Preanesthetic Assessment

The preanesthetic assessment of the thoracic aorta surgical patient ideally begins before admission to the operating room (OR). The first consideration is whether the planned procedure is emergent, urgent, or elective. For urgent or emergent operations, it is most efficient to assign team members specific tasks for rapid and comprehensive patient and OR preparation. For example, one team member can review the patient chart and diagnostic studies to formulate an anesthetic plan. A second team member can interview the patient and obtain informed consent. The remaining team members simultaneously can prepare the OR, apply physiologic monitors, secure intravascular access, and send laboratory specimens including blood for cross-matching.

The second consideration is to determine the aortic diagnosis because its extent and physiologic consequences dictate both anesthetic management and surgical approach. Aortic diseases proximal to the left carotid artery typically are approached via a median sternotomy, whereas aortic diseases distal to this point usually are approached via a left thoracotomy or thoracoabdominal incision. Although an aortic diagnosis often is established in advance, at times a definitive diagnosis must be verified after OR admission by direct review of diagnostic studies or by subsequent TEE. In every case, a review of the operative plan with the surgical team facilitates thorough anesthetic preparation. Direct review of adequate aortic diagnostic imaging studies not only verifies the operative diagnosis but also determines the surgical possibilities (ACC/AHA Class I recommendation; level of evidence C).¹ The anatomic details of an aortic disease permit the anesthesiologist to anticipate potential perioperative difficulties, including likely postoperative complications.

The systematic assessment of each organ system in the aortic surgical patient should focus on how it will affect the conduct of anesthesia and surgery. The baseline functional reserve of each organ system determines the likely perioperative complications and allows ranking of organ-protective strategies. It is reasonable to obtain further tests to quantitate the functional reserve of affected organ systems, for example, neurocognitive testing, brain imaging, noninvasive carotid artery imaging, pulmonary function testing, echocardiography, and cardiac catheterization (ACC/AHA Class IIa recommendation; level of evidence C).¹ For example, significant cerebrovascular disease affects blood pressure management to ensure adequate cerebral perfusion. Significant cardiac compromise typically increases the risks for heart failure, myocardial ischemia, and arrhythmias. Significant lung disease often is predictive for postoperative respiratory failure, pneumonia, or both. Significant renal insufficiency affects fluid management, triggers the avoidance of nephrotoxic drugs, and customizes the dosing of renally cleared drugs. Hepatic disease and hematologic dysfunction are risk factors for perioperative bleeding and transfusion. Severe aortic atheroma is a major risk factor for atheroembolism and consequent stroke and limb ischemia.

Because myocardial ischemia is an important predictor of perioperative outcome, it has featured prominently in the guidelines for thoracic aortic diseases. Patients with evidence of myocardial ischemia should undergo further evaluation to determine the extent and severity of coronary artery disease (CAD; ACC/AHA Class I recommendation; level of evidence C).¹ If significant CAD is responsible for an acute coronary syndrome, then coronary revascularization is indicated before or concomitant with the thoracic aortic procedure (ACC/AHA Class I recommendation; level of evidence C).¹ Concomitant coronary artery bypass grafting (CABG) is reasonable in patients who have not only stable but significant CAD, but who are also scheduled to undergo surgery for diseases of the ascending aorta or aortic arch, or both (ACC/AHA Class IIa recommendation; level of evidence C).¹ In contrast, the benefit of coronary revascularization is less clear in patients who have stable but significant CAD and who are scheduled to undergo surgical intervention for descending thoracic aortic disease (ACC/AHA Class IIb recommendation; level of evidence C).¹

Preoperative Medications

Preoperative medications typically provide detailed information about concomitant medical conditions. As a general rule, all cardiac, pulmonary, and antiseizure medications should be continued up until the morning of surgery. Angiotensin-converting enzyme inhibitors and angiotensin-receptor blockers should be discontinued the day before surgery to minimize the risk for perioperative vasoplegia and adverse outcomes.^5,6 All oral hypoglycemic agents should be discontinued the night before surgery to avoid hypoglycemia. If possible, metformin should be discontinued the day before surgery to minimize the risks for severe lactic acidosis associated with exposure to iodinated contrast agents or perioperative hypovolemia. If a patient is receiving insulin, up to 50% of the typical morning dose should be given the day of surgery with subsequent close glucose monitoring. Warfarin (Coumadin) should be discontinued for approximately 5 days before surgery for full recovery of coagulation function as verified by a normalized international normalized ratio.⁷ If this is not possible, then the patient should be admitted for heparinization until shortly before surgery. Patients chronically exposed to low-molecular-weight heparin, aspirin, adenosine diphosphate platelet-receptor inhibitors (clopidogrel and prasugrel), and platelet glycoprotein IIb/IIIa inhibitors (abciximab, eptifibatide, tirofiban) are typically at increased risk for perioperative bleeding. Optimally, aspirin and clopidogrel should be discontinued at least 5 to 7 days before surgery to allow adequate recovery of platelet function for perioperative hemostasis.⁷

Finally, the consequences for anesthetic procedures must be carefully considered. For example, coagulopathy caused by organ dysfunction or concomitant medication, or both, increases the risks for hemorrhagic complications associated with neuraxial techniques such as lumbar CSF drainage and epidural analgesia. Cervical spine or esophageal disease may prohibit the use of intraoperative TEE. Aortic pathologies may produce an intrathoracic mass effect to complicate tracheal intubation, selective lung ventilation, and/or hemodynamic stability after anesthetic induction.

Anesthetic Management

Overall, the anesthetic plan including techniques, drugs, and monitoring should be individualized to enhance the conduct of the procedure including perfusion technique, hemodynamic monitoring, and preservation of organ function (ACC/AHA Class I recommendation; level of evidence C).¹ Because thoracic aortic procedures may result in massive bleeding and cardiovascular collapse, it is essential to have immediate availability of packed red blood cells, large-bore vascular access, invasive blood pressure monitoring, and central venous access. Pulmonary artery catheterization assists in the management of cardiac dysfunction associated with CPB, DHCA, and PLHB. Intraoperative TEE is indicated in thoracic aortic procedures, including endovascular interventions, in which it assists in hemodynamic monitoring, procedural guidance, and endoleak detection (ACC/AHA Class IIa recommendation; level of evidence B).¹

A rationale exists for choosing to cannulate the left or right radial artery for intra-arterial blood pressure monitoring. Right radial arterial pressure monitoring will often detect compromised flow into the innominate artery because of aortic cross-clamping too near its origin. Right radial arterial pressure monitoring makes sense in procedures that require clamping of the left subclavian artery. Left radial arterial pressure monitoring is indicated when selective antegrade cerebral perfusion (ACP) is planned via the right axillary artery. At times, bilateral radial arterial pressure monitoring may be required. Femoral arterial pressure monitoring allows the assessment of distal aortic perfusion in procedures with PLHB.

Large-bore peripheral intravenous cannulation (e.g., two 16-gauge catheters) secures vascular access for rapid intravascular volume expansion. Rapid transfusion is desirable via an intravenous set with a fluid warming device. Alternatively, large-bore central venous cannulation can be utilized for volume expansion. If a pulmonary artery catheter (PAC) is required, a second introducer sheath dedicated to volume expansion also can be placed in the same central vein. Central venous cannulation with ultrasound guidance often increases speed and safety, especially in emergencies.⁸ Both a urinary and a nasopharyngeal temperature probe are required for monitoring the absolute temperature of the peripheral and core, as well as the rates of change during deliberate hypothermia and subsequent rewarming. The rectum is an alternative site for monitoring peripheral temperature, and the PAC can provide core temperature monitoring.

The induction of general anesthesia requires careful hemodynamic monitoring with anticipation of changes because of anesthetic drugs and tracheal intubation. Appropriate vasoactive drugs should be immediately available as required. Concomitant vasodilator infusions often are discontinued before anesthetic induction. Because etomidate does not attenuate sympathetic responses with no direct effects on myocardial contractility, it may be preferred in the setting of hemodynamic instability. Thereafter, titration of a narcotic such as fentanyl and a benzodiazepine such as midazolam will provide maintenance of general anesthesia. In elective cases, anesthetic induction can proceed with routine intravenous hypnotics, followed by narcotic titration for attenuation of the hypertensive responses to tracheal intubation and skin incision. Antibiotic therapy optimally should be completed in most cases at least 30 minutes before skin incision to achieve adequate bactericidal tissue levels.

General anesthetic maintenance is typically with a balanced technique, and neuromuscular blockade is achieved by titration of a nondepolarizing muscle relaxant. Anesthetics can be reduced during moderate hypothermia and then discontinued during deep hypothermia. With concomitant electroencephalographic (EEG) and/or somatosensory-evoked potential (SSEP) monitoring, anesthetic signal interference is minimized with the avoidance of barbiturates, bolus propofol, and doses of inhaled anesthetic greater than 0.5 minimum alveolar concentration. Propofol infusion, narcotics, and neuromuscular blocking drugs do not interfere with SSEP monitoring. With intraoperative motor-evoked potential (MEP) monitoring, high-quality signals are obtained when the anesthetic technique comprises total intravenous anesthesia with propofol and a narcotic such as remifentanil without neuromuscular blockade. Neuromonitoring (EEG, SSEP, MEP) in thoracic aortic procedures is not only compatible with contemporary anesthetic techniques but is also reasonable when the resulting data will guide perioperative management (ACC/AHA Class IIa recommendation; level of evidence B).¹ The decision to utilize this monitoring modality should be based on procedural urgency, institutional resources, patient needs, and planned operative technique (ACC/AHA Class IIa recommendation; level of evidence B).¹

In most cases, the duration of general anesthesia continues for several hours after admission to the intensive care unit (ICU) to permit a controlled anesthetic emergence. If epidural analgesia is used intraoperatively, a dilute solution of local anesthetic and narcotic is preferred to minimize postoperative hypotension from a concomitant sympathectomy and to minimize motor blockade to permit serial neurologic assessment of lower extremity function. Neuraxial anesthetic techniques are not recommended in patients at risk for neuraxial hematoma in the setting of concomitant thienopyridine antiplatelet therapy, low-molecular-weight heparins, and clinically significant anticoagulation (ACC/AHA Class III recommendation; level of evidence C).^1,7

The potential for significant bleeding and rapid transfusion is always relevant in thoracic aortic procedures. Consequently, it is prudent to have fresh frozen plasma and platelets available for ongoing replacement during massive red blood cell transfusion. The time delay associated with standard laboratory testing severely limits the intraoperative relevance of these data to guide transfusion. Strategies to decrease bleeding and transfusion in these procedures include timely preoperative cessation of anticoagulants and platelet blockers, antifibrinolytic therapy, intraoperative cell salvage, biologic glue, activated factor VII, and avoidance of perioperative hypertension. It is reasonable to have an institutional algorithmic approach to the management of bleeding and transfusion for thoracic aortic surgery (ACC/AHA Class IIa recommendation; level of evidence C).¹ This algorithm will depend significantly on institutional variations in point-of-care coagulation testing, blood component availability, and access to recombinant factor VII (ACC/AHA Class IIa recommendation; level of evidence C).¹

The antifibrinolytic lysine analogs, ε-aminocaproic acid or tranexamic acid, are commonly utilized in thoracic aortic surgery with and without DHCA. The concerns with aprotinin are now historical because it was widely withdrawn from clinical practice after a large randomized trial demonstrated its significant mortality risk in the setting of high-risk cardiac surgery, including thoracic aortic surgery with DHCA.^9,10 Even more recently, high-dose tranexamic acid has been correlated with a significantly increased risk for seizures after cardiac surgery.^11,12 Based on the lessons from aprotinin, further adequately powered trials should examine the safety of lysine analogs in thoracic aortic surgery.^9–12 Recombinant activated factor VII is a synthetic agent that accelerates hemostasis by binding with tissue factor at the site of tissue injury. Although this agent has demonstrated efficacy for hemostatic rescue in massive bleeding during thoracic aortic surgery, recent meta-analysis suggest further study for adequate delineation of its perioperative safety.^13,14

Postoperative Care

After completion of the operation, the patient should be transported directly from the OR to the ICU. The continuation of care from the OR to the ICU should be seamless and protocol based.¹⁵ In the absence of complications, early anesthetic emergence is preferable for early assessment of neurologic function. If delayed anesthetic emergence is indicated, then sedation and analgesia can be provided. Common early complications include hypothermia, coagulopathy, delirium, stroke, hemodynamic lability, respiratory failure, metabolic disturbances, and renal failure. Frequent clinical and laboratory assessment are essential to manage this dynamic postoperative recovery, including the safe conduct of tracheal extubation. The management of blood glucose levels has been standardized with a recent guideline from the Society of Thoracic Surgeons (STS).¹⁶ The chest roentgenogram allows confirmation of endotracheal tube and intravascular catheter position, as well as the diagnosis of acute intrathoracic pathologies. Antibiotic prophylaxis is continued for 48 hours after surgery to minimize surgical infection risk.

Diagnostic Imaging for Thoracic Aortic Aneurysms

The chest radiograph may suggest a thoracic aortic aneurysm with features such as a widened mediastinum, enlarged aortic knob, dilated descending thoracic aorta, aortic calcifications, leftward tracheal deviation, upward deviation of the left mainstem bronchus, and/or new left pleural effusion. Typically, transthoracic echocardiography can provide a reasonable examination of the thoracic aorta, although the acoustic windows are limited by the lungs. The contemporary imaging modalities of choice are CT, MRI, and TEE. Computed tomographic angiography (CTA) images the thoracic aorta during the arterial phase of an intravenous radiocontrast agent injection. It defines vascular anatomy and surrounding nonvascular structures. Aneurysm leak is detected as extravascular contrast extravasation. This imaging modality has multiple advantages such as high resolution, wide availability, rapid acquisition, imaging in patients with metallic implants, and generation of volumetric aortic images for stent design. Because CTA requires iodinated contrast agents, it carries a risk for contrast nephropathy that can be attenuated by administration of acetylcysteine and sodium bicarbonate.²² (See Chapters 2 and 3.)

Contrast-enhanced magnetic resonance angiography with gadolinium also images the entire thoracic aorta in fine detail. Although the spatial resolution of magnetic resonance angiography is slightly inferior to CTA, it does allow for degrees of tissue and fluid characterization. The disadvantages of magnetic resonance angiography include its limited availability, lack of imaging in patients with metallic implants, imaging difficulty in the setting of continuous hemodynamic monitoring, and the time required for image acquisition. Its advantages are the avoidance of ionizing radiation and the lack of renal toxicity.^1,17

TEE can image the thoracic aorta from the aortic valve to the distal ascending aorta and from the distal aortic arch to the proximal abdominal aorta. The distal ascending aorta and proximal aortic arch cannot be reliably imaged by TEE because the intervening trachea and left mainstem bronchus obstruct the acoustic window; this is known as the “blind spot” of TEE.²³ It is possible to overcome this blind spot with modalities such as imaging across the trachea temporarily filled with a saline-filled balloon (the A-view) and utilizing an expanded aortic view.^23,24 The advantages of TEE include its portability, its real-time interpretation, its compatibility at the bedside and in the OR, and its multiple imaging modalities for complete aortic and cardiac assessment. Its disadvantages include the requirement for sedation or general anesthesia and the risks for upper gastrointestinal injury.²⁵

Surgical Considerations for Thoracic Aortic Aneurysms

Surgical repair aims to replace the aortic aneurysm with a tube graft to prevent further aneurysmal complications (Table 21-5). The first indication for thoracic aortic aneurysm resection is whenever the aneurysm is symptomatic regardless of size (ACC/AHA Class I recommendation; level of evidence C).^1,17 Symptoms often herald the onset of rupture or dissection and should be interpreted as an urgent indication for surgery. A symptomatic presentation occurs in about 5% of patients. Unfortunately, the first symptom in the remaining 95% of patients often is death.

TABLE 21-5 Indications for Surgical Repair of Thoracic Aortic Aneurysms

The second indication for resection is aortic diameter. In the ascending aorta, a diameter of 6.0 cm is the critical hinge point after which the risk for aneurysm rupture increases exponentially. Consequently, surgical resection is recommended in the ascending aorta when the diameter reaches 5.5 cm (ACC/AHA Class I recommendation; level of evidence C).^1,17 In patients with genetically mediated aortopathies (Marfan syndrome, bicuspid aortic valve, familial thoracic aortic aneurysm or dissection; vascular Ehlers-Danlos syndrome; and Turner syndrome), surgical resection is recommended at a lower ascending aortic diameter of 5.0 cm (ACC/AHA Class I recommendation; level of evidence C).^1,17 Ascending aortic aneurysms with diameters less than 5.5 cm but with an annual growth rate in diameter greater than 0.5 cm/yr qualify for surgical resection (ACC/AHA Class I recommendation; level of evidence C).¹ It is reasonable to consider prophylactic replacement of the aortic root and ascending aorta in a woman with Marfan syndrome who is planning a pregnancy and who has an aortic root or ascending aortic diameter larger than 4.0 cm (ACC/AHA Class IIa recommendation; level of evidence C).¹ In adults with the aggressive aortopathy of the Loeys-Dietz syndrome, it is reasonable to consider proximal thoracic aortic repair when the internal aortic diameter exceeds 4.2 cm (ACC/AHA Class IIa recommendation; level of evidence C).^1,26 The ascending aortic aneurysm diameter also must be indexed to body size.²⁷ For example, if the maximal cross-sectional area of the aortic root or ascending aorta (in square centimeters) divided by the patient’s height (in meters) exceeds a ratio of 10, then surgical repair is a reasonable option (ACC/AHA Class IIa recommendation; level of evidence C).¹ The rationale behind indexing the aortic dimensions to body size is that shorter adults dissect and rupture their aortas at smaller diameters.^1,27 Furthermore, those patients who are undergoing open aortic valve procedures and who have an aortic root or ascending aortic diameter larger than 4.5 cm should be considered for concomitant aortic replacement resection (ACC/AHA Class I recommendation; level of evidence C).¹

The hinge point for rupture in the descending thoracic aorta is a diameter of 7.0 cm.¹⁷ Consequently, surgical resection is recommended in thoracoabdominal aneurysms when the aortic diameter exceeds 6.0 cm or less when it is associated with a connective tissue disorder such as Marfan syndrome (ACC/AHA Class I recommendation; level of evidence C).¹ In patients who have aneurysmal degeneration of the descending thoracic aorta associated with prior dissection and/or a connective tissue disorder, surgical resection is recommended when the aortic diameter is more than 5.5 cm (ACC/AHA Class I recommendation; level of evidence B).¹ Patients with aneurysms of the descending thoracic aorta should be considered for thoracic endovascular aortic repair (TEVAR) when technically feasible (ACC/AHA Class I recommendation; Level of Evidence B).^1,20

Aneurysms of the ascending aorta and aortic arch are approached from a median sternotomy incision. Standard CPB can be used for the repair of aneurysms limited to the aortic root and ascending aorta that do not extend into the aortic arch by cannulating the distal ascending aorta or proximal aortic arch and applying an aortic cross-clamp between the aortic cannula and the aneurysm. Aneurysms that involve the aortic arch require CPB with temporary interruption of cerebral perfusion (DHCA). Neuroprotection strategies in this setting include deep hypothermia, selective ACP, and retrograde cerebral perfusion (RCP). Aortic aneurysms of the descending thoracic aorta require lateral thoracotomy for surgical access. Aneurysmal resection requires cross-clamping with or without distal aortic perfusion.

Surgical Repair of Ascending Aortic and Arch Aneurysms

The type of surgical repair depends on aortic valve function and the aneurysm extent. Perioperative TEE can evaluate the aortic valve structure and function to guide and assess the surgical intervention (reimplantation, repair, replacement). Furthermore, TEE can assess the diameters of the aortic root, ascending aorta, and aortic arch to guide intervention. The most common aortic valve diseases associated with ascending aortic aneurysm are bicuspid aortic valve or AR caused by dilation of the aortic root (Figure 21-1). If the aortic valve and aortic root are normal, a simple tube graft can be used to replace the ascending aorta. If the aortic valve is diseased but the sinuses of Valsalva are normal, an aortic valve replacement combined with a tube graft for the ascending aorta without need for reimplantation of the coronary arteries can be performed (Wheat procedure; Figure 21-2; ACC/AHA class I recommendation; level of evidence C).¹

Figure 21-1 Transesophageal echocardiographic (TEE) midesophageal long-axis images of the aortic valve demonstrating aneurysmal dilation of the aortic root and ascending aorta (A). Doppler color-flow imaging (B) demonstrating severe aortic regurgitation caused by outward tethering of the aortic valve cusps by the aortic aneurysm. Ao, aorta; LV, left ventricle.

Figure 21-2 Replacement of the ascending aorta with a prosthetic tube graft for ascending aortic aneurysm or type A aortic dissection (A, B, F).

In the presence of aortic valvular disease, the aortic valve can be replaced (C–E) or repaired (not shown). Extension of the aneurysm or dissection into the aortic arch may require replacement of part or all of the aortic arch with a prosthetic tube graft (not shown). A small rim of the native aortic root containing the right and left coronary ostia was left behind in this repair.

(Adapted from Downing SW, Kouchoukos NT: Ascending aortic aneurysm. In Edmunds LH [ed]: Cardiac Surgery in the Adult. New York, McGraw-Hill, 1997, p 1176, by permission.)

If disease also involves the aortic valve and the aortic root, the patient requires aortic root replacement and aortic valve intervention. If technically feasible, the aortic valve can be reimplanted with a modified David technique, which includes graft reconstruction of the aortic root with reimplantation of the coronary arteries (ACC/AHA Class I recommendation; level of evidence C).^1,28 If not feasible, aortic root replacement with a composite valve-graft conduit is indicated (Bentall procedure; Figure 21-3; ACC/AHA Class I recommendation; level of evidence C).¹ Aortic root replacement requires coronary reimplantation or aortocoronary bypass grafting (Cabrol technique; Figure 21-4).

Figure 21-3 Replacement of the entire aortic root with a composite valved conduit for ascending aortic aneurysm.

The underside of the aortic arch was also incorporated into the prosthetic graft. The right and left coronary arteries were reimplanted into the graft (A–C). Alternatively, the aortic root can be replaced with a cryopreserved homograft or porcine bioprosthesis (not shown).

(Adapted from Griepp RB, Ergin A: Aneurysms of the aortic arch. In Edmunds LH [ed]: Cardiac Surgery in the Adult. New York, McGraw-Hill, 1997, p 1209, by permission.)

Figure 21-4 Replacement of the entire aortic root with a composite valved conduit for ascending aortic aneurysm combined with end-to-end anastomosis of the right and left coronary arteries to an 8-mm or 10-mm prosthetic tube graft that was then anastomosed to the aortic root (A, B).

(Adapted from Downing SW, Kouchoukos NT: Ascending aortic aneurysm. In Edmunds LH [ed]: Cardiac Surgery in the Adult. New York, McGraw-Hill, 1997, p 1181, by permission).

Repairing aortic aneurysms that extend into or involve the aortic arch requires CPB with DHCA with or without perfusion adjuncts. For ascending aortic aneurysms that involve only the proximal aortic arch, partial arch replacement (hemiarch technique) is reasonable in which a tubular graft is interposed between the ascending aorta or aortic root and the underside of the aortic arch (ACC/AHA Class IIa recommendation; level of evidence B).¹ Ascending aorta with hemiarch reconstruction often is performed using DHCA with or without ACP/RCP to make the distal anastomosis feasible without cross-clamping (“open technique”). In patients who have isolated aortic arch aneurysms and who have a low operative risk, arch replacement is reasonable when the arch diameter exceeds 5.5 cm (ACC/AHA Class IIa recommendation; level of evidence B).¹ Total aortic arch replacement is reasonable in aneurysms that involve the entire arch (ACC/AHA Class IIa recommendation; level of evidence B).¹ Ascending aortic aneurysms that extend through the aortic arch into the descending aorta can be repaired with the “elephant trunk” technique (Figure 21-5; ACC/AHA Class IIa recommendation; level of evidence B).^1,29 Aortic arch aneurysms that extend into the aortic branch vessels may require repair with branched or trifurcated tube grafts to permit separate anastomosis to the innominate, left carotid, and left subclavian arteries.³⁰ In patients with aortic arch aneurysms and concomitant severe comorbidity, recent guidelines support an endovascular repair technique (Class IIb recommendation; level of evidence C).^1,20 However, in patients who have aortic arch aneurysms and who have reasonable surgical risk, the recent guidelines advise against an endovascular repair technique (Class III recommendation; level of evidence A).^1,20

Figure 21-5 Elephant trunk procedure for prosthetic graft replacement of the ascending aorta, aortic arch, and descending thoracic aorta.

The aortic aneurysm or dissection is opened its entire length and extended through the aortic arch (A, B). The prosthetic tube graft is implanted with its distal end extending into the descending thoracic aorta, “elephant trunk” (C, D). The graft is pulled back into the arch for implantation of the arch branch vessels and construction of the proximal anastomosis (D, E). In the second stage of the procedure, the descending thoracic aorta is replaced by constructing a proximal graft-to-graft anastomosis (not shown).

(From Doty DB: Aortic aneurysm. In Brown M, Baxter S [eds]: Cardiac Surgery: Operative technique. St. Louis, Mosby-Year Book, 1997, p 324.)

Anesthetic Management for Ascending Aorta and Arch Aneurysms

The conduct of general anesthesia in this setting has specific concerns. The imaging studies should be reviewed for aneurysm compression of mediastinal structures such as the right pulmonary artery and left mainstem bronchus (Figure 21-6). Prevention of hypertension increases forward flow in AR and minimizes the risk for aneurysm rupture. A right radial arterial catheter is preferred for most cases. If arterial cannulation of the right axillary, subclavian, or innominate artery is planned for CPB and ACP, bilateral radial arterial catheters often are required to measure cerebral and systemic perfusion pressures. Nasopharyngeal, tympanic, and bladder temperatures are important for estimating brain and core temperatures for monitoring the conduct of DHCA. Monitoring of jugular bulb venous oxygen saturation and the EEG may reflect cerebral metabolic activity to guide the conduct of DHCA. Intraoperative TEE is essential to guide and assess the surgical interventions. In patients with AR, TEE can assist in the conduct of CPB by guiding placement of cannulae such as the retrograde cardioplegia cannula (coronary sinus) and by monitoring left ventricular (LV) volume to ensure that the LV drainage cannula keeps the ventricle collapsed. Intraoperative TEE is reasonable in thoracic aortic procedures, including endovascular interventions, in which it assists in hemodynamic monitoring, procedural guidance, and endoleak detection (ACC/AHA Class IIa recommendation; level of evidence B).¹

Figure 21-6 Computed tomographic angiogram of the chest demonstrating a large ascending aortic aneurysm (Ao) causing compression of the right pulmonary artery (RPA), distal trachea, and left main stem bronchus (LMB).

Neuroprotection Strategies for Temporary Interruption of Cerebral Blood Flow

The risk for stroke is substantial during the cerebral ischemia that accompanies aortic arch reconstruction.³¹ The first mechanism is cerebral ischemia due to hypoperfusion or temporary circulatory arrest during aortic arch repair. The second mechanism is cerebral ischemia due to embolization secondary to CPB and atheroma. Arterial emboli causes include air introduced into the circulation from open cardiac chambers, vascular cannulation sites, or arterial anastomosis. Atherosclerotic particulate debris may be released during clamping and unclamping of the aorta, the creation of anastomoses in the ascending aorta and aortic arch, or the excision of severely calcified and diseased cardiac valves. CPB may result in the microparticulate aggregates of platelets and fat. The turbulent high-velocity blood flow out of the aortic cannula used for CPB also may dislodge atherosclerotic debris within the aorta. Retrograde blood flow through a diseased descending thoracic aorta as a consequence of CPB conducted with femoral artery cannulation may cause retrograde cerebral embolization. For all these reasons, strategies to provide neurologic protection are essential in thoracic aortic operations (Box 21-2).

Deep Hypothermic Circulatory Arrest

The brain is exquisitely susceptible to ischemic injury within minutes after the onset of circulatory arrest because it has a high metabolic rate, continuous requirement for metabolic substrate, and limited reserves of high-energy phosphates. The physiologic basis for deep hypothermia as a neuroprotection strategy is to decrease cerebral metabolic rate and oxygen demands to increase the period that the brain can tolerate circulatory arrest.³² Existing evidence indicates that autoregulation of cerebral blood flow is maintained during deliberate hypothermia with alpha-stat blood gas management without compromise of clinical outcome.³³ Direct measurement of cerebral metabolites and brainstem electrical activity in adults undergoing DHCA with RCP at 14°C indicated the onset of cerebral ischemia after only 18 to 20 minutes (Figure 21-7).³⁴ Despite this observation, the large body of experimental evidence and clinical experience with the deliberate hypothermia suggest that it is the single most important intervention for preventing neurologic injury in response to circulatory arrest.

Figure 21-7 Changes in brainstem (N18) somatosensory-evoked potential amplitudes (dots) after initiation of deep hypothermic circulatory arrest with retrograde cerebral perfusion superimposed on the change in brain oxygen extraction ratio (OER) in patients without strokes (circles; n = 19), preoperative strokes (triangles; n = 4), intraoperative strokes (squares; n = 3), and both preoperative and intraoperative strokes (asterisks; n = 1). The N18 somatosensory-evoked potential decayed to half its original amplitude at 16 minutes after interruption of antegrade cerebral perfusion. The OER decreased to half its maximal value of 0.66 also at 16 minutes after interruption of antegrade cerebral perfusion.

(Adapted from Cheung AT, Bavaria JE, Pochettino A, et al: Oxygen delivery during retrograde cerebral perfusion in humans. Anesth Analg 88:14, 1999.)

Despite the proven efficacy of hypothermia for operations that require circulatory arrest, no consensus exists on an optimal protocol for the conduct of deliberate hypothermia for circulatory arrest. A strategy to protect the brain during aortic arch surgery must be a high priority in the perioperative management of these procedures to prevent stroke and optimize cognitive function (ACC/AHA Class I recommendation; level of evidence C).¹ Although the average nasopharyngeal temperature for DHCA may be about 18° C, the optimal temperature for DHCA has not been established.^31,32 A challenge in the selection of the ideal temperature for DHCA is the inability to directly measure the brain temperature. In an EEG-based approach to this question, the median nasopharyngeal temperature for electrocortical silence was 18° C, although a nasopharyngeal temperature of 12.5° C or cooling on CPB for at least 50 minutes achieved electrocortical silence in 99.5% of cases (Figure 21-8).³⁵ Although the EEG functions well as a physiologic end point for cerebral metabolic suppression during cooling for DHCA as part of an institutional protocol, its outcome benefit remains to be demonstrated in a randomized trial.^15,31,36 A jugular bulb venous oxygen saturation greater than 95% measured using an oximetric catheter represents an alternative physiologic end point to detect maximum cerebral metabolic suppression for DHCA.³⁷ It is important to note that deep hypothermia to a set temperature (mean = 19°C) as an end point for DHCA without EEG or jugular bulb venous oxygen saturation has been associated with excellent neurologic outcomes in recent series.^38,39 In addition to systemic hypothermia produced by extracorporeal circulation, topical hypothermia by packing the head in ice also has been incorporated in leading institutional DHCA protocols to minimize passive warming of the head.^38,39 When providing topical hypothermia, care should be exercised to protect the eyes, nose, and ears from frostbite by protecting these vulnerable areas. Recent clinical studies support the practice of limiting the duration of straight DHCA to shorter than 45 minutes to avoid the associated significant increases in stroke and mortality risks.³¹ The technique of DHCA alone is a reasonable approach for neuroprotection during aortic arch surgery in the setting of adequate institutional experience (ACC/AHA Class IIa recommendation; level of evidence B).¹

Figure 21-8 The relation between electroencephalographic activity to minutes of cooling (top) and nasopharyngeal temperature (bottom) before deep hypothermic circulatory arrest in 109 patients undergoing thoracic aortic operations requiring circulatory arrest. Electrocortical silence (ECS) was achieved by electroencephalogram (EEG) in all patients after 50 minutes of cooling or at a nasopharyngeal temperature of 12.5° C. At a nasopharyngeal temperature of 18° C, only 50% of patients had ECS by EEG.

(Adapted from Stecker MM, Cheung AT, Pochettino A, et al: Deep hypothermic circulatory arrest: I. Effects of cooling on electroencephalogram and evoked potentials. Ann Thorac Surg 71:19, 2001, by permission of the Society of Thoracic Surgeons.)

The conduct of DHCA extends CPB duration with consequent risks for coagulopathy and embolization. Rewarming increases cerebral metabolic rate and can aggravate neuronal injury during ischemia/reperfusion. Consequently, it is important to rewarm gradually by maintaining a temperature gradient of no more than 10° C in the heat exchanger and avoiding cerebral hyperthermia (nasopharyngeal temperature > 37.5°C). The current guidelines advise against cerebral hyperthermia in aortic arch procedures (ACC/AHA Class III recommendation; level of evidence B).¹

Retrograde Cerebral Perfusion

RCP is performed by infusing cold oxygenated blood into the superior vena cava cannula at a temperature of 8° C to 14° C via CPB (Figure 21-9). The internal jugular venous pressure is maintained at less than 25 mm Hg to prevent cerebral edema. Internal jugular venous pressure is measured from the introducer port of the internal jugular venous cannula at a site proximal to the superior vena cava perfusion cannula and zeroed at the level of the ear. The patient is positioned in 10 degrees of Trendelenburg to decrease the risk for cerebral air embolism and prevent trapping of air within the cerebral circulation in the presence of an open aortic arch. RCP flow rates of 200 to 600 mL/min usually can be achieved. The potential benefits of RCP include partial supply of cerebral metabolic substrate, cerebral embolic washout, and maintenance of cerebral hypothermia.⁴⁰ Although RCP has been associated with excellent clinical results in aortic arch repair, it has not become the standard technique for neuroprotection in DHCA.^15,41 A recent large, single-center study (1991–2007; N = 1107; RCP in 82%) evaluated the role of RCP in proximal thoracic aortic repair. The perioperative rates for mortality and stroke in this series were 10.4% and 2.8%, respectively. The application of RCP was significantly protective against mortality (odds ratio, 0.42; 95% confidence interval, 0.25-0.70; P = 0.0009) and stroke (odds ratio, 0.35; 95% confidence interval, 0.15-0.81; P = 0.02).⁴² Despite the lack of randomized trials, RCP is safe and easily implemented in aortic arch repair as an adjunct to maintain cerebral hypothermia, provide partial metabolic substrate delivery, and decrease the risk for cerebral embolization.^36–42 The technique of DHCA with RCP is a reasonable approach for neuroprotection during aortic arch surgery in the setting of adequate institutional experience (ACC/AHA Class IIa recommendation; level of evidence B).¹

Figure 21-9 Extracorporeal perfusion circuit used to deliver retrograde cerebral perfusion.

The bridge (D) is clamped during cardiopulmonary bypass. After initiation of deep hypothermic circulatory arrest, clamps are placed on the venous return line (A), the proximal arterial cannula (B), and inferior vena caval cannula (C), and the bridge (D) is unclamped to permit retrograde perfusion into the superior vena cava.

(Adapted from Bavaria JE, Woo YJ, Hall RA, et al: Retrograde cerebral and distal aortic perfusion during ascending and thoracoabdominal aortic operations. Ann Thorac Surg 60:347, 1995, by permission of the Society of Thoracic Surgeons.)

Selective Antegrade Cerebral Perfusion

Selective ACP should be considered for aortic arch repairs longer than 45 minutes.³¹ ACP typically is initiated during DHCA by selective cannulation of the right axillary artery, right subclavian artery, innominate artery, or left common carotid artery (Figure 21-10).⁴³ In transverse aortic arch reconstruction procedures, ACP can be accomplished by inserting individual perfusion cannulae into the open end of the aortic branch vessels after opening the aortic arch. After reattachment of the aortic arch branch vessels to the vascular graft, ACP can be provided through a separate arm of the vascular graft or by direct cannulation of the graft. A functional circle of Willis may provide contralateral brain perfusion during interruption of antegrade perfusion in the innominate, left carotid, or left subclavian arteries during construction of the vascular anastomoses. ACP with oxygenated blood at 10° C to 14° C at flow rates in the range of 250 to 1000 mL/min typically achieves a cerebral perfusion pressure in the range of 50 to 80 mm Hg.

Figure 21-10 Extracorporeal perfusion circuit used for selective antegrade cerebral perfusion.

After achieving deep hypothermia on cardiopulmonary bypass, individual cannulas are inserted into the coronary, innominate, and left carotid arteries for selective antegrade perfusion of the heart and brain.

(From Bachet J, Teodori G, Goudot B, et al: Replacement of the transverse aortic arch during emergency operations for type A acute aortic dissection. J Thorac Cardiovasc Surg 96:878, 1988.)

Unilateral ACP via right axillary arterial cannulation is a popular technique for adult aortic repair.⁴³ This technique assumes an adequate circle of Willis; however, the anatomic completeness of the circle of Willis does not guarantee adequate cerebral cross-perfusion during aortic arch repair.^44,45 Consequently, it remains essential to monitor the contralateral hemisphere in unilateral ACP with modalities such as cerebral oximetry, carotid artery scanning, and transcranial Doppler.^46–48

Given that ACP may be unilateral or bilateral, there remains controversy about which ACP technique is superior.⁴⁹ A recent literature review combined 17 studies for a total sample size of 3548 patients; 83.1% with bilateral ACP and 16.9% with unilateral ACP.⁵⁰ Although the stroke rates were less than 5% regardless of technique, the period of safe ACP was significantly prolonged with bilateral ACP (86–164 minutes) compared with unilateral ACP (30–50 minutes). The evidence favors bilateral ACP in the setting of aortic arch repair times longer than 60 minutes.⁵⁰

Pilot clinical series in adult aortic arch repair also have been undertaken in the setting of ACP with moderate hypothermic circulatory arrest (MHCA; systemic temperature = 25° C).^51,52 A large, single-center study (1999–2006; N = 501 [36.1% emergency cases]; median age, 64 years; 63.9% male sex) evaluated perioperative outcomes with this technique.⁵³ With a perioperative mortality rate of 11.6%, multivariate predictors for mortality included age and CPB time. The stroke rate was 9.6% with operative time and renal dysfunction as its multivariate predictors for stroke. The rate of temporary neurologic dysfunction was 13.4%, its multivariate predictors including MHCA duration (odds ratio, 1.015; p = 0.01). Although MHCA with cold ACP appears to be an adequate technique for adult aortic arch repair, its safety is limited in the settings of the elderly, multiple comorbidities, and extended operative time. The safety of aortic arch repair recently was further demonstrated with bilateral ACP and a greater mean MHCA temperature of 28° C (2002–2008; N = 229; mean age, 70.8 ± 9.7 years; 68.1% male sex).⁵⁴ Although MHCA with ACP appears to be a reasonable technique for adult aortic arch repair, its safety for ischemic protection of the spinal cord and kidney are still questioned.^55,56 The technique of DHCA with ACP is a reasonable approach for neuroprotection during aortic arch surgery in the setting of adequate institutional experience (ACC/AHA Class IIa recommendation; level of evidence B).¹

Descending Thoracic and Thoracoabdominal Aortic Aneurysms

Surgical therapy for thoracic and TAAAs is to replace aneurysmal aorta with a prosthetic tube graft. Surgical access is via lateral thoracotomy or thoracoabdominal incision. Despite recent advances, major surgical challenges remain because the typical patient is elderly with multiple significant comorbidities (Table 21-6). The risks for spinal, mesenteric, renal, and lower extremity ischemia are significant due to thromboembolism, loss of collateral vascular networks, temporary interruption of blood flow, and reperfusion injury. The risks for wound dehiscence and respiratory failure remain significant because of the large incisions and diaphragmatic division, as well as injuries to the phrenic and recurrent laryngeal nerves. Consequently, TAAA repair is high risk (Table 21-7).⁵⁸

TABLE 21-6 Preoperative Features in Patients with Thoracoabdominal Aortic Aneurysm (N = 1220)

Data from Coselli JS, LeMaire SA, Miller CC 3rd, et al: Mortality and paraplegia after thoracoabdominal aortic aneurysm repair: A risk factor analysis. Ann Thorac Surg 69:409, 2000.

TABLE 21-7 Clinical Outcomes of Thoracoabdominal Aortic Aneurysm (TAAA) Repair (United States: 1988–1998)

TAAA, thoracoabdominal aortic aneurysm.

* Incidence of paraplegia not reported.

Data from Cowan JA, Dimick JB, Henke PK, et al: Surgical treatment of intact thoracoabdominal aortic aneurysms in the United States: Hospital and surgeon volume-related outcomes. J Vasc Surg 37:1169, 2003; and Cowan JA, Dimick JB, Wainess RM, et al: Ruptured thoracoabdominal aortic aneurysm treatment in the United States: 1988 to 1998. J Vasc Surg 38: 312, 2003.

Aneurysms of the descending thoracic aorta are classified by considering which third(s) of the descending thoracic aorta is (are) involved.¹ Extent A involves the proximal third, extent B involves the middle third, and extent C involves the distal third. If more than one third is involved, then the extent is classified according to which thirds are involved, for example, an aneurysm involving the proximal two-thirds is classified as extent AB. Essentially, multisegment aneurysms can be classified as proximal or distal because these extents influence the risk for spinal cord ischemia after surgical repair, whether open or endovascular.

Aneurysms of the thoracoabdominal aorta typically are defined by the Crawford classification (Figure 21-11). Extent I TAAA begins at the left subclavian artery and ends below the diaphragm, but above the renal arteries. Extent II TAAA involves the entire descending thoracic aorta and ends below the diaphragm at the aortic bifurcation. Extent III TAAA begins in the lower half of the descending thoracic aorta and ends below the diaphragm at the aortic bifurcation. Extent IV TAAA is confined to the entire abdominal aorta. If an extent I or extent II TAAA involves the distal aortic arch, its surgical replacement often requires DHCA for the proximal anastomosis. The Crawford classification stratifies operative risk and guides perioperative management (Table 21-8). Open repair of TAAA typically is accomplished by one of three major techniques; (1) aortic cross-clamping, (2) aortic cross-clamping with a Gott shunt, and (3) aortic cross-clamping with PLHB or partial CPB (Figure 21-12).

Figure 21-11 Crawford classification of thoracoabdominal aortic aneurysm extent.

(From Coselli JS: Descending thoracoabdominal aortic aneurysms. In Edmunds LH [ed]: Cardiac Surgery in the Adult. New York, McGraw-Hill, 1997, p 1232.)

Figure 21-12 Operative techniques for repair of thoracic or thoracoabdominal aortic aneurysms.

In the clamp-and-sew technique, the distal aorta is not perfused (A). Alternatively, distal aortic perfusion during repair can be provided by a passive Gott shunt (B), partial left heart bypass (C), or partial cardiopulmonary bypass (D). Deep hypothermic circulatory arrest may be necessary if the proximal cross-clamp cannot be safely applied in aneurysms extending into the distal aortic arch (not shown).

(From O’Connor CJ, Rothenberg DM: Anesthetic considerations for descending thoracic aortic surgery: Part II. J Cardiothorac Vasc Anesth 9:734, 1995.)

Partial Left-Heart Bypass

The control of both proximal and distal aortic perfusion during TAAA repair is achieved with PLHB. This technique requires left atrial cannulation, usually via a left pulmonary vein (see Figure 21-12C). Oxygenated blood from the left atrium flows through the CPB circuit into the distal aorta or a major branch via the arterial cannula.⁶¹ The CPB circuit can include a heat exchanger, membrane oxygenator, and/or a venous reservoir. The degree of heparinization for PLHB is minimal with heparin-coated circuits without an oxygenator. Full systemic anticoagulation with ACT greater than 400 seconds is required for CPB circuits with membrane oxygenators and heat exchangers.⁶⁴ During PLHB, the proximal mean arterial pressure (MAP; radial artery) is generally maintained in the 80 to 90 mm Hg range. Flow rates in the range of 1.5 to 2.5 L/min typically maintain a distal aortic MAP in the 60 to 70 mm Hg range, monitored via a femoral arterial catheter.⁶⁴ Sequential advancement of the aortic cross-clamp during PLHB permits segmental aortic reconstruction with a decrease in end-organ ischemia. The advantages of PLHB include control of aortic pressures and systemic temperature, reliable distal aortic perfusion, and selective antegrade perfusion of important branch vessels (Figure 21-13).⁶¹ Its disadvantages include increased expense, increased complexity, and requirement for systemic anticoagulation (see Table 21-9). An alternative technique uses partial CPB by femoral vein to femoral artery perfusion with or without an oxygenator. This can allow for distal perfusion without the need for cannulation of the heart or aorta. However, it does not offer the control that is achieved with proper PLHB.

Figure 21-13 Extracorporeal perfusion circuit for repair of an extensive thoracoabdominal aortic aneurysm. Cannulation of the left atrium and femoral artery provides distal aortic perfusion by partial left heart bypass. Visceral perfusion can be provided by selective cannulation of the celiac, superior mesenteric, and renal arteries.

(Adapted from Coselli JS: Descending thoracoabdominal aortic aneurysms. In Edmunds LH [ed]: Cardiac Surgery in the Adult. New York, McGraw-Hill, 1997, p 1237.)

Endovascular Stent Graft Repair of Thoracic Aortic Aneurysms

TEVAR was established for the management of thoracic aortic aneurysms and now has recent management guidelines.²⁰ Endovascular stent grafts are tube grafts reinforced by a wire frame that are collapsed within a catheter for delivery and deployment within the aortic lumen. The principle of TEVAR is that the deployed stent complex spans the length of diseased aorta to exclude blood flow into the aneurysm cavity. TEVAR requires a landing zone for each end of the tubular graft. Endoleak is defined as blood flow within the aneurysm but outside the endovascular graft (Table 21-10).

TABLE 21-10 Classification of Endoleaks

Type	Cause of Perigraft Flow	Consequences and Therapeutic Strategy
I	Inadequate seal at proximal and/or distal landing zone	Systemic blood pressure is transmitted to aneurysm with risk for rupture: timely repair is indicated.
II	Retrograde flow from aortic branches into aneurysm	It may thrombose. If aneurysm is expanding, aortic branch embolization is indicated.
III	Structural failure of stent, e.g., perforations, fractures	Systemic blood pressure is transmitted to aneurysm with risk for rupture: timely repair is indicated.
IV	Stent graft fabric porosity	This usually occurs at implantation and disappears with anticoagulation reversal.
V	Aneurysm expansion without obvious endoleak (“endodistention”)	The endovascular repair can be strengthened with a second stent.

Data from Hiratzka LF, Bakris GL, Beckman JA, et al: 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with thoracic aortic disease: Executive summary. A report of the American College of Cardiology Foundation, American Heart Association Task Force on Practice Guidelines, American Association for Thoracic Surgery, American College of Radiology, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society for Vascular Medicine. Circulation 121:e266–e369, 2010.

The current guidelines from the STS suggest TEVAR for aneurysms of the descending thoracic aorta when the aortic diameter is larger than 5.5 cm (Class IIa recommendation; level of evidence B, when the patient has significant comorbidity; Class IIb recommendation; level of evidence C, when the patient has no significant comorbidity).²⁰ When the aortic diameter is less than 5.5 cm, the STS guidelines advise against TEVAR (Class III recommendation; level of evidence C).²⁰ In the setting of TAAA, the STS guidelines support TEVAR in patients with severe comorbidity (Class IIb recommendation; level of evidence C).²⁰ In patients with severe comorbidity and aortic arch aneurysm with distal extension, the STS guidelines support an endovascular repair technique (Class IIb recommendation; level of evidence C).^1,20 In patients who have reasonable surgical risk and who have aortic arch aneurysms with distal extension, the STS guidelines advise against an endovascular repair technique (Class III recommendation; level of evidence A).^1,20

Endovascular stent graft repair for isolated descending thoracic aortic aneurysms with a proximal landing zone that involves the left subclavian artery can be accomplished using a two-stage procedure (Figure 21-14). In the first stage, the left subclavian artery can be divided and anastomosed onto the left common carotid artery. This first stage of the procedure provides a proximal landing zone, allowing the deployment of the endovascular stent graft over the left subclavian artery branch in the distal aortic arch in the second stage of the procedure without compromising flow through the vessel. Multiple recent meta-analyses have demonstrated the outcome importance of not sacrificing the left subclavian artery during TEVAR to avoid the risks for stroke, paraplegia, and left upper extremity ischemia.^67–69 The recent guidelines from the Society of Vascular Surgery strongly support this principle but also recognize that in urgent TEVAR for life-threatening acute aortic syndromes, left subclavian artery coverage is unavoidable.⁷⁰

Figure 21-14 Intraoperative angiogram demonstrating an isolated saccular aneurysm (double arrows) of the thoracic aorta (A). The left subclavian artery (single arrow) was previously divided and transposed onto the left carotid artery to create a proximal landing site for endovascular stent repair (A). Intraoperative angiogram (B) after deployment of the endovascular stent graft (C) demonstrated exclusion of the aneurysm.

There are currently two major options for endovascular TAAA repair, namely, total TEVAR and hybrid TEVAR. Total endovascular TAAA repair requires customized stents that preserve major aortic branches with fenestrations or side branches. Recent series have demonstrated the safety and efficacy of this TEVAR modality in high-risk TAAA patients.^71–73 In hybrid TAAA repair, the landing zone for the nonfenestrated endovascular graft is created by aortic debranching procedures, for example, the renal and mesenteric arteries are anastomosed to the iliac arteries. Recent multiple series and meta-analyses have demonstrated the safety and efficacy of this TEVAR modality in high-risk patients.^74–78 This hybrid approach also has been utilized in aortic arch reconstruction for high-risk patients with aortic arch aneurysms.⁷⁹ Furthermore, TEVAR recently has extended proximally for therapy of select aneurysms of the ascending aorta.^80,81 In summary, TEVAR for TAAA, whether wholly endovascular or hybrid, is in recent clinical development with an established niche in patients with excessive operative risk. It is likely that these technologies will mature further in the coming years. This maturation of TEVAR for diseases of the descending thoracic aorta likely will be rapid given that recent meta-analysis (N = 5888, 42 nonrandomized studies) demonstrated that TEVAR as compared with open aortic repair reduced perioperative mortality (odds ratio, 0.44; 95% confidence interval, 0.33–0.59), paraplegia (odds ratio, 0.42; 95% confidence interval, 0.28–0.63), pneumonia, cardiac complications, renal failure, bleeding, and transfusion, as well as length of hospital stay.⁸²

Anesthetic Management for Thoracoabdominal Aortic Aneurysm Repair

The anesthetic management of patients undergoing TAAA repair often requires selective right lung ventilation in the setting of a major left thoracotomy and anesthetic interventions to prevent spinal cord ischemia. Right radial arterial pressure monitoring typically is preferred, especially if the aortic repair involves clamping the left subclavian artery or surgical endovascular access via the left brachial artery. Femoral arterial pressure monitoring is required when distal aortic perfusion is planned either with PLHB or a Gott shunt. Hemodynamic monitoring with a PAC usually is helpful for the management of the concomitant specialized perfusion techniques already discussed. The anesthetic plan must allow for spinal cord monitoring with SSEPs, MEPs, or both to account for decreases in renal function and include a plan for postoperative analgesia.

Lung Isolation Techniques

Selective ventilation of the right lung with concomitant left lung collapse during TAAA repair enhances surgical access and protects the right lung from left lung bleeding. Collapse of the left lung typically is achieved when the left main bronchus is intubated either with a double-lumen endobronchial tube (DLT) or a bronchial blocker. Routine fiberoptic bronchoscopic guidance guarantees the effectiveness of either technique. The increased length of the left mainstem bronchus facilitates placement of a left-sided DLT and subsequently anchors it during surgery. Endobronchial blockade is achieved with one of the following devices: the Arndt blocker, the Cohen blocker, or the Univent tube (Figure 21-15).⁸³ Wire-guided endobronchial blocking catheters permit the balloon-tipped catheter to be guided and positioned precisely in the left mainstem bronchus with a fiberoptic bronchoscope. The advantages of a left DLT include the ability to apply selective continuous positive airway pressure to the left lung. Its disadvantages include increased difficulty in difficult airways and bronchial injury in distorted endobronchial anatomy. The major advantage of endobronchial blockade is its compatibility with an existing standard 8.0-mm endotracheal tube. This is advantageous in emergencies and in difficult airways.⁸³ The disadvantages of endobronchial blockade include increased time for left-lung collapse and dislodgement during surgery. The majority of patients will require temporary postoperative mechanical ventilation, usually via a single-lumen endotracheal tube. ICU personnel often are unaccustomed to managing patients with DLTs with their risks for malposition, airway obstruction, and difficulty with airway secretions. Endotracheal tube exchange may be challenging if there is airway edema. An endotracheal tube exchange catheter in combination with direct laryngoscopy often facilitates safe endotracheal tube exchange.⁸⁴ It is recommended that in the setting of upper airway edema, DLTs are not routinely exchanged for single-lumen tubes (ACC/AHA Class III recommendation; level of evidence C).¹

Figure 21-15 Single-lung ventilation for thoracic or thoracoabdominal aortic aneurysm repair requiring a left thoracotomy can be accomplished using a Cohen bronchial blocker inserted through a standard endotracheal tube (A), an Arndt wire-guided bronchial blocker inserted through a standard endotracheal tube (B), a Univent endotracheal tube with an integrated bronchial blocker (C), or a left-sided double-lumen endobronchial tube (D).

Paraplegia after Thoracoabdominal Aortic Aneurysm Repair

Paraplegia after TAAA repair is a devastating complication. The temporary interruption of distal aortic perfusion and sacrifice of spinal segmental arteries during TAAA repair are central events in the pathogenesis of spinal cord ischemia and paraplegia. There are multiple contributing factors (Table 21-11).⁸⁵ The typical level of spinal cord ischemia after TAAA is midthoracic and is associated with a high perioperative mortality. There are many management strategies for prevention of this devastating complication after TAAA (Table 21-12).^1,85

TABLE 21-11 Factors That Contribute to Paraplegia after Thoracic or Thoracoabdominal Aortic Procedures

TABLE 21-12 Minimizing Paraplegic Risk after Thoracic or Thoracoabdominal Aortic Procedures

The spinal cord arterial supply provides a partial explanation for the clinical features of paraplegia after TAAA repair (Figure 21-16).^85,86 The anterior spinal artery supplies the anterior two thirds of the spinal cord, and the posterior spinal arteries supply the posterior third. Branches from each vertebral artery join to form the anterior spinal artery that descends along the midline of the anterior surface of the spinal cord. The anterior spinal artery sometimes is discontinuous and fed in a variable extent by radicular arteries derived from ascending cervical, deep cervical, intercostal, lumbar, and sacral segmental arteries. The posterior spinal arteries also are derived from the vertebral arteries and receive collateral supply from posterior radicular arteries. The terminal cord segments are supplied by radicular arteries that arise from the internal iliac and sacral arterial network. The thoracolumbar spinal cord typically has multiple arterial sources with a clinical vulnerability to significant ischemia. In this watershed region, an important blood supply is derived from a large radicular artery (intercostal arteries T9-T12 in 75% of patients, T8-L3 in 15%, and L1-L2 in 10%).^87,88 This important artery is known as the arteria magna or the artery of Adamkiewicz. Ischemia in the anterior spinal artery territory classically causes motor paralysis with preservation of proprioception.⁸⁵ Clinical experience, however, has demonstrated that spinal cord ischemia after TAAA repair is variable, asymmetric, and can affect motor or sensory function, or both.^85,89

Figure 21-16 The arterial supply to the spinal cord is provided by the anterior spinal artery and paired posterior spinal arteries that branch off the vertebral arteries (A).

Radicular arterial branches off the descending thoracic aorta provide collateral arterial supply to the anterior and posterior spinal arteries (B). The arteria magna or artery of Adamkiewicz refers to a large radicular branch located between the T9 and L2 vertebral levels that supplies the anterior spinal artery (B).

Paraplegia is defined as lower extremity motor weakness with muscle strength weaker than gravity. Paraparesis is defined as lower extremity weakness with muscle power that allows movement at least against gravity (Table 21-13).⁸⁹ Spinal cord ischemia may have an immediate onset, defined as lower extremity weakness on emergence from anesthesia within 24 hours of the procedure.^85,89 Delayed-onset spinal cord ischemia is defined as lower extremity weakness that follows a normal postoperative neurologic examination after emergence from anesthesia. In the largest series of TAAA repairs ever reported (N = 2286; 1986–2006), the incidence rate of symptomatic spinal cord ischemia was 3.8%, with 63% of these cases having an immediate onset and 37% a delayed onset.⁶¹ Multiple series have indicated that delayed-onset spinal cord ischemia can present days, weeks, or even months after TAAA repair.^61,85,89,90

TABLE 21-13 Description of Lower Extremity Weakness Caused by Spinal Cord Ischemia

Data from Greenberg RK, Lu Q, Roselli E, et al: Contemporary analysis of descending thoracic and thoracoabdominal aneurysm repair: A comparison of endovascular and open techniques. Circulation 118:808, 2008.

Immediate-onset paraplegia likely is a consequence of spinal cord ischemia, leading to infarction that occurred during surgery. In contrast with delayed-onset paraplegia, recovery with intervention in immediate-onset paraplegia has not been consistently demonstrated. This lack of therapeutic response likely indicates that irreversible spinal cord injury has occurred. Consequently, strategies to prevent immediate-onset paraplegia are directed toward intraoperative spinal cord protection (Box 21-3). The objective of intraoperative spinal cord monitoring is to detect spinal cord ischemia for immediate intervention to improve spinal cord perfusion. Distal aortic perfusion maintains spinal cord function during aortic cross-clamping and improves the ability to monitor spinal cord integrity during surgery with SSEP or MEPs.

Delayed-onset paraplegia indicates that, although the spinal cord was protected intraoperatively, it remains vulnerable to ischemia after surgery. Although the causes of this syndrome are incompletely understood, it often is preceded by hypotension.⁹¹ Strategies to minimize delayed-onset paraplegia concern the prevention of perioperative hypotension, early anesthetic emergence for early and subsequent serial neurologic assessment, and lumbar CSF drainage (Box 21-4). Given the catastrophic sequelae of permanent paraplegia after TAAA repair, all reasonable attempts to treat delayed-onset paraplegia can be justified.

Arterial Pressure Augmentation

The optimization of SCPP for spinal cord protection is recommended as part of an institutional perioperative protocol (ACC/AHA Class IIa recommendation; level of evidence B).¹ This recommendation also recognized the variety of suitable techniques such as maintenance of proximal aortic pressure and distal aortic perfusion with the caveat that technique selection often is a function of institutional experience.¹ In keeping with this recommendation are the principles of arterial pressure augmentation and CSF drainage for prevention and management of postoperative spinal cord ischemia (Figure 21-17).⁹⁰ Spinal cord ischemia after TAAA repair is more likely in the setting of hypotension because the spinal arterial collateral network has been reduced due to factors such as intercostal artery sacrifice.^91,100,101 Recent surgical techniques to preserve SCPP include selective intraoperative spinal cord perfusion and intercostal artery revascularization with interposition grafts.^102,103

Figure 21-17 Systolic, mean, and diastolic blood pressures in the period surrounding the onset (E) and recovery (R) from delayed-onset paraplegia in three patients after thoracoabdominal aortic aneurysm repair. Autonomic nervous system dysfunction caused by spinal cord ischemia may have contributed to the decrease in arterial pressure during the events. Arterial pressures were augmented with vasopressor therapy (bottom). Vasopressor requirements decreased after recovery from spinal cord ischemia.

(From Cheung AT, Weiss SJ, McGarvey ML, et al: Interventions for reversing delayed-onset postoperative paraplegia after thoracic aortic reconstruction. Ann Thorac Surg 74:417, 2002, by permission of the Society of Thoracic Surgeons.)

SCPP is estimated as the MAP minus the lumbar CSF pressure. In general, the SCPP should be maintained greater than 70 mm Hg after TAAA repair, that is, a MAP of 80 to 100 mm Hg.^85,90,100 Because spinal cord ischemia often involves the thoracolumbar cord, it often is accompanied by a significant sympathectomy known as spinal vasodilatory shock.^1,85,90 Early intervention to treat hypotension with vasopressor therapy may counter the autonomic nervous system dysfunction accompanying spinal cord ischemia and also augment SCPP. As in the treatment of neurogenic shock, high-dose vasopressor therapy with norepinephrine, phenylephrine, epinephrine, and/or vasopressin typically is required to restore systemic vascular resistance and spinal cord perfusion, with a MAP in the 80 to 100 mm Hg range.⁹⁰ Recovery from spinal cord ischemia often is heralded by recovery of systemic vascular tone and a decreasing vasopressor requirement. Therapeutic hypertension, as discussed here, for the management of spinal cord ischemia after TAAA must be weighed against the risks for arterial bleeding.

Intraoperative Neurophysiologic Monitoring

Neurophysiologic monitoring of the spinal cord (SSEPs and/or MEPs) is recommended as a strategy for the diagnosis of spinal cord ischemia so as to allow immediate intraoperative neuroprotective interventions such as intercostal artery implantation, relative arterial hypertension, and CSF drainage (ACC/AHA Class IIb recommendation; level of evidence B).¹ This management strategy may prevent immediate-onset postoperative paraplegia. SSEP monitoring is performed by applying electrical stimuli to peripheral nerves and recording the evoked potential that is generated at the level of the peripheral nerves, spinal cord, brainstem, thalamus, and cerebral cortex.¹⁰⁴ Because SSEP monitors posterior spinal column integrity, MEPs have been advocated because they monitor the anterior spinal columns that are typically at risk during TAAA repair. MEP monitoring is performed by applying paired stimuli to the scalp and recording the evoked potential that is generated in the anterior tibialis muscle.^105,106 (See Chapter 16.)

Paraplegia caused by spinal cord ischemia significantly dampens lower extremity evoked potentials as compared with the upper extremity (Figure 21-18). Intraoperative comparison of upper and lower extremity evoked potentials distinguishes spinal cord ischemia from the generalized effects of anesthetics, hypothermia, and/or electrical interference. As discussed earlier, the anesthetic must be designed for minimal interference with the selected neuromonitoring strategy. Although SSEPs can reliably exclude spinal cord ischemia with a negative predictive value of 99.2%, their sensitivity for its detection is only 62.5%, with no clinically useful predictive value for delayed-onset paraplegia.¹⁰⁷ A recent study (N = 233) compared both MEPs and SSEPs for spinal cord monitoring in extensive descending thoracic and TAAA repairs.¹⁰⁸ Both monitoring modalities had a nearly 90% correlation for spinal cord infarction (correlation statistic = 0.896; P < 0.0001), as well as a 98% negative predictive value for immediate-onset paraplegia. Furthermore, reversible changes in MEPs and SSEPs had no correlation with permanent paraplegia. In summary, despite the theoretic advantages of MEPs for monitoring the at-risk anterior spinal columns, in practice, this most recent data set suggests that SSEPs alone suffice for clinical purposes, and that MEPs did not add significantly to clinical management.¹⁰⁸ This assessment also is reflected in the neuromonitoring recommendations of the latest thoracic aortic disease guidelines.¹

Figure 21-18 Intraoperative somatosensory-evoked potential (SSEP) recordings from the lower (left) and upper (right) extremities that demonstrated spinal cord ischemia during thoracoabdominal aortic aneurysm repair.

Disappearance of SSEP signals from the right (R) and left (L) lower extremities recorded at the cortex (R1, R2, R3, L1, L2, L3) and spine (R4, L4) with preservation of SSEP signals from the lumbar plexus (R5, L5) and popliteal nerves (R6, L6) indicated the acute onset of spinal cord ischemia. Upper extremity SSEP signals were maintained during the episode. The light gray tracings were the baseline SSEP signals used for comparison.

Renal Protection during Thoracoabdominal Aortic Aneurysm Repair

Even though there has been major progress in TAAA repair, renal dysfunction remains common and still independently predicts for adverse clinical outcomes.^61,114 The thoracic aortic guidelines recommend preoperative hydration and intraoperative mannitol administration as reasonable nephroprotective strategies in extensive distal open thoracic aortic repairs, including TAAA repair (ACC/AHA Class IIb recommendation; level of evidence C).¹ Furthermore, intraoperative cold renal perfusion with blood or crystalloid is recommended as a reasonable intraoperative nephroprotective strategy during TAAA repair (ACC/AHA Class IIb recommendation; level of evidence C).^1,115,116 The administration of furosemide, mannitol, or dopamine for the sole purpose of renal preservation is not recommended in distal thoracic aortic repairs (ACC/AHA Class IIb recommendation; level of evidence B).¹ Rhabdomyolysis from lower extremity ischemia was recently identified as a mechanism for renal dysfunction after TAAA repair.^117–119 The maintenance of lower extremity perfusion bilaterally during distal aortic perfusion has been shown to ameliorate this rhabdomyolysis with a significant nephroprotective effect.

Postoperative Analgesia after Thoracoabdominal Aortic Aneurysm Repair

It is well recognized that the extensive thoracoabdominal incision is very painful. Because epidural analgesia has proved outcome utility in this type of extensive incision, it typically is part of the analgesic plan after TAAA repair.¹²⁰ The timing of epidural catheter placement and analgesia must take into account the perioperative anticoagulation status of the patient to minimize the risk for neuraxial hematoma.⁷ Furthermore, the epidural analgesia regimen should be formulated for a predominantly sensory block to allow serial motor assessment of the lower extremities and to minimize systemic vasodilation from a sympathectomy. For example, bupivacaine, 0.05%, combined with fentanyl, 2 μg/mL, can be initiated at a basal rate of 4 to 8 mL/hr after the patient exhibits normal neurologic function.⁹⁰ Bolus administration of concentrated local anesthetic through the epidural catheter should be discouraged to avoid sympathetic blockade and associated hypotension. The epidural catheter can be inserted before surgery, at the time of surgery, or in the postoperative period.

Anesthetic Management for Thoracic Endovascular Aortic Repair

TEVAR has revolutionized the management of descending thoracic and TAAAs with significant clinical outcome benefit.^20,82 The anesthetic management is based on the principles of care for patients undergoing endovascular abdominal aortic repair, but with the additional concerns of spinal cord ischemia and stroke.¹²¹ Typically, these patients undergo a balanced general anesthetic with invasive blood pressure monitoring and central venous access. The right radial artery is preferred for blood pressure monitoring, given that the left subclavian artery frequently may be covered and/or the left brachial artery may be accessed as part of the procedure.^67–70 PAC monitoring may be helpful in the setting of significant cardiac disease. TEE is reasonable in TEVAR in which it may assist in hemodynamic monitoring, procedural guidance, and endoleak detection (ACC/ACC Class IIa recommendation; level of evidence B).¹ As discussed earlier, if spinal cord monitoring is planned (SSEPs and/or MEPs), the anesthetic technique must be designed not to interfere with their signal quality.

The risk factors for stroke after TEVAR include a history of prior stroke, mobile aortic arch atheroma, and TEVAR of the proximal or entire descending thoracic aorta.^121,122 Therefore, the detection of mobile atheroma in the aortic arch is an important TEE finding in TEVAR because it predicts a greater stroke risk. The risk factors for spinal cord ischemia after TEVAR include perioperative hypotension (decreased SCPP), prior abdominal/descending thoracic aortic procedures (compromised spinal collateral arterial network), and coverage of the entire descending thoracic aorta (significant loss of intercostal arteries).^121,123 Consequently, indications for CSF lumbar drainage in TEVAR include planned extensive coverage of the descending thoracic aorta, history of prior abdominal/descending thoracic aortic procedures, and postoperative paraparesis/paraplegia despite relative hypertension.^121,123 Lumbar CSF drainage is a strongly recommended spinal cord protection strategy for TEVAR in patients with identified risk factors (ACC/AHA Class I recommendation; level of evidence B).^1,121–123

Type A Aortic Dissection

Aortic dissections that involve the ascending aorta (Stanford type A) are considered surgical emergencies (Box 21-5) (ACC/AHA Class I recommendation; level of evidence B).¹ The mortality rate without emergency surgery is about 1% per hour for the first 48 hours, 60% by about 1 week, 74% by 2 weeks, and 91% by 6 months (Figure 21-22).^1,124,125 Immediate surgical intervention significantly improves the mortality rate (Table 21-15), especially in patients younger than 80 years.^1,124–126 The principal causes of mortality include rupture, cardiac tamponade, myocardial ischemia from coronary dissection, severe acute AR, stroke caused by brachiocephalic dissection, and malperfusion syndromes including renal failure, ischemic bowel, and limb ischemia (Table 21-16). The type of preoperative presentation in type A dissection significantly determines operative mortality, prompting a clinical classification developed at the University of Pennsylvania (Penn classification: Table 21-17).¹²⁷ An aortic dissection less than 2 weeks old is classified as acute and older than 2 weeks is classified as chronic. This distinction is clinically important because after 2 weeks, mortality risk has plateaued and thus emergency surgery is not necessarily indicated.

Figure 21-22 Thirty-day mortality in 464 patients from the International Registry of Aortic Dissection (IRAD) stratified by medical and surgical treatment in both type A and type B aortic dissection.

(From Nienaber CA, Eagle KA: Aortic dissection: New frontiers in diagnosis and management. Part I: From etiology to diagnostic strategies. Circulation 108:631, 2003.)

TABLE 21-15 Mortality in Acute Aortic Dissection According to Dissection Type and Management

Data from Hagan PG, Nienaber CA, Isselbacher EM, et al: The International Registry of Acute Aortic Dissection (IRAD). New insights into an old disease. JAMA 283:897, 2000.

TABLE 21-16 Complications of Acute Stanford Type A Aortic Dissection (n = 513)

Data from Bossone E, Rampoldi V, Nienaber CA, et al: Usefulness of pulse deficit to predict in-hospital complications and mortality in patients with acute type A aortic dissection. Am J Cardiol 89:851, 2002.

TABLE 21-17 Penn Classification of Ischemic Presentations in Acute Stanford Type A Aortic Dissection

Data from Augoustides JG, Geirsson A, Szeto W, et al: Observational study of mortality risk stratification by ischemic presentation in patients with acute type A aortic dissection: The Penn classification. Nat Clin Pract Cardiovasc Med 6:140, 2009

Type B Aortic Dissection

Aortic dissections confined to the descending thoracic aorta (Stanford type B) should be managed medically unless there are life-threatening complications present such as malperfusion, aortic rupture, as well as severe pain and/or hypertension despite aggressive medical therapy (ACC/AHA Class I recommendation; level of evidence B).^1,124 Mortality with medical management in this type of aortic dissection is significantly lower than perioperative mortality (see Table 21-15).^1,124,125 The greater operative mortality is due to the severe complications of type B aortic dissection and the operation itself. TEVAR for the therapy of complicated acute type B dissection is highly recommended (STS guideline: Class I recommendation; level of evidence A).^1,20

Aortic Intramural Hematoma

Aortic intramural hematoma (IMH) is a variant of the classic aortic dissection (Table 21-18).^1,124,125 IMH has no intimal flap with no obvious intimal tear on aortic imaging. This class of intimal tear comprises about 17% of all dissections, with a 30-day mortality rate of 24%: 36% in type A IMH and 12% with type B IMH (P < 0.05).¹²⁶ Surgical management of type A IMH reduces mortality rate by 61.1% (14% vs. 36%; P = 0.02). Medical management for type B IMH reduced mortality fourfold (8% vs. 33%; P < 0.05).¹²⁶ Surgical indications in type A IMH include ascending aortic diameter larger than 50 mm or IMH thickness more than 12 mm. Surgical indications in type B IMH include rapid progression, rupture, or severe clinical symptoms despite aggressive medical therapy. It is, therefore, reasonable to manage IMH similar to classic aortic dissection in the corresponding thoracic aortic segment (ACC/AHA Class IIa recommendation; level of evidence C).¹ Although IMH may be caused by rupture of the vas vasorum in the aortic wall without intimal hematoma, there are frequently small intimal tears that are beyond the resolution of current aortic scanners and are only identifiable on close aortic inspection during surgery or autopsy.^1,127–130

TABLE 21-18 Aortic Intramural Hematoma

Clinical Diagnosis and Imaging Studies for Aortic Dissection

Aortic dissection is more common in men and has a peak incidence in later life.^1,124,125 It often has an earlier onset in the setting of Marfan syndrome, Ehlers-Danlos syndrome, Loeys-Dietz syndrome, bicuspid aortic valve, aortic coarctation, and familial aortic dissection.^1,124,125 It also is commonly associated with hypertension but less so with atherosclerosis.¹⁷ Further predisposing factors include pregnancy, cocaine abuse, arteritis, aortic trauma, and aortic instrumentation.¹

The pain of aortic dissection typically is severe, abrupt in onset, and has a ripping, tearing, or stabbing quality (ACC/AHA Class I recommendation; level of evidence B).¹ Highly suggestive physical findings include a pulse deficit, a systolic blood pressure limb differential greater than 20 mm Hg, focal neurologic deficit, and a new murmur of AR (ACC/AHA Class I recommendation; level of evidence B).¹ Besides a chest radiograph (ACC/AHA Class I recommendation; level of evidence C) and an electrocardiogram (ACC/AHA Class I recommendation; level of evidence B), urgent and definitive aortic imaging (TEE, CT, MRI) is strongly recommended in suspected aortic dissection (ACC/AHA Class I recommendation; level of evidence B).¹ A negative chest radiograph should not delay aortic imaging, especially in patients suspected of presenting with aortic dissection (ACC/AHA Class I recommendation; level of evidence B).¹ The selection of an aortic imaging modality should be guided by patient and institutional variables, including immediate test availability (ACC/AHA Class I recommendation; level of evidence C).¹ If initial aortic imaging is negative in the setting of high clinical suspicion for dissection, a second imaging study should be arranged (ACC/AHA Class I recommendation; level of evidence C).¹

The most common imaging study is contrast-enhanced spiral CT or CTA because it is widely available. Typical findings in acute aortic dissection include an intimal flap, luminal displacement of intimal calcifications, and aortic dilation (Figure 21-23).^124,125 IMH appears as a crescent-shaped high-attenuation thickening of the aortic wall in noncontrast CT (Figure 21-24).^124,125 CT can demonstrate rupture, branch-vessel involvement, and false lumen extent. Although MRI has a near 100% sensitivity and specificity, and is widely available, it also takes significantly longer than CT (Figure 21-25).^1,124,125

Figure 21-23 Computed tomographic angiogram in a patient with a type A aortic dissection.

Axial images of the chest (A) demonstrated an intimal flap that extended from the ascending aorta (double arrows) into the descending thoracic aorta (single arrow). Sagittal reconstruction (B) demonstrated the presence of an intimal flap in the descending thoracic aorta (single arrows).

Figure 21-24 Computed tomographic angiogram of the chest (A) and transesophageal echocardiographic upper esophageal short-axis images of the aorta (B) demonstrating an aortic intramural hematoma that extended from the ascending aorta into the descending thoracic aorta. A crescent-shaped or circumferential thickening of the aortic wall is diagnostic for aortic intramural hematoma. Ao, aorta.

Figure 21-25 Magnetic resonance imaging of the chest with gadolinium contrast injection in a patient with a type A aortic dissection. The dissection extended into the innominate artery (I), left carotid artery (LC), left subclavian artery (LS), and into the descending aorta (arrows).

At experienced centers, TEE provides high-resolution aortic images with comparable sensitivity and specificity to MRI and CT.^1,124,125 Furthermore, TEE can look for complications by interrogating the aortic valve (AR severity and mechanism), assessing ventricular function including regional wall motion for coronary dissection, and diagnosing cardiac tamponade and pericardial effusion. Aortic dissection appears on TEE examination as an undulating intimal flap within the aorta separating a true and false lumen (Figure 21-26). It is sometimes difficult to distinguish the true lumen from the false lumen, but the true lumen tends to be smaller with pulsatile high-velocity flow in systole. Doppler color-flow imaging can detect flow communication between the true and false lumens at intimal tear sites. Aortic IMH appears as an echo-dense crescent-shaped thickening (>7 mm) of the aortic wall that may contain echolucent pockets of noncommunicating blood (see Figure 21-24). TEE also may distinguish clinical mimickers of aortic dissection and can assess the thoracic aortic anatomy in detail to guide surgical decision making.^131,132

Figure 21-26 Transesophageal echocardiographic midesophageal long-axis image of the aortic valve (A) and short-axis image of the ascending aorta (B) in a patient with a type A aortic dissection.

An intimal flap separating the true lumen (TL) of the aorta with the false lumen (FL) was demonstrated in the aortic root and ascending aorta. Extension of the dissection into the aortic root may cause aortic regurgitation or coronary insufficiency.

Anesthetic Management for Aortic Dissection

Acute aortic dissection is a medical emergency. Acute medical management is directed at treatment of pain and decreasing the arterial pressure with antihypertensive agents. Vasodilator therapy should be initiated to decrease wall stress with control of heart rate and blood pressure (ACC/AHA Class I recommendation; level of evidence C).¹ In the presence of acute AR, β-blockers should be used with caution because they block the compensatory tachycardia (ACC/AHA Class I recommendation; level of evidence C).¹ In the absence of contraindications, β-blockers should be titrated to a heart rate of 60 beats/min (ACC/AHA Class I recommendation; level of evidence C).¹ Esmolol is a particularly useful β-blocker because it has a short pharmacologic half-life and can be rapidly titrated. Esmolol can be administered as an initial bolus of 5 to 25 mg intravenously, followed by a continuous infusion of 25 to 300 μg/kg/min. In patients with β-blocker contraindications, heart rate control should be gained with titration of nondihydropyridine calcium channel blockers such as verapamil or diltiazem (ACC/AHA Class I recommendation; level of evidence C).¹ Alternatively, labetalol, a drug that has a 1:7 ratio of β-blocker to α-blocker activity, can be administered as a 20 to 80 mg intravenous bolus followed by an infusion at 0.5 to 2.0 mg/min. Metoprolol, a cardioselective β-blocker, may be advantageous in patients with reactive airway disease who are sensitive to β-adrenergic antagonists. Metoprolol is administered at a dose of 5 to 15 mg intravenously every 4 to 6 hours. If the systolic blood pressure remains greater than 120 mm Hg with adequate heart rate control, then vasodilators (e.g., nitroprusside at a dosage of 0.5 to 2.0 μg/kg/min or nicardipine at a dose of 1 to 15 mg/hr) should be titrated for further reductions of blood pressure while still maintaining adequate vital organ perfusion (ACC/AHA Class I recommendation; level of evidence C).¹ Vasodilator therapy should not be initiated before heart rate control to avoid the associated reflex tachycardia that might aggravate the aortic dissection (ACC/AHA Class III recommendation; level of evidence C).¹

In general, the anesthetic management of type A aortic dissection resembles the management of ascending aortic aneurysms that require DHCA. The anesthetic management of type B aortic dissections resembles the management of TAAA repair. Large-bore intravenous catheters are essential for intravenous medications and rapid volume expansion. A radial arterial catheter for invasive blood pressure monitoring is preferred over a femoral artery catheter to allow for CPB cannulation, depending on surgeon preference. If a pulse deficit is detected, the site for arterial pressure monitoring should be chosen to best represent the central aortic pressure. A central venous or PAC to monitor CVP, pulmonary artery pressure, and cardiac output is useful. TEE insertion is performed after anesthetic induction.

Critically unstable patients should be resuscitated by standard ACC/AHA guidelines or by securing the airway, providing mechanical ventilation, and administering drugs to support the circulation. Emergent TEE should follow to verify the diagnosis of type A aortic dissection and to detect cardiac tamponade, hypovolemia, AR, and/or heart failure. If TEE detects cardiac tamponade, immediate sternotomy with preparations to institute CPB via femoral artery cannulation should be performed. Opening the pericardium and relief of cardiac tamponade can be followed by hypertension causing aortic rupture.

The induction of general anesthesia in hemodynamically stable patients with aortic dissection should proceed in a cautious manner. The dose of intravenous antihypertensive drugs may need to be reduced at the time of anesthetic induction to prevent severe hypotension when combined with anesthetic drugs. Hypotension also may occur on anesthetic induction in response to the attenuation of sympathetic nervous system tone or decreased cardiac preload caused by venodilation and positive pressure ventilation in patients with preexisting concentric left ventricular hypertrophy. The hypertensive response to endotracheal intubation, TEE probe insertion, and sternotomy should be anticipated and attenuated with narcotic analgesics.

Surgical Treatment of Stanford Type A Aortic Dissection

Surgical repair for type A aortic dissection requires resection of the proximal extent of the dissection. A partially dissected aortic root may be repaired with aortic valve resuspension. A destroyed aortic root must be replaced with a composite graft or a valve-sparing root replacement. In the setting of a DeBakey type II dissection, the entire dissected aorta merits replacement. CABG sometimes is necessary for aortic dissections that involve the coronary ostia. These surgical principles are all highly recommended (ACC/AHA Class III recommendation; level of evidence C).¹

Although femoral arterial cannulation is popular for CPB, recent evidence suggests that it is associated with adverse clinical outcomes including death, stroke, and malperfusion syndromes.^133,134 Cannulation of the distal ascending aorta or the axillary artery (ideally with an end-to-end graft) has been associated with significantly enhanced clinical outcome as compared with standard femoral arterial cannulation.^133,134 It remains important to monitor cerebral perfusion throughout the operative procedure for detection and correction of acute malperfusion.^46–48

In DeBakey type I dissections, the dissected descending thoracic aorta often undergoes aneurysmal degeneration and is responsible for significant aorta-related mortality in the long term.¹³⁵ Consequently, long-term outcomes after extensive type A dissection would be significantly improved if this distal aortic degeneration could be prevented.^135,136 Recent clinical series have demonstrated the efficacy and safety of anterograde stenting of the descending thoracic aorta during open aortic arch repair for DeBakey type 1 aortic dissection.^137–139 This technique is also known as the endovascular stented elephant-trunk technique or the frozen elephant-trunk technique. The long-term aneurysmal degeneration of the descending thoracic aorta is prevented by immediate stenting in the acute dissection phase; thus, favorable long-term aortic remodeling is facilitated.

Integrated Management of Stanford Type B Aortic Dissection

Uncomplicated type B aortic dissection currently has the best clinical outcome when managed medically.²⁰ Medical therapy for type B aortic dissection is directed at control of systemic hypertension to prevent aortic aneurysm formation, aortic rupture, and extension of the aortic aneurysm (ACC/AHA Class I recommendation; level of evidence C).¹ Combination therapy with a diuretic, β-blocker, angiotensin-converting enzyme inhibitor, or other antihypertensive agents usually is necessary to achieve and maintain blood pressure less than 130/80 mm Hg. All patients after repair of type A aortic dissection also should be managed aggressively with antihypertensive therapy because many are left with a residual distal aortic dissection after repair. Serial imaging of the aorta is necessary to detect expansion of the aortic lumen and aneurysm development that may warrant surgical correction.

In the presence of life-threatening complications, TEVAR has emerged as a preferred alternative therapy to surgery.^{20,82,140,141} A recent landmark randomized trial demonstrated that, in the short term, TEVAR added no survival advantage over medical management for uncomplicated type B aortic dissection.¹⁴² However, because TEVAR did improve aortic remodeling in this trial, further adequately powered trials are indicated to test whether this translates into better aortic outcomes.¹⁴³ Malperfusion syndromes associated with type B dissection also can be managed with intimal fenestration.¹⁴⁴