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Diseases of the thoracic aorta can occasionally be managed with medical treatment and surveillance, whereas others require surgical intervention. Depending on the disease process, some surgeries may be performed electively, whereas others are truly emergency operations.
Aortic surgery is complex, and therefore it requires an anesthetic tailored to the specific goals for hemodynamics, neuromonitoring, and cerebral/spinal cord perfusion.
Thoracic aortic aneurysms can cause compression of the trachea, left mainstem bronchus, right ventricular outflow tract, right pulmonary artery, or esophagus.
Deliberate hypothermia is the most important therapeutic intervention to prevent cerebral ischemia during temporary interruption of cerebral perfusion during aortic arch reconstruction.
Early detection and interventions to increase spinal cord perfusion pressure are effective for the treatment of delayed-onset spinal cord ischemia after thoracic or thoracoabdominal aortic aneurysm repair.
Severe atheromatous disease or thrombus in the thoracic or descending aorta is a risk factor for stroke.
Stanford type A dissection, involving the ascending aorta and aortic arch, is a surgical emergency. Stanford type B dissection, confined to the descending thoracic or abdominal aorta, should be managed medically when possible.
When adequate preoperative imaging is lacking, intraoperative transesophageal echocardiography can be used to diagnose type A dissection or traumatic aortic injuries that require emergency surgery.
Intraoperative transesophageal echocardiography and ultrasound imaging of the carotid arteries are useful for the diagnosis of aortic regurgitation, cardiac tamponade, myocardial ischemia, or cerebral malperfusion, complicating type A aortic dissection.
Newer endovascular approaches to the management of thoracic aortic disease continue to have a great impact on both elective and emergent aortic surgery.
Thoracic aortic diseases typically require surgical intervention ( Box 17.1 ). Acute aortic dissections, rupturing aortic aneurysms, and traumatic aortic injuries are surgical emergencies. Subacute aortic dissection and expanding aortic aneurysms require urgent surgical intervention. Stable thoracic or thoracoabdominal aortic aneurysms (TAAAs), aortic coarctation, or atheromatous disease causing embolization may be addressed surgically on an elective basis. The volume of thoracic aortic procedures has grown steadily because of factors such as increased public awareness, an aging population, earlier diagnosis, multiple advances in imaging, and advances in surgical techniques, including endovascular stenting. Medical centers have emerged that specialize in thoracic aortic diseases, resulting in improved management and survival. This progress has created a set of patients who later require reoperation for long-term complications such as valve or graft failure, pseudoaneurysm at anastomotic sites, endocarditis, and/or progression of the original disease process into the residual native aorta.
Aneurysm
Congenital or developmental
Marfan syndrome, Ehlers-Danlos syndrome
Degenerative
Cystic medial degeneration
Annuloaortic ectasia
Atherosclerotic
Traumatic
Blunt and penetrating trauma
Inflammatory
Takayasu arteritis, Behçet syndrome, Kawasaki disease
Microvascular diseases (polyarteritis)
Infectious (mycotic)
Bacterial, fungal, spirochetal, viral
Mechanical
Poststenotic, associated with an arteriovenous fistula
Anastomotic (postarteriotomy)
Pseudoaneurysm
Aortic dissection
Stanford type A
Stanford type B
Intramural hematoma
Penetrating atherosclerotic ulcer
Traumatic aortic injury
Aortic coarctation
The anesthetic management of thoracic aortic diseases has unique considerations, including the temporary interruption of blood flow, often resulting in ischemia of major organ systems. Critical components of anesthetic management include the maintenance of organ perfusion, protection of vital organs during ischemia, and monitoring and management of end-organ ischemia. As a result, the vigilant and skillful anesthesiologist contributes significantly to the overall success of these operations. The procedures performed by the thoracic aortic team for organ protection, such as partial left-heart bypass (PLHB) for distal aortic perfusion, cardiopulmonary bypass (CPB) with deep hypothermic circulatory arrest (DHCA), selective cerebral perfusion, and lumbar cerebrospinal fluid (CSF) drainage, are practiced routinely in no other area of medicine.
Patients undergoing thoracic aortic surgery require the common considerations for the safe use of anesthesia and perioperative care that are addressed in this section ( Box 17.2 ).
Urgency of the operation (emergent, urgent, or elective)
Pathology and anatomic extent of the disease
Median sternotomy vs thoracotomy vs endovascular approach
Mediastinal mass effect
Airway compression or deviation
Aortic valve disease
Cardiac tamponade
Coronary artery stenosis
Cardiomyopathy
Cerebrovascular disease
Pulmonary disease
Renal insufficiency
Esophageal disease (contraindications to transesophageal echocardiography [TEE])
Coagulopathy
Prior aortic operations
Warfarin (Coumadin)
Antiplatelet therapy
Antihypertensive therapy
Hemodynamic monitoring
Proximal aortic pressure
Distal aortic pressure
Central venous pressure
Pulmonary artery pressure and cardiac output
TEE
Neurophysiologic monitoring
Electroencephalography
Somatosensory-evoked potentials
Motor-evoked potentials
Jugular venous oxygen saturation
Lumbar cerebrospinal fluid pressure
Body temperature
Single-lung ventilation for thoracotomy
Double-lumen endobronchial tube
Endobronchial blocker
Potential for bleeding
Large-bore intravenous access
Blood product availability
Antifibrinolytic therapy
Antibiotic prophylaxis
Hypothermia
Hypotension
Hypertension
Bleeding
Spinal cord ischemia
Stroke
Renal insufficiency
Respiratory insufficiency
Phrenic nerve injury
Diaphragmatic dysfunction
Recurrent laryngeal nerve injury
Pain management
Identification of the aortic diagnosis is paramount 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 operating room (OR) admission by direct review of diagnostic studies or by subsequent transesophageal echocardiography (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. The anatomic details of an aortic disease permit the anesthesiologist to anticipate potential perioperative difficulties, including likely postoperative complications.
Inherent in surgical procedure is the potential for massive bleeding and cardiovascular collapse. Therefore, it is essential to have immediate availability of packed red blood cells and clotting factors, 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 A rationale exists for choosing to cannulate the left or right radial artery for intraarterial blood pressure monitoring. Right radial arterial pressure monitoring will often detect compromised flow into the brachiocephalic artery because of aortic cross-clamping too near its origin. Right radial arterial pressure monitoring also 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; however, a right-sided catheter may be preferred for ACP if direct brachiocephalic cannulation is used by the surgeon. 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 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. Both a urinary and a nasopharyngeal temperature probe are required for monitoring the absolute temperature of the periphery 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 and has 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 intravenous and inhalation anesthetic 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.
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; however, viscoelastic tests are being used with greater frequency to determine coagulation needs. 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. The antifibrinolytic lysine analogs, epsilon-aminocaproic acid or tranexamic acid, are the commonly utilized blood conservation agents in thoracic aortic surgery with and without DHCA. Recombinant activated factor VII is a synthetic agent that accelerates thrombin production leading to hemostasis, and it may be considered for the management of intractable nonsurgical bleeding after CPB that is unresponsive to routine therapy. Although this agent has demonstrated efficacy in complex aortic surgery, concerns for arterial thrombotic events remain, requiring further trials to investigate perioperative safety. Finally, the use of fibrinogen concentrates in the management of coagulopathy continue to be investigated in cardiac surgery, with recent evidence suggesting decreased intraoperative bleeding when fibrinogen concentrates are used as a first-line therapy for coagulopathy after major aortic surgery.
With the exception of some endovascular aortic procedures, patients often remain intubated and sedated at the completion of the operation, when they are transported directly from the OR to the intensive care unit (ICU). The continuation of care from the OR to the ICU should be seamless and protocol-based. 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. The chest roentgenogram allows confirmation of endotracheal tube and intravascular catheter position, as well as the diagnosis of acute intrathoracic pathologies. Common early complications include hypothermia, coagulopathy, delirium, stroke, hemodynamic lability, respiratory failure, metabolic disturbances, and renal failure. Frequent clinical and laboratory assessment is essential to manage this dynamic postoperative recovery, including the safe conduct of tracheal extubation. Given the risks associated with hyperglycemia after cardiac surgery, management of blood glucose levels should be standardized, with more recent data to suggest more liberal control (glucose less than 180 mg/dL) is acceptable with good outcomes. Antibiotic prophylaxis is typically continued for 48 hours after surgery to minimize surgical infection risk.
A thoracic aortic aneurysm is a permanent localized thoracic aortic dilatation that has at least a 50% diameter increase and three aortic wall layers. Localized dilatation of the thoracic aorta less than 150% of normal is termed ectasis. Annuloaortic ectasia is defined as isolated dilatation of the ascending aorta, aortic root, and aortic valve annulus. Pseudoaneurysm or a false aneurysm is a localized dilation of the aorta that does not contain all three layers of the vessel wall and instead consists of connective tissue and clot. Pseudoaneurysms are caused by a contained rupture of the aorta or arise from intimal disruptions, penetrating atheromas, or partial dehiscence of the suture line at the site of a previous aortic prosthetic vascular graft.
Thoracic aortic aneurysms are common and are the 15th most common cause of death in people older than 65. This disease process is virulent ( Box 17.3 ) but indolent because it typically grows slowly at an approximate rate of 0.1 cm/year. The most common reason for more rapid degeneration is acute aortic dissection. Besides acquired risk factors such as hypertension, hypercholesterolemia, and smoking, current evidence points to the strong influence of genetic inheritance. The aneurysm's location and extent determine the operative strategy and related perioperative complications. Aneurysms of the aortic root and/or ascending aorta commonly are associated with a bicuspid aortic valve. Dilation of the aortic valve annulus, aortic root, and ascending aorta pulls the aortic leaflets apart and causes central aortic regurgitation (AR). Aneurysms involving the aortic arch require temporary interruption of cerebral blood flow to accomplish the operative repair. Endovascular stent repair is an established therapy for aneurysms isolated to the descending thoracic aorta; however, ascending aorta stents have been employed in certain patients considered too high-risk for open surgery. Repair of descending thoracic aortic aneurysms requires the sacrifice of multiple segmental intercostal artery branches that compromises spinal cord perfusion and results in a significant risk for postoperative paraplegia from spinal cord ischemia.
Aortic rupture
Aortic regurgitation
Tracheobronchial and esophageal compression
Right pulmonary artery or right ventricular outflow tract obstruction
Systemic embolism from mural thrombus
Thoracic aortic aneurysms mostly are asymptomatic and frequently are discovered incidentally. Common symptoms of thoracic aortic aneurysm include chest and back pain caused by aneurysmal dissection, rupture, or bony erosion. The intrathoracic “mass effect” from a large thoracic aortic aneurysm can compress local structures to cause hoarseness (recurrent laryngeal nerve), dyspnea (trachea, mainstem bronchus, pulmonary artery), central venous hypertension (superior vena cava syndrome), and/or dysphagia (esophagus). Rupture of thoracic aortic aneurysms is a surgical emergency and is often accompanied with acute pain with or without hypotension. Although rupture of an ascending aortic aneurysm may cause cardiac tamponade, rupture in the descending thoracic aorta may cause hemothorax, aortobronchial fistula, or aortoesophageal fistula.
Surgical repair aims to replace the aortic aneurysm with a tube graft to prevent further aneurysmal complications. For thoracic aortic aneurysm resection, indications include whenever the aneurysm is symptomatic regardless of size, evidence of rupture, an ascending aneurysm diameter greater than 5.5 cm, or descending aneurysm greater than 7.0 cm. 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. Additionally, 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 (class I recommendation; level of evidence B).
Patients with aneurysms of the descending thoracic aorta should be considered for thoracic endovascular aortic repair (TEVAR) when technically feasible. 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 open surgical access. Aneurysmal resection requires cross-clamping with or without distal aortic perfusion.
The type of surgical repair depends on aortic valve function and the aneurysm location and 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 ( Fig. 17.1 ). 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. If disease involves both 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, which includes graft reconstruction of the aortic root with reimplantation of the coronary arteries. If not feasible, aortic root replacement with a composite valve-graft conduit is indicated (Bentall procedure). Aortic root replacement requires coronary reimplantation or aortocoronary bypass grafting (Cabrol technique).
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. Prevention of hypertension increases forward flow in AR and minimizes the risk for aneurysm rupture. The preference for a left or right radial arterial catheter depends on the surgeon's approach to arch repair. Occasionally, bilateral radial arterial catheters can allow for simultaneous monitoring of cerebral and systemic perfusion pressures if arterial cannulation of the right axillary, subclavian, or brachiocephalic artery is planned for CPB and ACP. 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 electroencephalogram 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.
The risk for stroke is substantial during the cerebral ischemia that accompanies aortic arch reconstruction. 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 embolic 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 17.4 ), and there exists a great degree of variation in the approaches used to protect and monitor brain function.
Deep systemic hypothermia
Topical cerebral cooling
Retrograde cerebral perfusion
Selective antegrade cerebral perfusion
Cerebral hyperthermia prevention during rewarming
The brain is extremely 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. 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. 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. Despite this observation, the large body of experimental evidence and clinical experience with deliberate hypothermia suggest that it is the single most important intervention for preventing neurologic injury in response to circulatory arrest.
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. Although the average nasopharyngeal temperature for DHCA may be about 18°C, the optimal temperature for DHCA has not been established. 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.
The conduct of DHCA extends CPB duration with consequent risks for coagulopathy and embolization. Rewarming increases cerebral metabolic rate and can aggra‑vate 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).
Although clinical studies would 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, the use of adjunct perfusion techniques for neuroprotection has allowed surgeons to work for longer periods of time in a safe manner. Similarly, these cerebral perfusion adjuncts have led to increased use of moderate degrees of hypothermia (20.1°C to 28.0°C). RCP is a cerebral perfusion technique performed by infusing cold oxygenated blood into the superior vena cava cannula at a temperature of 8°C to 14°C via CPB. 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 catheter at a siteproximal 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/minute usually can be achieved. The potential benefits of RCP include partial supply of cerebral metabolic substrate, cerebral embolic washout, and maintenance of cerebral hypothermia.
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