Epidural anesthesia and analgesia for coronary artery bypass graft surgery: still forbidden territory?

The application of epidural analgesia as an adjunct to general anesthesia continues to enjoy enthusiastic support among clinicians. Evidence of improved postoperative pulmonary function (1), favorable changes in bowel recovery after abdominal surgery (2,3), reduced hypercoagulability and graft thromboses after peripheral vascular surgery (4–6), and fewer thromboembolic complications after total joint arthroplasty (7), have reinforced the view that perioperative epidural neuraxial blockade not only provides superior analgesia (8), but also attenuates postoperative morbidity and mortality (9). The successful use of thoracic epidural analgesia/anesthesia (TEA) for the treatment of angina and ischemic heart disease (10–12) and the favorable results of improved analgesia when TEA is used after thoracotomy (1) have prompted investigations of TEA for cardiac surgery (13–15) with the expectation that cardiac sympathectomy and improved pulmonary function from enhanced analgesia will reduce the incidence of perioperative myocardial ischemia and infarction. Unfortunately, no studies of adequate size and statistical power have evaluated outcome when TEA is used during coronary artery bypass graft (CABG) surgery, nor has the fear of epidural hematoma formation and paraplegia subsided despite the absence of a single reported case of epidural hematoma after cardiac surgical procedures involving TEA (16). In this issue, Scott et al. (17) present the first randomized, prospective evaluation of the impact of perioperative TEA on outcome in a large series of patients undergoing CABG. In their unblinded analysis of 400 patients with normal ventricular function undergoing CABG, Scott et al. (17) assessed the postoperative impact of TEA using 0.5% bupivacaine and clonidine administered via thoracic epidural catheters placed immediately before surgery. Their results indicate a reduction in the incidence of supraventricular arrhythmias (SVA), postoperative confusion, lower respiratory tract infections, and renal failure in TEA-treated patients compared with a control group treated with a targetcontrolled postoperative infusion of alfentanil. In addition, they also observed that TEA-treated patients were more often extubated within 4 h of arrival in the intensive care unit. Several aspects of their study, as well as the controversial issue of TEA for cardiac surgery, merit scrutiny. The authors previously reported a similar effect of TEA on the incidence of SVA in a retrospective investigation of 218 patients undergoing CABG (18). Using a similar protocol in their current analysis of 418 patients, they chose the incidence of arrhythmias as the basis of their power analysis, estimating their study had a 90% power to detect a reduction in arrhythmias from 25% to 10%. The confirmation of fewer SVA with TEA is the most noteworthy and compelling (although not unexpected) finding of this report. Other investigators have reported lower catecholamine levels and slower heart rates after CABG in TEA-treated patients (14,19), a predictable consequence of cardiac sympathectomy. One confounding feature of Scott et al’s protocol is the inclusion of clonidine in the epidural infusion, since clonidine reduces sympathetic tone and heart rate (20,21). Although the epidural dose used (6–9 g/h) is less than previously reported IV doses (70 g/h) (20), the isolated impact of TEA with local anesthetic becomes less clear. In addition, postoperative -adrenoreceptor blockade significantly reduces the incidence of SVA after cardiac surgery (22), and it can be reasonably argued that perioperative administration of -adrenergic blocking drugs achieves the same outcome at less cost and with fewer serious risks than TEA. The second notable finding of this study was the reduced incidence of lower respiratory tract infections, a result attributed to improved analgesia and enhanced ventilatory function; the latter outcome was supported by greater inspiratory lung volumes in a subset of patients in the TEA versus Control groups (985 mL vs 733 mL, respectively). Although the voluntary nature of these measurements and the lack of blinded evaluators weaken the causal link between TEA and improved ventilatory function, they represent Department of Anesthesiology, Rush Medical College, RushPresbyterian-St. Luke’s Medical Center, Chicago, Illinois Accepted for publication May 4, 2001. Address correspondence to Christopher J. O’Connor, MD, Department of Anesthesiology, Rush Medical College, RushPresbyterian-St. Luke’s Medical Center, Chicago, IL 60612. Address e-mail to coconnor@rush.edu.