Thoracic Epidural Anesthesia as the Last Option for Treating Angina in a Patient Before Coronary Artery Bypass Surgery

Abstract

Ischemic cardiomyopathy in a patient with medically refractory unstable angina is a difficult clinical scenario. Unfavorable anatomy and/or comorbidity can prohibit the safe performance of angioplasty or coronary artery bypass (CAB) surgery. Thoracic epidural anesthesia (TEA) has been used successfully to stabilize patients with unstable angina refractory to maximum medical therapy [1]. TEA has also been used during and after CAB surgery in patients with preserved left ventricular function [2,3]. We describe a patient with intractable angina, poor ventricular function, and complicated comorbidities who received TEA for angina, later underwent CAB surgery using TEA in combination with general anesthesia, and continued to receive TEA for postoperative pain relief. Case Report A 68-yr-old man was transferred from another hospital with persistent angina at rest 4 days after a non-Q wave myocardial infarction. The patient had been treated with heparin, nitroglycerin, morphine, and metoprolol intravenously (IV) and aspirin by mouth without improvement from his anginal symptoms. His comorbidities included hypertension, peripheral vascular disease, a prior cerebrovascular accident with left-sided weakness, prior dual-chamber paced, dual-chamber sensed, dual-chamber response pacemaker implantation for complete heart block, hematuria, and acute tubular necrosis superimposed on chronic renal insufficiency. The patient underwent cardiac catheterization on admission, during which his blood pressure was 74/48 mm Hg, and his pulmonary capillary wedge pressure was 20 mm Hg. His electrocardiogram showed atrial and ventricular pacing at 80 bpm. Coronary angiography revealed a proximal 95% stenosis of the left anterior descending artery, a total occlusion of the circumflex artery at its midpoint with collateral filling by obtuse marginal branches, and a 40% occlusion of the right coronary artery. Transthoracic echocardiography showed global hypokinesis, anteroseptal dyskinesis, and inferior akinesis. His ejection fraction (EF) by multiple-uptake gated acquisition scan was 20%, and a resting thallium scintigraphy scan showed redistribution in the anterior and anteroseptal walls. His chest radiograph was significant for mild pulmonary edema. Abnormal laboratory values included a serum creatinine level of 5.7 mg/dL, a blood urea nitrogen level of 39 mg/dL, and red blood cells on urinalysis. The cardiac surgical service was consulted to consider CAB surgery. The operative risk was deemed prohibitively high and medical therapy was maximized with IV morphine, nitroglycerin, heparin, and atenolol, and with the use of intraaortic balloon pump counterpulsation. The patient's blood pressure improved to 98/60 mm Hg and remained stable over the next 3 days. However, his angina persisted, suggesting ongoing ischemia, and TEA was offered as a last therapeutic option. The patient was weaned from intraaortic balloon pump support, and the heparin infusion was stopped without a change in the patient's hemodynamic parameters or symptoms. Six hours after discontinuing the heparin infusion, an epidural catheter was placed at the T2-T3 level with the patient in the lateral decubitus position. The epidural space was identified via the midline approach and the catheter's position confirmed by the outline of a bolus of radioopaque dye into the epidural space. The catheter was tunneled for 6 cm under the skin to protect against displacement and lessen the chance of infection. Following catheter placement, a 5-mL bolus of 0.25% bupivacaine completely relieved the patient's angina. Arterial blood pressure and heart rate remained unchanged and IV nitrates and morphine were discontinued. Because the patient's angina recurred in between epidural catheter boluses, an infusion of 0.0625% bupivacaine with 100 micro g/mL of morphine was started at 4 mL/h. During the following 15 days, the patient remained pain free except on two occasions, in which "breakthrough" pain was treated with a bolus of 5 mL of 0.25% bupivacaine. Myocardial enzyme panels drawn after the episodes of breakthrough pain were within normal limits. Two weeks after admission, the acute tubular necrosis and hematuria had resolved and he was able to ambulate without pain. Four-vessel CAB surgery, with intraoperative and postoperative TEA, was planned for Day 16 of his admission. After induction of general anesthesia, an epidural infusion of 0.5% bupivacaine with 100 micro g/mL of morphine at 5 mL/h was started, supplemented by IV boluses of sufentanil and midazolam. The patient separated from cardiopulmonary bypass with 0.025 micro g [center dot] kg-1 [center dot] min-1 of epinephrine and 50 micro g/min of nitroglycerin. Hemodynamic parameters prebypass, during bypass, and postbypass were stable. On arrival in the intensive care unit, the concentration of bupivacaine was halved. The patient was tracheally extubated 18 h postoperatively. On postoperative Day 2, the bupivacaine concentration was halved again to 0.125% and continued until postoperative Day 5. The patient did not use any IV opioids postoperatively. He was discharged from the hospital 8 days after surgery. Discussion We describe a patient in whom TEA was the last therapeutic option available for stabilization prior to CAB surgery. TEA was continued with excellent intraoperative and postoperative clinical outcomes. Angina is mediated via sympathetic afferent nerve fibers, and thus a TEA-induced sympathectomy can be used to effectively treat this manifestation of myocardial ischemia [4,5]. There is concern that TEA may alleviate chest pain but mask ongoing myocardial ischemia. However, numerous animal and human studies have demonstrated the beneficial effects of TEA on the determinants of myocardial ischemia. Tsuchida et al. [6] demonstrated in dogs with experimentally induced ischemia that TEA attenuated the S-T segment elevation, the myocardial lactate production, and the decrease in subendocardial pH. Vikmo et al. [7] were able to reverse ischemic S-T segment changes from coronary occlusion in a canine model with TEA. Davis et al. [8] demonstrated improved regional endocardial perfusion and a smaller infarct using TEA in a dog model with experimentally induced ischemia. Klassen et al. [9] found that coronary blood flow during TEA was redistributed in favor of the endocardium in normal and ischemic dog hearts. Kock et al. [10] examined the effect of TEA on the determinants of myocardial oxygen supply and demand during exercise stress tests in patients receiving beta-adrenergic blockers. The same patients underwent two stress tests, the first without TEA and the second with TEA. The patients had larger EFs, fewer regional wall motion abnormalities, and less significant S-T segment depression during the exercise stress test with TEA than during the test without TEA. They also had lower rate-pressure products, lower systolic pressures, and lower diastolic pressures when receiving TEA during the test. Detrimental effects of TEA on myocardial supply may result from decreased preload if the sympathectomy extends beyond the distribution of the high thoracic dermatomes (T1-T5). For this reason, we ensure that the position of the epidural catheter tip is at the T1-T3 level with an epidurogram. There is also a report of S-T segment elevation occurring during thoracic surgery under TEA, which was attributed to coronary vasospasm from unopposed vagal tone [11]. Another concern is whether the coronary vasodilation resulting from the sympathectomy causes coronary steal. Blomberg et al. [4] measured an increase in the diameter of stenotic vessels during TEA, but no such dilation in the nonstenotic segments in humans. This response was limited to epicardial vessels. The use of thoracic epidural infusion for control of pain after an acute myocardial infarction is not without precedent. Toft and Jorgensen [12] used continuous TEA with 0.25% bupivacaine at an infusion rate of 6.1 mL/h to control pain in 14 patients for 12 to 42 h. We chose to continue epidural anesthesia during surgery because of the benefits from TEA on intraoperative hemodynamic parameters, postoperative recovery, and the stress response to surgery. Liem et al. [2] found that TEA during CAB surgery in patients with EFs more than 40% improved myocardial blood flow, decreased myocardial oxygen demand, and dilated stenosed arteries intraoperatively. This study also found more stable hemodynamic parameters during separation from bypass with TEA when compared with patients receiving general anesthesia alone. The intraoperative and postoperative stress response was decreased in the TEA group, as measured by a combination of plasma cortisol, norepinephrine, and epinephrine levels [13]. Postoperatively, patients in the TEA group were extubated sooner, had better visual analog scores for pain, and a lower incidence of tachycardia and myocardial ischemia [14]. Kirno et al. [15] confirmed these findings by showing that the addition of TEA to general anesthesia during CAB surgery in patients with EFs greater than 50% reduced the sympathetic stress response to sternotomy, as measured by plasma norepinephrine levels and hemodynamic parameters, when compared with general anesthesia alone. Epidural hematoma is an uncommon but potentially catastrophic complication of epidural catheter placement in patients undergoing systemic anticoagulation. Rao and El-Etr [16] found no epidural hematomas among 3164 patients who received epidural anesthesia and perioperative IV heparin for peripheral vascular surgery. Rough and Dougherty [17], however, noted seven spinal hematomas in 342 anticoagulated patients undergoing continuous spinal anesthesia and found that aspirin therapy, therapeutic anticoagulation within 1 hour of catheter insertion, and traumatic catheter insertion were risk factors for hematomas. Although our patient was taking aspirin throughout his stabilization period, Horlocker et al. [18] have determined the contribution of antiplatelet drugs to the risk of epidural hematoma to be minimal. We allowed this patient's partial thromboplastin time to normalize prior to catheter insertion and placed the catheter well in advance of the 24 h advocated in the literature [19] before systemic heparinization for cardiopulmonary bypass. The risk of infarction after stopping a heparin infusion, albeit temporarily, in patients with unstable angina is great and must be considered on a case-by-case basis. Our patient's symptoms did not worsen after heparin withdrawal and heparin was not restarted after catheter placement because TEA relieved the pain completely. Although we have no echocardiographic or other direct evidence that TEA improved his ischemic cardiomyopathy, normal myocardial enzyme panels obtained after initiating TEA and the complete relief of symptoms suggest there was no infarct progression. Our patient's intraoperative course was characterized by stable hemodynamic parameters with minimal inotropic or vasoactive drug support. He required no postoperative IV opioids for pain. We did not encounter evidence of decreased preload or coronary vasospasm during the course of TEA. Studies using bolus dosing of the epidural catheter at preset intervals have found that the dosing interval may be increased with time and that the pain-free interval outlasts the duration of drug effect [20]. Since we used a continuous infusion of local anesthetic in this patient, we cannot substantiate these findings. We find angina prophylaxis with a continuous infusion more effective than bolus administration in patients who become panicked at the onset of angina. We have not noted tachyphylaxis in patients who have had their infusions running continuously for up to 36 days, but this is undergoing further study. There is evidence that an alpha2-agonist-mediated sympathectomy may provide an alternative to TEA for protection from myocardial ischemia. Ellis and colleagues [21] found that clonidine premedication lessened intraoperative myocardial ischemia in noncardiac surgery, whereas Dorman et al. [22] found less S-T segment depression during the sternotomy to cross-clamp period in patients premedicated with clonidine for CAB surgery. The smooth operative course reported herein suggests that the benefits of TEA derived from studies of patients with preserved left ventricular function may be extrapolated to patients with lower EFs. This case further substantiates the role of TEA in the management of patients with severe ischemic heart disease. A close working relationship among cardiac anesthesiologists, cardiologists, and cardiothoracic surgeons is essential for success with this therapy.