|Year : 2014 | Volume
| Issue : 2 | Page : 170-176
Monitoring the effects of propofol and sevoflurane on cerebral oxygen supply-demand balance using transcranial Doppler sonography and jugular bulb saturation in pediatric open heart surgery
Gamal Z. El-Morsy1, Alaaeldin M. Eldeeb1, Mohamed Adel F Elgamal2, Ashraf Abdelrahman3
1 Department of Anesthesia and Surgical Intensive Care, Mansoura University, Mansoura, Egypt
2 Department of Cardiothoracic Surgery, Faculty of Medicine, Mansoura University, Mansoura, Egypt
3 Department of Radiology, Mansoura University Children Hospital, Mansoura, Egypt
|Date of Submission||23-Nov-2013|
|Date of Acceptance||18-Dec-2013|
|Date of Web Publication||31-May-2014|
Alaaeldin M. Eldeeb
Department of Anesthesia and Surgical Intensive Care, Faculty of Medicine, Mansoura University, Mansoura
Source of Support: None, Conflict of Interest: None
Increasing awareness of neurologic abnormalities associated with congenital heart surgical intervention has heightened investigations for prevention of neurologic injury during the perioperative period. This study investigated the effects of propofol and sevoflurane on cerebral oxygen supply demand balance using transcranial Doppler sonography and jugular bulb saturation in pediatric open heart surgery.
After obtaining institutional approval and a written consent from parents, 60 children who were admitted for elective open cardiac surgery for correction of congenital heart disease using CPB were included in this study. Children were randomized into two groups; group (P) and group (S). Induction of Anesthesia was achieved by 5 μg/Kg I.V. fentanyl, propofol 2- 2.5 mg/Kg (in propofol or P group) or sevoflurane 2-3 MAC (in sevoflurane or S group). Anesthesia was maintained by propofol infusion between 75-100 μg/kg/min in P group or sevoflurane 2 MAC in S group. Calculated parameters from the blood gas variables included cerebral metabolic rate of oxygen (CMRO 2 ), cerebral extraction of oxygen (CeO 2 ) and cerebral blood flow equivalent (CBF). Arterial blood gases (ABG) and velocities of flow were monitored by Trancranial Doppler at 5 time points : before the surgery, before CPB, during CPB (after establishment of full flow), after CPB and after recovery. Neurological examination and CT scan were done before surgery and 2 days after that.
There is no significant difference between the two groups in demographic data. Children in propofol group showed lower heart rate values after induction and after CPB than those in sevoflurane group. Mean arterial pressure was statistically higher in sevoflurane group compared with propofol group after induction. Children in sevoflurane group showed significantly higher; velocity maximum, velocity mean and pulsatile index, in the after induction and after bypass periods than those in propofol group. Velocity minimum showed no difference between the two groups. SjvO 2 , CMRO 2 , CeO 2 and CBF was significantly different after induction in sevoflurane group compared with propofol group. Perioperative blood gases showed no difference between the studied groups.
Compared with propofol anesthesia, sevoflurane anesthesia provides a wider margin of safety against impaired cerebral oxygenation and better preservation of systemic hemodynamics. Moreover, cerebral oxygen saturation may not reflect changes in cerebral oxygenation as monitored by jugular venous oxygen tension measurement in children undergoing CPB.
Keywords: Pediatric cardiac surgery, transcranial doppler, jugluar bulb saturation
|How to cite this article:|
El-Morsy GZ, Eldeeb AM, Elgamal MF, Abdelrahman A. Monitoring the effects of propofol and sevoflurane on cerebral oxygen supply-demand balance using transcranial Doppler sonography and jugular bulb saturation in pediatric open heart surgery. Ain-Shams J Anaesthesiol 2014;7:170-6
|How to cite this URL:|
El-Morsy GZ, Eldeeb AM, Elgamal MF, Abdelrahman A. Monitoring the effects of propofol and sevoflurane on cerebral oxygen supply-demand balance using transcranial Doppler sonography and jugular bulb saturation in pediatric open heart surgery. Ain-Shams J Anaesthesiol [serial online] 2014 [cited 2021 Oct 27];7:170-6. Available from: http://www.asja.eg.net/text.asp?2014/7/2/170/133425
| Introduction|| |
Increasing awareness on neurologic abnormalities associated with congenital heart surgical intervention has heightened investigations for prevention of neurologic injury during the perioperative period . This injury may be attributed to the imbalance between cerebral oxygen supply and demand, embolic ischemic events, postischemic reperfusion injury, direct drug toxicity, and inflammatory pathways ,. The increased attention toward brain functioning has generated increased utility of neurologic monitors that are used for detection of cerebral hypoxia, perfusion abnormalities, and electrophysiological derangements .
Possible approaches include monitoring of superior vena cava or jugular venous oxyhemoglobin saturation (SjvO 2 ), regional cerebral oxygen saturation by near infrared spectroscopy, cerebral blood flow velocity (CBFV) by transcranial Doppler, electroencephalography, and processed electroencephalography . These modalities could enhance the ability to prevent injury that results from hypoxia, ischemia, emboli, hypocarbia, hypotension, and hyperthermia .
Propofol is a rapid-acting intravenous anesthetic, causing a dose-dependent reduction in cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO 2 ) consumption. Sevoflurane, an inhalational anesthetic agent, shows an intrinsic dose-dependent cerebral vasodilatory effect. Several studies have demonstrated how it increases the CBF and decreases the cerebrovascular resistance ,. In this study, we tried to evaluate the effects of propofol and sevoflurane on cerebral oxygen supply-demand balance using transcranial Doppler sonography and jugular bulb saturation in pediatric open heart surgery.
| Patients and methods|| |
After institutional approval and written informed consent from parents, 60 male and female pediatric patients, ASA II and III, aged 3-5 years who were admitted for elective open cardiac surgery for correction of congenital heart disease using cardiopulmonary bypass (CPB) were included in this study. This study was conducted in Mansoura University Children Hospital from May 2012 to June 2013. Children with multiple congenital anomalies, hepatic or renal dysfunction, or neurological or metabolic diseases were excluded from the study.
Cardiovascular functions were assessed for children. Complete blood count, electrolyte, arterial blood gas, coagulation profile, liver and renal function tests, and urine analysis were performed. Neurological examination performed by ASQ (http://www.brookespublishing.com/asq) and radiological examination [including brain computed tomography (CT)] were performed before and 2 days after surgery.
During the preoperative clinic visit, consent was obtained; height, weight, and oxygen saturation were recorded. According to the hospital policy, all children were fasting for at least 2-4 h before the procedure, and they arrived in the operative room with an intravenous catheter in situ. All children were premedicated when they were with their parents in a room outside the operative room with intravenous dose of midazolam (Dormicum; Hoffmann-La Roche Ltd, Basel, Switzerland) 0.1 mg/kg over a 5-min period, given by the attending anesthesiologist just before the procedure, and then the anesthesiologist accompanied the child to the operative room.
On arrival to the operative room and before induction of anesthesia, all patients were connected to the standard monitors that included five-lead ECG, ECG leads II and V5, noninvasive arterial pressure, and a digital pulse oxymetry. Heart rate (HR) and mean arterial pressure) MAP) were recorded every 5 min for the duration of surgery.
After the measurement of baseline HR and MAP, all patients received atropine 0.01 mg/kg intravenously and were preoxygenated with 100% oxygen by face mask .Patients were randomized by the sealed envelope method into two groups (n = 30): group P and group S.
Induction of anesthesia was achieved by administration of intravenous fentanyl 5 g/kg, propofol 2-2.5 mg/kg (in the propofol or P group), or sevoflurane 2-3 MAC (in the sevoflurane or S group). Rocuronium 0.9 mg/kg intravenous was used for muscle relaxation. Children were mechanically ventilated, after loss of consciousness, by positive-pressure ventilation through face mask at a rate of 20-28 breathes/min with 50% O 2 . End-tidal CO 2 , monitored by capnograph, was maintained between 30-35 mmHg.
In group P, anesthesia was maintained by propofol infusion between 75 and 100 g/kg/min . The propofol emulsion was diluted 1 : 1 with 5% dextrose solution, and the induction dose was preceded by intravenous lidocaine (0.1 ml/kg of a 0.1% solution).
In group S, anesthesia was maintained with sevoflurane 2 MAC.
Fentanyl 0.05 g/kg/min was given, in either group, to maintain blood pressure within 75-80% of its basal value and entropy value between 45 and 55, with infusion requirements for rocuronium 0.3 mg/kg/min to maintain muscle relaxation.
Arterial blood gases were recorded at five time points: before the surgery, before CPB, during CPB (after establishment of full flow), after CPB, and after recovery. Spontaneous regaining of the heart function, need for DC shocks, and the duration of inotropic and/or vasopressor requirements to wean the heart from CPB were recorded in all patients.
A retrograde jugular bulb catheter was inserted for cerebral hemodynamic measurements and blood sampling. Meanwhile, the head of the child was kept in the neutral position; a single lumen 4 Fr catheter was introduced in a retrograde manner into the right internal jugular vein using the Seldinger technique. The catheter was advanced until the resistance of root of jugular blub was felt then withdrawn about 1 cm, and its tip was adjusted at the base of the skull by fluoroscopy. Heparinized normal saline was used for continuous flushing of the catheter and a pressure transducer was connected to catheter to measure the jugular bulb pressure. Central venous pressure was monitored by the right subclavian vein.
Arterial and jugular bulb blood samples were withdrawn simultaneously. Calculated parameters from the blood gas variables included CMRO 2 , cerebral extraction of oxygen (CeO 2 ), and cerebral blood flow equivalent (CBF). The difference between arterial and jugular oxygen saturation was calculated to estimate CeO 2 . CBF, which is an index of flow/metabolism relationship, was calculated as the reciprocal of arteriojugular oxygen content difference . CMRO 2 , CeO 2 , and CBF were calculated using the following formulas, respectively: CMRO 2 = avDO 2 × PaCO 2 /100, where avDO 2 is the arteriojugular oxygen content difference ; CeO 2 = (SaO 2−SjO 2 )/SaO 2 , where SaO 2 is the arterial oxygen saturation ; and CBF = 1/avDO 2 .
Velocities of flow were monitored by transcranial Doppler at five time points: before the surgery, before CPB, during CPB (after establishment of full flow), after CPB, and after the surgery in the ICU (after 2 days). Neurological examination and CT scan were performed before surgery and 2 days after that. Entropy was used to assess the depth of anesthesia. It was collected with an M-ENTROPYTM module of the S/5TM Anesthesia Monitor (DatexOhmeda, Madison, United States).
Statistical analysis of data was performed using Excel program for figures and statistical package for the social sciences (SPSS, version 17; SPSS Inc., Chicago, Illinois, USA). The data were described as mean±SD for quantitative data and frequency and proportion for qualitative data. The data were analyzed to test statistically significant difference between the groups. The Student t-test was used to compare between two groups for quantitative data. Paired t-test was used to compare with the basal figures. The c2 -test was used for qualitative data. P value was significant if less than or equal to 0.05 at 95% confidence interval.
| Results|| |
Sixty children completed this study with no dropouts. There was no significant difference between the two groups in demographic data [Table 1].
Children in the propofol group showed higher HR values after induction and after CPB than those in the sevoflurane group. Otherwise, the MAP was statistically higher in the sevoflurane group compared with the propofol group after induction [Table 2].
|Table 2: Heart rate (beats/min) and mean arterial pressure (mmHg) in the studied groups|
Click here to view
Children in the sevoflurane group showed significantly higher velocity maximum, velocity mean, and pulsatile index, during the after induction and after bypass periods than those in the propofol group [Figure 1],[Figure 2],[Figure 3] and [Figure 4]. Velocity minimum showed no difference between the two groups.
SjvO 2 , CMRO 2 , CeO 2 , and CBF were significantly higher after induction in the sevoflurane group compared with the propofol group [Table 3].
|Table 3: Perioperative jugular oxygen saturation and calculated cerebral parameters in the studied groups|
Click here to view
Perioperative blood gases showed no difference between the studied groups [Table 4]).
Duration of inotropic support, spontaneous recovery of conscious level, and need for DC shock were insignificant between both groups. Preoperative and postoperative neurological examination and CT were of no significance between the two groups [Table 5].
|Table 5: Duration of inotropic support, spontaneous recovery of conscious level, need for DC shock, postoperative neurological examination, and computed tomography study in the studied groups|
Click here to view
| Discussion|| |
SjvO 2 has been used for indirect monitoring of global cerebral oxygen use to guide physiologic management decisions in many clinical settings. SjvO 2 will reflect the balance between supply and demand. Therefore, SjvO 2 reflects CBF/CMRO 2 ratio ,.
In awake healthy humans, SjvO 2 normally ranges from 50 to 75%. Cerebral hypoperfusion is indicated by value less than 50%, whereas cerebral ischemia usually occurs with values less than 40% ,.
The brain extracts a great amount of oxygen resulting in low SjvO 2 , whenever the metabolic demand exceeds cerebral oxygen supply, such as condition with low CBF. In the current study, sevoflurane increases CBFV and has higher SjvO 2 than propofol, suggesting that wider margin of safety against impaired cerebral oxygenation under conditions of impaired cerebral perfusion, such as in CPB, could be achieved by sevoflurane anesthesia ,.
Van Hemelrijck et al.  reported that, the reduction in CMRO 2 seemed to be less than that in CBF during propofol anesthesia, although their study was performed using anesthetized baboons. Collectively, CBF/CMRO 2 ratio may be reduced during propofol anesthesia. In contrast, CBF/CMRO 2 ratio seems to be maintained or increased during sevoflurane anesthesia, although the effect of sevoflurane on CBF may vary depending on the experimental conditions .
The present study showed that the HR is lower after induction in the propofol group when compared with the sevoflurane group. This may be because of the fact that propofol caused a resetting of baroreceptors to allow a slower HR, despite decreased arterial blood pressures. Cullen et al.  and Shan et al.  in their studies support this finding.
Another finding in this study is that the MAP is lower in the propofol group than in the sevoflurane group. Propofol is known to decrease MAP, whereas sevoflurane maintains it. This may be explained by the fact that it causes decrease in systemic vascular résistance (SVR), negative inotropic effect, and resetting of baroreceptors ,,. This finding is supported by previous studies ,,.
The principal finding of the study is that CBFV was decreased in the propofol-anesthetized patients group as compared with the sevoflurane-anesthetized patients group during the surgery. This is in accordance with previous studies, which found that propofol causes reduction in CBFV ,,,,.
Basil et al.  and kuroda et al.  in their studies proved that sevoflurane has cerebral vasodilator effect and increases CBFV, which is in agreement with the present study. However, in contrast to our study, Cho et al.  in their study stated that sevoflurane decreased CBFV; this may be because of the different MAC used.
The CBFV reduction by propofol within the middle cerebral artery can be explained by several mechanisms, such as vasoconstricting effect of propofol on the small resistance arterioles, decreasing HR and MAP, decreasing the CMRO 2 , and suppressing effect on endothelium-dependent relaxation that might reduce the steady-state CBFV, in that order. In contrast, all volatile anesthetic agents are known to cause direct cerebral vasodilatation, and it has been suggested that desflurane and sevoflurane may be a more potent cerebral vasodilator than other volatile agents ,. This finding is in agreement with the results of previous studies conducted by Kaisti et al.  and Engelhard and Werner .
Another important finding in the present study is that SjvO 2 is much higher in sevoflurane anesthesia when compared with propofol anesthesia.
A possible explanation of higher SjvO 2 in the sevoflurane group is greater cerebral oxygen delivery owing to smaller reduction in MAP and cerebral perfusion pressure. Cerebral vasodilator effect of sevoflurane significantly increases regional CBF with respect to regional CMRO 2 , leading to increased cerebral arterial volume fraction and increased arterial/venous ratio. In contrast, propofol reduces regional CBF and regional CMRO 2 to the same extent, thus decreasing the cerebral blood volume in the human brain .
Other studies conducted by Munoz et al.  and Kawano et al.  support our findings.
Several reports have shown that cerebral oxygen desaturation is associated with postoperative cognitive decline .
Despite the high prevalence of SjvO 2 desaturation in the P/R group, which may be related to global ischemia, no new major neurologic deficits were observed during the early postoperative period. One may thus argue that there were some methodological problems or the established criteria for 'global ischemia' were simply wrong .
The severity and duration of ischemia are critical determinants of tissue damage, and viability-time thresholds must be exceeded to produce stroke, suggesting that propofol anesthesia provides marginally adequate cerebral oxygenation without inducing neurologic dysfunction.
One of the limitations to our study is the absence of cerebral pathology, which could modify the response. In addition, we used total intra venous anesthesia (TIVA) in the propofol group instead of target-controlled infusion (TCI) because of limited resources.
In conclusion, our study suggests that a wider margin of safety against impaired cerebral oxygenation and better preservation of systemic hemodynamics could be provided by sevoflurane anesthesia rather than by propofol anesthesia. Moreover, cerebral oxygen saturation may not reflect the changes in cerebral oxygenation as monitored by jugular venous oxygen tension measurement in children undergoing CPB.
| Acknowledgements|| |
Conflicts of interest
| References|| |
|1.||Majnemer A, Limperopoulos C, Shevell M, Rohlicek C, Rosenblatt B, Tchervenkov C. Health and well-being of children with congenital cardiac malformations, and their families, following open-heart surgery. Cardiol Young 2006; 16:157-221. |
|2.|| Shaaban-Ali M, Harmer M, Vaughan RS, Dunne JA, Latto IP. Changes in jugular bulb oxygenation in patients undergoing warm coronary artery bypass surgery (34-37 degrees C). Eur J Anaesthesiol 2001; 18:93-99. |
|3.|| Zhao W, Belayev L, Ginsberg MD. Transient middle cerebral artery occlusion by intraluminal suture: II. Neurological deficits, and pixel-based correlation of histopathology with local blood flow and glucose utilization. J Cereb Blood Flow Metab 1997; 17:1281-1371. |
|4.|| Andropoulos DB, Stayer SA, Diaz LK, Ramamoorthy C. Neurological monitoring for congenital heart surgery. Anesth Analg 2004; 99:1365-1440. |
|5.|| George M, Nancy S. Perioperative neuromonitoring in pediatric cardiac surgery: techniques and targets. Pediatr Cardiol 2010; 29:123-130. |
|6.|| Artru AA, Shapira Y, Bowdle TA. Electroencephalogram, cerebral metabolic, and vascular responses to propofol anesthesia in dogs. J Neurosurg Anesthesiol 1992; 4:99-109. |
|7.|| Steur RJ, Perez RS, De Lange JJ. Dosage scheme for propofol in children under 3 years of age. Paediatr Anaesth 2004; 14:462-467. |
|8.|| Newell DW, Aaslid R, Stooss R, Seiler RW, Reulen HJ. Evaluation of hemodynamic responses in head injury patients with transcranial Doppler monitoring. Acta Neurochir (Wien) 1997; 139:804-817. |
|9.|| Strauss GI, Møller K, Holm S, Sperling B, Knudsen GM, Larsen FS. Transcranial Doppler sonography and internal jugular bulb saturation during hyperventilation in patients with fulminant hepatic failure. Liver Transpl 2001; 7:352-358. |
|10.||1Jaggi JL, Cruz J, Gennarelli TA. Estimated cerebral metabolic rate of oxygen in severely brain injured patients. Available tool for clinical monitoring. Crit Care Med 1995; 23:66-71. |
|11.||1Cruz J. Combined continuous monitoring of systemic and cerebral oxygenation in acute brain injury: preliminary observations. Crit Care Med 1993; 21:1225-1232. |
|12.||1Kuroda Y, Murakami M, Tsuruta J, Murakawa T, Sakabe T. Preservation of the ration of cerebral blood flow/metabolic rate of oxygen during prolonged anesthesia with isoflurane, sevoflurane and halothane in humans. Anesthesiology 1996; 84:555-561. |
|13.||1Matta BF, Lam AM, Mayberg TS, Shapira Y, Winn HR. A critique of the intraoperative use of jugular venous bulb catheters during neurosurgical procedures. Anesth Analg 1994; 79:745-750. |
|14.||1Yoshitani K, Kawaguchi M, Sugiyama N, Sugiyama M, Inoue S, Sakamoto T, Kitaguchi K, Furuya H. The association of high jugular bulb venous oxygen saturation with cognitive decline after hypothermic cardiopulmonary bypass. Anesth Analg 2001; 92:1370-1376. |
|15.||1Macmillan CS, Andrews PJ. Cerebrovenous oxygen saturation monitoring: practical considerations and clinical relevance. Intensive Care Med 2000; 26:1028-1036. |
|16.||1Gopinath SP, Cormio M, Ziegler J, Raty S, Valadka A, Robertson CS. Intraoperative jugular desaturation during surgery for traumatic intracranial hematomas. Anesth Analg 1996; 83:1014-1021. |
|17.||1Beck DH, Doepfmer UR, Sinemus C, Bloch A, Schenk MR, Kox WJ. Effect of sevoflurane and propofol on pulmonary fraction during one-lung ventilation for thoracic surgery. Br J Anaesth 2001; 86:38-43. |
|18.||1Kaisti KK, Långsjö JW, Aalto S, Oikonen V, Sipilä H, Teräs M, et al. Effects of sevoflurane, propofol, and adjunct nitrous oxide on regional cerebral blood flow, oxygen consumption, and blood volume in humans. Anesthesiology 2003; 99:603-613. |
|19.||1Van Hemelrijck J, Fitch W, Mattheussen M, Van Aken H, Plets C, Lauwers T. Effect of propofol on cerebral circulation and autoregulation in the baboon. Anesth Analg 1990; 71:49-54. |
|20.||2Cullen PM, Turtle M, Prys-Roberts C, Way WL, Dye J. Effect of propofol anesthesia on baroreflex activity in humans. Anesth Analg 1987; 66:1115-1135. |
|21.||2Shah A, Adaroja RN. Comparison of haemodynamic changes with propofol and sevoflurane anesthesia during laparoscopic surgery. Natl J Med Res 2011; 1:76-79. |
|22.||2Katzung BG. Basic and clinical pharmacology. New York, NY: Lange Medical Books/McGraw-Hill; 2001. |
|23.||2Claeys MA, Gepts E, Camu F. Haemodynamic changes during anesthesia induced and maintained with propofol. Br J Anaesth 1988; 60:3-9. |
|24.||2Coates DP, Monk CR, Prys-Roberts C, Turtle M. Hemodynamic effects of the infusion of the emulsion of propofol during nitrous oxide anesthesia in humans. Anesth Analg 1987; 66:64-70. |
|25.||2Monk CR, Coates DP, Prys-Roberts C, Turtle MJ, Spelina K. Haemodynamic effects of a prolonged infusion of propofol as a supplement to nitrous oxide Anesthesia. Studies in association with peripheral arterial surgery. Br J Anesth 1987;59: 954-1009. |
|26.||2Eng C, Lam AM, Mayberg TS, Lee C, Mathisen T. The influence of propofol with and without nitrous oxide on cerebral blood flow velocity and CO, reactivity in humans. Anesthesiology 1992; 77:872-881. |
|27.||2Vandesteene A, Trempont V, Engelman E, Deloof T, Focroul M, Schoutens A, de Rood M. Effect of propofol on cerebral blood flow and metabolism in man. Anesthesia 1988; 43: 42-45. |
|28.||2Alkire MT, Haier RJ, Barker SJ, Shah NK, Wu JC, Kao YJ. Cerebral metabolism during propofol anesthesia in humans studied with positron emission tomography. Anesthesiology 1995; 82:393-403. |
|29.||2Johnston AJ, Steiner LA, Chatfield DA, Coleman MR, Coles JP, Al-Rawi PG, Menon DK, Gupta AK. Effects of propofol on cerebral oxygenation and metabolism after head injury. Br J Anesth 2003; 91:781-787. |
|30.||3Matta BF, Heath KJ, Tipping K, Summors AC. Direct cerebral vasodilatory effects of sevoflurane and isoflurane. Anesthesiology 1999; 91:677-680. |
|31.||3Kuroda Y, Murakami M, Tsuruta J, Murakawa T, Shiroyama Y. Effects of sevoflurane and isoflurane on the ratio of cerebral blood flow/metabolic rate for oxygen in neurosurgery. J Anesth 2000; 14,128-134. |
|32.||3Cho S, Fujigaki T, Uchiyama Y, Fukusaki M, Shibata O, Sumikawa K. Effects of sevoflurane with and without nitrous oxide on human cerebral circulation. Anesthesiology 1984; 85:757-60. |
|33.||3Oshima T, Karasawa F, Satoh T. Effects of propofol on cerebral blood flow and the metabolic rate of oxygen in humans. Acta Anaesthesiol Scand 2002; 46:831-836. |
|34.||3Sponheim S, Skraastad Ø, Helseth E, Due-Tønnesen B, Aamodt G, Breivik H. Effects of, 0.5 and1.0 MAC isoflurane, sevoflurane and desflurane on intracranial and cerebral perfusion pressures in children. Acta Anesthesiol Scand 2003; 47:932-940. |
|35.||3Engelhard K, Werner C. The effects of general anesthesia and variations in hemodynamics on cerebral perfusion. Appl Cardiopulm Pathophysiol 2009; 13:157-159. |
|36.||3Muñoz HR, Núñez GE, de la Fuente JE, Campos MG. The effect of nitrous oxide on jugular bulb oxygen saturation during remifentanil plus target-controlled infusion propofol or sevoflurane in patients with brain tumors. Anesth Analg 2002; 94:389-392. |
|37.||3Kawano Y, Kawaguchi M, Inoue S, et al. Jugular bulb oxygen saturation under propofol or sevoflurane/nitrous oxide anesthesia during deliberate mild hypothermia in neurosurgical patients. J Neurosurg Anesthesiol 2004; 16:6-10. |
|38.||3Kawano Y, Kawaguchi M, Inoue S, Horiuchi T, Sakamoto T, Yoshitani K, Furuya H, Sakaki T. Jugular bulb oxygen saturation under propofol or sevoflurane/nitrous oxide anesthesia during deliberate mild hypothermia in neurosurgical patients. J Neurosurg Anesthesiol 2004; 16:6-10. |
|39.||3Kadoi Y, Saito S, Goto F, Fujita N. Decrease in jugular venous oxygen saturation during normothermic cardiopulmonary bypass predicts short-term postoperative neurologic dysfunction in elderly patients. J Am Coll Cardiol 2001; 38:1450-1455. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]