Current Reviews for Nurse Anesthetists

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2 Current Reviews for Nurse Anesthetists Publisher And Editor-in-Chief FRANK MOYA, MD Coral Gables, Florida Editorial Board Advisory Board Chuck Biddle, CRNA, PhD Richmond, Virginia Linda Callahan, CRNA, PhD Klamath Falls, Oregon Nancy Gaskey-Spears CRNA, PhD Gastonbury, Connecticut Joseph A. Joyce, CRNA, BS Winston-Salem, North Carolina Mary Jeanette Mannino, CRNA, JD Laguna Niguel, California Maria Garcia-Otero, CRNA, PhD Coral Gables, Florida Sandra Ouellette, CRNA, Med, FAAN Winston-Salem, North Carolina Charles Barton, MSN, MEd Akron, Ohio Carol G. Elliott, CRNA, MPA, PhD Kansas City, Kansas Linda J. Kovitch, CRNA, MSN Bedford, Massachusetts Frank T. Maziarski, CRNA Seattle, Washington Charles Moss, CRNA, MS Larkspur, Colorado Laura Wild-McIntosh, CRNA, MSN Hillsboro, New Jersey Monte Lichtiger, MD Coral Gables, Florida Associate Publishers Joan McNulty Elizabeth Moya, JD Assistant Editor Linda G. Williams Assistant Publishers Barbara McNulty Donna Scott Circulation Assistants Carrie Scott Tiffany Lazarich Myriam Montes Kimberly Gutierrez Sponsor Frank Moya Continuing Education Programs, LLC Subscription Office - Editorial Office Current Reviews Frank Moya, M.D S.E. First Avenue 1450 Madruga Ave Ft. Lauderdale, FL Suite 207 Coral Gables, FL Phone: (954) Fax: (800) Accreditation This program has been prior approved by the American Association of Nurse Anesthetists for 26 CE credits; Code Number 33802; Expiration Date May 31, Approved by Frank Moya Continuing Education Programs, LLC. Provider approved by the California Board of Registered Nursing, Provider Number CEP 1754, for 26 contact hours and Florida Board of Nursing, Provider Number FBN 2210 for 26 contact hours. In Accordance with AANA directives, you must get 80% of the answers correct to receive one credit for each lesson and if there is a failure, there is no retaking. Disclosure Policy Frank Moya Continuing Education Programs, LLC, in accordance with the Accreditation Council for the Continuing Medical Education s (ACCME) Standards for Commercial Support, will disclose the existence of any relevant financial relationship a faculty member, the sponsor or anyone else who may be in a position to control the content of this Activity has with any commercial interest. BEFORE STARTING, PLEASE SEE LAST PAGE OF LESSON TO READ WHETHER THERE ARE ANY RELEVANT RELATIONSHIPS TO DISCLOSE AND, IF SO, THE DETAILS OF THOSE RELATIONSHIPS. Current Reviews is intended to provide it s subscribers with information that is relevant to anesthesia providers. However, the information published herein reflects the opinions of it s authors and does not represent the views of Current Reviews in Clinical Anesthesia, Current Reviews for Nurse Anesthetists, or Frank Moya Continuing Education Programs, LLC. Anesthesia practitioners must utilize their knowledge, training and experience in their clinical practice of anesthesiology. No single publication should be relied upon as the proper way to care for patients. The information presented herein does not guarantee competency or proficiency in the performance of procedures discussed. Copyright 2015 by Current Reviews. Reproduction in whole or in part prohibited except by written permission. All rights reserved. Information has been obtained from sources believed to be reliable, but it s accuracy and completeness, and that of the opinions based therein are not guaranteed. Printed in U.S.A. Current Reviews is published biweekly by Current Reviews, 1828 S.E. First Avenue, Ft. Lauderdale, FL POSTMASTER: Send address changes to Current Reviews, 1828 S.E. First Avenue, Ft. Lauderdale, FL

3 Anesthesia and the Patient with Carotid Artery Disease Terrence L. Trentman, MD Associate Professor of Anesthesiology Mayo Clinic Arizona Phoenix, Arizona LESSON OBJECTIVES Upon completion of this lesson, the reader should be able to: 1. Discuss the epidemiology and pathophysiology of carotid artery disease. 2. List imaging options for patients with carotid artery disease. 3. List Class I guidelines for selection of patients for carotid revascularization. 4. Discuss the risks of shunt use during carotid endarterectomy (CEA) surgery. 5. Explain how carotid sinus manipulation may affect blood pressure. 6. Describe elements of the preoperative exam for patients undergoing carotid revascularization. 7. List and contrast neurologic monitoring options during CEA. 8. Discuss anesthetic goals during CEA surgery, including ventilation, blood pressure, glucose and temperature control. 9. Discuss the greatest long-term risk for CEA patients. 10. List common postoperative problems after CEA. Current Reviews for Nurse Anesthetists designates this lesson for 1 CE contact hour in pharmacology/therapeutics. Introduction Many patients with carotid artery disease will present for carotid endarterectomies (CEA) or other procedures, so it is vital that anesthesia providers understand the management of this challenging patient population. Nationally, stroke is the fourth most common cause of death after heart disease, cancer and respiratory conditions, with 15-20% of ischemic strokes due to carotid artery disease. Intracranial atherosclerosis is less common than extracranial atherosclerosis, which most commonly occurs at the bifurcation of the internal and external carotid arteries. Carotid artery disease is more frequently an embolic problem than one of complete occlusion of the artery. Emboli from the carotid artery cause amaurosis fugax (monocular blindness) or transient ischemic attacks (TIAs) manifested by paresthesia, clumsiness, or speech changes. Cerebral artery disease, including carotid artery stenosis, is about one-third as common as coronary artery disease in the United States. However, about 8.5% of patients will have both coronary and cerebral artery disease (Table 1). As discussed below, this combination of vascular disease creates management decision challenges for the anesthesia provider. This lesson will present an anatomic description of carotid artery disease, in addition to guidelines on management of patients with extracranial carotid stenosis. Based upon a review of current literature, discussion points in this lesson include: 1. When is CEA indicated vs. carotid artery stenting (CAS)? 2. How is a CEA performed as opposed to CAS? 3. What is the greatest risk to patients undergoing a CEA? 4. What neurologic monitoring options are available during CEA procedures? 5. What are the hemodynamic goals during and after cross clamping the carotid artery? 6. Is regional anesthesia better than general anesthesia for CEA? Curr Rev Nurs Anesth 38(7):81-92,

4 Diagnosing Carotid Artery Disease A diagnosis of carotid artery disease is based upon symptoms of a transient ischemic attack, or results of screening patients with risk factors, including advanced age, smoking, hypertension and hyperlipidemia. A carotid bruit may be heard over the neck; however, cardiac valvular noise can be transmitted to the carotids, so this is not a particularly sensitive test. For those suspected of having carotid disease, the most common test is the duplex ultrasound, which has a sensitivity of 94% and a specificity of 92% for carotid artery stenosis greater than 60% (the gold standard is digital subtraction angiography). A positive carotid ultrasound is usually followed by CT angiography or magnetic resonance angiography (Figure 1). Management Guidelines In 2011, the American College of Cardiology Foundation and the American Heart Association published their guidelines on the management of patients with extracranial carotid artery disease. The recommendations were classified as follows: 1. Class I recommendation means that the benefit far outweighs the risk of the treatment, and the treatment should be performed. 2. Class IIa means the benefit outweighs the risk, but additional studies are needed. It is reasonable to perform the treatment. 3. Class IIb means the benefit outweighs or is equal to the risk, and more studies are needed; therefore, the treatment may be considered. 4. Class III means there is no benefit or even harm, and the treatment should not be performed. All patients should undergo medical management, including smoking cessation, use of aspirin, a statin and blood pressure management. Class I recommendations for carotid revascularization include patients who have had a nondisabling stroke or TIA within six months who are at average to low surgical risk. These patients should undergo a CEA, assuming that they have greater than 70% of stenosis of the internal carotid artery by ultrasound or greater than 50% stenosis by angiography. Carotid artery stenting (CAS) is an alternative to CEA in this patient population (Table 2). Class IIa recommendations include performing CEA in asymptomatic patients with greater than 70% stenosis if their perioperative risk is low. CAS can be chosen instead of CEA in this patient population if the anatomy is unfavorable for CEA. Class IIb guidelines include prophylactic CAS in asymptomatic patients who have significant stenosis (70% by ultrasound or 60% by angiography). However, the benefit of intervention in this asymptomatic patient population (vs medical therapy) is not well established. Class III guidelines include patients where carotid revascularization is not recommended. This includes patients with less than 50% stenosis, chronic total occlusion of the artery, or patients with severe disability caused by a cerebral infarct. A number of factors should be considered in evaluating these patients; most importantly, their greatest long-term risk is myocardial ischemia. As the reader can surmise, some controversy surrounds the management of patients with asymptomatic carotid artery disease. It is reasonable to screen asymptomatic patients for carotid stenosis when they have known or strongly suspected coronary artery disease. Also, patients who have a bruit or known carotid stenosis greater than 50%, known vascular disease or > 2 risk factors (e.g., age, smoking and dyslipidemia) can be screened with an ultrasound. In addition, patients who are scheduled for a CABG should undergo screening if they have at least one risk factor such as left main coronary disease, peripheral vascular disease, smoking, age > 65 years, carotid bruit or prior TIA or stroke. Particularly challenging are those patients with symptomatic carotid artery disease AND coronary Table 1 Epidemiology and Pathophysiology of Carotid Artery Disease # Stroke is the 4 most common cause th of death # Among patients who have coronary disease, 8.5% will also have carotid disease # Of ischemic strokes, 15-20% are caused by carotid disease # Extracranial is more common than intracranial atherosclerosis # Carotid disease is usually an embolic rather than an occlusive problem # Transient ischemic attack (TIA) presents as paresthesias, clumsiness, speech changes and/or weakness # Amaurosis fugax is monocular blindness 84 Current Reviews for Nurse Anesthetists

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8 This is vital because ischemic or under-perfused regions of the brain may have lost their normal autoregulation. However, the most common cause of stroke is embolism, not hypoperfusion. Nonetheless, during the cross clamp phase of a CEA, anesthesia providers commonly use fluids and vasopressors (e.g., phenylephrine) to maintain blood pressure at normal to approximately 20% above the patient s baseline (unless contraindicated). Unfortunately, augmenting blood pressure can increase the risk of myocardial ischemia. Most important during the cross clamp phase of a CEA is to avoid hypotension, particularly if no shunt is used. What follows is a description of various neurologic monitoring options during CEA (Table 4). The Awake Patient. Having the patient awake and communicating during a CEA is the gold standard of neurologic monitoring. The patient and surgeon must be comfortable with this approach, and frequent communication with the patient is required. Verbal and strength testing is carried out during the procedure every 2 to 5 minutes, usually with a handgrip (squeeze toy) and patient responses to questions. The procedure may be carried out under regional anesthesia with local anesthetic augmentation as needed. This approach is difficult if the patient is claustrophobic, anxious, unable to lay flat or coughing. If a complication develops, airway access may be difficult. Carotid Stump Pressure. In this approach, the surgeon places a needle or balloon catheter in the distal carotid artery to measure the pressure. A pressure of at least 40 mmhg may be equally reliable and as cost effective as EEG. If there is adequate stump pressure, the surgeon may decide not to shunt. However, stump pressure may not correlate with cerebral perfusion pressure. The ischemic threshold for brain tissue may vary from patient to patient; therefore, it is difficult to know how much stump pressure is needed in a patient. Electrocephalogram (EEG). This is carried out with scalp electrodes. EEG deterioration begins below a cerebral blood flow of 15 ml/ min/100 grams of brain tissue. Ipsilateral EEG attenuation, slowing or both are seen in ischemia. If evidence of ischemia is seen, the surgeon can place a shunt and the anesthesia provider can increase blood pressure. However, the EEG is sensitive to changes in anesthetic depth and drugs such as propofol and barbiturates. If the anesthetic depth is adjusted during EEG monitoring, the technician should be advised. Bilateral EEG changes should result from changes in anesthetic depth (ischemia is unilateral). It is noteworthy that the EEG is more effective at monitoring cortical rather than deep brain structures. Also, many patients have baseline EEG abnormalities, making the evaluation of EEG changes difficult. Somatosensory Evoked Potentials (SSEP). This form of monitoring evaluates cortical potentials after stimulation of a peripheral nerve. It is more effective at evaluating deep brain structures than EEG. A 50% decrease in amplitude or a 10% increase in latency is considered significant. A constant, light level of anesthesia is required during SSEP monitoring. Overall, EEG and SSEP have similar sensitivity and specificity for cerebral ischemia. Transcranial Doppler (TCD). TCD measures middle cerebral artery flow velocity through the thin petrous bone, and it can also detect embolic signals. TCD predictors of stroke after a CEA include emboli during wound closure, > 90% decrease in systolic velocity at cross clamp placement, and/or > 100% increase in the pulsatility index at cross clamp release. TCD is operator dependant and 10-15% of patients cannot be monitored due to a poor temporal region window. Cerebral Oximetry (Near Infrared Spectroscopy, NIRS). Cerebral oximetry monitors cerebral oxygen saturation of the frontal lobe. NIRS is easy to apply and non-invasive. With awake monitoring as the gold standard, a > 10% drop in cerebral oxygen saturation has been shown to have high sensitivity and specificity for cerebral ischemia. Other Perioperative Management Considerations Ventilation management during CEA is important. Hypercarbia can be detrimental due to dilatation of normal vessels and potential steal from hypoperfused areas. Conversely, hypocarbia may result in cerebral vasoconstriction. Therefore, normocarbia should be maintained during CEA surgery. Table 4 Neurologic Monitoring Options During Carotid Endarterectomy # Assess the awake patient (verbal response, contralateral hand grip) # Carotid stump pressure (40-50 mm Hg?) # Electroencephalogram (EEG) # Somatosensory evoked potentials (SSEP) # Transcranial Doppler (TCD) # Cerebral oximetry = Near infrared spectroscopy (NIRS) 88 Current Reviews for Nurse Anesthetists

9 Hyperglycemia is associated with worse neurologic outcomes after cerebral ischemia. Therefore, blood glucose should be monitored throughout the perioperative period and maintained within reasonable levels. For example, at the author s institution, blood glucose levels between mg/dl is acceptable. This is particularly important as many patients with cerebral vascular disease will also be diabetic. In terms of volatile agents, isoflurane, sevoflurane and desflurane all reduce the cerebral metabolic rate of oxygen (CMRO 2). There may be advantages to less soluble agents like sevoflurane and desflurane in terms of rapid wake-up. There are reports of administration of barbiturates during CEA surgery, as these drugs may provide cerebral protection during periods of ischemia. Thiopental decreases CMRO 2 by 50%. While a barbiturate bolus could be given before cross clamping of the carotid artery, there is no evidence of better outcomes with this technique and delayed emergence is likely. Hypothermia can also depress neuronal activity and decrease CMRO 2. A 2-3 degree temperature decrease will reduce ischemic damage. However, there is no evidence of benefit of hypothermia during CEA and the logistics of cooling are considerable. Also, shivering increases myocardial oxygen demand. In terms of monitoring, arterial lines are commonly used. Transesophageal echocardiogram (TEE) monitoring is an option but logistically difficult to insert and use during this particular procedure. Intravenous access must be adequate to support the use of infusions (both a vasopressor and vasodilator). New neurologic deficits need to be investigated, including evaluating for patency of the newly repaired carotid artery and CT scanning of the brain. Minimal premedication is ideal, because the goal is an awake patient ready for neurological evaluation at the end of surgery. The preoperative blood pressure range and pulse information should be obtained before the surgery begins. Minimizing long-acting opiates is also desirable to reduce sedation at the end of the procedure (Table 5). If regional anesthesia is selected, a superficial cervical plexus block can be performed by infiltrating local anesthetic just behind the posterior border of the sternocleidomastoid muscle. The surgical field covers the C2-4 dermatomes. Deep cervical plexus blocks do not contribute to patient comfort and have been associated with complications. The GALA trial, published in Lancet in 2008, showed no difference in outcome for general versus local anesthesia in over 3,500 patients. Similarly, a Cochrane review from 2013 looked at over 4,500 operations and showed no statistically significant difference in 30-day death or stroke for those patients undergoing local versus regional anesthesia for CEA. Table 5 Anesthetic Considerations During CEA # Routine arterial line plus ability to titrate infusions to increase or decrease blood pressure # While carotid artery is cross clamped, maintain blood pressure ~ 20% above baseline # Maintain normocarbia # Avoid hyperglycemia (worsens neurologic outcome) # Barbiturate bolus before cross clamping may decrease CMRO 2, but no evidence of better outcomes, and slower wake-up # Cooling patient is logistically difficult and is not associated with benefit # Carotid sinus stimulation can cause hypotension and bradycardia # Goal: rapid wake-up and early neurologic assessment Post Procedure Management In the postoperative period, a number of management challenges may develop (Table 6). Although hypotension is possible, hypertension is more common. Less frequent are cranial nerve injuries including vagus, hypoglossal, mandibular and posterior auricular nerve injuries. In NASCET, 101/1,415 patients developed a wound hematoma, 4 of which were severe enough to cause death or permanent disability. The hyperperfusion syndrome consists of headache and hypertension. This occurs in 6-11% of patients because of loss of brain autoregulation and increased brain perfusion after removal of the carotid plaque. The carotid sinus controls baroreceptor reflexes and responds to increased arterial pressure with bradycardia and vasodilation. This reflex can be triggered during surgery as the surgeon manipulates the carotid bifurcation. The surgeon can infiltrate the area with local anesthetic to blunt this response. However, after removal of the plaque, the sinus may detect increased blood pressure leading to hypotension. More common is postoperative hypertension due to denervation of the baroreceptor fibers in the artery. The denervated carotid sinus receives less stimulation and responds as if the blood pressure is low. Therefore, careful hemodynamic monitoring should continue in the immediate postoperative period. In the author s practice, patients are monitored at least overnight in the step-down unit. Curr Rev Nurs Anesth 38(7):81-92,

10 Table 6 Post-Carotid Endarterectomy Concerns # New neurologic deficits, requiring imaging and/or neck exploration # Hemodynamic instability (hypertension more common than hypotension) # Cranial nerve injury # Neck hematoma # Hyperperfusion syndrome (headache, hypertension, cerebral edema, seizures) # Myocardial ischemia Poor preoperative blood pressure control predicts postoperative hypertension. Hypertension and tachycardia are associated with myocardial ischemia, the greatest risk to patients after CEA. Hypertension can be associated with cerebral edema, hemorrhage and seizures. Post-CEA hypertension is associated with adverse outcomes; whereas, hypotension and bradycardia are not. In the immediate postoperative period, a blood pressure greater than 140/90 should be treated and continuous ECG monitoring should be carried out, knowing that myocardial ischemia will occur in up to 15% of CEA patients. If the patient is hypotensive, residual anesthetic is a possible cause, as well as too much antihypertensive medication or possible resetting of the baroreceptors. If patients have multiple risk factors, including a history of stroke, congestive heart failure, renal failure, hypertension, dysrhythmia and/or MI, they should be considered for the ICU postoperatively. As noted above, most patients in NASCET who suffered an adverse outcome were identified within 8 hours of surgery. Summary Carotid artery disease is common and associated with coronary artery disease. The greatest perioperative risk remains myocardial ischemia. It is important for the anesthesia provider to discuss with the surgeon the plan for neurologic monitoring and shunting. Since there is no benefit to regional over general anesthesia, this decision can be based upon provider preference and patient factors including anxiety and ability to lie flat. Cerebral perfusion pressure is a key to the successful outcome of CEA. Blood pressure should be maintained at normal to approximately 20% above baseline during the cross clamp period with normocarbia and an anesthetic technique tailored for a rapid wake up. Postoperative blood pressure control, stroke, and myocardial ischemia remain important considerations. Terrence L. Trentman, MD, Department of Anesthesiology, Mayo Clinic Arizona, Phoenix, Arizona. trentman.terrence@mayo.edu References Augoustides J. Advances in the management of carotid artery disease: focus on recent evidence and guidelines. Journal of Cardiothoracic and Vascular Anesthesia 26: , Brott T. et al. Stenting versus endarterectomy for treatment of carotid-artery stenosis (CREST). N Eng J Med 363:11-23, Ferguson G. et al. The North American symptomatic carotid endarterectomy trial (NASCET). Stroke 30: , Lewis S. et al. General anaesthesia versus local anaesthesia for carotid surgery (GALA): a multicentre, randomized controlled trial. Lancet 372: , Roffi M. et al. Carotid artery stenting vs. endarterectomy. European Heart Journal 30: , (Good review of CAS vs. CEA) Unic-Stojanovic D. et al. General versus regional anesthesia for carotid endarterectomy. Journal of Cardiothoracic and Vascular Anesthesia 27: , Vaniyapong T. et al. Local versus general anaesthesia for carotid endarterectomy. Cochrane Database of Systematic Reviews Dec Terrence L. Trentman, MD. Dr. Trentman graduated from Tulane University School of Medicine and completed an internship, anesthesiology residency and pain fellowship at Mayo Clinic, Rochester, Minnesota. He now practices at Mayo Clinic in Arizona and is a member of the liver transplant team. He divides his time between the general operating room including ultrasound guided regional anesthesia, and the chronic pain clinic. 90 Current Reviews for Nurse Anesthetists

11 Tips for your Clinical Practice: Key Points # Stroke is the fourth leading cause of mortality in the United States, and carotid arterial disease is responsible for 15-20% of ischemic strokes; approximately 8.5 % of patients have both cerebral and coronary artery disease. # Recommendations for carotid revascularization range from Class I (> 70% occlusion; benefit far outweighs risk; non-disabling stroke or TIA within six months; average to low surgical risk) to Class III (< 50% occlusion; no benefit or even harm; chronic total occlusion or severe disability; carotid revascularization not recommended). # For patients with symptomatic carotid artery and coronary artery disease and > 80% carotid stenosis, CAS or CEA may be considered prior to or concurrently with CABG. # In preparation for anesthesia and surgery patients should continue statins, aspirin and antihypertensive drugs (particularly beta-blockers). Baseline blood work and blood chemistries should be checked, and a cardiac evaluation should be obtained. # The circle of Willis is complete in < 50% of patients; cross clamping of the carotid artery may precipitate additional neurologic deficits and/or a permanent stroke. # Neurological monitoring and shunt insertion do not change the risk of stroke. # Although debated for many decades, hyper- and hypocarbia should be avoided during CEA. Blood glucose should be maintained at mg/dl. # Hypothermia and thiopental administration decrease CMRO 2, but better outcomes have not been demonstrated for either intervention. # Postoperative hypotension may reflect residual anesthetic or excessive administration of antihypertensive drugs. Robert R. Kirby, M.D. Professor Emeritus of Anesthesiology University of Florida, College of Medicine FRANK MOYA CONTINUING EDUCATION PROGRAMS, INC. & FACULTY DISCLOSURE THIS AUTHOR S AND FMCEP S SPECIFIC DISCLOSURES: The author / faculty has indicated that there is no relevant financial interest or relationship with any commercial interest. The author / faculty has indicated that, as appropriate, he/she has disclosed that a product is not labeled for the use under discussion, or is still under investigation. As a matter of policy, FMCEP does not have any relevant financial interest or relationship with any commercial interest. In addition, all members of the staff, Governing Board, Editorial Board and CME Committee who may have a role in planning this activity have indicated that there is no relevant financial interest or relationship with any commercial interest. Current Reviews is intended to provide its subscribers with information that is relevant to anesthesia providers. However, the information published herein reflects the opinions of its authors. Anesthesia practitioners must utilize their knowledge, training and experience in their clinical practice of anesthesiology. No single publication should be relied upon as the proper way to care for patients. DESIGNATON OF SPECIFIC CONTENT AREAS: Current Reviews for Nurse Anesthetists (CRNA) is designed to meet the standards and criteria of the American Association of Nurse Anesthetists (AANA) for the prior-approved continuing medical education activity, Provider-Directed Independent Study, also known as home study. CRNA is an approved program provider. CRNA has designated the lessons which meet specific content areas such as pharmacology, HIV/AIDS, etc. However, only the Board of Nursing of an individual State is the final authority in the determination of whether or not these lessons meet the State s licensure requirements. Curr Rev Nurs Anesth 38(7):81-92,

12 MARK ONLY THE ONE BEST ANSWER PER QUESTION ON YOUR ANSWER CARD. MARK THIS PAGE AND KEEP FOR YOUR RECORDS. 7 In accordance with AANA directives, you must get 80% of the answers correct to receive one credit for each lesson, and if there is a failure, there is no retaking. POST-STUDY QUESTIONS 1. Amaurosis fugax can be caused by carotid artery emboli and is defined as: G A. Transient clumsiness. G B. Monocular blindness. G C. Arm or leg weakness that lasts less than 24 hours. G D. Speech changes. 2. A carotid bruit: G A. Almost always emanates from the cardiac valves. G B. Is used to diagnose coronary artery disease. G C. Is highly sensitive for carotid stenosis > 70%. G D. Is an abnormal sound auscultated over the carotid artery. 3. Class I recommendations for carotid revascularization include which of the following: G A. Less than 50% stenosis in symptomatic patients. G B. TIA within 6 months with low surgical risk. G C. Total occlusion of the artery. G D. Severe disability caused by a cerebral infarct. 4. In NASCET, the majority of surgical adverse events occurred: G A. Intraoperatively or within 8 hours after surgery. G B. 30 days or more postop. G C. 90 days or more postop. G D. 7 days or more postop. 5. In CREST: G A. Carotid stent (CAS) patients had a higher rate of MI. G B. CAS patients had fewer strokes than endarterectomy (CEA) patients. G C. No difference was found in the composite endpoint, CAS vs. CEA. G D. Overall, CEA patients had the best long-term results. 6. During CEA surgery, shunting: G A. Is considered standard of care. G B. Is the only reasonable response to electroencephalogram (EEG) changes. G C. Lowers the risk of stroke. G D. Can cause air emboli. 7. The most common cause of stroke during CEA surgery is: G A. Embolism. G B. Hypotension. G C. Shunt use. G D. Hypertensive hemorrhage. 8. The gold standard of neurologic monitoring during CEA surgery is: G A. Carotid stump pressure. G B. Electroencephalogram (EEG). G C. The awake patient. G D. Transcranial Doppler (TCD). 9. Ventilation during CEA surgery should be managed to achieve: G A. Hypercarbia to dilate cerebral blood vessels. G B. Hypocarbia to constrict normal cerebral vessels and drive blood toward stenotic areas. G C. A mild to moderate respiratory alkalosis. G D. Normocarbia. 10. Carotid sinus fibers in the artery wall can be damaged during CEA surgery, most commonly resulting in postoperative: G A. Hypotension. G B. Hypertension. G C. Tachycardia. G D. New neurologic deficits. Moving? Please notify us at least six weeks before you move to your new address, so you won t miss any issues of your subscription. The post office will not forward your subscription to Current Reviews for Nurse Anesthetists. Phone: (954) Fax: (954) or (800)