Management of Postoperative Arrhythmias

Management of Postoperative Arrhythmias Robert W Rho) Charles R. Bridges) and Dusan Kocovic Arrhythmias occur commonly in patients after cardiac surgery. Atrial fibrillation is the most common arrhythmia in the postoperative period; it accounts for significant morbidity to the patient and prolonged hospital stays, and it contributes significantly to the cost of hospitalization. It occurs more commonly in elderly men and in patients undergoing valvular procedures. Beta blockers are effective agents that keep patients from developing postoperative atrial fibrillation and help maintain ventricular rate control. Prophylaxis with antiarrhythmic agents such as amiodarone and sotalol and recently with atrial pacing have shown promise in recent randomized trials. Patients with atrial fibrillation that persists for longer than 48 hours appear to be at a greater risk for cerebroembolic events and should receive anticoagulation unless a contraindication exists. Although frequent premature ventricular contractions and nonsustained ventricular tachycardia (NSVT) occur frequently in patients after cardiac surgery, sustained ventricular tachycardia and ventricular fibrillation are rare and are associated with a poor prognosis. Polymorphic ventricular tachycardia may occur in the setting of myocardial ischemia, metabolic disturbances, and drug toxicities (including antiarrhythmic agents used to treat atrial fibrillation). Poor left ventricular function is a potent risk factor for sudden death in patients with NSVT. Patients with persistent NSVT and ischemic cardiomyopathy with left ventricular ejection fractions of less than 40% should undergo electrophysiologic testing. Conduction abnormalities that may be encountered in patients after cardiac surgery are rarely life threatening. Patients who have undergone valve replacement or repair are at higher risk of developing significant bradyarrhythmias that may require temporary pacing. Copyright © 2000 by W.H. Saunders Company Key words: Atrial fibrillation, atrial flutter, ventricular tachycardia, coronary artery bypass graft, conduction abnormality, pacemaker.

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ardiac arrhythmias are a frequently encountered complication of cardiac surgery and contribute significantly to the morbidity and mortality of postoperative cardiac patients. Atrial fibrillation is the most frequent arrhythmia encountered in the early postoperative period, occurring in up to 30% of patients after coronary artery bypass (CABG) surgery. Bradyarrhythmias are frequently encountered after valvular surgery and may necessitate temporary or permanent pacemaker therapy. Although ventricular ectopy and nonsustained ventricular tachycardia are frequently seen postoperatively, sustained ventricular arrhythmias are relatively uncommon after coronary bypass or valvular surgery. Sustained ventricular arrhythmias after cardiac surgery are associFrom the Division qfCardiovascular Medicine, Hospital qfthe University qfPennsylvania, Philadelphia, PA. Address reprint requests to Dusan Kocovic, MD, Associate Profossor qf Medicine, Division qfCardiovascular Medicine, Hospital qfthe Universi~)' qf Pennsylvania, 3400 Spruce St, 9 Founders, CardioMscular Division, Philadelphia, PA 19104. E-mail: [email protected]. COjJyright © 2000 ~Y WE. Saunders Company 1043-0679/00/1204-0014$10.00/0 doi:10.1053/stcs.2000.21117

ated with a poor prognosis. Despite advancements in surgical technique and anesthesia and changes in methods of myocardial protection, the incidence of arrhythmias postoperatively has not changed significantly. This article addresses the epidemiology, pathogenesis, diagnosis, and treatment of arrhythmias encountered in the postoperative period after cardiac surgery.

Atrial Fibrillation and Atrial Flutter Epidemiology Atrial fibrillation is the most common arrhythmia encountered in the early postoperative period. It occurs in up to 30% of patients after coronary bypass surgeryl-5 and in up to 64% of patients after valvular surgery.6 Among patients undergoing valvular surgery, patients with mitral valve operations and with postoperative pericardial effusions are more likely to have a postoperative course complicated by atrial fibrillation.6-7 The peak incidence of atrial fibrillation occurs on the second or third postoperative day.2,3 The incidence of atrial flutter postoperatively is not well established. Studies of atrial flutter often

Seminars in Thoracic and Cardiovascular Surgery, Vol 12, No 4 (October), 2000: pp 349-361

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combine atrial flutter with atrial fibrillation because of their clinical similarities and because the two arrhythmias often coexist within the same patient. Atrial flutter may represent up to one third of atrial arrhythmias postoperatively.8 Although postoperative atrial fibrillation is often transient and benign, it may be associated with more serious consequences including stroke, myocardial ischemia, congestive heart failure, and hemodynamic collapse. Furthermore, the presence of atrial fibrillation contributes significantly to length of intensive care unit stay, total duration of hospitalization, and health care expenditures.3,4 Many investigators have studied clinical risk factors identifying patients who are at high risk for developing atrial fibrillation postoperatively. The most consistent risk factor in these studies is age. I -5 This is not surprising, because advanced age is a potent risk factor for atrial fibrillation in the general population. 9 Zaman et al 2 reported that only 1 in 29 patients (3.4%) aged 50 to 54 years developed atrial fibrillation versus 19 in 45 patients (42.2%) aged 70 to 74 years. The odds of developing atrial fibrillation increased 1.48-fold (95% confidence interval [CI], 1.24-1.77) for each 5-year increase in age and 3.8-fold (95% CI, 2.00-7.23) for those aged over 60 years compared with patients less than 60 years of age. 2 Similarly, Mathew et al4 reported a 24% increase in the odds of developing postoperative atrial fibrillation for every 5-year increase in age. 4 Atrial dilatation, fibrosis, and the loss of side-to-side electrical coupling between myocytes have been associated with increased age and result in slowing of atrial conduction and nonuniform anisotropic conduction. These alterations in the electrophysiologic properties may predispose the aged heart to atrial arrhythmias. 2,4,10 Efforts to identify preoperative clinical variables other than age have yielded conflicting results. A prior history of atrial fibrillation, postoperative use of beta blockers (a negative risk factor), beta-blocker withdrawal, signal-averaged P wave duration (SAPD) (greater than 155 ms), male sex, and concomitant valvular heart disease are factors that appear to have the most consistent association with postoperative atrial fibrillation. 2-4.6.11 Zaman et al reported an overall incidence of postoperative atrial fibrillation in 28.2% of 326 patients undergoing coronary artery bypass surgery. In a stepwise logistic regression analysis of preoperative variables, SAPD of greater than 155 was also an independent risk factor (odds ratio [OR], 5.37; 95% CI, 3.1-9.3). SAPD greater than

155 ms had a positive predictive accuracy of 49% but a negative predictive accuracy of 89%. Age and male sex were also independent risk factors for postoperative atrial fibrillation in this study.2 Mathew et al4 reported an overall incidence of postoperative atrial fibrillation of 27% in a large multicenter population of 2,417 patients undergoing coronary artery bypass with or without concomitant valvular surgery. (Of these patients, 90% underwent CABG and 10% underwent CABG combined with valvular surgery). Independent predictors of postoperative atrial fibrillation included advanced age (OR, 1.24 per 5-year increase in age; 95% CI, 1.18-1.31), male sex (OR, 1.59; 95% CI, 1.09-1.81); prior history of atrial fibrillation (OR, 2.28; 95% CI, 1.74-3.00), and a history of congestive heart failure (OR, 1.31; 95% CI, 1.041.64). Neither ejection fraction nor left ventricular end diastolic pressures were predictive of atrial fibrillation in this study."' Other studies have also shown no association between elevated left ventricular end diastolic function and decreased ejection fraction and postoperative atrial fibrillation. 1,5 Several studies have shown that beta blockers, when administered before or immediately after surgery, are effective for preventing atrial fibrillation. Beta-blocker withdrawal has been associated with a significant increase in the incidence of postoperative atrial tachyarrhythmias. 12,13 Postoperative atrial fibrillation and atrial flutter are usually temporary problems that resolve without the need for antiarrhythmic medications or direct current cardioversion. Episodes are usually paroxysmal and recurrent, and in patients without a prior history of atrial fibrillation or atrial flutter, they rarely last beyond 4 to 6 weeks. Despite improvement in surgical technique, anesthesia, and myocardial protection during cardiopulmonary bypass, the incidence of these arrhythmias may be increasing,3 which may in part be caused by the increasing age of patients undergoing cardiac procedures.

Pathogenesis Atrial fibrillation is thought to occur as the result of multiple wavelets wandering through the atrial myocardium around functional and anatomic barriers. Enlarged atria, slow conduction, short refractory periods, and anisotropic atrial tissue (nonuniformities in refractoriness and/or conduction velocities) favor the propagation of multiple wavelets manifesting clinically as atrial fibrillation. 14,15 Atrial flutter is thought to occur as a result of a single macro-reentry circuit, which usually involves the tricuspid

Management ofPostoperative Arrhythmias

annulus, the cristae terminalis, and the eustachian ridge as anatomic barriers to conduction. 16-19 Conditions favoring atrial fibrillation postoperatively are multiple and include the presence of circulating catecholamines, autonomic imbalance, electrolyte abnormalities, pericardial inflammation, inadequate atrial protection from cardioplegia during bypass, and atrial enlargement from volume overload and impaired hemodynamics encountered in the postoperative period.

Diagnosis Most cases of atrial fibrillation are easily diagnosed by the surface 12-lead electrocardiogram. Atrial fibrillation is characterized by an irregularly irregular rhythm and a lack of organized P waves. At times atrial fibrillation can appear well organized in lead Vb giving the appearance of flutter waves and leading clinicians to mistakenly diagnose the rhythm as atrial flutter. Atrial flutter is characterized by an undulating saw-tooth pattern in the inferior leads (leads II, III, and aVF). Absence of flutter waves in the inferior leads make the diagnosis of atrial flutter unlikely. The rate of the flutter waves is usually 300 bpm. In the postoperative setting, the atrioventricular (AV) node usually conducts 2: 1 to the ventricle, and therefore the ventricular rate is usually 150 bpm in atrial flutter. Atrial flutter is the most likely arrhythmia when a narrow complex regular tachyarrhythmia with a rate of 150 bpm is encountered (Fig 1).

Prophylaxis Beta blockers. Several randomized studies have reported a beneficial effect of beta blockers on the prevention of atrial fibrillation after CABG.12,13,20 Furthermore, withdrawal of beta blockers in patients going for cardiac surgery is associated with an increased risk of postoperative atrial fibrillation. 13,21 Because of the preponderance of evidence supporting the efficacy of beta blockers, all patients without contraindication to beta-blocking agents should be placed on beta-blocking agents before cardiac surgery. Patients who have been on beta-blocking agents previously should remain on beta blockade throughout the postoperative course. Magnesium supplementation. Hypomagnesemia occurs commonly after CABG surgery. Hypomagnesemia in patients post-CABG surgery is associated with a higher incidence of supraventricular arrhythmias. 22 Magnesium levels should be checked in the

351

early postoperative period and serum levels should be maintained above 2.0 mEq/dL. Antiarrhythmic drugs. Amiodarone has recently been shown to be effective in the prophylaxis of postoperative atrial fibrillation. In a double-blind, randomized study of 124 patients treated with amiodarone (64 patients) versus placebo (60 patients), Daoud et al 23 reported that 25% of patients treated with amiodarone developed atrial fibrillation versus 53% of patients treated with placebo (P = .003). There were no adverse events in patients treated with amiodarone, and there was a significant reduction in hospitalization cost for patients treated with amiodarone. There were more patients treated with beta blockers in the amiodarone group (26/64 versus 18/60 patients), and patients treated with amiodarone were younger (57 versus 61 years of age) in this study.23 Guarnieri et aF4 reported in a randomized, double-blind study of intravenous amiodarone versus placebo (amiodarone given immediately postoperatively at 1 g/d for 2 days) that atrial fibrillation occurred in 47% of the placebo group and 35% of the amiodarone-treated group (P = .01). The length of hospital stay was not reduced by amiodarone therapy.24 Sotalol has been shown in several studies to lower the incidence of atrial fibrillation in postoperative CABG patients. 25 ,26 Gomes et aF6 randomly selected 85 patients to receive either sotalol or a placebo. Patients treated with sotalol had a 12.5% incidence of atrial fibrillation versus 38% incidence in the placebo group; however, more patients underwent valve surgery in the placebo group (18% versus 10%). There were no torsades de pointes or change in duration of hospital stay in this small study.26 In patients who are at high risk for developing atrial fibrillation or are known to be unable to tolerate atrial fibrillation hemodynamically, prophylactic therapy with amiodarone or sotal01 may be a reasonable option. Atrial pacing. Atrial pacing may exert its antiarrhythmic effect by preventing bradycardia and irregular heart rates, suppressing atrial premature beats, promoting more uniform tissue repolarization, and, in the case of multi site pacing, preventing asynchronous and nonuniform activation that may promote areas of functional block and set up a substrate for functional reentry.v Several studies have recently been published evaluating atrial pacing alone or with adjunctive betablocker therapy, pacing sites (right-atrial versus biatrial pacing), and dynamic overdrive pacing (focusing on optimized suppression of premature atrial contrac-

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Figure 1. (A)Atrial fibrillation with organized atrial activation in lead Vi. Note the lack of organization in the inferior leads (ill, aVF). This arrhythmia could be mistaken for atrial flutter and antitachycardia pacing would not be successful. (B) Atrial flutter with 2-to-l conduction. Note the organized saw-tooth pattern in the inferior leads. Antitachycardia pacing may be successful in cardioverting this arrhythmia to sinus rhythm.

tions) . Gerstenfeld et aI28 reported no difference in atrial pacing alone in 61 patients randomized to no pacing, right-atrial pacing, and biatrial pacing. However, in patients treated with beta blockers, the

incidence of atrial fibrillation in the paced groups was significantly less than that of the control group. There was no significant difference between rightatrial pacing and biatrial pacing in this study. Green-

Management qfPostoperative Arrh)·thmias

berg et aF9 randomized 154 patients into 4 groups: (1) control group with no atrial pacing, (2) rightatrial pacing, (3) left-atrial pacing, and (4) biatrial pacing. Atrial fibrillation occurred in 37% of the control group and in 17% of the paced group (P = .005). There was no significant difference between right-atrial, left -atrial, or biatrial pacing in this study.29 Monitoring of the effectiveness of left-atrial pacing was not rigorously performed in these two studies. Fan et apo randomized 132 patients after CABG surgery into 4 groups: (1) biatrial pacing, (2) leftatrial pacing, (3) right-atrial pacing, or (4) no pacing. Patients were paced for 5 days postoperatively and daily pacing and sensing thresholds of each lead were assessed. The incidence of postoperative atrial fibrillation was significantly reduced in the biatrial pacing group (12.5%) when compared with the other 3 groups (left-atrial pacing, 35.4%; right-atrial pacing, 33.3%; no pacing, 41.9% [P < .05]). Pwave dispersion was also significantly reduced in the biatrial pacing group.30 Daoud et aPl randomized 118 patients who underwent CABG, valvular surgery, or both into 3 groups: (1) right-atrial pacing at 45 bpm (RA-AAI), (2) right-atrial triggered pacing at a rate of more than 85 bpm (RA-AAT), and (3) biatrial triggered pacing at a rate of more than 85 bpm (Bi-AAT). Biatrial pacing had a significant reduction in postoperative atrial fibrillation (10%) when compared with the RA-AAT group (32%; P = .01) and the RA-AAI group (28%; P = .02). There was no difference between the RA-AAT group versus the RA-AAI group (P = .8).31 Levy et aP2 randomized 130 patients to either biatrial pacing (80 bpm for 4 days) or no pacing. They reported a significant reduction in atrial fibrillation (duration of more than 1 hour) with biatrial pacing (13.8%) versus no pacing (38.5%) (P = .001). Spencer et al33 prospectively randomized patients with a history of paroxysmal atrial fibrillation and an indication for a permanent pacemaker into conventional high right-atrial pacing versus Bachmann's bundle pacing. Bachmann's bundle pacing significantly reduced the P wave duration compared with high right-atrial pacing (123 ± 18 ms versus 160 ± 28 ms;P < .05) and was associated with a lower incidence of atrial fibrillation at 12 months (21% versus 41%) (P = .004).33

Management The goals of treatment of atrial fibrillation and atrial flutter are (1) to control ventricular rate, (2) to convert and maintain sinus rhythm, and (3) to prevent thromboembolic complications. The best approach to the management of patients with postoperative

353

atrial fibrillation is tailored to the individual patient. Initial assessment of the patient should include (1) the patient's hemodynamics, (2) the patient's symptoms, (3) the ventricular rate, (4) the electrocardiogram for evidence of ischemia, and (5) the duration of atrial fibrillation. In patients who are clinically stable, rate control is the first priority. Beta blockers are the first choice of therapy in the postoperative setting unless a contraindication exists (severe reactive airway disease). If the patient has a contraindication to beta blockers, diltiazem, verapamil, and digitalis may be used as alternatives. Digitalis is a poor single choice for rate control, because circulating catecholamines may easily overwhelm its vagotonic effects on the AV node. In patients who have persistent atrial fibrillation or frequent recurrence of atrial fibrillation for greater than 48 hours duration, an antiarrhythmic agent may be considered (usually procainamide or amiodarone) and anticoagulation should be started. Because most cases of atrial fibrillation are self limited and rarely last beyond 4 to 6 weeks, antiarrhythmics and anticoagulation can usually be stopped after I to 2 months of therapy. In patients with atrial flutter for whom atrial pacing is readily available (existing dual-chamber pacemaker or an atrial epicardial lead), rapid atrial pacing may be used to terminate atrial flutter. 16,34-39 This procedure is performed by pacing at a slightly shorter pacing interval than the flutter rate. Overdrive pacing is attractive because it causes little discomfort to the patient, but it is limited in its modest efficacy, and furthermore, atrial fibrillation may be induced in up to 70% of patients. 36.38 Improvement in cardioversion efficacy with significant reduction in the induction of atrial fibrillation can be achieved with the addition of a class IA antiarrhythmic agent before atrial overdrive pacing. The efficacy of combination therapy is reported to be approximately 70% to 100%.35,36,39 The majority of patients in atrial flutter with hemodynamic embarrassment will ultimately require direct-current cardioversion. Direct-current cardioversion may only provide transient benefit in the postoperative setting, and adjunctive treatment with an antiarrhythmic agent may be necessary to sustain sinus rhythm. In patients with persistent atrial fibrillation or frequent paroxysms of atrial fibrillation despite betablocker therapy, an antiarrhythmic drug is often initiated with the intention of cardioverting and maintaining patients in sinus rhythm. Currently there are no large randomized clinical trials that provide guidance as to most efficacious antiarrhyth-

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mic agent in the postoperative CABG patient. Common antiarrhythmic agents used in patients with postoperative atrial fibrillation include procainamide and amiodarone. In patients who are completely revascularized and have normal ejection fractions, intravenous sotalol and propafenone have also been used. (Intravenous formulations currently are not available in the United States.)40·41 Ibutilide fumarate was tested in a randomized fashion in 302 patients with atrial fibrillation or flutter occurring 1 to 7 days after cardiac surgery. Ibutilide (1.0 mg intravenously) resulted in a significantly higher conversion rate when compared with placebo (57% versus 15%; P = .0001). The conversion efficacy was much higher with atrial flutter than with atrial fibrillation. Patients who received ibutilide had a higher incidence of polymorphic ventricular tachycardia (1.8%) when compared with those who received placebo (1.2%).~2 Embolic stroke is a well-known complication of atrial fibrillation. Patients with left-ventricular dysfunction, a prior history of thromboembolism, and hypertension are at greater risk of thromboembolic stroke. There is convincing evidence that atrial fibrillation is associated with post-CABG cerebroembolic stroke. Creswell et all reported that patients with

postoperative atrial fibrillation had a 3.3% incidence of stroke versus a 1.4% incidence in patients without postoperative atrial fibrillation (P < .0005). Taylor et al43 reported a significantly higher incidence of atrial fibrillation in patients who suffered strokes or transient ischemic attacks than in patients who did not have a neurologic event (60% versus 18%, P < .005%). In a similar study, Reed et al44 reported that 54% of patients who suffered post-CABG stroke had atrial fibrillation versus 28% of patients without neurologic events. The OR for stroke in patients with atrial fibrillation was 3.0 (95% CI, 1.4-6.7). Patients in whom atrial fibrillation persists for longer than 48 hours should be anticoagulated with heparin unless a contraindication to heparin anticoagulation exists (Fig 2). Atrial flutter is usually managed similarly to atrial fibrillation; however, there are some important management considerations that are unique to atrial flutter. In atrial flutter, rapid atrial pacing may be efficacious in terminating the arrhythmia, especially when combined with a class IA antiarrhythmic agent. Antiarrhythmic drugs should be used with caution in atrial flutter because sufficient slowing of the flutter rate may result in I: I conduction across the AV node, which is already capable of more rapid conduction

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Management ifPostoperative Arrhythmias

because of circulating catecholamines in the postoperative setting. This tachyarrhythmia is usually not hemodynamically tolerated and may degenerate into ventricular fibrillation. It is important that patients treated with antiarrhythmic therapy be placed on medications that will sufficiently slow AV conduction (eg, beta blockers, calcium channel blockers, digoxin).

Ventricular Tachyarrhythmias Epidemiology Sustained ventricular tachycardia (VT) and ventricular fibrillation (VF) occur infrequently after CABG and are associated with a significant mortality rate. 45 Topol et al46 reported an incidence ofVT and/or VF in 0.7% of patients (12/1675) after CABG. Ten of the 12 patients (83%) had a prior myocardial infarction. Three of the 12 patients (25%) had documented graft closure. At 11 ± 4 months follow-up time, 2 patients died and 4 patients had implantable cardiac defibrillators. Kron et al47 reported an incidence ofVT or VF of 1.4% of patients (18/1251) during the first 6 weeks after open heart surgery. The event occurred within the first 48 hours in 72% of patients (13/18). They reported an overall mortality rate of 44% (8/18) among patients with postoperative VT or VF. Steinberg et al48 reported an incidence of new-onset sustained VT in 3.1% of patients (12/382) after CABG. Only lout of 12 patients had a perioperative myocardial infarction. The in-hospital mortality rate was 25%. Patients who developed VT were more likely to have prior myocardial infarction (92% v 50%, P < .01), severe congestive heart failure (56% v 21 %, P < .01), and an ejection fraction below 0.40 (70% v 29%, P < .01), a bypass graft across a noncollateralized occluded vessel (1.5 v 0.42,P < .01), and a bypass graft across a noncollateralized occluded vessel to an infarct zone (1.5 v 0.17, P < .01). Thus, sustained VT and VF after CABG surgery occurs in 0.7% to 3.1 % of patients and is associated with a high mortality rate. Patients who have had reperfusion to a chronic infarct zone and depressed left-ventricular function with congestive heart failure appear to be at greatest risk of developing VT/YF postoperatively. Cardiac ischemia is an important cause ofVT/YF. 49 Single ventricular premature depolarizations (VPDs) and nonsustained ventricular tachycardia (NSVT, defined as 3 or more VPDs in succession with no associated hemodynamic instability) occur frequently after CABG surgery. NSVT has been reported in 17% to 58% of post-CABG patients. 50,51 Single VPDs and NSVT that occur early in the postoperative period are rarely associated with sustained

355

VT or sudden death. Patients with NSVT that persists postoperatively and a left ventricular ejection fraction of less than 0.40 are at higher risk of sudden death. 52

Pathogenesis Postoperative ventricular tachyarrhythmias that occur in the first few days after cardiac surgery are often provoked by a number of predisposing conditions. These include electrolyte abnormalities such as hypokalemia and hypomagnesemia, metabolic acidosis, drugs such as sympathomimetics, antiarrhythmics used to treat other arrhythmias (atrial fibrillation), perioperative ischemia, and low cardiac output states. 46.47 ,49-51 Treatment and removal of these underlying factors often eliminate further recurrences of ventricular tachyarrhythmias. Myocardial ischemia is an important cause of postoperative sustained VT and VF.49 VF/polymorphic VT is more indicative of ischemia, and the possibility of graft spasm or thrombosis should be carefully investigated. Kron et al47 reported that 4 of 6 patients (66%) with postoperative VF had an acute ischemic event. Topol et al46 identified at least one occluded vein graft in 3 of 12 patients (25%) who developed VT or VF after CABG surgery. Many patients who have undergone CABG surgery have had prior infarcts that may predispose them to ventricular arrhythmias. The underlying mechanism of monomorphic VT is re-entry that involves a fixed substrate consisting of normal myocardium interspersed with islands of poorly conducting fibrotic scar. Because the substrate is fixed and conduction velocity is constant, the morphology of the VT is uniform and the rate is relatively stable.

Diagnosis In patients who tolerate the arrhythmia hemodynamically, the diagnosis ofVT/YF is made by the surface 12-lead electrocardiogram. On the 12-lead surface electrocardiogram, features with the greatest specificity for VT include atrioventricular dissociation, positive QRS concordance, axis less than 90° to ± 180°, a QRS duration of more than 160 ms with a left bundle branch block (LBBB) pattern in Vb and a QRS duration of more than 140 ms with a right bundle branch block (RBBB) pattern in VI' The presence of fusion beats and capture beats also support the presence ofVT53 (Fig 3).

Management Few systematic data are available to define the optimal management of VT/polymorphic VT in the

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postoperative setting. Because polymorphic vr is more indicative of ischemia, acute graft occlusion should be considered and ruled out. Acute treatment of this arrhythmia includes direct current cardioversion, intravenous lidocaine, and a quick and thorough assessment and correction of underlying metabolic or electrolyte abnormalities and drug toxicities. Patients with sustained vr should be cardioverted and considered for an implantable cardiac defibrillator with adjunctive antiarrhythmic therapy (amiodarone) if frequent bouts of the vr are encountered. Patients with frequent premature ventricular contractions require no further therapy than elimination of precipitating factors. In a similar fashion, NSvr in patients with normal left-ventricular function also requires no specific treatment. Patients with NSvr and ischemic cardiomyopathies with a left-ventricular ejection fraction of less than 0.40 and inducible sustained monomorphic vrwith programmed stimulation are considered to be at an increased risk for sudden death. The MUSTT (Multicenter Unsustained Iachycardia Irial) trial showed the superiority of implantable cardioverter defibrillator (ICD) implantation to antiarrhythmic drug therapy as measured in 5-year mortality (24% v 55%, P < .00 I) in this population of patients. 52 It is not clear how soon after CABG surgery electrophysiologic testing should be performed, because many of these arrhythmias disappear with reversal of the postoperative factors promoting the arrhythmias. The MUSTT trial excluded patients who had NSvr only within 4 days of CABG surgery. Patients who survive the initial sustained vrm episode and have no identifiable predisposing condition, regardless of left-ventricular function, should probably be treated aggressively with electrophysiologic study and consideration of an implantable defibrillator. Recurrent sustained vr and VF are associated with a poor prognosis after CABG surgery. Patients with these conditions should be evaluated for ICD implantation. ICD implantation is contraindicated in patients with frequent recurrences of vrm. In patients with recurrent sustained vr that is hemodynamically stable, catheter ablation may be performed with a 70% success rate. Antiarrhythmic

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therapy serves an adjunctive role to ICD implantation in patients who can be adequately suppressed with antiarrhythmic therapy (Fig 4).

Conduction Disturbances Epidemiology Postoperative conduction disturbances have been reported in up to 60% of patients after CABG surgery. 54 The incidence of postoperative conduction abnormalities has increased but is not associated with increased mortality.55 The majority of conduction abnormalities seen after CABG surgery resolve spontaneously and rarely require implantation of a permanent pacemaker. 55,56 Common conduction defects seen postoperatively include complete bundle branch blocks, hemiblocks, various degrees of AV block, and sinus node dysfunction. The most frequent conduction abnormality encountered postoperatively is the presence of a new RBBB. Baerman et aI55 prospectively followed 93 consecutive patients undergoing CABG surgery. Forty-six patients (49%) had a new conduction defect postoperatively. The presence of RBBB was seen in 16 of 93 of patients (17%). Of these patients, 81 % had resolution of the RBBB at the time of hospital discharge. RBBB and left anterior hemiblock (IAHB) were seen in 14 of 93 of patients (15%). Of these patients, 38% had resolution of RBBB/LAHB at the time of discharge. LBBB was seen in 8 of 93 patients (9%), with 50% of these patients having resolution of the LBBB at hospital discharge. Third-degree AV block was seen in 4 of 93 patients (4%), with 25% of these 4 patients having resolution of third-degree AV block at the time of discharge. Cold blood cardioplegic solution was used in all patients in this series. Three of the patients with persistent third-degree heart block had a permanent pacemaker implanted. At 2 months follow-up, all 3 of these patients were no longer in AV block.55 In a retrospective study of 200 consecutive patients undergoing CABG surgery, Wexelman et al 57 reported new conduction abnormalities in 45 of200 patients (22.5%). Cold blood cardioplegic solution was used during cardiopulmonary bypass.

Figure 3. (A) Monomorphic ventricular tachycardia: The consistent beat-to-beat morphology in monomorphic ventricular tachycardia suggests a fixed substrate (a scar from a previous infarction) through which re-entry occurs. (B) Polymorphic ventricular tachycardia: Myocardial ischemia is a common cause of this arrhythmia, although electrolyte abnormalities, rewarming, acid-base disorders, and other metabolic factors may be culprits in the early postoperative period. (C) Nonsustained ventricular tachycardia is defined as 3 or more successive ventricular beats and less than 30 seconds of asymptomatic ventricular tachycardia.

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Lasting > 30seconds Symptoms or decreased BP

I. DC cardioversion I. Correct electrolytes I . DC cardioversion if there is 2. Aggressive ischemia workup 2. Rule out ischemia (EKG) hemodynamic compromise (consider cardiac catheterization) 3 Eliminate arrhythmogenic drugs 2. Start IV lidocaine or Amiodarone 3. Correct electrolytes drugs in . 4. Rule out Ischemia patients with a prolonged QT. 5. Eliminate arrhythmogenic drugs (ie: dopamine, epinephrine, etc.)

! ~~~~~:~:~:~~~:OgeniC :

If the arrhythmia persists:

1. Consider cardiac catheterization 2. EP evaluation depending on clinical situation.

1

Persistent

Clinical Follow-up

VT > 4 days·

"EF>4 EF t: 400/0 EP study +/-ICD

Figure 4. Proposed general algorithm for the management of postoperative ventricular tachycardia. (Based on the MUSTI trial. 52 )

The distribution of conduction abnormalities included RBBB (47%), RBBB/IAHB (8%), RBBB/firstdegree atrioventricular block (2%), LAHB (11 %), LBBB (18%), RBBB/lAHB/first-degree atrioventricular block (5%). At 14 months follow-up there was no difference in mortality in patients with conduction abnormalities versus those without.57 Chu et aP4 studied the incidence and prognostic effect of new perioperative ventricular conduction abnormalities in 913 patients undergoing CABG surgery. He reported an incidence of conduction abnormalities in 156/913 (17%) of patients. The development of conduction abnormalities, including isolated new LBBB, did not worsen the survival rate in patients followed up for 3 years after surgery. Conduction system disturbances are associated with the type of cardioplegic solution used. Gundry et aP8 reported that conduction disturbances occurred in 41 of 179 patients (23%) who received crystalloid cardioplegia versus 141 of 289 patients (49%) who received blood cardioplegia. Perioperative complete heart block requiring permanent pacemaker implantation occurred in 20 patients with crystalloid cardioplegia versus 67 patients with blood cardioplegia (P < .002). Lower concentrations of blood in blood

cardioplegia solution are associated with lower rates of conduction abnormalities. Gundry et aP8 reported that only 8 of 90 patients (9%) had conduction abnormalities with 2: I blood cardioplegic mixture versus 141 of 289 patients (49%) with 4:1 blood cardioplegia. More importantly, no patients had perioperative complete heart block in the 2: 1 cardioplegia group versus 67 of 289 (23%) in the 4: 1 blood cardioplegia group. The difference in conduction abnormalities are thought to occur as the result of high viscosity at low temperatures in blood cardioplegia. Conduction abnormalities occur more frequently in valvular surgery because of the proximity of the conduction system to the aortic and mitral valves. Moore et aP9 reported a 4% incidence of complete heart block in patients undergoing aortic valve replacement and a I % incidence of complete heart block in patients undergoing mitral valve replacement.

Management The decision to implant a permanent pacemaker is individualized for a given patient. There is no estab-

359

Management qfPostoperative Arrhythmias

Post operative Bradyarrhythmias

j

Stop all A V nodal drugs

Complete heart block or Symptomatic 2nd degree AVB Symptomatic sinus node dysfx

No

Yes

1

1

1

Clinical follow up

Epicardial pacing Temporary pacing wire Check daily thresholds

Persisting> 4-7 days?

Consider Permanent pacemaker (Majority of conduction abnormalities improve after coronary artery bypass surgery)

Figure 5. Proposed general algorithm for the management of postoperative bradyarrhythmias.

lished consensus on when the decision to implant a permanent pacemaker should be made. Patients in complete heart block should be managed initially with epicardial or transvenous temporary pacing. Drugs that suppress AV nodal function (digoxin, beta blockers, calcium channel blockers) should be discontinued. The patient's underlying rhythm should be checked daily until the fourth or fifth postoperative day. Patients with persistent AV block in the absence of medications slowing AV nodal conduction should be considered for permanent pacemaker implantation. The incidence of heart block after a prosthetic tricuspid valve replacement is unknown. Patients who have undergone tricuspid valve replacement should have epicardial leads placed intraoperatively because insertion of a endocardial lead through a prosthesis is contraindicated. Placement of a lead via the coronary sinus into a cardiac vein may be a viable option for these patients who become pacer dependent and an epicardial lead is not available (Fig 5).

Conclusion Arrhythmias occur commonly in patients after cardiac surgery. Atrial fibrillation is the most common arrhythmia in the postoperative period, and it accounts for significant morbidity to the patient and prolonged hospital stays and contributes significantly to the cost of hospitalization. It occurs more commonly in elderly men and in patients undergoing valvular procedures than in patients undergoing CABG alone. Beta blockers are effective agents as prophylaxis to keep patients from developing postoperative atrial fibrillation and in maintaining ventricular rate control. Prophylaxis with antiarrhythmic agents such as amiodarone and sotalol and, recently, with atrial pacing have shown promise in recent randomized trials. Patients with persistent atrial fibrillation for longer than 48 hours appear to be at a greater risk for cerebroembolic events and should receive anticoagulation unless a contraindication exists.

360

Rho, Bridges, and Kocovic

Although frequent premature ventricular contractions occurs frequently in patients after cardiac surgery, sustained ventricular tachycardia is rare and is associated with a poor prognosis. Polymorphic ventricular tachycardia may occur in the setting of myocardial ischemia, metabolic disturbances, and drug toxicities (including antiarrhythmic agents used to treat atrial fibrillation). Poor left ventricular function is a potent risk factor for sudden death in patients with NSVT. Patients with persistent NSVT and ischemic cardiomyopathy with left ventricular ejection fractions of less than 40% should undergo electrophysiologic testing. Conduction abnormalities may be encountered in patients after cardiac surgery and are rarely lifethreatening. Patients who have undergone valve replacement or repair are at higher risk of developing significant bradyarrhythmias, which may require temporary pacing. These patients may rarely require permanent pacemaker implantation before discharge from the hospital. The majority of conduction abnormalities encountered after cardiac surgery resolve spontaneously. The decision to implant a permanent pacemaker into patients with persistent heart block or sinus node dysfunction is made on an individual basis.

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