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Anesth Analg 2002;95:266-272 © 2002 International Anesthesia Research Society
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Abstract |
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Preexisting diabetes mellitus is one of the major factors related to adverse postoperative neurological disorders after cardiac surgery. In previous reports, we found that diabetic patients more often experienced cerebral desaturation than nondiabetic patients during normothermic cardiopulmonary bypass (CPB). The purpose of this study was to examine the effects of increasing mean arterial blood pressure (MAP) by the administration of phenylephrine on internal jugular venous oxygen hemoglobin saturation (SjvO2) during tepid CPB in diabetic patients. We studied 20 diabetic patients scheduled for elective coronary artery bypass graft surgery and, as a control, 20 age-matched nondiabetic patients. After the induction of anesthesia, a fiberoptic oximetry catheter was inserted into the right jugular bulb to monitor SjvO2. After measuring the baseline partial pressure of the arterial and jugular venous blood gases and cardiovascular hemodynamic values, MAP was increased by the repeated administration of a 10-µg bolus of phenylephrine until it reached 100% of baseline values. There was a significant difference in SjvO2 value between the Diabetic and Control groups after the administration of phenylephrine (Diabetic group, 56% ± 6%; Control group: 60% ± 4%) (P < 0.05). There was a significant difference in the arterial-jugular oxygen content difference value between the Diabetic and Control groups after the administration of phenylephrine (diabetic group, 4.9% ± 0.6%; Control group, 4.5% ± 0.4%) (P < 0.05). We subdivided the Diabetic group into three groups (Diet Therapy group [n = 4], Glibenclamide group [n = 10], and Insulin-Dependent group [n = 6]). There was a significant difference in the mean slopes of SjvO2 versus cerebral perfusion pressure for increasing cerebral perfusion pressure between the Insulin-Dependent group and the other groups (Dunnett test: P = 0.04). Increasing MAP had no effects on the SjvO2 value in insulin-dependent patients during tepid CPB.
IMPLICATIONS: We examined the effects of increasing mean arterial blood pressure (MAP) by the administration of phenylephrine on internal jugular venous oxygen saturation (SjvO2) during tepid cardiopulmonary bypass in diabetic patients and found that increasing MAP had no effect on the SjvO2 value in insulin-dependent patients.
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Introduction |
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Preexisting diabetes mellitus is one of the major factors related to adverse postoperative neurological disorders after cardiac surgery (1). The mechanisms of postoperative cognitive decline in diabetic patients after cardiac surgery, however, are not fully understood (1). One of the mechanisms of adverse cognitive decline in diabetic patients after cardiac surgery might be related to the cerebral desaturation state caused by hypoperfusion during cardiopulmonary bypass (CPB).
Croughwell et al. (2) reported that patients with diabetes mellitus had abnormal cerebral autoregulation during hypothermic CPB. They found that desaturation state, estimated by jugular venous oxygen saturation (SjvO2) of <50%, was more often observed in diabetic patients than in nondiabetic patients during the rewarming period after hypothermic CPB. We found that diabetic patients more often experienced cerebral desaturation than nondiabetic patients during normothermic CPB (3)
Recently, there have been several studies to attempt to ameliorate cerebral oxygenation during CPB (4–7). Hanel et al. (5) reported that mild hypercapnia during the rewarming period could prevent cerebral desaturation. Grubhofer et al. (8) reported that increasing the cerebral perfusion pressure (CPP) induced increases in the SjvO2 in nondiabetic patients under hypothermic CPB. We found that moderate hypothermia (32°C) could prevent cerebral desaturation in diabetic patients (9).
Because tepid (from 34.5°C to 35.0°C) and normothermic (>35°C) CPB methods are widely used, it is important to examine whether we would be able to ameliorate the cerebral oxygenation during tepid or normothermic CPB, especially in diabetic patients. However, there has been no study determining whether increasing the CPP would induce increases in the SjvO2 in diabetic patients under tepid CPB. The purpose of this study was to examine the comparative effects of increasing mean arterial blood pressure (MAP) by the administration of phenylephrine on SjvO2 in diabetic and nondiabetic patients during tepid CPB.
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Methods |
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This study had the approval of the ethics committee of our institution, and written, informed consent was obtained from all patients. Twenty diabetic patients consecutively scheduled for elective coronary artery bypass graft were studied. Patients with diabetes mellitus were defined as patients who were medically treated with antidiabetic therapy, such as diet, oral, or insulin therapy. Fasting blood sugar and glycosylated hemoglobin should be well controlled in all diabetic patients by diet, oral antidiabetic drug, or insulin therapy because uncontrolled diabetes mellitus is considered a risk for postoperative wound infection.
Patients with a history of cerebrovascular disease, psychiatric illness, renal disease (creatinine concentration of >2.0 mg/dL), or active liver disease (glutamine oxaloacetate transaminase or glutamine pyruvate transaminase of >40 U/dL) were excluded. Patients with moderate to severe atherosclerotic lesions in the ascending aorta or with carotid artery stenosis, confirmed by preoperative ultrasonography and magnetic resonance imaging, were also excluded. As a control, 20 age-matched nondiabetic patients consecutively scheduled for elective coronary artery bypass graft were studied.
All patients received 10 mg of diazepam orally 1 h before anesthesia. Anesthesia was induced with 0.2 mg/kg of midazolam, 10 µg/kg of fentanyl, and 0.2 mg/kg of vecuronium, and the trachea was intubated. After the induction of anesthesia, a pulmonary arterial catheter (Vigilance®; Swan-Ganz CCO Thermodilution Catheter; Baxter, Irvine, CA) was inserted via the right internal jugular vein. For continuous monitoring of SjvO2, a 4.0F fiberoptic oximetry oxygen saturation catheter (Dual-Lumen Oximetry Catheter®; Baxter) was inserted into the right jugular bulb with a modified Seldinger technique. This catheter was connected to an analysis system (ExplorerTM system; Baxter) and calibrated in vivo by drawing a blood sample from the catheter. The position of the jugular bulb catheter tip was verified by radiograph film. The correctly positioned catheter tip should be cranial to a line extending from the atlanto-occipital joint space and caudal to the lower margin of the orbit. The SjvO2 data were collected and processed in a monitor-computer interface and were displayed and stored every 5 s in an Apple Macintosh computer (Apple Inc., Cupertino, CA).
The partial pressures of the arterial and jugular venous blood gases were analyzed with a Stat Profile Ultmita® (NOVA Biomedical Co., Boston, MA) and cooximeter (OSM3, Hemoximeter®; Radiometer Co, Copenhagen). All patients were ventilated with oxygen 50% and nitrogen 50%. PETCO2 was monitored (Ultima®; Datex, Helsinki, Finland) and maintained between 35 and 40 mm Hg. Anesthesia was maintained with a large dose of fentanyl (total dosage of fentanyl, 88.6 ± 15.4 µg/kg, mean ± SD). Muscular relaxation was maintained by the intermittent administration of vecuronium. No volatile anesthetic was administered. The tympanic temperature was continuously monitored by Mon-a-Therm® (Mallinckrodt Co., St. Louis, MO).
The CPB circuit was primed with a crystalloid, nonglucose-containing solution, and a nonpulsatile pump flow rate of 2.2 to 2.5 L · min-1 · m-2 was maintained. A membrane oxygenator and a 40-µm arterial line filter were used, and PaCO2 uncorrected for temperature was adjusted to normocapnic levels (35 to 40 mm Hg) by varying fresh gas flow to the membrane oxygenator (alpha-stat regulation).
The target tympanic temperatures were from 34.5°C to 36.0°C. The limit on maximal inflow temperature was set at 37.0°C. Hematocrit was maintained at >0.20 on CPB, with the addition of blood as necessary.
The study was performed during the stable CPB period (approximately 30 min after the start of CPB). According to the regimen of Grubhofer et al. (8), after the baseline partial pressure of the arterial and jugular venous blood gases and cardiovascular hemodynamic values were measured, MAP was increased by the repeated administration of a 10-µg bolus of phenylephrine until it reached 100% of baseline values, with an allowed maximum of 100 mm Hg. The study end point was defined as MAP at 100% of baseline values that was maintained at least 60 s. The data obtained were analyzed later by an individual who was also blinded to patient grouping.
CPP was defined as MAP minus internal jugular venous pressure. Internal jugular venous pressure was measured by monitoring pressure at the distal end of the SjvO2 catheter. Intraoperative epiaortic ultrasonography confirmed that none of the patients had moderate or severe atherosclerotic lesions in the ascending aorta.
The Mini-Mental Status Examination was performed for both groups on the day before the operation and 1 mo after the surgery. This examination consists of 16 questions to test disorders of language, right-left orientation, and ability to perform complex commands (10). The scores ranged from 0 to 56 points.
All data were expressed as mean ± SD. Paired Student’s t-tests, Mann-Whitney U-tests, and Dunnett’s test were used for analysis. Statistical significance was set at P < 0.05.
After the study was completed, we evaluated the sample size. The sample size calculation was based on the hypothesis that the SjvO2 value in Control patients would be increased by 10% compared with that in Diabetic patients. The sample size provides 80% power to detect a 20% difference between groups with a 5% probability of Type I error. All calculations were performed on a Macintosh computer with SPSS (SPSS, Inc, Chicago, IL) and StatView 5.0 software packages (Abacus Concepts, Inc., Berkeley, CA).
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Results |
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There were no significant demographic differences between the two groups (Table 1). There was no significant difference in the phenylephrine dosage required to induce MAP to reach 100% of baseline values (Control group, 49.1 ± 10 µg; Diabetic group, 54.5 ± 12 µg; Mann-Whitney U-test, P = 0.24). There was no significant difference in time from the induction of MAP to reach 100% of baseline values (Control group, 7.1 ± 1.6 min; Diabetic group, 7.6 ± 1.7 min; Mann-Whitney U-test, P = 0.21). Table 2 shows the individual data of diabetic patients.
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There were no significant differences in internal jugular venous pressure, tympanic temperature, PaCO2, hemoglobin concentration, or pump flow between the two groups either before or after treatment (Tables 3 and 4). The oxygen saturation values measured by the optical catheter (SjvO2) and in sampled blood measured by the blood gas analyzer were compared. SjvO2 and oxygen saturation in sampled blood correlated well (y = 11.945 + 0.743x; r2 = 0.601; P < 0.0001).
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Figure 1, A and B shows the individual data of Control and Diabetic patients after the administration of phenylephrine. Figure 1C shows a typical case after the administration of phenylephrine. SjvO2 values in the Diabetic group did not change after the administration of phenylephrine. In contrast, the SjvO2 value in the Control group was increased after the administration of phenylephrine (SjvO2 value before treatment, 55% ± 3%; SjvO2 value after the administration of phenylephrine, 60% ± 4%) (P < 0.05) (Tables 3 and 4). There was a significant difference in SjvO2 values between the Diabetic and Control groups after the administration of phenylephrine (Diabetic group, 56% ± 6%; Control group, 60% ± 4%) (P < 0.05).
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The arterial-jugular oxygen content difference (AjDO2) in the Diabetic group did not change after the administration of phenylephrine. In contrast, the AjDO2 value in the Control group was decreased after the administration of phenylephrine (AjDO2 value before treatment, 5.0% ± 0.3%; AjDO2 value after the administration of phenylephrine, 4.5% ± 0.4%) (P < 0.05) (Tables 3 and 4). There was a significant difference in AjDO2 values between the Diabetic and Control groups after the administration of phenylephrine (Diabetic group, 4.9% ± 0.6%; Control group, 4.5% ± 0.4%) (P < 0.05).
Figure 1, A and B shows the effect of CPP on SjvO2 during normothermic CPB in the Diabetic (Fig. 1A) and Control (Fig. 1B) groups. There was no significant difference in the mean slopes of SjvO2 versus CPP for increasing CPP between the two groups (Diabetic group, 0.064% ± 0.08%/mm Hg; Control group, 0.086% ± 0.06%/mm Hg; Mann-Whitney U-test, P = 0.37).
Because of the heterogeneous population of patients with diabetes mellitus in this study, we subdivided the diabetes group into three groups (Table 4). There was a significant difference in the mean slopes of SjvO2 versus CPP for increasing CPP between the Insulin group and the other three groups (Dunnett test, P = 0.04).
The Mini-Mental Status Examination was performed for both groups on the day before the operation and 1 mo after the surgery. There was no significant difference in examination scores on the day before the operation and 1 mo after the surgery among the four groups (a day before the operation: Diet Therapy group, 49 ± 7; Glibenclamide group, 48 ± 6; Insulin-Dependent group, 47 ± 7; Control group, 49 ± 8; at 1 mo after the surgery: Diet Therapy group, 46 ± 5; Glibenclamide group, 46 ± 7; Insulin-Dependent group, 46 ± 7; Control group, 48 ± 9).
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Discussion |
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Croughwell et al. (2) reported that lower values for internal SjvO2 at the end of rewarming during CPB were associated with cognitive deficits four to eight days after surgery. In a previous report, we showed that reduced SjvO2 in elderly patients during normothermic CPB was associated with short-term postoperative cognitive dysfunction (11). These articles suggested that it might be important to ameliorate the reduced SjvO2 during CPB.
The administration of phenylephrine could have increased the SjvO2 value in nondiabetic patients in this study. Grubhofer et al. (8) report that increasing the CPP (from 47 ± 8.2 mm Hg to 93 ± 16 mm Hg) induced increases in the SjvO2 value by 4.9% and induced a calculated increase in the cerebral blood flow (CBF) by 19.9% in nondiabetic patients during hypothermic CPB. They indicated that phenylephrine was effective for increasing the CBF. Our study is in part consistent with the findings of Grubhofer et al. (8). The administration of phenylephrine during tepid CPB was effective in increasing the SjvO2 in nondiabetic patients, but not in diabetic patients.
In previous studies (3,9), we found that SjvO2 in diabetic patients during normothermic CPB was lower, compared with that in controls. This observation was also reported by Croughwell et al. (2). This is the first report to examine whether increasing MAP would improve the reduced SjvO2 in diabetic patients during tepid CPB. However, we demonstrated no effects on the SjvO2 value by the administration of phenylephrine in insulin-dependent diabetic patients. Several mechanisms may be speculated to explain our observation. Pallas and Larson (12) showed that diabetic patients had impaired endothelial-dependent responses that were related to morphological and functional changes linking the vascular endothelium and the vascular smooth muscle. More specifically, vascular responses to both the calcium-dependent pathways of vasoconstriction and the nitric oxide pathways of vasorelaxation significantly differ between diabetic and nondiabetic patients. Because we did not examine the molecular mechanisms regarding no effect of increasing MAP on SjvO2, further study is necessary to confirm whether these findings are associated with an impaired endothelial-dependent response in diabetic patients.
We did not measure pressure-flow autoregulation in the brain during CPB in this study, and this deserves discussion. There have been some controversial results regarding the pressure-flow autoregulation in the brain during CPB (13–19). Newman et al. (13) reported that MAP in the range of 51–75 mm Hg had a small effect on CBF during both hypothermic and normothermic CPB. In contrast, Sadahiro et al. (19) reported that CBF was constant when MAP was higher than 50 mm Hg in an animal model. Roger et al. (15) reported that CBF was unchanged as MAP increased from 56 ± 7 mm Hg to 84 ± 7 mm Hg after the administration of phenylephrine. In our Control group, we found that the AjDO2 value was decreased after the administration of phenylephrine. The tympanic temperature was unchanged at the pre- and posttreated periods. If the cerebral metabolic rate for oxygen (CMRO2) was assumed to be constant after the administration of phenylephrine, decreased AjDO2 might indicate an increase in CBF after the administration of phenylephrine. These findings were inconsistent with those of Sadahiro et al. (19) and Roger et al. (15) The reasons for this contradictory result are unknown. However, this discrepancy might be in part attributable to the differences in the demographic data of the subjects, anesthetic drugs, pump flow rate, and hemodilution (14,17). In contrast to Control patients, no change in AjDO2 was observed after the administration of phenylephrine in Insulin-Dependent patients. This finding might indicate the loss of the normal coupling of CBF and CMRO2 in insulin-dependent patients and is in part consistent with the finding of Croughwell et al. (2). Croughwell et al. found greater desaturation during rewarming in diabetic than in nondiabetic patients and reported that the periods of desaturation were associated with increased oxygen extraction and loss of the normal coupling between CBF and CMRO2. Our data confirmed that pressure-flow autoregulation in insulin-dependent patients was impaired during tepid CPB.
In this study, we did not measure CBF directly. Thus, it cannot be excluded that increased or decreased AjDO2 indicated a change in CBF. Additionally, the CMRO2 is influenced by the depth of anesthesia and the brain temperature. Therefore, we cannot confirm whether CBF was truly unaltered after the administration of phenylephrine in this study.
We found a significant difference in the mean slopes of SjvO2 versus CPP for increasing CPP between the Insulin-Dependent group and the other groups. This implied that heterogeneity in the Diabetic group significantly influenced our results. Insulin-dependent patients are so few in number that it cannot be concluded that increasing MAP by the administration of phenylephrine has no effect on the improvement of the reduced SjvO2 values during CPB in all diabetic patients. Further study is necessary to confirm whether increasing MAP has a beneficial effect on the reduced SjvO2 value during CPB in diabetic patients.
It remains controversial whether SjvO2 during CPB is indicative of the cerebral oxygenation state (20,21). Moreover, it remains controversial whether reduced SjvO2 is associated with postoperative cognitive dysfunction (11,20,21). Further study is needed to identify the possible beneficial intervention necessary to improve the cerebral oxygenation in insulin-dependent patients during CPB.
In this study, diabetic patients had SjvO2 values similar to those of control patients. In previous studies (3,9), we found that diabetic patients had lower SjvO2 values during CPB than control patients. The discrepancy between this study and the other studies might in part be attributable to the differences in temperature management during CPB or to different anesthetics drugs, as well as to the heterogeneous population of patients with diabetes mellitus in this study. First, we did not observe a decrease in tympanic temperature at the start of CPB in this study. Our previous study (11) showed that the decrease in tympanic temperature at this time point observed in previous studies had a significant effect on the decrease in SjvO2 values at 20 minutes after the start of CPB. Second, we used large doses of fentanyl for anesthesia in this study. In contrast, we used propofol-based anesthesia in previous studies. Nandate et al. (22) reported the different effects of anesthetic drugs on SjvO2 values. Finally, as shown in Table 4, the heterogeneous population of patients with diabetes mellitus had a great effect on the results.
In hypertensive patients, the flow-pressure autoregulatory curve is shifted rightward, so that higher levels of CPP are needed to maintain adequate CBF (17). Because most patients in this study had hypertension, this might have affected our results.
Robson et al. (20) provided evidence that jugular bulb catheters were not very accurate during CPB, possibly because of increased vessel wall contact. However, in a previous publication (21) and in this study, we investigated the accuracy of our oximetric catheter system and found an excellent correlation between oximetry catheter values for SjvO2 and simultaneous SjvO2 values obtained from samples of jugular venous blood measured in a cooximeter.
In conclusion, increasing MAP by the administration of phenylephrine has no effect on SjvO2 values in insulin-dependent patients during tepid CPB.
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Acknowledgments |
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Supported in part by a grant from the Japanese Ministry of Science and Education (YK).
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References |
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