Carotid disease is usually a problem of embolization (transient attacks of monocular blindness, transient ischemic attacks) and less often occlusion or insufficiency (cervical bruit). The most common noninvasive test is carotid duplex ultrasonography followed by confirmatory angiography.

1. Management of Asymptomatic Carotid Stenosis. The optimal treatment of asymptomatic carotid stenosis is controversial. (Many question the role of carotid endarterectomy [CEA] in asymptomatic patients.)
2. Management of Symptomatic Carotid Stenosis. CEA, in conjunction with aspirin therapy, has proven superior to medical therapy alone
3. Preoperative Evaluation and Preparation for Carotid Endarterectomy.
   1. Most patients presenting for CEA will be taking aspirin, which should be continued throughout the perioperative period.
   2. Many patients will also be taking another antiplatelet therapy (clopidogrel). The benefit of continuing other agents at the time of CEA must be balanced against the risk of bleeding.
4. Monitoring and Preserving Neurologic Integrity
   1. The intraoperative goals of protecting the brain and the heart often conflict. (Increasing arterial blood pressure to augment cerebral blood flow increases the oxygen demand of the heart.) The rationale behind maintaining a stable, high-normal blood pressure throughout the procedure is based on the assumption that blood vessels in ischemic or hypoperfused areas of brain have lost normal autoregulation. Nonetheless, hypotension and hypoperfusion are not the most common cause of stroke after CEA; embolic events may be even more important and often occur postoperatively.
   2. On balance, it is probably beneficial in the absence of neurologic monitoring (bispectral index, electroencephalography, Transcutaneous Doppler [TCD], SSEP) to avoid hypotension during the period of cross-clamping, particularly if no shunt is used. Intravenous fluid and vasopressors such as phenylephrine can be used to maintain blood pressure between normal and 20% above baseline. (Augmentation of blood pressure has been associated with an increased incidence of MI.)
   3. If information from the awake patient or reliable monitoring shows good cerebral blood flow, the anesthesiologist may choose to use less vasopressor and to maintain a lower blood pressure during the period of temporary carotid occlusion than would be otherwise feasible.
   4. Hypercapnia during CEA may be detrimental if it dilates vessels in normal areas of the brain while vessels in ischemic brain areas that are already maximally dilated cannot respond. The net effect, then, is a “steal” phenomenon (diversion of blood flow from hypoperfused brain regions to normally perfused brain regions). Conversely, hypocarbia may cause vasoconstriction and extend any area of cerebral ischemia. Most authorities therefore recommend the maintenance of normocarbia. Most recommend maintenance of normocarbia.
   5. Almost all commonly used anesthetic agents reduce cerebral metabolism, thereby decreasing the brain's requirements for oxygen, yet the notion that reduced cerebral metabolism is associated with cerebral protection has been challenged.
      1. Barbiturates may offer a degree of brain protection during periods of regional ischemia.
      2. Both etomidate and propofol decrease brain electrical activity and thus decrease cellular oxygen requirements. Etomidate preserves cardiovascular stability and may be beneficial in a patient population whose cardiac reserves are often limited. Propofol also allows rapid awakening of the patient and neurologic assessment at the end of surgery.
   6. Hypothermia can depress neuronal activity sufficiently to decrease cellular oxygen requirements below the minimum levels normally required for continued cell viability. In theory, hypothermia represents the most effective method of cerebral protection. Even a mild decrease in temperature of about 2° to 3°C at the time of arterial hypoxemia may reduce ischemic damage to the brain.
   7. Surgeons who never use shunts usually rely on expedient surgery to avoid neurologic problems and do not report worse overall outcome statistics than those who use shunts. Placement of a shunt is associated with an embolism-related stroke rate of at least 0.7% from the dislodgment and embolization of atheroma.
5. Anesthetic and Monitoring Choices for Elective Surgery (Table 39-6: Prevention of Perioperative Myocardial Infarction in Vascular Surgery Pateints)
6. Carotid angioplasty and stenting is usually performed in the vascular interventional suite by a team involving vascular surgeons, cardiologists, or radiologists. (Anesthesiologists may be asked to provide sedation and monitoring in complex cases.) The patient needs to be arousable and responsive so that serial neurologic examinations can be conducted.
   1. Cerebral emboli are a risk of angioplasty (protect with proximal flow blockage and distal filters).
   2. Periprocedural antiplatelet therapy (aspirin, clopidogrel, or ticlopidine) is the standard of care.
7. Postoperative Management (Table 39-7: Postoperative Management Following Carotid Endarterectomy)
8. Management of Emergent Carotid Surgery
   1. The patient who awakens with a major new neurologic deficit or who develops a suspected stroke in the immediate postoperative period represents a surgical emergency.
   2. For patients undergoing neck exploration for a wound hematoma after CEA, a tracheostomy or cricothyroidotomy tray should be immediately available.
   3. Esmolol is particularly useful to control hyperdynamic cardiovascular responses during awake intubation.

Anesthesia for Vascular Surgery

1. Vascular Disease: Epidemiologic Medical and Surgical Aspects
2. Chronic Medical Problems and Management in Vascular Surgery Patients
3. Other Medical Problems in Vascular Surgery
4. Organ Protection in Vascular Surgery Patients
5. Carotid Endarterectomy
6. Aortic Reconstruction
7. Lower Extremity Revascularization