Anesthetic Management

Anesthetic management goals for carotid endarterectomy include protection of the heart and brain from ischemic

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I routinely monitor leads II and V₅ for detection of rhythm disturbances and ST segment changes. On-line ST segment analysis is particularly helpful and is used routinely. Placement of an intra-arterial catheter for beat-to-beat blood pressure monitoring is used in all patients. Central venous and pulmonary artery catheters are usually unnecessary for carotid surgery. If such monitors are used, the subclavian or femoral insertion sites are most practical because inadvertent carotid puncture could compromise blood flow as a result of hematoma. In my experience, the most common reason for central access is difficult or inadequate peripheral access. Intravenous access for fluid and drug administration can be accomplished with a single, secure, medium-bore (16-gauge) catheter. Given that both arms will be tucked to the patient's side, the intravenous catheter must run well after patient positioning.

General Anesthesia

Any of the commonly used induction agents, maintenance anesthetics, and short- to intermediate-acting non-depolarizing muscle relaxants can be safely used during carotid endarterectomy, given that stable hemodynamics are maintained and the patient is awake at the end of the procedure. My induction technique using sufentanil is as follows. After placement of routine monitors and oxygen by face mask, a sufentanil infusion (0.5 to 1.0 μg/kg) is initiated. If the patient becomes at all sedated during the planned 10- to 15-minute infusion period, as evidenced by slowed speech or delayed response to questioning, the infusion is discontinued. No additional opioids are administered intraoperatively. Induction of anesthesia is accomplished with incremental doses of thiopental (≤8 mg/kg) followed by succinylcholine, unless contraindications exist. Etomidate or propofol may also be used. Esmolol is particularly effective in blunting the increases in heart rate and blood pressure during laryngoscopy and intubation and is used liberally during the induction period. ^[591] Blood pressure responses during and after endotracheal intubation are unpredictable in this patient population, and the clinician must be prepared for immediate treatment of extremes in blood pressure. My preference is to use short-acting drugs, such as phenylephrine (50 to 100 μg) for hypotension and sodium nitroprusside (5 to 25 μg), for hypertension. Patients with poorly controlled hypertension (diastolic blood pressure > 100 mm Hg) require special care. These patients are often intravascularly volume depleted and may have significant hypotension with induction. Administration of fluids intravenously (5 mL/kg), careful titration of anesthetics, and immediate treatment of hypotension are especially important.

Anesthesia is maintained with 50% nitrous oxide in oxygen and low-dose (i.e., less than one-half minimum alveolar concentration [MAC]) potent inhaled anesthetics. Isoflurane may be preferred because fewer ischemic electroencephalographic (EEG) changes occur during carotid occlusion when compared with halothane^{[592] [593]} or enflurane.^{[592] [593] [594]} Studies using EEG and regional cerebral blood flow (rCBF) measurements suggest that the critical rCBF (the rCBF below which EEG changes of cerebral ischemia occur) is lower for isoflurane than for halothane or enflurane.^{[592] [593]} Sevoflurane may be a good alternative, as its critical rCBF in patients undergoing endarterectomy is similar to that determined with isoflurane^[595] and it may facilitate a more rapid emergence.^[596] I typically use vecuronium for muscle relaxation because the procedure rarely lasts longer than 90 minutes. I do not use cervical plexus block or request local anesthetic infiltration for skin incision because the surgical stimulation is minimal and is frequently necessary to support blood pressure. A combined remifentanil and propofol anesthetic technique has been reported but offered little advantage over inhalational anesthesia.^[597]

Despite only modest surgical stimulation, hemodynamic fluctuations are common during carotid endarterectomy. Blood pressure and heart rate are controlled within predetermined and individualized ranges during the surgical procedure with short-acting agents whenever possible (esmolol, phenylephrine, nitroglycerin, and sodium nitroprusside). It is generally accepted that blood pressure should be maintained in the high-normal range throughout the procedure and particularly during the period of carotid clamping in an attempt to increase collateral flow and to prevent cerebral ischemia. In patients with contralateral internal carotid artery occlusion or severe stenosis, induced hypertension to approximately 10% to 20% above baseline is advocated during the period of carotid clamping when neurophysiologic monitoring is not used. Blood pressure preservation or augmentation can be accomplished by maintaining light levels of general anesthesia or by administering sympathomimetic drugs, such as phenylephrine and ephedrine. Caution must be exercised when using vasopressors to augment blood pressure during carotid endarterectomy because the increases in blood pressure and heart rate may increase myocardial oxygen requirements and increase the risk of myocardial ischemia^[598] or infarction.^[599]

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Surgical manipulation of the carotid sinus with activation of baroreceptor reflexes can cause abrupt bradycardia and hypotension. Cessation of surgical manipulation promptly restores hemodynamics, and infiltration of the carotid bifurcation with 1% lidocaine usually prevents further episodes.^[602] Infiltration may, however, increase the incidence of intraoperative^[602] and postoperative^[603] hypertension. I do not advocate routine infiltration of the carotid bifurcation.^[604]

With closure of the deep fascial layers in the neck, isoflurane is discontinued, nitrous oxide is increased to 70%, and ventilation is controlled manually. On application of the surgical dressings, neuromuscular reversal agents are administered, and oxygen is increased to 100%. At this time, I decrease external stimuli to the patient by quieting the room, turning off overhead surgical lights, and placing the patient in a head-up recumbent position. Ventilation is gently assisted until the patient spontaneously opens his or her eyes or moves. With rare exceptions, all patients are extubated after neurologic integrity is established. Neurologic deficits on emergence require immediate discussion with the surgeon about the need for angiography or reoperation. The period of emergence and extubation may be associated with marked hypertension and tachycardia, which may require aggressive pharmacologic intervention. Tight hemodynamic control during this period is likely to be more demanding than during induction.^[601] Greater hemodynamic stability and decreased pharmacologic intervention during emergence have been reported in patients undergoing carotid endarterectomy with propofol as compared with isoflurane. ^[601] A significantly lower incidence of myocardial ischemia on emergence was found in the propofol group compared with the isoflurane group (1 of 14 versus 6 of 13). Of particular note, all patients with myocardial ischemia on emergence had systolic blood pressures greater than 200 mm Hg.

Regional and Local Anesthesia

Regional and local anesthetic techniques for carotid endarterectomy have been in use for more than 40 years,^[605] and many centers consider these to be the techniques of choice.^{[606] [607]} Regional anesthesia is accomplished by blocking the C2 to C4 dermatomes by use of a superficial and deep cervical plexus block (see Chapter 44 ). Adequate anesthesia can be obtained with an isolated superficial cervical plexus block, possibly due to spread of local anesthetic to the cervical nerve roots.^[608] Local infiltration of the surgical field can also provide the necessary sensory blockade. Regional anesthesia allows continuous neurologic assessment of the awake patient, which is believed to be the most sensitive method for detecting inadequate cerebral perfusion and function.^[609] Other advantages that have been reported include avoidance of expensive cerebral monitoring, reduced need for shunting,^{[563] [610] [611] [612]} greater stability of blood pressure and decreased vasopressor requirements,^{[570] [611] [613]} and reduced hospital costs.^{[569] [610] [613] [614]}

Local or regional anesthesia requires significant patient cooperation throughout the procedure and is best maintained with constant communication and gentle handling of tissues. Supplemental infiltration of local anesthetic by the surgeon, especially at the lower border and ramus of the mandible, is frequently helpful. Sedation, if used at all, must be kept to a minimum to allow continuous neurologic assessment. Levels of consciousness, speech, and contralateral hand grip are assessed throughout the procedure. Hand grip can be assessed with the use of a squeaky-toy. I control blood pressure at or near preoperative levels by use of the same agents used for patients receiving general anesthesia. Blood pressure augmentation with phenylephrine is employed when patients have neurologic changes during carotid artery test clamping or after shunt placement. A 2- to 3-minute test clamp in the awake patient allows prompt identification of patients who would benefit from shunt placement. ^[615] Patient acceptance of regional anesthesia is high,^[616] as evidenced by a 92% preference for repeat cervical plexus block for future carotid endarterectomy.^[617] The surgical drapes are "tented" over the head and face areas to minimize claustrophobic anxiety. It has been suggested that no absolute contradiction to regional anesthesia for carotid endarterectomy exists.^[606] In our practice, my colleagues and I avoid regional anesthesia under the following circumstances: strong preference for general anesthesia expressed by the patient (i.e., claustrophobia), language barriers that make communication difficult, and difficult vascular anatomy. Difficult anatomy is usually manifested by a patient with a short neck and a high (more cephalad) bifurcation that may require vigorous submandibular retraction.

Regional versus General Anesthesia

Most reports comparing local or regional anesthesia with general anesthesia indicate no differences in perioperative stroke or death rate on the basis of anesthetic technique.^{[569] [606] [607] [610] [613] [614] [618] [619] [620] [621]} Three reports have found an increased incidence of perioperative stroke in patients under general anesthesia.^{[570] [612] [622]} An increased incidence of cardiopulmonary complications in patients under general anesthesia has been reported in five studies. ^{[610] [613] [618] [621] [623]} Potential disadvantages of local or regional anesthesia include inability to use pharmacologic cerebral protection with anesthetics, patient panic or loss of cooperation, seizure or loss of consciousness with carotid clamping, and inadequate access to the airway if conversion to general anesthesia becomes necessary. The incidence of serious complications from cervical plexus block is low; however, near-toxic levels of local anesthetic have been reported in nearly half of patients after superficial and deep cervical plexus block.^[624] Although no major complications related to local anesthetic toxicity occurred, some caution should be used when requesting the surgeon to supplement with additional local anesthetic. Phrenic nerve paresis is common after cervical plexus block^[625] and is of little clinical consequence except in patients with severe chronic obstructive pulmonary disease or contralateral diaphragmatic dysfunction. Rates of conversion from regional anesthesia to general anesthesia of approximately 2% to 6% have been reported.^{[606] [609] [626]} In patients undergoing carotid endarterectomy under

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Intraoperative neurologic changes during carotid endarterectomy under local or regional anesthesia occur in 2.4% to 24% of patients.^{[626] [628] [629]} Patients undergoing carotid endarterectomy under cervical plexus block who experience intraoperative neurologic changes are six times more likely (6.6% versus 1.1%) to have a postoperative stroke.^[626] Compared with general anesthesia, regional anesthesia for carotid endarterectomy may be associated with increased levels of blood catecholamines.^[630] A high incidence of tachycardia has been reported in patients undergoing regional anesthesia for carotid endarterectomy.^[617] No large-scale, prospective, randomized trials have evaluated whether neurologic or cardiac outcomes differ with regional versus general anesthesia. The ultimate decision to use one technique over the other must be based on the surgeon's and the anesthesiologist's experience and the patient's preference.

Carbon Dioxide and Glucose Management

Cerebrovascular carbon dioxide reactivity is part of the complex autoregulatory system to control cerebral blood flow. Normal cerebral autoregulation responds to acute changes in PaCO₂ by decreasing cerebral blood flow (i.e., vasoconstriction) with hypocapnia and increasing cerebral blood flow (i.e., vasodilatation) with hypercapnia. In patients with carotid artery stenosis or occlusion, ipsilateral cerebral blood flow may be impaired because of poor intracerebral collateral blood flow. In the setting of poor collateralization and resultant cerebral hypoperfusion, cerebral resistance vessels in the hypoperfused territories will dilate in an effort to maintain cerebral blood flow. These chronically dilated resistance vessels may demonstrate a diminished or absent (i.e., vasomotor paralysis) cerebral blood flow response to carbon dioxide. Impaired cerebrovascular reactivity to hypercapnia may play a significant role in the development of stroke ipsilateral to carotid stenosis or occlusion.^{[631] [632]} Although it might be expected that impaired carbon dioxide reactivity would increase the risk of cerebral ischemia after carotid artery clamping, the results of intraoperative cerebral monitoring suggest no such relationship exists.^[633] Impaired cerebrovascular reactivity to carbon dioxide significantly improves after carotid endarterectomy. ^[633]

Control of ventilation and carbon dioxide during general anesthesia is a matter of some controversy. Hypercapnia may cause a steal phenomenon (i.e., shunting of blood away from hypoperfused territories with dilated vasculature) and is generally avoided. Hypocapnia, with its associated cerebral vasoconstriction, has been advocated to promote a reversal of this steal phenomenon. However, there is little clinical evidence for this reverse steal effect.^[634] Experimental data does not support the use of hypocapnia as a therapeutic maneuver to produce a favorable redistribution of blood flow during focal cerebral ischemia. ^[635] In this rat model of focal cerebral ischemia, hypocapnia (PaCO₂ of 23) actually increased the size of the region at risk for ischemia.^[635] It is common practice therefore to maintain normocapnia or mild hypocapnia during carotid endarterectomy.

There is evidence of increased ischemic injury to neural tissue when ischemia occurs in the presence of hyperglycemia. Although there are no good outcome studies in humans, it is appropriate to maintain a blood glucose level below 250 mg/dL in patients undergoing carotid endarterectomy.^[636] If hyperglycemia is treated with insulin preoperatively or intraoperatively, blood glucose level should be carefully monitored, especially during general anesthesia, to avoid the dangers of hypoglycemia.