Standard ASA monitors are applied for surgery on the aorta. EKG should monitor leads II and V5 (for ischemia). A Foley catheter is routinely placed to monitor urine output. Arterial catheters are placed in all patients. These allow for rapid assessment of blood pressure, management with appropriate medication/interventions (cross clamping), and frequent laboratory analysis. Placement sites should be coordinated with the surgeon according to his/her approach/technique. Dynamic variation in the arterial wave form with positive pressure ventilation may be observed as an indicator of volume status.

Venous access should include at least one large-bore peripheral IV and central venous access (CVP or PA catheter, more commonly a triple lumen catheter). This allows for infusion of vasoactive/ionotropic medications, resuscitative fluids/blood products, and measurement of central venous pressure. Transesophageal echocardiography may be used to monitor cardiac function, guide fluid management, and detect myocardial ischemia and for anatomical assessments on the aorta, heart, and lungs. Cerebrospinal fluid drains are usually reserved for surgery on the thoracic aorta. Somatosensory evoked potentials and motor evoked potentials have been used during surgery on the aorta to detect spinal cord ischemia.

General anesthesia is required for surgery on the aorta. An epidural is commonly placed preoperatively, but is usually used for analgesia after the aortic cross clamp is removed and the patient is stabilized. The goal of anesthetic induction is to avoid wide variations in blood pressure and heart rate. During induction, blood pressure may drop significantly secondary to hypovolemia and limited cardiac reserve. However, with intubation, heart rate and blood pressure may increase. Therefore, induction medications should be tailored to avoid hemodynamic instability. Patients with ruptured AAA may be severely hypovolemic, and therefore, profound hypotension may occur with induction of anesthesia. Induction should occur with the abdomen prepped, the drapes placed, and the surgeon ready to enter the abdomen to gain control of the aorta and raise the blood pressure.

Most surgical approaches can be facilitated by using a single-lumen endotracheal tube. A double-lumen tube or endobronchial blocker may be used for surgery on the thoracic aorta to improve surgical exposure. Anesthesia is usually maintained by using volatile anesthetic agents, muscle relaxants, and narcotics.

Cross clamping of the aorta causes an immediate increase in systemic vascular resistance (vasoconstriction) and afterload and also venous return and mean arterial pressure (Fig. 27.2). This response is directly proportional to the level of aortic clamping with infrarenal < suprarenal < thoracic. These changes are mediated by an impedance to blood flow and increased circulating catecholamines. Vasodilating drugs (volatile inhalational agent, nitroglycerin, nitroprusside) may be used to counteract this response and decrease the afterload strain placed on the heart. Monitoring of cardiac function and hemodynamics is critical during this portion of the surgery. It should be remembered that any vasodilating drugs used to treat proximal hypertension will exacerbate hypotension and ischemia distal to the aortic clamp.

Unclamping is associated with hypotension secondary to decreased systemic vascular resistance and venous return (peripheral shift of blood volume), washout of ischemic metabolites, and vasoplegia. Treatment options include fluid loading prior to unclamping, vasoactive/ionotropic medications (phenylephrine), and gradual release of the cross clamp.

Postoperatively, patients are admitted in the intensive care unit. Patients who are hemodynamically stable may be extubated in the operating room. Epidural analgesia is initiated for pain control and helps to decrease requirements for intravenous opioids, improve lung function, and decrease the duration of postoperative ileus. For additional pain control, intravenous narcotics and nonsteroidal anti-inflammatory drugs should be used as needed.

Symptoms and signs of myocardial ischemia (adequate beta-blocker therapy), renal function, bleeding, mesenteric or bowel ischemia (blood in stool), or neurologic impairment should be followed closely. Bleeding is major concern during aortic surgery. Anatomic sources include acute rupture, leaking anastomotic sites, or perforation of surrounding organs or vasculature. Constant observation of the field and communication with the surgeon are critical aspects of management. Other sources of bleeding include hypothermia, dilution of coagulation factors, disseminated intravascular coagulation, inadequate anticoagulant reversal, and platelet dysfunction.

Postoperative renal failure, which is more common in patients with preexisting renal disease, is a major complication following aortic surgery and may be the strongest predictor of mortality. Renal failure is more common with suprarenal than infrarenal aortic clamping. Pharmacologic interventions to prevent renal failure include the administration of mannitol (0.5 g/kg) or furosemide (prior to cross clamping), and fenoldopam or low-dose dopamine (after release of cross clamp). None, however, have been shown to decrease the risk of renal failure. Other interventions include limiting cross clamp time, mild hypothermia (infusion of 4 °C Ringer lactate), and adequate hydration and maintaining adequate perfusion pressure (avoid hypotension).

Paraplegia secondary to spinal cord ischemia is a major concern after thoracic aortic repair. Long cross clamping times associated with interruption of blood flow or hypoperfusion from the anterior spinal artery leads to spinal cord ischemia. There is loss of motor and pin-prick sensation, but preservation of vibration and proprioception. Spinal cord ischemia may be prevented by monitoring somatosensory and motor evoked potentials. Methods to decrease the incidence of paraplegia are extracorporeal circulation, use of heparin-coated shunts, placement of CSF lumbar drain, administration of methylprednisolone and mannitol, mild hypothermia, and decreased cross clamping time.

Endovascular stent grafting is an alternative to open aortic repair. With the development of new graft material and technology, almost any portion of the aorta can be stented. The aorta is typically accessed through a femoral or iliac artery. Under fluoroscopy, the diseased portion of the aorta is identified, surround vascular branches are mapped, and the graft deployed. Once in place, the graft is assessed for leak or rupture. As compared to open aortic repair, endovascular aortic repair is associated with decreased blood loss, fluid shifts, and cardiac, renal, and pulmonary morbidity. It also decreases the length of ICU and hospital stay. Although short-term outcome may be improved, on 1-year follow-up, there is no significant difference in outcomes.

Other than standard ASA monitors, a large-bore intravenous line, and an arterial catheter, is usually placed for continuous measurement of blood pressure and laboratory analysis. General, regional (spinal, epidural, or combined), or local anesthesia can be used for endovascular aortic repair. The choice usually depends on the patient, surgeon, or anesthesiologist. Vasoactive medications and blood products should be readily available. Complications of endovascular aortic repair are listed in Table 27.1. In the event of difficulty with repair, preparation and planning must be made for possible conversion to open aortic repair.

The carotid arteries supply blood flow to the anterior circulation of the brain, while the vertebral arteries supply blood flow to the posterior circulation of the brain. These two circulations communicate at the Circle of Willis via the posterior communicating arteries. The Circle of Willis functions as a source of collateral blood flow in the event of occlusion of one of its contributing branches.

Carotid stenosis results from progressive build-up of plaque in the wall of the carotid artery, the most common site being the origin of the internal carotid artery (Fig. 27.3). The deleterious nature of atheromatous plaque in the carotid artery is twofold. Firstly, progressive narrowing of the lumen restricts blood flow through the artery. Secondly, this area is a potential source for thromboembolism to the brain.