Anesthesia for Vascular Surgery

Difficulty swallowing with ipsilateral Horner syndrome (i.e., ptosis, miosis, exophthalmos, reduced sweating) can be from damage of which cranial nerve A. VII B. IX C. X D. XI E. XII

B.

A graft wall fabric porosity is considered what type of leak A. I B. II C. III D. IV

D.

Which of the following are two of the most common sites of chronic atherosclerosis. A. Suprarenal B. Juxtarenal C. Infrarenal D. Iliac

C & D Aortoiliac Occlusive Disease - The infrarenal aorta and the iliac arteries are two of the most common sites of chronic atherosclerosis. Because of the diffuse and progressive nature of aortoiliac atherosclerosis, plaque enlargement may reduce blood flow to the lower extremities below a critical level and result in symptoms of ischemia. Unlike patients with aortic aneurysmal disease, patients undergo surgery for aortoiliac occlusive disease only if they are symptomatic. Surgical intervention is indicated for disabling intermittent claudication and limb-threatening ischemia. Intervention is directed toward restoring peripheral pulsatile circulation to relieve claudication and toward preventing amputation. Patients with localized aortoiliac occlusive disease typically have claudication because collateral circulation adequate to prevent critical lower extremity ischemia usually exists. Perioperative mortality is lower in patients undergoing aortoiliac reconstruction than in those undergoing abdominal aortic surgery. - Therapeutic options for managing aortoiliac occlusive disease include anatomic or direct reconstruction (i.e., aortobifemoral bypass), extraanatomic or indirect bypass grafts (i.e., axillofemoral bypass), and catheter-based endoluminal techniques (i.e., percutaneous transluminal angioplasty with or without stent insertion). Aortobifemoral bypass is viewed as the gold standard in treating aortoiliac occlusive disease. Extraanatomic bypass grafts are generally reserved for specific indications, usually patients with infection, failure of previous reconstruction, or prohibitive risk. Reduced long-term patency and inferior functional results are frequently the trade-off for lower perioperative morbidity and mortality. Catheter-based endoluminal techniques, such as percutaneous transluminal angioplasty, are used for relatively localized disease and may be reasonable alternatives to aortobifemoral bypass in 10% to 15% of patients with aortoiliac occlusive disease. Renal and Visceral Arterial Insufficiency - Atherosclerosis is the most common cause of renal artery stenosis. Occlusive lesions are located almost exclusively in the proximal segment and orifice of the renal artery and are usually an extension of aortic atherosclerosis. Fibromuscular dysplasia is an important, but less common, cause of renal artery stenosis and most frequently involves the distal two thirds of the renal arteries. Hemodynamically significant renal artery stenosis may cause hypertension by activation of the renin-angiotensin-aldosterone system, and bilateral involvement may result in renal failure. Patients with renovascular hypertension 2118frequently have poorly controlled hypertension despite maximal medical therapy. These patients often have severe bilateral renal artery stenosis and may have recurrent congestive heart failure or flash pulmonary edema. Indications for intervention include control of hypertension and salvage of renal function. Operative interventions include aortorenal bypass, extraanatomic bypass (hepatorenal or splenorenal bypass), or transaortic endarterectomy. Suprarenal or supraceliac aortic cross-clamping is frequently required for open operative interventions. Percutaneous transluminal angioplasty with stenting of the renal artery is used as the first-line treatment in selected patients. - Stenosis at the origin of the celiac and mesenteric arteries occurs as a result of extension of aortic atherosclerosis. The inferior mesenteric artery is by far the most commonly involved, followed by the superior mesenteric artery and the celiac artery. Occlusion of a single vessel rarely causes ischemic symptoms because of the extensive nature of visceral collateralization. However, occlusion or significant stenosis of any two vessels may compromise collateral flow sufficiently to give rise to chronic visceral ischemia. Operative repair of visceral artery stenosis is reserved for symptomatic patients. Operative interventions include transaortic endarterectomy and bypass grafts, which frequently require supraceliac aortic cross-clamping. Mortality rates for such procedures range from 7% to 18%. To avoid the high mortality associated with open repair, percutaneous transluminal angioplasty with stenting has increasingly been applied in patients with chronic visceral ischemia. Acute visceral artery occlusion can be caused by an embolus or, less commonly, by thrombosis. To avoid the extremely high mortality associated with acute visceral ischemia, diagnosis and surgical intervention must occur before gangrene of the bowel develops.

Which of the following aneurysm repair is approved for an endovascular approach A. Ascending aorta B. Aortic aorta C. Descending thoracic aorta D. Aortic valve

C. Endovascular Technique - The endovascular approach can be undertaken without the large incisions, extensive dissections, prolonged aortic cross-clamp times, and significant blood loss and fluid shifts associated with open repair. The arterial access site for endovascular stent-graft placement is selected on the basis of vessel size and degree of obstructing atherosclerotic disease. The technique most commonly requires bilateral transverse groin incisions to expose the common femoral arteries. In patients with severely diseased femoral or iliac arteries, balloon angioplasty or local endarterectomy can be performed to allow passage of the delivery system. Adjunctive retroperitoneal procedures may be necessary in up to 20% of patients during endovascular AAA. Indications include small external iliac arteries that limit femoral access and a concomitant iliac artery aneurysm that precludes distal fixation of the stent-graft in the common iliac artery. In these cases, a transverse lower abdominal incision with retroperitoneal dissection exposes the iliac artery, and a synthetic conduit is sutured (end to side or end to end) onto the common iliac 2137artery. The delivery system is endoluminally placed into the aorta through this iliac conduit. At the termination of the procedure, the conduit can be ligated, attached to the external iliac artery (interposition graft), or attached to the common femoral artery (iliofemoral bypass graft). Although adjunctive retroperitoneal procedures may allow a larger number of patients to undergo endovascular aortic repair, such procedures are associated with an increased risk for complications, greater blood loss, longer procedure time, and longer hospital length of stay than endovascular repair with standard femoral access. Obviously, the advantage of endovascular techniques being less invasive than open repair is reduced when adjunctive procedures are required. - Adjunctive procedures may also be needed with endovascular repair of the thoracic aorta. One series involving patients with a spectrum of aortic disease reported that 25% of patients needed open surgical access to the aorta and 21% needed left subclavian-carotid transposition to provide an adequate proximal fixation site. Although adjunctive surgical procedures may be needed, the technical skill required for endovascular aortic surgery is primarily catheter based. Thus, appropriately trained cardiologists, radiologists, and vascular surgeons can deliver endovascular treatment of aortic disease. A multispecialty approach is commonly used and offers patients the expertise of both surgical and catheter-based specialists. Even though no standard has been set, the requirements for endovascular aortic surgery are the same wherever it is performed. The standard operating room environment is ideal from the surgical and anesthesia standpoint, particularly when conversion to an open repair is required. The operating room must be equipped with endovascular supplies, portable radiologic imaging tools, and an angiographic table. Angiographic suites often have superior radiographic imaging tools and angiographic tables and are better equipped to deal with ionizing radiation. The superior imaging may reduce radiation exposure and decrease contrast dye loads. In an effort to provide an optimized environment for multispecialty endovascular intervention, many centers are constructing sophisticated operative angiographic suites in or adjacent to the operating room. - Endovascular stent-grafting of the aorta requires preprocedural diagnostic imaging to precisely evaluate and delineate the aortic anatomy. CTA and MRA have been established as the gold standard for preprocedural evaluation. For AAAs, length and diameter of the proximal neck, location of important aortic and iliac side branches (accessory renal arteries, inferior mesenteric artery, and hypogastric arteries), and distal fixation site characteristics must be determined. Significant aneurysm neck angulation, short neck length, large neck diameter, and severe aortic calcification currently exclude many patients from endovascular repair. - Endovascular stent-grafts are often custom-made for each patient based on aortic anatomy. Each endovascular stent-graft delivery device has a unique method of deployment, and many individual variations in technique are possible. First-generation endografts were not fully stented and required balloon expansion of the proximal portion at the time of deployment. Metal hooks in the proximal portion were embedded into the aortic wall with balloon inflation, which resulted in complete aortic occlusion, not unlike aortic cross-clamping. These unsupported endografts were prone to complications such as migration and kinking. Distal migration during proximal endograft deployment was particularly troublesome with intrathoracic endograft placement. Induced hypotension, adenosine-induced asystole, and induced ventricular fibrillation have all been used successfully to reduce endograft migration during deployment. Current-generation endografts are fully stented (i.e., stent-grafts) and self-expanding. Balloon expansion is not required at the time of deployment. Stent-graft migration at the time of deployment is largely prevented, and associated complications are reduced. A unique trilobed aortic balloon can be used to expand the stent-graft for aortic apposition after deployment without complete aortic occlusion. Though no longer a requirement, mild induced hypotension (with nitroglycerin or sodium nitroprusside) can be used selectively during stent-graft deployment. - Hybrid procedures (a combination of open surgical and endovascular stenting) have expanded the endovascular approach to include aortic aneurysms involving major branches that originate from the aorta. Type IV TAA repair can be accomplished with open visceral and renal bypass followed by stent-graft implantation over the "debranched" visceral segment. Similar approaches are being used to treat complex aneurysms that involve the aortic arch. Hybrid procedures rarely require aortic cross-clamping. In patients with aneurysmal disease of the entire aortic arch, the traditional "elephant trunk" procedure has been combined with a second-stage stent-graft procedure of the descending thoracic aorta. The distal end of the elephant trunk serves as the proximal attachment site for the stent graft. Anesthetic Management - Local, regional, and general anesthesia techniques have all been described for endovascular aortic repair shortly after its introduction. Several regional techniques have been used, including paravertebral, spinal, continuous spinal, epidural, and combined spinal and epidural. General anesthesia was commonly used with early-generation devices because the surgical procedure times were often long. As centers have gained experience with newer-generation devices, procedure times have been reduced and local and regional techniques are used more often, most commonly with IV sedation. A sedation technique using dexmedetomidine with local anesthesia has been reported.100 Despite procedural advances and the established feasibility of local and regional anesthesia, these techniques have not become accepted on a large scale. An analysis of anesthesia type based on data from the EUROSTAR registry (5557 endovascular repairs of infrarenal aortic aneurysm) reported the use of local, regional, and general anesthesia in 6%, 25%, and 69% of patients, respectively.101 The influence of anesthesia type on outcome based on the EUROSTAR data indicates that the use of local or regional anesthesia may reduce ICU admission, hospital length of stay, and early complications.101 Further analysis of high-risk patients from this registry 2138suggests that a mortality benefit may exist when local or regional anesthesia is used.102 A retrospective analysis of 229 endovascular AAA repairs using local anesthesia with IV sedation or general anesthesia reported similar rates of cardiac and pulmonary morbidity.103 Reduced intraoperative fluid requirements103,104 and less vasopressor support104 have been reported with the use of local anesthesia. Given the retrospective nature of these reports and the significant selection bias regarding assignment of anesthetic technique, specific recommendations regarding the use of local, regional, and general anesthesia are premature. As with open aortic repair, maintenance of vital organ perfusion and function by the provision of stable perioperative hemodynamics is probably more important to overall outcome than is the choice of anesthetic technique. I commonly use a general anesthetic technique for endovascular aortic repair in patients requiring extensive groin dissection or any retroperitoneal dissection and those requiring complex repairs, where conversion to open repair may be more likely. A balanced technique using relatively short-acting agents maximizes management flexibility. Opioid requirements are usually minimal (fentanyl 2 to 4 μg/kg), and postoperative pain is easily managed. Esmolol, sodium nitroprusside, nitroglycerin, and phenylephrine should be available and used to maintain appropriate hemodynamics. Epidural and spinal anesthesia are used selectively based primarily on patient and surgeon preference. - Placement of a radial artery catheter should be routine for all endovascular aortic repairs. It should be placed on the right side because a catheter may be placed percutaneously in the left brachial artery for aortic angiography. Central venous and pulmonary artery catheter monitoring are rarely used. Two large-bore peripheral IV catheters are recommended. Although blood loss and fluid requirements are not usually excessive, the potential for rapid blood loss is real. The possibility of acute aortic rupture necessitates the availability of fluids, blood, and a rapid infusion device. Catheterization of the bladder is required for most procedures. Monitoring of urine output can help guide fluid management, particularly when large volumes of heparinized flush solution and radiographic contrast material are used and when diuretics (i.e., mannitol or furosemide) are administered. Fluid management is directed primarily at maintaining normovolemia. Isotonic HCO3− infusion is often used in patients with renal dysfunction to reduce the incidence of contrast-induced nephropathy.105 Active patient warming is frequently necessary to prevent hypothermia, particularly with longer procedures. - Endovascular repairs involving the descending thoracic aorta require additional preparation and monitoring. These procedures are often performed in the operating room under general anesthesia. Although current-generation devices are much less prone to graft migration during deployment, pharmacologically (i.e., sodium nitroprusside or nitroglycerin) induced hypotension (i.e., systolic blood pressure < 100 mm Hg) is commonly used during deployment. TEE monitoring is frequently used and can be extremely helpful in identifying proximal and distal stent-graft landing zones, entry and exit points of dissections, true and false lumens, and aneurysm exclusion. Paraplegia is a recognized complication after endovascular repair of the descending thoracic aorta and is reported to be as high as 8%.88 Concomitant or previous abdominal aortic repair and long-segment thoracic aortic exclusion appear to be important risk factors. Postoperative hypotension may play a role as well. CSF drainage reverses delayed-onset neurologic deficit after endovascular TAA repair,89 prompting some centers to use perioperative CSF drainage in all high-risk patients. Intraoperative spinal evoked potential monitoring plus temporary (15 minutes) balloon occlusion of the thoracic aorta before stent-graft deployment is a means to evaluate the patient's risk for spinal cord ischemia.106

Which of the following is a late complication fof endovascular repair for aneurysm A. Acute renal failure B. MI C. Stroke D. Limb occlusion

D. Early Complications - In addition to primary endoleaks, early complications include access vessel trauma, inadvertent stent deployment over vital branch vessel, aneurysm rupture, pelvic and lower extremity ischemia, acute renal failure, MI, stroke, paraplegia, and postimplantation syndrome (PIS). PIS is a weakly defined yet relatively common condition associated with features of a systemic inflammatory response such as leukocytosis, fever, and elevation of inflammatory mediators. Although transient and usually well tolerated, PIS is associated with an increased length of hospital stay. Late Complications - Late complications are most often related to endoleak but also include degeneration of the proximal neck, limb occlusion, device migration or fatigue (kinking or collapse), endograft infection, aneurysm enlargement, open conversion, and rupture. Lifelong surveillance imaging is mandatory for the early detection and management of these complications. Approximately 20% of patients will require catheter-based or limited surgical reintervention after endovascular infrarenal aortic aneurysm repair. Outcomes - Endovascular repair of AAAs was originally developed to provide a treatment option for patients considered to be poor surgical candidates. Early studies reported better hemodynamic stability, reduced stress response, decreased rate of systemic complications and shorter postoperative length of stay, and improved respiratory function and analgesic control than with open aortic repair. Based on these early reports and without the benefit of long-term outcome data or randomized clinical trials, endovascular aneurysm repair has been applied to a large proportion of patients with AAAs. Large retrospective cohort studies and prospective registries subsequently established the safety and efficacy of endovascular repair. Several prospective randomized controlled trials in Europe and the United States followed to answer several critical questions related to the broad application of endovascular technology in patients fit and unfit for open repair. - A meta-analysis of 163 studies involving 28,862 patients assessed safety and efficacy outcomes after endovascular repair of asymptomatic AAA.108 The operative mortality was 3.3%. Technical success (complete aneurysm exclusion) rate was 82.7%. The rate for primary conversion to open repair was 3.8%, and for secondary conversion to open repair 3.4% (overall 5.4%). The postoperative rupture rate was 1.3% and was associated with a 44.4% mortality rate. A type I endoleak developed in 10.5% of patients, with an annual rate of 8.4%. A type II, III, or IV endoleak developed in 13.7% of patients, with an annual rate of 10.2%. A definite improvement in outcome was reported over the study period (1992 to 2002). Another meta-analysis involving 19,804 patients undergoing endovascular repair of infrarenal aortic aneurysm between 2000 and 2004 reported a 30-day mortality rate of 1.6% and 2.0% in randomized and nonrandomized trials, respectively.109 Device deployment was successful in 97.6% of patients. Technical success was achieved in 81.9% at discharge and 88.8% at 30 days. Secondary intervention to treat endoleak or to maintain graft patency was required in 16.2% of patients. - In a study of 45,660 Medicare beneficiaries who underwent either endovascular or open repair of an AAA between 2001 and 2004, perioperative mortality was lower after endovascular repair (1.2% versus 4.8%), and the reduction in mortality increased with age (8.5% difference for those 85 years or older).97 Conversion from endovascular repair to open repair occurred in 1.6% of patients. Endovascular repair was associated with fewer major complications, shorter length of hospital stay (3.4 days versus 9.3 days), and a greater likelihood of being discharged home (94.5% versus 81.6%). Late survival was similar between cohorts, although the survival curves did not converge until after 3 years. By the fourth year, rupture was more likely to occur after endovascular repair (1.8% versus 0.5%), as was aneurysm-related intervention (9.0% versus 1.7%). Prospective randomized controlled trials comparing endovascular and open repair of asymptomatic infrarenal AAA (in patients fit for open repair) have been undertaken to determine comparative morbidity and mortality, and the need for reintervention. A recent meta-analysis of all prospective, randomized trials (2899 patients) reported short-term (30-day), intermediate-term (up to 2 years), and long-term (3 years or longer) outcomes.110 The primary conversion rate for endovascular repair was 0.6%. Length of hospital stay and ICU stay were shorter with endovascular repair. There were no differences in perioperative complications, including stroke, MI, and renal failure. The 30-day all-cause mortality was less with endovascular repair (relative risk [RR]: 0.35, 95% confidence interval [CI]: 0.19 to 0.64). At intermediate follow-up, the all-cause mortality had a nonsignificant difference (RR: 0.78, 95% CI: 0.57 to 1.08), the aneurysm-related mortality was lower (RR: 0.46, 95% CI: 0.28 to 0.74), and the reintervention rate higher (RR: 1.48, 95% CI: 1.06 to 2.08) for endovascular repair compared to open repair. At long-term follow-up, no difference was found in all-cause mortality (RR: 0.99, 95% CI: 0.85 to 1.15) or aneurysm-related mortality (RR: 1.58, 95% CI: 0.20 to 12.74) whereas the difference in reintervention persisted (RR: 2.54, 95% CI: 1.58 to 4.08). The Endovascular Aneurysm Repair (EVAR)-2 trial was designed to compare endovascular repair versus no intervention in patients deemed unfit for open AAA repair.111 A total of 338 patients with AAAs greater than 5.5 cm, older than 60 years of age, and deemed unfit for open repair because of comorbid conditions were randomized to undergo endovascular repair or no intervention. All patients received best medical treatment for their comorbid conditions. Operative mortality (30 day) for the endovascular group was 9%. The overall mortality rate at 4 years was 64%, and no difference was found between the endovascular group and the no-intervention group in aneurysm-related mortality or all-cause mortality. Although more deaths from aneurysm rupture occurred in the no-intervention group, the initial high mortality in the endovascular group resulted in no late differences in mortality. The authors concluded that endovascular repair did not improve survival over no intervention, had little effect on health-related quality of life, and was associated with a need for continued monitoring and reintervention, 2140at substantially increased cost. In-hospital mortality for the highest risk patients undergoing endovascular aortic aneurysm repair in the United States may be lower than that reported in EVAR-2, suggesting that these high-risk patients should not be denied endovascular repair.112

Most carotid artery stenting procedures are performed with what kind of anesthesia A. General B. Regional C. Neuraxial D. Local

D. Endovascular Treatment of Carotid Disease: Carotid Artery Stenting - Endovascular treatment of carotid disease is an innovation in evolution for stroke prevention and currently involves percutaneous transluminal angioplasty and stenting. Significant procedural advancements include the use of dual antiplatelet therapy, self-expanding stents, and emboli protection devices. Over the last decade, major randomized clinical trials comparing carotid endarterectomy with carotid artery stenting have been published. A recent systematic review of randomized trials (16 trials involving 7572 patients) found that endovascular treatment (including balloon angioplasty or stenting) was associated with an increased risk for periprocedural stroke or death compared with endarterectomy.174 Of note, the increase in risk appeared to be limited to patients 70 years of age and older. Endovascular treatment was associated with lower risks for MI, cranial nerve palsy, and access site hematomas. The rate of ipsilateral stroke after the periprocedural period was not different between treatment groups. Among patients unfit for surgery, the rate of death or stroke did not differ between endovascular treatment and medical care. Updated guidelines provide specific recommendations for revascularization of symptomatic and asymptomatic patients.131 - The carotid artery stenting procedure consists of the following steps: femoral access, aortic arch angiogram, selective cannulation of the common carotid artery origin and angiogram, guidewire advancement into the external carotid artery, carotid sheath placement and advancement into the common carotid artery, placement of embolic protection device, balloon angioplasty of lesion, advancement of stent delivery catheter across dilated lesion, deployment of self-expanding stent, balloon dilatation of stent, completion angiogram, and access site management. The femoral artery approach is considered standard, but brachial artery and high radial artery access have been reported with high procedural success. Embolic protection devices are considered mandatory and include distal protection in the form of a filter or occlusion balloon and proximal protection in the form of flow interruption or flow reversal. Cardiologists and radiologists currently perform a large percentage of these procedures in specialized endovascular suites. - Most carotid artery stenting procedures are performed under local anesthesia with light or no sedation to facilitate patient cooperation and continuous neurologic assessment. In addition to routine monitors, an arterial line is placed for continuous blood pressure monitoring. Some degree of hemodynamic instability is common in patients during and after carotid artery stenting. Bradycardia and hypotension occur much more frequently after carotid artery stenting with balloon angioplasty than without angioplasty.175 A recent, large retrospective study reported asystole in 4.9% of patients after carotid stenting.176 Asystole was more likely to occur in patients undergoing a right-sided procedure, in those with significant contralateral stenosis, and in those with a reduced left ventricular ejection fraction. The administration of prophylactic atropine before balloon inflation decreases the incidence of intraoperative bradycardia and cardiac morbidity in primary carotid stenting patients.177

An AAA that has a diameter of 6-7 has a ruputre risk of A. 20 B. 30 C. 40 D. 50

a.

These endoleaks are associated with an increased risk for rupture and are almost uniformly treated aggressively. A. Type I B. Type II C. Type III D. Type IV E. Type V

A & B Complications Endoleak - The inability to obtain or maintain complete exclusion of the aneurysm sac from arterial blood flow, termed endoleak, is a complication specific to endovascular aortic repair. The concern is that any pressurization of the aneurysm sac (i.e., endotension) can lead to aneurysm enlargement and rupture. Endoleaks can be detected by arteriography, computed tomographic scanning, magnetic resonance imaging, and duplex ultrasound scanning. A classification system developed for endoleak describes four distinct types.107 Type I endoleak occurs when the seal between the stent-graft and the aortic wall at the proximal or distal attachment sites is inadequate. Type II endoleak occurs when there is retrograde filling of the aneurysm sac from patent intercostal, lumbar, inferior mesenteric, or testicular arteries. Type III endoleak is due to structural failure of the stent-graft that allows blood to flow directly into the aneurysm sac. The structural failure may be due to tears in the graft fabric or separation of individual components of a modular endograft. Type IV endoleak relates directly to the porosity of the graft material. Type V endoleak refers to persistent pressurization of the aneurysm sac after endovascular repair without an identified leak on imaging studies. Endoleaks are also classified as primary (after deployment) or secondary (after initial seal). - The rate of occurrence of endoleak depends on many factors, including the endograft device, the method of deployment, vascular anatomy, and progression of disease. Management of endoleak after endograft placement is controversial and ranges from observation with periodic imaging surveillance to immediate endovascular or surgical correction. Types I and III endoleaks are associated with an increased risk for rupture and are almost uniformly treated aggressively. Although type II endoleaks do not often require urgent treatment and many spontaneously thrombose, they are associated with aneurysm enlargement. Type IV endoleaks are usually self-limited and rarely require specific treatment. Type V endoleaks require intervention if aneurysm growth is detected. Endovascular extension grafts, coil embolization, and conversion to open repair have been used successfully to repair endoleaks.

This is the most commonly used distal aortic perfusion technique A. Left heart bypass B. Right heart bypass

A. Left Heart Bypass - Maintaining lower body perfusion with the use of retrograde distal aortic perfusion reduces ischemic injury and improves outcome, provided the pressure is high enough to perfuse the organs. The simplest method of providing distal aortic perfusion is a passive conduit or shunt. The heparin-bonded Gott shunt was developed to avoid the need for systemic heparinization and is used to divert flow passively from the left ventricle or proximal descending thoracic aorta to the distal aorta. Some centers place a temporary axillary-to-femoral artery graft to function as a shunt during aortic cross-clamping. - Partial bypass, also referred to as left heart bypass or left atrial-to-femoral bypass, is the most commonly used distal aortic perfusion technique (Fig. 69-11). This technique allows adjustment of blood flow and usually draws blood 2132from the left atrium and returns blood to the left femoral artery. A centrifugal pump is used (Biomedicus, Eden Prairie, Minn), and full-dose systemic heparin is not needed because the circuit is coated with heparin. The typical heparin dose for partial bypass is 100 units/kg. With this technique, an oxygenator is unnecessary because only the left side of the heart is bypassed. Insertion of a heat exchanger into the circuit allows cooling and warming, which is beneficial but not absolutely essential. Variations of left heart bypass include cannulating the aortic arch or proximal descending thoracic aorta instead of the left atrium. With this circuit, the left ventricle is relieved of the increased afterload during aortic cross-clamping. With left atrial cannulation, the left ventricle is relieved of preload and cardiac output is reduced. Either way, proximal hypertension is controlled, the work of the ventricle is decreased, and perfusion is provided to the distal aorta. My colleagues and I have had even greater success with cannulation of a pulmonary vein instead of the left atrium. This method accomplishes the same effect as with atrial cannulation but is associated with less atrial irritability. When hypothermia (30° C) is combined with atrial cannulation, approximately 15% of patients experience new atrial fibrillation. Although most patients revert to sinus rhythm on rewarming, direct cardioversion may be required. - During left heart bypass, it is essential that arterial blood pressure be monitored above and below the aortic cross-clamps. I simultaneously display radial and femoral artery pressure and aim for a mean arterial pressure of 80 to 100 mm Hg above the cross-clamp and at least 60 mm Hg below the cross-clamp. Careful control of intravascular volume, bypass pump flow, and vasoactive drugs is required to achieve the target blood pressures. Management of left heart bypass requires continuous communication and cooperation between the surgeon, anesthesiologist, and perfusionist. We typically set the initial pump flow to approximately 50% of the patient's cardiac output with application of the proximal aortic clamp. Flow is then adjusted to maintain target proximal and distal pressures. Administration of vasodilators is very infrequently required at this stage. With no vital organ ischemia, the surgeon can complete the proximal anastomoses in an unhurried fashion. With sequential aortic clamping, intercostal arteries can be reimplanted with minimal adjustments of pump flow. Pump flow is eventually reduced significantly during reimplantation of the visceral and renal arteries. At this time, distal perfusion is only to the lower extremities. We routinely use moderate hypothermia (32° C) during bypass to protect the vital organs during obligate periods of ischemia. After completion of the distal anastomoses, pump flow is increased, and the patient is actively warmed to 37° C.

The advantages of this monitoring are that it is inexpensive, relatively easy to obtain, and continuously available during carotid clamping (dynamic stump pressure). A. Carotid artery stump pressure B. Regional cerebral blood flow C. EEG D. SSEP E. TUD F. Cerebral oxygenation

A. Neurologic Monitoring and Cerebral Perfusion - Intraoperative monitoring for cerebral ischemia or hypoperfusion and, more recently, for cerebral emboli during carotid endarterectomy is controversial (see also Chapter 49). Monitoring techniques include internal carotid artery stump pressure determinations, rCBF measurements, EEG monitoring, SSEP monitoring, transcranial Doppler ultrasonography (TCD), and cerebral oximetry monitoring. The rationale for the use of such monitoring is based on the need to prevent intraoperative strokes. The primary clinical utility of cerebral monitoring is to identify patients who may benefit from shunting during the period of arterial clamping. Secondarily, cerebral monitoring is used to identify patients who may benefit from blood pressure augmentation or change in surgical technique. Despite a tremendous amount of investigative effort, only limited data support the assumption that cerebral monitoring actually improves patient outcome after carotid endarterectomy. To further complicate the issue, several large series have reported excellent results from carotid endarterectomy with routine shunting, routine no shunting, and selective shunting using one or more of the methods discussed later. In a review, the mean reported stroke rate with routine shunting was 1.4% and for routine no shunting was 2%.165 The mean perioperative stroke rates for selective shunting were 1.6% using stump pressure, 1.6% using EEG, 1.8% using SSEP, and 4.8% using TCD.165 Carotid Artery Stump Pressure - The internal carotid artery stump pressure represents the back-pressure resulting from collateral flow through the circle of Willis via the contralateral carotid artery and the vertebrobasilar system. The advantages of monitoring carotid stump pressure are that it is inexpensive, relatively easy to obtain, and continuously available during carotid clamping (dynamic stump pressure). Despite these advantages, few centers use stump pressure monitoring. A recent single center report of 1135 consecutive carotid endarterectomies under general anesthesia used a stump pressure of below 45 mm Hg as a guide for selective shunting.166 The 30-day stroke rate was 3% for patients selectively shunted (21%), 0.5% for patients not shunted (79%), and 1% overall. The overall 30-day mortality was 0.5%. Of note, no patient had a stroke caused by global intraoperative cerebral hypoperfusion. A recent prospective randomized trial comparing routine shunting versus selective shunting based on stump pressure below 40 mm Hg in 200 patients undergoing carotid endarterectomy under 2153general anesthesia found both methods were associated with an infrequent perioperative stroke rate (0% versus 2%).167 The two strokes in the selective shunting cohort were related to carotid artery thrombosis. No patients died perioperatively. Although an old method, stump pressure monitoring appears to have survived the test of time.

Residual hypothermia in the early postoperative period is associated with an __________ incidence of myocardial ischemia and cardiac morbidity A. increased B. decreased

A. Postoperative Management of Vascular Surgery Patients - Vascular surgery patients require special attention during the postoperative period because most complications occur postoperatively and other problems may arise that require immediate attention. Conventional practice is to monitor all vascular surgery patients in an ICU setting after surgery. Some centers have set up specialized vascular step-down units in which lower risk patients can be evaluated frequently by specialized nursing staff. There are, however, no clinical trials to support this practice. Myocardial ischemia and cardiac morbidity occur most frequently in the postoperative period. Patients should be carefully monitored for signs and symptoms of myocardial ischemia, realizing that up to 90% of ischemic episodes are asymptomatic. Troponin surveillance may be beneficial in high-risk patients. The determinants of myocardial O2 supply and demand should be optimized for all patients (Fig. 69-18) to prevent ischemia before it develops. β-Blocker and statin therapy should be continued throughout the postoperative period. Dysrhythmias are common and may be secondary to ischemia or to sympathectomy associated with regional anesthesia. - Besides myocardial ischemia and cardiac morbidity, other problems include coagulopathy, from either residual 2156heparin or dilutional coagulopathy after massive transfusion. Even in the absence of coagulopathy, bleeding through fresh vascular anastomoses may occur when significant postoperative hypertension is untreated. Hypovolemia occurs after aortic surgery as a result of significant third-space fluid loss and bleeding. Hypovolemia may lead to hypotension and hypoperfusion of vital organs or lower extremity vascular grafts. Graft occlusion in the lower extremities occurs in 3% to 10% of patients after lower extremity or aortic surgery and should be recognized immediately and surgically corrected. Lower extremity pulses should be checked at hourly intervals. Some patients require the administration of heparin or dextran to prevent thrombosis when the surgical repair is questionable or when patients have diffuse atherosclerotic disease. - Residual hypothermia in the early postoperative period is associated with an increased incidence of myocardial ischemia and cardiac morbidity; therefore, body temperature should be carefully monitored and controlled in all vascular surgery patients. In the early postoperative period, vascular surgery patients have a twofold to threefold greater incidence of myocardial ischemia when core temperature is less than 35° C.178 Even mild hypothermia of approximately 35° C is associated with a 200% to 700% increase in norepinephrine levels,179,180 generalized vasoconstriction,181 and increased blood pressure in postoperative patients.179 Shivering occurs and increases total-body O2 consumption by approximately 40% in the typical elderly vascular patient.182 In a prospective randomized trial, the relative risk for early postoperative cardiac morbidity was reduced by 55% when normothermia was maintained by use of a forced-air warming system.183 - The stress response needs to be controlled in the postoperative period. This includes preventing the potential triggers for myocardial ischemia such as pain, anemia, hypothermia, hemodynamic extremes, and ventilatory insufficiency. In mechanically ventilated patients, the weaning period is especially stressful, and myocardial ischemia occurs frequently during this time. Careful sedation and expeditious weaning are desirable. When possible, extubation in the operating room is less stressful and is preferable for carotid and lower extremity vascular surgery patients. For more invasive surgical procedures (TAA and AAA), postoperative mechanical ventilation is usually necessary. - Vascular surgery continues to challenge the anesthesiologist, given the significant physiologic stress superimposed on a relatively elderly patient population with a high incidence of coexisting disease. Clinical studies and society guidelines provide insight into the preoperative assessment and optimization of cardiac risk, the implications of anesthetic technique, and the diagnosis, prevention, and treatment of myocardial ischemia in vascular surgery patients. These studies and guidelines have improved our ability to care for vascular surgery patients with reduced morbidity and better overall outcome.

Which vessel is the most used graft for femoral-popliteal bypass surgery A. great sapehnous vein B. umbilical vein C. cephalic vein D. basilic vein

A. Surgical Management - Accepted treatments of lower extremity arterial disease include both nonoperative and operative modalities. Nonoperative options include lifestyle and risk factor modification, exercise programs, and pharmacologic therapy. Operative options include percutaneous endovascular modalities and surgical reconstruction. Endovascular techniques include more established therapies such as intraarterial thrombolytic therapy, balloon catheter embolectomy, transluminal balloon angioplasty, and angioplasty and stent placement, as well as new technologies such as novel angioplasty balloons, atherectomy and laser angioplasty systems, cryotherapy, and placement of nitinol and drug-eluting stents. Surgical procedures include endarterectomy, bypass grafting (primary or revision), and amputation. - Lower extremity arterial reconstruction is performed both for severe disabling claudication and critical limb ischemia (limb salvage). The choice of operative approach depends primarily on the location and distribution of arterial occlusions. Several surgical approaches are used in patients with lower extremity arterial insufficiency. For occlusion distal to the inguinal ligament, a femoral-popliteal bypass with an autologous great saphenous vein (reversed) graft is most often the procedure of choice. Graft patency rates with this approach are reported to be 59% at 5 years and 38% at 10 years. The saphenous vein may be used in situ (not reversed), but this technique is more demanding and requires excision of the valves to allow adequate flow. Human umbilical vein and polytetrafluoroethylene grafts can be used when an autologous saphenous vein is unavailable, which is often the case when patients have previously undergone coronary artery bypass or lower extremity bypass. The cephalic and basilic veins from the upper extremities are sometimes used as a graft. Harvesting vein from the upper extremities has obvious implications with regard to IV catheter placement and the use of regional anesthesia. - In patients with aortoiliac disease who are not candidates for aortobifemoral bypass because of coexisting medical diseases, an extraanatomic procedure (axillofemoral or femorofemoral bypass) is an alternative approach that is thought to be a less stressful procedure. Distal arterial reconstruction with a bypass to the tibial, peroneal, or pedal vessels is almost exclusively performed for limb salvage. Prosthetic grafts have very high failure rates, and every attempt is made to harvest adequate autologous vein.

Surgical manipulation of the carotid sinus with activation of the baroreceptor reflexes can cause A. Tachycardia B. Bradycardia C. Hypertension D. Hypotension

B & D General Anesthesia - Any of the drugs commonly used to induce anesthesia, maintenance anesthetics, and nondepolarizing muscle relaxants can be used safely during carotid endarterectomy, given that stable hemodynamics are maintained and the patient is awake at the end of the procedure. A conventional technique is as follows. Sedative premedication (e.g., midazolam) has the potential to compromise early neurologic assessment and is universally avoided. After placement of routine monitors and administration of O2 by facemask, small doses of opioid (e.g., fentanyl 0.5 to 1 μg/kg) are administered during arterial line placement. Induction of anesthesia is accomplished with incremental dosages of propofol supplemented with additional opioid (total fentanyl dose 2 to 4 μg/kg). Etomidate also may be used and is preferred in patients with limited cardiac reserve. Neuromuscular relaxation with a short-acting to intermediate-acting nondepolarizing muscle relaxant such as vecuronium facilitates tracheal intubation. Esmolol is particularly effective in blunting the increases in heart rate and blood pressure during laryngoscopy and endotracheal intubation and is used liberally during the induction period. Arterial 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 of anesthesia. Administration of fluids intravenously (5 mL/kg), careful titration of anesthetics, and immediate treatment of hypotension are especially important. - Anesthesia is maintained with 50% N2O in O2 and low-dose (i.e., less than half the minimum alveolar concentration [MAC]) inhaled volatile anesthetics. Isoflurane is often preferred because fewer ischemic electroencephalographic (EEG) changes occur during carotid occlusion than with halothane or enflurane. 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. Sevoflurane is a good alternative because its critical rCBF in patients undergoing endarterectomy is similar to that determined with isoflurane152 and it may facilitate more rapid emergence.153 Additional opioid is rarely administered after skin incision. I do not use a cervical plexus block or request local anesthetic infiltration for skin incisions because the surgical stimulation is minimal and arterial blood pressure needs to be frequently supported. A combined remifentanil and propofol anesthetic technique has been reported but offered little advantage over inhaled anesthetics.154 - Despite only modest surgical stimulation, hemodynamic fluctuations are common during carotid endarterectomy. Arterial blood pressure and heart rate are controlled within predetermined and individualized ranges during the surgical procedure with short-acting drugs whenever possible (esmolol, phenylephrine, nitroglycerin, and sodium nitroprusside). Arterial 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 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. Arterial 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. Some 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 O2 requirements, as well as the risk for myocardial ischemia155 or infarction. The restrictive use of vasopressors for specific instances of cerebral ischemia has been advocated.156 In one report, induced hypertension during the period of carotid occlusion was not associated with myocardial ischemia.157 - Surgical manipulation of the carotid sinus with activation of the baroreceptor reflexes can cause abrupt bradycardia and hypotension. Cessation of surgical manipulation promptly restores the hemodynamics, and infiltration of the carotid bifurcation with 1% lidocaine usually prevents further episodes. Infiltration may, however, increase the incidence of both intraoperative and postoperative hypertension. I do not advocate routine infiltration of the carotid bifurcation.158 - With closure of the deep fascial layers in the neck, isoflurane is discontinued, N2O is increased to 70%, and ventilation is controlled manually. On application of the surgical dressings, drugs used to reverse neuromuscular blockade (i.e., neostigmine) are administered, and O2 is increased to 100%. At this time external stimuli to the patient are decreased by quieting the room, turning off the overhead surgical lights, and placing the patient in a head-up recumbent position. Ventilation is gently assisted until the patient exhibits spontaneous eye opening or movement. With rare exceptions, all tracheas are extubated after neurologic integrity is established. Neurologic deficits on emergence require immediate discussion with the surgeon about the need for angiography, reoperation, or both. 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. Greater hemodynamic stability and decreased pharmacologic intervention during emergence have been reported in patients undergoing carotid endarterectomy 2151with propofol versus isoflurane. In addition, a significantly less frequent incidence of myocardial ischemia on emergence was found in the propofol group than in the isoflurane group (1 of 14 versus 6 of 13). Of particular note, all patients with myocardial ischemia on emergence had systolic blood pressure higher than 200 mm Hg.

Regional techniques be delayed at least 12 to 24 hours after the last dose of A. Heparin B. LMWH C. Aspirin D. Plavix

B. Preoperative Preparation and Monitoring - Preoperative assessment and optimization of cardiac risk were discussed previously (see also Chapters 38 and 39). It is extremely important that long-term cardiac and respiratory medications be given the morning of surgery. Continuing chronic β-adrenergic blocker therapy is particularly important because acute withdrawal can be associated with significant morbidity. Current, recent, and anticipated use of hemostasis-altering drugs should be established and discussed with the surgical team. In most instances, antiplatelet therapy with aspirin should be continued. Preoperative termination of other antiplatelet therapy, such as thienopyridine derivatives, should be made on an individual basis. - Monitoring for lower extremity arterial revascularization should include an intraarterial catheter that permits continuous blood pressure monitoring to optimize coronary artery and lower extremity graft perfusion, as well as blood sampling for diagnostic laboratory testing. A urinary bladder catheter is usually indicated because the duration of the procedure may be long and urine output may be useful for assessing intravascular volume and cardiac output. Although central venous catheters are not necessarily helpful in routine cases, central venous pressure monitoring should be considered for patients with significant renal dysfunction, in whom intravascular volume should be carefully monitored, and for patients with significantly impaired ventricular dysfunction or congestive heart failure. In these patients, pulmonary artery catheter monitoring may be helpful, but given the relatively low potential for blood loss and third-space fluid loss with lower extremity vascular procedures, the pulmonary artery catheter is usually reserved for patients with active congestive heart failure or unstable angina. Our criteria for using invasive hemodynamic monitoring have been described previously.39 As discussed earlier, computerized ST-segment monitoring is helpful in monitoring for myocardial ischemia. Regional Versus General Anesthesia - The most appropriate regimen of intraoperative anesthesia and postoperative analgesia for high-risk patients undergoing vascular surgery remains controversial. Competing concerns regarding both the quality and escalating costs of perioperative care have challenged clinicians to establish practice standards that are both safe and efficient. Postoperative complications after vascular surgery are common and have an adverse impact on both clinical outcome and resource use. Improvement in clinical outcome and reduced use of medical resources in patients undergoing vascular surgery may result from the use of one particular regimen of anesthesia and analgesia over another. If such improvement can be achieved, selection of the most appropriate anesthetic and analgesic regimen would then be of great benefit to patients, providers, payers, and society. - The question of whether regional or general anesthesia is preferable for vascular surgery has been debated for years. Early nonrandomized trials were inadequately designed to answer the questions. They were prone to significant bias because many clinicians had the unsupported belief that regional anesthesia was safer for patients with advanced cardiac or pulmonary disease. Even the prospective studies must be interpreted cautiously because many suffer from deficiencies in design and methodology, including nonuniform patient populations,78,115,116 lack of 2143standardization or control of perioperative treatments,† use of nonequivalent modalities for postoperative pain relief,74,78,81,115-117 and possible investigator bias.‡ Many clinical trials have attempted to optimize the delivery and management of anesthetic techniques, which may mask the true risks associated with the anesthetic. An example is the strict hemodynamic control, transfusion thresholds, and postoperative analgesia regimens that have been used in clinical trials.39,40 The physician must also appreciate that the overall complication rates reported in clinical trials may seem high, but this may be explained by the aggressive surveillance commonly used in clinical trials. In general, it is often best to choose the anesthetic and analgesic techniques that are most familiar to a particular institution—for example, because unfamiliarity and mismanagement of epidural catheters can cause serious complications. I think that overall optimization of perioperative care, rather than anesthetic or analgesic selection, is the most important factor in improving outcome after vascular surgery. In some situations, one anesthetic technique (regional or general) is preferable to the other. The patient may have a preference for one technique over another based on multiple factors. Regional techniques should be avoided in patients who are uncooperative, demented, or unable to lie flat. Needle or catheter placement can be difficult in patients with severe spine deformity or previous spinal instrumentation. Local infection, neurologic disease affecting the lower part of the body, and hemostasis-altering drugs are all considered, to varying degrees, a contraindication to regional anesthesia. Anticoagulant and antiplatelet therapy is common in the vascular surgery population and often precludes the use of spinal or epidural techniques. Symptomatic bleeding within the neuraxis (spinal or epidural hematoma) is a potentially devastating complication of neuraxial anesthesia that can lead to permanent neurologic injury. I view preoperative anticoagulation with heparin or warfarin and any active thrombolytic therapy as contraindications to the use of spinal and epidural anesthesia. In patients in whom such agents have recently been discontinued, very careful consideration should be given on an individual basis before performing neuraxial techniques. The anesthesiologist must take into consideration the specific drug used, the duration of discontinuance, current coagulation status, and concomitant administration of medications affecting hemostasis. The use of regional techniques during intraoperative systemic heparinization does not appear to represent a significant risk. Although it has been recommended that surgery be canceled when blood is obtained through the neuraxial needle, support for this recommendation is lacking. Much more importantly, it has also been recommended that epidural catheters not be removed until anticoagulants have been discontinued in the postoperative period.118 The use of and indications for low-molecular-weight heparin (LMWH) continue to increase, and evidence suggests a significant risk for spinal or epidural hematoma when regional techniques are used in conjunction with these drugs. Current recommendations suggest that regional techniques be delayed at least 12 to 24 hours after the last dose of LMWH.118 The use of antiplatelet agents is a complex topic, and it is important to note the pharmacologic differences among the drugs when regional techniques are desired.118 Although some centers routinely check a bleeding time in patients who have taken aspirin in the 7 days before a planned regional anesthetic technique, no evidence indicates that bleeding time is useful in this setting. In general, when a regional technique is desired for a patient with any question of a coagulation abnormality, spinal anesthesia with the smallest diameter needle is preferable to epidural anesthesia. A comprehensive consensus report on neuraxial anesthesia and anticoagulation is available and should be read by all clinicians.118 - Given the relative risks associated with neuraxial anesthesia in patients receiving anticoagulant or antithrombolytic therapy, some clinicians advocate the broader use of peripheral nerve blocks, such as sciatic, femoral, popliteal, and ankle (see also Chapter 57). Continuous catheter techniques can be used to provide both anesthesia and postoperative analgesia. High-resolution ultrasound imaging of neural structures, percutaneous electrode guidance, and the use of stimulating catheters have been introduced into clinical practice. Peripheral nerve blocks are probably associated with fewer systemic and neuraxial side effects, but little clinical information is available in the vascular surgical population. Because of the large volume of local anesthetics frequently used for peripheral nerve blocks, the issue of systemic toxicity must be considered. Caution should be considered with the use of peripheral nerve block in an anticoagulated patient, particularly when the neural structures are deep or located in close proximity to vascular structures. - Because regional anesthesia does not require airway instrumentation, neuromuscular blocking agents, or volatile agents, it has traditionally been a prevailing belief that regional anesthesia is preferable in patients with significant pulmonary disease. Although it is true that instrumentation of the airway may precipitate bronchospasm or increase the risk for nosocomial infection, general anesthesia with endotracheal intubation does allow complete airway and ventilation control, the ability to effectively administer inhaled bronchodilators, and the ability to easily suction airway secretions. A reduction in time to extubation after aortic surgery is a fairly consistent theme with regional anesthesia and analgesia, but this does not appear to have any impact on clinically relevant pulmonary outcomes.40,74,78,83 - Epidural analgesia has been championed over parenteral opioid analgesia as a means of optimizing postoperative pulmonary function by improving pain control and respiratory muscle function. Although epidural analgesia can provide excellent postoperative pain control and may improve postoperative lung function (i.e., increased tidal volume and vital capacity), clinical studies do not support a consistent finding of improved pulmonary outcomes. Overall, little evidence from well-designed clinical studies exists to demonstrate improved pulmonary outcome with regional anesthesia and analgesia.119 Because postoperative maneuvers to increase mean lung volumes are of proved benefit in preventing postoperative pulmonary complications, it has been recommended that maneuvers to encourage deep breathing, such as deep-breathing 2144exercises, incentive spirometry, and chest physiotherapy, should be the focus of preventive efforts.119 - Cardiac morbidity is the most common cause of death in patients undergoing surgery, and the incidence of perioperative cardiac morbidity is 10 times more frequent in vascular surgery patients than in nonvascular surgery patients.5 Eleven prospective randomized trials evaluating the effects of regional versus nonregional anesthesia or analgesia in vascular surgical patients have reported on cardiac outcomes and death. Three studies (Bode and associates,117 Christopherson and co-workers,39 and Cook and colleagues,120) compared pure regional (spinal or epidural) versus general anesthetic techniques in lower extremity vascular patients. Tuman and colleagues116 compared combined epidural and general versus general anesthetics in aortic and lower extremity surgical patients. Six studies (Baron and co-workers,74 Bois and co-workers,80 Boylan and associates,83 Davies and associates,76 Garnett and colleagues,80 and Norris and colleagues40) compared epidural and nonepidural anesthetic or analgesic techniques (or both) in aortic surgical patients. Fleron and co-workers80 compared intrathecal opioid versus IV analgesia in aortic surgical patients. Of note, only the report by Norris and associates40 had a double-blinded design. The results of these studies, involving more than 1300 patients, are shown in Table 69-8. - In summary, no study demonstrated any difference in outcome with regard to mortality, MI, myocardial ischemia, or congestive heart failure. Only the study by Tuman and colleagues116 reported a difference in cardiac outcome. Outcome was significantly improved by epidural anesthesia and analgesia, but only when more subtle outcomes (i.e., dysrhythmias) were included. Christopherson and co-workers39 (i.e., the Perioperative Ischemia Randomized Anesthesia Trial [PIRAT]) and Norris and associates40 (i.e., PIRAT II) found no difference in cardiac events or myocardial ischemia as detected by continuous Holter monitoring over a 3-day postoperative period. In these studies from my institution, strict intraoperative and postoperative protocols were used to guide and optimize perioperative management and postoperative analgesia. Bode and colleagues117 described the largest randomized trial, which included a spinal anesthesia group in addition to general and epidural groups. There were no differences in cardiac events in any of the three groups. Of note, a failed spinal or epidural technique in this trial was associated with 9% mortality, as opposed to 2% for all successful general and regional anesthetics.116 - One of the most interesting and clinically significant findings in these randomized trials is the beneficial effect of regional anesthesia on lower extremity graft patency in the postoperative period. Two of the studies (Tuman and colleagues116 and Christopherson and co-workers39) reported a fivefold greater incidence of graft occlusion after general (relative to regional) anesthesia. Most graft occlusions occurred in the first 1 to 3 days after surgery, after which the established difference in the incidence of graft occlusion between anesthetic techniques was maintained over time (6 weeks and beyond) (Fig. 69-15). This time course suggests that anesthetic technique may have played a role in graft occlusion. Bode's group121 reported an overall very low incidence of graft occlusion, but differences in hemodynamic management, surgical technique, and the patient population may explain these findings. For example, intraoperative intravascular angioscopy was used to inspect the grafts to confirm patency before completion of surgery, and all patients were cared for in an intensive care setting for 48 hours after surgery. Thus, optimization of care with respect to graft patency may negate any beneficial effect of regional techniques. It is also important to keep in mind that none of these studies were specifically designed to evaluate surgical outcome (i.e., graft patency) 2145in a prospective manner. A retrospective review of more than 300 primary femoropopliteal-tibial bypass procedures reported no differences in graft thrombosis rates for epidural (14%) or general anesthesia (9.4%).122 - The proposed mechanism for the benefit of regional anesthesia is the effect of the anesthetic technique on coagulation. General anesthesia is associated with a hypercoagulable state in the early postoperative period, whereas regional anesthesia attenuates this effect. Tuman and colleagues116 demonstrated this by thromboelastography and Rosenfeld and co-workers123 by increased plasminogen activator inhibitor (Fig. 69-16) and fibrinogen levels. Fibrinolysis is decreased after general anesthesia and is normal after regional anesthesia. These findings may be related to attenuation of the surgical stress response with regional anesthesia because a link appears to exist among stress, catecholamines, and acute-phase reactants, such as plasminogen activator inhibitor and fibrinogen.123-125 Platelet reactivity is also enhanced in the presence of a stress response.125 Another important mechanism for the increased lower extremity graft patency with regional anesthesia may be the increased lower extremity blood flow associated with sympathectomy. - In the postoperative period, Breslow and associates126 demonstrated differences in the adrenergic response with general versus regional anesthesia (Fig. 69-17). Epinephrine and norepinephrine are increased after general anesthesia relative to regional anesthesia. The cortisol response after general anesthesia is also greater than after regional anesthesia.126 This stress response is associated with increased blood pressure and hemodynamic liability during the intraoperative and early postoperative periods after general anesthesia compared with regional anesthesia.40,127 When the hemodynamic parameters are controlled pharmacologically, however, no difference is found related to anesthetic technique in myocardial ischemia or cardiac morbidity.39,40,117 - Postoperative pain is recognized as one of the many factors contributing to the surgical stress response. In studies comparing epidural analgesia with parenteral opioid analgesia for control of postoperative pain after major surgery, improved pain control with epidural techniques is often reported. A recent meta-analysis review supports the view that epidural analgesia provides better postoperative analgesia than parenteral opioids.128 However, the historical studies that form the basis of the meta-analysis review have often neglected to control, specify, and, most importantly, optimize treatment in the nonepidural arms of their studies. Unfortunately, this issue remains a significant limitation in more recent trials.78,129 Epidural analgesic techniques will probably continue to outperform "suboptimal" nonepidural analgesic techniques. I believe that IV patient-controlled analgesia is the optimal mode of delivery for opioid analgesia and should be used as the nonepidural arm for all postoperative pain studies. Postoperative epidural analgesia does not consistently outperform IV patient-controlled opioid analgesia. Of particular note, patient-controlled epidural analgesia outperforms both intermittent-bolus and continuous-infusion epidural analgesia. Thus, the mode of delivery is an important factor with both epidural and parenteral opioid analgesia. The clinician also needs to keep in mind that the superior pain control reported with epidural techniques is relative, with adequate pain control consistently reported for parenteral analgesia. In the only double-blinded trial in vascular surgery patients, Norris and colleagues40 reported no difference in postoperative pain scores in patients randomized to either patient-controlled epidural analgesia or 2146patient-controlled IV analgesia after aortic surgery. In this trial, postoperative pain management (i.e., epidural and IV) was optimized, continued for 72 hours, and managed by an acute pain service. Postoperative epidural catheter failure may occur in up to 6% of patients.

Which of the following is the most reliable method of neuroprotection from ischemic injury. during aortic cross clamping A. CSF drainage B. Hypothermia C. Barbiturates D. Corticosteroids

B. Anesthetic Technique - No single anesthetic technique is best for TAA repair. Usually, balanced anesthesia is provided with a combination of an opioid, a low-dose potent volatile anesthetic, a benzodiazepine, and a muscle relaxant. A total IV technique may be optimal if transcranial MEP monitoring is used. Induction of general anesthesia should be slow and controlled. Hypertension should be avoided because acute stress on the aneurysm can cause rupture. The heart rate should be maintained at or below baseline because myocardial ischemia is often related to the heart rate. Extubation should always take place in the ICU and only after a significant period of hemodynamic and metabolic stability. The postoperative analgesic regimen should focus on pain control and stable hemodynamics. Spinal Cord Ischemia and Protection - Paraplegia is a devastating complication of aortic surgery. The incidence of paraplegia is reported to be 0.5% to 1.5% for coarctation repair, 0% to 10% for thoracic aneurysm repair, 10% to 20% for thoracoabdominal repair, and as high as 40% for extensive dissecting TAA repair. The spinal cord receives its blood supply from two posterior arteries (≈25%) and one anterior spinal artery (≈75%) (Fig. 69-12). The posterior spinal arteries, which supply the sensory tracts in the spinal cord, receive flow from the posterior and inferior cerebellar arteries, the vertebral arteries, and the posterior radicular arteries. The anterior spinal artery, which supplies the motor tracts in the spinal cord, is formed by two branches of the intracranial portion of the vertebral arteries. The upper cervical segment of the spinal cord receives most of its blood flow from the vertebrals. The thoracic portion of the anterior 2133spinal artery is supplied by the anterior radicular arteries (one or two cervical, two or three thoracic, and one or two lumbar). The largest of the radicular arteries is called the great radicular artery (GRA) or the artery of Adamkiewicz. The GRA is the major blood supply to the lower two thirds of the spinal cord. The segmental supplier of the GRA is variable (T5-L5) but is located between T9 and T12 in approximately 75% of cases. The variation in origin of the GRA explains why even infrarenal aortic aneurysm repair is associated with a 0.25% incidence of paraplegia. The specific impact of extensive segmental artery sacrifice on spinal cord perfusion during TAA repair is poorly understood. - Various methods can facilitate preventing ischemic injury to the spinal cord. Distal aortic perfusion with extracorporeal support reduces the incidence of paraplegia. Any of the various methods of distal bypass are likely to be beneficial when the anticipated cross-clamp time is longer than 30 minutes, but they are probably not beneficial when cross-clamp time is less than 20 minutes. CSF drainage is frequently used to improve spinal cord perfusion during TAA repair and is often used in combination with distal aortic perfusion. Spinal cord perfusion pressure is defined as distal mean aortic pressure minus CSF pressure or central venous pressure, whichever is greatest. Autoregulation of spinal cord blood flow is similar to cerebral autoregulation, and blood flow is relatively constant over the range of 50 to 125 mm Hg. During hypoxia or hypercapnia, autoregulation is lost, and flow becomes linearly related to perfusion pressure. Thus, significant flow may remain even at very low perfusion pressure. Drainage of CSF is important because CSF pressure often increases (by 10 to 15 mm Hg) with cross-clamping of the descending thoracic aorta. The increase in CSF pressure reduces spinal cord perfusion pressure and increases the likelihood of ischemic spinal cord injury. Despite evidence from animal studies that CSF drainage protects the spinal cord, clinical use of this technique is controversial. One randomized trial reported a reduced incidence of paraplegia, but another reported no benefit. Most of the evidence in support of CSF drainage comes from nonrandomized historical cohort studies in which the technique is used in combination with other adjuncts, such as intrathecal papaverine and hypothermic partial bypass. Coselli and colleagues88 offered the strongest evidence supporting the efficacy of CSF drainage. They conducted a prospective, randomized clinical trial to evaluate the impact of CSF drainage on the incidence of spinal cord injury after Crawford type I and II TAA repair. CSF drainage resulted in an 80% reduction in the relative risk for a postoperative deficit. Nine patients in the control group (13%) had paraplegia or paraparesis versus only two patients in the CSF drainage group (2.6%). Left heart bypass, moderate heparinization, permissive mild hypothermia, and reimplantation of patent intercostal and lumbar arteries were performed in both treatment groups. The target CSF pressure was 10 mm Hg. CSF drainage also reverses delayed-onset neurologic deficit after open and endovascular TAA repair.89 - Although CSF drainage is widely used during TAA repair, it has risks. Potential complications include headache, meningitis, chronic CSF leakage, spinal or epidural hematoma, and subdural hematoma. The possibility of intraspinal pathologic processes should be considered in any patient with a postoperative lower extremity neurologic deficit. A retrospective review of 230 patients who underwent TAA repair with CSF drainage at my institution reported eight subdural hematomas (3.5%).90 High-volume CSF drainage was identified as a risk factor for its occurrence. Six patients had subdural hematomas detected during hospitalization, with an associated mortality of 67%. Two patients were seen in a delayed fashion, and both required an epidural blood patch to control chronic CSF leakage. 2134 Hypothermia is probably the most reliable method of neuroprotection from ischemic injury. By reducing O2 requirements by approximately 5% for each degree centigrade, a twofold prolongation of tolerated cross-clamp time is achieved by cooling even to mild hypothermia (34° C). Because the reduction in metabolic rate is linearly related to temperature, moderate or profound hypothermia provides even greater protection. Both systemic and regional spinal cord cooling is beneficial. Systemic hypothermia can been achieved with either full cardiopulmonary bypass (with or without DHCA) or partial bypass. Cooling to 30° to 32° C with left atrial-to-femoral bypass in conjunction with CSF drainage was associated with no permanent neurologic sequelae in a series of 20 patients despite a relatively long average cross-clamp time (≈70 minutes).91 My colleagues and I have since used this technique in more than 600 patients cooled to 32° C, with a 5% incidence of paraplegia. Although some risk is incurred when a beating heart is subjected to moderate hypothermia, the benefits appear to outweigh the risks. Supraventricular and ventricular dysrhythmias respond well to cardioversion or mild warming to 33° to 34° C. Regional cooling of the spinal cord by cold perfusion of the GRA with blood or crystalloid provides significant protection during spinal ischemia in animal models. Regional cooling is beneficial in humans who received epidural infusions of 4° C saline. Even if active cooling is not used, it is advantageous to allow patients to passively cool to 33° to 34° C during TAA repair. With passive cooling, the challenge is rewarming after the surgical repair. This is most easily accomplished with the use of a forced-air blanket over the upper part of the body. The lower body region should not be actively warmed because warming ischemic tissue increases metabolic requirements, acidosis, and ischemic injury. - Many drugs have been studied in an attempt to reduce the incidence of ischemic spinal cord injury. Barbiturates provide significant protection. Corticosteroids provide protection in dogs but were beneficial in humans only when they were combined with CSF drainage. Calcium channel blockers were not consistently shown to be protective against spinal cord ischemia. N-methyl-D-aspartate (NMDA) receptor antagonists have been investigated because ischemic injury appears to be related to increased levels of excitatory amino acids (particularly glutamate), which allow increased permeability to Ca2+ ions and high intracellular Ca2+ concentrations. Dextrorphan (a noncompetitive NMDA receptor antagonist) shows promise during spinal cord ischemia. Magnesium, another NMDA receptor antagonist, improves recovery from spinal cord ischemia in rat and dog models when administered intrathecally. Naloxone is protective in patients with traumatic spinal cord injuries and in a rabbit model of spinal ischemia. Naloxone also shows promise when combined with CSF drainage in patients undergoing TAA repair. Intrathecal papaverine appears to be protective, especially when combined with CSF drainage. Other agents under investigation include levosimendan, allopurinol, adenosine, ziconotide, activated protein C, and desferrioxamine. Other than the use of corticosteroids and naloxone at a few centers, most of these agents are considered investigational - Preoperative spinal cord angiography has been used in patients with TAA. The rationale for this highly invasive angiographic procedure is that precise identification of intercostal arteries giving rise to the GRA will allow focused reimplantation of these vessels during surgical repair and help prevent spinal cord injury. Selective intercostal angiography identifies the GRA when an intercostal branch is found making a cephalad hairpin turn to enter the spinal canal and supply a midline longitudinal artery (i.e., the anterior spinal artery) (Fig. 69-13). The GRA can be identified in 43% to 86% of patients studied with traditional angiography. Higher detection rates for GRA localization have been reported with computed tomographic angiography (CTA) and magnetic resonance angiography (MRA), with the latter achieving rates of nearly 100%.92 2135 - The importance of reimplanting the intercostal arteries identified as supplying the GRA is not universally accepted. Even in patients with an identified and reimplanted GRA, spinal cord injury is not always prevented. Some investigators have concluded that preoperative localization of the GRA has little impact on neurologic outcome after TAA repair. A report from my institution93 found no improvement in overall neurologic outcome with preoperative spinal cord angiography, but it offered important insight regarding the type of aneurysm, identification of the GRA, and neurologic outcome. In patients undergoing TAA repair for extensive degenerative aneurysms, spinal cord injury occurred in 0 of 45 patients versus 10 (12%) of 81 patients with and without an identified GRA, respectively. In contrast, identification of the GRA was not helpful in the case of chronic expanding aortic dissection, with 3 (15%) of 20 patients versus 3 (6%) of 49 patients suffering spinal cord injury with and without an identified GRA, respectively. The investigators hypothesized that mural thrombus in degenerative aneurysms results in the occlusion of many intercostal arteries and favors the development of extensive paravertebral collateral channels (see Fig, 69-13). Identification of a GRA allows focused reimplantation with uniform success. In patients with chronic dissection, most intercostal arteries are patent, collateralization is minimal, and reimplantation of one or two intercostal arteries may be insufficient to supply blood flow to the spinal cord. This collateral blood supply concept is further supported by clinical studies demonstrating that clamping the segmental supplier to the GRA during TAA repair does not produce critical spinal cord ischemia in the majority of patients.94 Sufficient collateral blood supply, independent of the GRA, must therefore exist to maintain spinal cord integrity. - Delayed-onset neurologic deficits are common after TAA repair.95 In a large series of 2368 TAA repairs, 93 (3.9%) patients had postoperative paraplegia or paraparesis, 34 (37%) of whom initially had intact spinal cord function but a deficit developed later.96 Preoperative renal dysfunction, acute dissection, and extent type II TAA are significant predictors of delayed neurologic deficit. Postoperative hypotension and CSF drain malfunction may play an important role in the development of these deficits. Neurologic function can frequently be recovered by maintaining an optimal arterial blood pressure and CSF drainage.

This is done during carotid endarterectomy are obtained by IV or ipsilateral carotid artery injection of radioactive xenon and analysis of decay curves obtained from detectors placed over the area of the ipsilateral cortex supplied by the middle cerebral artery. A. Carotid artery stump pressure B. Regional cerebral blood flow C. EEG D. SSEP E. TUD F. Cerebral oxygenation

B. Regional Cerebral Blood Flow - rCBF measurements during carotid endarterectomy are obtained by IV or ipsilateral carotid artery injection of radioactive xenon and analysis of decay curves obtained from detectors placed over the area of the ipsilateral cortex supplied by the middle cerebral artery. Measurements are typically obtained before, during, and immediately after carotid clamping. This technology, combined with the EEG monitoring, has provided important insight into the relationship between rCBF and EEG evidence of cerebral ischemia and the critical rCBF associated with various anesthetics.168,169 The critical rCBF varies depending on the volatile anesthetic used. In patients receiving N2O plus a volatile anesthetic, rCBF is approximately 20, 15, 10, and 10 mL/100 g of brain tissue per minute for halothane, enflurane, isoflurane, and sevoflurane, respectively.152,168,169 The expense and the expertise required to make and interpret these blood flow measurements have limited the use of this technology to only a few centers. Electroencephalography - Many centers advocate intraoperative use of EEG monitoring for the detection of cerebral ischemia and subsequent selective shunting (see also Chapter 49). The full 16-channel strip-chart EEG and the processed (compressed spectral array) EEG monitor are used for this purpose. Although the processed EEG monitor is more easily interpreted, it is less sensitive than the raw EEG monitor. Significant ischemic EEG changes occur in 7.5% to 20% of monitored patients during carotid clamping under general anesthesia. Significant EEG changes occur more frequently in patients with contralateral carotid disease than in those without (14.3% versus 5.1%). The presence of a contralateral carotid occlusion may increase the rate of significant ischemic EEG changes to nearly 50% during carotid clamping. Because contralateral occlusion is highly predictive of ischemic EEG changes with carotid clamping, it has been recommended that EEG monitoring be eliminated in this circumstance. Ischemic EEG changes may also be seen with shunt malfunction, hypotension, or cerebral emboli. - When the electroencephalogram is used for cerebral ischemia monitoring during carotid endarterectomy, a stable physiologic and anesthetic milieu is mandatory. Isoflurane, desflurane, and sevoflurane produce similar ECG changes at equipotent levels and, when used at 0.5 MAC, allow for reliable ECG cerebral ischemia monitoring. The clinical usefulness of intraoperative EEG monitoring for ischemia during carotid endarterectomy is limited by several factors. First, it may not detect subcortical or small cortical infarcts. Second, false-negative results (i.e., neurologic deficit with no ischemic EEG changes intraoperatively) are not uncommon. Patients with preexisting stroke or reversible neurologic deficits may have a particularly high incidence of such results. Third, EEG monitoring is not specific for ischemia and may be affected by changes in temperature, blood pressure, and anesthesia depth. Fourth, false-positive results (i.e., no perioperative neurologic deficit with significant ischemic EEG changes intraoperatively) occur because not all cerebral ischemia uniformly proceeds to infarction. Finally, intraoperative EEG monitoring is inherently limited because most intraoperative strokes are thought to be thromboembolic and most perioperative strokes occur postoperatively. At present, no consistent data demonstrate that EEG monitoring is clearly superior to other methods of intraoperative cerebral monitoring or that the use of EEG monitoring improves outcome.

Which of the following should be maintained during CEA as anesthetic management A. Hypercapnia B. Hypocapnia C. Hyperglycemia D. Hypoglycemia

B. Carbon Dioxide and Glucose Management - Cerebrovascular CO2 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 CO2. Impaired cerebrovascular reactivity to hypercapnia may play a role in the development of stroke ipsilateral to carotid stenosis or occlusion. Although one might expect that impaired CO2 reactivity would increase the risk for cerebral ischemia after carotid artery clamping, the results of intraoperative cerebral monitoring suggest that no such relationship exists. Impaired cerebrovascular reactivity to CO2 will significantly improve after carotid endarterectomy. - Control of ventilation and CO2e 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, little clinical evidence exists for this "reverse" steal effect. Additionally, experimental data do not support the use of hypocapnia as a therapeutic maneuver to produce a favorable redistribution of blood flow during focal cerebral ischemia. Indeed, in this animal model of focal cerebral ischemia, hypocapnia (PaCO2 of 23 mm Hg) actually increased the size of the region at risk for ischemia. It is therefore common practice to maintain normocapnia or mild hypocapnia during carotid endarterectomy. - Evidence demonstrates increased ischemic injury to neural tissue when ischemia occurs in the presence of hyperglycemia. Data from The Johns Hopkins Hospital found that operative-day glucose greater than 200 mg/dL at the time of carotid endarterectomy was associated with an increased risk for perioperative stroke or transient ischemic attack, MI, and death.147 Thus, until additional data become available, it may be beneficial to maintain a blood glucose level below 200 mg/dL in patients undergoing carotid endarterectomy. If hyperglycemia is treated with insulin preoperatively or intraoperatively, the blood glucose level should be carefully monitored, especially during general anesthesia, to avoid the dangers of hypoglycemia.

A dilutional coagulopathy in which platelets become deficient after approximately one blood volume of replacement develops during A. Massive fluid resuscitation B. Massive transfusion C. Massive plasma transfusion D. Desmopressin therapy

B. Coagulation and Metabolic Management - Coagulopathy is a frequent complication during TAA repair. A dilutional coagulopathy in which platelets become deficient after approximately one blood volume of replacement develops during massive transfusion (see also Chapters 61 and 62). At between one and two blood volumes of replacement, coagulation factors are diluted to levels low enough to increase bleeding. Other contributing factors are residual heparin; ischemia of the liver, in which most coagulations factors are produced; and persistent hypothermia after weaning from bypass. With the early use of fresh frozen plasma and platelets, severe coagulopathy often can be avoided. The prothrombin time, partial thromboplastin time, fibrinogen level, and platelet count should be measured frequently. Cryoprecipitate may be necessary to correct coagulopathy, especially when the prothrombin time and partial thromboplastin time are prolonged and hypervolemia prevents the administration of significant volumes of fresh frozen plasma. When coagulopathy persists despite these efforts, ε-aminocaproic acid is beneficial as antifibrinolytic therapy, and desmopressin can be given to increase circulating levels of von Willebrand factor and factor VIII. Normothermia should be achieved by complete rewarming before separation from bypass, by increasing ambient temperature after separation from bypass, and by forced-air warming over the upper body skin surface. - Analysis of arterial blood gases and electrolyte levels should be performed frequently. Sodium bicarbonate should be given to treat the metabolic acidosis that occurs during and after cross-clamping. Hyperkalemia should be treated aggressively, especially in oliguric or anuric 2136patients. Calcium chloride and sodium bicarbonate are the primary acute treatments of hyperkalemia.

This appear to be the major mechanism of perioperative neurologic complications and most occur in the postoperative period in CEA A. Hemodynamic factor B. Thromboembolic

B. Postoperative Considerations - Most neurologic complications (transient and permanent) after carotid endarterectomy are explained by intraoperative embolization, hypoperfusion during carotid clamping, and postoperative embolization or thrombosis from the endarterectomy site. It is generally accepted that most neurologic complications are related to surgical technique. Thromboembolic (rather than hemodynamic) factors appear to be the major mechanism of perioperative neurologic complications and most occur in the postoperative period. Neurologic complications attributable to carotid artery thrombosis may occur with an incidence as frequent as 3.3% and are associated with a high rate of major stroke or death despite immediate operative intervention. Other important, but less common neurologic complications include intracerebral hemorrhage and cerebral hyperperfusion. The reported incidence of intracerebral hemorrhage after carotid endarterectomy ranges from 0.4% to 2.0%. Most intracerebral hemorrhages occur 1 to 5 days after the operation and are associated with significant morbidity and mortality. - Hypertension is common in the postoperative period after carotid endarterectomy. Not surprisingly, patients with poorly controlled preoperative hypertension often have severe hypertension postoperatively. The causes are not well understood, but surgical denervation of the carotid sinus baroreceptors is probably contributory. Regional anesthesia is associated with less hypertension. Other causes of postoperative hypertension, such as hypoxemia, hypercapnia, bladder distention, and pain, should be excluded or treated. Because neurologic and cardiac complications may be associated with postoperative hypertension, blood pressure should be aggressively controlled to near preoperative values after surgery. Short-acting drugs are the safest and most effective. Patients with persistent hypertension can be converted to longer-acting IV or oral agents before discharge from the ICU. Postoperative cerebral hyperperfusion syndrome is an abrupt increase in blood flow with loss of autoregulation in the surgically reperfused brain and is manifested as headache, seizure, focal neurologic signs, brain edema, and possibly intracerebral hemorrhage. Unfortunately, little is actually known about the cause and management of this syndrome. Typically, this syndrome does not occur until several days after carotid endarterectomy. Patients with severe postoperative hypertension and severe preoperative internal carotid artery stenosis are believed to be at increased risk for this syndrome. However, more recent data do not corroborate this common belief and suggest that recent contralateral carotid endarterectomy may be predictive of cerebral hyperperfusion.171 Postoperative hypotension occurs almost as frequently as hypertension after carotid endarterectomy. Carotid sinus baroreceptor hypersensitivity or reactivation probably plays an important role. Postoperative hypotension may be more common after regional anesthesia. To avoid cerebral and myocardial ischemia, hypotension should be corrected promptly. Cardiac output is frequently normal or elevated and systemic vascular resistance reduced in hypotensive patients after carotid endarterectomy. Intensive surveillance for evidence of myocardial and cerebral ischemia and judicious use of fluids and vasopressors are recommended for postoperative hypotension. In most cases the hypotension resolves over a period of 12 to 24 hours. - Cranial and cervical nerve dysfunction after carotid endarterectomy is well documented in the literature. Although most injuries are transient, permanent injuries can lead to significant disability. Patients should be examined for injury to the recurrent laryngeal, superior laryngeal, hypoglossal, and marginal mandibular nerves shortly after extubation. Unilateral recurrent laryngeal nerve injury may result in ipsilateral true vocal cord paralysis in the paramedian position. Although most patients have hoarseness and an impaired cough mechanism, the injury is usually well tolerated. However, bilateral recurrent laryngeal nerve injury and resultant bilateral vocal cord paralysis can result in life-threatening upper airway obstruction. This situation must be anticipated in 2155patients who have previously undergone contralateral carotid endarterectomy or neck surgery. Carotid body denervation may occur after carotid endarterectomy as a result of surgical manipulation. Unilateral loss of carotid body function may result in an impaired ventilatory response to mild hypoxemia and is rarely of clinical significance. Bilateral carotid endarterectomy is associated with loss of the normal ventilatory and arterial pressure responses to acute hypoxia and an increased resting partial pressure of arterial CO2. In this situation, the central chemoreceptors are the primary sensors for maintaining ventilation, and serious respiratory depression may result from opioid administration. Fortunately, most patients require little more than acetaminophen or ketorolac for postoperative pain. Wound hematoma probably occurs more frequently than reported in the literature. In the North American Symptomatic Carotid Endarterectomy Trial,136 5.5% of patients had wound hematomas. Most cases are the result of venous oozing and require little more than external compression for 5 to 10 minutes. Expanding hematomas require prompt evaluation at the bedside and immediate evacuation if airway compromise is evident. Aggressive postoperative blood pressure control may help reduce the incidence of hematoma. - Although some clinicians believe that intensive care monitoring is not routinely required after carotid surgery, a significant number of patients do require intensive monitoring and active intervention. I think all patients should be monitored in an intensive care setting for at least 8 hours after carotid endarterectomy, because most events requiring intervention occur within this timeframe.172,173

What is the safe limit for deep hypothermic circulatory arrest A. 30 min B. 60 min C. 90 min D. 120 min

C. Deep Hypothermic Circulatory Arrest - Complex aneurysms involving the aortic arch often require elective cardiopulmonary bypass with an interval of deep hypothermic (15° C) circulatory arrest (DHCA) because cerebral blood flow is transiently interrupted during surgery (see also Chapter 67). Bypass can be accomplished by cannulation of the femoral artery and the femoral vein (i.e., femoral-femoral bypass). During the interval of DHCA, some centers also use anterograde (i.e., innominate artery) or retrograde (i.e., internal jugular vein) selective cerebral perfusion with cold oxygenated blood to extend the safe maximum duration of circulatory arrest. Without this technique, 45 to 60 minutes is thought to be the safe limit of DHCA, but 90 minutes has been reported with selective cerebral perfusion. - DHCA also may be necessary whenever the location, extent, or severity of aortic disease precludes placement of a proximal aortic clamp during thoracic or thoracoabdominal aortic repair. This is often the case in patients with previous aortic arch repair, in which adhesions and scarring make application of the proximal aortic cross-clamp difficult or impossible during TAA repair. DHCA eliminates the need for proximal aortic clamping and allows a bloodless field for the proximal aortic anastomosis. Some centers advocate the routine use of DHCA during complex aortic reconstruction because deep hypothermia may provide better end-organ and spinal cord function. This potential benefit must be carefully weighed against the risks associated with prolonged cardiopulmonary bypass and circulatory arrest. After completion of the proximal anastomosis and intercostal artery-to-graft anastomoses under DHCA, the aortic graft is cannulated and bypass flow is reestablished to the upper part of the body. During a period of hypothermic low bypass flow, the distal anastomoses are completed and then rewarming is initiated.

Which of the following is the most common cause of peripheral arterial disease. A. Embolism B. Thromboangitis obliterans C. Atherosclerosis D. Fibromuscular dysplasia

C. Lower Extremity Revascularization - Lower extremity arterial insufficiency, or peripheral arterial disease, is a common condition that affects as many as 10 million people in the United States, and its incidence is increasing annually. Because individuals with lower extremity peripheral arterial disease are most often asymptomatic or have symptoms other than classic intermittent claudication, the true prevalence of the disease is unknown. In a population-based study of individuals 55 years of age and older, the prevalence of peripheral arterial disease was 19.1% (16.9% in men and 20.5% in women). The prevalence of peripheral arterial disease in primary care practices in the United States is frequent (29%), and the condition is often unrecognized (44%). Arterial disease of the upper extremity does occur but is much less common than lower extremity involvement. - Atherosclerosis is the most common cause of peripheral arterial disease. Risk factors for atherosclerosis of the lower extremity are the same as for other vascular areas and include advanced age, male sex, hypertension, smoking, hyperlipidemia, and diabetes. Infrainguinal atherosclerosis may involve the femoral artery, popliteal artery, and any of the infrapopliteal arteries. The superficial femoral artery is the most common site of major atherosclerotic involvement below the inguinal ligament. Nonatherosclerotic causes of peripheral arterial disease include embolism, thromboangiitis obliterans (Buerger disease), immune arteritis, radiation arteritis, giant cell arteritis, adventitial cystic disease, fibromuscular dysplasia, and homocysteinemia. - As previously noted, peripheral arterial disease is a very strong indicator of generalized atherosclerosis and is a risk marker for other vascular conditions, including CAD, cerebrovascular disease, and aneurysmal disease. For example, patients with concomitant CAD and peripheral arterial disease have a higher prevalence of triple-vessel coronary disease than do patients with CAD alone. Additionally, over 20% of patients with peripheral arterial disease have a 70% or greater carotid artery stenosis. It is well documented that patients with peripheral arterial disease are at higher risk for cardiovascular morbidity and mortality than individuals without peripheral arterial disease. The increased cardiovascular risk may not be entirely due to atherosclerosis because these patients may have an enhanced prothrombotic state secondary to platelet activation113 and a high prevalence of diverse hypercoagulable states.114 The natural history of atherosclerotic lower extremity peripheral arterial disease is illustrated in Figure 69-14.

Acute ischemia needs to be evaluated rapidly because irreversible tissue injury can occur within how many hours A. 1-3 B. 2-4 C. 3-5 D. 4-6

D. Acute Arterial Occlusion - Acute peripheral arterial occlusion occurs primarily as a result of embolism and thrombosis. Pseudoaneurysm after invasive procedures in which the femoral artery is cannulated is a much less common cause of acute ischemia. The vast majority of emboli to the lower extremity originate in the heart, with intermittent atrial fibrillation and myocardial infarction being the most common causes of emboli. Although rheumatic heart disease is now a rare cause of embolic occlusion, prosthetic heart valves may be a source of emboli. Other causes of embolization include bacterial endocarditis, atrial myxoma, paradoxical venous emboli, and atheromatous debris from proximal aneurysms. Arterial emboli often lodge at vessel bifurcations. Common sites in the lower extremity include the femoral artery bifurcation, iliac artery bifurcation, and popliteal artery. - Thrombotic occlusions probably outnumber embolic occlusions by a ratio as high as 6:1. Acute arterial thrombosis of native vessels almost always occurs in the setting of severe and long-standing atherosclerosis. It can be viewed as the terminal event in the progression of atherosclerosis. Thrombosis of vascular bypass grafts is common and may result in acute ischemia. The high prevalence of diverse hypercoagulable states in patients with peripheral arterial disease may predispose such patients to thrombosis.114 The clinical computed tomography manifestation of acute arterial occlusion varies depending on the location of the obstruction and the extent of collateral circulation. In patients with a sudden onset of acute extremity ischemia, the occlusion often occurs abruptly and without the preexisting development of collateral pathways. Although ischemic symptoms are often more severe in patients with embolic occlusion than in patients with thrombotic occlusion, differentiation between embolic and thrombotic occlusion may be difficult. Acute occlusion of a previously patent extremity artery is a dramatic event characterized by pulselessness, pain, pallor, paresthesia, and paralysis (the five Ps). Absence of pulses and pallor are early manifestations. The sudden onset of pain is very common, and it may be intense. Motor weakness and paresthesia are usually late manifestations of severe ischemia. - Acute ischemia needs to be evaluated rapidly because irreversible tissue injury can occur within 4 to 6 hours. Initial management usually involves immediate anticoagulation to prevent propagation of thrombus, stabilization and control of coexisting medical conditions, and arteriography. Immediate surgical revascularization is generally indicated in the profoundly ischemic extremity. Patients with embolization to a nonatherosclerotic extremity are frequently managed with femoral thromboembolectomy under local anesthesia. Management of patients with peripheral arterial disease who are suspected of having thrombotic occlusion requires arteriography to determine the severity and anatomic location of the occlusion. Angioplasty or thrombolytic therapy may be performed in conjunction with arteriography. Intraarterial thrombolysis is often used as an initial intervention in an effort to unmask the culprit lesion responsible for the occlusive event. Patients are frequently scheduled for lower extremity bypass surgery the following day, pending evaluation of lower extremity blood flow. The frequent use of heparin anticoagulation and thrombolytics has significant implications for the anesthesiologist because regional anesthesia is not an option in an anticoagulated patient. 2141Morbidity and mortality rates in this patient population are frequent, particularly in patients requiring significant operative intervention.

This is the most common peripheral vascular surgical procedure performed in the United States A. AAA B. FEM-POP C. EVAR D. CEA

D. Indications - Endarterectomy of the carotid bifurcation has been used to reduce symptoms and prevent stroke for more than 50 years. Although the efficacy of carotid endarterectomy for prevention of ipsilateral stroke in patients with and without symptoms has been demonstrated in large-scale randomized clinical trials,136,137 multiple factors including perioperative risk, comorbidities, and life expectancy must be considered in the overall assessment. In centers of excellence, it is a low-risk procedure with excellent long-term durability. Carotid endarterectomy is the most common peripheral vascular surgical procedure performed in the United States, with an estimated 130,000 procedures performed annually. The rate and number of carotid endarterectomies have fluctuated significantly since the early 1970s. With marked growth in the specialty of vascular surgery and an expanding list of surgical indications, the number of carotid endarterectomies performed in nonfederal hospitals increased from 15,000 in 1971 to 107,000 in 1985 and then declined substantially over the next 5 to 6 years. The decline was probably due to publications questioning the indications for the procedures and isolated reports citing excessively frequent rates of operative morbidity and mortality. - In 1992, a marked increase in the number of carotid endarterectomies occurred after the results of two large-scale, prospective randomized trials were published. The North American Symptomatic Carotid Endarterectomy Trial (NASCET) and the European Carotid Surgery Trial both reported definitive results for symptomatic patients with high-grade carotid stenosis (70% to 99%).136,138 In NASCET, follow-up at 2 years showed a stroke rate for surgical patients of 9% versus 26% for medical patients. This 2148benefit of carotid endarterectomy has persisted at 8 years of follow-up.139 In the European Carotid Surgery Trial, the long-term stroke rate was 2.8% for surgical patients, excluding a perioperative stroke and death rate of 7.5%, and 16.8% for medically managed patients. The efficacy of carotid endarterectomy in asymptomatic patients with carotid stenosis has been evaluated in five randomized trials.137,140-143 The Carotid Artery Surgery Asymptomatic Narrowing Operation Versus Aspirin trial, the first to publish its results, concluded that carotid endarterectomy was not indicated for asymptomatic patients with 50% to 90% carotid stenosis.140 Unfortunately, this study was seriously flawed and the results questioned. The Mayo Asymptomatic Carotid Endarterectomy Study was terminated early because of a significantly increased number of MIs and transient cerebral ischemic events in the surgical group.141 Most of these events were not related to the surgery itself but rather to the absence of aspirin in the surgical group. The Department of Veterans Affairs trial was designed to compare the effects of carotid endarterectomy plus aspirin versus medical treatment (i.e., aspirin) in asymptomatic male patients with 50% or greater carotid stenosis.142 This trial demonstrated a significant reduction in ipsilateral neurologic events in the surgical group (8%) versus the medical group (20.6%). However, the combined incidence of stroke and death was not different between study groups. The Asymptomatic Carotid Atherosclerosis Study (ACAS) demonstrated that patients with asymptomatic carotid stenosis (≥60%) who were treated with carotid endarterectomy and aspirin have a reduced 5-year risk for ipsilateral stroke compared with patients treated with aspirin alone (5.1% versus 11.0%).137 These results reflect only a 5.9% absolute risk reduction in 5 years, which is just above 1% per year. Of note, improvement in outcome for patients randomized to undergo endarterectomy in this trial did not reach significance until 3 years after surgery. The European Asymptomatic Carotid Surgery Trial, the largest trial to date, largely replicated the results of ACAS, but in a somewhat more pragmatic setting.143 This trial demonstrated that patients with asymptomatic carotid stenosis (≈70%) on ultrasound who were treated by immediate carotid endarterectomy plus medical treatment have a reduced 5-year risk for stroke compared with patients treated with medical therapy alone (6.4% versus 11.8%). Of note, half of this 5-year benefit involved disabling or fatal strokes. - Although landmark randomized clinical trials have defined individuals who are likely to benefit from carotid endarterectomy (and set the standard for developing evidence-based practice guidelines throughout the world), it has been suggested that the significant increase in the number of carotid endarterectomies performed over the last decade may be due in part to the extrapolation of trial results to patients and settings not directly supported by the trials. For example, both NASCET and ACAS restricted enrollment to patients younger than 80 years of age, and both trials carefully selected institutions and surgeons to optimize the results of surgery. Additionally, subgroup analysis of ACAS could not demonstrate a significant benefit for women.137 - With the advent of a second interventional treatment modality, percutaneous carotid angioplasty and stenting (discussed later), and the evolution of intensive medical therapy, this issue has become more complex. Carotid Endarterectomy - The strong association between stroke and carotid artery disease is well known. The principal cause of carotid artery disease is atherosclerosis, which most commonly involves the bifurcation of the common carotid artery with frequent extension into both the internal and external carotid arteries. The clinical manifestations of carotid artery disease represent a spectrum of conditions, with fatal or debilitating stroke secondary to cerebral infarction at one end of the spectrum and ranging successively through nondebilitating stroke, transient ischemic attack, and amaurosis fugax (transient attack of monocular blindness) to an asymptomatic bruit. Cerebrovascular sequelae of carotid atherosclerosis may result either from embolization of thrombus or atheromatous debris or from a reduction in flow (hypoperfusion) secondary to stenosis. The latter probably accounts for less than 10% of the cerebrovascular sequelae of carotid atherosclerosis. Although much is known about the genesis and evolution of atherosclerosis, significantly less is known about the circumstances that lead to plaque instability and rupture. Regardless of the mechanism, the degree of cerebral injury depends on such factors as plaque morphology, characteristics of the embolus, duration of hypoperfusion, cerebrovascular vasoreactivity, integrity of the circle of Willis, and cerebral collateral circulation. A multisociety guideline is available for the management of carotid artery disease.131 Stroke is a major public health burden worldwide. It is the fourth leading cause of death and the leading cause of serious, long-term disability in the United States. Stroke is also a major contributor to health care costs. The direct and indirect costs of stroke in the United States in 2008 are estimated at $65.5 billion.132 Approximately 780,000 people experience a new (≈600,000) or recurrent (≈180,000) stroke each year in the United States.132 Annually, more than 950,000 hospitalizations and 165,000 deaths occur from stroke. Well-defined risk factors exist in patients with stroke, the most important of which is hypertension. Approximately 83% of strokes are ischemic (i.e., cerebral thrombosis or embolism), and 7.6% of ischemic strokes result in death within 30 days of initial evaluation.133 Extracranial atherosclerotic disease accounts for up to 20% of all ischemic strokes. Less than 20% of strokes are preceded by a transient ischemic attack. Despite a well-documented decline in stroke mortality, the annual incidence rate of stroke may be increasing. This increase is probably due to growth in high-risk populations. The incidence of perioperative stroke in unselected patients, patients with asymptomatic carotid bruit, and patients with at least 50% carotid stenosis undergoing general anesthesia and surgery is approximately 0.1%, 1.0%, and 3.6%, respectively. - Although treatment options to reverse the effect of acute ischemic stroke are limited, outcomes may be improved with appropriate therapy. The only approved therapy is IV recombinant tissue plasminogen activator. Given the narrow 3- to 4.5-hour treatment window from the onset of symptoms, prompt evaluation and diagnosis of ischemic stroke are critical. With the exception of acute stroke after carotid endarterectomy, surgical treatment of patients with acute ischemic stroke is controversial and not generally recommended because of limited data and perceived high risk. Endovascular treatment of patients with acute ischemic stroke is undergoing intense investigation. Emergency angioplasty and stenting, mechanical disruption of arterial clot, and mechanical extraction of thrombi are interventions currently being evaluated.134 The AHA and American Stroke Association have guidelines for the early management of patients with ischemic stroke.135

Disabling claudication corresponds to a ABI of A. 1.0 B. 0.9 C. 0.6 D. 0.5 E. 0.2

D. Chronic Arterial Occlusion - Chronic arterial insufficiency is most often secondary to long-standing atherosclerosis in which the arterial lumen of the lower extremity becomes progressively stenosed by atherosclerotic plaque. When the stenosis approaches total occlusion, the marked reduction in blood flow leads to thrombotic occlusion. Hemodynamically significant stenosis and total-vessel occlusion commonly exist in the lower extremity with no or very minimal symptoms. The development of collateral vessels around a stenosed or occluded arterial segment often prevents clinical symptoms until multiple occlusions exist in major vessels. Thus, most patients with peripheral arterial disease are asymptomatic. Patients with symptoms most commonly have mild intermittent claudication—pain or fatigue in the muscles of the lower extremity caused by exertion and relieved with rest. The pain usually occurs in the muscle group distal to the site of arterial insufficiency. With disease progression, severe disabling intermittent claudication or rest pain—critical limb ischemia—can develop. - Noninvasive testing with the ankle-brachial index (ABI) is the clinical standard for documenting the presence and severity of peripheral arterial disease. The ABI is determined by dividing ankle systolic pressure by brachial systolic pressure. Normally, the ABI is between 1.0 and 1.1; a value less than 0.9 indicates arterial disease proximal to the point of measurement. The ABI approximates the degree of arterial insufficiency; claudication occurs with indexes ranging from 0.3 to 0.9, disabling claudication or rest pain with indexes less than 0.5, and gangrenous extremities with indexes less than 0.2. - One of the most important aspects of peripheral arterial disease is that it is a very strong marker for early mortality. In patients with peripheral arterial disease the risk for amputation is much less than the risk for death. 2142A low ABI is a strong predictor for disease progression, but it is also one of the strongest risk factors for all-cause mortality. Claudication is associated with a high rate of mortality but is relatively benign in terms of lower extremity outcome.

This is based on the response of the sensory cortex to electrical impulses from peripheral sensory nerve stimulation. A. Carotid artery stump pressure B. Regional cerebral blood flow C. EEG D. SSEP E. TUD F. Cerebral oxygenation

D. Somatosensory Evoked Potentials SSEP monitoring is based on the response of the sensory cortex to electrical impulses from peripheral sensory nerve stimulation. The sensory cortex, being primarily supplied by the middle cerebral artery, is at risk during carotid artery clamping. SSEP monitoring, unlike EEG monitoring, is able to detect subcortical sensory pathway ischemia. Characteristic SSEP tracings (i.e., decrease in amplitude, increase in latency, or both) occur with decreased rCBF and are abolished in primates when flow decreases to less than 12 mL/100 g of brain tissue per minute. No specific reduction in amplitude or increase in latency has been established as a physiologic marker of impaired rCBF under operative conditions in humans. Anesthetics, hypothermia, and blood pressure may affect SSEPs significantly, and false-negative results have been reported. The validity of SSEPs as an intraoperative monitor of cerebral ischemia during carotid endarterectomy has not been definitively established. Transcranial Doppler Ultrasonography TCD allows continuous measurement of mean blood flow velocity and detection of microembolic events in the middle cerebral artery (see also Chapter 49). These parameters have important clinical implications because most perioperative neurologic deficits are thought to be thromboembolic in origin. With TCD, intraoperative embolization has been detected in more than 90% of patients undergoing carotid endarterectomy. Most intraoperative emboli are characteristic of air and are not associated with adverse neurologic outcomes. TCD may provide useful information regarding shunt function, malfunction, and the incidence of emboli during shunt insertion. Embolization during carotid artery dissection may indicate plaque instability and the need for early carotid artery clamping. Embolization during dissection and wound closure is associated with operative stroke. One center has reported that combined TCD monitoring and completion angiography resulted in a reduction in the intraoperative stroke rate from 4% to 0%. Early postoperative embolization has been detected in more than 70% of patients after carotid endarterectomy and is exclusively particulate in nature. Most TCD-detected emboli occur in the first 2 to 3 hours after surgery. Persistent particulate embolization in the early postoperative period has been shown to predict thrombosis and the development of a major neurologic deficit. Frequent early postoperative TCD embolic signals have been demonstrated to be highly predictive of early postoperative ipsilateral focal 2154cerebral ischemia. Intervention with dextran has been shown to reduce and ultimately stop sustained embolization after carotid endarterectomy. Perioperative microembolization is more common in women and patients with symptomatic carotid disease. TCD monitoring has been reported to detect early asymptomatic carotid artery occlusion and hyperperfusion syndrome after carotid endarterectomy. Although TCD monitoring holds some promise, conclusive evidence demonstrating improved outcome has not been reported. Additionally, the high rate of technical failures significantly limits the clinical utility of this monitoring modality.170 Cerebral Oxygenation Direct monitoring of cerebral oxygenation can be obtained with jugular bulb venous monitoring. Such monitoring allows determination of the arterial-jugular venous O2 content difference and jugular venous O2 saturation and therefore provides information on global cerebral O2 metabolism. Jugular venous samples are obtained from a catheter inserted into the jugular bulb ipsilateral to the surgical site. Continuous fiberoptic jugular venous oximetry catheters are available as well. Significant technical and methodologic shortcomings have limited the clinical application of this monitoring during carotid endarterectomy. Near-infrared spectrophotometry is a noninvasive technique that allows continuous monitoring of regional cerebral O2 saturation through the scalp and skull. Similar to pulse oximetry, cerebral oximetry is based on the different absorption characteristics of the near-infrared spectrum of oxygenated and deoxygenated hemoglobin. However, unlike pulse oximeters, cerebral oximeters measure the O2 saturation of hemoglobin in the entire tissue bed (i.e., brain tissue and arterial and venous blood), which is predominately venous blood, and therefore approximates venous blood O2 saturation. A commercially available cerebral oximetry sensor is applied to the forehead skin ipsilateral to the surgical site, and regional cerebral O2 saturation from a small sample of the frontal cortex below the sensor is provided. To date, wide patient-to-patient variability in baseline cerebral O2 saturation and the lack of a clinical threshold of a decrease in cerebral O2 saturation predictive of the need for shunt placement have impeded the widespread use of this novel monitoring modality.

Which of the following is a part of an optimal renal protection during TAA surgery A. Furosemide B. Dopamine C. Fenoldopam D. Mannitol

D. Renal Ischemia and Protection - Renal failure after TAA repair results from preexisting renal dysfunction, ischemia during cross-clamping, thrombotic or embolic interruption of renal blood flow, and hypovolemia and hypotension. Approximately 6% of patients require postoperative dialysis, even in centers with the most clinical experience. The associated mortality can be high. The primary predictor of postoperative renal failure is preoperative renal dysfunction. The duration of cross-clamp time is very important with the clamp-and-sew technique. - Retrograde distal aortic perfusion techniques are widely used to preserve renal function during the cross-clamp period. Adequate bypass flow and arterial blood pressure are essential for maintaining renal function. Systemic and regional hypothermia, by reducing O2 requirements, protects the kidneys during ischemia. Some centers advocate the use of DHCA in the treatment of distal TAAs (i.e., extent type III and IV) to preserve renal function. - The role of pharmacologic protection is somewhat controversial. Mannitol 12.5 to 25 g/70 kg is often given before cross-clamping. Mannitol improves renal cortical blood flow and the glomerular filtration rate in animal models of ischemia. Endothelial cell swelling is decreased, and an osmotic diuresis occurs. Evidence demonstrates free radical scavenging with mannitol and subsequent protection from ischemia in animals. Loop diuretics are sometimes given, but these drugs have been less effective than mannitol in experimental models. In clinical studies, the prophylactic use of loop diuretics has not been shown to improve outcome or reduce the need for dialysis for patients with acute renal failure. Dopamine given in low doses (1 to 3 μg/kg/minute) dilates renal blood vessels and increases renal blood flow and urine output. Despite these beneficial effects, whether dopamine provides renal protection during ischemia is not clear. Fenoldopam mesylate, a selective dopamine type 1 agonist that preferentially dilates the renal and splanchnic vascular beds, has shown some promise as a renoprotective drug. At the present time, optimal renal protection during TAA surgery should rely on hypothermia, mannitol, and prevention of hypotension and hypoperfusion of the kidneys.

True or False Aspirin therapy should be discontinued before CEA procedure

False Anesthetic Management - Anesthetic management goals for carotid endarterectomy include protection of the heart and brain from ischemic injury, control of the heart rate and arterial blood pressure, and ablation of the surgical pain and stress responses. These goals must be achieved with another important goal in mind—to have an awake patient at the end of surgery for the purpose of neurologic examination. The preoperative visit is particularly important in patients undergoing carotid surgery. During this visit, a series of arterial blood pressure and heart rate measurements are obtained from which acceptable ranges for perioperative management can be determined. Patients are instructed to continue all long-term cardiac medications up to and including the morning of surgery. Aspirin therapy should be continued throughout the perioperative period. As noted earlier, discontinuation of aspirin therapy may be related to an increased rate of MI and transient ischemic events in patients undergoing carotid endarterectomy. When patients arrive at the hospital on the day of surgery, they are queried regarding any new cardiovascular or cerebrovascular symptoms. Long-term cardiovascular medications not taken at home should be administered in the preoperative holding area whenever possible. Patient reassurance is particularly important at this time because anxiety is associated with increases in heart rate, systemic vascular resistance, and myocardial O2 consumption, which in this patient population could precipitate myocardial ischemia. - ECG monitoring should include continuous leads II and V5 for detection of rhythm disturbances and ST-segment changes. Online ST-segment analysis can be particularly helpful. An intraarterial catheter for beat-to-beat blood pressure monitoring should be considered routine. Noninvasive arterial blood pressure measurement in the contralateral arm is recommended. Central venous and pulmonary artery catheters are rarely indicated for carotid surgery. The rare patient with uncompensated heart failure or recent MI with ongoing ischemia requiring emergent surgery is a possible exception. If such monitors are used, the subclavian or femoral insertion sites are most 2150practical 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. IV access for fluid and drug administration can be accomplished with a single, secure, medium-bore (16-gauge) catheter. Because both arms will be tucked to the patient's sides, the IV catheter must run well after patient positioning.

True or False A variety of anesthesia techniques, including general anesthesia, regional (i.e., epidural or spinal) anesthesia, and combined techniques, are widely used for lower extremity reconstruction.

True Anesthetic Management - A variety of anesthesia techniques, including general anesthesia, regional (i.e., epidural or spinal) anesthesia, and combined techniques, are widely used for lower extremity reconstruction. General anesthesia is usually delivered with use of a balanced technique consisting of opioids, volatile inhaled anesthetics, N2O, and neuromuscular blockade. Induction of anesthesia should proceed in a controlled fashion such that a stable hemodynamic profile is maintained. Maintenance of anesthesia may be accomplished with a low-dose inhaled anesthetic (i.e., isoflurane, desflurane, or sevoflurane) in 50% N2O and opioid (fentanyl 3 to 5 μg/kg). Because virtually all patients are extubated in the operating room, high doses of opioid are generally avoided. The goal is to maintain stable hemodynamics and prevent myocardial ischemia during the intraoperative and postoperative periods. Judicious use of β-blockers and vasoactive drugs is often necessary. Regional anesthesia can be accomplished with spinal or epidural techniques. Disadvantages of spinal anesthesia include the limited duration of action in the setting of a surgical procedure that is somewhat unpredictable in length and complexity. The level of sympathetic block is somewhat less controllable than with the epidural technique. Hypotension can occur with either technique and should be treated promptly with judicious use of fluids and vasopressors. An advantage of an epidural technique is the ability to continue drug delivery into the postoperative period for analgesia and attenuation of the stress response. A lumbar epidural catheter is ideal for lower extremity vascular procedures. The dermatomes that need to be anesthetized are innervated at the same level where the catheter is inserted, because the incision is usually in the L1 to L4 region. Small volumes of local anesthetic are recommended because a T10 block is generally sufficient. Usually, 9 to 12 mL (including the test dose) is sufficient for the initial dose, and more drug is given as needed. Because vascular surgery patients are generally advanced in age and thus prone to higher block levels, larger doses may result in high sympathetic blockade with significant hypotension.130 A high sympathetic block is problematic because of decreased coronary perfusion and excessive fluid and vasopressor requirements. Congestive heart failure may result in the postoperative period when the sympathectomy resolves and the intravascular space contracts. When administering an epidural test dose, careful attention should be directed to both heart rate and blood pressure. Blood pressure may be a more reliable indicator of an intravascular injection because vascular surgery patients may have little or no increase in heart rate as a result of β-blocker therapy and decreased β-adrenergic responsiveness secondary to aging. When hypotension results from sympathectomy, a low-dose phenylephrine infusion is helpful in reducing IV fluid requirements. I think this approach is more physiologic than administration of large fluid volumes. Postoperative Considerations - Pain and anxiety require especially careful attention in the postoperative period because the stress response and myocardial ischemia are of greatest concern at this time. Intravascular volume should be optimized, significant anemia avoided (hemoglobin maintained at > 9.0 g/dL), and heart rate and arterial blood pressure carefully 2147controlled. Computerized ST-segment analysis is helpful in identifying ischemic changes. Peripheral pulses should be checked frequently to verify lower extremity graft patency. Increasing arterial blood pressure augmentation and anticoagulants may be necessary when peripheral perfusion is limited. Urgent surgery may be required to reopen clotted or stenotic grafts. Postoperative analgesia can be provided by IV or epidural opioids delivered by patient-controlled analgesia or epidural opioids with local anesthetics delivered by continuous infusion or patient-controlled analgesia. For epidural patient-controlled analgesia, a dilute concentration of local anesthetic should be used to allow neurologic evaluation of the lower extremities to rule out spinal or epidural hematoma. Bupivacaine 0.0625% is ideal in this regard. Fentanyl 5 μg/mL can be added and the solution infused at 2 mL/hr, with an on-demand (patient-controlled analgesia) bolus of 2 to 4 mL and a lockout interval of 10 minutes.

True or False The perioperative stroke and death rate for carotid endarterectomy needs to be very low to maintain the beneficial effects of surgery over medical therapy alone.

True Perioperative Morbidity and Mortality - Although the randomized trials just noted have demonstrated a protective effect of carotid endarterectomy on ipsilateral stroke, the critical determinants of benefit for any given patient must include the overall perioperative event rate and expected long-term survival. Thus, the perioperative stroke and death rate for carotid endarterectomy needs to be very low to maintain the beneficial effects of surgery over medical therapy alone. Further, to compensate for the perioperative risk associated with surgery, the patient must have a reasonable life expectancy (12 to 18 months). The 30-day stroke and death rate of 2.3% for asymptomatic patients in ACAS (1987 to 1993) and 5.0% for symptomatic patients in NASCET (1988 to 1991) are often cited as benchmarks. More recent reports suggest a considerably less frequent event rate. For example, a prospective database study of 13,316 carotid endarterectomies performed in 2007 and 2008 reported a 30-day stroke and death rate of 1.3% in asymptomatic patients and 2.9% in symptomatic patients.144 The 30-day mortality was significantly more frequent in patients who developed a stroke than in those who did not (12.9% versus 0.6%). Patients with high-risk anatomy, such as restenosis and contralateral carotid arterial occlusion, have the highest risk for perioperative stroke and death. Neurologic deficits occur more commonly in patients with poorly controlled preoperative hypertension and in those with hypertension or hypotension postoperatively. The incidence of perioperative MI in patients undergoing carotid endarterectomy ranges from 0% to 5%. Recent reports suggest the incidence of MI is relatively low. The General Anesthesia versus Local Anesthesia for Carotid Surgery (GALA) trial (discussed later) results reported only 13 patients of 3526 (0.37%) had a perioperative MI.145 The four fatal perioperative MIs accounted for only 8.9% of the total 30-day mortality. Although the role of carotid endarterectomy in patients older than 80 years of age remains a concern, recent reports suggest that carotid endarterectomy can be performed safely in the very elderly and those deemed high risk, with combined stroke or death rates being comparable to those found in randomized trials (NASCET and ACAS). Preoperative Assessment - The optimal preoperative assessment for patients undergoing carotid endarterectomy continues to be debated (see also Chapter 38). Patients with recently symptomatic carotid disease present a particular challenge because strong evidence exists to support surgical intervention within 2 weeks after manifestation of symptoms, thus limiting the time available for evaluation and optimization of relevant comorbidities as well as the initiation of new medications.146 The medical management of patients with asymptomatic carotid disease should be optimized and includes β-blockers, statins, and antiplatelet agents. Poorly controlled hypertension should be addressed with 2149the patient's internist. The gradual decreasing of the arterial blood pressure over several weeks before surgery will restore intravascular volume, reset cerebral autoregulation to a more normal range, and improve perioperative management. Poorly controlled diabetes also warrants preoperative optimization, which may improve perioperative outcome.147 - CAD is common in patients undergoing carotid endarterectomy and is a leading cause of both early and late mortality. Hertzer and co-workers148 performed coronary angiograms in 506 patients scheduled for carotid endarterectomy and found significant (>70%) stenosis in one or more coronary artery, CAD in 83% of patients suspected of having CAD, and CAD in 40% thought to have no CAD. Despite the known frequent incidence of CAD in patients undergoing carotid endarterectomy, preoperative studies for the evaluation of myocardial function or ischemic potential are rarely undertaken. Exceptions to this practice are patients with unstable angina, recent MI with evidence of ongoing ischemia, decompensated congestive heart failure, and significant valvular disease. In general, specialized cardiac testing would be unlikely to result in cancellation of the procedure or alter perioperative management. Further, the relatively infrequent overall rates of perioperative nonfatal and fatal MI after carotid endarterectomy make aggressive strategies leading to prophylactic coronary revascularization less appealing.145 A recent clinical trial reported on the safety and efficacy of coronary angiography and revascularization in preventing postoperative cardiac ischemic events after carotid endarterectomy. In a randomized fashion, 426 patients with no history of CAD were randomized to either coronary angiography before carotid endarterectomy (216 patients) or carotid endarterectomy without coronary angiography (210 patients). In the angiography group, 68 patients had a significant stenosis of the coronary arteries and underwent revascularization with PCI (66 patients) or CABG (2 patients). PCI was performed 1 to 8 days before surgery and always consisted of angioplasty and stenting. No patients in the angiography group had a postoperative cardiac ischemic event or complication related to PCI, whereas 9 patients in the group without angiography had an ischemic event (one fatal MI and eight ischemic events treated medically). Although all PCI patients received dual-antiplatelet therapy, no major bleeding or neck hematomas were observed. Long-term follow-up was not reported. Patients with combined carotid stenosis and CAD requiring coronary revascularization represent somewhat of a management dilemma because it is often unclear which disease should be treated first.149 The severity of carotid and coronary disease must be evaluated in terms of clinical symptoms and anatomic lesions, and a decision must be made to perform a combined, staged (carotid endarterectomy first), or reverse-staged (CABG first) procedure. Carotid revascularization is recommended before CABG (staged procedure) in patients with symptomatic carotid disease and bilateral severe asymptomatic carotid stenosis. The optimal management of severe unilateral asymptomatic carotid stenosis in patients undergoing CABG is unclear. The only randomized clinical trial to date randomized 185 patients with severe unilateral asymptomatic carotid stenosis undergoing CABG to a staged or combined procedure (94 patients) or a reverse-staged procedure (90 patients).150 Although the perioperative mortality rates were equivalent (∼1.0%), the 90-day stroke and death rates were significantly lower in the staged and combined group (1.0% versus 8.8%). Given the overall paucity of high-quality evidence, management of an individual patient should be guided by careful assessment of the relative severity of the coronary and carotid disease with particular emphasis on both surgeon-specific and institution-specific results in these patient populations. Carotid artery angioplasty and stenting is widely being applied as an alternative revascularization modality before staged CABG. More recently, a combined procedure (carotid angioplasty/stenting and CABG) has been introduced. In a small feasibility and safety study (90 patients), carotid artery angioplasty and stenting under local anesthesia followed immediately by CABG reported a 30-day stroke and death rate of 2.2%.151

True or False Regional and local anesthesia allows continuous neurologic assessment of the awake patient, which is widely considered to be the most sensitive method for detecting inadequate cerebral perfusion and function

True Regional and Local Anesthesia - Regional and local anesthetic techniques for carotid endarterectomy have been in use for more than 50 years, and many centers consider them to be the techniques of choice. Regional anesthesia is accomplished by blocking the C2 to C4 dermatomes by use of a superficial, intermediate, deep, or combined cervical plexus block (see also Chapter 57). Adequate anesthesia can be obtained with an isolated superficial or intermediate cervical plexus block, likely as a result of spread of local anesthetic to the cervical nerve roots.159 Local infiltration of the incisional site and surgical field can also provide the necessary sensory blockade. A recent systematic review including over 10,000 cervical plexus blocks for carotid endarterectomy found that the deep (or combined) block was associated with a higher serious complication rate rated to the injecting needle compared with a superficial (or intermediate) block (0.25% versus 0%).160 The conversion rate to general anesthesia was also higher with the deep block (2.1% versus 0.4%). No difference was found in the incidence of serious systemic complications between the blocks. Although the incidence of serious complications from a cervical plexus block is infrequent, near-toxic levels of local anesthetic occurs in almost half of patients after superficial and deep cervical plexus block.161 Although no major complications related to local anesthetic toxicity occurred, some caution should be exercised when requesting the surgeon to supplement with additional local anesthetic. - Regional and local anesthesia allows continuous neurologic assessment of the awake patient, which is widely considered to be the most sensitive method for detecting inadequate cerebral perfusion and function. Awake monitoring reduces the need for shunting and avoids the expense associated with indirect monitors of cerebral perfusion. Other advantages that have been reported include greater stability of blood pressure and decreased vasopressor requirements, reduced operative site bleeding, and reduced hospital costs. Potential disadvantages of local or regional anesthesia include an 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 should conversion to general anesthesia be necessary. The reported incidence of intraoperative neurologic changes during carotid endarterectomy under local or regional anesthesia varies widely (2.4% to 24%). Rates of conversion from regional anesthesia to general anesthesia of approximately 2% to 6% have been reported. Phrenic nerve paresis is common after cervical plexus block and is of little clinical consequence except in patients with severe COPD or contralateral diaphragmatic dysfunction. - Regional and local 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. The surgical drapes are "tented" over the head and face area to minimize claustrophobic anxiety. Levels of consciousness, speech, and contralateral handgrip are assessed throughout the procedure. If both arms are tucked to the patient's side, handgrip can be assessed with the use of a squeaky toy. Blood pressure is augmented with phenylephrine when patients exhibit neurologic changes during carotid artery test clamping or after shunt placement. A 2- to 3-minute test clamp in awake patients allows prompt identification of those who would benefit from shunt placement. Patient acceptance of regional anesthesia is frequent and common, as evidenced by a 92% preference for repeat cervical plexus block for future carotid endarterectomy. Perhaps, no absolute contradiction to regional anesthesia for carotid endarterectomy exists. 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 and may require vigorous submandibular surgical retraction. Regional Versus General Anesthesia - For decades, the impact of anesthetic technique on outcome for carotid endarterectomy has been debated and studied. Until recently, nonrandomized studies dominated and largely supported that regional anesthesia was associated with significant reductions in the risk for perioperative death, stroke, MI, and pulmonary complications.162 The lack of randomized data was addressed with the landmark GALA trial.145 This multicenter, randomized controlled trial included 3526 patients with symptomatic or asymptomatic internal carotid stenosis from 95 medical centers in 24 countries. Patients were randomly assigned to carotid endarterectomy under general anesthesia (1753 patients) or local anesthesia (1773 patients) between 1999 and 2007. The primary outcome was a composite of perioperative death, MI, and stroke (including retinal infarction). The main finding was that anesthetic technique was not associated with a significant difference in the composite end point (4.8% for general versus 4.5% for local). Anesthetic technique was not associated with a significant difference in secondary outcomes, including duration of surgery, duration of ICU stay, length of hospital stay, or quality of life at 1 month after surgery. Other outcomes, including cranial nerve injury (10.5% versus 12.0%), wound hematoma (8.3% versus 8.5%), wound hematoma requiring reoperation (2.6% versus 2.3%), and chest infection, (2.0% versus 1.9%) were similar between patients receiving general anesthesia and local anesthesia, respectively. Of note, 4.4% of patients under local anesthesia (93% received a cervical plexus block) had complications that lead to cancellation of surgery or conversion to general anesthesia. Important limitations of the GALA trial include lack of standardization, absence of blinding, and possible investigator bias. Using patient-level data from the GALA trial, a recent report found that local anesthesia had a cost-effectiveness benefit over general anesthesia.163 2152 - Although randomized clinical trials, such as GALA, are considered to be the gold standard in clinical research, the conclusions are not always generalizable and therefore may not reflect actual practice in treating unselected patients. A recent report from a large international vascular registry, including 20,141 carotid endarterectomies performed in 10 countries between 2003 and 2007, found that anesthetic technique had no effect on perioperative mortality (0.5% overall) or stroke rate (1.5% overall).164 These real-world results complement the data from the GALA trial. Thus, using major perioperative complications as a guide, there is no reason to routinely prefer one anesthetic technique over the other for carotid endarterectomy. The ultimate decision to use general anesthesia or regional anesthesia should be based on surgeon and the anesthesiologist experience and patient preference.

Which Crawford type of aneurysm is at greatest risk for paraplegia A. Type I B. Type II C. Type III D. Type IV

B. Thoracoabdominal Aortic Surgery - Open repair of the thoracoabdominal aorta is widely regarded as the most challenging surgical procedure in terms of overall anesthetic and perioperative management. Surgical repair is required for a spectrum of disease, including degenerative aneurysm, acute and chronic dissection, intramural hematoma, mycotic aneurysm, pseudoaneurysm, penetrating aortic ulcer, coarctation, and traumatic aortic tear. Since the first thoracoabdominal aortic aneurysm (TAA) repair in 1955, tremendous advances have been made in the field. These advances have led to significant reductions in operative mortality and perioperative complications. However, even in centers where numerous procedures are performed, morbidity and mortality are frequent, especially in patients with dissecting or ruptured aneurysms. To successfully care for these patients, the anesthesiologist must be knowledgeable in the areas of one-lung ventilation; extracorporeal circulatory support, including circulatory arrest; renal and spinal cord protection; induced hypothermia; invasive hemodynamic monitoring, including TEE; massive transfusion; and management of coagulopathy. Intraoperative management requires a team effort with intimate cooperation among surgeons, anesthesiologists, perfusionists, nurses, and electrophysiologic monitoring staff. Endovascular stent-graft repair of lesions that affect the descending thoracic and thoracoabdominal aorta is evolving rapidly. As discussed later, accumulating experience with stent-graft repair of thoracic aortic aneurysm, dissection, and traumatic tear has demonstrated this modality to be an effective alternative to open repair for select patients. Etiology and Classification - Aneurysms of the thoracoabdominal aorta occur primarily because of atherosclerotic degenerative disease (80%) and chronic aortic dissection (17%).84 The remainder 2128are caused by either trauma or connective tissue diseases involving the aortic wall from conditions such as Marfan syndrome, cystic medial degeneration, Takayasu arteritis, or syphilitic aortitis.85 The true incidence of TAA is unknown, but population studies suggest a prevalence much less than that of infrarenal AAA. Degenerative and dissecting TAAs differ in their associated risk factors, extent of aortic involvement, and natural history. Thus, complete characterization of each TAA is required to formulate a comprehensive treatment plan. Development of both degenerative and dissecting TAAs is ultimately related to weakening of the aortic wall. Although the natural history of TAA without surgery is uncertain, enlargement tends to be progressive and nonoperative management is generally associated with a poor prognosis. With progressive enlargement, nutritional blood flow to the aorta is compromised. The increasing diameter is associated with increased wall tension, even when arterial pressure is constant (law of Laplace). The frequent incidence of associated systemic hypertension enhances aneurysm enlargement. - Degenerative and dissecting TAAs are symptomatic at initial evaluation in 57% and 85% of patients, respectively. The most common initial complaint is back pain. Additional symptoms can be caused by compression of organs or structures adjacent to the aneurysm. Aortic rupture, as a manifestation of TAA, occurs with equal frequency (9%) in both degenerative and dissecting aneurysms. Rupture of the thoracic and abdominal segments occurs with equal frequency and primarily in patients with aneurysms larger than 5 cm. Surgical repair is usually recommended when aneurysm diameter exceeds 6 cm, but earlier repair may be offered to patients with Marfan syndrome and those with a strong family history of an aortic aneurysm. In addition to cause, aneurysms of the thoracoabdominal aorta may be classified according to their anatomic location. In 1986, Crawford and colleagues,84 recognizing the correlation between aneurysm extent and clinical outcome, proposed a classification based on the extent of aortic involvement (Fig. 69-9). The Crawford classification defines aneurysms as types I, II, III, and IV and is appropriately applied to aneurysms of all causes (degenerative and dissecting). Type I aneurysms involve all or most of the descending thoracic aorta and the upper abdominal aorta. Type II aneurysms involve all or most of the descending thoracic aorta and all or most of the abdominal aorta. Type III aneurysms involve the lower portion of the descending thoracic aorta and most of the abdominal aorta. Type IV aneurysms involve all or most of the abdominal aorta, including the visceral segment. Types II and III are the most difficult to repair because they involve both the thoracic and the abdominal segments of the aorta. Patients with Crawford type II aneurysms are at greatest risk for paraplegia and renal failure from spinal cord and kidney ischemia during cross-clamping. Even with extracorporeal circulatory support, an obligatory period occurs when blood flow to these organs is interrupted because the origin of the blood flow is between the cross-clamps. For this reason, protective measures to prevent ischemic injury are important in reducing morbidity. - Aortic dissection, with or without aneurysm formation, has likewise been classified according to the extent of aortic involvement. The most widely used classification, proposed by DeBakey and colleagues, defines aortic dissection as types I, II, and III (Fig. 69-10). Type I aneurysms begin in the ascending aorta and extend throughout the entire aorta. These lesions are usually repaired via a two-stage approach, with the first procedure on the ascending aorta and aortic arch and the second procedure on the descending thoracic aorta. Type II aneurysms are confined to the ascending aorta. Both types I and II often involve the aortic valve and cause aortic regurgitation, and sometimes they involve the ostia of the coronary arteries. Type III aneurysms begin just distal to the left subclavian artery and extend either to the diaphragm (type IIIA) or to the aortoiliac bifurcation (type IIIb). Another commonly used classification of aortic dissection is the Stanford classification. This more simplified 2129classification divides aortic dissection into those that involve the ascending aorta (Stanford type A) and those that do not involve the ascending aorta (Stanford type B). Aortic dissection is also classified by duration, with those less than 2 weeks classified as acute and those greater than 2 weeks classified as chronic. This classification has very significant mortality implications, with much higher mortality in the acute phase. - Acute aortic dissection involving the ascending aorta (DeBakey types I and II, Stanford type A) is a surgical emergency that requires immediate cardiac surgical repair (see also Chapter 67). Acute dissections involving the descending aorta (DeBakey type III, Stanford type B) are most often treated conservatively (i.e., arterial blood pressure, heart rate, and pain control) because surgical repair has no proved benefit over medical or interventional treatment in stable patients. Early surgical intervention may be required for a variety of reasons, including aneurysmal formation, impending rupture, organ or leg ischemia, and inadequate response to medical therapy. In approximately 20% to 40% of patients with chronic aortic dissection, significant aneurysmal dilatation of the descending thoracic or thoracoabdominal aorta will develop.

True or False EVAR is the treatment of choice for the majority of patients with an AAA.

True Endovascular Aortic Aneurysm Repair In 1991, the first endovascular stent grafting (EVSG) procedure was performed to repair an infrarenal aortic aneurysm. The development of this technique allows surgeons to repair an AAA in a less invasive manner. Severe cardiac and respiratory pathology make as many as 30% of patients with aortic aneurysms poor surgical candidates.119 EVAR was initially developed to help patients with severe coexisting disease who were not considered viable surgical candidates. Presently, EVAR is the treatment of choice for the majority of patients with an AAA.120 In high risk patients having elective AAA repair, the 30-day and 1-year mortality rates are significantly decreased with EVAR as compared to OSR.121 Schermerhorn suggests that the patient population who may benefit most from EVAR are high-risk patients.121 Patients who are prone to aortic aneurysm development commonly have coexisting diseases, as listed in Box 28.10. - Endovascular aortic repair is associated with improved 30-day outcomes (all-cause mortality, readmission, surgical site infection, pneumonia, and sepsis) as compared to OSR.122-124 In one study, the 30-day mortality rate was 1.7% in the EVAR group versus 4.7% in the OSR group. Secondary interventions most often caused by endoleak were more common in the EVAR group (9.8% versus 5.8%).125 However, there was no significant difference between the groups with respect to 2-year survival. A comparison of EVAR versus OSR showed that mortality was 0.6% and mean length of stay (LOS) was 5.8 days for EVAR, whereas in-hospital mortality for OSR was 4.6%, and the average LOS was 11.9 days.126 EVAR is associated with decreased procedure duration, a decreased need for transfusion of blood and blood products, a shorter duration of hospitalization, and decreased morbidity compared to OSR.127 Perioperative mortality after EVAR has remained similar in recent years despite improvements in techniques, devices, and proficiency. Randomized trials such as the Endovascular Aneurysm Repair 1 (EVAR 1), Dutch Randomized Endovascular Aneurysm Management (DREAM), and Open versus Endovascular Repair (OVER) trials showed lower 30-day mortality rates for EVAR as compared to OSR. However, late mortality rates (24-36 months postoperatively) are similar for EVAR and OSR.128 - Reinterventions occur more frequently after EVAR than after OSR.129 The primary reason for a secondary corrective procedure is due to endoleak. Endoleak is a term that is used to describe the inability of the EVSG to isolate blood flow into the aneurysm sac. Endoleak has been determined to be a significant risk factor for late open conversion. The overall risk of late failure is approximately 3% per year.124 EVAR is also being used to treat patients with TAAs. The mortality rate for EVAR for elective DTAA repairs range from 3.5% to 12.5%, as compared with an open approach, where mortality is approximately 10%.130 Reports also show that EVAR has a low incidence (0% to 6%) of spinal cord ischemia and paraplegia.131 Potential explanations for the decreased incidence of spinal cord trauma as compared to OSR are (1) no thoracic aortic cross-clamping and (2) no prolonged periods of extreme hypotension. Perioperative hypotension (MAP less than 70 mm Hg) was a significant predictor of spinal cord ischemia in patients undergoing EVAR for TAA132 - The overall mortality rate for patients with a ruptured AAA who are alive when diagnosed in emergency departments is 40% to 70%.133 Since the 1950s, mortality from ruptured AAAs has only decreased 3.5% per decade.134 Patient survival after emergency repair with EVAR has increased from 2005 to 2011. A significant improvement is noted particularly in those patients who survive the first 24 hours postoperatively.135 The 30-day mortality rate after AAA rupture is estimated to be 10% to 45%.136 Even though secondary interventions and ESVG surveillance are required, the use of EVAR for both ruptured AAAs and TAAs in patients with suitable anatomy is a lifesaving option.137 Medical centers that consider EVAR for ruptured AAA repair must have immediate CT imaging capabilities, trained endovascular teams, adequate endovascular supplies, and a specially arranged surgical suite.

Which of the following is not an effect of statin therapy A. Antiarrhythmic B. Antiinflammatory C. Plaque-stabilizing D. Antioxidant

A Perioperative Statin Therapy - In addition to their lipid-lowering properties, statins have beneficial antiinflammatory, plaque-stabilizing, and antioxidant effects (see also Chapter 39). Over the last decade, statin use has emerged as a promising strategy for the prevention of perioperative cardiovascular complications in patients undergoing vascular surgery.48 This approach is supported by the double-blind, placebo-controlled DECREASE-III trial. Unfortunately, controversy exists regarding this trial because of scientific misconduct identified by a recent investigation by Erasmus University.19 Statin use can help preserve renal function after aortic surgery and improve graft patency after lower extremity bypass surgery. - Although current guidelines recommend the use of statins in all patients with peripheral arterial disease, the optimal timing and dosing of statins for perioperative use has not been established. Because no intravenous (IV) preparations are available, statins should be given that have a prolonged half-life or a slow-release formula.49 Interruption of statin therapy after aortic surgery can increase cardiac risk.49,50 Data from the DECREASE III trial suggest that this risk may be avoided if the interruption is brief (2 days) and an extended-release statin is used.42 Current ACC/AHA guidelines should guide overall use. Because side effects can occur and are difficult to assess clinically in the perioperative period, serial measurements of creatine kinase and liver function are advisable until safety has been established.

Cross-clamping of the aorta in such location in relation to the diaphragm results in the most profound increases in arterial blood pressure unless diverting circulatory support or IV vasodilators are used. A. Above B. At the level C. Below

A & B Aortic Cross-Clamping - The pathophysiology of aortic cross-clamping is complex and depends on many factors, including level of the cross-clamp, status of the left ventricle, degree of periaortic collateralization, intravascular blood volume and distribution, activation of the sympathetic nervous system, and anesthetic drugs and techniques. Most abdominal aortic reconstructions require clamping at the infrarenal level. However, clamping at the suprarenal and supraceliac levels is required for suprarenal aneurysms and renal or visceral reconstructions and is frequently necessary for juxtarenal aneurysms, inflammatory aneurysms, and aortoiliac occlusive disease with proximal extension. These higher levels of aortic occlusion have a significant impact on the cardiovascular system, as well as on other vital organs rendered ischemic or hypoperfused. Ischemic complications may result in renal failure, hepatic ischemia and coagulopathy, bowel infarction, and paraplegia. With endovascular aortic repair now common, an increasing proportion of patients undergoing open repair have anatomically complex aneurysms, many of which require suprarenal cross-clamping.60 Hemodynamic and Metabolic Changes - The hemodynamic and metabolic changes associated with aortic cross-clamping are summarized in Box 69-1. The magnitude and direction of these changes are complex, dynamic, and vary among experimental and clinical studies. However, several important factors must be considered (Box 69-2). The systemic cardiovascular consequences of aortic cross-clamping can be dramatic, depending primarily on the level at which the cross-clamp is applied. Arterial hypertension above the clamp and arterial hypotension below the clamp are the most consistent components of the hemodynamic response to aortic cross-clamping at any level. The increase in arterial blood pressure above the clamp is primarily due to the sudden increase in impedance to aortic blood flow and the resultant increase in systolic ventricular wall tension or afterload. However, factors such as myocardial contractility, preload, blood volume, and activation of the 2119sympathetic nervous system also may be important.61 Cross-clamping of the aorta at or above the diaphragm results in the most profound increases in arterial blood pressure unless diverting circulatory support or IV vasodilators are used.

Protamine administration is associated with a reduction in A. Blood pressure B. Heart rate C. Bleeding complications D. Major thrombotic outcomes

A & C Anesthetic Management - The anesthetic objectives for vascular surgery are similar to those for any type of elective procedure: to provide analgesia and amnesia, to facilitate surgical intervention, and to minimize operative morbidity and mortality. Goals that are specific to CEA include maintaining cerebral and myocardial perfusion and oxygenation, minimizing the stress response, and facilitating a smooth and rapid emergence. However, it may be difficult to maintain the integrity of one system without adversely affecting the other. For example, raising the arterial blood pressure to augment cerebral perfusion can increase myocardial oxygen demand, which may lead to ischemia. In addition, significantly decreasing blood pressure can lead to cerebral hypoperfusion. Therefore, the anesthetic goal is to optimize perfusion to the brain, minimize myocardial workload, ensure cardiovascular stability, and allow for rapid emergence. Anticoagulation is achieved via administration of heparin (50-100 units/kg) prior to carotid artery cross-clamping. The decision to administer protamine upon completion of the surgical procedure is based on the surgeon's impression. Protamine administration is associated with a reduction in bleeding complications without increasing major thrombotic outcomes, including stroke, MI, or death after CEA.200 Protamine administration is associated with hypotension. Anaphylaxis is a rare but life-threatening side effect. An understanding of the physiology of the cerebrovascular system is important for optimal anesthetic management. Fig. 28.13 illustrates the anatomy of structures in this region. This knowledge enables the selection of appropriate monitoring and anesthetic techniques that will protect and improve cerebral and myocardial perfusion.

These are the most common complications observed postoperatively in patients recovering from abdominal aortic reconstruction A. Respiratory B. Hepatic C. Renal D. Cardiac E. Cerebral

A, C, D Postoperative Considerations - Cardiac, respiratory, and renal failure are the most common complications observed postoperatively in patients recovering from abdominal aortic reconstruction. Cardiovascular function must be closely monitored in the ICU for at least 24 hours after surgery. Maintaining adequate blood pressure, intravascular fluid volume, and myocardial oxygenation is paramount during this period. MI frequently contributes to postoperative morbidity and mortality; serial cardiac enzyme analysis may be justified. Pharmacologic agents used in the treatment of hypertension or hypotension must also be available. - Most patients require ventilatory assistance during the postoperative period. Vigilant monitoring of respiratory function is mandatory, especially when epidural catheters are used for postoperative analgesia. To address the significant number of serious postoperative complications, which are noted in Box 28.5, intensive and continuous assessment of the patient condition is vital. Patients are admitted to the ICU for high-acuity monitoring and care. Postoperative Considerations for Patients Having Abdominal Aortic Aneurysm Repair • Continue invasive hemodynamic monitoring • Treat acute blood pressure extremes, arrhythmias (atrial fibrillation) • Assess for postoperative myocardial infarction • Provide ventilatory management with weaning and extubation • Assess for abdominal compartment syndrome • Evaluate hemoglobin, hematocrit, coagulation status, and adequacy of volume replacement • Assess blood urea nitrogen/creatinine and urine output • Institute deep vein thrombosis prophylaxis per protocol

This is the more common approach to AAA repair A. Transperitoneal B. Retroperitoneal C. Anteroperitoneal D. Lateroperitoneal

A.

AAAs are two to six times more common in A. Men B. Women

A. Abdominal Aortic Aneurysms Incidence - The incidence of AAA is estimated to be between 3% and 10% for patients over 50 years of age in the western world.38 Improved detection of AAAs is the result of increased screening of asymptomatic aneurysms by noninvasive diagnostic modalities such as computed tomography (CT), magnetic resonance imaging (MRI), and ultrasonography. The occurrence of AAAs has increased because of the increased age of the general population and the vascular changes that occur as a result of aging.39 AAAs are two to six times more common in men than in women, and are two to three times more common in white men than in black men.38 Women with AAAs are being treated at older ages and typically have AAAs that are smaller in diameter, as compared to men.40 In men, AAAs most frequently begin to occur at 50 years of age and peak at 80 years of age.41 Conditions and Traits Associated With Development of Abdominal Aortic Aneurysm • Smoking • Older age • Gender (more common in males than in females) • Family history • Coronary artery disease • High cholesterol • Chronic obstructive pulmonary disease • Height (per 7 cm interval) • Hypertension • Peripheral vascular occlusive disease • Caucasian

During carotid artery cross-clamping, maintaining the MAP at __% or greater of the patient's preoperative mean pressure decreases postoperative cognitive dysfunction A. 20 B. 40 C. 60 D. 80

A. Blood Pressure Control - The presence of hypertension in patients with cerebrovascular disease is well known. Therefore, one of the most challenging aspects of care associated with anesthesia for CEA is blood pressure control. Patients with cerebral insufficiency are vulnerable to perioperative blood pressure instability. Hypotension occurs in 10% to 50% of patients who undergo CEA, and is believed to be the result of carotid sinus baroreceptor stimulation. Conversely, 10% to 66% of patients experience hypertension, which is attributed to surgical manipulation of the carotid sinus.198 Preoperative blood pressure control, volume status, and depth of anesthesia can also contribute to intraoperative hemodynamic instability. During carotid artery cross-clamping, maintaining the MAP at 20% or greater of the patient's preoperative mean pressure decreases postoperative cognitive dysfunction.199 - Blood pressure control must begin in the preoperative phase. All patients should continue taking their antihypertensive medications until the time of surgery. Patients with systolic blood pressure greater than 180 mm Hg may be at increased risk of stroke and death.182 Additional pharmacologic agents may be required in the preoperative period, especially during the insertion of intravenous and intra-arterial catheters, to reduce increases in heart rate and blood pressure. The induction of anesthesia, the initial incision, dissection, manipulation of the carotid sinus, and emergence from anesthesia are all events that precipitate blood pressure fluctuations. The use of pharmacologic adjuncts, such as short-acting β-adrenergic blockers, may stabilize blood pressure during induction and emergence. Continuous intravenous use of nitroglycerin or sodium nitroprusside should be available to treat hypertension. Patients with chronic hypertension are predisposed to dramatic decreases in blood pressure after the induction of general anesthesia. This condition must be treated promptly, and can be successfully managed by providing intravenous fluids or administering appropriate vasopressors. Hypotension and bradycardia, which result from carotid sinus baroreceptor manipulation, may be inhibited by stopping surgical stimulation, infiltrating the region with local anesthesia, and, if necessary, administering an anticholinergic

This constitutes the gold standard in identifying neurologic deficits related to carotid artery cross-clamping. A. EEG B. Carotid stump pressure C. SSEP D. TCD

A. Cerebral Monitoring - In addition to standard monitoring, direct intra-arterial pressure must be continuously assessed via arterial line placement. During CEA, hemodynamic variability frequently occurs. Owing to the high incidence of CAD and neurovascular disease in this patients having a CEA, prompt and tight control of blood pressure is imperative. - During repair, the carotid artery cross-clamp is applied distally and proximally to the carotid incision. Various monitoring techniques have been proposed for assessing the adequacy of CBF during this maneuver. A summary of select cerebral monitoring techniques is presented in Box 28.14. Each of these monitoring modalities has limitations; the most sensitive and specific measure of adequate CBF is responsiveness in an awake patient. - Electroencephalogram (EEG) monitoring constitutes the gold standard in identifying neurologic deficits related to carotid artery cross-clamping.175,187 EEG has demonstrated reliability in monitoring cortical electrical function.188 Loss of β-wave activity, loss of amplitude, and emergence of slow-wave activity are all indicative of neurologic dysfunction. Limitations surrounding EEG monitoring include (1) the effect of blood pressure, temperature, and anesthetic agents on monitoring, and (2) the fact that this modality only detects EEG changes on the superficial layers of the brain and not in deep cortical structures such as the brainstem. Carotid stump pressure has been used as a means of assessing collateral flow.189 After the carotid cross-clamp is placed, blood flow from the nonoperative carotid artery and the basilar artery provides blood flow to the circle of Willis. A catheter is placed into the distal portion (above the cross-clamp) of the operative internal carotid artery, and the pressure can be monitored. Carotid stump pressure is a gross measurement of the pressure within the circle of Willis. A carotid stump pressure of less than 40 to 50 mm Hg reflects neurologic hypoperfusion and is a criterion for shunt placement. However, there is no correlation between stump pressures and EEG changes.177 In a study by Harada,190 a carotid stump pressure of less than 50 mm Hg had a positive predictive value for only 36% of patients who exhibited ischemic changes on EEG during carotid artery cross-clamping. A combination of stump pressure and either Transcranial Doppler (TCD) or EEG appears to improve the detection of cerebral ischemia during carotid artery cross-clamping.191 - Somatosensory-Evoked Potential (SSEP) monitoring can be used to identify inadequate CBF during cross-clamping; however, false-positive results can occur. In addition, SSEPs reflect the sensory integrity of the spinal cord and the brain; therefore, a motor deficit can occur despite a normal SSEP waveform. Additionally, there are no values for decreased amplitude and increased latency that definitively correlate with cerebral ischemia. Monitoring both SSEP and EEG is more sensitive for predicting perioperative deficits as compared to using either monitoring modality in isolation. Patients who experience perioperative strokes are 17 times more likely to have a change in either EEG or SSEP than other patients.192 Transcranial Doppler (TCD) velocity monitoring has been used to detect adverse cerebral events during CEA. TCD is noninvasive and measures cerebrovascular dynamics through the CBF velocity. The use of TCD during CEA to determine if carotid shunt placement is necessary is a reliable method to decrease adverse neurologic outcomes.193 TCD can also be used during the postoperative period to detect ischemia and the presence of cerebral hyperperfusion syndrome (CHS). Near-infrared spectroscopy (NIRS) measures cerebral oxygenation. A greater than 20% reduction in regional cerebral oxygenation coincides with regional and global cerebral ischemia during CEA.194 Despite the established advantages of using NIRS monitoring in cardiac surgery, its routine use is less established during noncardiac procedures. Both NIRS and TCD monitoring are independently accurate in predicting the need for selective shunting by detecting cerebral ischemia during CEA and general anesthesia.195 As compared with stump pressure monitoring, cerebral oximetry more accurately predicts cerebral oxygenation.196 Box 28.14 outlines the cerebral monitoring modalities that can be used during general anesthesia for CEA.

Renal insufficiency more commonly occurs with which cross clamping A. Suprarenal B. Juxtarenal C. Infrarenal D. Iliac

A. Effects on Regional Circulation Acute Kidney Injury. - Tissues that are distal to the aortic clamp are underperfused. Renal insufficiency and acute renal failure are severe complications associated with abdominal aortic reconstruction. Suprarenal and juxtarenal cross-clamping are associated with a higher incidence of altered renal dynamics and can decrease renal blood flow by as much as 80%. However, significant reductions in renal blood flow occur even when aortic cross-clamping is performed below the renal arteries. Infrarenal aortic cross-clamping is associated with a 40% decrease in renal blood flow.38 Thus, renal insufficiency more commonly occurs with suprarenal as compared to infrarenal cross-clamping. AKI may occur in as many as 18% of patients undergoing aortic aneurysm repair. Preoperative evaluation of renal function is the best method of assessing and anticipating which patients may develop postoperative renal dysfunction. Preexisting renal impairment is common after elective infrarenal EVAR, and preoperative renal function appears to be the main factor associated with AKI. A complete evaluation of renal function is required during the preoperative period, and patients with a low glomerular filtration rate should be managed with more aggressive renal protection interventions.73 - Suprarenal cross-clamp times longer than 30 minutes increase the risk of postoperative renal failure. Even though renal blood flow is restored after unclamping, prolonged effects associated with ischemic reperfusion injury (IRI) occur. The injury caused to the renal tubular epithelium decreases the glomerular filtration rate. This effect may lead to acute renal failure, which is fatal in 50% to 90% of patients who have undergone aneurysmectomy.74 Clamp position above the renal arteries is predictive of severe AKI in patients treated with open surgical repair (OSR).75 AKI is common problem after elective infrarenal EVAR, and preoperative renal function appears to be the main factor associated with AKI. AKI is associated with higher mortality rates and long-term cardiovascular events after surgery.75,76 The administration of renal-dose dopamine, mannitol, sodium bicarbonate, and/or loop diuretics has not been scientifically proven to preserve or improve renal function postoperatively. The use of balanced crystalloid solutions and hyperchloremic solutions decreases the incidence of AKI.77 Minimizing the use of nephrotoxic medications such as nonsteroidal antiinflammatory drugs and aminoglycoside antibiotics preoperatively is prudent. Intraoperative renal perfusion with cold solution appears to have a renal protective effect and decrease the incidence of AKI.78 Atrial natriuretic peptide (ANP) causes vasodilatation of the preglomerular artery, inhibition of the angiotensin axis, and prostaglandin release, which promotes renal vascular dilation. During the AKI reflow period, the natriuretic effect of ANP could be useful in preventing tubular obstruction in patients undergoing major surgery such as cardiovascular surgery.77 The most important interventions to protect from AKI are aggressive hemodynamic stabilization and minimization of aortic clamp times, which have proven efficacy.79

What is the most common cause of aneurysm A. atherosclerosis B. aortic dissection C. inflammation D. infection

A. Etiology - Atherosclerosis is the most common cause of aneurysmal pathology. Atherosclerotic lesions occur most often in the descending and distal thoracic aorta, and are most often classified as fusiform. Less common causes include aortic dissection and various mechanical, inflammatory, and infectious processes. The various causes of aortic aneurysms are classified in Box 28.8. Etiology of Thoracoabdominal Aortic Aneurysms Degenerative • Nonspecific (commonly considered arteriosclerotic), dysplastic (80%) Mechanical (Hemodynamic) • Dissections (15% to 20%) • Poststenotic • Arteriovenous fistula • Blunt or penetrating trauma Connective Tissue • Ehlers-Danlos syndrome • Marfan syndrome Inflammatory (Noninfectious) • Takayasu disease • Behçet syndrome • Reiter syndrome • Kawasaki disease • Microvascular disorder (e.g., polyarteritis) • Ankylosing spondylitis • Rheumatoid aortitis • Periarterial inflammatory disease (e.g., pancreatitis) Infectious • Tuberculosis • Bacterial • Fungal • Spirochetal (syphilis) Anastomosis • Postarteriotomy • Postoperative pseudoaneurysm

Carotid artery stenosis is the primary cause of approximately __% of all strokes A. 20 B. 40 C. 60 D. 80

A. Morbidity and Mortality - The surgical outcomes reported for CEA vary due to differences in patient populations and varying degrees of surgical expertise. Other variables that cannot be stratified in studies but may affect patient outcomes include the state of collateral flow through the circle of Willis, the presence of concurrent atherosclerotic disease in the cerebral vasculature, the size and morphology of the offending plaque, the specific presenting symptoms, and the presence of concurrent cardiovascular disease.174 Carotid artery stenosis is the primary cause of approximately 20% of all strokes.175 The recommended acceptable perioperative stroke rates are less than 3% in asymptomatic patients, less than 5% in symptomatic patients, and 10% or less in patients with recurrent disease or existing strokes.176 Morbidity rates related to CEA have been reported to be at or below these recommended limits.176,177 The perioperative MI rate of 2% to 5% illustrates the global nature of atherosclerotic disease and represents the greatest contribution to overall morbidity. The perioperative mortality rate for CEA is approximately 0.5% to 2.5%,178,179 and the long-term postoperative stroke incidence ranges from 1% to 3% per year.180 In a multicenter cohort of black and white adults in the United States, the incidence and mortality rates associated with a stroke decreased from 1987 to 2011. The decreases varied across age groups, but were similar across sex and race.181

Patients having vascular surgery are at _________ risk for developing a venous thromboembolism (VTE) during the postoperative period A. Increased B. Decreased

A. Postoperative Considerations - Postoperative pain management is important to consider after peripheral vascular surgery. Most clinicians agree that postoperative administration of narcotics not only provides patient comfort, but also contributes to cardiac stability. The use of epidural opioids and local anesthetics in patients recovering from vascular surgery is an important component of postoperative care because pain can greatly enhance sympathetic nervous system stimulation. Despite a decrease in discomfort during the postoperative course, these patients must be monitored for possible adverse events, such as MI, hypotension, or respiratory depression, which could be attributed to the administration of epidural opioids and local anesthetics. Acute pain increases inflammatory mediators such as creatinine kinase, C-reactive protein, interleukin (IL)-6, and tumor necrosis factor, which can lead to regional blood flow alterations, organ dysfunction, and cell death.35 - Patients having vascular surgery are at increased risk for developing a venous thromboembolism (VTE) during the postoperative period. In one study, VTE was detected in 18.1% of patients with aortoiliac obstruction and 21.0% of patients after AAA repair.36 The incidence of VTE continued to be elevated after discharge. All methods intended to prevent the formation of deep vein thrombosis (DVT), including pharmacologic management, should be employed throughout the postoperative period. Low molecular weight heparin is frequently used to bridge the time between withholding oral anticoagulants and surgery. It is important to restart oral anticoagulant medications postoperatively after the risk of bleeding is decreased to minimize DVT and VTE. Increased postoperative hematocrit concentration is associated with an increased risk of 30-day mortality from DVT and pulmonary embolism.37

This is the single most significant risk factor influencing long-term survivability in patients with vascular disease A. CAD B. MI C. Carotid stenosis D. Stroke

A. Presence of Concurrent Disease Preoperative Management - The presence of underlying CAD in patients with vascular disease has been well documented. Reports suggest that CAD exists in more than 50% of patients who require abdominal aortic reconstruction, and is the single most significant risk factor influencing long-term survivability.8,91,92 MIs are responsible for 40% to 70% of all fatalities that occur after aneurysm reconstruction.6,46 Preoperative cardiac evaluation begins with the identification of risk factors that may contribute to adverse cardiac events and subsequent death. When preoperative CAD exists, an increased incidence of postoperative adverse cardiac complications has been demonstrated.93 - The end-point of any method of preoperative cardiac evaluation for aneurysmectomy is identification of functional cardiac limitations. Depending on the degree of cardiac dysfunction, preoperative optimization of cardiac function may range from simple pharmacologic manipulation to surgical intervention. The American College of Cardiology and the American Hospital Association guidelines on perioperative cardiovascular evaluation and care for noncardiac surgery are generally followed when preparing patients for these procedures. Optimizing patient preoperative pathophysiologic states, as described in Box 28.4, minimizes the overall rate of morbidity and mortality.

Compared with the conventional surgical method, advantages of the endovascular approach to AAA repair include the following except A. decrease aortic cross-clamping time B. improved hemodynamic stability C. decreased incidence of embolic events D. decreased blood loss

A. Procedure - The most significant intraoperative advantages with EVAR as compared to OSR are the absence of aortic cross-clamping and the absence of an incision that extends from the xiphoid process to the pubis. EVAR involves deployment of an ESVG within the aortic lumen. The graft restricts blood flow to the portion of the aorta where the aneurysm exists. This procedure is also performed for patients who have TAAs or TAAAs. Cannulation of both femoral arteries is performed. As seen in Fig. 28.6, a guide wire is threaded through the iliac artery to the level of the aneurysm. Next, a sheath is inserted over the guide wire and positioned at the aneurysm location through the use of fluoroscopy. The proximal end of the sheath must extend beyond the aneurysm, and care must be taken to avoid occlusion of the renal arteries. Once the sheath is deployed, radial force or fixation mechanisms such as hooks or barbs on the stent become embedded into the aortic wall to prevent stent migration (Fig. 28.7). - The surgical procedure may take place in a traditional operating room or an interventional radiology suite. Compared with the conventional surgical method, advantages of the endovascular approach include the absence of aortic cross-clamping, improved hemodynamic stability, decreased incidence of embolic events, decreased blood loss, a reduced stress response, decreased incidence of renal dysfunction, and decreased postoperative discomfort.138,139 Systemic anticoagulation with heparin (50 to 100 units/kg) is administered prior to catheter manipulation.140 Administration of a broad spectrum antibiotic is recommended prior to surgery. The anesthetic techniques that can be used for EVAR include general anesthesia, neuraxial blockade, or local anesthesia with sedation.141 - Local anesthesia with sedation, as compared to general anesthesia, is associated with decreases in nonfatal cardiac morbidity, respiratory complications, renal failure, and overall mortality.142,143 There is also decreased pulmonary morbidity as compared with general anesthesia, and local anesthesia with sedation is associated with a shorter LOS as compared with general and neuraxial anesthesia.144 The goals for intraoperative management for EVAR include maintaining hemodynamic stability, providing analgesia and anxiolysis, and being prepared to rapidly convert to an open procedure. Local or neuraxial anesthesia is associated with fewer ICU admissions, decreased length of hospitalization, and fewer systemic complications, as compared to general anesthesia.145 In an alternative analysis, there was no difference in 30-day mortality associated with either local anesthesia or general anesthesia provided for EVAR. However, shorter operative times, shorter length of hospitalization, and fewer postoperative complications were associated with a local anesthetic technique.146 - With infrarenal or suprarenal EVAR, creatinine clearance values can decrease by 10% in the first year.147 However, proximal endovascular graft migration can occur, causing renal artery occlusion and postoperative renal failure.148 Fenestrated EVSGs that are constructed to allow blood to flow to the renal arteries can be used safely for those patients who have juxtarenal or suprarenal aortic aneurysms.149 Plasma catecholamine concentrations and mediators of the systemic immune response are decreased in patients who undergo the endovascular approach as compared with patients who undergo conventional repair.150,151 Pearson determined that plasma cortisol release was lower in patients having EVAR than in those having traditional open AAA repair.152 The EVAR group also developed significantly less sepsis and had a lower incidence of systemic immune response syndrome. Complications that can arise from the EVAR approach include endograft thrombosis, migration, or rupture; graft infection; iliac artery rupture; and lower extremity ischemia.153 Fatal cerebral embolism resulting in sudden respiratory arrest has occurred during EVAR.154 Box 28.11 lists potential complications associated with EVAR.

Risk Factors Associated With an Increased Risk of Mortality in Patients With Abdominal Aortic Aneurysm Rupture include the following except A. Male B. Black C. CHF D. Renal failure

A. Risk Factors Associated With an Increased Risk of Mortality in Patients With Abdominal Aortic Aneurysm Rupture • Increased age • Women • Nonwhite race • Insurance status (higher for those who self-pay or are on Medicaid in the United States) • Comorbid conditions • Congestive heart failure • Renal failure • Valvular heart disease

Afterload reduction during aortic cross clamping, most commonly accomplished with the use of A. Sodium nitroprusside B. Isoflurane C. Amrinone D. Nitroglycerin

A. Therapeutic Strategies - Patients with preexisting impaired ventricular function and reduced coronary reserve are most vulnerable to the stress imposed on the cardiovascular system by aortic cross-clamping. Rational therapeutic strategies to prevent the deleterious effect of aortic cross-clamping primarily include measures to reduce afterload and maintain a normal preload and cardiac output. Vasodilators, positive and negative inotropic drugs, and controlled intravascular volume depletion (i.e., phlebotomy) may be used selectively. - Patients with impaired ventricular function requiring supraceliac aortic cross-clamping are the most challenging. Myocardial ischemia, reflecting an unfavorable balance between myocardial O2 supply and demand, may result from the hemodynamic consequences of aortic cross-clamping. Controlled (i.e., slow clamp application) supraceliac aortic cross-clamping is important to avoid abrupt and extreme stress on the heart. Both afterload and preload reduction are often required. Afterload reduction, most commonly accomplished with the use of sodium nitroprusside (predominantly an arteriolar dilator), is necessary to unload the heart and reduce ventricular wall tension. In a large series of patients requiring cross-clamping of the descending thoracic aorta, stable left ventricular function was maintained with sodium nitroprusside during cross-clamping. Sodium nitroprusside most likely allowed adequate intravascular volume before unclamping, which resulted in stable unclamping hemodynamics. Although isoflurane can provide hemodynamics comparable to those provided by sodium nitroprusside during thoracic aortic cross-clamping, I do not advocate its use to control proximal hypertension in patients with significantly impaired ventricular function. Though not widely used, amrinone provides hemodynamic control equivalent to that of sodium nitroprusside during abdominal aortic surgery. A normal preload is equally important and involves careful IV fluid titration and vasodilator administration. Nitroglycerin is commonly used because it increases venous capacity more than does sodium nitroprusside. - In patients without evidence of left ventricular decompensation or myocardial ischemia during supraceliac aortic cross-clamping, a proximal aortic mean arterial pressure of up to 120 mm Hg is acceptable. The surgeon may request lower proximal arterial pressure if friable aortic tissue is encountered. Blood flow below the aortic clamp depends on pressure and decreases further during therapy with vasodilators. In this setting, vital organs and tissues distal to the clamp are exposed to reduced perfusion pressure and blood flow. Though infrequent, maintenance of adequate cardiac output may require active intervention with inotropic drugs.

False aneurysms only involve which layer of the aorta A. tunica adventitia B. tunica media C. tunica intima

A. Thoracic Aortic Aneurysms - The mortality associated with elective thoracic aneurysm repair is 22%, and if rupture occurs, it increases to 54%.103 Patients with aortic dissections have a predicted survival of only 3 months if they do not undergo surgical repair, because the incidence of rupture is high.104 Aneurysms have been described for hundreds of years, but not until 1951 did the development of the arterial prosthesis lead to successful bypass options.105 The refinement of endovascular stent grafts, surgical and perfusion techniques, and intraoperative management have contributed to improved surgical outcomes. Classification - Aneurysms of the thoracic aorta may be classified with respect to type, shape, and location. Typically, aneurysms involving all three layers of the arterial wall—tunica adventitia, tunica media, and tunica intima—are considered to be true aneurysms. In comparison, aneurysms that solely involve the adventitia are termed false aneurysms. The shape of the lesion also can serve as a means of characterizing aneurysms. Fusiform aneurysms have a spindle shape and result in dilation of the aorta. Saccular aneurysms are spherical dilations and are generally limited to only one segment of the vessel wall. Aortic dissection is the result of a spontaneous tear within the intima that permits the flow of blood through a false passage along the longitudinal axis of the aorta. If an aortic dissection is extensive, it is difficult for the surgeon to isolate the aneurysm and secure a graft, due to the weakened aortic wall. There are two major classification schemes for aortic dissections, based on the location. These are the DeBakey and Stanford classifications (Table 28.6). Thoracoabdominal aortic aneurysms (TAAA) are classified using the Crawford classification, as shown in Fig. 28.4.

The most common complication associated with Carotid Artery Stenting is A. Bradycardia B. Thromboembolism C. MI D. Horner Syndrome

Anesthetic Considerations - The anesthetic technique used most often for patients having CAS is local anesthesia at the femoral insertion site, minimal sedation, antithrombotic therapy, and observation for hypotension and bradycardia.238 Anticoagulation is initiated with a heparin bolus (50-100 units/kg) to maintain an activated clotting time greater than 250 seconds.239 Balloon inflation in the internal carotid artery can stimulate the baroreceptor response, resulting in prolonged bradycardia and hypotension. Glycopyrrolate or atropine can be given prior to inflation to offset this vagal response. Fluoroscopy will be used throughout the surgery, so it is important that all operating room personnel are protected with lead shielding. - Complications associated with CAS are listed in Box 28.16. The most common complication associated with this procedure is stroke caused by thromboembolism.240 Interventions for a patient with an acute stroke include airway and hemodynamic management. Immediate CT scan and identification of the presence of an embolus is critical. Neurologic deficits are significantly reversible if CBF is restored within 2 hours. Treatment with catheter-directed recombinant tissue plasminogen activator is approved for acute ischemic stroke that is believed to be caused by an embolus. Catheter-based thrombectomy using snares or balloon angioplasty to restore blood flow and remove the thromboembolic material has also been used successfully. - Patients typically remain in the postanesthesia care unit for 30 minutes after carotid stent placement and are then transferred to a monitored floor. A carotid duplex scan is performed prior to discharge, and then routinely obtained at 6 weeks, 6 months, 1 year, and then yearly. Patients remain on aspirin therapy for anticoagulation for life.241

The most common site for atherosclerosis are the following except A. Coronary arteries B. Carotid Body C. Abdominal aorta D. Iliac artery

B - The perioperative management of patients undergoing vascular surgery is one of the most challenging and controversial areas in the field of anesthesiology. Given the frequent occurrence of coexisting disease in elderly patients (see also Chapter 80), the hemodynamic and metabolic stress associated with arterial cross-clamping and unclamping, and the ischemic insults to vital organs, including the brain, heart, kidneys, and spinal cord, perioperative morbidity and mortality are more frequent with vascular surgery than with most other surgical procedures. Anesthesia care must focus on preservation of vital organ function, with a strong emphasis on the heart, which is the single most important cause of morbidity after vascular surgery. The clinical controversies associated with vascular surgery are diverse and involve aspects of preoperative, surgical, anesthetic, and postoperative management. The controversy associated with routine preoperative screening for coronary artery disease (CAD), as well as appropriate treatment if detected, has particular importance (see also Chapters 38 and 39). A specific anesthetic technique has not been established because vascular procedures often lend themselves to local, regional, general, or combined techniques. - In the 1970s, vascular surgery was recognized as a risk factor for perioperative cardiac morbidity. In the 1980s, the focus shifted to risk stratification in an effort to identify patients who were at the most frequent risk for morbid outcomes. In the 1990s, intensive clinical investigation involving anesthetic technique, sympatholytic drugs, hemodynamic control, and analgesic technique was undertaken and provided important insight into the prevention, treatment, and mechanisms of cardiac and other morbidity. During this time, a guideline-based approach to health care was initiated, primarily in the United States (see also Chapter 102). Over the last decade, a paradigm shift occurred away from routine preoperative screening for CAD with a focus on risk stratification and invasive treatment of CAD to an intensive strategy of perioperative cardiac risk reduction using medications and risk factor modification (see also Chapters 38 and 39). Additionally, over the last decade the multidisciplinary field of endovascular surgery has provided less invasive approaches or alternatives to conventional vascular reconstruction. These less invasive procedures, initially offered to patients traditionally considered unfit for open surgery, are being widely applied to the larger cohort of patients undergoing vascular surgery. The goal of this chapter is to review issues related to the perioperative care of patients undergoing vascular surgery and to address the underlying controversies. For simplicity, the five major categories of vascular surgical procedures are discussed separately: abdominal aortic surgery, thoracoabdominal aortic surgery, endovascular aortic surgery, lower extremity vascular surgery, and carotid surgery. Atherosclerosis - Cardiovascular diseases place an enormous burden on health care systems worldwide and are the leading cause of death and disability in the United States. Their underlying pathologic process is atherosclerosis, a slowly progressing chronic disorder of the arterial wall that compromises the blood supply to any or all of the vital organs or the extremities and leads to the clinical manifestations of myocardial infarction (MI), stroke, and gangrene. The lesions of atherosclerosis occur primarily in large and medium-sized arteries and tend to form at sites with disturbed laminar flow, such as branch points. The most common sites are the coronary arteries, carotid bifurcation, abdominal aorta, and iliac and femoral arteries (Fig. 69-1). Although atherosclerotic lesions result from a variety of complex pathogenetic processes, progression of atherosclerosis occurs in several stages. The initial lesion of atherosclerosis, the fatty streak, starts in early childhood and is initiated by intimal accumulation of low-density lipoprotein (LDL) particles. The fatty streak lesion consists largely of T cells and lipid-laden macrophages called foam cells. With the progressive accumulation of apoptotic and degenerated foam cells, cell debris, and cholesterol crystals, the fatty streak progresses to an atheromatous plaque with a necrotic lipid core. A more complex lesion develops with the formation of a fibrous cap of variable thickness composed of collagen and proliferated smooth muscle cells. The advanced lesions of atherosclerosis represent a progression of the fibroatheromatous plaque, with an expanded lipid-rich core, accumulation of calcium, and disruption of endothelial integrity. Physical disruption of the plaque's fibrous cap permits contact between flowing blood elements, including platelets and coagulation proteins, and the highly thrombogenic material located in the lesion's lipid core, such as collagen and tissue factor, which results in thrombus formation (i.e., atherothrombosis) or, in the case of intraplaque hemorrhage, plaque progression. Atherothrombosis may lead to complete vascular occlusion at the site of plaque rupture or detach to become an embolus that can block blood flow distal to its origin. - The American Heart Association Committee on Vascular Lesions has provided a numerical classification of histologically defined atherosclerotic lesion types.1 Figure 69-2 outlines the most updated classification.2 Lesion types I, II, and III are always small and clinically silent. With the development of type IV lesions, the pathways to clinical disease vary (see Fig. 69-2). Although lesions IV through VI may progress such that they obstruct the lumen of a medium-size or large artery and produce a clinical event (i.e., MI, ischemic stroke, or extremity ischemia), the clinical manifestations of atherosclerotic disease are most often associated with type VI lesions. The criteria for type VI histology are often interrelated and include one or more of the following: surface defect, hematoma, and thrombosis. Regression of lipid from lesion types IV, V, and VI may result in lesion morphology similar to that of type VII and VIII lesions. - Established risk factors for atherosclerosis-related cardiovascular disease are male gender, age, family history of premature cardiovascular disease, high levels of LDL cholesterol, low levels of high-density lipoprotein (HDL) cholesterol, diabetes, obesity, hypertension, and smoking. Newer and emerging risk factors include homocysteine, fibrinogen, lipoprotein(a), apolipoproteins B and A-I, and high-sensitivity C-reactive protein (hsCRP). Atherosclerosis usually has no early warning signs, making primary prevention difficult and often delaying risk modification until the 2108disease has progressed to an advanced stage. Established pharmacologic strategies against atherosclerosis are largely limited to treating hypertension and hyperlipidemia and controlling hemostasis to prevent thrombotic complications. Inhibitors of hydroxymethylglutaryl coenzyme A (i.e., statins) are the lipid-modifying drugs of choice and their efficacy in lowering LDL cholesterol and the risk for cardiovascular events is well established in large outcome-based clinical trials.3 Antiplatelet drugs, including aspirin and thienopyridines such as clopidogrel, are widely used to prevent vascular events in patients with cardiovascular disease. - Inflammation in the arterial wall plays a fundamental role in both atherogenesis and atheroprogression.4 Serum markers of inflammation, such as hsCPR, are being used in cardiovascular risk stratification. hsCPR levels are correlated with risk for death and MI and with the development of peripheral vascular disease. As a result of this new understanding, inflammation has become a therapeutic target in the prevention and treatment of atherosclerosis and its complications. Statins have important antiinflammatory modes of action that are independent of LDL cholesterol lowering. For example, treatment with statins decreases hsCRP in patients with atherosclerosis by 13% to 50% in contrast to placebo, and decreased levels of hsCRP while receiving statins is associated with improved clinical outcome.

Prevention of cerebral ischemia in CEA can be accomplished by A. Decreasing collateral flow B. Increasing collateral flow C. Decreasing cerebral metabolic requirements D. Increasing cerebral metabolic requirements

B & C Cerebral Protection - The major objective during carotid artery revascularization is to maintain cerebral CBF and oxygenation. Prevention of cerebral ischemia can be accomplished in one of two ways: by increasing collateral flow (placement of intraluminal shunt) or by decreasing cerebral metabolic requirements (anesthetic medications). Multiple interventions are available for cerebral protection, including avoiding hyperglycemia, hemodilution, maintenance of normocarbia, and tight control of arterial blood pressure. Anesthetics, except for etomidate, have cerebral protective properties and may be used to minimize the degree of cerebral ischemia. Shunt placement is commonly used to allow blood to flow proximally and distally to the carotid cross-clamp during intimal plaque dissection. Potential complications associated with carotid shunt placement are depicted in Fig. 28.12. - Cerebral ischemic events are most often the result of embolic complications, and frequently occur during the postoperative period. The need for shunt placement is based on surgeon preference and information obtained using intraoperative monitoring techniques to determine CBF. Furthermore, propofol decreases CMRO2 to 40% below normal values.114 Dexmedetomidine also decreases cerebral oxygen consumption and CBF in animal models.197 During transient focal ischemia, propofol decreases the CMRO2, which results in cerebral protection. The disadvantages of administering propofol during CEA surgery include myocardial depression and hypotension. The inhalation agents also decrease CMRO2 in a dose-dependent fashion. Nitrous oxide should be avoided due to the potential for pneumocephalus from microbubble expansion after carotid artery unclamping.175,182

Which Debakely classificaiton Originates in the ascending aorta; confined to this segment A. Type I B. Type II C. Type III D. Type IV

B.

Which of the following is not a Criteria for High Risk in Abdominal Aortic Aneurysm Repair A. Older than 70 years B. Male C. History of MI D. Diabetes

B.

The splanchnic organs contain nearly ___% of the total blood volume, nearly two thirds (>800 mL) of which can be autotransfused from the highly compliant venous vasculature into the systemic circulation within seconds. A. 15 B. 25 C. 35 D. 45

B. - Changes in cardiac output and filling pressure with aortic cross-clamping are not consistent and require an integrated approach in understanding the direction and magnitude of such changes (Fig. 69-5). Cross-clamping of the proximal descending thoracic aorta increases mean arterial, central venous, mean pulmonary arterial, and pulmonary capillary wedge pressure by 35%, 56%, 43%, and 90%, respectively, and decreases the cardiac index by 29%.62 Heart rate and left ventricular stroke work are not significantly changed. Supraceliac aortic cross-clamping increases mean arterial pressure by 54% and pulmonary capillary wedge pressure by 38%.63 Ejection fraction, as determined by two-dimensional echocardiography, decreases by 38%. Despite normalization of systemic and pulmonary capillary wedge pressure with anesthetic agents and vasodilator therapy, supraceliac aortic cross-clamping causes significant increases in left ventricular end-systolic and end-diastolic area (69% and 28%, respectively), as well as wall motion abnormalities indicative of ischemia in 11 of 12 patients (Table 69-6). Aortic cross-clamping at the suprarenal level causes similar but smaller cardiovascular changes, and clamping at the infrarenal level is associated with only minimal changes and no wall motion abnormalities. - The marked increases in ventricular filling pressure (preload) reported with high aortic cross-clamping have been attributed to increased afterload and redistribution of blood volume, which is of prime importance during thoracic aortic cross-clamping. The splanchnic circulation, an important source of functional blood volume reserve, is central to this hypothesis. The splanchnic organs contain nearly 25% of the total blood volume, nearly two thirds (>800 mL) of which can be autotransfused from the highly compliant venous vasculature into the systemic circulation within seconds.64 Primarily because of smaller splanchnic venous capacitance, blood volume is redistributed from vascular beds distal to the clamp to the relatively noncompliant vascular beds proximal to the clamp (see Fig. 69-5). Both passive and active mechanisms lower splanchnic venous capacitance with thoracic aortic cross-clamping. Cross-clamping the aorta above the splanchnic system dramatically reduces splanchnic arterial flow, which produces a significant reduction in pressure within the splanchnic capacitance 2120vessels.52 This decreased pressure allows the splanchnic veins to passively recoil and increase venous return to the heart and blood volume proximal to the clamp. Thoracic aortic cross-clamping also results in significant increases in plasma epinephrine and norepinephrine, which may enhance venomotor tone both above and below the clamp. The splanchnic veins are highly sensitive to adrenergic stimulation. The major effect of catecholamines on the splanchnic capacitance vessels is venoconstriction, which actively forces out splanchnic blood, reduces splanchnic venous capacitance, and increases venous return to the heart.52 - Several animal studies support the blood volume redistribution hypothesis. Cross-clamping the thoracic aorta in dogs results in marked increases in mean arterial pressure and end-diastolic left ventricular pressure (84% and 188%, respectively) and no significant change in stroke volume.65 In this same experimental model, simultaneous cross-clamping of the thoracic aorta and the inferior vena cava resulted in no significant change in mean arterial pressure or preload (Fig. 69-6). Stroke volume was reduced by 74%. By transfusing blood (above the clamps) during this period of simultaneous clamping, the authors reproduced the hemodynamic effect of thoracic aortic cross-clamping alone. This study also demonstrated that thoracic aortic cross-clamping is associated with a significant and dramatic increase (155%) in blood flow above the level of the clamp whereas no change in blood flow occurred with simultaneous aortic and inferior vena cava clamping. In other animal models, the proximal aortic hypertension and increased central venous pressure occurring after thoracic aortic cross-clamping were completely reversed by phlebotomy.66 Aortic cross-clamping at the thoracic and suprarenal levels in dogs both resulted in proximal aortic hypertension, but only occlusion at the thoracic level increased central venous pressure.67 In this study, thoracic aortic occlusion increased blood volume in organs and tissues proximal to the clamp whereas no such increase occurred with suprarenal aortic cross-clamping. These experimental data strongly support the hypothesis of blood volume redistribution during aortic cross-clamping and help explain the marked differences in hemodynamic responses observed after aortic cross-clamping at different levels.63 Afterload-dependent increases in preload also occur with aortic cross-clamping, usually in the setting of impaired myocardial contractility and reduced coronary reserve. The impaired left ventricle may respond to increased afterload with an increase in end-systolic volume and a concomitant reduction in stroke volume (afterload mismatch). The reduction in stroke volume may be due to limited preload reserve, myocardial ischemia, or inability of the heart to generate a pressure-induced increase in contractility (the Anrep effect). If right ventricular function remains normal, the preclamp right ventricular stroke volume added to the increased left ventricular end-systolic volume results in left ventricular dilation and elevated end-diastolic volume. If corrective measures are not undertaken, overt left ventricular overload may result, with severe peripheral organ dysfunction and pulmonary edema. - Most clinical studies indicate that cardiac output decreases with thoracic aortic cross-clamping (without vasodilator therapy or diverting circulatory support), whereas most animal studies show no significant change or an increase in cardiac output. However, the status of the left ventricle clearly plays a major role. Whereas a normal intact heart can withstand large increases in volume without significant ventricular distention or dysfunction, an impaired heart with reduced myocardial 2121contractility and coronary reserve may respond to such increase in volume conditions with marked ventricular distention as a result of acute left ventricular dysfunction and myocardial ischemia. Although impaired myocardial contractility and reduced coronary reserve are rare in animal experiments, such disorders are frequent in the elderly population undergoing aortic reconstruction. The increase in ventricular loading conditions seen with thoracic and supraceliac cross-clamping62,63 in the clinical setting may increase left ventricular wall stress (afterload), with resultant acute deterioration of left ventricular function and myocardial ischemia. Impaired subendocardial perfusion caused by high intramyocardial pressure may be the cause of wall motion abnormalities and changes in ejection fraction. Reflex mechanisms causing immediate feedback inhibition may also explain the reduction in cardiac output with aortic cross-clamping. For example, baroreceptor activation resulting from increased aortic pressure should depress the heart rate, contractility, and vascular tone. Thoracic aortic cross-clamping with the use of vasodilator therapy to normalize ventricular loading conditions maintains or increases cardiac output.68 The metabolic effects of aortic cross-clamping are summarized in Box 69-1. Cross-clamping of the thoracic aorta decreases total-body O2 consumption by approximately 50%. For reasons that are unclear, O2 consumption decreases in tissues above the clamp. In clinical studies, increased mixed venous O2 saturation occurs with aortic cross-clamping above the celiac axis. This increase in mixed venous O2 saturation may be explained by a reduction in O2 consumption that exceeds the reduction in cardiac output, thus decreasing total body O2 extraction. Central hypervolemia and increased arteriovenous shunting in tissues proximal to the aortic clamp may play a role in reducing total body O2 extraction. Arterial blood pressure, blood flow, and O2 consumption distal to a thoracic aortic cross-clamp decrease by 78% to 88%, 79% to 88%, and 62%, respectively, from baseline values before clamping. Blood flow through tissues and organs below the level of aortic occlusion is dependent on perfusion pressure and is independent of cardiac output. Administration of sodium nitroprusside to maintain proximal aortic pressure above the cross-clamp at preclamp levels has been shown to further reduce arterial pressure distal to the clamp by 53%. As discussed later, these data have significant implications regarding vital organ protection during aortic cross-clamping. - The cardiovascular response to infrarenal aortic cross-clamping is less significant than with high aortic cross-clamping (see Table 69-6). Although several clinical reports have noted no significant hemodynamic response to infrarenal cross-clamping, the hemodynamic response generally consists of increases in arterial pressure (7% to 10%) and systemic vascular resistance (20% to 32%), with no significant change in heart rate. Cardiac output is most consistently decreased by 9% to 33%. Reported changes in ventricular filling pressure have been inconsistent. Blood volume redistribution may affect preload with infrarenal aortic cross-clamping (see Fig. 69-5). In this situation, blood volume below the clamp shifts to the compliant venous segments of the splanchnic circulation above the clamp, thereby dampening the expected increase in preload. The preload changes with infrarenal aortic cross-clamping also may depend on the status of the coronary circulation. Patients with severe ischemic heart disease responded to infrarenal aortic cross-clamping with significantly increased central venous (35%) and pulmonary capillary (50%) pressure, whereas patients without CAD had decreased filling pressure. Echocardiographically detected segmental wall motion abnormalities occur in up to 30% of patients during infrarenal aortic reconstruction, with over 60% occurring at the time of aortic cross-clamping. Patients with aortoiliac occlusive disease may have less hemodynamic response to infrarenal aortic cross-clamping than do patients with AAA disease, perhaps as a result of more extensive periaortic collateral vascularization.

The majority of endoleaks in EVAR are what type A. I B. II C. III D. IV

B. - Endovascular graft design and durability continue to improve. Graft devices are either unibody (come in one piece) or modular (come in multiple pieces). The endograft fabric is either woven polyester (Dacron) or polytetrafluoroethylene. There is no significant difference in biologic response when comparing these two materials.155 The graft skeleton is constructed of stainless steel, Nitinol, or Elgiloy (Fig. 28.8). Nitinol stents are popular because they exhibit minimal shortening after deployment when exposed to body temperature. There is considerable interest and research involving drug-eluting stents. Researchers have shown in initial clinical trials that restenosis rates are improved with the newer-generation endovascular stents.156,157 EVSGs have undergone modifications to meet anatomic challenges and improve patient outcomes. In the past, endovascular repair has been limited to infrarenal AAAs and isolated TAAs. The advent of fenestrated and branched endografts have made endovascular repair of thoracoabdominal and juxtarenal aneurysms possible. Fenestrated ESVGs are safe and effective in short- and mid-term postoperative follow-up.158 Continued evolution of endograft technology will maximize the benefit and minimize complications in patients with a range of aneurysmal disease. - Endoleak (Fig. 28.9), which was noted earlier as persistent blood flow and pressure (endotension) between the endovascular graft and the aortic aneurysm, is a serious complication of this procedure. Types of endoleaks are listed in Table 28.7 and shown in Fig. 28.10. Endoleak diagnosed by postoperative CT scan has been reported to occur in 15% to 52% of patients.159 The majority of endoleaks are type II, and 70% close spontaneously within the first month after implantation.160 Type II endoleaks are caused by collateral retrograde perfusion and are associated with long-term complications. Type I and type III endoleaks are caused by device-related problems and most often occur soon after EVSG implantation.161 The most frequent interventions used to correct these complications include implantation of a second endograft or open repair.162 One long-term study has demonstrated that EVAR yields good results as compared to an open repair, but the overall durability of the open surgical procedure is superior.163

Contraindications to elective repair include the following except A. intractable angina pectoris B. recent stroke C. severe pulmonary dysfunction D. chronic renal insufficienc

B. Abdominal Aortic Reconstruction Patient Selection - As a result of recent advances in surgical and anesthetic techniques, the 30-day perioperative mortality rate associated with elective open repair of AAAs is estimated to be 3% to 4.5%.59 Most patients with abdominal aneurysms, including the elderly, are considered surgical candidates. Although advanced age contributes to an increased incidence of morbidity and mortality, age alone is not a contraindication to elective aneurysmectomy.60 However, physiologic age is more indicative of increased surgical risk than chronologic age. Contraindications to elective repair include intractable angina pectoris, recent MI, severe pulmonary dysfunction, and chronic renal insufficiency.61 Patients with stable CAD and coronary artery stenosis of greater than 70% who require nonemergent AAA repair do not benefit from revascularization if β-blockade has been established.44 Table 28.1 lists characteristics that define high-risk patients; however, in most cases, the presence of an AAA warrants surgical intervention.53 - The dimensions of an aneurysm can change over time. AAAs expand by approximately 4 mm/yr.62 Aneurysmal vessel dimensions correspond to the law of Laplace: where T = wall tension, P = transmural pressure, and r = vessel radius. As the radius of a vessel increases, the wall tension increases. Wall tension is directly proportional to the vessel radius and intraluminal pressure and inversely proportional to wall thickness. Therefore, the larger the aneurysm, the higher the likelihood of spontaneous rupture. As previously stated, aneurysms measuring more than 4 to 5 cm in diameter generally require surgical intervention, but aneurysms measuring less than 4 to 5 cm should not be considered benign, and monitoring of the condition is indicated.44 An aneurysm has the potential to rupture regardless of its size. As the diameter of the aneurysm increases in size, the risk of rupture increases, as shown in Table 28.2.1 In contradiction to the current thought that increased wall shear stress increases the risk of aortic rupture, it has been shown that aortic rupture may occur more often at sites with low wall shear stress, due to blood flow recirculation resulting in thrombus deposition, aortic wall degeneration, and eventual rupture.63 Due to increased wall stress at the bifurcation of the aorta and the iliac arteries, AAAs most frequently develop in the infrarenal aorta, although approximately 5% to 15% involve the suprarenal aorta. It is estimated that approximately 40% of AAAs also involve the iliac arteries.1

This is the single most important determinant of paraplegia and renal failure with the clamp-and-sew technique. A. Surgical technique B. Duration of the clamp time C. Blood loss D. Perioperative hemodynamics

B. Anesthetic Management Simple Aortic Cross-Clamping - Descending thoracic and thoracoabdominal aortic surgery can be performed without extracorporeal support (i.e., left heart bypass or cardiopulmonary bypass). The "clamp-and-sew" technique has had relatively favorable outcomes, but these cases are from institutions with extensive clinical experience and the shortest cross-clamp times. Advocates of this technique favor its surgical simplicity. However, the benefits of avoiding the complexity and complications of bypass must be weighed against the risk for vital organ ischemia and complications such as renal failure and paraplegia. - Other than the location and extent of the aneurysm, the duration of cross-clamping on the aorta is the single most important determinant of paraplegia and renal failure with the clamp-and-sew technique. Clamp times of less than 20 to 30 minutes are associated with almost no paraplegia. When clamp times are between 30 and 60 minutes (the vulnerable interval), the incidence of paraplegia increases from approximately 10% to 90% as time progresses. Because clamp times are typically in this range or longer, specific adjuncts directed against end-organ ischemic complications are often used. Such adjuncts include epidural cooling for spinal cord protection, regional hypothermia for renal protection, and in-line mesenteric shunting to reduce visceral ischemia. - When the simple clamp-and-sew technique is used, application of the aortic cross-clamp results in significant proximal hypertension, which requires active pharmacologic intervention. Management strategies have been discussed previously in the section on abdominal aortic reconstruction. Briefly, both sodium nitroprusside and isoflurane have been used successfully to control the proximal hypertension associated with high aortic cross-clamping. Isoflurane is best reserved for patients with good myocardial function. Vasodilators, such as sodium nitroprusside, must be used with caution because they can result in significant overperfusion of the body proximal to the clamp and very low pressures distally. Nitroglycerin can be used to normalize preload and cardiac filling and thus reduce ventricular wall tension. Although nitroglycerin does not control proximal hypertension well as a single agent, it is very helpful when used in combination with sodium nitroprusside. Management of aortic unclamping has been discussed earlier.

What is the most consistent hemodynamic response to aortic unclamping A. Decrease myocardial contractility B. Decrease blood pressure C. Decrease central venous pressure D. Decrease cardiac output

B. Aortic Unclamping The hemodynamic and metabolic effects of aortic unclamping are listed in Box 69-3. The hemodynamic response to unclamping depends on many factors, including the level of aortic occlusion, total occlusion time, use of diverting support, and intravascular volume. Hypotension, the most consistent hemodynamic response to aortic unclamping, can be profound, particularly after removal of a supraceliac cross-clamp (Fig. 69-7). Reactive hyperemia in tissues and organs distal to the clamp and the resultant relative central hypovolemia are the 2123dominant mechanisms of the hypotension. Washout of vasoactive and cardiodepressant mediators from ischemic tissues, as well as humoral factors, may also contribute to the hemodynamic responses after unclamping the aorta. These humoral factors and mediators, which may also play a role in organ dysfunction after aortic occlusion, include lactic acid, renin-angiotensin, O2 free radicals, prostaglandins, neutrophils, activated complement, cytokines, and myocardial-depressant factors.61 - Avoidance of significant hypotension with unclamping requires close communication with the surgical team, awareness of the technical aspect of the surgical procedure, and appropriate administration of fluids and vasoactive drugs. It is essential that correction of preoperative fluid deficits, maintenance of intraoperative fluid requirements, and replacement of blood loss be accomplished before unclamping. Vasodilators, if used, should be gradually reduced and discontinued before unclamping. The inspired concentrations of volatile anesthetics should be decreased. Moderate augmenting of intravascular volume by administration of fluids (∼500 mL) during the immediate prerelease period is indicated for infrarenal unclamping. More aggressive intravascular fluid administration is required in the period immediately preceding supraceliac unclamping. Maintaining increased central venous or pulmonary capillary wedge pressure during the cross-clamp period is not indicated and may result in significant overtransfusion of fluids and blood products. If significant hypotension results, gradual release of the aortic clamp and reapplication or digital compression are important measures in maintaining hemodynamic stability during unclamping. Although vasopressor requirements are minimal after release of the infrarenal clamp, significant support is often needed after the removal of supraceliac clamps. Caution must be observed when vasopressor support is used in this setting because profound proximal hypertension may occur if reapplication of the cross-clamp is required above the celiac axis. In addition, hypertension should be avoided to prevent damage to or bleeding from the vascular anastomoses.

The equivalent of at least __ units of washed blood must be recovered for Intraoperative cell salvage to be cost-effective. A. 1 B. 2 C. 3 D. 4

B. Autologous Blood Procurement - Elective abdominal aortic reconstruction may result in substantial blood loss and warrants the routine crossmatching of 4 to 6 units of packed red blood cells (RBCs). Suprarenal aneurysms and other more complex aortic reconstructions often demand even greater allogeneic blood availability. Over the last 2 decades, concerns regarding the safety, availability, and acceptability of allogeneic blood have led to greater use of autologous blood procurement (see also Chapters 61 and 63). Preoperative autologous donation, intraoperative cell salvage, and acute normovolemic hemodilution have all been used during aortic surgery to reduce or eliminate exposure to allogeneic blood and the associated risks for transfusion-related complications. - Intraoperative cell salvage is the most widely used technique and in some centers is considered routine. The equipment is expensive and requires significant training and expertise. An early, nonrandomized study reported a 75% reduction in the number of allogeneic RBC units transfused during elective aortic surgery with the use of cell salvage. Later randomized studies have reported conflicting results. The routine use of cell salvage during aortic surgery may not be cost-effective ($250 to $350 per case), and thus it may best be reserved for a select group of patients with an expected large blood loss. The equivalent of at least 2 units of washed blood must be recovered for this technique to be cost-effective. A cost-effective option is to use the cell salvage reservoir for blood collection and activate the full salvage process only if large blood loss occurs. - Acute normovolemic hemodilution is often used in conjunction with intraoperative cell salvage during aortic surgery. Two randomized studies reported that the combined use of hemodilution and cell salvage reduced the allogeneic blood requirement in patients undergoing aortic surgery. As with cell salvage alone, this benefit is probably greater with procedures involving higher blood loss. Another randomized study found that the combined use of the two techniques during aortic surgery was cost neutral in comparison to standard allogeneic transfusion. Hemodilution does not worsen myocardial ischemia and may improve hemodynamic tolerance to aortic cross-clamping in patients with CAD.

This is the second most common vascular operation performed in the United States every year A. Coronary revascularization B. Carotid endarterectomy C. Open AAA repair D. EVAR

B. Cerebrovascular Insufficiency and Carotid Endarterectomy - Carotid endarterectomy (CEA) is the second most common vascular operation performed in the United States every year (the first being coronary revascularization). Cerebrovascular accidents (strokes) are the third leading cause of death in the United States.167 More strokes are caused by cerebral ischemia than by intracranial hemorrhage. In carotid atherosclerotic disease, subintimal fatty plaques can increase in size over time and incrementally occlude the vascular lumen, which results in decreased cerebral blood flow (CBF). The plaque may rupture and release fibrin, calcium, cholesterol, and inflammatory cells. This phenomenon can lead to abrupt occlusion of the lumen from thrombosis due to platelet activation, or an embolus may form and decrease CBF distal to the carotid artery. In each scenario, an abrupt decrease in CBF leads to transient ischemic attacks (TIAs) or strokes. Note the anatomic details associated with the removal of plaque and the involvement within the layers of the carotid artery in Fig. 28.11. - More than half of all strokes are preceded by a TIA. The Framingham study reported that the risk of a stroke was 30% 2 years after a TIA had occurred and approximately 55% 12 years after a TIA had occurred.168 It is this increased risk of stroke associated with TIA that provides the rationale for the use of CEA, the surgical procedure in which the internal carotid artery is incised and the plaque within the carotid arterial lumen is removed to improve CBF.

Which laryngeal nerve is most susceptible to be affected in a descending thoracic aneurysm A. Right B. Left

B. Descending Thoracic and Thoracoabdominal Aneurysms Preoperative Assessment - Patients who undergo major vascular surgery are often elderly and have varying degrees of concurrent disease. Most patients who develop a descending thoracic aortic aneurysm (DTAA) are asymptomatic. Operative surgical decisions are based on the size, extent, and rate of expansion of the aneurysm. For patients with degenerative aortic disease, surgical repair is advised for aneurysms 6 cm or larger. Independent risk factors for DTAA include pain, increased age, COPD, renal insufficiency, aneurysm size, and aneurysm expansion rate.110 - The importance of a thorough preoperative evaluation cannot be overemphasized. Special attention should be directed toward cardiac, renal, and neurologic function. Although most fatalities related to thoracic aortic surgery are cardiac in origin, renal and neurologic dysfunction contribute to poor surgical outcomes.111 Preoperative renal dysfunction is directly related to postoperative renal failure, and is thought to be one of the strongest contributors to renal deterioration after surgery.83,111 Neurologic function should be carefully assessed in the preoperative phase. Paraplegia is one of the most devastating consequences of thoracic aortic surgery, and any alteration in lower-extremity function should be noted. Hoarseness related to compression of the recurrent laryngeal nerve should be assessed and documented. The left recurrent laryngeal nerve is most susceptible due to its close proximity to the aortic arch. Bilateral recurrent laryngeal nerve compression or damage can result in respiratory compromise.

Amaurosis fugax, as seen in high grade carotid artery stenosis, is manifested as A. TIA B. Monocular blindness C. Aphasia D. Facial drooping on one side

B. Diagnosis - The neurologic symptoms associated with cerebral vascular dysfunctions such as TIAs and strokes are often related to decreased CBF. Whereas there are multiple causes for symptoms such as lightheadedness, altered levels of consciousness, aphasia, and acute motor deficits, these deficits warrant testing to determine if carotid stenosis is present. Asymptomatic carotid bruits may be a sign of carotid artery disease. However, not all carotid bruits indicate the presence of significant carotid artery disease. Amaurosis fugax manifests as monocular blindness and occurs in 25% of patients with high-grade carotid artery stenosis. This syndrome is believed to be caused by microthrombi that migrate into the internal carotid artery and decrease the blood supply of the optic nerve via the ophthalmic artery. Standard diagnostic imaging techniques used to assess the extent of carotid disease include duplex ultrasonography, digital subtraction angiography, CT angiography, and magnetic resonance angiography.185 Preoperative Assessment - The presence of concurrent CAD and carotid stenosis is well documented. Although stroke is a devastating consequence of CEA, MI contributes more often to poor surgical outcomes than stroke. Although coronary angiography may not be justified in all patients undergoing CEA, a systematic approach for identifying CAD and its subsequent risks should be performed before elective surgery. - Patients with no significant medical history, normal physical examination, and normal electrocardiography should proceed directly to surgery; these patients have low surgical risks. When abnormal cardiac information is obtained, further evaluation should be performed. The presence of significant comorbidities will determine the extent to which further preoperative testing is appropriate. Box 28.13 lists preoperative risk factors in patients having CEA. Preoperative pharmacologic optimization for patients with vascular and cardiac disease is discussed earlier in this chapter. Vascular surgery is associated with an increased risk of major adverse cardiac events.186 For a complete discussion of cardiac optimization, see Preoperative Evaluation and preparation of the patient. (Chapter 20) The ACCF/AHA recommendations for perioperative cardiac assessment are in Table 28.8. Preoperative Risk Factors for Patients Scheduled for CEA • Neurologic (cerebrovascular accident) • Coronary artery disease • Hypertension • Diabetes • Renal disease • Thromboembolism

In AAA repair, fluid replacement should be sufficient to maintain normal cardiac filling pressures and cardiac output, and a urine output of at least __ mL/kg per hr A. 0.5 B. 1 C. 1.5 D. 2

B. Fluid Management - Maintaining intravascular volume may be an extreme challenge during abdominal aortic resections. Controversy exists regarding whether the administration of crystalloids or colloids affects the overall incidence of morbidity and mortality. Crystalloids may be used for replacing basal and third-space losses at an approximate rate of 10 mL/kg per hr. Blood losses initially can be replaced with crystalloids at a ratio of 3:1. The combination of crystalloid and colloid administration is also acceptable. Regardless of the choice of fluid, volume replacement must be dictated by physiologic parameters. Fluid replacement should be sufficient to maintain normal cardiac filling pressures and cardiac output, and a urine output of at least 1 mL/kg per hr. Patients with limited cardiac reserve can develop congestive heart failure if hypervolemia occurs. As mentioned previously, cell-saver blood retrieval is commonly used, and the use of two large-bore intravenous lines in addition to a central venous catheter is warranted. Goal-directed fluid therapy may help to optimize a patient's intravascular volume and hemodynamic status. Hemodynamic Alterations - Hemodynamic changes are likely to occur throughout the procedure. Adequate preoperative sedation should be given before the placement of invasive monitoring equipment. Fluctuations in heart rate and blood pressure should be anticipated during induction and intubation. Preoperative replacement of fluid deficits prevents exaggerated responses to vasodilating induction agents. For patients with adequate left ventricular function, hemodynamic stability can be preserved with a "slow" and controlled induction using higher doses of opioids and sympathomimetic agents if hypotension develops. The response to mesenteric traction (discussed previously) is also associated with stimulation of the celiac reflex, which results in bradycardia and hypotension.

Patients scheduled for which surgery have a frequent incidence of right and left arm arterial blood pressure differences. A. Abdominal Aneurysm repair B. Carotid surgery C. Femoral endarterectomy D. Brachial artery repair

B. Hemodynamic Monitoring - The appropriate level of invasive hemodynamic monitoring (see also Chapter 45) in patients undergoing vascular surgery is a controversial issue. Multiple considerations determine the need for monitoring and are often not the same for all vascular patients. Given the frequency of coexisting disease, the potential for fluid shifts and blood loss, and the physiologic changes associated with cross-clamping and unclamping, virtually all patients undergoing major vascular surgery should be monitored with an intraarterial catheter. This allows beat-to-beat blood pressure monitoring, accurate determination of diastolic pressure, and sampling of arterial blood for diagnostic purposes. The radial artery is most commonly selected for cannulation because of its superficial location and the presence of collateral circulation. The need to verify collateral blood flow is questionable. The Allen test can be used to assess collateral flow in the palmar arch, but evidence suggests that ischemic injury can occur in patients with a normal Allen test result and that no injury occurs in patients with an abnormal Allen test result when the radial artery is cannulated. When the radial artery is difficult to cannulate, the ulnar or axillary arteries are alternative sites. The axillary artery can be cannulated by the Seldinger technique, but extreme care should be taken to avoid injecting air when flushing an axillary catheter because the tip may lie close to or inside the aortic arch and thus allow air to enter the cerebral circulation. Whenever possible, the femoral arteries should be avoided in patients with peripheral vascular disease. - Vascular surgery patients often have a large discrepancy in arterial blood pressure between the right and left arms as a result of atherosclerotic lesions in the subclavian or axillary arteries; such discrepancy results in a falsely low arterial blood pressure in the ipsilateral arm.51 Patients scheduled for carotid surgery have a frequent incidence of right and left arm arterial blood pressure differences. To avoid pseudohypotension, arterial blood pressure should be verified in both arms, and the arm with the higher pressure should be used for monitoring during surgery. Both arms may have falsely low arterial blood pressure as a result of bilateral disease. In this case, the femoral artery may be the best option for monitoring. - The utility of central venous and pulmonary artery catheters for hemodynamic monitoring of patients during vascular surgery is controversial. The surgical procedure often determines the degree of fluid shifting and blood loss and thus the usefulness of invasive monitoring. The patient's underlying cardiac, pulmonary, and renal status also need to be considered. Although cardiovascular function is highly dependent on adequate ventricular filling (i.e., the heart cannot pump out more blood than it receives), values of central venous pressure and pulmonary artery occlusion pressure do not correlate with values of measured circulating blood volume.52 Additional information, such as stroke volume and cardiac output, are often important when extreme stress is placed on an already impaired heart. The indications for central venous pressure and pulmonary artery catheter monitoring are discussed in further detail in the subsequent sections. The role of TEE (see also Chapter 46) in the perioperative period has expanded rapidly over the last decade. TEE is useful in identifying anatomic and functional cardiac abnormalities and is a sensitive monitor for detection of myocardial ischemia. During complex aortic reconstruction, TEE provides important real-time information on cardiac filling and function and is particularly useful when unexplained hemodynamic instability is encountered.

These aneurysms are located at the level of the renal arteries, but they spare the renal artery orifice. A. Suprarenal B. Juxtarenal C. Infrarenal

B. Juxtarenal and Suprarenal Aortic Aneurysms - Although most AAAs occur below the level of the renal arteries, 2% extend proximally and involve the renal or visceral arteries.98 Juxtarenal aneurysms are located at the level of the renal arteries, but they spare the renal artery orifice. More proximal suprarenal aneurysms include at least one of the renal arteries, and may involve visceral vessels. The effects of aortic cross-clamping for juxtarenal or suprarenal aneurysms are similar to those for infrarenal aortic occlusions; however, the magnitude of hemodynamic alterations increases, as the aorta is clamped more proximally. - Renal failure, although possible during infrarenal aortic cross-clamping, occurs more often because of suprarenal aortic occlusion. Maintaining adequate intravascular volume and administering osmotic and loop diuretics may minimize renal ischemia and dysfunction. - Paraplegia is possible when the blood supply to the spinal cord is interrupted by aortic cross-clamping at or above the level of the diaphragm. Increasing the MAP or decreasing cerebrospinal fluid (CSF) pressure by placing a catheter in the subarachnoid space to drain CSF may be used as a means to increase spinal cord perfusion pressure.98 Total body hypothermia and multimodal neurological monitoring, including SSEPs and MEPs, can be used to decrease the incidence of paraplegia. Early detection and intervention for spinal cord ischemia can decrease the incidence of permanent paraplegia after endovascular stent-grafting of the descending thoracic aorta. Neurologic deficits can become evident weeks after surgery. Routine SSEP monitoring, serial neurologic assessment, arterial pressure augmentation, and CSF drainage may benefit patients at risk for paraplegia.99 Box 28.6 summarizes the complications that may result from juxtarenal or suprarenal aortic occlusion. Potential Complications of Juxtarenal or Suprarenal Aortic Occlusion • Renal failure • Hemorrhage • Distal arterial occlusion • Infarction • Pulmonary or cardiac dysfunction • Impotence • Paraplegia • Thrombosis • Pseudoaneurysm formation • Aortoenteric fistula

This is the most common reason for poor outcomes in noncardiac surgery for patients with vascular disease. A. Perioperative Stroke B. Perioperative MI C. Perioperative Renal failure D. Perioperative Shock

B. Patient Preparation - Perioperative MI is the most common reason for poor outcomes in noncardiac surgery for patients with vascular disease. Optimization of myocardial oxygen supply and demand and modification of cardiac risk factors are the major goals of preoperative risk reduction. β-Blockers and statins are the important preoperative pharmacologic treatments for medical management.17,19 Prophylactic coronary revascularization does not reduce the incidence of perioperative cardiac events.64 Preoperative cardiac testing is recommended only if interpretation of the results will change anesthetic management.15,65,66 - Preoperative fluid loading and restoration of intravascular volume are perhaps the most important techniques used to enhance cardiac function during abdominal aortic aneurysmectomies. Reliable venous access must be secured if volume replacement is to be accomplished. Large-bore intravenous lines and central lines can be used to infuse fluids or blood. Massive hemorrhage is an ever-present threat; therefore, the availability of blood and blood products should be ensured. Provisions for rapid transfusion and intraoperative blood salvage should be confirmed.

Which of the following is a leading cause of perioperative mortality at the time of vascular surgery A. COPD B. CAD C. Renal Failure D. Stroke

B. Preoperative Evaluation Coexisting Disease - Patients undergoing vascular surgery have a frequent incidence of coexisting disease, including diabetes mellitus, hypertension, renal impairment, and pulmonary disease, all of which should be assessed and, if possible, optimized before surgery (see also Chapters 38 and 39). Because of the systemic nature of atherosclerotic disease, patients with vascular disease frequently have arterial disease affecting multiple vascular territories. CAD is the leading cause of perioperative mortality at the time of vascular surgery, and long-term survival after vascular procedures is significantly limited by the frequent occurrence of morbid cardiac events.5 Less than 10% of patients who undergo vascular surgery have normal coronary arteries, and more than 50% have advanced or severe CAD. Unrecognized MI (determined by wall motion abnormalities at rest in the absence of a history of MI) and silent myocardial ischemia (determined by stress-induced wall motion abnormalities in the absence of angina) often occur in vascular surgery patients (23% and 28%, respectively) and are associated with increased long-term mortality and adverse cardiac events.6 Left ventricular systolic dysfunction is five times more common in patients with vascular disease than in matched controls.7 It is not clear whether any specific category of vascular disease is associated with a greater likelihood of coexisting CAD. Some investigators have shown a similar incidence and severity of CAD in patients with aortic, lower extremity, and carotid disease. Others have shown that patients with lower extremity vascular disease are more likely to have significant CAD and to experience perioperative morbidity. Medical therapy is the cornerstone of the management of CAD. Perioperative and Long-Term Cardiac Outcomes - Preoperatively, the potential for MI and death in patients undergoing vascular surgery must be considered (Table 69-1). Nonfatal and fatal MIs are the most important and specific outcomes that determine perioperative cardiac morbidity. When multiple recent studies are pooled, the 2109overall prevalence of perioperative MI and death is 4.9% and 2.4%, respectively. When outcomes are assessed over the long term (2 to 5 years), the prevalence of MI and death is 8.9% and 11.2%, respectively. This perioperative and long-term morbidity and mortality persist despite aggressive medical and surgical therapy.8 - Guideline-Based Approach A guideline-based approach to health care is relatively new and originated primarily in the United States. The American College of Cardiology (ACC) Foundation and the American Heart Association (AHA) jointly produced guidelines in the area of cardiovascular disease for more than 2 decades. The ACC/AHA Task Force on Practice Guidelines published "Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery" in 1996. This evidence-based approach to perioperative evaluation and management was updated in 2002 and 2007,9,10 and in 2009.11 New guidelines will be published in 2014. A stepwise approach (simplified from the 2007 guidelines) to perioperative cardiac evaluation and care for noncardiac surgery is provided in Chapter 38. The authors emphasize that the purpose of the preoperative evaluation is not to give medical clearance but rather to perform an evaluation of the patient's current medical status; make recommendations concerning the evaluation, management, and risk for cardiac problems; and provide a clinical risk profile that the patient and caregivers can use in making treatment decisions that may influence perioperative and longer term cardiac outcomes. The overriding theme of the perioperative guidelines is that intervention is rarely 2110necessary to simply lower the risk associated with surgery unless such intervention is indicated irrespective of the preoperative context. Thus, preoperative testing should not be performed unless it is likely to influence patient care. The particular challenge that the vascular surgery patient presents is emphasized throughout the document. Aspects of the updated guidelines and their evidence-based approach will be discussed throughout this chapter.

This arterial catheter is used for aneurysms involving the proximal descending thoracic aorta A. Left radial B. Right radial C. RIght femoral D. Left femoral

B. Preoperative Preparation and Monitoring - Open surgical TAA repair requires extensive preoperative evaluation and planning. The evaluation and management of coexisting cardiac and pulmonary disease are discussed earlier in this chapter. Before the day of surgery, the anesthesiologist and vascular surgeon should discuss, at a minimum, extent of the aneurysm and technique of surgical repair, plans for distal aortic perfusion, monitoring for spinal cord ischemia, renal and spinal cord protection, hemodynamic monitoring, and ventilation strategy. Blood loss during TAA repair can be profound, and the need for massive transfusion must not be underestimated. This author routinely has 15 units of packed RBCs and 15 units of thawed fresh frozen plasma immediately available in the operating room, and additional units must be readily obtainable. I use a large cooler to store blood products on ice in the operating room so that they can be returned to the blood bank if not used. Platelets should be readily available as well. A dedicated critical care technician is helpful in assisting with laboratory testing and retrieving products from the blood bank (also see Chapter 61). Large-bore IV access is obviously important, especially if partial bypass (in contrast to full bypass) is planned, 2130because it is difficult or impossible for the perfusionist to administer fluid or blood products into the closed partial bypass circuit. This author routinely inserts three 8.5-Fr catheters into the internal jugular and antecubital veins. One of these accepts a pulmonary artery catheter, and the other two are connected to a rapid infuser system that allows the delivery of up to 1500 mL/minute of blood products at a temperature of 37° to 38° C. A right radial arterial catheter is used for aneurysms involving the proximal descending thoracic aorta because occasionally the cross-clamp is placed proximal to the left subclavian artery, thus occluding flow to the left upper extremity. When distal aortic perfusion techniques are used, I monitor arterial blood pressure distal to the cross-clamps. This can be accomplished with the placement of a right femoral arterial catheter, or the surgical team can place a catheter directly into the femoral artery or distal aorta. This catheter monitors perfusion pressure to the kidneys, spinal cord, and mesenteric circulation during the time when the cross-clamps are high on the descending aorta and the lower body region is perfused by a shunt or bypass circuit. Radial and femoral arterial pressure should be simultaneously displayed on the anesthesiologist's monitor and a monitor visible to the surgeons and the perfusionists. TEE is used routinely during TAA repair (see also Chapter 46). When TEE is used by a properly trained individual, assessment of left ventricular end-diastolic volume, myocardial ischemia, and valvular function is possible. It is also possible to determine the size and the extent of the aneurysm. A double-lumen endobronchial tube should be inserted for the purpose of one-lung ventilation (see also Chapter 66). One-lung ventilation provides optimal visualization of the surgical field and reduces retraction-related trauma to the left lung. A left-sided endobronchial tube is optimal because it is more easily positioned and less likely to become malpositioned. Additionally, risk exists for occluding the right upper lobe bronchus with a right-sided tube. I position all double-lumen tubes under direct vision using a fiberoptic bronchoscope because it facilitates quick and definitive placement and allows direct visualization of the distal trachea and mainstem bronchi. Occasionally, when the left mainstem bronchus is compressed by a large aneurysm, the lumen does not accommodate an endobronchial tube. In this situation, a right-sided endobronchial tube might be necessary. Rarely, the right mainstem bronchus may be compressed by a large aneurysm. The double-lumen tube is usually changed, if possible, to a single-lumen tube at the completion of surgery. This facilitates ICU management of pulmonary hygiene and reduces resistance to breathing during weaning in the postoperative period. The airway is often edematous after surgery, and it may be difficult or impossible to change the double-lumen tube without tube-changing catheters. - Many centers use electrophysiologic monitoring with somatosensory evoked potentials (SSEPs) or motor evoked potentials (MEPs) to monitor for spinal cord ischemia (see also Chapter 49). These monitoring techniques may be helpful in both identifying the important intercostal arteries that perfuse the spinal cord and confirming successful reimplantation into the aortic graft. If spinal cord ischemia is identified, cross-clamps can often be repositioned, upper or lower body blood pressure can be increased to augment perfusion through collateral channels, or other measures may be taken to protect the spinal cord (i.e., cerebrospinal fluid [CSF] drainage, induced hypothermia, or intrathecal pharmacologic agents). These techniques are discussed later. Three general problems exist with SSEP monitoring when used during TAA repair. First, sensory monitoring is more likely to detect lateral and posterior sensory column ischemia and is a poor monitor for the anterior motor column. As a result, paraplegia can occur despite normal SSEP signals. Second, inhaled anesthetics and hypothermia can significantly interfere with SSEP signals. Third, ischemia affects peripheral nerves, and ischemia in the lower extremities delays conduction from the usual stimulation sites (e.g., posterior tibial nerve). To eliminate the peripheral nerves as a confounding factor, spinal stimulation via a lumbar epidural electrode can be used, which may be more specific for ischemic injury than peripheral monitoring alone. Lower extremity and peripheral nerve ischemia can be avoided with the use of distal aortic perfusion techniques. To avoid lower extremity ischemia from occlusion of the left femoral artery at the insertion site of the retrograde perfusion cannula, some surgeons suture a small-caliber graft onto the femoral artery (end to side) for insertion of the cannula, which allows both antegrade and retrograde perfusion. These limitations of SSEP monitoring probably accounted for the lack of improvement in neurologic outcome in a large prospective series of TAA repairs. In this same series, the incidence of false-negative responses was 13% and that of false-positive responses was 67%, thus making identification of critical spinal arteries impossible. The transcranial MEP technique has been used successfully to monitor the anterior columns of the spinal cord. The technique is relatively simple and can be viewed as a "train-of-four" for the brain and spinal cord. Electrical stimulation over the motor cortex activates α-motor neurons, and evoked electromyographic responses are obtained in lower extremity muscle. Only electromyogenic responses are specific for the status of the motor neurons in the anterior horn gray matter. Bilateral recording needles should be placed in the popliteal fossae (i.e., popliteal nerve) and bilateral surface electrodes over the gastrocnemius and tibialis anterior muscles. Bilateral stimulating needles are routinely placed in the popliteal fossae to monitor direct muscle responses and the level of neuromuscular blockade. During aortic cross-clamping, MEPs are monitored every minute. A reduction in MEP amplitude to less than 25% of baseline is considered an indication of spinal cord ischemia and requires corrective measures. Because signal averaging is not required and the anterior horn cells react with an almost immediate functional loss after the onset of ischemia, the technique can be used to rapidly identify intercostal arteries supplying the spinal cord. Additionally, the technique can be used to evaluate the adequacy of distal aortic perfusion and the patency of reimplanted critical intercostal arteries. Careful titration of a short-acting neuromuscular blocker is required to maintain a stable level of neuromuscular blockade. Complete neuromuscular blockade makes MEP monitoring impossible. I use a continuous infusion 2131technique to maintain electrical muscle amplitude at approximately 50% of baseline. Isoflurane, desflurane, sevoflurane, and N2O depress synaptic conduction and significantly decrease the amplitude of myogenic MEPs. Although modifications of the stimulating technique have improved monitoring with inhaled anesthetics somewhat, a total IV anesthetic technique may be optimal. Fentanyl and ketamine have little effect on myogeneic MEPs and have been used successfully as a combined anesthetic in a large series of patients undergoing TAA repair with MEP monitoring.87 This series of 210 consecutive patients had the lowest rate of neurologic deficit (2.4%) and permanent paraplegia (1.4%) reported.87 - Body temperature should be monitored at two sites (core and peripheral) to assess cooling and warming when bypass techniques are used. However, an important difference exists between full and partial bypass with regard to temperature monitoring. With full bypass, perfusion is usually into the ascending aorta, and typically the upper body core temperature (i.e., nasopharynx or esophagus) cools and warms fastest, whereas the lower body temperature changes more slowly. With partial bypass, the opposite is true. The blood from bypass is returned into the femoral artery, and the lower part of the body (i.e., rectum or bladder) changes before the upper part changes. This difference is important to recognize to achieve complete cooling and warming because the lagging temperature should be the end point for cooling and warming.

The most influential interventions used to protect the spinal cord during thoracic aortic cross-clamping include the following except A. routine CSF drainage (CSF pressure < 10 mm Hg) B. endorphin receptor agonist C. Moderate intraoperative hypothermia (< 35°C) D. avoiding hypotension (MAP > 90 mm Hg

B. Spinal Cord Ischemia - Neurologic dysfunction is a serious complication associated with thoracic aortic aneurysms (TAA) reconstruction. Spinal cord injury is categorized into immediate and delayed paraplegia. The incidence of immediate paraplegia with DTAA ranges from 0% to 3% if surgery is performed with adjunctive procedures or clamp times are less than 10 minutes. However, the incidence of paraplegia and/or paresis for patients having TAA repair is 7.1% ± 6.1% (range 0%-32%).112 Impending spinal cord injury depends on the type of aneurysm, surgical technique, cross-clamp time, and use of spinal cord protection interventions.113 The exact incidence of delayed paraplegia is unknown, but it is believed that as many as 25% of all spinal cord injuries are delayed. The primary preoperative risk factors for delayed paraplegia include type 2 aneurysms, emergency procedures, number of sacrificed segmental segments, and renal failure. The main postoperative factors include hemodynamic instability caused by atrial fibrillation, bleeding, multiorgan failure, and sepsis.110 - Several techniques have been successfully applied in an effort to decrease the incidence of neurologic dysfunction after thoracic aortic surgery. These include SSEP and MEP monitoring, CSF drainage, hypothermia, reattachment of intercostal arteries, and distal aortic perfusion. Systemic hypothermia and selective cooling of the spinal cord may lengthen ischemic time intervals; however, the clinical benefits of these hypothermia methods are unclear.114 The use of various bypass mechanisms and distal shunts may minimize the length of aortic occlusion time. - Spinal cord perfusion pressure can be estimated by calculating the arterial blood pressure minus the CSF pressure. During aortic clamping, CSF pressure increases whereas arterial pressure decreases distal to the clamp. The spinal cord perfusion pressure can therefore be manipulated by altering arterial blood pressure and draining CSF through the intrathecal catheter.114,115 The most influential interventions used to protect the spinal cord during thoracic aortic cross-clamping include (1) routine CSF drainage (CSF pressure < 10 mm Hg), (2) endorphin receptor blockade (naloxone infusion), (3) moderate intraoperative hypothermia (< 35°C), (4) avoiding hypotension (MAP > 90 mm Hg), and (5) optimizing cardiac function.116 It is postulated that increased levels of excitatory amino acid neurotransmitters bind to opioid receptors in the spinal cord and induce spinal cord edema. Therefore, administration of naloxone may inhibit edema formation. Avoiding the use of sodium nitroprusside is indicated, as arterial dilation may cause a "steal phenomenon," further decreasing spinal cord blood flow. - Methods for detecting spinal cord ischemia were discussed previously. The intraoperative use of SSEPs and MEPs can provide early identification of neurologic dysfunction, but these monitoring modalities do not ensure spinal cord integrity. Factors that contribute to the development of neurologic deficits include the level of aortic clamp application, ischemic time, embolization or thrombosis of a critical intercostal artery, failure to revascularize intercostal arteries, and the urgency of surgical intervention.114,115 Delayed paraplegia may also be the result of IRI, although the exact mechanism of injury has not been proven.110,117,118 Additional complications of thoracoabdominal aortic reconstruction are listed in Box 28.9.

These drugs have cardioprotective effects, as they reduce vascular inflammation, decrease the incidence of thrombogenesis, enhance nitric oxide bioavailability, stabilize atherosclerotic plaques, and lower lipid concentrations. A. Beta blockers B. Statin C. Antiplatelet medication D. Calcium channel blockers

B. Statins. - It has been suggested that statins decrease perioperative mortality in patients with vascular disease by decreasing adverse cardiovascular and cerebrovascular events and death.18 These drugs have cardioprotective effects, as they reduce vascular inflammation, decrease the incidence of thrombogenesis, enhance nitric oxide bioavailability, stabilize atherosclerotic plaques, and lower lipid concentrations. It is reasonable to start a statin drug in this patient population. If prescribed, a statin should be instituted 30 days prior to the surgical procedure and continued throughout the postoperative period.15 Statin therapy that is started preoperatively and continued through discharge has been associated with reduced 30-day mortality and an absolute 18% improvement in 5-year survival after vascular surgery.18,19 Specifically, patients who were prescribed statins and then underwent endovascular aortic aneurysm repair (EVAR) had greater residual aneurysm sac regression within the first years postoperatively.20 Antiplatelet Medications. - It has been unclear whether patients having noncardiac surgery who are at increased risk for MI should receive aspirin throughout the perioperative period. The results of current evidence and the Perioperative Ischemic Evaluation 2 (POISE-2) research trial indicate that perioperative aspirin does not prevent MI and does not alter the risk of a perioperative cardiovascular event.21 The outcomes were unchanged for those subjects who took aspirin for a prolonged period compared to those who started aspirin prior to surgery. Aspirin did, however, increase the risk of major bleeding. In patients who have been on a long-term aspirin regimen and have aspirin withheld during the perioperative period, it is important to ensure that aspirin is restarted after the increased risk period for bleeding has passed (i.e., 8-10 days after surgery). On the basis of currently available literature, aspirin should not be administered to patients undergoing surgery unless there is a definitive guideline-based primary or secondary prevention indicated.22,23 - The presence of concurrent pulmonary, renal, neurologic, and endocrine dysfunction should be identified, and measures should be taken to improve organ function before surgery. Acute kidney injury (AKI) is common during the perioperative period in patients undergoing vascular surgery, and this condition is associated with a high risk for cardiovascular-specific mortality comparable to that seen with chronic kidney disease.24 Strategies used to help prevent perioperative AKI are discussed later in this chapter. Preoperatively, the greater the number of comorbidities that exist, the greater the risk of morbidity and mortality during the perioperative period.

Which approach does not cause mesenteric traction syndrome A. Transperitoneal B. Retroperitoneal C. Anteroperitoneal D. Lateroperitoneal

B. Surgical Approach - The standard surgical approach for elective abdominal aortic reconstruction is a transperitoneal incision. The advantages of this route include exposure of infrarenal and iliac vessels, ability to inspect intraabdominal organs, and rapid closure.87 Unfavorable consequences associated with the transperitoneal approach include increased fluid losses, prolonged ileus, postoperative incisional pain, and pulmonary complications. - The retroperitoneal approach is an alternative to the standard route. Its advantages include excellent exposure (especially for juxtarenal and suprarenal aneurysms and in obese patients), decreased fluid losses, less incisional pain, and fewer postoperative pulmonary and intestinal complications. In addition, the retroperitoneal approach does not elicit mesenteric traction syndrome.87 The reported limitations of this approach are the unfamiliarity of surgeons with this technique, poor right distal renal artery exposure, and the inability to inspect the integrity of the abdominal contents. Table 28.5 compares the standard and retroperitoneal surgical approaches. After cross-clamping, the aneurysm is incised, and a synthetic graft is sewn distally and proximally to the aneurysm. The aortic adventitia is then resewn over the synthetic graft (Fig. 28.3).

Deflation of which lung is necessary during repair of thoracic aneurysms A. Right B. Left

B. Treatment - As previously described, a high mortality rate is associated with the rupture of thoracic aneurysms. Therefore, early detection and surgical intervention make a significant contribution to long-term survival. Hemodynamic compromise and increased complexity of the aneurysm are associated with increased postoperative mortality. The surgical approach and the method of aneurysm resection vary according to the location of the lesion within the thoracic aorta. Resection of the ascending aorta and graft replacement necessitate the use of complete cardiopulmonary bypass or partial cardiopulmonary bypass (atrial-femoral: left atrial cannulation to a centrifugal pump, and reinfusion to a femoral artery cannula). If extracorporeal circulation is not indicated, heparin (50-100 units/kg) is required prior to aortic cross-clamping. For complete cardiac bypass, total systemic heparinization with 400 units/kg is necessary, and monitoring of activated clotting time is needed.106 Depending on the proximity of the aneurysm to the aortic arch, the aortic valve may require replacement. Surgical resection of lesions in the transverse arch compromises cerebral perfusion, although various bypass techniques, combined with profound hypothermia and circulatory arrest, have been used.107 Aneurysms of the descending aorta may be resected after application of an aortic cross-clamp. However, perfusion to distal organs can be compromised during this procedure. Arterial line and pulse oximetry monitoring should occur on the right side because impingement of the left subclavian artery, which provides blood flow to the left hand, is possible. A double lumen tube is placed, and deflation of the left lung is necessary to avoid left lung contusion and improve the surgical operating conditions. The patient is positioned in the left lateral decubitus position, and a left-sided thoracotomy is accomplished. The extent of the thoracotomy is determined by the extent of the aneurysm. A lower thoracic incision is associated with a decreased incidence of postoperative pulmonary dysfunction.108

The use of thoracic epidural analgesia (TEA) in patients having coronary artery bypass surgery decreases the incidence of A. Renal complication B. Coagulopathy C. Respiratory complication D. Supraventricular arrhythmias

C & D Regional Anesthesia. - The use of epidural anesthesia for abdominal aneurysmectomies is commonly considered. The benefits of epidural use include decreased preload and afterload, preserved myocardial oxygenation, reduced stress response, excellent muscle relaxation, decreased incidence of postoperative thromboembolism, increased graft flow to the lower extremities, decreased pulmonary complications, and improved postoperative analgesia. Potential disadvantages include anticoagulation and the possibility of epidural hematoma, as well as severe hypotension during blood loss or un-clamping if local anesthesia is administered intraoperatively.34,95 - The use of thoracic epidural analgesia (TEA) in patients having coronary artery bypass surgery decreases the incidence of postoperative supraventricular arrhythmias and respiratory complications. General anesthesia with TEA does not increase the risk of mortality, MI, or neurological complications compared to GA alone.96 Combination Techniques. - The use of a combined general anesthesia and epidural anesthesia provides the benefits of epidural anesthesia with the ability to provide amnesia and controlled ventilation. Due to neuraxial blockade, a "light" GA can be administered. Postoperative epidural analgesia improves postoperative respiratory function and blood flow to distal tissues. Furthermore, postoperative epidural analgesia reduces postoperative pain and pulmonary complications in patients with chronic obstructive pulmonary disease (COPD), as compared to general anesthesia alone after open aneurysm repair.97 However, the major risks associated with neuraxial anesthesia are subarachnoid or epidural hemorrhage (resulting in hematoma after heparinization) and hypotension, which may be difficult to treat, especially during an episode of acute blood loss. - In summary, all the aforementioned anesthetic techniques can be used safely and can demonstrate positive outcomes. Even more important than anesthetic selection is the clinical management of each patient. Observation, accurate interpretation, and immediate intervention to minimize dramatic hemodynamic variability during the anesthetic process reduces morbidity and mortality to a much greater extent than selection of a superior anesthetic technique.

Patients with poor (<4 METs) or unknown functional capacity and three or more clinical risk factors who are scheduled for intermediate-risk surgery is considered what class A. I B. IIa C. IIb D. III

C.

Which of the following metabolic changes decrease during aortic unclamping A. Lactate B. Body oxygen consumption C. Temperature D. Activated complement

C.

Which of the following metabolic changes increase in aortic cross clamping A. Oxygen total body consumption B. Total body carbon dioxide production C. Mixed venous oxygen saturation D. Total body oxygen extraction

C.

In EVARs, these are the most likely causes of late aneurysm rupture A. Catheter migration B. Microembolization C. Endoleak D. Graft Tear

C. - As described in the EVAR 1 study, reinterventions due to endoleak were required in three times as many patients who had EVAR as compared to an open procedure. Of these endoleaks requiring reintervention, 7% were discovered within 1 month of implantation, and another 13% occurred within 4 years postoperatively.148 A comparison of outcomes evaluating EVAR and open AAA repair in nearly 40,000 patients has been reported. Perioperative mortality (≤ 30 days postoperative) and the risk of mortality 3 years postoperatively were lower after EVAR compared with OSR. At 3 years postoperatively, the risk of mortality was similar to patients having an OSR. Follow-up interventions were more common after EVAR, most often due to the ESVG. Lastly, the risk of rupture was greater with EVAR within an 8-year postoperative period.122 - As EVSG-related endoleaks are the most likely causes of late aneurysm rupture, post-EVAR surveillance is an important factor in avoiding the risk of late aneurysm rupture.164 A large proportion of late ruptures are amenable to endovascular treatment. Postoperative follow-up care for patients who have undergone EVAR is vital, because long-term outcomes have not been quantitatively established. Physical examination and contrast-enhanced CT scans are recommended at 1, 6, 12, and 18 months postoperatively, and then annually.165 Additionally, abdominal x-rays should be obtained on a regular basis. Lifelong radiographic evaluation and surveillance is necessary to monitor aneurysm size, graft migration, and endoleak. Intensive follow-up care, the need for reinterventions, and the cost of the endograft make EVAR more expensive than open repair.166

Which of the following should not be done as a part of temperature control in patients undergoing aortic aneurysm A. Forced air warm-blanket B. Warmed fluids C. Lower body warmed D. BLood warmer

C. Anesthetic Drugs and Techniques - A variety of anesthetic techniques, including general anesthesia, regional (epidural) anesthesia, and combined techniques, have been used successfully for abdominal aortic reconstruction. Combined techniques most commonly use a lumbar or low thoracic epidural catheter in addition to a "light" general anesthetic. Local anesthetics, opioids, or, more commonly, a combination of the two may be administered by bolus or continuous epidural infusion. Maintenance of vital organ perfusion and function by the provision of stable perioperative hemodynamics is more important to overall outcome than is the choice of anesthetic drug or technique.40 Therefore, the specific anesthetic technique for patients undergoing abdominal aortic reconstruction is important insofar as it allows rapid and precise control of hemodynamic parameters. Given the frequent incidence of cardiac morbidity and mortality in patients undergoing aortic reconstruction, factors that influence ventricular work and myocardial perfusion are of prime importance. - Induction of general anesthesia should ensure that stable hemodynamics are maintained during loss of consciousness, laryngoscopy and endotracheal intubation, and the immediate postinduction period. A variety of IV anesthetics (propofol, etomidate, thiopental) are suitable. The addition of a short-acting, potent opioid such as fentanyl 3 to 5 μg/kg) usually provides stable hemodynamics during and after induction of anesthesia. Volatile anesthetics may be administered in low concentrations before endotracheal intubation during assisted ventilation as an adjunct to blunt the hyperdynamic response to laryngoscopy and endotracheal intubation. Esmolol 10 to 25 mg, sodium nitroprusside 5 to 25 μg, nitroglycerin 50 to 100 μg, and phenylephrine 50 to 100 μg should be available for bolus administration during induction if needed to maintain appropriate hemodynamics. Maintenance of anesthesia may be accomplished with a combination of a potent opioid (fentanyl or sufentanil) and an inhaled anesthetic (sevoflurane, desflurane, or isoflurane) (i.e., balanced anesthesia). Patients with severe left ventricular dysfunction may benefit from a pure opioid technique, but a balanced anesthetic technique allows the clinician to take advantage of the most desirable characteristics of potent opioids and inhaled volatile anesthetics while minimizing their undesirable side effects. Nitrous oxide can be used to supplement either an opioid or an inhaled anesthetic. I typically use low-dose isoflurane in 50% N2O and fentanyl 12 to 18 μg/kg. Approximately 50% of the opioid dose is administered during induction of anesthesia and before skin incision. When epidural local anesthetics are used, this author uses the same technique and reduces the fentanyl dose to 6 to 8 μg/kg. Various regional anesthetic and analgesic techniques have been used effectively during and after aortic reconstruction. For over 2 decades, interest has focused on 2126the use of regional anesthetic and analgesic techniques to reduce the incidence of perioperative morbidity in patients undergoing aortic reconstruction. The benefits of combined general and epidural anesthesia intraoperatively, with or without epidural analgesia continued into the postoperative period, remain controversial.40,74-78 Moreover, studies that have reported improved outcome do not determine whether the benefit results from the intraoperative anesthetic technique or the postoperative analgesic regimen (or a combination of the two). In a randomized trial using epidural morphine in patients undergoing aortic surgery, Breslow and associates79 found attenuation of the adrenergic response and a less frequent incidence of hypertension in the postoperative period. A large randomized trial reported no reduction in nonsurgical complications with the use of intrathecal opioid.80 The effects of the anesthetic or analgesic technique on the incidence of perioperative myocardial ischemia have received considerable attention. Four randomized trials, with nearly 450 combined patients undergoing aortic reconstruction, failed to demonstrate a reduction in the incidence of perioperative,40,81 intraoperative,82 or postoperative77 myocardial ischemia when epidural techniques were used. Additionally, randomized trials have not demonstrated a reduction in the incidence of cardiovascular, pulmonary, or renal complications after aortic surgery with the use of epidural techniques.40,74,76,77,83 - The duration and intensity of postoperative care after aortic surgery are critically dependent on the physiologic derangements incurred during the perioperative period (i.e., depression of consciousness, hypothermia, excessive intravascular fluids, incisional pain, ileus, and respiratory depression), as well as on the development of certain less common, but more severe postoperative complications (i.e., MI, pneumonia, sepsis, renal failure, and decreased tissue perfusion). Length of hospital stay may therefore be considered the outcome variable most directly proportional to an integrated final negative effect of all significant perioperative morbidity (excluding in-hospital death) and the variable most likely to be altered by the anesthetic or analgesic technique. Randomized trials have not demonstrated any reduction in length of hospital stay after aortic surgery with the use of regional techniques.∗ Norris and colleagues40 reported the results of a randomized clinical trial comparing alternative combinations of intraoperative anesthesia (i.e., general or combined epidural and general) and postoperative analgesia (i.e., IV patient-controlled analgesia or epidural patient-controlled analgesia) with respect to length of stay after abdominal aortic surgery. Two unique features of the trial included a factorial design (Fig. 69-8), which allowed the inclusion of all four combinations of intraoperative anesthesia and postoperative analgesia and the ability to separate the influence of time period and technique, and a double-blind design, which helped eliminate investigator and treating physician bias. The study rigorously protocolized perioperative management, standardized postoperative surgical care, and optimized postoperative pain management. Although the overall length of stay was much shorter (median, 7.0 days) than that reported in other studies,74,75,77,83 we were not able to demonstrate a reduction in length of stay or direct medical costs based on anesthetic or analgesic technique (Table 69-7). The overall incidence of postoperative complications in the trial was low and not different based on anesthetic or analgesic technique. Postoperative pain was well controlled overall, with similar pain scores in both analgesic treatment groups. Thus, if perioperative care and pain relief are optimized, epidural anesthetic and analgesic techniques for aortic surgery offer no major advantage or disadvantage over general anesthesia and IV patient-controlled analgesia. - The use of epidural local anesthetics in combination with general anesthesia during aortic reconstruction poses several problems, including hypotension at the time of aortic unclamping and the need for increased intravascular fluid and vasopressor requirements. Supraceliac aortic cross-clamping may significantly exaggerate these disadvantages, and, as a result, some clinicians avoid epidural local anesthetics for such procedures. Epidural opioids without local anesthetics can be used for procedures requiring supraceliac aortic cross-clamping. Epidural local anesthetic can be given later, after aortic unclamping, when hemodynamics and intravascular volume have stabilized. For low thoracic or high lumbar epidural catheters, the initial bolus should be limited to 6 to 8 mL of local anesthetic. Additional local anesthetic is administered by continuous infusion at 4 to 6 mL/hr with adjustments based on hemodynamics and inhaled anesthetic requirements during surgery. Although elective aortic reconstruction via the retroperitoneal approach using straight epidural anesthesia (no general anesthetic) has been reported, this technique is not recommended for routine use. - Emergence from anesthesia should be conducted after restoration of circulation and establishment of adequate organ perfusion. Hemodynamic, metabolic, and temperature homeostasis must be achieved before skin 2127closure; otherwise, patients should be transported to the intensive care unit (ICU) with their trachea intubated and their ventilation controlled. Early extubation of the trachea is not generally attempted in patients with supraceliac aortic cross-clamp times longer than 30 minutes, patients with poor baseline pulmonary function, or patients requiring large volumes of blood or crystalloid during surgery. At the start of skin closure, inhaled anesthetics are discontinued, N2O is increased to 70%, and any residual neuromuscular blockade is reversed. I routinely insert a large nasal airway after induction of anesthesia, but before systemic heparinization in all patients for whom extubation is planned in the operating room. Hypertension and tachycardia are aggressively controlled during emergence by the use of short-acting drugs such as esmolol, nitroglycerin, and sodium nitroprusside. Patients are placed in a recumbent, head-up position, and N2O is discontinued. If spontaneous ventilation is adequate, the trachea is extubated. Some centers advocate extubation of all patients in the ICU after a period of stability has been established. In these cases, mild sedation with a benzodiazepine such as midazolam is appropriate. Temperature Control - Postoperative hypothermia is associated with many undesirable physiologic effects and may contribute to adverse outcomes (see also Chapter 54). Normothermia should be maintained before skin incision by increasing ambient temperature in the operating room, applying warm cotton blankets, and warming IV fluids. If significant hypothermia occurs early in the procedure, normothermia is extremely difficult to achieve, and emergence and tracheal extubation may be delayed. During surgery, all fluids and blood products should be warmed before administration. A forced-air warming blanket should be applied over the upper part of the body. The lower part of the body should not be warmed because doing so can increase injury to ischemic tissue distal to the cross-clamp by increasing metabolic demands.

Aortic Cross-Clamp Release causes hemodynamic alterations such as the following except A. SVR decrease B. Decrease preload C. Increase afterload D. Reactive hyperemia

C. Aortic Cross-Clamp Release - While the aorta is occluded, metabolites that are liberated as a result of anaerobic metabolism (such as serum lactate) accumulate below the aortic cross-clamp and induce vasodilation. As the cross-clamp is released, SVR decreases, and blood is sequestered into previously dilated veins, decreasing venous return. Reactive hyperemia causes transient vasodilation secondary to the presence of tissue hypoxia, release of adenine, and liberation of an unknown vasodepressor substance that may act as a myocardial depressant and peripheral vasodilator.74 This combination of events results in decreased preload and afterload. The hemodynamic instability that may ensue after the release of an aortic cross-clamp is called declamping shock syndrome.84 Evidence demonstrates that venous endothelin (ET), and specifically (ET)-1, may be partially responsible for the hemodynamic alterations that accompany declamping shock syndrome. Venous ET-1 has a positive inotropic effect on the heart and a vasoconstricting effect on blood vessels. Table 28.4 summarizes the most commonly observed hemodynamic responses to aortic unclamping and therapeutic interventions. - The magnitude of the response to unclamping the aorta may be manipulated. Although SVR and MAP decrease, intravascular volume may influence the direction and magnitude of the change in cardiac output. Restoration of circulating blood volume is paramount in providing circulatory stability before release of the aortic clamp.64,74,85 The site and duration of cross-clamp application, as well as the gradual release of the clamp, influence the magnitude of circulatory instability. For this reason, it is vital that communication between the anesthetist and the surgical team occurs. Partial release of the aortic cross-clamp over time often results in less severe hypotension. Vasopressors and/or inotropic agents are administered to help minimize hypotension. An algorithm depicting the systemic hemodynamic response to aortic unclamping is shown in Fig. 28.2. - Ischemic reperfusion injury is a complex metabolic process that occurs during application of the cross-clamp (ischemia) and unclamping of the aorta (reperfusion). IRI is characterized by metabolic, thrombotic, and inflammatory components. Cells that comprise tissues remain metabolic despite low blood flow, and they liberate cytotoxic mediators during anaerobic metabolism. During cellular ischemia, reactive oxygen species and increased intracellular calcium further inhibit mitochondrial activity and adenosine triphosphate generation. Specific body tissues vary in terms of the time it takes for their cells to become necrotic. The degree of cellular necrosis is primarily determined by the duration of ischemia. The no-reflow phenomenon occurs when the microvasculature is occluded by platelets, neutrophils, and thrombi, causing inadequate perfusion and further increasing cellular necrosis.1 Reinstituting blood flow increases inflammatory cell influx and cytotoxic substance wash-out into the central circulation.82 Myocardial stunning and dysrhythmias can occur due to decreased cellular energy, increased reactive oxygen metabolites, and increased intracellular calcium, necessitating inotropic support.86 Other manifestations associated with IRI include tissue edema, acute respiratory distress syndrome, compartment syndrome, bacterial translocation, renal failure, and multisystem organ failure.1

Which of the following decrease during aortic cross clamping A. SVR B. MAP C. CO D. PAOP

C. Aortic Cross-Clamping - Abdominal aortic reconstruction is one of the most challenging situations for the anesthetist, due to the frequency and degree of hemodynamic variability during cross-clamping and unclamping of the aorta. This is further complicated by the fact that most patients having an aortic aneurysm repair are elderly and have varying degrees of coexisting disease. Perhaps the most dramatic physiologic change occurs with the application of an aortic cross-clamp. Temporary aortic occlusion produces various hemodynamic and metabolic alterations. Hemodynamic Alterations - The hemodynamic effects of aortic cross-clamping depend on the application site along the aorta, the patient's preoperative cardiac reserve, and the patient's intravascular volume. The most common site for cross-clamping is infrarenal, because most aneurysms appear below the level of the renal arteries. Less common sites of aneurysm development are the juxtarenal and suprarenal areas. - During aortic cross-clamping, hypertension occurs above the cross-clamp, and hypotension occurs below the cross-clamp. Aortic cross-clamping increases plasma levels of catecholamines, aldosterone, cortisol, prostaglandins, and other stress hormones that are associated with a sympathetic nervous system response. There is an absence of blood flow distal to the cross-clamp in the pelvis and lower extremities.6 An increase in afterload causes the left ventricular myocardial wall tension to increase, which in turn increases myocardial oxygen demand. Patients with poor left ventricular function are at risk for developing congestive heart failure during this period. Mean arterial pressure (MAP) and systemic vascular resistance (SVR) also increase. Cardiac output may decrease or remain unchanged. Pulmonary artery occlusion pressure (PAOP) may increase or remain unchanged. Table 28.3 summarizes the physiologic changes associated with aortic cross-clamping. - Patients with adequate cardiac reserve commonly adjust to sudden increases in afterload without the occurrence of adverse cardiac events. However, patients with ischemic heart disease or ventricular dysfunction are unable to fully compensate, as a result of the hemodynamic alterations. The increased left ventricular wall stress attributed to aortic cross-clamp application may contribute to decreased global ventricular function and myocardial ischemia. Clinically, these patients experience increases in PAOP in response to aortic cross-clamping. Aggressive pharmacologic intervention is required for restoration of cardiac function during this time. An algorithm that depicts the systemic hemodynamic responses to aortic cross-clamping is shown in Fig. 28.1.

This is the most common factor that contributes to the progression of the an aortic dissection A. Atherosclerosis B. Vagal maneuver C. Hypertension D. Tachycardia

C. Aortic Dissection - Aortic dissection is characterized by a spontaneous tear of the vessel wall intima, permitting the passage of blood along a false lumen. Although the cause of dissections is unclear, lesions that were thought to be related to cystic necrotic processes may actually be caused by variations in wall integrity. Hypertension is the most common factor that contributes to the progression of the lesion. Manipulation of the ascending aorta during cardiac surgery may be associated with aortic dissection.109 The symptoms of aortic dissection are the result of interruption of blood supply to vital organs. The most serious complication is aneurysm rupture. Diagnosis can be accomplished by the previously mentioned noninvasive techniques. - Treatment of dissecting aortic lesions depends on their location within the thoracic aorta (Fig. 28.5). Type A lesions have the highest incidence of rupture and require immediate surgical intervention. Type B lesions may initially be managed medically, with the administration of arterial dilating and β-adrenergic blocking agents - In summary, surgical resection of thoracic aortic lesions enhances long-term survival. Refinement of surgical techniques and improvements in perfusion technology have reduced the overall mortality rate. The surgical method used is dependent on the location of the aortic lesion. Anesthesia for aneurysms of the ascending and transverse aorta requires cardiopulmonary bypass.

Postoperative pulmonary complications are potentially serious in patients undergoing vascular surgery, with the most significant morbidity seen in patients undergoing A. Carotid procedure B. Closed aortic procedure C. Open aortic procedure D. Lower extremity procedure

C. Assessment of Pulmonary Function - Postoperative pulmonary complications are potentially serious in patients undergoing vascular surgery, with the most significant morbidity seen in patients undergoing open aortic procedures (see also Chapters 67 and 103). The most important pulmonary complications are atelectasis, pneumonia, respiratory failure, and exacerbation of underlying chronic disease. Given the prevalence of cigarette smoking in this population, chronic obstructive pulmonary disease (COPD) and chronic bronchitis are common and, when present, place the patient at increased risk for postoperative pulmonary complications. When clinical assessment suggests severe pulmonary compromise, pulmonary function tests may be useful in evaluating and optimizing respiratory function (see also Chapters 39 and 51). Preoperative analysis of arterial blood gases should be used to establish a baseline for postoperative comparison. Baseline hypercapnia (partial pressure of arterial carbon dioxide > 45 mm Hg) indicates a more frequent risk for postoperative morbidity. Bronchodilator therapy may be indicated on the basis of results of pulmonary function tests, although the risk for β-adrenergic agonist-induced arrhythmia or myocardial ischemia also must be considered. Preoperative treatment with a short course of glucocorticoids (prednisone 40 mg/day for 2 days) may be helpful for patients with significant COPD or asthma. Evidence of pulmonary infection should be treated with appropriate antibiotics. Although improved pulmonary outcome with regional anesthesia is not clear, patients with significant pulmonary disease may benefit from epidural techniques. Use of these techniques in the postoperative period helps avoid respiratory depression from systemic opiates (see also Chapter 98). Pulmonary complications in the postoperative period are difficult to avoid. Incentive spirometry and continuous positive airway pressure do provide benefit.31 Given proper pulmonary care, even patients with severe pulmonary insufficiency, however, may undergo aortic surgery with acceptable morbidity and mortality outcomes.32 Assessment of Renal Function - Chronic renal disease is common in vascular surgery patients and is associated with an increased risk for death and cardiovascular disease (see also Chapters 37 and 52).33 Chronic renal disease strongly predicts long-term 2114mortality in patients with symptomatic lower extremity arterial occlusive disease irrespective of disease severity, cardiovascular risk, and concomitant treatment.34 Cardiovascular disease is independently associated with a decline in renal function and the development of kidney disease.35 Serum creatinine and creatinine clearance are used to assess renal function perioperatively. A preoperative serum creatinine level more than 2 mg/dL is an independent risk factor for cardiac complications after major noncardiac surgery.36 Preoperative creatinine clearance less than 60 mL/minute is an independent predictor of both short-term and long-term mortality after elective vascular surgery.37 Perioperative β-adrenergic blocker38 and statin37 administration decrease risk for death in vascular surgery patients with renal impairment. Atherosclerotic disease in the abdominal aorta or renal arteries may compromise renal blood flow and renal function. Conversely, renal artery stenosis causes hypertension through renin-induced and angiotensin-induced vasoconstriction. Hypertension itself may cause renal insufficiency or failure. Diabetic nephropathy is also common (see also Chapter 39). Superimposed on baseline abnormalities in renal function are the preoperatively and intraoperatively administered angiographic dyes, which are directly nephrotoxic. Renal ischemia occurs with interruption of renal blood flow from aortic cross-clamping. Even with infrarenal aortic cross-clamps, renal blood flow may decrease despite normal systemic arterial blood pressure and cardiac output. Embolic plaque can be showered into the renal arteries, especially when suprarenal aortic cross-clamps are applied and released. Fluctuations in intravascular volume and cardiac output can compromise renal perfusion during the intraoperative and postoperative periods. In one series of more than 500 patients, the prevalence of acute renal failure was 7% after abdominal aortic reconstruction.

This cerebral moniroting assesses perfusion pressure in the operative carotid artery A. Electroencephalogram (EEG) B. Somatosensory-evoked potential (SSEP) C. Carotid stump pressure (CSP) D. Transcranial Doppler (TCD)

C. Cerebral Monitoring Modalities During General Anesthesia for CEA • Electroencephalogram (EEG): assesses cortical electrical function • Somatosensory-evoked potential (SSEP): assesses sensory-evoked potentials • Carotid stump pressure (CSP): assesses perfusion pressure in the operative carotid artery • Transcranial Doppler (TCD): assesses blood flow velocity in the middle cerebral artery • Cerebral oximetry: assesses cerebral regional oxygen saturation (near-infrared spectroscopy) CEA, Carotid endarterectomy.

Which of the following is not a complication associated with carotid artery stenting A. Stroke B. Hypotension C. Tachycardia D. Horner syndrome

C. Complications Associated With Carotid Artery Stenting • Stroke • Myocardial ischemia/infarction • Bradycardia • Hypotension • Deformation of expandable stent • Stent thrombosis • Horner syndrome • Cerebral hyperperfusion syndrome • Carotid artery dissection • Carotid artery rupture • Hemorrhage resulting from anticoagulation

Anesthetic agents, with the exception of _________, decrease the cerebral metabolic rate of oxygen consumption (CMRO2). A. Propofol B. Midazolam C. Ketamine D. Thiopental

C. Intraoperative Considerations Cerebral Physiology - CBF can remain relatively constant at different cerebral perfusion pressures as a result of cerebrovascular autoregulation. Cerebral perfusion pressure can be expressed as the difference between MAP and intracranial pressure (ICP). During CEA, ICP is usually not elevated; therefore, MAP plays the predominant role in determining cerebral perfusion pressure. When MAP is maintained between 60 and 160 mm Hg, CBF remains constant. However, the adverse effects of chronic systemic hypertension shift the patient's cerebral autoregulatory curve to the right, and therefore a higher than normal MAP may be required to ensure adequate cerebral perfusion. CBF is also influenced by arterial carbon dioxide and oxygen concentrations, as well as anesthetic agents. Profound hypocarbia causes cerebral vascular constriction by decreasing CBF. Cerebral steal can occur with hypercarbia as it leads to cerebral vascular dilation in cerebral vessels. However, in those areas of the brain that are at risk of developing ischemia caused by atherosclerotic plaques, the cerebral vessels are maximally dilated. Therefore, causing profound cerebral vascular dilation decreases CBF and increases the potential for regional ischemia. Inhalation agents increase CBF due to cerebral vascular dilation in a dose-dependent fashion. Anesthetic agents, with the exception of ketamine, decrease the cerebral metabolic rate of oxygen consumption (CMRO2). - Normal CBF is approximately 50 mL/100 g per min. Neuronal function is generally maintained at levels greater than 25 mL/100 g per min. Blood flow that is less than this critical value jeopardizes cellular function. Decreased perfusion and ischemia can be reflected in changes in consciousness. Cellular death occurs at levels less than 6 mL/100 g per min, as evidenced by the flattening seen on an electroencephalogram. - Carotid occlusive disease jeopardizes the cerebral perfusion pressure in the ipsilateral artery. Ischemia leads to the disruption of autoregulation and compensatory vasodilation, and thus blood flow becomes pressure-dependent. During CEA, a primary goal is to ensure adequate CBF by maintaining and, if necessary, augmenting MAP.

If the aneurysm involves the thoracic region or the distal aortic arch, which arterial line monitoring is preferred A. Right femoral B. Left femoral C. Right radial D. Left radial

C. Intraoperative Management Monitoring - Intraoperative monitoring devices used for thoracoabdominal aneurysm resection are the same as for those used for abdominal aneurysmectomies. Direct intra-arterial blood pressure and pulmonary artery pressure monitoring is standard during extracorporeal circulation. If the aneurysm involves the thoracic region or the distal aortic arch, right radial arterial line monitoring is preferred, because left subclavian arterial blood flow may be compromised during surgery. The use of TEE is suggested for cardiac monitoring in patients with myocardial dysfunction. An indwelling urinary catheter is used for assessing renal function. To facilitate exposing the descending thoracic aorta, a double-lumen endotracheal tube is inserted to allow for one-lung ventilation. As a result, careful monitoring of oxygenation is mandatory. Routine use of pulse oximetry may be limited if the left subclavian artery is manipulated; therefore, the right hand, the ear, or the nasal passages should be used for monitoring oxygen saturation. Finally, a lumbar intrathecal catheter is inserted to access CSF pressure. SSEPs and/or MEPs are often used to monitor and detect neurologic dysfunction.

Mesenteric traction syndrome is associated with the following except A. Hypotension B. Tachycardia C. Decrease CO D. Facial flushing

C. Metabolic Alterations - After the application of an aortic cross-clamp, the lack of blood flow to distal structures creates an hypoxic and ischemic environment. In response to tissue ischemia, metabolites such as cytokines, prostaglandins, nitric oxide, and arachidonic acid are formed and released into circulation Furthermore, anaerobic metabolism leads to the accumulation of serum lactate. The release of arachidonic acid derivatives may be a contributing factor leading to cardiac instability and myocardial depression during aortic cross-clamping.38 Thromboxane A2 synthesis, which is accelerated by the application of an aortic cross-clamp, may be responsible for the decrease in myocardial contractility and cardiac output that occurs. - Traction on the mesentery is a surgical maneuver used for exposing the aorta. Mesenteric traction syndrome is associated with this procedure. Decreases in blood pressure and SVR, tachycardia, increased cardiac output, and facial flushing are common responses to mesenteric traction. Although the cause of this syndrome is unknown, it has been associated with high concentrations of 6-keto-prostaglandin F1α, a stable metabolite of prostacyclin, at the time of mesenteric traction.71 The 6-keto-prostaglandin F1α levels and hemodynamic stability return to pre-clamp values as reperfusion occurs. - The neuroendocrine response to major surgical stress is believed to be mediated by cytokines such as IL-1B, IL-6, and tumor necrosis factor, as well as plasma catecholamines and cortisol.72 These mediators are thought to be responsible for triggering the inflammatory response that results in increased body temperature, leukocytosis, tachycardia, tachypnea, and fluid sequestration. Patients who have an exaggerated plasma stress mediator release have longer operative and cross-clamp times and require a greater number of blood transfusions.

Optimization of Body Systems Prior to Abdominal Aortic Aneurysm Repair include the following except A. Control hypertension B. Smoking cessation C. Avoid steroid supplementation D. Glycemic control

C. Optimization of Body Systems Prior to Abdominal Aortic Aneurysm Repair Cardiac Evaluation • Quantify risk factors and optimize cardiac function • Institute appropriate β-blocker • Institute statin therapy • Control hypertension • Institute appropriate anticoagulation therapy Pulmonary Evaluation • Advise smoking cessation • Perform radiologic tests and pulmonary function testing as indicated • Institute pharmacologic therapy, which may include corticosteroids and bronchodilators Renal Evaluation • Assess electrolytes, creatinine, and glomerular filtration rate Adrenal Evaluation • Provide steroid supplementation for patients at risk for acute adrenal crises Deep Vein Thrombosis Prophylaxis • Administer pharmacologic prophylaxis • Provide graduated compression stockings • Provide intermittent pneumatic compression • Provide enous foot pumps Musculoskeletal Evaluation • Assess range of neck motion prior to airway management • Assess functional limitations for positioning to avoid postoperative paresthesia Endocrine Evaluation • Provide short- and long-term glycemic control (mandatory), due to the increased incidence of diabetes Miscellaneous Considerations • Order laboratory assessments—complete blood count, coagulation panel, electrolyte panel, blood urea nitrogen, creatinine, albumin, blood sugar, liver function tests, type and crossmatch six units packed red blood cells

The patients who benefit most from CEA are those with stenosis of greater than __% A. 30 B. 50 C. 70 D. 90

C. Patient Selection - The risks associated with CEA and stroke must be measured against the risks associated with undergoing medical management. The patients who benefit most from CEA are those with stenosis of greater than 70%; it is less beneficial in symptomatic patients with 50% to 69% stenosis.175 Surgical intervention is most beneficial in men who are older than 75 and are within 2 weeks of their last ischemic event.182 As mentioned previously, the Framingham study identified the incidence of stroke after TIAs and demonstrated an increased risk of stroke in patients with untreated disease. Preoperative neurologic dysfunction was found to be the most significant factor for predicting postoperative stroke incidence (4%). Several conditions that can increase the risk of perioperative complications include severe preoperative hypertension, CEA performed in preparation for coronary artery bypass, angina, internal carotid artery stenosis near the carotid siphon, age older than 75 years, and diabetes mellitis.183,184 Box 28.12 identifies various factors that contribute to morbidity during CEA. Factors Contributing to Morbidity During Carotid Endarterectomy • History of stroke • Operative timing • Hyperglycemia • Multiple comorbidities • Age • Contralateral carotid artery disease • Progressing stroke • Ulcerative lesion • Intraoperative hemodynamic instability • Surgery with shunt • Surgery without shunt

Therefore, hemoglobin concentrations should be maintained at greater than ____ g/dL in vascular patients, especially those at significant risk for ischemic cardiac morbidity. A. 3 B. 6 C. 9 D. 12

C. Perioperative Myocardial Ischemia Etiology and Prevention - Ischemic cardiac morbidity is the most common cause of perioperative death in the United States5 (see also Chapter 39). Myocardial ischemia in the perioperative period is a strong predictor of adverse cardiac events after vascular surgery. Myocardial ischemia results from an imbalance between myocardial oxygen supply and demand, for which many causes exist during the perioperative period. Virtually every determinant of myocardial O2 supply and demand can be altered by factors common with vascular surgery, including intravascular fluid shifts, blood loss, pain, increased release of catecholamines, hypothermia, altered coagulability, and ventilatory insufficiency. Tachycardia, intravascular hypervolemia, and anemia are particularly detrimental because they simultaneously decrease O2 supply and increase O2 demand. The prevention and treatment of perioperative myocardial ischemia require careful control of these and other determinants of myocardial O2 supply and demand, as well as other physiologic changes that can precipitate ischemia. Table 69-5 summarizes eight studies showing the relative incidence of preoperative, intraoperative, and postoperative myocardial ischemia. The two studies with the most infrequent rates of intraoperative myocardial ischemia followed a protocol that included rigorously controlled intraoperative heart rate and arterial blood pressure. 39,40 Norris and associates40 continued this "tight" hemodynamic control into the postoperative period and reported a lower rate (15%) of postoperative myocardial ischemia. Excellent control of perioperative hemodynamics, especially heart rate (<85 beats/minute), likely decreases the incidence of myocardial ischemia. An even slower heart rate control (<70 beats/minute) may reduce myocardial ischemia after vascular surgery41; some added risk exists with this approach.42 The heart rate should clearly be controlled, but also the underlying cause should be determined. The common recommendation is to maintain arterial blood pressure within 20% of baseline. However, a more rational approach that appropriately addresses patients with hypertension or hypotension is described in Figure 69-4. Perioperative statin therapy also reduces the incidence of myocardial ischemia after vascular surgery.43 - The optimal hematocrit value for vascular surgery patients is not clear. An increased incidence of myocardial ischemia and cardiac morbidity occurs in vascular surgery patients if hemoglobin concentrations are less than 9.0 g/dL in the early postoperative period. Therefore, hemoglobin concentrations should be maintained at 2115greater than 9.0 g/dL in vascular patients, especially those at significant risk for ischemic cardiac morbidity. Accordingly, a "liberal" transfusion trigger should be considered (see also Chapter 61). Monitoring for Myocardial Ischemia - Three methods are used to detect myocardial ischemia during the perioperative period: surface electrocardiogram (ECG), transesophageal echocardiography (TEE), and pulmonary artery catheterization (see also Chapters 45 to 47). The sensitivity and specificity for detection of ischemia, the level of training required, and the cost of these methods differ and are important considerations. Monitoring for ischemia is important during and after vascular surgery. Ischemia may lead to infarction, especially when the ischemia is sustained over time (>2 hours).44 Accordingly, the clinical determinants of myocardial O2 supply and demand should be optimal in an attempt to resolve the ischemic condition. - Serial measurement of cardiac-specific biomarkers in the postoperative period is used to monitor for myocardial injury after vascular surgery. Measurement of cardiac troponin T or I facilitates the detection of myocardial damage over less specific biomarkers and allows the detection of very small injury. Data from the CARP and Ventavis Inhalation With Sildenafil to Improve and Optimize Pulmonary Arterial Hypertension (VISION) trials support the use of perioperative cardiac troponin as a means of stratifying high-risk patients after vascular surgery.45,46 Although not supported by current guidelines, routine surveillance of cardiac troponin after vascular surgery probably should be used for the detection of cardiac events and postoperative risk stratification.47

This is the most common cause of peripheral vascular occlusive disease A. Arteriosclerosis B. Aneurysm C. Atherosclerosis D. Vasculitis

C. Peripheral Vascular Disease - Atherosclerosis is the most common cause of peripheral vascular occlusive disease. This degenerative process involves the formation of atheromatous plaques that may obstruct the vessel lumen resulting in a reduction in distal blood flow. The pathophysiologic process is systemic, progressive, and primarily affects the arteries due to plaque formation, which can lead to stenosis and potentially occlusion of the vascular lumen; thrombosis from hypercoagulability, resulting in acute organ ischemia; embolism from microthrombi or atheromatous debris; and weakening of the arterial wall, resulting in aneurysm formation. Atherosclerosis is an inflammatory condition that is partially caused by cholesterol plaques, which occur within arteries. In response to cholesterol plaques, immune cells such as macrophages and monocytes liberate proinflammatory cytokines, which leads to a progressive increase in the size of plaques. The lipid cap which envelopes the plaque can rupture, resulting in intraluminal thrombosis or plaque emboli. The most common risk factors associated with atherosclerosis are shown in Box 28.1. Endothelial dysfunction is a potential cause of increased hemodynamic variability during anesthesia. Smoking, elevated proinflammatory mediators, and diabetes mellitus are major risk factors in the pathogenesis of atherosclerosis in the arterial tree. Typical symptoms associated with peripheral occlusive disease include claudication, skin ulcerations, gangrene, and impotence.1 The extent of disability is primarily influenced by the development of collateral blood flow. The mortality rate in patients with vascular disease is two- to sixfold higher than in the general population.2 Hypercoagulability resulting from platelet interaction with leukocytes and other cells that modulate the immune response plays a major role in the development of atherosclerosis.3,4 Researchers have discovered heritable genetic factors that predispose patients to developing vascular disease.5 - Treatment for peripheral occlusive disease may range from pharmacologic therapy to surgery. Surgical therapy includes transluminal angioplasty, endarterectomy, thrombectomy, endovascular stenting, and arterial bypass. Some common surgical maneuvers used to bypass occlusive lesions are aortofemoral, axillofemoral, femorofemoral, and femoropopliteal procedures. Bypass techniques may be classified as inflow or outflow procedures, depending on the level of the obstruction, with the dividing axis occurring at the level of the groin. Temporary occlusion of the operative artery is mandatory during surgical bypass, as this temporarily further reduces blood flow and oxygen delivery. The development of collateral circulation provides alternative vascular blood flow in patients with occlusive disease.6,7 Initially, angiogenesis or the development of new vessels supplies collateral blood flow that is sufficient to meet tissue oxygen demands. As the disease progresses, the blood flow is decreased, and the oxygen supply is unable to meet the tissues' demand, which could result in myocardial dysfunction, neurologic dysfunction, renal dysfunction, and/or limb ischemia.

Signs and symptoms of cerebral hyperperfusion syndrome include the following except A. Headache B. Visual disturbance C. Transient blindness D. Seizures

C. Postoperative Considerations - Perhaps the most common problem experienced in the postoperative period is hypertension. Although the specific cause remains unclear, postoperative hypertension is likely related to changes in sensitivity of the carotid baroreceptor reflex. A systolic blood pressure greater than 180 mm Hg is associated with an increased incidence of TIA, stroke, or MI.183 Patients with a systolic blood pressure of 145 mm Hg or less have fewer postoperative complications.169 A postoperative blood pressure of 140/80 mm Hg or less is recommended.222 Chronic hypertension during the postoperative period can lead to the development of cerebral hyperperfusion syndrome (CHS) as described below. Postoperative hypertension often resolves within 24 hours after surgery. Postoperative hypotension is less common but can be more difficult to treat because raising the blood pressure increases myocardial oxygen demand. Reestablishing normal pressures can be accomplished by careful titration of fluids and vasopressors. - Although an uncommon complication, carotid artery hemorrhage can occur in the postoperative phase. Hemorrhage is a devastating event that requires immediate surgical intervention. One of the initial manifestations of hemorrhage may be upper airway obstruction, which may make reintubation difficult due to tracheal deviation. Emergency management of a patient with airway compromise as a result of carotid artery hemorrhage and hematoma includes immediate evacuation of the hematoma. In addition, recurrent laryngeal nerve damage can occur, which routinely manifests as inspiratory stridor. Respiratory insufficiency can be problematic for patients who have preexisting respiratory conditions. Tension pneumothorax also can occur, because the apices of the lungs extend above the clavicles toward the surgical site. Treatment includes immediate lung re-expansion via chest tube insertion or needle decompression. Damage to the carotid body can lead to blunting of the chemoreceptor reflex, and therefore supplemental oxygen should be administered. Lastly, CHS may result from increased blood flow to the brain as a result of a loss of cerebral vascular autoregulation. The mechanism of action that causes this phenomenon is unclear; however, it is hypothesized that CHS may occur as a result of chronic cerebral ischemia or altered cerebrovascular autoregulation. Signs and symptoms of CHS include severe headache, visual disturbances, altered level of consciousness, and seizures. CHS may occur more often in patients who have had a contralateral CEA within the last 3 months and undergo a second CEA for occlusion on the ipsilateral side.223 - The incidence of postoperative stroke after CEA was discussed previously. Unfortunately, even after successful revascularization of the carotid artery, occlusion can recur at a rate of 3% per year.179 Although symptoms are present in only a small percentage of patients (3% to 5%), the incidence of recurrent carotid stenosis may be much larger than that reported, because asymptomatic cases may be overlooked.223 As many as 25% of patients experience a neurocognitive decline up to 1 month after surgery. Patients who are predisposed to this decline are those with diabetes and advanced age.224 The exact mechanism responsible for postoperative cognitive dysfunction has not been scientifically identified. Postoperative complications associated with CEA are listed in Box 28.15. - Owing to the anatomic location of and potential neurologic complications after CEA, post-emergence neurologic integrity should be assessed. In addition to neurocognitive functioning, clinical assessment of cranial nerve function should be performed (Table 28.9). The anatomic locations of the cranial nerves in relation to the internal, external, and common carotid arteries are shown in Fig. 28.14 Postoperative Complications of Carotid Endarterectomy • Hemodynamic instability • Myocardial ischemia/infarction • Cerebral hyperperfusion syndrome • Stroke • Respiratory insufficiency • Recurrent/superior laryngeal nerve damage • Hematoma • Carotid body dysfunction • Tension pneumothorax • Acute carotid occlusion.

It has been estimated that __% of patients presenting for abdominal aortic aneurysm (AAA) repair have significant CAD A. 22 B. 32 C. 42 D. 52

C. Preoperative Evaluation - The atherosclerotic process in occlusive disease is not limited to peripheral arteries, and should be expected to be present in the coronary, cerebral, and renal arteries. More than half of the mortality associated with peripheral vascular disease results from adverse cardiac events.8 There is a clear association between the development of aortic aneurysms and coronary artery disease (CAD).9 It has been estimated that 42% of patients presenting for abdominal aortic aneurysm (AAA) repair have significant CAD.10 Preoperative cardiovascular evaluation and treatment is beneficial for reducing not only perioperative risk but also late cardiovascular events. After elective AAA repair, the 5-year survival rate and incidence of major adverse cardiovascular events is 86%.11 Cardiac pathology, which often occurs in this patient population, must be managed aggressively to optimize cardiac functioning and decrease morbidity and mortality from cardiac causes. Preoperative Pharmacologic Management β-Blockade. - The advantages of β-blockade, as it relates to factors that affect myocardial oxygen supply and demand, have been extensively studied in patients with peripheral vascular disease The use of β-blockers is recommended in patients at high risk for myocardial ischemia and infarction.12 For patients having an AAA repair, there is a tenfold decrease in cardiac morbidity associated with adequate preoperative β-blockade.13 β-Blockade therapy should be instituted days to weeks before surgery and titrated to a target heart rate between 50 and 60 beats per minute (bpm).14 Perioperative β-blockade started within one day or less before noncardiac surgery prevents nonfatal myocardial infarctions (MIs), but increases the risk of hypotension, bradycardia, stroke, and death. Initiating β-blockade between 2 and 7 days before surgery may be preferable, but there is a lack of scientific data to support the benefit of beginning therapy more than a month in advance.15 Vascular surgery patients with limited heart rate variability after receiving β-blockers exhibit less cardiac ischemia and decreased postoperative troponin values and have a decreased mortality from all causes 2 years postoperatively.16 For patients taking β-blockers, these medications should be continued up to the day of surgery and during the postoperative period.17

Which of the following is not a risk factor Related to the Development of Atherosclerotic Lesions A. Hypertension B. Obesity C. Female D. Hyperlipidemia

C. Risk Factors Related to the Development of Atherosclerotic Lesions • Advanced age • Smoking • Hypertension • Diabetes mellitus • Insulin resistance • Obesity • Family history and genetic predisposition • Physical inactivity • Sex (males at greater risk than females) • Homocysteine • Elevated C-reactive protein • Elevated lipoprotein • Hypertriglyceridemia • Hyperlipidemia

The most common abnormalities detected by intraoperative TEE include the following except A. hypovolemia B. low ejection fraction C. left ventricular failure D. segmental wall motion abnormalities E. pulmonary embolus

C. Routine Monitoring - Standard monitoring methods include electrocardiography (with display of lead II for detection of dysrhythmias and the precordial V5 lead for analysis of ischemic ST-segment changes), pulse oximetry, and capnography. An esophageal stethoscope allows for continuous auscultation of heart and breath sounds, as well as temperature monitoring. Placement of an indwelling urinary catheter is necessary for continuous measurement of urinary output and renal function. Neuromuscular function should be routinely monitored. Invasive Monitoring - Maintaining cardiac function is crucial for a successful surgical outcome. Cardiac function should be closely monitored during abdominal aortic reconstruction. Invasive blood pressure monitoring permits beat-to-beat analysis of the blood pressure, immediate identification of hemodynamic alterations related to aortic clamping, and access for blood sampling. However, information obtained from PACs has been shown to have low sensitivity and low specificity in detecting myocardial ischemia when compared with electrocardiography and TEE. As previously discussed, PACs are not routinely indicated unless a specific purpose warrants their use.26 By detecting changes in ventricular wall motion, TEE provides a sensitive method for assessing ventricular wall motion abnormalities. TEE is a primary method of intraoperative cardiac assessment in patients undergoing surgery on the heart and the aorta.65,67 Wall motion abnormalities also occur much sooner than electrocardiographic changes during periods of reduced coronary blood flow.52 When TEE is used to guide intraoperative hemodynamic management, patients with left ventricular diastolic dysfunction have a decreased incidence of developing congestive heart failure and atrial fibrillation.68,69 The most common abnormalities detected by intraoperative TEE include hypovolemia, low ejection fraction, right ventricular failure, segmental wall motion abnormalities, and pulmonary embolus.70 Myocardial ischemia poses the greatest risk of mortality after abdominal aortic reconstruction. Intraoperative monitoring may enable earlier detection and intervention during ischemic cardiac events.

Ischemia of the colon is most often attributed to manipulation of which artery A. Celiac B. Superior mesenteric C. Inferior mesenteric D. Hypogastric

C. Spinal Cord Ischemia. - Spinal cord damage causing paraplegia can occur during aortic occlusion. The incidence of paraplegia during thoracic and thoracoabdominal aneurysm repair is estimated to be between 1% and 13%.80 Longitudinal blood flow to the spinal cord includes (1) two posterior and two posterolateral arteries supplying blood to the dorsal or sensory portion of the spinal cord (20% of spinal cord blood flow) and (2) one anterior spinal artery supplying blood to the anterior or motor portion of the spinal cord (80% of spinal cord blood flow). Transverse blood flow originating from the aorta is via the greater radicular artery (artery of Adamkiewicz). The exact location of this artery is variable and depends on an individual's specific anatomical characteristics. The artery most often originates between spinal segments T8-T12, but it can originate as low as L2 in a small segment of the population. This explains why the presence of paraplegia with aortic cross-clamping is unpredictable. Interruption of blood flow to the greater radicular artery in the absence of collateral blood flow has been identified as a factor that can cause paraplegia in patients having AAA repair. The incidence of neurologic complications increases as the aortic cross-clamp is positioned higher or more proximal to the heart. Somatosensory-evoked potential (SSEP) monitoring has been advocated as a method of identifying spinal cord ischemia. However, SSEP monitoring reflects dorsal (sensory) spinal cord function, and does not provide information regarding the integrity of the anterior (motor) spinal cord.6 Motor-evoked potential (MEP) monitoring is capable of determining anterior cord function. This monitoring modality relies on intact neuromuscular functioning for analysis, which limits its use in abdominal aortic aneurysmectomies, because neuromuscular blocking drugs are routinely used. Alternative methods for reliable evaluation of spinal cord ischemia are still under investigation.81 - Spinal cord protection strategies include distal aortic perfusion, cerebrospinal fluid drainage, and mild hypothermia. Maintenance of normotension (systolic ≥ 120 mm Hg) through the second postoperative day decreased the incidence of paraplegia during thoracic aortic reconstruction.82,83 - Ischemic colon injury is a well-documented complication associated with abdominal aortic resections. Ischemia of the colon is most often attributed to manipulation of the inferior mesenteric artery, which supplies the primary blood supply to the left colon. This vessel is often sacrificed during surgery, and blood flow to the descending and sigmoid colon depends on the presence and adequacy of the collateral vessels. Increased intraabdominal pressure has also been implicated in ischemic colon injury. Mucosal ischemia occurs in 10% of patients who undergo AAA repair. In less than 1% of these patients, infarction of the left colon necessitates surgical intervention.74

The most common symptoms of ruptured AAAs include the following except A. abdominal pain B. hypotension C. pulsatile abdominal mass D. syncope

D. Ruptured Abdominal Aortic Aneurysm - A high mortality rate of 80% to 90% is associated with a ruptured AAA, whereas postoperative mortality is estimated to range from 40% to 50%.100 The mortality after surgery to repair a ruptured AAA does not vary based on the type of surgical repair (open versus endovascular).101 The most common symptoms of ruptured AAAs include a triad of severe abdominal discomfort or back pain, altered level of consciousness caused by hypotension, and a pulsatile abdominal mass.102 Other common symptoms include syncope, groin or flank pain, hematuria, and groin hernia. Risk factors associated with an increase in mortality in patients with a ruptured AAA are noted in Box 28.7. - Hypotension and a history of cardiac disease are two factors associated with the poorest prognosis.51 Patients with these symptoms should be immediately transferred to the operating room for surgical exploration. When hypotension is absent, more time is available for comprehensive preoperative assessment and testing. However, decompensation and cardiovascular collapse can occur rapidly. - Once the patient arrives in the operating suite, performing a brief preoperative evaluation to establish peripheral and central venous access is a priority. Provisions for fluid, blood, and blood product administration is necessary, as rapid massive hemorrhage is a distinct possibility. The use of blood salvaging techniques and the ability to rapidly infuse blood and fluids are indicated. Insertion of an arterial line is essential, as significant fluctuations in blood pressure should be expected. Vasopressors such as phenylephrine and epinephrine given as a bolus and by infusion should be available. Hemodynamic stability must be the primary objective, and anesthetic induction and maintenance agents must be selected on a case-by-case basis. - Cardiovascular stability is the primary focus until blood loss from the proximal aorta is controlled by surgical intervention. Fluid resuscitation can begin with crystalloids; colloids and blood products can be administered as they become available. Intraoperative blood salvage provisions should be available. Coagulation studies and other laboratory tests including hemoglobin, hematocrit, and ionized calcium values should be obtained. Calcium is a positive inotrope, which is necessary for myocardial contractility. Large amounts of citrate used as a preservative in banked blood bind calcium ions and result in relative hypocalcemia. Decreased myocardial contractility--as evidenced by hypotension, increased left ventricular end-diastolic pressure, and increased central venous pressure--can be caused by hypocalcemia. Increased bleeding can also be caused by intraoperative hypocalcemia. If hypocalcemia occurs, calcium chloride can be administered, as guided by ionized calcium levels. Dilutional thrombocytopenia is the most common reason for coagulopathy to develop after massive intravenous fluid and blood administration. The use of fresh frozen plasma has been shown to decrease the total transfusion requirement and the incidence of coagulopathies.37 - The hemodynamic effects of aortic cross-clamping and release are similar to those for elective surgery; however, responses may be extreme, especially if hypotension exists when the clamp is released. Most patients require large amounts of fluid and blood replacement, and therefore postoperative mechanical ventilation is recommended. Patients experiencing hypovolemic shock are exquisitely sensitive to the cardiodepressant and vasodilatory effects of anesthetic agents. Titration of anesthetic agents and the use of vasopressors and or positive inotropes are warranted. Additionally, ventilation may be difficult due to surgical displacement of the diaphragm cephalad. This will decrease lung expansion and functional residual capacity and increase peak pressures. Because positive pressure ventilation decreases venous return, hypotension can occur. Minimizing peak inspiratory pressures and administering higher concentrations of oxygen will help maximize venous return and maintain oxygen saturation. Manual initiation of a positive pressure breath will improve alveolar recruitment and distention.

Which of the following patient condition is Carotid Artery Stenting better A. Advance age B. Severe renal dysfunction C. Intolerance of antiplatelet agents D. COPD

D.

Intraoperative monitoring for Thoracoabdominal Aortic Aneurysm Repair should focus on the following ischemia except A. myocardial B. neurologic C. renal D. pulmonary

D. Anesthetic Management - The principles of perioperative management of TAAs and DTAAs are similar to those previously discussed for abdominal aortic aneurysmectomies. Anesthetic selection should be based on the presence of concomitant disease processes, with the objective of maintaining cardiovascular stability and minimizing morbidity and mortality. Intraoperative monitoring should focus on detection of myocardial, neurologic, and renal ischemia. The hemodynamic consequences of aortic cross-clamping should be attenuated by the use of pharmacologic adjuncts. Restoration of circulating blood volume minimizes the hemodynamic alterations caused by the release of the aortic clamp. For a comprehensive summary of anesthetic management for AAA repair, see the earlier section on anesthetic management for thoracic aortic aneurysm. Postoperative Considerations - After surgery is completed, if a double-lumen endotracheal tube was used, it should be replaced with a standard endotracheal tube to provide a secure airway because postoperative ventilatory assistance is usually required. Airway anatomy may become edematous during surgery, causing difficulty with ventilation and reintubation. Under these circumstances, the double-lumen endotracheal tube may be left in place. Replacement of the endotracheal tube can proceed in the postoperative period after the airway edema has dissipated. Recurrent laryngeal nerve dysfunction can contribute to breathing difficulties after extubation. - Close observation of neurologic, circulatory, pulmonary, and renal status is warranted in the postoperative phase. Hemodynamic control is vital to maintaining perfusion to vital organs without creating excessive demands on the heart or the aortic graft. Careful monitoring of respiratory status aided by arterial blood gas analysis is indicated. Epidural analgesia with the use of local anesthetics, narcotics, or both can be administered for pain relief.

Advantages of a regional technique in CEA include the following except A. improved patient satisfaction B. decreased cost C. minimization of potential postoperative cognitive effects D. ability to administer cerebral protectants

D. Anesthetic Selection - The longstanding question has been whether there is an advantage of regional versus general anesthesia for CEA. The General Anesthetic versus Local Anesthetic for Carotid Surgery Trial (GALA), as well as a Cochrane meta-analysis, indicate no significant difference between the two anesthetic techniques.201,202 The anesthetic selection is based on the surgeon's preference, the patient's condition, and the preoperative evaluation. Advantages of a regional technique are that an awake patient can respond to commands and allow for continuous assessment of neurologic function. If the patient's level of consciousness decreases as a result of cerebral hypoperfusion, surgeons can then place a shunt. Other potential benefits include improved patient satisfaction, decreased cost, and minimization of potential postoperative cognitive effects associated with general anesthesia.203-205 Disadvantages include patient agitation and inability to remain still, minimal airway control, seizure or stroke during carotid artery clamping, and limited ability to give anesthetic medications. Advantages of general anesthesia include the ability to perform more extensive and difficult surgical procedures, better airway control, the ability to administer cerebral protectants, and improved blood pressure control.175,182

Which of the following decreases with an epidural technique in vascular surgery A. endocardial perfusion B. hemodynamic stability C. atrioventricualr oxygen differentiation D. renovascular constriction

D. Benefits of the Epidural Technique in Vascular Surgery Endocrine • Inhibits surgical stress response • Inhibits epinephrine and cortisol release • Inhibits hyperglycemia • Inhibits lymphopenia and granulocytosis • Causes nitrogen sparing • Blocks sympathetic tone • Inhibits inflammatory mediator release Cardiovascular • Decreases myocardial oxygen demand and afterload • Increases endocardial perfusion at ischemic zone • Increases hemodynamic stability • Decreased blood loss • Decreases general anesthetic medication requirements • Redistributes blood to lower extremities Pulmonary • Decreased effect on FVC, FEV1, and PEFR • Decreases ventilation perfusion mismatch • Improves atrioventricular oxygen differentiation • Decreases pulmonary postoperative complications • Decreased incidence of thromboembolism Renal • Increases blood flow in the renal cortex • Decreases renovascular constriction Geriatric • Inhibits physiologic stress • Improves postoperative mental status Miscellaneous • Allows earlier extubation, ambulation, and discharge • Improves postoperative pain control FEV1, Forced expiratory volume in 1 second; FVC, forced vital capacity; PEFR, peak expiratory flow rate.

How long should one wait post uncomplicated MI before going to undergo uncomplicated procedures A. 1-3 weeks B. 2-4 weeks C. 3-5 weeks D. 4-6 weeks

D. Cardiac Risk Assessment - The preoperative cardiac assessment presents an opportunity to initiate and optimize pharmacologic management, perform appropriate diagnostic and therapeutic interventions, and adjust overall care to decrease not only perioperative risk but also long-term risks from cardiovascular events. The challenge for clinicians is to accurately assess risk for cardiac morbidity while maintaining a cost-effective, clinically relevant, and evidence-based strategy. The ACC/AHA stepwise approach considers vascular surgery distinct from other noncardiac surgical procedures and is reviewed in detail in Chapter 38. Only issues specific to vascular surgery are reviewed in this chapter. - After assessment of cardiac risk, the additional challenge exists of modifying perioperative management to reduce risk by adjusting or adding cardiac medications (e.g., β-adrenergic blocker), direct coronary intervention (e.g., percutaneous coronary intervention [PCI] or coronary artery bypass grafting [CABG]), modifying or intensifying perioperative management (e.g., invasive hemodynamic monitoring), or changing preoperative plans (e.g., performing endovascular aortic repair rather than open aortic repair). Coordination is essential among surgeons, anesthesiologists, and cardiologists, each of whom may have different criteria for risk assessment and different objectives for risk modification. Clinical Risk Indices - Assessing cardiac risk in patients before vascular surgery is a controversial and difficult task (see also Chapters 37 and 38). Although risk indices are a cost-effective screening method for determining which patients may require further cardiac evaluation (i.e., additional risk stratification with noninvasive technologies), the high pretest probability of CAD in vascular surgery patients makes the risk index somewhat less useful. Vascular surgery-specific indices have been recently developed to optimize the prediction of perioperative mortality12 and cardiac morbidity13 in patients undergoing elective and urgent vascular surgery. Risk indices do not provide specific risk prediction for individuals, but rather place patients in general risk categories, most commonly designated as low (cardiac risk generally < 1%), intermediate (cardiac risk of 1% to 5%), or high (cardiac risk often > 5%). Clinical risk variables identified by logistic regression in vascular surgery cohorts can be used along with noninvasive cardiac testing to optimize preoperative assessment of cardiac risk before vascular surgery. From the registry of the Coronary Artery Revascularization Prophylaxis (CARP) trial, the absence of multiple preoperative cardiac risk variables identifies patients with the best long-term survival after elective vascular surgery.14 Previous Myocardial Infarction - In patients undergoing cardiac evaluation before vascular surgery, unrecognized MI (determined by rest wall motion abnormalities and no history of MI) is highly prevalent (23%) and associated with increased long-term cardiac risk.6 Diabetes and heart failure are important predictors of unrecognized MI. Current guidelines recommend waiting 4 to 6 weeks after an uncomplicated MI before proceeding with elective surgery11 and risk stratification with stress testing and assessment of ventricular function during this period.15 Vascular surgery is often not elective, and urgent or emergent surgery may be required for patients with symptomatic aortic aneurysm, crescendo transient ischemic attacks from carotid disease, or limb-threatening ischemia from iliac or femoral occlusive disease. In these instances, the patient must proceed to surgery with careful perioperative medical management and surveillance. Previous Coronary Artery Bypass Surgery Patients who have undergone prior (<5 years) CABG and are without current symptoms of angina or heart failure appear to have a relatively infrequent incidence of cardiac morbidity after noncardiac surgery. However, previous coronary revascularization may not provide the same level of protection against MI and death after major vascular surgery. Results from the randomized, prospective CARP trial demonstrated that an aggressive strategy of prophylactic coronary artery revascularization before vascular surgery in patients with stable cardiac symptoms does not improve short-term outcome or long-term survival.8 At 2.7 years after randomization, mortality was 22% and 23% in patients with and without revascularization, respectively. Postoperative MI, defined by increased troponin levels, occurred in 12% and 14% of patients with and without revascularization, respectively. Among those randomized to revascularization, patients undergoing CABG had fewer perioperative (6.6% versus 16.8%) and late postoperative (9.9% versus 23.7%) MIs than did patients undergoing PCI despite more diseased vessels in the CABG group (3.0 versus 2.2).16 Completeness of the revascularization procedure (CABG > PCI) was the predominant variable accounting for this difference. The Dutch Echocardiographic Cardiac Risk Evaluation Applying Stress Echocardiography (DECREASE)-V Pilot Study investigated in a randomized fashion the role of prophylactic coronary revascularization in high-risk (three or more clinical risk variables and extensive stress-induced on noninvasive cardiac testing) patients undergoing major vascular surgery, although concern has been raised about the integrity of investigations from the Poldermans group at Erasmus University.17-19 Preoperative coronary revascularization was not associated with improved short-term or long-term outcome compared with best medical treatment.17 No significant difference was found in the composite end point of all-cause death or nonfatal MI at 30 days (43% versus 33%) or during 1-year follow-up (49% versus 44%) between patients randomized to revascularization or no revascularization. Unlike the CARP trial, no difference was observed in the incidence of perioperative cardiac events between patients treated with CABG or PCI. The results of these 2111two randomized trials are congruent with the current ACC/AHA guidelines on perioperative management11 and CABG.20 Specifically, preoperative revascularization should be reserved for patients with unstable cardiac conditions or advanced coronary disease, for whom a survival benefit with CABG has been established. Periprocedural complications after CABG are substantially more frequent in patients with peripheral arterial disease than in those without such disease.21 These complications may preclude or alter the timing of subsequent vascular surgery.

Which of the following is the most common complication of Thoracoabdominal Aortic Aneurysm Repair A. Hemorrhage B. Graft thrombosis C. Graft infection D. Respiratory failure

D. Complications Following Thoracoabdominal Aortic Aneurysm Repair Early Complications • Respiratory failure (most common complication) • Hemorrhage • Myocardial infarction • Congestive heart failure • Early paraplegia • Embolization/thrombosis • Distal artery occlusion • Bowel ischemia • Sexual dysfunction • Infection • Renal failure • Cerebrovascular accident Late Complications • Delayed paraplegia • Graft thrombosis • Fistula formation • False aneurysm • Graft infection

Which of the following can occur from impingement by the aneurysm on the left recurrent laryngeal nerve A. pain B. stridor C. cough D. hoarseness

D. Diagnosis - The symptomatology of thoracic aneurysms is often related to the site of the lesion and its compression of adjacent structures. Pain, stridor, and cough may result from compression of thoracic structures. A change in the quality of one's voice, resulting in hoarseness, can occur from impingement by the aneurysm on the left recurrent laryngeal nerve. This can occur because the left recurrent larynx nerve bifurcates from the vagus nerve at the level of the aortic arch. Symptoms related to aortic insufficiency may be observed in aneurysms of the ascending aorta. An upper mediastinal mass may be an incidental finding on conventional chest radiography in an asymptomatic patient. Further investigation with noninvasive methods such as CT scan and MRI can describe the specific anatomic characteristics and location of the aneurysm.

Which of the following is not a Factor That May Influence the Magnitude and Direction of Physiologic Changes Occurring With Aortic Cross-Clamping A. Body Temperature B. Volume status C. Left ventricular function D. Vasoconstrictors

D. Factors That May Influence the Magnitude and Direction of Physiologic Changes Occurring With Aortic Cross-Clamping Level of aortic cross-clamp Species differences Anesthetic agents and techniques Use of vasodilator therapy Use of diverting circulatory support Degree of periaortic collateralization Left ventricular function Status of the coronary circulation Volume status Neuroendocrine activation Duration of aortic cross-clamp Body temperature

Ischemic stroke accounts for approximately ___% of first-time strokes and is primarily caused by atheromatous plaques. A. 20 B. 40 C. 60 D. 80

D. Indications - Since 1954, specific indications for and expected outcomes of CEA have been the subject of heated debate. Ischemic stroke accounts for approximately 80% of first-time strokes and is primarily caused by atheromatous plaques. The initial indication for CEA was symptomatic stenosis but not complete occlusive carotid disease. This presentation occurs in most patients who undergo carotid surgery. Some centers have extended the indications to include evolved ("nondense"), nonhemorrhagic strokes and asymptomatic severe stenosis or lesser stenosis associated with contralateral occlusive disease. The North American Symptomatic CEA Trial concluded that CEA for patients with recent hemispheric TIAs and high-grade stenosis (70% to 99%) had a risk reduction of 65% for the development of an ipsilateral stroke 2 years after surgery, compared with patients whose conditions were medically managed.169 The Executive Committee for the Asymptomatic Carotid Atherosclerosis Study demonstrated that asymptomatic patients with at least 60% carotid artery stenosis who underwent CEA had a 53% lower 5-year risk of ipsilateral stroke than patients who were treated medically.170 Other widely reported large-scale studies including the Asymptomatic Carotid Atherosclerosis Study (ACAS) and the European Asymptomatic Carotid Surgery Trial (EACST) demonstrated a benefit of CEA with medical therapy (aspirin and atherosclerotic risk factor reduction) over medical therapy alone for patients with carotid stenosis in the 60% to 99% range.171,172 These trials showed a similar absolute and relative reduction in risk for stroke of approximately 5% and 50%, respectively, at 5 years for CEA over medical therapy. Symptomatic patients are at a higher risk than asymptomatic patients for perioperative adverse events. However, the benefit of CEA in patients with recent ipsilateral carotid territory symptoms and moderate to severe carotid stenosis is much greater than the benefit of CEA in asymptomatic patients.173

The most common complication associated with Thoracoabdominal aortic repair is A. Neurological B. Renal C. Cardiovascular D. Pulmonary

D. Morbidity and Mortality - Despite tremendous development in surgical and anesthetic technique, mortality, and complication rates remain frequent for open surgical repair of TAA. Patients who undergo replacement of the entire thoracoabdominal aorta (Crawford extent type II) have the most frequent perioperative risk. Contemporary mortality rates reported from large institutions range from 5% to 14%. Statewide and nationwide mortality rates may be considerably more frequent (∼20%). The perioperative mortality rate may significantly underestimate the risk associated with TAA repair. In a large statewide series, the mortality with elective TAA repair was 19% at 30 days and 31% at 365 days.86 - The incidence of paraplegia or paraparesis in patients undergoing surgical repair of TAA is reported to be 3.8% to 40%, depending on complex factors such as anatomic location, the duration of cross-clamping, the use of protective measures, the degree of dissection, and whether the aneurysm has ruptured. Extensive dissecting TAA repair carries the highest risk for neurologic deficit. A contemporary report of 210 consecutive open TAA repairs reported three patients with paraplegia and two with temporary paraparesis for an overall rate of neurologic deficit of 2.4% (1.4% permanent).87 Renal failure occurs in 3% to 30% of patients, depending on similar factors noted earlier. Overall, approximately 6% of patients need postoperative dialysis after TAA repair, which is associated with high mortality (30% to 60%). Gastrointestinal complications occur in approximately 7% of patients and are associated with a mortality approaching 40%. Not surprisingly, pulmonary complications are the most common problem associated with TAA repair. The incidence of postoperative pulmonary insufficiency approaches 50%, with 8% to 14% of patients requiring tracheostomy. As with all other vascular surgical procedures, cardiac complications are common and a leading cause of perioperative mortality. In general, perioperative mortality and major complication rates after open isolated descending thoracic aortic replacement are lower than those described for TAA repair.

Criteria for surgical intervention for AAA include the following except A. ruptured AAA B. a 4 to 5 cm AAA with greater than 0.5 cm enlargement in less than 6 months C. patients who are symptomatic for AAA D. and a 4-cm AAA or greater for elective repair for patients with a reasonable life expectancy

D. Mortality - Elective AAA repair is one of the most frequent vascular surgical procedures, with approximately 40,000 operations performed in the United States annually.43 Mortality rates for elective abdominal aortic aneurysmectomies have decreased since the 1970s. The present mortality rate ranges from 1% to 11%, although it is most commonly estimated at 5%. This is compared with mortality rates of 18% to 30% in the 1950s.38,44-47 Even with the advent and increased frequency of EVAR, long-term mortality rates are similar, at approximately 15% to 17%.48 Advanced detection capabilities, earlier surgical intervention, extensive preoperative preparation, refined surgical techniques, higher quality hemodynamic monitoring, improved anesthetic techniques, and aggressive postoperative management have all contributed to this improvement in surgical outcomes. Data suggest that the risk of rupture is low for AAAs less than 4 cm in diameter, but the risk dramatically increases for AAAs with a 5-cm diameter or greater. Surgical intervention is recommended for AAAs 5.5 cm or greater in diameter.49 Unfortunately, mortality rates for patients with undetected or untreated ruptured aortic aneurysms have not followed the trend of those who have surgical intervention. Estimates of mortality resulting from ruptured AAAs vary from 35% to 94%.43,50-52 Combining prehospital mortality with operative mortality, the overall mortality for AAA rupture is 80% to 90%. The 5-year mortality rate for individuals with untreated AAAs is 81%, and the 10-year mortality rate is 100%.53 Other criteria for surgical intervention for AAA include ruptured AAA, a 4 to 5 cm AAA with greater than 0.5 cm enlargement in less than 6 months, patients who are symptomatic for AAA, and a 5-cm AAA or greater for elective repair for patients with a reasonable life expectancy. Early detection and elective surgical intervention can be lifesaving, because elective surgical mortality is less than 5% in most studies.54

Which of the following hemodynamic parameters increases during aortic cross-clamping A. Cardiac output B. Renal blood flow C. Oxygen consumption D. Pulmonary occlusion pressure

D. Physiologic Changes With Aortic Cross-Clamping∗ and Therapeutic Interventions Hemodynamic Changes ↑ Arterial blood pressure above the clamp ↓ Arterial blood pressure below the clamp ↑ Segmental wall motion abnormalities ↑ Left ventricular wall tension ↓ Ejection fraction ↓ Cardiac output† ↓ Renal blood flow ↑ Pulmonary occlusion pressure ↑ Central venous pressure ↑ Coronary blood flow Metabolic Changes ↓ Total body oxygen consumption ↓ Total body carbon dioxide production ↑ Mixed venous oxygen saturation ↓ Total body oxygen extraction ↑ Epinephrine and norepinephrine • Respiratory alkalosis‡ • Metabolic acidosis Therapeutic Interventions Afterload reduction Sodium nitroprusside Inhalational anesthetics Amrinone Shunts and aorta-to-femoral bypass Preload reduction Nitroglycerine Controlled phlebotomy Atrial-to-femoral bypass Renal protection Fluid administration Distal aortic perfusion techniques Selective renal artery perfusion Mannitol Drugs to augment renal perfusion Other Hypothermia ↓ Minute ventilation Sodium bicarbonate

Which of the following increases following aortic corss clamping A. Venous return B. Arterial blood pressure C. Mixed venous oxygen saturation D. Pulmonary artery pressure

D. Physiologic Changes With Aortic Unclamping∗ and Therapeutic Intervention Hemodynamic Changes ↓ Myocardial contractility ↓ Arterial blood pressure ↑ Pulmonary artery pressure ↓ Central venous pressure ↓ Venous return ↓ Cardiac output Metabolic Changes ↑ Total body oxygen consumption ↑ Lactate ↓ Mixed venous oxygen saturation ↑ Prostaglandins ↑ Activated complement ↑ Myocardial-depressant factor(s) ↓ Temperature Metabolic acidosis Therapeutic Interventions ↓ Inhaled anesthetics ↓ Vasodilators ↑ Fluid administration ↑ Vasoconstrictor drugs • Reapply cross-clamp for severe hypotension • Consider mannitol • Consider sodium bicarbonate

Which of the following is a systemic complication associated with EVAR A. Microembolization B. Endoleak C. Allergy to contrast dye D. Postimplantation syndrome

D. Potential Complications Associated With EVAR Graft and Deployment Complications • Failed deployment • Microembolization • Migration/occlusion of major branch arteries (i.e., renal, mesenteric) • Aortic perforation/aneurysm rupture • Aortic dissection • Hematoma formation • Endoleak • Stenosis/kink/thrombosis • Graft tear • Damage to access arteries (femoral → iliac) • Infection Radiologic Implications • Radiation exposure • Allergy to contrast dye • Renal insufficiency from contrast dye Systemic Complications • Neurologic (CVA, paraplegia) • Cardiac morbidity/mortality • Pulmonary insufficiency • Renal insufficiency • Postimplantation syndrome CVA, Cardiovascular accident; EVAR, endovascular aneurysm repair.

One limiting factor for the use of Regional anesthesia in CEA is A. Hemodynamic instability B. Coagulopathy C. Cardiac dysfunction D. Patient acceptance

D. Regional Anesthesia. - A regional anesthetic (RA) technique during CEA requires a deep and superficial cervical plexus block, which is accomplished by anesthetizing cervical nerves II to IV.175 Superficial cervical blocks do not anesthetize the region at the angle of the mandible, which is innervated by the trigeminal nerve. Local infiltration may be required. As noted previously, the greatest advantage of RA is the ability to directly assess neurologic function in an awake individual. Assessing level of consciousness is the most effective method of assessing the adequacy of CBF and detecting cerebral ischemia. In fact, assessment of consciousness in the awake patient may be more sensitive than conventional EEG in detecting cerebral ischemia. Corson206 reviewed data from 399 patients who underwent CEA in which GA and RA were used. The authors concluded that perioperative strokes occurred less often when RA was administered, especially in high-risk patients. McCarthy207 compared middle cerebral artery blood flow velocity using transcranial Doppler monitoring in patients undergoing CEA with either local or GA. It was determined that preservation of cerebral circulation was better maintained in patients who received local anesthesia.208-211 In addition, 67% of the GA group and 15% of the local anesthesia group received shunts.212 RA resulted in fewer hemodynamic fluctuations and fewer intraoperative vasoactive medication requirements as compared with GA during perioperative management of CEA.213 However, despite these seemingly physiologic advantages, no differences were observed in outcomes between the local and GA groups. The use of RA has been associated with shorter operative times, fewer cardiopulmonary complications, and a shorter duration of postoperative hospitalization. - One limiting factor for the use of RA is patient acceptance. The individual is mildly sedated; therefore, preoperative education is essential, and patient cooperation during surgery is vital. Anxiety, fear, and apprehension can initiate sympathetic stimulation, and as a result, extreme hemodynamic responses can occur. Deep sedation, which can be required in an apprehensive patient, may confound the neurologic assessment, negating the advantages of a regional technique. Additionally, hypercarbia can result from hypoventilation, and dysphoria is more likely to occur. Furthermore, converting to a GA technique once surgery has begun can be problematic. Symptoms indicating that adequate cerebral perfusion has been compromised include dizziness, contralateral weakness, decreased mentation, and loss of consciousness. In the event that this scenario occurs, immediate shunt placement is warranted. If symptoms associated with cerebral hypoperfusion do not resolve rapidly with shunt placement, emergent airway management is necessary. General Anesthesia. - Although the use of RA has numerous advantages, GA is also used during CEA. Perhaps the greatest benefit of this technique is that it counters the most cited disadvantage of regional anesthesia: lack of patient tolerance during the procedure. GA promotes a motionless field during surgery. In addition, inhalation agents may provide hemodynamic stability and may have beneficial effects on cerebral circulation.214 By decreasing cerebral and cardiac metabolism, the inhalation agents provide a degree of protection against ischemia, an effect that is called anesthetic preconditioning.215-217 - There is no scientific evidence to suggest that patient outcome is improved when inhaled agents are used, compared to narcotic-based techniques. In studies of inhalation agents, the critical regional CBF (the blood flow measurement for which EEG signs of ischemia occur) during isoflurane anesthesia was less than when other volatile anesthetics were used.214,218 The effects of sufentanil on cerebral hemodynamics were similar to those of isoflurane.219 Remifentanil can be used, and its rapid metabolism improves neurologic recovery. The inhalation agents may alter the monitoring methods used for detecting cerebral ischemia, such as EEG and SSEP monitoring. In these cases, GA may require modification, and direct communication between the anesthesia and surgical teams is vital. When carotid artery cross-clamping without shunting occurs, MAP values must be 20% or greater of the patient's preoperative MAP to help ensure adequate cerebral perfusion through the contralateral carotid artery and decrease the possibility of postoperative cognitive dysfunction.199 The use of nitrous oxide during CEA can potentially increase the incidence of a clinically significant pneumocephalus. During shunt placement and carotid artery cross-clamp release, microbubbles can be entrained into the carotid artery blood flow. Nitrous oxide is also known to cause hyperhomocysteinemia. Increased homocysteine can increase the postoperative cardiac risk and long-term mortality and increase the potential for carotid artery restenosis.220,221 If nitrous oxide is used, it should be discontinued before removal of the carotid artery cross-clamp.175,182 - In summary, there is no scientific consensus supporting the notion that a specific anesthetic technique is superior in decreasing perioperative morbidity and mortality post-CEA. Ensuring adequate cerebral and cardiac perfusion by treating hypertensive and hypotensive episodes aggressively is important. An anesthetic plan that allows for a rapid assessment of neurologic function at the completion of surgery should be selected.

Which of the following is generally considered to be the most effective means of renal protection during and after aortic cross-clamping. A. Dopamine B. Mannitol C. Fenoldopam D. Maintenance of intravascular volume

D. Renal Function and Protection - Preservation of renal function is of significant importance during aortic reconstructive surgery. Acute renal failure occurs in approximately 3% of patients undergoing elective infrarenal aortic reconstruction, and mortality resulting from postoperative acute renal failure is more frequent than 40%. Despite significant improvements in the perioperative care of these patients, the frequent incidence of morbidity and mortality resulting from acute renal failure has remained largely unchanged over the last several decades. Most of the morbidity associated with significant postoperative renal dysfunction is nonrenal. - The adequacy of renal perfusion "cannot" be assumed by urine output. Although urine output is closely monitored and often augmented during aortic surgery, intraoperative urine output does not predict postoperative renal function. Procedures requiring aortic cross-clamping above the renal arteries dramatically reduce renal blood flow. Experimental studies report an 83% to 90% reduction in renal blood flow during thoracic aortic cross-clamping. Infrarenal aortic cross-clamping in humans is associated with a 75% increase in renal vascular resistance, a 38% decrease in renal blood flow, and a redistribution of intrarenal blood flow toward the renal cortex. These rather profound alterations in renal hemodynamics occurred despite no significant change in systemic hemodynamics, and they persisted after unclamping. The sustained deterioration in renal perfusion and function during and after infrarenal aortic cross-clamping has been attributed to renal vasoconstriction, but the specific pathophysiologic process remains unknown. Renal sympathetic blockade with epidural anesthesia to a T6 level does not prevent or modify the severe impairment in renal perfusion and function that occurs during and after infrarenal aortic cross-clamping. Although plasma renin activity is increased during aortic cross-clamping, pretreatment with converting enzyme inhibitors before infrarenal aortic cross-clamping does not attenuate the decreased renal blood flow and glomerular filtration rate. Other mediators, such as plasma endothelin, myoglobin, and prostaglandins, may contribute to the decreased renal perfusion and function after aortic cross-clamping. Acute tubular necrosis accounts for nearly all the renal dysfunction and failure after aortic reconstruction. The degree of preoperative renal insufficiency remains the strongest predictor of postoperative renal dysfunction. In 2122addition to aortic cross-clamping-induced reductions in renal blood flow, ischemic reperfusion injury, intravascular volume depletion, embolization of atherosclerotic debris to the kidneys, and surgical trauma to the renal arteries all contribute to renal dysfunction. Mannitol, loop diuretics, and dopamine are used clinically in an attempt to preserve renal function during aortic surgery. Significant controversy exists regarding the use of these drugs, as well as the mechanisms by which they may offer a protective effect. Although not proved, pharmacologic "protection" before aortic cross-clamping is believed to be beneficial, and is therefore given. The use of mannitol 12.5 g/70 kg to induce osmotic diuresis before aortic cross-clamping is ubiquitous in clinical practice. Mannitol improves renal cortical blood flow during infrarenal aortic cross-clamping and reduces ischemia-induced renal vascular endothelial cell edema and vascular congestion. Other mechanisms by which mannitol may be beneficial include acting as a scavenger of free radicals, decreasing renin secretion, and increasing renal prostaglandin synthesis. - Loop diuretics and low-dose dopamine (1 to 3 μg/kg/minute) are used to protect the kidneys from aortic cross-clamp-induced injury by increasing renal blood flow and urine output intraoperatively. Routine use of these drugs is common for patients with preoperative renal insufficiency and for procedures requiring suprarenal aortic cross-clamping. Intraoperative use of these drugs requires increased surveillance of intravascular volume and electrolytes during the postoperative period. Therapy with these drugs could actually be harmful because of hypovolemia and resultant renal hypoperfusion. In addition, dopamine's positive inotropic and chronotropic activity may cause tachycardia and increase myocardial O2 consumption in patients with limited coronary reserve. Although I have virtually abandoned the prophylactic use of dopamine, diuretics are often given to patients with low urine output after aortic unclamping, particularly those maintained on chronic diuretic therapy. - Fenoldopam mesylate, a selective dopamine type 1 agonist that preferentially dilates the renal and splanchnic vascular beds, has shown some promise as a renoprotective drug. However, its role in the prevention of renal dysfunction after aortic surgery is not known. Statin use is associated with preserved renal function after aortic surgery requiring suprarenal aortic cross-clamping.69 Remote ischemic preconditioning reduces the incidence of renal impairment after open aortic surgery.70 Optimal systemic hemodynamics, including maintenance of intravascular volume, is generally considered the most effective means of renal protection during and after aortic cross-clamping. The goal is to achieve a preload adequate to allow the left ventricle to cope with cross-clamping-induced changes in contractility and afterload while maintaining cardiac output. However, in providing such therapy, excessive intravascular volume should be avoided, because it may lead to inappropriate increases in preload or pulmonary edema in patients with decreased myocardial reserve.

This is the risk factor that is most highly correlated with AAA. A. Older age B. Family history C. Gender D. Smoking

D. Risk Factors - The incidence of AAAs in a given population depends on the presence of risk factors (Box 28.3). Independent risk factors thought to be causes rather than markers for the development of an AAA include age, gender, and smoking. Smoking is the risk factor that is most highly correlated with AAA. In cigarette smokers, the incidence of AAAs increases fivefold.38 There is an association between chronic inflammation and angiopathology. The specific mechanism that links inflammation and vascular disease has not been definitively established, but elevated cytokine levels appear to play a central role.42

Which of the following is not an established risk factor for abdominal aortic aneurysm A. Increasing age B. Smoking C. Family history D. Women

D/ Abdominal Aortic Reconstruction - Anesthesia for conventional abdominal aortic reconstruction requires an understanding of the pathophysiology, extensive knowledge of the surgical procedure, the ability to interpret sophisticated hemodynamic data, and skillful pharmacologic control and manipulation of hemodynamics. Preoperative and intraoperative communication with the surgical team is essential. All open operative procedures on the abdominal aorta and its major branches require large incisions and extensive dissection, clamping and unclamping of the aorta or its major branches, varying duration of organ ischemia-reperfusion, significant fluid shifts and temperature fluctuations, and activation of neurohumoral and inflammatory responses. The major objectives of surgical treatment of the aorta are to relieve symptoms, reduce the frequency of associated complications, and in the case of aortic aneurysm, prevent rupture. Over the last two decades, the growth and development of catheter-based technology for the treatment of peripheral arterial disease have generated tremendous interest for less invasive methods to treat aortic disease. Endovascular aortic aneurysm repair (discussed later) has become an established less invasive alternative to conventional open repair, and its use has expanded to more than 75% of elective repairs and 30% of rupture repairs.53 The endovascular field continues to evolve rapidly with new devices, innovations, and indications for aortic disease. Natural History and Surgical Mortality Abdominal Aortic Aneurysm - Abdominal aortic aneurysms (AAAs) occur frequently in elderly men, with an incidence approaching 8% (see also Chapter 80). Increasing age, smoking, family history of AAA, and atherosclerotic disease are established risk factors. Although the prevalence is less frequent in women, the risk factors for AAA are similar to those in men. More than 30,000 deaths result from rupture of AAAs each year in the United States.54 The number of hospital discharges each year with the first diagnosis of aortic aneurysm is nearly 70,000. Approximately 40,000 patients undergo repair of AAA each year in the United States, at a cost likely to exceed a billion dollars. The incidence of AAA appears to be increasing and is age and gender dependent. AAA is a multifactorial disease associated with aortic aging and atherosclerosis. Although no unified concept of pathogenesis exists, genetic, biochemical, metabolic, infectious, mechanical, and hemodynamic factors may 2117contribute to the development of AAA disease. Adventitial elastin degradation (elastolysis), a hallmark of AAA formation, may be the primary event. Chronic inflammation plays a fundamental role in the destruction of connective tissue in the aortic wall. Concomitant aortoiliac occlusive disease is present in approximately 20% to 25% of patients with AAA. Approximately 5% of patients undergoing abdominal aortic resection have inflammatory aneurysms. Rare causes of AAA disease include trauma, mycotic infection, syphilis, and Marfan syndrome. Most AAAs are detected incidentally when imaging is performed for other reasons or through screening programs. The natural history of AAA disease is progressive enlargement and ultimate rupture and death. The diameter and rate of expansion of asymptomatic AAAs are the best predictors of the risk for rupture. Current guidelines emphasize that it is not possible to recommend a single threshold diameter for operative intervention that can be generalized to all patients. Yet, elective repair should be undertaken in all patients with AAA 6 cm or larger in diameter. Although some controversy exists regarding elective AAA repair when its diameter is in the 5.5- to 5.9-cm range, the risk for rupture of a 5.5-cm aneurysm (per year) is equal to or greater than the risk for perioperative mortality, and thus surgical repair is indicated. The 1-year incidence of probable rupture in patients refusing or unfit for elective repair is 9.4%, 10.2%, and 32.5% for aneurysms 5.5 to 5.9 cm, 6.0 to 6.9 cm, and 7.0 cm or greater, respectively.55 - Over 90% of AAAs are less than the current threshold (5.5 cm) for surgical repair at the time of detection. Randomized controlled trials in patients with AAAs 4.0 to 5.5 cm in diameter have provided important insight into the natural history of small asymptomatic aortic aneurysms.56 Four trials have demonstrated that surveillance of small aneurysms (4.0 to 5.5 cm) is a safe management option and that early repair (open or endovascular surgery) did not result in any long-term survival benefit. Surgical repair is often considered if small aneurysms become symptomatic or expand more than 0.5 cm in a 6-month period. Although significant interest exists in medical treatment (e.g., antibiotics, β-adrenergic blockers, statins) to delay or reverse expansion of small aneurysms, evidence for a protective effect is limited.57 Aneurysms less than 4.0 cm in diameter are thought to be relatively benign in terms of rupture and expansion. - Perioperative mortality from elective resection of infrarenal AAAs has progressively declined from 18% to 20% during the 1950s, 6% to 8% in the mid-1960s, 5% to 6% in the early 1970s, and 2% to 4% in the 1980s, at which time it plateaued. A publication of data from 1000 consecutive elective open infrarenal abdominal aneurysm repairs over a 15-year period reported a perioperative mortality rate of 2.4%.58 Hertzer and co-workers59 reported a mortality rate of 1.2% for 1135 consecutive elective open infrarenal abdominal aortic repairs at the Cleveland Clinic. This single-center mortality rate is considerably less than the mortality rates of 5.6% to 8.4% reported from large national data sets. These more frequent mortality rates on the national level suggest that all of the technologic and treatment advances over the last 2 decades have not had an impact on outcomes of patients requiring open AAA repair. Regionalization of patient care and endovascular treatments currently hold the most promise for improvement in operative mortality. For ruptured AAAs, perioperative mortality has not changed significantly over the last 4 decades and remains nearly 50%, with few exceptions. Including patients with rupture who die before reaching a hospital, the overall mortality rate after rupture may very well exceed 90%. The long-term durability of open infrarenal AAA repair is excellent and well established. The incidence of late graft complications is infrequent (0.4% to 2.3%). Postoperative survival rates after repair of nonruptured AAA are 92% at 1 year and 67% at 5 years.

True or False A more invasive surgical approach for the treatment of carotid artery stenosis is carotid artery angioplasty and stenting (CAS).

False Carotid Artery Angioplasty Stenting - A less invasive surgical approach for the treatment of carotid artery stenosis is carotid artery angioplasty and stenting (CAS). Controversy exists regarding the degree of success that this procedure affords as an alternative to CEA. The best application of CAS is still evolving and many studies comparing stenting with endarterectomy are ongoing. Best practices regarding proper patient selection, technique, and timing of the procedure are still being explored.225,226 The current incidence of stroke after CEA is approximately 2%. A meta-analysis noted that, compared to CAS, CEA decreases the risk of stroke at 30 days, increases the risk of MI, and does not have an effect on the risk of death.227 - The first large multicenter randomized controlled trial comparing CEA versus CAS was the Stenting and Angioplasty with Protection Patients at High Risk for Endarterectomy (SAPPHIRE) trial.228 The rate of event-free survival at 1-year post-surgery was 88% for the CAS group and 79.9% for the CEA group. The stroke rate after 1 year was lower in the CAS group as compared with the CEA group (6.2% versus 7.9%, respectively). As for cardiac morbidity, the rate of MI for CAS versus CEA was 1.9% versus 6.6% at 30 days postoperatively. Overall, cardiac morbidity was 3% for CAS and 6.2% for CEA. The conclusion drawn from the SAPPHIRE trial was that CAS does not yield inferior outcomes as compared with CEA. However, the study methodology was criticized and some experts questioned whether the results could be replicated.229 A new 3-year follow-up report of the SAPPHIRE study group indicates that in patients with severe carotid artery stenosis and increased surgical risk, no significant difference could be shown in long-term outcomes between patients who underwent CAS with an emboli-protection device and those who underwent endarterectomy.230 - The Endarterectomy versus Angioplasty with Symptomatic Severe Carotid Stenosis (EVA-3S) trial was designed to compare the outcomes from CAS versus CEA. The study population included patients with symptomatic carotid stenosis of at least 60%. The study was stopped early because of a high incidence of stroke and death (9.6% compared with 3.9% for CEA at 30 days after surgery). The conclusion was that CEA was superior to CAS for this patient population when considering risk of stroke at 30 days and 6 months postoperatively.231 Another randomized controlled trial, the Stent-Protected Angioplasty versus Carotid Endarterectomy (SPACE) trial, yielded high but similar statistics for 30-day stroke death rates (6.8% for CAS and 6.3% for CEA).232 The goal of the Carotid Revascularization Endarterectomy versus Stenting Trial (CREST), a randomized controlled trial, was to determine which procedure (CAS or CEA) was more effective in preventing stroke and death. Inclusion criteria were patients who were symptomatic and had greater than 50% carotid artery stenosis and those who were asymptomatic with greater than 60% carotid artery stenosis. The preliminary results from the first stage of the trial, which included 1000 patients, are encouraging and compare favorably with CEA. The rate of death or stroke from any cause during the 30 days after the procedure was 3% for asymptomatic patients under 80 years of age and 2.7% for symptomatic patients under 80 years of age.233 Initial indications were that CAS was associated with an increased incidence of stroke in octogenarians. However, it has now been determined that the incidence of stroke resulting from CAS is similar to the CEA results for all age groups.234 The CREST data show that the health-related quality of life in patients who underwent CAS is superior to those who underwent CEA for up to 1 year postoperatively.235 The CREST study was conducted over a ten-year period. It was determined that there were no significant differences between patients that had CEA versus CAS with respect to stroke, MI, and death.236 - Case selection guidelines for CAS are listed in Table 28.10. Prior to CAS, a high-resolution MRI is taken of the patient's aortic arch and carotid arteries, as well as a cerebral angiogram. This allows evaluation of the individual anatomy and angiopathology of the aortic arch, brachiocephalic artery (for right carotid artery stent), or left common carotid artery. The type of sheaths, stents, and cerebral embolic protection device needed can then be determined. Femoral artery access is obtained, and a sheath is then threaded through the aortic arch and into the operative carotid artery. The guide wire/embolic protection device is advanced through the sheath and positioned across the stenotic region. An embolic protection device sequesters emboli during angioplasty and stenting to avoid distal occlusion in cerebral arteries (Fig. 28.15). A distal embolic protection device lowers the risk of intraoperative and postoperative adverse events.237 This filter-like device is inserted distal to the area of stenosis prior to the angioplasty and stent deployment to catch microthrombi and pieces of plaque that could lodge within the brain. Angioplasty with a 5-mm balloon dilates the carotid artery, then the stent is deployed. The guide wire/device wire is removed after angiographic confirmation that carotid artery dissection or occlusion has not occurred. Fig. 28.16 shows carotid artery patency after angioplasty and stent placement.

True or False Not all inhalation anesthetics may depress the myocardium and cause hemodynamic instability.

False Intraoperative Management Anesthetic Selection - Several anesthetic techniques are available for abdominal aortic resections. Although each technique has its advantages and disadvantages, no single technique has been proven to be definitively superior. Anesthetic selection should be based on the following objectives: providing optimum analgesia and amnesia, facilitating relaxation, maintaining hemodynamic stability, preserving renal blood flow, and minimizing morbidity and mortality. General Anesthesia. - Circulatory stability is especially desirable for patients undergoing AAA reconstruction, especially for those with CAD. All inhalation anesthetics may depress the myocardium and cause hemodynamic instability. Therefore high concentrations of inhalation agents should not be used in patients with a moderate to severe decreased ejection fraction. The degree of myocardial depression is dose-dependent, and therefore it is acceptable to administer inhalation agents at lower inhaled concentrations. Beneficial effects attributed to inhalation agents include the ability to alter autonomic responses, reversibility, rapid emergence, potentially earlier extubation, neurologic protection, and cardioprotection.33 Cardiovascular stability provided by opioids has been well-documented, and this feature is especially attractive for patients with ischemic heart disease and ventricular dysfunction. Provision of intense analgesia for the initial postoperative period after major abdominal vascular surgery (i.e., administration of neuraxial opioid) does not alter the combined incidence of major cardiovascular, respiratory, and renal complications.94 Despite the absence of direct myocardial depression, the sympathetic nervous system inhibition that ensues may decrease SVR and heart rate. Therefore, especially in an individual with a moderate to severely decreased ejection fraction, narcotics should be carefully titrated to the patient's hemodynamic response.

True or False The effectiveness of pulmonary artery catheters (PACs) in improving patient outcomes has been proven

False Monitoring - The extent of perioperative monitoring should be based on the presence of coexisting disease and the type of surgery. Clearly, the detection of myocardial ischemia should be a primary objective in patients with vascular disease. Methods for assessing cardiac function include electrocardiography, pulmonary artery pressure, and transesophageal echocardiography (TEE) monitoring. The effectiveness of pulmonary artery catheters (PACs) in improving patient outcomes remains controversial. Many randomized controlled trials have been performed to assess whether they offer any benefit. It was determined that PAC monitoring had no effect on mortality or length of hospital stay. Additionally, there were higher rates of pulmonary embolism, pulmonary infarction, and hemorrhage in the PAC group.25-27 Furthermore, PACs have not been associated with decreased inoperative mortality or morbidity, and they are associated with increases in the duration of ventilation and length of stay in the intensive care unit (ICU) following cardiac surgical procedures.26 Specific indications for the use of PAC may be indicated (e.g., complex cardiac surgery).28 - Due to the global nature of atherosclerotic disease, some degree of systemic cardiovascular disease in patients with peripheral vascular disease should be assumed.10 Patients with hypertension and/or angiopathology rely on increased mean arterial pressures to perfuse their vital organs. Thus, cerebral and coronary autoregulation occurs within a higher range compared to patients without peripheral occlusive vascular disease (60-140 mm Hg). Short, sustained periods of hypotension can result in cardiac or neurologic ischemia. Direct intra-arterial blood pressure monitoring allows for near-real-time determination of blood pressure values, and is warranted because information ascertained from an arterial line, such as fluid volume status, acute fluctuations in blood pressure caused by surgical intervention, and titration of vasopressor/vasodilator medications, guides treatment decisions. - In the future, the use of noninvasive hemodynamic monitoring modalities may prove to decrease morbidity and mortality by allowing the anesthetist to make anesthetic choices based on another important factor: cardiac output. Titration of vasoactive medications and guiding intravenous fluid therapy could improve survivability in this patient population. More scientific evidence will be needed on the subject prior to making practice guideline recommendations.

True or False β-adrenergic blockers should be used as the initial or primary treatment of tachycardia caused by perioperative events, such as hypovolemia, anemia, pain, or infection, because these conditions require prompt treatment of the underlying cause.

False Perioperative β-Adrenergic Blocker Therapy - Perioperative β-adrenergic blocker therapy is an important and controversial topic, particularly in patients undergoing vascular surgery, and is reviewed more fully in Chapters 38 and 39. Patients receiving chronic β-adrenergic blocker therapy should continue taking β-adrenergic blockers throughout the perioperative period. However, β-adrenergic blockers should not be used as the initial or primary treatment of tachycardia caused by perioperative events, such as hypovolemia, anemia, pain, or infection, because these conditions require prompt treatment of the underlying cause. Treatment of tachycardia caused by the sympathetic stimulation associated with surgical stress should be considered in high-risk patients, particularly those with known ischemic potential (i.e., ischemia on preoperative testing). Hypotension and bradycardia should be avoided. Acute initiation of large-dose β-adrenergic blockade in the perioperative period should be avoided. If a decision is made to initiate β-blocker treatment in the perioperative period in an effort to reduce cardiac risk, the safest approach may be to initiate therapy with a small dose and titrate to effect over a 7- to 10-day period before the planned surgery. Perioperative β-adrenergic blocker therapy can decrease the number of patients referred for preoperative cardiac testing. However, such testing should not be eliminated, and its risk-to-benefit ratio should be carefully assessed.

True or False A reduction in the rate of MI, stroke, and respiratory failure was found when epidural anesthesia was used in patients undergoing aortic surgery

True Anesthetic Selection - The anesthetic technique chosen for patients having vascular surgery depends on the type of surgical procedure to be performed and the presence of coexisting disease. Maintaining consistent hemodynamic control and avoiding significant episodes of intraoperative hypertension and hypotension are vital to (1) maintaining oxygen delivery to vital organs, (2) decreasing the possibility of increased myocardial oxygen consumption, and (3) decreasing the potential for hemorrhagic stroke. In certain instances, infiltration of local anesthetic and intravenous sedation may be sufficient, whereas more invasive surgical procedures require the use of general anesthesia. Regional anesthesia for surgery on the lower extremities may decrease the overall morbidity and mortality associated with this patient population. Numerous studies have failed to yield demonstrative evidence that any single anesthetic technique decreases morbidity and mortality following vascular surgery. A comprehensive meta-analysis combining data from 141 studies involving 9559 patients suggested a 30% reduction in mortality for those patients who received a combined general anesthetic (GA) and epidural combination. A reduction in the rate of MI, stroke, and respiratory failure was found when epidural anesthesia was used in patients undergoing aortic surgery.29 A major study has been conducted to evaluate various end-points associated with major vascular surgery.30 None of these studies have definitively concluded that superior outcomes depend on the anesthetic technique used.31 A positive consideration for administering inhalation and intravenous anesthetic agents is that anesthetic medications decrease the rate of oxygen demand and help to protect neurologic and cardiac tissue in patients having noncardiac surgery.32 In addition, a meta-analysis reviewing epidural analgesia versus opioids for postoperative pain relief in patients undergoing abdominal aortic surgery showed an overall decreased rate of MI in those patients who received epidural analgesia.33 Epidural analgesia provided during the postoperative period has significant physiologic advantages. Specific benefits of using an epidural for major abdominal vascular surgery are summarized in Box 28.2. In addition, many patients having vascular surgery are receiving anticoagulant therapy and will receive heparin intraoperatively; therefore there is a risk that neuraxial anesthesia could lead to epidural hematoma formation.34

True or False Evidence suggests that there is no difference with respect to 30-day mortality between a hematocrit of 24% and a hematocrit of 30% in patients having cardiac surgery

True Management of Fluid and Blood Loss - Extreme loss of extracellular fluid and blood should be expected during repair of AAAs. The degree of surgical and evaporative losses and third-spacing will determine the magnitude of the patient's fluid volume deficit. Furthermore, the surgical approach, the duration of the surgery, and the experience of the surgeon affect the total blood loss. Most blood loss occurs because of back-bleeding from the lumbar and inferior mesenteric arteries after the vessels have been clamped and the aneurysm is opened.88 Anticoagulation with the use of heparin also contributes to blood loss. Excessive bleeding, however, can occur at any point during surgery, and blood replacement is often necessary during open abdominal aortic resections. - Owing to the heightened awareness of transfusion-related morbidity, the use of autologous blood via a cell saver system is a standard procedure. Presently, three options are available for administering autologous transfusions: preoperative deposit, intraoperative phlebotomy and hemodilution, and intraoperative blood salvage. Ideally, patients donate their own blood to minimize the intraoperative use of homologous blood products and the subsequent risk of transfusion-related viruses. With anemia and decreased hemoglobin, oxygen transport is decreased, thus placing the patient with systemic vascular disease at increased risk for MI and stroke. Autotransfusion blood-salvaging systems may be used for replacing intraoperative blood loss. In a study at the Mayo Clinic in which intraoperative autologous red cell salvage was used, 75% less banked blood was transfused. In a prospective study of 100 patients who underwent elective abdominal aortic resections, 80% of patients received only their own blood.88 An increased number of banked red blood cell units infused is an independent risk factor for poor outcome after cardiac surgery.89 Evidence suggests that there is no difference with respect to 30-day mortality between a hematocrit of 24% and a hematocrit of 30% in patients having cardiac surgery.90

True or False PCI probably should be limited to patients with unstable active CAD.

True Previous Percutaneous Coronary Intervention - The role of prophylactic percutaneous coronary revascularization in the preoperative management of vascular surgery patients is controversial.8,17 PCI probably should be limited to patients with unstable active CAD.11 Patients with peripheral vascular disease are often not ideal candidates for PCI. These interventions require placement of a large-diameter introducer sheath in the femoral artery, which predisposes to pseudoaneurysm and compromised blood flow to the lower extremities.22 PCI can be performed through the brachial artery, but it is technically difficult. PCI in patients with peripheral arterial disease, as opposed to those without peripheral arterial disease, is associated with less frequent procedural success, more frequent in-hospital cardiovascular complications, and mortality.23 Current guidelines indicate that PCI before noncardiac surgery, including vascular surgery, is of no value in preventing perioperative cardiac events, except in patients in whom PCI is independently indicated for unstable active cardiac conditions.11 - The optimal interval between PCI and subsequent vascular surgery is unknown (see also Chapters 37 and 38). Current perioperative guidelines provide a comprehensive review of this topic and offer recommendations based on clinical data and expert opinion.11 The type of coronary intervention, the need for dual antiplatelet therapy, the risk for bleeding from surgery, the risk in terminating antiplatelet therapy, and the urgency of the surgery all must be carefully considered. Noninvasive Diagnostic Cardiac Testing - Accurate clinical assessment of the pretest probability of significant CAD is extremely important. In general, noninvasive cardiac testing before vascular surgery is best directed at patients considered to be at intermediate clinical risk. Such testing should not be undertaken if it is unlikely to alter patient management and should not be considered as a preliminary step leading to coronary revascularization. A revascularization procedure is rarely needed solely for the purpose of getting a patient through the perioperative period. Extensive cardiac evaluation before vascular operations can result in morbidity, delays, and patient refusal to undergo vascular surgery. A complete review of this subject is found in Chapter 38. Cardiac Catheterization and Prophylactic Revascularization - The largest series on outcome in vascular surgery patients is that of Hertzer and colleagues24 from the Cleveland Clinic. These investigators performed cardiac catheterization in 1000 consecutive patients scheduled to undergo peripheral vascular surgery (aortic aneurysm resection, carotid endarterectomy, and lower extremity revascularization). The incidence and severity of CAD were assessed according to the following classification: normal coronary arteries; mild-to-moderate CAD with no lesion exceeding 70% stenosis; advanced, compensated CAD with one or more lesions exceeding 70% stenosis but with adequate collateral circulation; severe, correctable CAD with more than 70% stenosis in one or more coronary arteries; and severe inoperable CAD with greater than 70% stenosis in one or more coronary arteries and severe distal disease or poor ventricular function. The most remarkable findings were that only 8.5% of patients had normal coronary arteries and 60% had advanced or severe coronary lesions (>70% stenosis). Even when CAD was not suspected by the clinical history, more than a third of patients had advanced or severe coronary lesions (Table 69-2). - In the Hertzer series, patients with severe correctable CAD were offered CABG before their vascular surgery, patients with normal or mild-to-moderate CAD went directly to vascular surgery, and those with severe inoperable CAD were treated on an individual basis. Combined mortality rates over the immediate- and long-term (4.6-year follow-up) postoperative period are shown in Table 69-3.25 Of the 216 patients who underwent coronary revascularization (CABG), 12 (5.5%) died after this surgery. This mortality rate is more frequent than that reported for patients undergoing CABG surgery without peripheral vascular disease (1% to 2%). Perhaps the risks associated with CABG should be seriously considered as part of the preoperative evaluation of these patients. When overall early and late mortality (>5 years) is considered, death occurred in 12% versus 26% of patients who did or did not undergo CABG. Although these data 2112appear to support the beneficial effect of CABG on outcome, the mortality from CABG itself (5.5%) reduces its apparent benefits. - Two randomized clinical trials have been performed to determine the impact of prophylactic coronary artery revascularization on outcome after open aortic and lower extremity arterial vascular surgery.8,17 Of the 5859 patients screened in the CARP trial,8 1190 underwent coronary angiography based on a combination of clinical risk factors and noninvasive stress imaging data.26 The incidence and severity of CAD on these angiograms were 43% of patients had one or more major coronary arteries with at least a 70% stenosis suitable for revascularization (and were randomized to either revascularization or no revascularization before vascular surgery); 31% had nonobstructed coronary arteries; 18% had coronary stenosis considered unsuitable for revascularization; and 5% had left main coronary artery stenosis of 50% or more. The CARP trial showed that prophylactic revascularization (by CABG or PCI) was generally safe but did not improve long-term outcome after vascular surgery. Long-term mortality (2.7 years) was 22% in the revascularization group and 23% in the group considered inappropriate for revascularization (Fig. 69-3). Although the trial was not designed to test the short-term benefit of prophylactic revascularization, perioperative outcomes were not decreased, including death (3.1% versus 3.4%) and MI (12% versus 14%). The CARP trial results can be applied to most of the vascular surgery patients; however, they cannot be extrapolated to patients with unstable cardiac symptoms, left main coronary artery disease, aortic stenosis, or severe left ventricular dysfunction because these conditions excluded patients from study participation. The DECREASE-V trial17 screened 1880 vascular surgery patients, 430 of whom with three or more clinical risk factors underwent noninvasive stress testing using stress-echo or perfusion imaging. Patients with extensive stress-induced ischemia (26%) were randomly assigned to 2113revascularization or no revascularization. Coronary angiography showed two-vessel disease in 24%, three-vessel disease in 67%, and left main coronary artery disease in 8%. Prophylactic coronary revascularization (CABG or PCI) did not improve perioperative or long-term outcome (Table 69-4). The incidence of all-cause death or nonfatal MI at 30 days in patients who underwent revascularization or who did not was 43% versus 33%, respectively. The incidence of the composite end point at 1 year was similar, 49% versus 44%, respectively. As noted previously, this trial has come under scrutiny based on concerns of unfortunate scientific misconduct by the principal investigator. - The lack of benefit of prophylactic coronary revascularization in the CARP and DECREASE-V trials is difficult to reconcile with the more favorable data from Hertzer and co-workers24 and other studies (Coronary Artery Surgery Study [CASS]27 and Bypass Angioplasty Revascularization Investigation [BARI]28), but is consistent with current guideline recommendations.11 Clearly, issues are involved that go beyond critical coronary lesions; perhaps the current understanding of the pathophysiology of perioperative MI is incomplete. For example, perioperative MI may be caused by culprit lesions (i.e., vulnerable plaques with high likelihood of thrombotic complications) often located in coronary vessels without critical stenosis.29 For this type of MI (atherothrombotic), perioperative strategies aimed at reducing potential triggers of coronary plaque destabilization and rupture may be more appropriate than those leading to coronary revascularization. Demand ischemia is likely the predominant cause of perioperative MI, which has been confirmed by a recent angiographic study.30

It has been estimated that less than __% of AAAs are identified during routine physical examination. A. 10 B. 20 C. 30 D. 40

c. Diagnosis Physical Examination - Asymptomatic aneurysms may be detected during routine examination as a pulsatile abdominal mass. Smaller aneurysms are often undetected on routine physical examination. AAA screening rates remain below 50%. AAAs are frequently discovered incidentally by primary practitioners, and some patients undergo unnecessary ultrasound screening.55 It has been estimated that less than 30% of AAAs are identified during routine physical examination. A more extensive scoring system that includes additional risk factors such as the presence of carotid artery or peripheral arterial disease, obesity, hypertension, smoking, diabetes, and increased age may increase the rate of detection to almost 90% of AAAs.56 Imaging - A minimally invasive method used to initially diagnose the presence of AAA is by ultrasound. Ultrasound is helpful to determine if a AAA is present, but it is not highly accurate in determining the extent of AAA or if rupture has occurred.57 CT angiography (CTA) allows for a more precise view of the aneurysm morphology, including aneurysm size, vessel wall integrity, and adjacent anatomic definition such as the iliac arteries. CTA has become the imaging test of choice for AAA because of its high quality resolution, rapid image acquisition, and wide availability.58 This information gained from CTA is valuable to the surgeon and interventional radiologist for initial determination of the surgical intervention (e.g., open or EVAR) and the extent of the distal and proximal aneurysm if an endovascular stent graft is to be implanted.