A Practical Approach to Cardiac Anesthesia

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CHAPTER 24. Anesthetic Management for Thoracic Aneurysms and Dissections

Thomas M. Skeehan and John R. Cooper, Jr.

Quick Links to Sections in this Chapter

–Classification and natural history

–Diagnosis

–Preoperative management of patients requiring surgery of the thoracic aorta.

–Surgical and anesthetic considerations

–Future trends.

See Related Case Study from Yao & Artusio's Anesthesiology

In the management of thoracic aortic surgery, the anesthesiologist may face a marked variability in the problems associated with etiology, type, and anatomic location of the surgical procedure. This chapter gives a concise overview of the pathophysiology of thoracic aortic surgery, an understanding of its surgical approaches and results, and a rational approach to the management of the patient undergoing thoracic aortic surgery.

  1. Classification and natural history

    1. Dissections. An aortic dissection occurs when blood penetrates the aortic intima and forms an expanding hematoma within the vessel wall, usually separating the intima and media to create a so-called false lumen or dissecting hematoma. The vessel lumen is not dilated and often is compressed by the advancing hematoma. In contrast, an aortic aneurysm involves dilation of all three layers of the vessel wall and has a highly different pathophysiology and implications for management. The term dissecting aneurysm, although commonly used, is often a misnomer.

      1. Incidence and pathophysiology

        1. Incidence. Aortic dissections have been estimated to cause one of every 10,000 hospital admissions. In large autopsy series, aortic dissection has been found in one of every 600 cases, and it was believed that dissections may have caused or contributed significantly to the mortality in up to 1% of these autopsy cases.

        2. Predisposing conditions. The medical conditions predisposing to aortic dissection are listed in Table 24.1 in their order of importance. Interestingly, atherosclerosis by itself may not contribute to the risk of subsequent dissection.

        3. Inciting event. The onset of aortic dissections has been associated with increased physical activity or emotional stress. Dissections also have been associated with blunt trauma to the chest; however, the temporal relationship of blunt trauma and subsequent dissections has not been well established. Dissections can occur without any physical activity. They also may occur during cannulation for cardiopulmonary bypass (CPB).

        4. Mechanism of aortic tear. An intimal tear is the initial event in aortic dissection. The intimal tear of aortic dissections usually occurs in the presence of a weakened aortic wall, predominantly involving the middle and outer layers of the media. In this area of weakening, the aortic wall is more susceptible to shear forces produced by pulsatile blood flow in the aorta. The most frequent locations of intimal tears are the areas experiencing the greatest mechanical shear forces, as listed in Table 24.2. The ascending and isthmic (just distal to the left subclavian artery) segments of the aorta are relatively fixed and thus subject the aortic wall to the greatest amount of mechanical shear stress. This explains the high incidence of intimal tears in these areas.

          In large autopsy series, however, up to 4% of dissections had no identifiable intimal disruption. In these cases, rupture of the vasa vasorum, the vessels that supply blood to the aortic wall, has been implicated as an alternative cause of dissections. The thin-walled vasa vasorum are located in the outer third of the aortic wall, and their rupture would cause the formation of a medial hematoma and propagation of a dissection in the presence of an already diseased vessel, without formation of an intimal tear.

        5. Propagation. Propagation of an aortic dissection can occur within seconds. The factors that contribute to propagation are the hemodynamic forces inherent in pulsatile flow: pulse pressure and ejection velocity of blood.

        6. Exit points. Exit points of dissections are found in a relatively small percentage of cases. Exit point tears usually occur distal to the intimal tear and represent points at which blood from the false lumen reenters the true lumen. The presence or absence of an exit point does not appear to have an impact on the clinical course.

        7. Involvement of arterial branches. The origins of the major branches of the aorta, including the coronary arteries, may be involved in aortic dissections. Their involvement ranges from the occlusion of their lumens by mechanical compression by the false lumen or propagation of the dissecting hematoma into the arterial branch. The incidence of involvement of arterial branches gathered from a large autopsy series is listed in Table 24.3.

      2. DeBakey classification of dissections (Fig. 24.1). This classification comprises three different types, depending on where the intimal tear is located and which section of the aorta is involved.

        FIG. 24.1 DeBakey classification of aortic dissections by location: type I, with intimal tear in the ascending portion and dissection extending to descending aorta; type II, ascending intimal tear and dissection limited to ascending aorta; type III, intimal tear distal to left subclavian, but dissection extending for a variable distance, either to the diaphragm (a) or to the iliac artery (b). (From DeBakey ME, Henly WS, et al. Surgical management of dissecting aneurysms of the aorta. J Thorac Cardiovasc Surg 1965;49:131, with permission.)


        1. Type I. The intimal tear is located in the ascending portion, but the dissection involves all portions (ascending, arch, and descending) of the thoracic aorta.

        2. Type II. The intimal tear is in the ascending aorta, but the dissection involves the ascending aorta only, stopping before the takeoff of the innominate artery.

        3. Type III. The intimal tear is located in the descending segment, and the dissection almost always involves the descending portion of the thoracic aorta only, starting just distal to the origin of the left subclavian artery. By definition, type III dissections can propagate proximally into the arch, but this is rare.

      3. Stanford (Daily) classification of dissections (Fig. 24.2). This classification is simpler than the DeBakey classification and has more clinical relevance.

        FIG. 24.2 Stanford (Daily) classification of aortic dissections. Type A describes a dissection involving the ascending aorta regardless of site of intimal tear (1, ascending; 2, arch; 3, descending). In type B, both the intimal tear and the extension are distal to the left subclavian. (From Miller DC, Stinson EB, et al. Aortic dissections. J Thorac Cardiovasc Surg 1979;78:367, with permission.)


        1. Type A. Type A dissections are those that have any involvement of the ascending aorta, regardless of where the intimal tear is located and regardless of how far the dissection propagates. Clinically, type A dissections run a more virulent course.

        2. Type B. Type B dissections are those that involve the aorta distal to the origin of the left subclavian artery.

      4. Natural history

        1. Mortality—untreated. The survival rate of untreated patients with aortic dissections is dismal, with a 2-day mortality of up to 50% in some series and a 6-month mortality approaching 90%. The usual cause of death is rupture of the false lumen and fatal hemorrhage. Other causes of death include progressive cardiac failure (aortic valve involvement), myocardial infarction, stroke, irreversible coma, and bowel gangrene (mesenteric artery occlusion).

        2. Surgical mortality. The overall surgical mortality is approximately 30%, but surgical therapy is often the only viable option for most of these patients.

    2. Aneurysms

      1. Incidence. Thoracic aortic aneurysms account for 1% to 4% of aneurysms seen at autopsy. Currently, approximately 60% involve the ascending aorta and 30% are localized to the descending aorta. Aneurysms involving the aortic arch exclusively make up less than 10% of the total.

      2. Classification by location and etiology. In general, the etiology and pathophysiology of aortic aneurysms are site dependent. The most common causes by region are medionecrosis in the ascending aorta and atherosclerosis in the arch and descending aorta. Other etiologies are listed in Table 24.4.

      3. Classification by shape

        1. Fusiform. Fusiform aneurysmal dilation involves the entire circumference of the aortic wall.

        2. Saccular. Saccular aneurysms involve only one portion of the aortic wall. Aortic arch aneurysms are commonly of this type.

      4. Natural history. The usual history of aortic aneurysms is that of progressive dilation and, in more than 50% of cases, rupture. The untreated 5-year survival is approximately 13%, depending on the size of the aneurysm at diagnosis. Other complications include mycotic infection, atheroembolism to peripheral vessels, and dissection. This last complication is rare, probably occurring in fewer than 10% of cases. Some predictors of poor prognosis are large size (greater than 10-cm maximum transverse diameter), presence of symptoms, and associated cardiovascular disease, especially coronary artery disease, myocardial infarction, or cerebral vascular accident.

    3. Thoracic aortic rupture (tear)

      1. Etiology. The overwhelming majority of thoracic ruptures are secondary to trauma and almost always involve a deceleration injury in a motor vehicle accident. Sudden deceleration places large mechanical stresses on the aortic wall at points where the aorta is relatively immobile. Rupture of the aorta in many cases leads to immediate exsanguination and death. However, in approximately 10% to 15% of cases, the integrity of the lumen is maintained by the adventitial covering of the aorta, and these patients are able to reach emergency care. Surgical treatment of these survivors is often successful.

      2. Location. The location of most ruptures of the thoracic aorta is the area just distal to the origin of the left subclavian artery (isthmus), due to the relative fixation of the aorta at this point by the ligamentum arteriosum (Fig. 24.3). The aorta also is fixed in the ascending portion just distal to the aortic valve, and this is the second most common site of rupture.

        FIG. 24.3 The heart and great vessels are relatively mobile in the pericardium, whereas the descending aorta is relatively fixed by its anatomic relations. The attachment of the ligamentum arteriosum enhances this immobility and increases the risk of aortic tear due to deceleration injury. (From Cooley DA, ed. Surgical treatment of aortic aneurysms. Philadelphia: WB Saunders, 1986:186, with permission.)


  2. Diagnosis

    1. Clinical signs and symptoms (Table 24.5)

      1. Dissections. The clinical presentation of aortic dissection usually is characterized by a dramatic onset and a fulminant course. Differences and clinical presentation of Stanford types A and B are listed in Table 24.5.

      2. Aneurysms. Aneurysms of the ascending, arch, or descending thoracic aorta often are asymptomatic until late in their course. In many circumstances, the presence of an aneurysm is not diagnosed until medical evaluation is conducted for an unrelated problem or for a problem related to a complication of the aneurysm.

      3. Traumatic rupture. Ruptures most commonly occur just distal to the left subclavian artery. In this setting, signs and symptoms are similar to those seen with aneurysms of the descending thoracic aorta if the patient survives the initial event.

    2. Laboratory diagnosis

      1. Electrocardiogram. A common finding for many patients with aortic disease is that of left ventricular hypertrophy, a condition correlating with a history of accompanying hypertension. The electrocardiogram (ECG) may show a pattern associated with ischemia or pericarditis caused by coronary artery occlusion or hemopericardium, respectively, in the setting of ascending aortic dissection.

      2. Chest x-ray film. A widened mediastinum is a classic x-ray finding in the presence of thoracic aortic pathology. Widening of the aortic knob is often seen, with disparate ascending-to-descending diameter. A double shadow has been described in the setting of aortic dissection, in which the false lumen actually is visualized.

      3. Serum chemistries. There are no specific laboratory findings with asymptomatic aneurysm. Dissection or rupture will produce a fall in hemoglobin. Dissections may cause elevation of cardiac enzymes (coronary artery occlusion), elevation of blood urea nitrogen and creatine (renal artery occlusion), and acidosis (low cardiac output or bowel ischemia).

      4. Computed tomographic scans and magnetic resonance imaging. Computed tomography is a useful tool for diagnosing aneurysm size and has replaced angiography in some instances. Magnetic resonance imaging has been found to be extremely sensitive and specific in terms of identifying the entry tear, false lumen, aortic regurgitation, and pericardial effusion associated with aortic dissections [1].

      5. Angiography. This technique remains the "gold standard" for determining the severity and extent of aneurysm and dissection. It can be used to determine the site of an intimal tear in the setting of dissecting hematoma, to assess aortic valve function, and to identify the distal and proximal spread of the lesion. In the case of ascending aortic pathology that will require CPB, the coronary anatomy can be delineated. Patients with disease of the thoracic aorta usually have concurrent coronary disease. Bypassing significant lesions would help to improve ventricular function for weaning from CPB. Aortography can diagnose the involvement of major vessels but rarely can identify the critical intercostal vessels that provide blood supply to the spinal cord (see Section IV.G).

      6. Transesophageal echocardiography. Transesophageal echocardiography (TEE) has a role in diagnosing and screening patients who are suspected of having an aortic dissection. It can be diagnostic if adequate images are obtained. Pulsed Doppler and color Doppler imaging will aid in diagnosing the presence, extent, and type of dissection in most cases. TEE has been found to be highly sensitive and specific in the diagnosis of aortic dissection. Identification of a mobile intimal flap provides a prompt bedside diagnosis that can be lifesaving. In addition, (a) entry and reentry tears can be defined; (b) aortic regurgitation can be identified and quantified; (c) assessment of left ventricular (LV) function can be made; (d) presence of pericardial effusion or cardiac tamponade can be identified; and (e) follow-up studies of the false lumen can be made after therapeutic intervention.

      7. Recommendation for diagnostic strategies. Nienaber et al. [2] and colleagues proposed a noninvasive imaging strategy for the diagnosis of thoracic aortic dissection. Magnetic resonance imaging, because of its high degree of sensitivity (98.3%) and specificity (97.8%), was recommended as the preferred diagnostic method in hemodynamically stable patients. For patients deemed unstable for this rather lengthy procedure (40 to 45 minutes), TEE, which has an average duration of about 15 minutes and sensitivity and specificity of 97.7% and 76.9%, respectively, is recommended for the unstable patient. Aortography, because of its inability to provide more critical information than the noninvasive methods and its higher incidence of complications, should remain as a diagnostic tool to be used only in select cases.

    3. Indications for surgical correction

      1. Ascending aorta

        1. Dissections. Currently, any acute type A dissection should be corrected surgically, given the virulent course and high mortality if left untreated.

        2. Aneurysms. Surgical indications for resection include the following:

          1. Presence of persistent pain despite a small aneurysm

          2. Involvement of the aortic valve producing aortic insufficiency

          3. Presence of angina due either to LV strain from aortic valve involvement or coronary artery involvement by the aneurysm

          4. Rapidly expanding aneurysm or an aneurysm greater than 10 cm in diameter, because the chance of rupture increases with increasing size

      2. Aortic arch

        1. Dissections. Acute dissection limited to the aortic arch is an indication for surgery (rare).

        2. Aneurysms. Because even elective surgical treatment for these types of aneurysms is more difficult and is associated with a higher morbidity and mortality, management tends to be more conservative. Surgical indications include the following:

          1. Persistence of symptoms

          2. Aneurysm greater than 10 cm in transverse diameter

          3. Progressive expansion of an aneurysm

      3. Descending aorta

        1. Dissection. Some controversy remains concerning the best treatment for an acute type B dissection. Due to similar mortality statistics for medical or surgical intervention, type B dissections often are treated medically in the acute phase, especially if the patient's concurrent disease would make surgical mortality prohibitively high. However, in patients with a type B dissection, the following complications should be treated surgically as they occur:

          1. Failure to control hypertension medically

          2. Continued pain (indicating progression of the dissection)

          3. Enlargement on chest x-ray film, computed tomographic scan, or angiogram

          4. Development of a neurologic deficit

          5. Evidence of renal or gastrointestinal ischemia

          6. Development of aortic insufficiency

            It should also be noted, as shown in Table 24.6, that 10-year survival for patients with medically managed type B dissections is similar to surgical survival for type A and B dissections together. Both of these managements compare favorably with the 10-year survival of patients with untreated aortic dissections.

        2. Aneurysm. Surgical indications include the following:

          1. Chronic aneurysm of the descending thoracic aorta that causes persistent pain or other symptoms

          2. Aneurysm greater than 10 cm in diameter

          3. Expanding aneurysm

          4. Leaking aneurysm (more fulminant symptoms)

  3. Preoperative management of patients requiring surgery of the thoracic aorta. Emergency preoperative management of aortic dissections is discussed below. However, emergency preoperative management for a leaking thoracic aneurysm and a contained thoracic rupture would be similar.

    1. Prioritizing: making the diagnosis versus controlling blood pressure. In the setting of a suspected dissecting hematoma, aortic tear, or leaking aneurysm, the first priority must always be to control the blood pressure (BP). Making the diagnosis with chest x-ray film or angiogram should occur only when proper monitoring, intravenous (IV) access, and therapy have been established. During the diagnostic procedure, the patient should be monitored closely, with a physician present as the clinical situation dictates. The anesthesiologist should become involved as early as possible to lend expertise in monitoring and in airway and hemodynamic management, should clinical deterioration occur before the patient reaches the operating room. Rapid diagnosis using TEE may save critical minutes in initiating definitive surgical treatment in this setting.

    2. BP control. The ideal drug to control BP would be a rapid acting, IV administered drug that has an ultra-short half-life and few if any side effects. Not only systolic and diastolic pressures but also the ejection velocity must be reduced because both of these factors have been shown to be important in the propagation of dissecting hematomas.

      1. Monitoring. It is imperative that these patients have the following: an ECG for detection of ischemia and dysrhythmias; two large-bore IV catheters; an arterial catheter in the proper location (to be discussed); and, if time permits, a central venous catheter or pulmonary artery (PA) catheter to follow filling pressures and to allow drug infusion.

      2. Agents

        1. Vasodilators

          1. Nitroprusside has emerged as the agent of choice for controlling the BP, because it is effective and easily regulated because of its short duration of action. It is given as an IV infusion, and central administration is optimal. The usual starting dose is 0.5 to 1 μg/kg/min, titrated to effect. Doses of 8 to 10 μg/kg/min have been associated with toxicity (see Chapter 2).

          2. Nitoglycerin causes direct vasodilation, but it is less potent than nitroprusside. It can be useful in the setting of myocardial ischemia with ascending aortic pathology. Dosages usually range from 1 to 4 μg/kg/min.

          3. Fenoldopam is a newer rapid-acting vasodilator that is a D1-like dopamine receptor agonist. It has little affinity for the D2-like, α1, or β adrenoreceptors. Fenoldopam causes vasodilation in many vascular beds, but it increases renal blood flow to a significant degree. Therefore, it may have some renal sparing effects while treating acute hypertension. Dosing starts at 0.05 to 0.1 μg/kg/min and can be incrementally increased to a maximum of 0.8 μg/kg/min.

        2. Decreasing ejection velocity. Decreasing ejection velocity becomes an important therapeutic consideration, especially if nitroprusside is used as the agent to lower BP. Nitroprusside will increase ejection velocity by increasing dP/dt and heart rate. For this reason, β-adrenergic blockade should be used with nitroprusside not only to decrease tachycardia but also to decrease contractility (see Chapter 2).

          1. Propranolol can be administered as an IV bolus of 1 mg, and doses of up to 4 to 8 mg may be required until the effect is seen.

          2. Labetalol, a combined α- and β-blocker, may offer a single alternative to the nitroprusside–propranolol combination. It should be given initially as a 20-mg loading bolus, and several minutes should be allowed for its effect to be seen. If no effect is seen, the dose should be doubled and several minutes allowed again for onset of effect. This process should be repeated up to a maximum dose of 40 to 80 mg every 10 minutes until a total dose of 300 mg is reached or until BP is controlled. Continuous infusion starting at 1 mg/min may be used, or a small bolus dose can be repeated every 10 to 30 minutes to maintain BP control.

          3. Esmolol is a short-acting β-blocking agent with a very short half-life that may be useful in this setting. It is administered as a bolus loading dose of 500 μg/kg over 1 minute and then continued as an infusion starting at 50 μg/kg/min, titrated to effect, to a maximum of 300 μg/kg/min. This drug is particularly advantageous in a patient with obstructive lung disease because it is β1-selective and its action can be terminated quickly if respiratory symptoms ensue.

      3. Desired endpoints. BP should be lowered to approximately 105 to 115 mm Hg systolic, and heart rate should be kept at 60 to 80 beats/min. If a PA catheter is in place, the cardiac index may be lowered to the 2 to 2.5 L/(min·m2) range because a hyperdynamic myocardium may promote the progression of a dissecting hematoma.

    3. Transfusion. A total of 8 to 10 units of blood should be typed and cross-matched before surgery. Use of blood scavenging devices has decreased the amount of banked blood used, but the logistics of processing scavenged blood, plus the clinical situation, may require that homologous transfusion still be used.

    4. Assessment of other organ systems

      1. Neurologic. The patient should be monitored closely to detect signs of any change in neurologic status, because deterioration in function is an indication for immediate surgical intervention.

      2. Kidneys. Renal function should be followed closely with insertion of a urinary catheter. If aortic dissection has been diagnosed, the development of anuria or oliguria in the setting of euvolemia is an indication for immediate surgical intervention.

      3. Gastrointestinal. Serial abdominal examinations should be performed. In addition, blood gas analysis should be done routinely to assess changes in acid–base status, because ischemic bowel can produce significant acidosis.

    5. Use of pain medications. Patients with aortic dissections may be anxious and in severe pain. Pain relief should be given not only to lessen suffering but also to aid in control of BP. It is important to avoid obtundation; otherwise, important changes in patient status will be missed. Worsening of back or abdominal pain may indicate expansion of the lesion or further dissection and is regarded by many surgeons as an emergent situation. In addition, propagation of a dissection into a head vessel may lead to a change in mental status that may be undetected if the patient is oversedated.

  4. Surgical and anesthetic considerations

    1. Goal of surgical therapy (for dissections, aneurysms, aortic rupture). The first major goal of treating acute aortic disruption must be to control hemorrhage. Once control is achieved, the objectives of management of both acute and chronic lesions are similar: to repair the diseased aorta and to restore relationships of major arterial branches.

      Elective repair of a thoracic aneurysm most often is accomplished by replacing the diseased segment of aorta with a synthetic graft and then implanting major arterial branches into the graft. With a dissection, in contrast, the major goal is to resect the segment of aorta containing the intimal tear. When this segment is removed, it is possible to obliterate the false lumen and interpose graft material. It may not be possible or necessary to replace all of the dissected portion of the aorta because, if the origin of dissection is controlled, reexpansion of the true lumen may compress and obliterate the false lumen. With contained aortic tears, the objective is to resect the area of the tear and either reanastomose the natural aorta to itself in an end-to-end fashion or use graft material for the anastomosis if there is insufficient natural aorta remaining.

    2. Overview of intraoperative anesthetic management (for dissections, aneurysms, aortic rupture)

      1. Key principles

        1. Managing BP. BP control must be maintained during the transition from the preoperative to the intraoperative period. Such control is important in light of the surgical and anesthetic manipulations that will profoundly affect BP.

        2. Monitoring of organ ischemia. The organs that must be monitored continuously for adequacy of perfusion are the central nervous system, heart, kidney, and lungs. The liver and gut cannot be monitored continuously, but their metabolic functions can be checked periodically.

        3. Treating coexisting disease. Patients with aortic pathology often have associated cardiovascular and systemic diseases, as outlined in Table 24.7.

        4. Controlling bleeding. Achieving hemostasis after CPB or with graft material in place poses special challenges, especially when the native tissue is damaged or diseased. Coagulation abnormalities and their treatment are discussed in Chapter 18.

      2. Induction and anesthetic agents. Because many of these patients come to surgery emergently, most are considered to have a full stomach and require rapid securing of the airway. On the other hand, these patients also require a smooth induction, because wide swings in hemodynamics may worsen the clinical situation. Usually a compromise is made using a controlled induction with cricoid pressure and manual ventilation. This "modified" rapid sequence induction allows some airway protection and expeditious titration of anesthetic drugs to control BP, the main goal being to secure the airway as quickly as possible with a minimum of hemodynamic perturbation. Use of nonparticulate antacids, H2-blockers, and metoclopramide should be considered before induction of anesthesia. Anesthetic considerations and agents are described more fully in Section IV.D. Despite all precautions, marked changes in hemodynamics are common and should be expected [3].

      3. Importance of site of lesion (Table 24.8). Although the principles of anesthetic induction and choice of anesthetic agents are similar for all aortic lesions, practical intraoperative management depends almost entirely on the site of the lesion.

    3. Ascending aortic surgery

      1. Surgical approach. The approach used for ascending aortic surgery is a midline sternotomy.

      2. Cardiopulmonary bypass. Because of the proximal involvement of the aorta and because the surgery often includes repair or replacement of the aortic valve, CPB is required.

        1. If the aneurysm ends in the proximal or midportion of the ascending aorta, the arterial cannula for CPB can be placed in the upper ascending aorta or arch.

        2. The usual site of cannulation is the femoral artery. This is required if the entire ascending aorta is involved because an aortic cannula cannot be placed distal to the pathology without jeopardizing perfusion to the great vessels.

        3. Venous cannulation usually can be performed through the right atrium; however, femoral venous cannulation may be necessary if the aneurysm is especially large.

      3. Aortic valve involvement. Frequently, either aortic valvuloplasty or aortic valve replacement is necessary with ascending aortic dissections or aneurysms. Which procedure is used depends on the degree of involvement of the sinuses of Valsalva and the aortic annulus.

      4. Coronary artery involvement. With an acute dissecting hematoma, the coronary arteries may be involved. Coronary occlusion usually takes the form of compression of the coronary lumen by the expanding false lumen and will require bypass grafting. Displacement of the coronary arteries from their normal position with enlargement of the aortic annulus will require reimplantation of their orifices into the graft wall or a vein bypass.

      5. Surgical techniques. An example of the usual cross-clamp placement used in surgery of the ascending aorta is shown in Figure 24.4. Note that placement of the distal clamp is more distal than would be the case for simple cross-clamping for coronary surgery and at times might even include a part of the innominate artery. If aortic insufficiency is present, a large portion of the cardioplegic solution infused into the aortic root will flow through the incompetent aortic valve instead of the coronaries, causing distention of the LV and loss of the myocardial preservative effects of cardioplegia. For these reasons, an immediate aortotomy must be performed and the coronary vessels infused individually with cold cardioplegia. Many centers use retrograde coronary perfusion for cardioplegia administration as an alternative technique to obviate this problem.

        FIG. 24.4 Circulatory support and clamp placement for surgery of the ascending aorta. Femoral arterial cannula usually is required, and distal clamp must be beyond the extent of pathology. Proximal clamp would be needed to provide cold cardioplegia to the aortic root, but placement of this clamp is not possible if the proximal aorta is involved. CPB, cardiopulmonary bypass. (From Benumof JL. Intraoperative considerations for special thoracic surgery cases. In: Benumof JL, ed. Anesthesia for thoracic surgery. Philadelphia: WB Saunders, 1987:384, with permission.)


        If the aortic valve and annulus both are normal, the diseased section of aorta is replaced with graft material. If the annulus is normal and the valve is incompetent, the valve may be resuspended or replaced. If both valve incompetence and annular dilation are present, either a composite graft (i.e., a tube graft with an integral artificial valve) or an aortic valve replacement with a graft sewn to the native annulus can be used. The coronary arteries must be reimplanted into the wall of the composite graft and may not require reimplantation when separate aortic valve replacement and grafts are used, depending on whether enough of the native sinus of Valsalva remains (Fig. 24.5). The posterior wall of the old aneurysm can be wrapped around the graft material and sewn in place to maximize hemostasis.

        FIG. 24.5 Surgical repair of ascending aortic aneurysm or dissection. A: Aortic valve has been replaced and the aorta is transected at native annulus, leaving "buttons" of aortic wall around coronary ostia. B: Graft material anastomosed to the annulus, with left coronary reimplantation. C: Completion of left and beginning of right coronary reimplantation. D: Completion of distal graft anastomosis. (From Miller DC, Stinson EB, Oyer PE, et al. Concomitant resection of ascending aortic aneurysm and replacement of the aortic valve—operative results and long-term results with "conventional" techniques in ninety patients. J Thorac Cardiovasc Surg 1980;79:394, with permission.)


        In patients with ascending dissections, the aortic root is opened and the site of the intimal tear is located. A section of the aorta that includes the intimal tear is excised, and the edges of the true and false lumens are sewn together. A section of graft is used to replace the excised portion of the aorta.

      6. Complications. Complications are those that occur with any procedure involving CPB and an open ventricle and include the following:

        1. Air emboli

        2. Atheromatous or clot emboli

        3. LV dysfunction secondary to ischemia

        4. Myocardial infarction or myocardial ischemia secondary to technical problems with reimplantation of the coronaries

        5. Renal or respiratory failure

        6. Clotting abnormalities

        7. Surgical hemostasis; bleeding from suture lines can be especially difficult to control.

    4. Anesthetic considerations for ascending aortic surgery

      1. Monitoring

        1. Arterial catheter placement. Because the right subclavian artery may be involved in either the disease process or the surgical repair, a left radial or femoral arterial catheter is inserted for monitoring BP.

        2. ECG. Five-lead, calibrated ECG should be used to monitor both leads II and V5.

        3. PA catheter. Because of the advanced age of many of these patients and the presence of severe systemic disease, a PA catheter can be a useful aid in management preoperatively and postoperatively, but it is not mandatory.

        4. Two-dimensional echocardiography. In addition to its preoperative diagnostic importance, TEE is a useful adjunct in the intraoperative management of these patients. The diagnosis of hypovolemia, hypocontractility, myocardial ischemia, intracardiac air, and valvular dysfunction can be made with TEE. Caution should be exercised when placing this probe in the presence of a large ascending aortic aneurysm.

        5. Neurologic monitors

          1. Electroencephalogram. For evaluating brain function, either raw or processed electroencephalographic data may be helpful for judging the adequacy of cerebral perfusion during CPB. Newer monitors such as the bispectral index may help to assess the depth of anesthesia during these procedures.

          2. Temperature. When correctly placed, a nasopharyngeal temperature probe gives the anesthesiologist an approximation of brain temperature. Rectal temperature also should be monitored.

        6. Renal monitors. As with all cases involving bypass, urine output should be monitored.

      2. Induction and anesthetic agents. See Table 24.9.

      3. Cooling and rewarming. Hypothermic CPB is used in most cases of ascending aneurysms. Deep hypothermic circulatory arrest (DHCA) is needed if the proximal arch is involved. If femoral cannulation is used and the femoral artery is small, a smaller cannula may be needed. This probably will delay cooling and rewarming, because lower blood flows are used to avoid excessive arterial line pressures. Extra time for cooling and rewarming must be allowed in this setting.

    5. Aortic arch surgery

      1. Surgical approach. The aortic arch is approached through a median sternotomy.

      2. Cardiopulmonary bypass. CPB is required, and femoral cannulation must be used in almost all cases.

      3. Technique. Typical placement of clamps for this procedure is shown in Figure 24.6. Note that the surgical technique dictates that the cerebral vessels be clamped to resect the aneurysmal or dissected section of aortic arch.

        FIG. 24.6 Representation of cannula and clamp placement for surgery of the aortic arch. Femoral bypass is used. Proximal clamp is placed to arrest the heart. Distal clamp isolates the arch so that the distal anastomosis can be performed. Middle clamp on major branches isolates the head vessels so that en bloc attachment to graft is possible. CPB, cardiopulmonary bypass. (From Benumof JL. Intraoperative considerations for special thoracic surgery cases. In: Benumof JL, ed. Anesthesia for thoracic surgery. Philadelphia: WB Saunders, 1987:384, with permission.)


        The attachments of the arch vessels usually are excised en bloc so that all three vessels are located on one "button" of tissue, as shown in Figure 24.7. This facilitates rapid reimplantation of vessels and reestablishment of blood flow. Once the distal anastomosis is completed, the surgeon sutures the button of arch vessels to the graft material. The clamp can be replaced more proximally, the arch portion of the graft de-aired, the distal aortic clamp removed, and flow reestablished to the cerebral vessels from the femoral CPB aortic cannula. Thus, the time of brain ischemia is minimized. The proximal anastomosis then is completed.

        FIG. 24.7 Aortic arch replacement. A: The distal suture line is completed first, followed by (B) reattachment of the arch vessels. C: Flow is reestablished to these vessels by moving the clamp more proximally. D: The proximal suture line is completed. (From Crawford ES, Saleh SA. Transverse aortic arch aneurysm—improved results of treatment employing new modifications of aortic reconstruction and hypokalemic cerebral circulatory arrest. Ann Surg 1981;194:186, with permission.)


      4. Cerebral protection. Resection of aortic arch aneurysms involves interruption or alteration of cerebral blood flow. Various surgical techniques have been used to prevent cerebral ischemia. All involve cooling the brain to reduce metabolic rate and the buildup of toxic metabolites.

        1. DHCA has been adopted by many surgeons as a technically advantageous way to repair aortic arch pathology, because blood flow is stopped and exposure maximized. DHCA requires core cooling to 15° to 22°C, depending on the exact technique used. Turning off the pump and partially draining the patient's blood volume into the pump provide a bloodless field with hypothermic brain protection for up to 45 minutes. This has improved results but is associated with longer bypass runs.

        2. Because of the time limits inherent with DHCA, some groups began using DHCA in conjunction with retrograde cerebral perfusion (RCP) through the superior vena cava as a method of brain protection. This technique has gained acceptance in many centers because it prolongs the "safe time" allowed for what can be a complicated reconstruction of the aortic arch and its vessels. Advantages of RCP include uniform cooling, efficient de-airing of the cerebral vessels (thus reducing the risk of embolism), and provision of oxygen and energy substrates. Outcome studies have identified the following risk factors for mortality and morbidity in RCP during DHCA: time on CPB, urgency of surgery, and patient age [4].

        3. Another technique that has been used with success is continuous anterograde cold blood cerebral perfusion. With this technique, the brain is selectively perfused via the brachiocephalic arteries with cold blood (6° to 12°C) while the patient is maintained at moderate core temperature. As shown in Figure 24.8, the cerebral perfusate is derived from the oxygenator and distributed via a separate roller pump, much the same as anterograde blood cardioplegia. This technique has largely supplanted the older technique of individual cannulation and perfusion of the carotid vessels because of technical considerations. Anterograde perfusion takes advantage of autoregulation of cerebral blood flow, which is thought to remain intact even at low temperature. With intact autoregulation, physiologic protection against ischemia of hyperperfusion will be active. One of the chief advantages of this technique is that DHCA is required only for completion of the distal anastomosis. Because of these advantages, some groups believe that continuous anterograde perfusion is the safest method of brain protection during aortic arch surgery [5].

          FIG. 24.8 Perfusion circuit for anterograde cerebral perfusion for aortic arch surgery. Venous blood from the right atrium drains to the oxygenator (Ox), and cooled to 28°C by heat exchange (E2) before passing via the main roller pump (P2) to a femoral artery. A second circuit derived from the oxygenator with a separate heat-exchanger (E1) and roller pump (P1) provides blood at 6° to 12°C to the brachiocephalic and coronary arteries. (From Bachet J, Guilmet D, Goudot B, et al. Antegrade cerebral perfusion with cold blood: a 13 year experience. Ann Thorac Surg 1999;67:1875, with permission.)


      5. Complications. Complications from this operation are similar to those with any procedure using CPB. Irreversible cerebral ischemia is a distinct possibility with this type of surgery. Hemostatic difficulties may be increased secondary to the multiple suture lines and long bypass time.

    6. Anesthetic considerations for aortic arch surgery

      1. Monitoring

        1. Arterial BP. An intraarterial catheter can be placed in either the right or left radial artery for prebypass management if the innominate or left subclavian arteries, respectively, are not involved. If both are involved, the femoral artery should be catheterized.

        2. Neurologic monitors

          1. Electroencephalography can be useful not only for ensuring that adequate cooling has been achieved but also for titration of the thiopental dose for brain protection.

          2. Nasal temperature will verify adequate brain cooling.

        3. Transesophageal echocardiography. TEE provides useful information similar to that for ascending aortic surgery (see Section IV.D.1), but care should be taken when placing the probe.

      2. Choice of anesthetic agents. See Table 24.9.

      3. Management of hypothermic circulatory arrest. The technique involves core cooling to 15° to 20°C, packing the head in ice, using other cerebral protective agents, avoiding glucose-containing solutions, and using proper monitoring. More details are provided in Chapter 23.

      4. Complications. Complications related to anesthesia for this procedure are uncommon. One is myocardial depression secondary to the use of thiopental for cerebral protection, and inotropic agents may be needed to wean the patient from CPB.

    7. Descending thoracic aortic surgery

      1. Surgical approach. Exposure of the descending aorta is accomplished through a left thoracotomy incision, usually between the fourth and fifth ribs. A double intercostal incision may be necessary for complete exposure (Fig. 24.9). The patient is placed in a full right lateral decubitus position with the hips slightly rolled to the left to allow access to the femoral vessels. When positioning the patient, it is important to provide protection to pressure points, including use of axillary roll, pillows between the knees, and pads for the head and elbows. It is important to maintain the occiput in line with the thoracic spine to prevent traction on the brachial plexus.

        FIG. 24.9 Surgical approach to an extensive aneurysm or dissection involving the descending thoracic aorta. A single musculocutaneous incision and a double intercostal incision are used. The standard proximal and distal intercostal incisions are made through the fourth and seventh intercostal spaces (ICS), respectively. A traumatic aortic rupture at the isthmus usually can be reached through a single intercostal incision. (From Cooley DA, ed. Surgical treatment of aortic aneurysms. Philadelphia: WB Saunders, 1986:63, with permission.)


      2. Surgical techniques. Whether an aneurysm, dissection, or rupture is being treated, the surgical technique involves placing cross-clamps above and below the lesion, opening the aorta, and replacing the diseased segment with a graft.

        1. Simple cross-clamping. Many groups report success with cross-clamping the aorta above and below the lesion without adjuncts to maintain distal perfusion. This technique has the advantage of simplifying the operation and reducing the amount of heparin needed (Fig. 24.10).

          FIG. 24.10 Illustration of simple cross-clamp placement for repair of descending aortic aneurysm or dissection. Distal clamp placement dictates that flow to the spinal cord and major organs proceeds through collateral vessels. (From Benumof JL. Intraoperative considerations for special thoracic surgery cases. In: Benumof JL, ed. Anesthesia for thoracic surgery. Philadelphia: WB Saunders, 1987:384, with permission.)


          Clamping the descending aorta produces marked hemodynamic changes: profound hypertension in the proximal aorta and hypotension below the distal clamp. The increase in afterload that occurs when the majority of the cardiac output goes only to the great vessels causes acute elevations in LV filling pressures and a progressive fall in cardiac output. The presumption is that LV failure will result if this afterload is maintained for any significant length of time. The acute increase in pressure proximal to the clamp can precipitate a catastrophic cerebral event (e.g., rupture of a cerebral aneurysm).

          Mean arterial pressure distal to the cross-clamp decreases to less than 10% to 20% of control. This decrease is paralleled by a decrease in renal blood flow and spinal cord blood flow. The presence of a chronic obstruction to flow and the resultant well-developed collateral flow (i.e., coarctation) will lessen the hemodynamic changes that usually are seen. Examples of BPs above and below a cross-clamp from a series of patients with different aortic pathologies are listed in Table 24.10.

          The use of an "open" technique of simple aortic cross-clamping has been advocated. With this technique, no distal cross-clamp is used, thereby allowing direct inspection of the distal aorta for thrombus or debris. More importantly, graft material can be anastomosed in an oblique fashion that incorporates the maximal number of intercostal arteries.

        2. Shunts. A method that provides decompression of the proximal aorta and perfusion of the distal segment involves placement of a heparin-bonded (Gott) extracorporeal shunt from the LV, aortic arch, or left subclavian artery to the femoral artery (Fig. 24.11). Systemic heparinization is not required. The advantage with this technique is that distal perfusion can be maintained while decompression of the proximal aorta is achieved. The major problems with this technique are technical difficulties with placement and kinking with inadequate distal flows. Two sizes of these shunts are available: 7 mm (5-mm inner diameter) and 9 mm (6-mm inner diameter). The limitations on flow imposed by these relatively small diameters interfere with the actual proximal ventricular decompression and augmentation of distal perfusion pressure that can be achieved.

          FIG. 24.11 Placement of a heparin-coated vascular shunt from proximal to distal aorta during repair of descending aneurysm or dissection. (From Benumof JL. Intraoperative considerations for special thoracic surgery cases. In: Benumof JL, ed. Anesthesia for thoracic surgery. Philadelphia: WB Saunders, 1987:384, with permission.)


        3. Extracorporeal circulation. Historically the first method used for distal perfusion and proximal decompression, extracorporeal circulation (ECC) is being used more often after a period of being out of favor at many centers. There are several ways to perform ECC; all involve removal of blood, passage of blood to an extracorporeal pump, and reinfusion of blood into the femoral artery to perfuse the aorta below the distal cross-clamp (Fig. 24.12). Blood can be returned to the pump from the femoral vein, which is technically the easiest site to use. However, this site requires placement of an oxygenator in the circuit. Alternatively, the left atrium or LV apex may be cannulated for blood return to the pump. The pump may be a standard double roller (positive displacement) or a centrifugal (kinetic) type.

          FIG. 24.12 Partial bypass (PB) [or extracorporeal circulation (ECC)] method for maintaining distal perfusion pressure and preventing proximal hypertension. Oxygenated blood can be taken directly from the left ventricle or atrium (or aortic arch) and pumped either by roller head or centrifugal pump into the femoral artery. Alternatively, unoxygenated blood can be taken from the femoral vein, passed through a separate oxygenator, and pumped into the femoral artery. Use of an oxygenator dictates the use of a full heparinizing dose. (From Benumof JL. Intraoperative considerations for special thoracic surgery cases. In: Benumof JL, ed. Anesthesia for thoracic surgery. Philadelphia: WB Saunders, 1987:384, with permission.)


          Each of these variations has disadvantages. Use of an oxygenator requires complete systemic heparinization, which is associated with increased incidence of hemorrhage, especially into the left lung. Left atrial or ventricular cannulation without an oxygenator may allow use of less heparin but carries an increased risk of air embolism. Table 24.11 summarizes the possible cannulation sites and major differences between heparinized shunts and ECC for distal perfusion.

      3. Complications of repair

        1. Cardiac. Cardiac disorders (myocardial infarction, dysrhythmia, or low-output syndrome) are a significant (20% to 40%) cause of death in patients with all types of descending aortic repair.

        2. Hemorrhage. This is a common cause of death (20% to 30%) in all types of repair of the descending aorta.

        3. Renal failure. The incidence of renal failure ranges from 4% to 9% among survivors, with a much higher incidence among nonsurvivors. The etiology is presumed to be a decrease in renal blood flow during aortic cross-clamping. However, renal failure may occur in the presence of apparently adequate perfusion (heparinized shunt or ECC). Preexisting impairment of renal blood flow from a dissection involving the renal arteries increases the incidence of renal failure.

        4. Paraplegia. Most case reviews report the incidence of paraplegia as being in the range from 6% to 10%. [6] This is probably the most devastating morbid event because it is irreversible. The cause is either interruption or prolonged hypoperfusion (more than 30 minutes) of the blood supply to the anterior spinal artery. The anterior spinal artery is formed from the vertebral arteries rostrally. As it descends, it also receives blood from radicular arteries, which arise from the intercostal arteries (Fig. 24.13). In a majority of patients, one of these radicular arteries, the great radicular artery (of Adamkiewicz), contributes a major portion of the supply to the midportion of the anterior spinal artery. Unfortunately, this vessel is almost impossible to identify angiographically or by inspection at operation. It may arise anywhere from T5 to below L1. These anatomic considerations place blood flow in this artery at higher risk intraoperatively and postoperatively. Interruption of flow in this vessel may lead to paraplegia, depending on the contribution available from other collaterals. An anterior spinal syndrome can result, in which motor function is lost (anterior horns) but some sensation remains intact (posterior columns).

          FIG. 24.13 Anatomic drawing of the contribution of the radicular arteries to spinal cord blood flow. If the posterior intercostal artery is involved in a dissection or is sacrificed to facilitate repair of aortic pathology, critical blood supply may be lost, causing spinal cord ischemia. (From Cooley DA, ed. Surgical treatment of aortic aneurysms. Philadelphia: WB Saunders, 1986:92, with permission.)


        5. Miscellaneous. Many other complications may arise. Some are a function of the type of pathology. For example, death from multiple organ trauma is a major factor in patients who survive traumatic rupture. Respiratory failure alone and as a component of multiple organ failure is more common with thoracic aortic disease than with abdominal aortic disease. Cerebrovascular accidents are seen in a small number of patients, as is left vocal cord paralysis due to recurrent laryngeal nerve damage.

    8. Anesthetic considerations in descending aortic surgery

      1. General considerations. Anesthesia for descending aortic surgery can be one of the most demanding cases because of the profound changes in numerous organ systems. This topic is summarized in several good reviews [7,8].

      2. Monitoring

        1. Arterial BP. A right radial or brachial arterial catheter is needed to monitor pressures above the cross-clamp because the left subclavian artery may be compromised by the cross-clamp. To assess perfusion distal to the lower aortic clamp, many anesthesia and surgical teams prefer to monitor pressure below the clamp also, which requires placement of a femoral arterial catheter. Should a partial bypass technique be used, the left femoral artery is cannulated for distal perfusion and the right femoral artery is used for BP monitoring.

        2. Ventricular function. Some operative teams prefer to monitor LV function during proximal cross-clamping and therefore insert a PA catheter to follow filling pressures and cardiac output.

        3. Other monitors. Additional monitors used are similar to those used for other thoracic procedures: ECG (standard lead V5 cannot be used because of the surgical approach), pulse oximetry, core temperature, and urine output. TEE would be useful to assess ventricular function and filling volumes during these cases, but anatomic interference by the probe in the surgical field may preclude its use.

      3. One-lung anesthesia. Double-lumen endobronchial tubes are recommended not only to improve surgical exposure but also to provide an element of patient safety. By collapsing the left lung, trauma to that lung is decreased. If manipulation during surgery causes hemorrhage into the airway, the contralateral (right) lung is protected from blood spillage. A left-sided tube is technically easier to place and is used often, but it may be impossible to insert in some patients because of aneurysmal distortion of the trachea or left main stem bronchus. Patients with aortic rupture may have a distorted left main stem bronchus. Right-sided tubes may be used, but proper alignment with the right upper lobe bronchus should be checked with a fiberoptic bronchoscope. Alternatively, tubes with an endobronchial blocker should be considered in cases where adequate placement of a double-lumen tube cannot be achieved. For a detailed description of double-lumen or endobronchial blocker tube placement and single-lung ventilation, see Chapter 25.

      4. Conduct of anesthesia before and during cross-clamping. Before the aorta is cross-clamped, mannitol (0.5 g/kg) should be infused to provide some renal protection during clamping. Even though a shunting procedure will be used, changes in the distribution of renal blood flow make mannitol administration prudent. In addition, sodium nitroprusside should be mixed and ready for infusion.

        After the clamp is applied, it is important to closely monitor acid–base status with serial arterial blood gas measurements. It is common for metabolic acidosis to develop due to hypoperfusion of critical organ beds, and this should be treated aggressively if the patient is normothermic. If simple cross-clamping without adjuncts is used, proximal hypertension should be controlled, again with the realization that distal organ flow may be diminished. In treating proximal hypertension, regional blood flow studies have shown that nitroprusside infusion may decrease renal and spinal cord blood flow in a dose-related fashion. Ideally, cross-clamp time (regardless of technique) should be less than 30 minutes, because the incidence of complications, especially paraplegia, begins to increase above this limit.

        If a heparinized shunt has been placed and proximal hypertension cannot be treated without producing subsequent distal hypotension (less than 60 mm Hg), the surgeon should be made aware that there may be a technical problem with shunt placement. If partial bypass (ECC) is used, the pump speed or venous return can be adjusted so that control of proximal hypertension can be maintained by adequate unloading while the lower body is simultaneously perfused. Usually little or no pharmacologic intervention is necessary in this case because the pump speed and manipulation of venous return provide rapid control of proximal and distal pressures. Table 24.12 lists the treatment options for several clinical scenarios during ECC.

        Before removal of the cross-clamp, a vasopressor should be available. The anesthesiologist must be constantly aware of the stage of operation so that major events such as clamping and declamping may be anticipated.

      5. Declamping shock. When simple cross-clamping of the aorta is used, subsequent unclamping can lead to serious and even life-threatening consequences, usually severe hypotension or myocardial depression. There are several theoretical causes of this declamping syndrome, including washout of acid metabolites, vasodilator substances, sequestration of blood in the lower extremities, and reactive hyperemia. The usual cause, however, is relative or absolute hypovolemia. To attenuate the effects of clamp removal, in the 10 to 15 minutes before unclamping of the thoracic aorta, the volume status of the patient should be optimized. This includes elevating filling pressures by infusing blood products, colloid, or crystalloids. Some advocate prophylactic bicarbonate administration just before clamp removal to minimize the myocardial depression caused by the acidosis that occurs following removal. It is advisable for the surgeon to release the cross-clamp slowly over a period of 1 to 2 minutes to allow enough time for compensatory changes to occur.

        Vasopressors may be needed to compensate for hypotension but must be used with care because even transient hypertension may result in significant bleeding. With a volume-loaded patient and slow clamp release, any significant hypotension usually is short lived and well tolerated. If hypotension is severe, the easiest maneuver is reapplication of the clamp to allow further volume infusion.

        If shunts or ECC is used, declamping hypotension usually is attenuated because the vascular bed below the clamp is less "empty." ECC also provides a means of rapid volume infusion if a reservoir is used.

      6. Fluid therapy and transfusion. Even patients undergoing elective repair of a descending aneurysm may be relatively hypovolemic, and fluid therapy should have the following aims: correct this fluid deficit, provide maintenance fluids, compensate for evaporative and "third space" losses, decrease red cell loss by mild hemodilution, and replace blood loss as needed.

        Despite proximal and distal control of the aorta, blood loss can be considerable in these cases due to back-bleeding from the intercostal arteries. These collateral vessels often are ligated on opening the aorta. Use of cell-scavenging devices has become common and has reduced the need for banked blood, but because massive losses may occur, banked blood may still be needed. As long as liver perfusion is adequate, even with a large blood loss, citrate toxicity usually is not a problem because of rapid "first pass" metabolism in the liver. Repair of a thoracic aneurysm with simple clamping, however, presents a unique situation—the liver is not perfused. In this circumstance, transfusion of large amounts of banked blood may rapidly produce citrate toxicity, resulting in myocardial depression that requires calcium chloride infusion.

      7. Spinal cord protection. Several methods have been espoused to provide protection of the spinal cord during cross-clamping in addition to ECC, shunts, and expeditious surgery [9].

        1. Maintaining perfusion pressure. Some groups prefer to maintain perfusion pressure of the distal aorta in the range from 40 to 60 mm Hg to increase blood flow to the middle and lower spinal cord. This practice should be regarded as controversial because at present there are few data on outcome supporting this position. No method used to maintain blood flow to the distal aorta (i.e., shunt or partial bypass) guarantees that spinal cord blood flow, and therefore function, will be maintained. Proximal and distal clamp placement to isolate the diseased aortic segment may include critical intercostal vessels that provide flow to the cord and whose loss is not compensated by distal perfusion. In addition, distal perfusion may be hindered by the presence of atherosclerotic disease in the abdominal aorta, a condition that may prevent significant flow to the kidneys and spinal cord. Last, these crucial vessels may be disrupted in gaining surgical exposure. One should never assume that the cord and kidneys are absolutely "protected" because a shunt or partial bypass has been used. The largest studies have shown no difference in the incidence of paraplegia regardless of the surgical adjunct used.

        2. Somatosensory-evoked potentials. Somatosensory-evoked potentials (SEPs) have been promoted as a means of assessing functional status of the spinal cord during periods of possible ischemia [10]. Briefly, SEPs monitor spinal cord function by stimulating a peripheral nerve and monitoring the response in the brainstem and cerebral cortex. Normal SEPs seem to ensure the integrity of the posterior (sensory) columns. However, SEPs have several shortcomings. First, during aortic surgery, it is the anterior (motor) horns that are more at risk. Perhaps for this reason, there have been reports of patients who had normal SEPs during cross-clamping and who subsequently were found to have paraplegia. Second, it must be remembered that many anesthetics, including all of the halogenated drugs, nitrous oxide, and several IV drugs (e.g., thiopental and propofol) will alter the amplitude and latency of the evoked potential. In addition, if simple cross-clamping is used, ischemia of the peripheral nerves will interfere with SEP interpretation.

          Other than being used as an intraoperative tool to help identify intercostal arteries that should be reimplanted to preserve spinal cord perfusion, SEP monitoring has not been shown to decrease the incidence of paraplegia.

        3. Motor-evoked potentials. Because of the noted deficiencies in SEP monitoring, the use of motor evoked potentials has been advocated as a superior monitor of spinal cord ischemia [11]. Motor evoked potentials can accurately monitor the integrity of the anterior horn of the spinal cord and currently are used during procedures of the spinal column. However, because access to the central nerve roots for direct stimulation is not possible in thoracic surgery, transcranial stimulation over the motor cortex has been used. In addition to being cumbersome, this method has been reported to trigger seizures in susceptible patients. However, some groups have experienced success in the application of this method.

        4. Hypothermia. Allowing the core temperature to be reduced to approximately 33° to 34°C will lower the metabolic rate of the spinal cord tissue and may provide some protection from reduced or interrupted blood flow. Adequate temperature reduction usually can be accomplished with topical cooling agents (cooling blankets, bags of crushed ice). Iced saline gastric lavage also may be used. Administration of even 1 or 2 units of cool banked blood (only if indicated) will lower the core temperature. Precise control of temperature is difficult. At temperatures below 32°C, the myocardium may become more irritable and prone to ventricular arrhythmias. These facts, plus the lack of improved outcome data, have resulted in sparse use of this technique.

        5. Spinal drains. Experimental data show that spinal cord damage may be mediated through the increase in cerebrospinal fluid (CSF) pressure that accompanies the reduction in spinal cord blood flow during cross-clamping. CSF pressure may be increased to as high as the mean distal arterial pressure. Because spinal cord blood flow is proportional to the mean arterial pressure minus the higher of the CSF or venous pressure, perfusion in this circumstance may be reduced to zero. A spinal drain would allow not only for measurement of the intraspinal pressure but also for therapeutic reduction of CSF pressure by its removal and an increase in spinal cord blood flow. As a note of caution, removal of CSF in the presence of an elevated intraspinal pressure may provide a gradient for herniation of cerebral structures. In addition, placement of a spinal drain followed by systemic heparinization may lead to the formation of an epidural hematoma as a rare complication. The use of spinal drains has increased because of the associated low morbidity and possible significant benefits [12]. To date, no controlled study has demonstrated a reduction in morbidity associated with the use of spinal drains.

        6. Other. Additional "protective" measures, such as IV steroids, pharmacologic suppression of spinal cord function through IV or intrathecal drug administration, local hypothermia, and free radical scavengers, are not widely used or are considered experimental.

      8. Prevention of renal failure. The etiologic cause of renal failure is thought to be ischemia from interruption of blood flow by clamping, although embolism remains another possibility. Use of CPB or a shunt may be protective, but superior outcome data are lacking, and renal failure still occurs despite these surgical adjuncts. Adequate volume loading should be used and probably is most important in renal protection. Mannitol may help, and because its use is innocuous in most patients it is recommended.

  5. Future trends. Just as the past 40 years of treatment of aortic diseases have been highlighted by innovation and the refinement of surgical and anesthetic techniques, so also will the future. The most promising surgical developments have been made in the area of intraluminal stenting of aneurysmal segments of the thoracoabdominal aorta [13]. Anesthetic developments will focus on refinements in the pharmacology and physiology of organ preservation. Advances in both areas should continue to improve survival in patients with what once was considered to be a lethal disease [14,15].

References

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  1. Hartnell GG. Imaging of aortic aneurysms and dissection: CT and MRI. J Thorac Imaging 2001;16:35–46.
  2. Nienaber CA, Von Kodolitsch Y, Nicolas V. The diagnosis of thoracic aortic dissection by noninvasive imaging procedures. N Engl J Med 1993;328:1–9.
  3. Cooper JR Jr, Skeehan TM, Cooley DA. Resection of a thoracic aneurysm in a 57-year-old male [case conference]. J Cardiothorac Vasc Anesth 1991;5:390–398.
  4. Ueda Y, Okita Y, Aomi S, et al. Retrograde cerebral perfusion for aortic arch surgery: analysis of risk factors. Ann Thorac Surg 1999;67:1879–1882.
  5. Bachet J, Guilmet D, Goudot B, et al. Anterograde cerebral perfusion with cold blood: a 13-year experience. Ann Thorac Surg 1999;67:1874–1878.
  6. Shenaq SA, Svensson LG. Paraplegia following aortic surgery.J Cardiothorac Vasc Anesth1993;7:81–94.
  7. O'Connor CJ, Rothenberg DM. Anesthetic considerations for descending thoracic aortic surgery: part I.J Cardiothorac Vasc Anesth1995;9:581–588.
  8. O'Connor CJ, Rothenberg DM. Anesthetic considerations for descending thoracic aortic surgery: part II.J Cardiothorac Vasc Anesth1995;9:734–737.
  9. Robertazzi RR, Cunningham JN Jr. Intraoperative adjuncts of spinal cord protection. Semin Thorac Cardiovasc Surg 1998;10:29–34.
  10. Robertazzi RR, Cunningham JN Jr. Monitoring of somatosensory evoked potentials: a primer on the intraoperative detection of spinal cord ischemia during reconstructive surgery.Semin Thorac Cardiovasc Surg1998;10:11–17.
  11. DeHaan P, Kalkman CJ, Jacobs MJ. Spinal cord monitoring with myogenic motor evoked potentials: early detection of spinal cord ischemia as an integral part of spinal cord protective strategies during thoracoabdominal aneurysm surgery. Semin Thorac Cardiovasc Surg 1998;10:19–24.
  12. Ling E, Arellano R. Systematic overview of the evidence supporting the use of cerebrospinal fluid drainage in thoracoabdominal aneurysm surgery for prevention of paraplegia. Anesthesiology 2000;93:1115–1122.
  13. Mitchell RS. Endovascular solutions for diseases of the thoracic aorta. Cardiol Clin 1999; 17:815–825.
  14. Oliver WC Jr, Nuttall G, Murray MJ. Thoracic aortic disease. In: Kaplan JA, ed.Cardiac anesthesia,4th ed. Philadelphia: WB Saunders, 1999:821–860.
  15. Gewertz BL, Schwartz LB, eds. Surgery of the aorta and its branches. Philadelphia: WB Saunders, 2000.