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Ann Thorac Surg 1995;60:1671-1677
© 1995 The Society of Thoracic Surgeons
Department of Anesthesiology and Section of Cardiothoracic Surgery, Department of Surgery, Mayo Clinic and Foundation, Rochester, Minnesota
Accepted for publication July 13, 1995.
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Abstract |
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Methods. Cerebral blood flow, metabolic rate, and oxygen delivery were measured in 60 patients randomized to normothermic (37°C) or hypothermic (27°C) cardiopulmonary bypass. The nitrous oxide saturation technique of Kety and Schmidt was used for cerebral blood flow determinations. Both temperature groups underwent moderate (31%) hemodilution.
Results. During normothermic cardiopulmonary bypass, cerebral blood flow increased secondary to hemodilution and decreased cerebral vascular resistance; a normal matching of oxygen demand and delivery was maintained. During hypothermic bypass, hemodilution and hypothermia had essentially equal, opposing effects on cerebral vascular resistance and blood flow. With hypothermia, brain oxygen demand and delivery were both reduced but not closely coupled.
Conclusions. From the standpoint of global cerebral perfusion and oxygenation, our data support the practice of ``warm'' heart operations. It clarifies the marked influence of hematocrit on cerebral blood flow and delineates the interaction of temperature and hematocrit on cerebral oxygen delivery. It also suggests that additional investigation to better define ``temperature-appropriate'' hemodilution during cardiopulmonary bypass is indicated.
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Introduction |
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The practice of cardiopulmonary bypass (CPB) in North America has been undergoing change during the past 3 years. Traditionally, CPB has been performed with induced hypothermia (25° to 32°C) because reductions in temperature lower tissue metabolic rate and have myocardial and cerebral protective effects [1]. Recently, many institutions have shifted their CPB practice to higher temperatures because warm cardioplegia with systemic normothermia improves myocardial function after CPB [2]. Although myocardial performance may be enhanced, there are significant concerns about the impact of normothermic CPB on the brain. A recent report [3] suggested that warm CPB may be associated with a higher incidence of neurologic injury than hypothermic CPB. There are also physiologic data that suggest normothermic bypass may be a cerebral stress [4, 5].
Cerebral venous oxygen saturation generally reflects the balance between cerebral oxygen delivery (CDO2) and consumption. Decreases in cerebral venous oxygen saturation have been documented during rewarming from hypothermic CPB [4, 6] and occurs with high frequency during early normothermic CPB [4]. An explanation of these results could be that the higher cerebral oxygen demand of warm bypass may not be coupled to reciprocal increases in CDO2.
Although measurements of cerebral blood flow (CBF) or cerebral metabolic rate for oxygen (CMRO2) cannot confirm or refute the safety of a temperature management strategy during cardiac operations, the measurement of CBF and CMRO2 is fundamental to demonstrate that this change in cardiac surgical practice has at least a prima facie physiologic acceptability with respect to the cerebral circulation. In this study, we measure CBF, CMRO2, and CDO2 in patients undergoing hypothermic and normothermic bypass, our goal being to assess the adequacy of cerebral oxygenation during normothermic CPB and better understand the relationship of temperature, CDO2, and hematocrit during CPB.
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Material and Methods |
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Anesthesia consisted of fentanyl and midazolam (loading dose, fentanyl 30 µg/kg and midazolam 100 µg/kg, followed by an infusion of fentanyl and midazolam, 0.3 and 0.4 µg • kg-1 • min-1, respectively). Infusion rate was reduced by 50% with the onset of CPB. Inspired oxygen fraction was maintained between 0.4 and 0.7. Arterial, pulmonary artery, and right atrial blood pressures, heart rate, end-tidal carbon dioxide concentrations, and nasopharyngeal temperature were continuously measured. A catheter was placed percutaneously in the right jugular bulb for sampling of cerebral venous blood. Catheter position was confirmed by fluoroscopy in all patients.
During CPB, a nonpulsatile pump flow of 2.2 to 2.4 L • min-1 • m-2 was maintained. Arterial carbon dioxide tension (PaCO2) was adjusted to normocapnic levels (35 to 40 mm Hg) without temperature correction (
-stat regulation). The bypass pump was primed to maintain a hematocrit of 23% or greater during CPB and a membrane oxygenator was used. Sodium nitroprusside or phenylephrine infusions were used during CPB to maintain a mean arterial blood pressure of 50 to 70 mm Hg. To maintain nasopharyngeal temperature at 27°, 32°, or 37°C, the perfusate was set at 25° to 26°, 32° to 33°, and 37° to 39°C, respectively.
Cerebral blood flow and the arteriovenous oxygen difference (AVDO2) were measured during four periods: (1) between sternotomy and aortic cannulation; (2) 30 minutes after the onset of CPB (37°C) in normothermic patients, and when a stable nasopharyngeal temperature of 27°C was achieved in hypothermic patients; (3) 60 minutes after the onset of CPB in normothermic patients, and at 32°C during rewarming in hypothermic patients; and (4) 30 minutes after weaning from CPB. Mean arterial blood pressure, pump flow rate during CPB, and nasopharyngeal temperature were stable for 5 minutes before measurements were made. Measurement of CBF and AVDO2 allowed subsequent calculation of CMRO2, CDO2, and the CDO2 to CMRO2 ratio. Cerebral vascular resistance was calculated as mean arterial blood pressure divided by CBF.
Cerebral blood flow was measured using the nitrous oxide (N2O) washin technique of Kety and Schmidt [7] according to previously established methods [8]. Ten percent N2O was introduced into the ventilator or oxygenator fresh gas flow with an air-oxygen mixture. Ten paired arterial and jugular bulb venous samples for N2O measurement were taken over the 15-minute saturation period [8]. During CPB, arterial blood was drawn from a shunt taken off the arterial inflow line of the CPB machine rather than the radial artery. The CBF was calculated from arterial and venous saturation curves fit to the measured N2O concentrations and integrated to infinity as follows [7, 8]:
 | (1) |
is the brain blood solubility coefficient for N2O; V(t) is the venous N2O reading at saturation; and 
(a - v)dt is the area circumscribed by the difference in the arterial and venous N2O concentration curves. All CBF values were normalized to a PaCO2 of 37 mm Hg by correcting measured values by 3% for each mm Hg difference in PaCO2 from 37 mm Hg [9, 10]. This was done so CBF comparisons could be made at equivalent PaCO2 values both within and between groups.
Cerebral Metabolism Measurement
The CMRO2 was determined from the product of the AVDO2 and the CBF, using the equation:
 | (2) |
Arterial and jugular bulb blood gas tensions and saturations were determined (IL-BGE Analyzer, IL 4-286 Co-Oximeter; Instrumentation Laboratories Inc, Boston, MA) during each CBF measurement period. Blood gas tensions were measured at 37°C and the arterial and venous blood oxygen tensions were subsequently back-corrected to a blood temperature of 27°C or 32°C when the patient was hypothermic. The formula of Severinghaus was used [8, 11]. The arterial and venous oxygen content (CxO2), CDO2, and CMRO2 at 27°C and 32°C were calculated after this temperature correction.
Arterial or venous oxygen content (CxO2):
 | (3) |
Cerebral oxygen delivery (CDO2):
 | (4) |
Arteriovenous oxygen content difference (AVDO2):
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For both temperature groups, within-group comparisons were performed using repeated-measures analysis of variance followed by Dunnett's test, when indicated. Between-group comparisons for each of the four study periods was performed using a Wilcoxon rank sum test. All data are expressed as mean ± standard deviation and p value less than 0.05 was considered significant. Complete sets of measurements for all four study periods were obtained in 30 of 30 normothermic patients. Cerebral blood flow and derived measurements were obtainable in 29 of 30 hypothermic patients during periods III and IV.
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Results |
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TopAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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), or with regard to any cerebral physiologic measurement (Figs 1–3, Table 2) (p >; 0.05 by rank-sum test).
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), all reported CBF values are normalized to a PaCO2 of 37 mm Hg so direct comparisons could be made.
In hypothermic (27°C) patients, CBF and cerebral vascular resistance did not differ from the value before CPB. Although, as body temperature declined with hypothermia, CMRO2 decreased (Figs 1, 2). During CPB with hemodilution at 27°C, arterial oxygen content and CDO2 were significantly decreased relative to the period before CPB (Fig 3). However, the ratio of CDO2 to CMRO2 was increased (Fig 4).
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). Cerebral vascular resistance decreased with rewarming (Table 2). Cerebral oxygen delivery remained less at 32°C than before CPB (Fig 3) and the CDO2 to CMRO2 ratio at 32°C remained higher than the control value (Table 2).
Thirty minutes after CPB (period IV), the hypothermic group demonstrated large increases in CBF relative to control or bypass values and large reductions in cerebral vascular resistance (Fig 1, Table 2). This occurred although the CMRO2 after CPB was not different from the CMRO2 before CPB (Fig 2). The CDO2 in the period after CPB also did not differ from the control value (Fig 3), nor did the CDO2 to CMRO2 ratio (Table 2).
In the normothermic group at 30 minutes of bypass (period II), CBF increased relative to the period before CPB as cerebral vascular resistance decreased (Table 2). The CMRO2 was unchanged (Figs 1 and 2). As in the cold group, arterial oxygen content decreased with bypass hemodilution, but with normothermia CDO2 was unchanged from control (Figs 3, 4). The ratio of CDO2 to metabolic rate was also unchanged (Table 2).
During period III in the normothermic group (60 minutes on CPB), the CBF remained higher, and cerebral vascular resistance lower than control, whereas the CMRO2 continued unchanged (Figs 1, 2), the CDO2 and the CDO2 to CMRO2 ratio were also unchanged (Figs 3, 4; Table 2).
After CPB, CBF and cerebral vascular resistance in the warm group remained greater than control, whereas the CMRO2 remained unchanged (Figs 1, 2). Likewise, the CDO2 and the CDO2 to CMRO2 ratio remained unchanged from before CPB (Table 2).
When the two groups were compared, they did not differ before bypass with respect to any cerebral physiologic value. During the first CPB period (period II), the ``warm'' and ``cold'' bypass groups differed with regard to temperature and all cerebral physiologic variables, although mean arterial blood pressure, PaCO2, and hemoglobin did not differ (Table 1). Cerebral blood flow, metabolic rate, and oxygen delivery were all higher in the normothermic group (Figs 1–3) and cerebral vascular resistance was lower. The ratio of CDO2 to demand was significantly higher in the cold group (Table 2). All cerebral physiologic measurements between groups differed at a level of p <; 0.001 by Wilcoxon rank-sum test.
During the second CPB period (period III), the normothermic and hypothermic groups differed with respect to temperature and each of the cerebral physiologic variables while the hemodynamic values, hemoglobin, and PaCO2 again did not differ between groups (Table 1). The CBF, CMRO2, and CDO2 were all higher in the warm group, whereas cerebral vascular resistance was lower (Figs 1–3, Table 2) (p <; 0.05 by Wilcoxon rank-sum test). During this period, the CDO2 to CMRO2 ratio did not differ between groups (Table 2).
After CPB, the hypothermic and normothermic groups differed only with respect to two variables. Thirty minutes after CPB the normothermic group had a higher nasopharyngeal temperature than the hypothermic group, and the hypothermic group had a higher arterial glucose concentration (Table 1).
Formal neurologic testing was not part of our study design; however, no patient in either temperature group demonstrated a focal neurologic deficit postoperatively. There was no perioperative morbidity.
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Comment |
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TopAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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). Third, after CPB both groups demonstrate high CBF and low cerebral vascular resistance, although CMRO2 is unchanged. This is presumably a function of persistent hemodilution. Cerebral oxygen delivery after CPB remains at control levels in the warm CPB group and returns to control levels in the cold CPB group. After CPB, cerebral oxygen supply and demand are closely matched. If global oxygen delivery is adequate during warm bypass, we are left to explain reports of low cerebral venous oxygen saturation during rewarming from hypothermia [4, 6] and during the early phase of normothermic CPB [6]. With rewarming, low cerebral venous oxygen saturation values may result from brain hyperthermia [12]. Measurements of brain oxygenation during stable temperatures may not be predictive of physiology when the brain is hyperthermic or when its temperature is actively changing, therefore, reports of low cerebral venous oxygen saturation values during rewarming are not inconsistent with our results. Similarly, initiation of normothermic CPB may be associated with an oxygenation stress [4, 5]. The transition to CPB is associated with hemodilution, a fall in mean arterial blood pressure, and with normothermic CPB, a rise in temperature. Aortic manipulation in this period probably also results in a cerebral embolic load. These acute changes may account for the low cerebral venous oxygen saturation values that we reported previously during the initial phase of warm CPB [4]. In this investigation, cerebral physiologic measurements were made after this transitional period of instability.
One might speculate that the higher CBF associated with warm bypass may predispose the cerebral circulation to a higher embolic load and a worsened neurophysiologic status when ischemia does occur. However, with normothermic CPB and hemodilution, blood flow to all organs is increased so it is unclear if a greater proportion of emboli will in fact be delivered to the central nervous system. This has yet to be documented. In addition, in this and a previous study [4], our temperature groups did not differ in neurologic outcome and larger prospective studies on neurologic outcome and bypass temperature have generated conflicting results [3, 13]. On the basis of presented data, we can only conclude that global cerebral oxygenation is well maintained with warm CPB.
This study differs from previous investigations on the relationship between temperature and cerebral physiology during human CPB in several ways. First, our CBF method, the Kety-Schmidt technique, differs from the xenon-133 washout technique that is typically used in human CPB studies [14]. The CBF and CMRO2 values we report using this technique are significantly higher than those reported with xenon-133 washout during bypass in humans [14] and our results more closely approximate predicted values [15, 16] and those obtained with a variety of techniques in humans [17, 18] and animal models [19, 20].
Second, our CBF results under hypothermic conditions differ from results obtained during hypothermia under nonbypass conditions [21]. We document an appropriate temperature-dependent decrease in CMRO2 but this was not associated with a decrease in CBF. Under nonbypass conditions, other investigators have demonstrated that a decrease in CMRO2 with hypothermia is associated with a decrease in CBF [21]. However, those non-CPB studies differ from our own because of the absence of hemodilution.
In this report, the hematocrit decreased approximately 31% with the onset of CPB (Table 1). Hemodilution increases CBF [22] secondary to a decrease in cerebral vascular resistance. Hemodilution and reduced temperature had offsetting effects on cerebral vascular resistance during cold bypass, therefore no change in CBF was seen. This effect of hemodilution on cerebral vascular resistance and CBF is evident in the normothermic group where hemodilution without temperature change occurs. In the normothermic group, a 30% decrease in hematocrit was associated with a 48% decrease in cerebral vascular resistance and a 43% increase in CBF. Therefore, if no hemodilution occurred during hypothermic bypass, our data suggest that hypothermia would have resulted in approximately a 50% decrease in CBF at 27°C. This is consistent with investigations under hypothermic conditions without hemodilution [21].
The results of three other CPB investigations are supportive of this interpretation. Hindman and colleagues [19] used microspheres to determine CBF in rabbits during hypothermic (27°C) CPB with moderate hemodilution and documented CBF values similar to ours. Schwartz and associates [23] obtained similar results using internal carotid xenon-133 injection in baboons during hypothermic (32°C) CPB, and Stephan and colleagues [24] in a clinical study using the Kety-Schmidt technique during hypothermic (26°C) CPB with moderate hemodilution obtained results nearly identical to our own.
This report also differs from many other cerebral physiologic studies because CDO2 is emphasized together with changes in CBF and CMRO2. Typically, the CBF to CMRO2 ratio is reported, with deviations from established values of 15 to 20 [14], being suggestive of pathophysiology. However, in the context of CPB, this relationship can be misleading because CPB hemodilution has a profound effect on CBF and is not reflected adequately in the CBF to CMRO2 ratio [25]. Hemodilution and decreasing cerebral vascular resistance explains the maintenance of CBF during cold bypass as well as the increase in CBF that occurs during warm bypass and in the period after CPB. Each of these results would be unexpected if one looked only at the predicted relationship between CMRO2 and CBF.
Because bypass results in relatively dramatic changes in hematocrit, the importance of CDO2, not simply CBF determinations, becomes evident. However, this is not sufficient to say that the brain primarily regulates CDO2 rather than CBF. During warm bypass, CBF rises with hemodilution and CDO2 is maintained at control levels, although during hypothermia neither CBF nor CDO2 appear to be coupled to brain oxygen demand.
In Figure 4, the CDO2 to CMRO2 ratio is plotted against CMRO2 for the 238 measurements obtained in this study. As CMRO2 is decreased with hypothermia, the CDO2 to CMRO2 ratio rises in an approximately logarithmic fashion. Both flow and oxygen delivery increase relative to CMRO2 as temperature is reduced. These data argue against either a normal coupling of CDO2 and CMRO2 (or CBF and CMRO2) during hypothermia. Similar conclusions can be drawn from the results of Michenfelder and Milde [20] who documented increasingly high CBF values relative to metabolic rate at equivalent and more extreme levels of CPB hypothermia in dogs. It is unclear if this is a result of a disturbance in a cerebral regulatory process or a function of changing biophysical characteristics of blood at reduced temperature.
Regardless of the mechanism, these results provide potential insights into management of hemodilution during hypothermic CPB. During hypothermia, CDO2 greatly exceeds oxygen demand, even with moderate hemodilution. Our data suggest that hemoglobin concentrations approaching 5 g/dL should be well tolerated at 27°C. A narrower margin for hematocrit will exist at normothermia as the compensatory increase in flow that can occur with hemodilution is limited. Therefore, hematocrit may need to be actively manipulated as temperature changes with cooling and rewarming. Further definition of ``temperature-appropriate hemodilution'' during CPB could have a significant impact on our practice.
This report supports the safety of normothermic bypass with respect to global cerebral oxygen supply and demand. During ``warm'' bypass, oxygen demand and delivery are closely coupled. It also demonstrates a significant excess of CBF and oxygen delivery relative to demand during hypothermia and indicates that flow-metabolism coupling is not well maintained under this condition. The results also suggest that greater degrees of hemodilution should be well tolerated during hypothermic CPB and that hyperemia after CPB is probably an expected consequence of hemodilution. Finally, the relevance of hematocrit and CDO2 calculations to studies of this type is emphasized.
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), normothermic group (
); n = 30 in all periods except periods III and IV of hypothermic group, where n = 29. *Identifies change from before cardiopulmonary bypass (CPB) within groups by repeated-measures analysis of variance followed by Dunnett's test (p <; 0.05). #Identifies between-group differences by Wilcoxon rank sum test (p <; 0.01). Values are mean ± standard deviation.
