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Anesth Analg 2003;96:1145-1149
© 2003 International Anesthesia Research Society

NEUROSURGICAL ANESTHESIA

Esmolol Blunts the Cerebral Blood Flow Velocity Increase During Emergence from Anesthesia in Neurosurgical Patients

Philippe Grillo, MD*, Nicolas Bruder, MD*, Pascal Auquier, MD{dagger}, Daniel Pellissier, MD*, and François Gouin, MD*

*Département d’Anesthésie-Réanimation and {dagger}Service de Santé Publique et de Biostatistiques, Marseille, France

Address correspondence and reprint requests to Pr Nicolas Bruder, Département d’anesthésie-réanimation, CHU Timone, 264 Rue Saint-Pierre 13385 Marseille Cedex, France. Address e-mail to nicolas.bruder{at}ap-hm.fr


   Abstract
Top
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Cerebral hyperemia has been demonstrated during emergence from anesthesia in neurosurgical patients, but its mechanism is speculative. We performed this study to test the hypothesis that this could be attributed to sympathetic overactivity. Thirty neurosurgical patients were included in a prospective, randomized, double-blinded study comparing esmolol, a short-acting ß-blocker, and a placebo. Esmolol (0.3 mg · kg-1 · min-1) was infused from the end of anesthesia to 15 min after extubation. Cerebral blood flow velocity (CBFV), mean arterial blood pressure, and heart rate were recorded before anesthesia, during anesthesia after surgery, at extubation, and 5–60 min after extubation. Cardiac output (COe) was estimated by using an esophageal Doppler from anesthesia to 60 min after extubation. CBFV, COe, and heart rate were significantly lower in the esmolol group. Mean arterial blood pressure was comparable between the groups. There was no correlation between CBFV and COe at any time point during the study. In conclusion, esmolol blunted the CBFV increase during emergence, confirming that sympathetic overactivity contributes to cerebral hyperemia during neurosurgical recovery.

IMPLICATIONS: Esmolol blunted the postoperative increase in cerebral blood flow velocity in neurosurgical patients. The origin of sympathetic hyperactivity and its potential deleterious consequences require further study.


   Introduction
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 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
Recovery from general anesthesia and extubation is a period of intense physiological stress for patients. Oxygen consumption, catecholamine blood concentration, blood pressure, and heart rate (HR) increase after intracranial surgery (1). Cerebral hyperemia was also demonstrated at extubation by a concomitant increase in cerebral blood flow velocity (CBFV) and jugular venous bulb saturation in oxygen (2). There was a 60%–80% increase in CBFV in the middle cerebral artery from preinduction value on extubation that persisted at a lower level for 1 h. This observation occurred after anesthesia with propofol or isoflurane. The mechanism of this cerebral hyperemic response was unclear. In this study, we hypothesized that the stress associated with emergence and resultant sympathetic stimulation could explain this finding. To test this hypothesis, we performed a prospective, randomized, double-blinded study, using esmolol, a short-acting ß-blocking drug, to blunt the effects of sympathetic stimulation. Because esmolol may decrease cardiac output (CO), the relationship between CBFV and CO changes was also studied.


   Materials and Methods
Top
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
After IRB approval and written informed consent, 30 patients, ASA physical status I or II, scheduled for elective intracranial surgery, were included in this study. The intracranial lesions were 16 meningiomas, 3 grade 0 aneurysms, 6 gliomas, 3 metastatic tumors, and 2 arteriovenous fistulas, and were equally distributed between the 2 groups. Patients requiring emergency surgery, with clinical symptoms of intracranial hypertension, treated for systemic hypertension, or having contraindications for ß-blocking therapy, were not included in the study. Patients were randomly allocated into two groups: Group P (placebo: saline), n = 15, or Group E (esmolol), n = 15. The medication was prepared in equivalent volumes by a nurse who did not participate in the study. The anesthesiologist was blinded to the medication infused. Anesthesia was maintained with IV fentanyl (5–10 µ/kg), desflurane (<5% expired), nitrous oxide (N2O) in oxygen (FIO2 = 0.5), and atracurium. The end-tidal CO2 value was maintained between 30 and 35 mm Hg during anesthesia. After completion of surgery, the administration of desflurane and N2O was stopped and a bolus of esmolol (0.5 mg/kg) or placebo was given. Then a continuous infusion of esmolol (0.3 mg · kg-1 · min-1) or placebo was infused until 15 min after extubation. Hypertension during emergence (systolic blood pressure >160 mm Hg >1 min) was treated with a 1-mg IV nicardipine bolus. Hypotension (systolic blood pressure <100 mm Hg >1 min) was treated with IV ephedrine. A 2-MHz ultrasound probe (EME TC 2-64) was used to measure the time-averaged blood flow velocity in the middle cerebral artery at a depth of 50 or 55 mm on the opposite side of surgery. The measurements were recorded in the operating room immediately before anesthesia, during anesthesia just after surgical closure of the skin under desflurane (2%–4% expired), in the recovery room at extubation, and 5, 10, 15, 30, and 60 min after extubation. An esophageal Doppler probe (ODM IITM, Laboratoires AbbottTM, Rungis, France) was placed after the induction of anesthesia for the measurement of aortic flow velocities and calculation of estimated CO (COe). CO2 was measured at the same times that CBFV was measured. The intensity of the esophageal Doppler signal varied, often markedly, with rotation of the probe. For the purpose of this study, the position with the maximal Doppler signal was searched for at the time of each CO measure. Mean arterial blood pressure (MAP) measured via a radial artery catheter and HR were recorded at the same times. The data were reported as mean ± SD. Data analysis used a general linear model taking into account the effect of time (SPSS software version 10.0, SPSS Science, Erkrath, Germany). Post hoc comparisons to baseline values (before anesthesia for CBFV or during anesthesia for COe) and comparisons between groups for age, weight, height, duration of anesthesia, temperature, and fentanyl doses used the Student’s t-test. Regression analysis was used to search for correlation between COe and CBFV. P < 0.05 was considered significant.


   Results
Top
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
The mean age (Group P: 47 ± 15 yrs, Group E: 52 ± 10 yrs), weight (Group P: 68 ± 16 kg, Group E: 65 ± 10 kg), height (Group P: 168 ± 6 cm, Group E: 165 ± 6 cm), duration of anesthesia (Group P: 263 ± 70 min, Group E: 249 ± 40 min), and body temperature at extubation (Group P: 36.5° ± 0.5°C, Group E: 36.6° ± 0.6°C) were similar between the two groups. The fentanyl doses were significantly larger in Group P than in Group E (Group P: 430 ± 160 µg, Group E: 340 ± 50 µg, P < 0.05). No fentanyl was administered during emergence. There was a statistically significant difference between the two groups for CBFV and COe and HR for all time periods after anesthesia (P < 0.05) (Fig. 1, Fig. 2 and Table 1). Time effect was significant (P < 0.01) for CBFV and COe, HR and MAP. CBFV values were significantly larger than baseline from extubation to 30 min after extubation in Group P and only at extubation in Group E. COe values increased in Group P from extubation to 60 min after extubation and decreased in Group E from 5 to 15 min after extubation compared with baseline values. Two patients in Group P and 1 patient in Group E required a 1-mg bolus of nicardipine during recovery. There was no correlation between CBFV and COe at any time point during the study period.



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  		Figure 1. Middle cerebral artery blood flow velocity (CBFV) before anesthesia (preop), during anesthesia (anesth), at extubation (extub), and 5–60 min after extubation (E + 5' to E + 60') in Group P (placebo) and Group E (esmolol) (mean ± SD). *P < 0.05 compared with preoperative (preop) value. #P < 0.05 statistically significant between groups.

 


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  		Figure 2. Estimated cardiac output (COe) during anesthesia after surgery (anesth), at extubation (extub), and 5–60 min after extubation (E + 5' to E + 60') in Group P (placebo) and Group E (esmolol) (mean ± SD). *P < 0.05 compared with the value recorded during anesthesia (anesth). #P < 0.05 statistically significant between groups.

 

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  		Table 1. Mean Arterial Blood Pressure (MAP) (mm Hg) and Heart Rate (HR) Before Anesthesia (Preop), during Anesthesia (Anesth), at Extubation (Extub), and 5 min to 60 min After Extubation (E + 5' to E + 60') in Group P (Placebo) and Group E (Esmolol)
 

   Discussion
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
This study shows that esmolol blunts the increase in CBFV during recovery from neurosurgical anesthesia, confirming our hypothesis that sympathetic stimulation contributes to cerebral hyperemia during emergence from craniotomy. Several mechanisms may explain the effect of esmolol on CBFV during recovery from anesthesia.

The involvement of ß-adrenergic receptors in the control of cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRO2) has been demonstrated in animals and humans. Direct injection of norepinephrine into the ventricles increased CBF and cerebral metabolism (3). In rats, previous adrenalectomy or the administration of a ß receptor-blocking drug limited the increase in CBF and CMRO2 induced by immobilization stress (4,5) . However, this effect was probably not directly related to a an increased concentration of circulating epinephrine because infusion of epinephrine does not increase CBF (6). Plasma catecholamines alone do not affect the cerebral circulation if the blood-brain barrier is intact and if cerebral pressure autoregulation is maintained (7,8) . When the permeability of the blood-brain barrier is altered by osmotic insult, IV infusion of epinephrine or norepinephrine increases CBF and CMRO2 (5). The permeability of the blood-brain barrier is altered in sepsis (9) or after the release of inflammatory substances such as histamine or bradykinin (10), which may explain the dose-related increase in CBFV and jugular venous bulb saturation in oxygen with dobutamine infusion in septic patients (11). Neurosurgical recovery is associated with sympathetic stimulation including an increase in catecholamine blood concentration (1). This adrenergic stimulation may increase CBF and CMRO2 in cases of central nervous system lesions or increase in the permeability of the blood-brain barrier, which can occur in neurosurgical patients because of intraoperative ischemia. Transient hypertension related to sympathetic stimulation after a painful stimulus can also elicit cerebrovascular autoregulation breakthrough and opening of the blood-brain barrier in rats (12). In these animals, a direct application of a ß-adrenergic receptor agonist to the brain parenchyma increased the permeability of the blood-brain barrier. This effect was prevented with a ß-adrenoreceptor antagonist (13). Factors related to anesthesia, such as hypocapnia and anesthetic technique, may enhance blood-brain barrier disruption (14). Thus, several causes may open the blood-brain barrier during emergence, leading to increased CBF through catecholamine release.

The origin of the brain sympathetic activation is not clear. Several mechanisms may be postulated. Cerebral sympathetic stimulation may increase CBF independently of systemic catecholamine release (15). A catecholamine activation has been demonstrated in the vasomotor center on emergence from anesthesia in rats (16). Halothane withdrawal increases the neuronal activity in the locus coeruleus which is a noradrenergic system that has been shown to modulate CBF (17). Although the significance of these experimental findings is not clear in humans, it is possible that central adrenergic stimulation may increase CBF even when the blood-brain barrier is intact. Another mechanism may involve intracerebral noradrenergics pathways. The cerebral vasculature is under sympathetic control through the stellate ganglion. However, in animals, cervical sympathetic stimulation reduces CBF and increases the cerebral vascular resistance (18,19) . In humans, stellate ganglion blockade increases CBF in the territory of the internal carotid artery (20). Thus, this mechanism cannot explain the effect of esmolol on CBFV in this study.

There was a marked difference in COe between the groups. Esophageal Doppler has been validated for the measurement of CO (21). Close agreement between this technique and thermodilution was shown for measurement of percentage changes in CO with a 95% confidence interval for the bias of -1.2%–2% (22). It is not possible to exclude an influence of CO on CBF or CBFV. However, the data from the literature do not support this hypothesis. In an animal study, Davis and Sundt (23) demonstrated that CBF changes occurred independently of CO variations. Isoproterenol produced a 38%–72% increase in CO without a change in CBF. In rats, nondilutional intravascular volume expansion producing a 138% ± 11% increase in CO did not increase CBF (24). In brain injured patients, Bouma and Muizelaar (25) measured simultaneously CO and CBF after manipulation of blood pressure and CO with phenylephrine, trimethaphan, and mannitol. They did not find any correlation between changes in CO and changes in CBF, regardless of the status of CBF pressure autoregulation. During exercise, ß1-adrenergic blockade limited the increase in CBFV but this effect disappeared after cervical sympathetic blockade (26), showing no direct relationship between CO and CBF. In our study, we did not find any correlation between CBFV and COe at any time period. Thus, CO changes are unlikely to explain the effect of esmolol on CBFV.

Although we did not find a statistically significant difference in MAP between the groups, it seems that esmolol attenuated MAP variations. Because CBF autoregulation is not an instantaneous process during MAP changes, it is possible that transient increases in MAP could induce transient increases in CBFV. Rapid increases in MAP are likely to occur at extubation but are usually not observed in neurosurgical patients when the painful stimulus caused by the presence of the tracheal tube has been removed. Five minutes after extubation, the MAP was stable in both groups and CBFV was higher than baseline only in Group P.

This study shows that sympathetic stimulation is an important cause of postoperative cerebral hyperemia, but other factors may have a role. Return to normocarbia after prolonged hypocarbia, intraoperative cerebral ischemia, or other mechanisms might contribute to postoperative CBF changes (27). Clinically, perioperative hypertension and cerebral hyperemia during neurosurgical recovery may theoretically lead to neurological complications such as intracranial bleeding and brain edema. After carotid endarterectomy, the risk of intracerebral hemorrhage in patients with hyperperfusion is >10 times that of patients without hyperperfusion (28). Cerebral hyperemia might also increase cerebral edema, which occurs in nearly 20% of neurosurgical patients (29). However, the clinical importance of postoperative cerebral hyperemia after neurosurgery is unknown. Severe hypertension (systemic blood pressure >200 mm Hg) predisposes patients recovering from intracranial surgery to intracranial hemorrhage (30,31) . But the risk associated with less severe hypertension has not demonstrated. Basali et al. (32) established a link between perioperative hypertension and intracranial hemorrhage after craniotomy in a retrospective case control study. Of particular interest was the very strong association between hypertension with intracranial hemorrhage when blood pressure remained in the normal range intraoperatively but became increased postoperatively. This suggested that loose surgical hemostasis performed at a low blood pressure may bleed when at a higher blood pressure.

Many drugs, such as calcium channel blockers or ß-blockers are able to control postoperative blood pressure after elective surgery. Morimoto et al. (33) showed that calcium channel blockers increased cerebral oxygenated hemoglobin and CBF during tracheal extubation caused by cerebral vasodilation. Thus, these drugs may increase CBF and intracranial pressure in patients with cerebral disorders despite blood pressure control. ß-Adrenergic blocking drugs are not cerebral vasodilators and have no significant effect on intracranial pressure (34). This might limit the deleterious consequences of postoperative sympathetic overactivity. There are few clinical data to support this hypothesis. However, Barron et al. (35) reviewed data obtained from 60,329 patients treated with tissue plasminogen activator who were enrolled in the National Registry of Myocardial Infarction 2. The early administration of ß-blockers (n = 23,749) was associated with a 31% reduction in the rate of intracranial hemorrhage. The authors hypothesized that ß-blockers inhibited vasodilation via their blockade of peripheral ß-adrenergic receptors and permitted catecholamine-mediated {alpha}-adrenoreceptor vasoconstriction, leading to a decrease in CBF. This reduction in intracranial hemorrhage rate was not observed with other hypotensive drugs such as nitroglycerin, angiotensin-converting enzyme inhibitors, or calcium channel blockers. After carotid endarterectomy, blood pressure control did not prevent hyperperfusion (36). These data support the idea that blood pressure control alone is insufficient to avoid cerebral hyperemia after neurosurgery.

In conclusion, we found that esmolol blunted the increase in CBFV during recovery from neurosurgical anesthesia. The decrease in CO after esmolol may be a limit to its use in patients with hypovolemia or heart failure. This study confirms our hypothesis that sympathetic stimulation contributes to cerebral hyperemia during emergence from craniotomy. ß-Blocking drugs may be considered to limit the hemodynamic changes of neurosurgical recovery, but further clinical studies are needed before recommending their systematic use in this setting.


   Acknowledgments
 
This study was supported by an institutional grant from the Assistance Publique–Hôpitaux de Marseille.


   References
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

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Accepted for publication December 26, 2002.




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins and Stanford University Libraries' HighWire Press®. Copyright 2003 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press