. In view of the great differences in the time it took the MAP to react to the administration of the vasopressor, the following time points were defined:

  1. Baseline, initiation of the phenylephrine bolus
  2. MAP at 150% of baseline values
  3. MAP at 200% of baseline values
  4. MAP decreased to baseline values
  5. 20 minutes after initiation of the phenylephrine bolus

After calibration of the jugular venous bulb catheter at a nasopharyngeal temperature of 29°C, jugular venous oxygen content was calculated continuously from the SjvO2 readings. According to the Fick principle, the reciprocal of the arterial-jugular venous blood oxygen content difference (1/ajDO2) was used as an equivalent for the cerebral blood flow, which can be determined repeatedly under the condition of an unchanged cerebral metabolic rate of oxygen [9]. The calculations of the relations between SjvO2, ajDO2, and cerebral blood flow are shown in Appendix 1.

Statistics
Data are presented as the mean plus or minus the standard deviation. In every patient, we analyzed continuous SjvO2 readings by linear regression, applied to both increases and decreases in mean CPP ( ). We performed the Wilcoxon signed-rank test to show statistically significant differences in the slopes from zero, and we compared the slopes for increasing CPP with the slopes for decreasing CPP. We performed the paired Student’s t-test for differences between baseline values and values at time points B, C, D, and E.

A p value of less than 0.05 was considered statistically significant. The SAS statistical software package (SAS Institute, Inc, Cary, NC) on a microcomputer was used for all analyses.


   Results
Top
 Abstract
 Introduction
 Material and Methods
 Results
Comment
 Appendix 1
 References
 
The mean age of the patients was 63 ± 11 years, the CPB time was 112 ± 39 minutes, and the aortic cross-clamp time was 64 ± 25 minutes. In 2 patients, no correct position of the jugular bulb catheter could be achieved, and in 1 patient, a short surgical procedure (one single vein bypass graft) limited cooling to 32°C. These 3 patients were excluded from further calculations. A mean of 27 ± 9.4 minutes after the initiation of CPB, the nasopharyngeal (29° ± 1.6°C) and vesical (29.9° ± 2.2°C) temperatures reached the level of moderate hypothermia. On observing no further change in the temperatures at 33 ± 8.1 minutes of CPB, we initiated the study protocol and began taking the measurements (Table 1).


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  		Time Course of Measured Variables During the Study Period1

 
During phenylephrine administration, CPP increased from 47 ± 8.2 to 93 ± 16 mm Hg and SjvO2 increased by 4.9%. After phenylephrine administration, CPP decreased to 58 ± 10 mm Hg and SjvO2 decreased by 5.9% (Table 1). Thus, the increase in CPP was followed by a significant increase in the cerebral blood flow equivalent, from 30.2 ± 16.8 to 36.2 ± 20.4 milliliters of blood per milliliter of oxygen. For time points A, C, and D, the individual SjvO2 values for each patient after the increase and decrease in CPP are plotted in Fig 1.



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  		The effect of cerebral perfusion pressure (CPP) on jugular venous bulb oxygenation saturation (SjvO2) during hypothermic cardiopulmonary bypass in 17 individual patients. The left side of the graph indicates changes in SjvO2 after an increase in CPP induced by phenylephrine infusion, and the right side shows the relation of SjvO2 and CPP after a decrease in CPP to baseline levels.

 
Mean slopes of SjvO2 versus CPP for both increasing and decreasing CPP were significantly different from zero, and individual slopes are listed in Table 2. The individual slopes in patients with a CPP below (n = 6) or above (n = 11) 50 mm Hg at baseline were not significantly different (0.095 ± 0.099 versus 0.105 ± 0.152 mm Hg; p = 0.87). In addition, intraindividual slopes for increasing and decreasing CPP were not significantly different (p = 0.19).


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  		Individual Slopes Determined by Linear Regression for the Dependence of Jugular Venous Bulb Oxygen Saturation on Cerebral Perfusion Pressure for Increases (Slope 1) and Decreases (Slope 2) in Cerebral Perfusion Pressure1

 
The cerebral blood flow equivalent and SjvO2 were significantly higher than baseline during increased CPP (time point B: p < 0.005; time point C: p < 0.003). Other controlled variables (eg, CPB pump flow, nasopharyngeal and vesical temperature, arterial hemoglobin concentration, PaO2, PaCO2) remained constant during the entire study period of 20 minutes (Table 1). A typical time course of measured values is plotted in Fig 2. After uneventful recovery from operation and anesthesia, none of the patients showed grossly detectable neurologic deficits.



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  		Plot of a continuous recording of measured variables in a typical case. Immediately after phenylephrine infusion, cerebral perfusion pressure (CPP) and jugular venous bulb oxygen saturation (SjvO2) increased. All temperatures remained constant over the 20-minute study period. At the end of the recording, CPP and SjvO2 reached stable levels similar to baseline values, suggesting an insignificant effect of changes in brain temperature on measured SjvO2 values. (CPB = cardiopulmonary bypass; T nas = nasopharyngeal temperature; T vesic = vesical temperature.)

 

   Comment
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
Appendix 1
 References
 
The principal finding of our investigation during moderate hypothermic CPB was a significant increase in SjvO2 as a result of an increase in CPP and a decrease in SjvO2 as a result of a decrease in CPP. According to the Fick principle, the cerebral metabolic rate of oxygen and the cerebral blood flow are the two most important determinants of SjvO2. A change in either of these variables could have been responsible for our observed results.

The cerebral metabolic rate of oxygen is influenced by the depth of anesthesia and the temperature of the brain. The depth of anesthesia can be assumed to have remained the same during the study period, whereas the temperature of the brain could not be measured reliably with routinely used monitor sites during hypothermic CPB [10]. Stone and colleagues [10] and Hindman and associates [11] found brain temperature to lag somewhat with blood temperature equilibration. At a nasopharyngeal temperature of 28°C, at least 16 minutes of routine perfusion techniques are required to achieve small brain-blood temperature gradients. We allowed 5 minutes for brain temperature equilibration; thus, the increase in SjvO2 that occurred during the initial increase in MAP could be attributed to further brain cooling. This effect, however, should also be present in the period of decreasing CPP, but this was not observed (Fig 2). Further, during 20 minutes of perfusion, nasopharyngeal and vesical temperatures did not change, suggesting that brain temperature equilibration was almost complete at the start of our study protocol.

The second important determinant of SjvO2 is cerebral blood flow. The significant dependence of SjvO2 and cerebral blood flow equivalent on CPP strongly suggests impaired cerebral pressure-flow autoregulation. This dependence differed considerably between individual patients, indicating that the impairment in autoregulation is a very individual reaction. An influence of CPP on cerebral blood flow also was observed by Mutch and co-workers [12] in dogs during changes in CPB pump flow and by Buijs and associates [13] in a human transcranial Doppler flow study. Newman and colleagues [14] reported a 4% increase in cerebral blood flow for every 10-mm Hg increase in MAP during hypothermia, which is in accordance with our results. In contrast, others have found cerebral pressure-flow autoregulation to be fairly well maintained during CPB [5][6][7]. However, exceptions were made for CPB performed using pH-stat blood gas management [5][6][15] and during deep hypothermia (12° to 25°C) in infants [16].

There appear to be several explanations for these conflicting results. First, the changes in cerebral blood flow estimated by our results are small, which probably explains our failure to detect the influence of MAP in previous studies. Second, our investigation of cerebral autoregulation is limited because measurements of cerebral blood flow by xenon-133 clearance methods cannot be performed continuously [9]. Autoregulation, however, is a vascular response that occurs within 15 to 30 seconds [4]. Hence, although SjvO2 is not a direct measurement of cerebral blood flow, it allows continuous determination of relative changes in cerebral blood flow in states of unchanged cerebral oxygen consumption. At least, human cerebral autoregulation in previous reference studies was investigated during nonpulsatile CPB. Although Sadahiro and co-workers [17] reported higher cerebral blood flow in dogs using pulsatile CPB, they observed no difference in autoregulation with pulsatile and nonpulsatile CPB. Consequently, our results also should be valid for nonpulsatile perfusion techniques.

The reliability of data derived from a jugular bulb catheter is an important concern. During three studies of CPB [3][18][19], this device was found to be an accurate method for continuous monitoring of SjvO2 that is not affected by temperature or hemodilution. We repeatedly observed wall artifacts in our patients during the first few minutes of CPB, but obtained stable signals from SjvO2 readings throughout the rest of the study period.

Jugular venous bulb oxygen saturation commonly is used as an index of the adequacy of cerebral oxygenation during CPB. Critically low SjvO2 values (<50%) found in normothermic, awake humans account for cerebral dysfunction and electroencephalographic slowing [20][21]. Jugular venous bulb oxygen saturation values of less than 50% are reported to occur frequently during normothermic CPB [22] and during rewarming from hypothermia [23]. Recently, Croughwell and colleagues [2] found an association between SjvO2 and postoperative cognitive decline. Jugular venous bulb oxygen saturation values can be obtained easily and, consequently, they may play an important role in the detection of impending cerebral ischemia and the use of therapeutic interventions. According to our results, it seems reasonable to prevent cerebral deoxygenation and ischemia through the use of phenylephrine during CPB. However, the lower limit of CPP at which this intervention is necessary to improve outcome remains to be defined.

In conclusion, we observed increases in SjvO2 as a result of increases in CPP induced by phenylephrine infusion. We interpret this finding as a sign of impaired cerebral autoregulation during hypothermic CPB. Whether this dependency has any implications for postoperative cerebral function remains to be elucidated, but it seems possible in patients who are at higher risk for cerebral hypoperfusion (eg, those with cerebrovascular disease) or in patients who have low SjvO2 values.


   Appendix 1
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Appendix 1
References
 
Calculations of relative changes in cerebral blood flow can be made from the arterial-jugular venous blood oxygen content difference (ajDO2) [9] if the cerebral metabolic rate of oxygen remains unchanged. This can be assumed during stable hypothermic CPB. Hence, all changes in cerebral blood flow will result in changes in SjvO2. The relation between cerebral blood flow, ajDO2, and SjvO2 is described as follows in the Fick equation:


where CMRO2 is the cerebral metabolic rate of oxygen (mL of oxygen · 100 g-1 · min-1), CBF is the cerebral blood flow (mL of blood · 100 g-1 · min-1), ajDO2 is the arterial-jugular venous blood oxygen content difference, SaO2 is the arterial oxygen saturation (%), SjvO2 is the jugular venous bulb oxygen saturation (%), Hb is the blood hemoglobin concentration (g/100 mL), and PaO2 is the partial pressure of O2 (mm Hg).


   References
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Appendix 1
 References
 

  1. Shaw PJ, Bates D, Cartlidge NEF, et al. Neurologic and neuropsychological morbidity following major surgery: comparison of coronary artery bypass and peripheral vascular surgery. Stroke 1987;18:700-707.[Abstract/Free Full Text]
  2. Croughwell ND, Newman MF, Blumenthal JA, et al. Jugular bulb saturation and cognitive dysfunction after cardiopulmonary bypass. Ann Thorac Surg 1994;58:1702-1708.[Abstract/Free Full Text]
  3. Andrews PJD, Colquhoun AD Detection of cerebral hypoperfusion during cardiopulmonary bypass. Anaesthesia 1994;49:949-953.[Medline]
  4. Strandgaard S, Paulson OB Cerebral autoregulation. Stroke 1984;15:413-416.[Free Full Text]
  5. Murkin JM, Farrar JK, Tweed WA, McKenzie FN, Guiraudon G Cerebral autoregulation and flow/metabolism coupling during cardiopulmonary bypass: the influence of PaCO2. Anesth Analg 1987;66:825-832.[Abstract/Free Full Text]
  6. Rogers AT, Stump DA, Gravlee GP, et al. Response of cerebral blood flow to phenylephrine infusion during hypothermic cardiopulmonary bypass: influence of PaCO2 management. Anesthesiology 1988;69:547-551.[Medline]
  7. Soma Y, Hirotani T, Yozu R, et al. A clinical study of cerebral circulation during extracorporeal circulation. J Thorac Cardiovasc Surg 1989;97:187-193.[Abstract]
  8. Bankier AA, Fleischmann D, Windisch A, et al. Position of jugular oxygen saturation catheter in patients with head trauma: assessment by use of plain films. Am J Roentgenol 1995;164:437-441.[Abstract/Free Full Text]
  9. Young WL, Newman MF, Amory D, Reves JG Cerebral blood flow values during cardiopulmonary bypass: relatively absolute or absolutely relative?. Ann Thorac Surg 1995;59:558-561.[Free Full Text]
  10. Stone JG, Young WL, Smith CR, et al. Do standard monitoring sites reflect true brain temperature when profound hypothermia is rapidly induced and reversed?. Anesthesiology 1995;82:344-351.[Medline]
  11. Hindman BJ, Funatsu N, Harrington J, et al. Differences in cerebral blood flow between alpha-stat and ph-stat management are eliminated during periods of decreased systemic flow and pressure. Anesthesiology 1991;74:1096-1102.[Medline]
  12. Mutch WAC, Sutton IR, Teskey JM, Cheang MS, Thomson IR Cerebral pressure-flow relationship during cardiopulmonary bypass in the dog at normothermia and moderate hypothermia. J Cereb Blood Flow Metab 1994;14:510-518.[Medline]
  13. Buijs J, Van Bel F, Nandorff A, Hardjowijono R, Stijnen T, Ottenkamp J Cerebral blood flow pattern and autoregulation during open-heart surgery in infants and young children: a transcranial, Doppler ultrasound study. Crit Care Med 1992;20:771-777.[Medline]
  14. Newman MF, Croughwell ND, Blumenthal JA, et al. Effect of aging on cerebral autoregulation during cardiopulmonary bypass. Association with postoperative cognitive dysfunction. Circulation 1994;90(Suppl 2):243-249.
  15. Patel RL, Turtle MRJ, Chambers DJ, Newman S, Venn GE Hyperperfusion and cerebral dysfunction. Effect of differing acid-base management during cardiopulmonary bypass. Eur J Cardiothorac Surg 1993;7:457-464.[Abstract/Free Full Text]
  16. Greeley WJ, Ungerleider RM, Smith LR, Reves JG The effects of deep hypothermic cardiopulmonary bypass and total circulatory arrest on cerebral blood flow in infants and children. J Thorac Cardiovasc Surg 1989;97:737-745.[Abstract]
  17. Sadahiro M, Haneda K, Mohri H Experimental study of cerebral autoregulation during cardiopulmonary bypass with or without pulsatile perfusion. J Thorac Cardiovasc Surg 1994;108:446-454.[Abstract/Free Full Text]
  18. Brown R, Wright G, Royston D A comparison of two systems for assessing cerebral venous oxyhaemoglobin saturation during cardiopulmonary bypass in humans. Anaesthesia 1993;48:697-700.[Medline]
  19. Nakajima T, Ohsumi H, Kuro M Accuracy of continuous jugular bulb venous oximetry during cardiopulmonary bypass. Anesth Analg 1993;77:1111-1115.[Abstract/Free Full Text]
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  23. 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;53:827-832.[Abstract/Free Full Text]



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