Anesthetic Management

ANESTHETIC MANAGEMENT

Surgery on the Ascending Aorta

Surgery on the ascending aorta routinely uses median sternotomy and CPB. The conduct of anesthesia is similar to that for cardiac operations involving CPB, but the intraoperative course may be complicated by long aortic cross-clamp times and large intraoperative blood losses. TEE is espe-cially useful. Blood loss can be reduced by adminis-tration of ε-aminocaproic acid or tranexamic acid. Concomitant aortic valve replacement and coro-nary reimplantation are often necessary (Bentall procedure). The radial artery cannulation site should be guided by the possible need for clamp-ing of either the subclavian or innominate arteries during the procedure. Nicardipine or nitroprusside may be used for precise blood pressure control. β-Adrenergic blockade should also be employed inthe presence of an aortic dissection. On the other hand, bradycardia worsens aortic regurgitation and should be avoided. The arterial inflow cannula for CPB is placed in a femoral artery for patients with dissections. In the event that sternotomy may rup-ture an aneurysm, prior establishment of partial CPB (using the femoral artery and femoral vein) should be considered.

Surgery Involving the Aortic Arch

These procedures are usually performed through a median sternotomy with deep hypothermic circula-tory arrest (following institution of CPB). Additional considerations focus on achieving optimal cerebralprotection with systemic and topical hypother-mia (above). Hypothermia to 15°C, barbiturate or propofol infusion to maintain a flat EEG, methyl-prednisolone or dexamethasone, mannitol, and phe-nytoin are also commonly administered (but there is vanishingly small evidence for efficacy of these drug treatments). The necessarily long rewarming peri-ods probably contribute to the larger intraoperative blood losses commonly observed after CPB.

Surgery Involving the Descending Thoracic Aorta

Surgery limited to the descending thoracic aorta may be performed through a left thoracotomy without CPB, with or without (so-called “clamp-and–run” technique) a heparin-impregnated left ventricular apex to femoral artery shunt; or using partial right atrium to femoral artery bypass. A thoracoabdomi-nal incision is necessary for lesions that also involve the abdominal aorta. One-lung anesthesia greatly facilitates surgical exposure. Correct positioning of the endobronchial tube (even with fiberoptic bron-choscopy) may be difficult because of distortion of the anatomy. A right-sided double-lumen tube or a regular endotracheal tube with a bronchial blocker may be necessary.

The aorta must be cross-clamped above and below the lesion. Acute hypertension develops above the clamp, with hypotension below when there is no shunt or partial bypass. Arterial blood pressure should be monitored from the right radial artery, as clamping of the left subclavian artery may be necessary. The sudden increase in left ventricular afterload after application of the aortic crossclamp during aortic surgery may precipitate acute left ventricular failure and myocardial ischemia, particularly in patients with underlying ventricular dysfunction or coronary disease; it can also exacer-bate preexisting aortic regurgitation. Cardiac output falls and left ventricular end-diastolic pressure and volume rise. The magnitude of these changes is inversely related to ventricular function. These effects can be ameliorated by the use of shunting or partial bypass. Moreover, the adverse effects of aor-tic clamping become less pronounced the more dis-tal on the aorta that the clamp is applied. A vasodilator infusion is often needed to prevent excessive increases in blood pressure. In patients with good ventricular function, increasing anes-thetic depth just prior to cross-clamping may also be helpful.

Excessive intraoperative bleeding may occur during these procedures. Prophylaxis with anti-fibrinolytic agents may be helpful. A blood scav-enging device (cell saver) for autotransfusion is routinely used. Adequate venous access and intraop-erative monitoring are critical. Multiple large-bore (14-gauge) intravenous catheters (preferably with blood warmers) are useful. Pulmonary artery cath-eterization and intraoperative TEE are often used. The period of greatest hemodynamic instability fol-lows the release of the aortic cross-clamp; the abrupt decrease in afterload together with bleeding and the release of vasodilating acid metabolites from the ischemic lower body can precipitate severe systemic hypotension and less commonly hyperkalemia. Decreasing anesthetic depth, volume loading, and partial or slow release of the cross-clamp are helpful in avoiding severe hypotension. A bolus dose of a vasopressor may be necessary. Sodium bicarbonate is often used, particularly for persistent severe meta-bolic acidosis (pH < 7.20) in association with hypo-tension. Calcium chloride may be necessary when symptomatic hypocalcemia follows massive transfu-sion of citrated blood products.

A. Paraplegia

Spinal cord ischemia can complicate thoracic aortic cross-clamping. The incidence of transient post-operative deficits and postoperative paraplegia are 11% and 6%, respectively. Increased rates are asso-ciated with cross-clamping periods longer than 30 min, extensive surgical dissections, and emer-gency procedures. The classic deficit is an anterior spinal artery syndrome with loss of motor function and pinprick sensation but preservation of vibration and proprioception. Anatomic variations in spinal cord blood supply are responsible for the unpredict-able occurrence and variable nature of deficits. The spinal cord receives its blood supply from the ver-tebral arteries and from the thoracic and abdomi-nal aorta. One anterior and two posterior arteries descend along the cord. Intercostal arteries feed the anterior and posterior arteries in the upper thoracicaorta. Textbook descriptions suggest that in the lower thoracic and lumbar cord, the anterior spinal artery is supplied by the thoracolumbar artery of Adamkiewicz. The truth is that a single large feed-ing artery usually cannot be identified. When pres-ent, this artery has a variable origin from the aorta, arising between T5 and T8 in 15%, between T9 and T12 in 60%, and between L1 and L2 in 25% of indi-viduals; it nearly always arises on the left side. It may be damaged during surgical dissection or occluded by the aortic cross-clamping. Monitoring motor and somatosensory evoked potentials may be useful in preventing paraplegia, but clearly surgical technique and speed are most important.

As noted earlier, use of a temporary heparin-coated shunt or partial CPB with hypothermia maintains distal perfusion and decreases the inci-dence of paraplegia, hypertension, and ventricular failure. Partial CPB has the disadvantage of requir-ing heparinization, which increases blood loss. Using a heparin-coated shunt precludes the need for heparinization. It is usually positioned proximally in the left ventricular apex and distally in a femoral artery. Other therapeutic measures that may be pro-tective of the spinal cord include methylpredniso-lone, mild hypothermia, mannitol, and drainage of cerebrospinal fluid (CSF) to reduce the CSF pressure in the spine; magnesium is also protective in some animal models. The efficacy of mannitol appears to be related to its ability to lower CSF pressure by decreasing its production. Spinal cord perfusion pressure is mean arterial blood pressure minus CSF pressure; the rise in CSF pressure following experi-mental cross-clamping of the aorta may explain how a mannitol-induced decrease in CSF pressure could improve spinal cord perfusion pressure dur-ing cross-clamping. Any protective effect of drain-age of CSF via a lumbar catheter may have a similar mechanism.

The excessive use of vasodilators to control the hypertensive response to cross-clamping may be a contributing factor in spinal cord ischemia, as drug actions also occur distal to the cross-clamp. Excessive reduction in blood pressure above the cross-clamp should therefore be avoided to prevent inadequate blood flow and excessive hypotension below it.

B. Kidney Failure

An increased incidence of kidney failure following aortic surgery is reported after emergency proce-dures, prolonged cross-clamping periods, and pro-longed hypotension, particularly in patients with preexisting kidney disease. A variety of “cocktails” have been employed in the hope of reducing the risk of kidney failure, including infusion of manni-tol (0.5 g/kg) prior to cross-clamping, furosemide, fenoldopam (or low-dose dopamine), etc. Low (renal)-dose dopamine or fenoldopam will increase renal blood flow and may be used as an adjunct for a persistently low urinary output after the cross-clamp is released, however there is no convincing evidence that these treatments alter renal outcomes.

Surgery on the Abdominal Aorta

Stents are most often placed via catheters inserted in a femoral artery. When an open technique is chosen, either an anterior transperitoneal or an anterolat-eral retroperitoneal approach can be used to access the abdominal aorta. Depending on the location of the lesion, the cross-clamp can be applied to the supraceliac, suprarenal, or infrarenal aorta. Heparin is usually administered prior to aortic clamping. Intraarterial blood pressure can be monitored from either upper extremity. In general, the more distally the clamp is applied to the aorta, the less the effect on left ventricular afterload. In fact, occlusion of the infrarenal aorta frequently results in minimal hemo-dynamic changes. In contrast, release of the clamp usually produces hypotension; the same techniques that were described earlier (see above) may be used. The large incision and extensive retroperitoneal sur-gical dissection increase fluid requirements beyond intraoperative blood loss. We recommend colloid to maintain intravascular volume and crystalloid for maintenance fluids. Fluid replacement may be guided by monitoring central venous pressure, noninvasive monitors of stroke volume, or TEE. Pulmonary artery catheters are rarely used.

Renal prophylaxis with mannitol should be considered, particularly in patients with preexist-ing renal impairment. Clamping of the infrare-nal aorta has been shown to decrease renal blood flow, which may contribute to postoperative kid-ney failure. The decrease in renal blood flow is not prevented by epidural anesthesia or blockade of the renin–angiotensin system.

Some centers use continuous epidural anesthe-sia combined with general anesthesia for abdominal aortic surgery. This combined technique decreases the general anesthetic requirement and appears to suppress the release of stress hormones. It also pro-vides an excellent route for administering postop-erative epidural analgesia. Systemic heparinization during surgery introduces concern regarding the risk of paraplegia secondary to an epidural hematoma; however, all credible studies suggest that there when the catheter is placed well in advance of hepariniza-tion and removed after reversal of anticoagulation there is no increased risk of neuraxial hematomas as a consequence of epidural catheter placement.

Postoperative Considerations

Those undergoing stenting may not require intu-bation either during or after the procedure. Most patients undergoing open surgery on the ascend-ing aorta, the arch, or the thoracic aorta will remain intubated and ventilated for 1–24 h postoperatively. As with cardiac surgery, the initial emphasis in their postoperative care should be on hemodynamic sta-bility and monitoring for postoperative bleeding. Patients undergoing open abdominal aortic surgery may be extubated at the end of the procedure. These patients typically continue to require a marked increase in maintenance fluids for several hours postoperatively.