Cardiac surgery: Postoperative arrhythmias

Mina K. Chung, MD

Arrhythmias are common after surgery, particularly after cardiac surgery. Atrial brillation is the most common arrhythmia encountered postoperatively, although ventricular arrhythmias and conduction disturbances can also occur. Older age is the most consistent predictor of postoperative atrial arrhythmias. -adrenergic blockers, amiodarone, and sotalol are the most effective at preventing postoperative atrial brillation. Sustained ventricular arrhythmias in the recovery period after cardiac surgery warrant aggressive therapy, usually with an implantable cardioverter-debrillator in the absence of reversible causes. Postoperative, nonsustained ventricular tachycardia in the setting of left ventricular dysfunction and ischemic coronary disease also

usually warrants risk stratication and possible treatment, often with electrophysiologic testing and implantation of an implantable cardioverter-debrillator, if sustained ventricular arrhythmias are induced. Transient bradyarrhythmias may be managed with temporary pacing wires placed at surgery, but signicant and persistent atrioventricular block or sinus node dysfunction can occur and indicate a need for permanent pacing. (Crit Care Med 2000; 28[Suppl.]:N136 N144) KEY WORDS: cardiac surgery; atrial brillation; postoperative arrhythmias; ventricular arrhythmias; pacemakers; bradyarrhythmias; coronary artery bypass surgery

broad range of rhythm disturbances can occur after cardiac surgery. Atrial brillation is the most common arrhythmia occurring after cardiac operations. Ventricular arrhythmias are less frequent, and may be precipitated by transient metabolic disturbances or ischemia, but generally are managed in the same manner as in nonpostoperative situations. Bradyarrhythmias may require temporary or permanent pacing. The current understanding and management of tachy- and bradyarrhythmias occurring after cardiac surgery will be reviewed in this article.

TACHYARRHYTHMIAS Atrial Arrhythmias

Despite identication of risk factors and efforts to determine effective prophylactic agents, postoperative atrial arrhythmias remain a prominent clinical problem. Recent studies report incidences of atrial arrhythmias after coronary artery bypass graft surgery to be 17% to 33% (1, 2), and even higher after valvular surgery (1, 3). Atrial brillation

From The Cleveland Clinic Foundation, Department of Cardiology, Cleveland, OH. Address requests for reprints to: Mina K. Chung, MD, Department of Cardiology, Cleveland Clinic Foundation, 9500 Euclid Avenue, Desk F-15, Cleveland, OH 44195. E-mail: [email protected] Copyright 2000 by Lippincott Williams & Wilkins

is the most common arrhythmia after cardiac surgery. The peak incidence occurs on postoperative days 2 and 3. Hospital length of stay after coronary artery bypass graft surgery can be extended by 2 4 days with additional costs of several thousand dollars per patient (1, 4, 5). In addition, postoperative atrial brillation increases the risk of stroke (1, 6) and mortality (6) after cardiac surgery. Pathogenesis and Risk Factors. Patients undergoing cardiac surgery often have the substrate of atrial enlargement or elevation in atrial pressures that may predispose to atrial brillation. The propagation of multiple reentrant circuits during atrial brillation can be promoted by larger atrial sizes that can support multiple circuits. Focal sources that can initiate atrial brillation have been identied, particularly in patients with lone atrial brillation (in the absence of structural heart disease) (7). These foci most commonly arise from the pulmonary veins. It is conceivable that atrial stretch, hypertension, volume and electrolyte shifts, and heightened catecholamine states could potentially trigger these foci. The relative contributions of reentrant vs. focal mechanisms to postoperative atrial arrhythmias have not been established. Factors that contribute to the development of atrial brillation after cardiac surgery do support these pathophysiologic concepts. These factors include

acute atrial changes occurring at the time of surgery, such as acute atrial enlargement, ischemia and infarction, hypertension, trauma from cannulation, hypomagnesemia, inammation caused by pericarditis, cardiopulmonary bypass and cross-clamp times, pulmonary vein venting, and blocker withdrawal (1, 5, 8, 9). Clinically, the incidence of postoperative atrial brillation in patients undergoing coronary artery bypass graft surgery consistently increases with higher age (1, 2, 5). Age-related structural or electrophysiologic changes appear to lower the threshold for atrial brillation in the elderly. Other reported risk factors for postoperative atrial brillation have included chronic obstructive pulmonary disease, cardiomegaly, left atrial enlargement, type of cardioplegia, right coronary artery stenosis, and sinus nodal or atrioventricular (A-V) nodal artery disease (1, 2, 10). Preoperative use of -adrenergic blockers (1, 2, 5) and digoxin (1) have been studied, but results are not consistent. blocker withdrawal has also been associated with postoperative supraventricular arrhythmias (9). A state of heightened catecholamine effect occurs because chronic blocker use leads to a higher density of -adrenergic receptors. Because atrial brillation is most prevalent 23 days after surgery, inammatory mechanisms have also been proposed. Unfortunately, clinical criteria,
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such as pericardial rubs, electrocardiogram changes, fever, and pleuritic chest pain correlate poorly with postoperative pericarditis and supraventricular arrhythmias, although one study reported that 63% of patients with pericardial effusions had supraventricular arrhythmias, compared with 11% of patients without effusions (11). The role of magnesium remains controversial. Magnesium levels frequently fall after cardiac surgery and low serum levels correlate with episodes of postoperative arrhythmias. However, administration of magnesium in multiple studies have produced varying results, ranging from effectiveness to borderline or negative effects. Success may require documentation and achievement of adequate magnesium blood levels (8). Electrophysiologic or electrocardiographic variables have been examined to preoperatively identify patients at risk for developing supraventricular arrhythmias. These include preoperative P wave duration by standard electrocardiogram or signal-averaged electrocardiogram and use of electrical stimulation to evaluate preoperative inducibility of atrial brillation (12). These methods have moderate sensitivity and specicity, but are not currently in widespread use. Prophylaxis. Multiple agents tested for their efcacy in the prevention of postoperative atrial arrhythmias have been reviewed (13). Studies of digoxin have been mixed, and a meta-analysis showed no benet (14). However, multiple randomized studies have demonstrated the consistent prophylactic effectiveness of blockers, including propranolol, timolol, metoprolol, nadolol, and acebutolol. Two meta-analyses demonstrated overall a substantial reduction in postoperative supraventricular arrhythmias with postoperative use of blockers (14, 15). Nevertheless, blockers have often been used in only a limited manner, presumably because of fear of hemodynamic or pulmonary intolerance. Few adverse effects have been reported, although most trials excluded patients with signicant obstructive lung disease, A-V nodal block greater than rst degree, and impaired left ventricular function. Sotalol, a class III antiarrhythmic agent with blocker activity, has been effective in reducing postoperative supraventricular arrhythmias (16, 17) and may be more effective than standard blockers (18). Caution is warranted to avoid hemodynamic adverse effects assoCrit Care Med 2000 Vol. 28, No. 10 (Suppl.)

ciated with its -blocking activity. These effects may require temporary pacing or reduction or discontinuation of the drug, although only rare proarrhythmia has been reported. Amiodarone prevents postoperative atrial brillation (19 23). Regimens have included: 4.5 g iv during the rst four postoperative days (19); 15 mg/kg after removal of the aortic cross-clamp for 24 hrs, then 600 mg orally in three divided doses for 5 days (20); preoperative oral amiodarone given for a minimum of 7 days (mean dose, 4.6 g) followed by 200 mg/day until discharge (21), and 2 g orally divided over 1 4 days before surgery and 400 mg daily for 7 days after surgery (22). Use of intravenous regimens may be limited by cost. Although 2 g of iv amiodarone given over the rst 2 days after cardiac surgery reduced postoperative atrial brillation in one study, hospital stay was not reduced (23). Other agents tested for prophylaxis of atrial brillation after surgery include: verapamil, diltiazem, magnesium, and procainamide. Studies have yielded generally negative or inconclusive results or were small, although procainamide at therapeutic levels may be benecial (24, 25). Right atrial or biatrial overdrive pacing has variable effectiveness in preventing postoperative atrial brillation (5, 26 30). In one report, atrial pacing in the AAI mode may even cause an increase instead of suppression of frequent atrial premature depolarizations (28). However, atrial pacing may be more effective in patients treated with blockers (26, 29). There is no additional benet to right atrial pacing by alternative site or biatrial pacing (26, 29). At this time, we do not advocate the use of routine AAI atrial overdrive pacing to suppress atrial arrhythmias after cardiac surgery, but concomitant use with blockers, particularly with improved consistent overdrive pacing algorithms might be of benet. An algorithm we have used at the Cleveland Clinic Foundation for prophylaxis of atrial brillation after cardiac surgery is shown in Figure 1. Patients eligible for blocker prophylaxis are treated with metoprolol for 5 days, monitored for occurrence of supraventricular tachyarrhythmias or side effects, and then tapered off over 3 days. Prophylactic regimens including amiodarone are also used. Diagnosis and Treatment. Atrial brillation usually presents with an abrupt

change in rhythm with loss of P waves. Onset of atrial brillation in the postoperative period is likely to be symptomatic because it is often associated with rapid ventricular rates. The diagnosis of atrial brillation, utter, or other forms of supraventricular tachycardia can be conrmed by using atrial electrograms obtained from the temporary atrial epicardial pacing wires that are often placed routinely at the time of cardiac surgery. Although postoperative atrial brillation often is self-limiting, symptoms, hemodynamic compromise, and risk of thromboembolism usually justies intervention. Hemodynamic effects are inuenced by the ventricular rate, the ventricular function, and arrhythmia duration. Treatment of postoperative atrial brillation is similar to treatment of acute onset atrial brillation in other situations. A general approach and algorithm for treatment of postoperative atrial brillation is shown in Figure 2. Clinical instability, manifested by hypotension, ischemia, or congestive heart failure, should prompt immediate synchronized electrical cardioversion, usually beginning with 200 J of energy. Atrial overdrive pacing can be attempted if atrial utter is the dominant rhythm. In the absence of the need for urgent cardioversion, control of the ventricular rate becomes of primary concern. Table 1 shows dosing regimens commonly used for ventricular rate control of atrial brillation. The goal is to achieve a heart rate of 70 100 beats/min. Commonly used agents include digoxin, blockers, and calcium-channel blockers. High postoperative sympathetic tone makes rate control with digoxin alone frequently suboptimal. In patients whose atrial arrhythmia persists 24 hrs, pharmacologic or electrical cardioversion should generally be attempted. The efcacy of antiarrhythmic agents in the setting of atrial brillation after cardiac surgery was reviewed (13): quinidine, 64%; procainamide, 61% to 87%; disopyramide, 48% to 85%; ecainide, 60% to 86%; propafenone, 43% to 76%; amiodarone, 41% to 93%; sotalol, 85%; dofetilide, 36% to 44%; and ibutilide, 57%. Table 2 shows dosing regimens that may be used for acute conversion of atrial brillation by using class I or III antiarrhythmic drugs. The availability of intravenous and oral forms makes procainamide a typical rst-line choice after rate control has been achieved. A loading dose of 10 15
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Figure 1. Algorithm for prevention of atrial brillation after cardiac surgery. CABG, coronary artery bypass graft; AV, atrioventricular; LV, left ventricular; LVEF, left ventricular ejection fraction; AF, atrial brillation; bid, twice a day; po, by mouth; NG, nasogastric; POD, postoperative day; AVB, atrioventricular block; CHF, congestive heart failure; qd, daily.

mg/kg iv at 50 mg/min is followed by a continuous infusion at 12 mg/min. Potential side effects include hypotension, QRS widening, and proarrhythmia (including QT prolongation and torsades de pointes). Oral sustained-release preparations can subsequently be used, typically at 2 4 g/day in 2 4 divided doses, depending on the preparation. Doses should be adjusted according to serum levels, which should be checked daily while the patient is receiving intravenous dosing. Levels of N-acetyl-procainamide (NAPA), an active metabolite of procainamide, can accumulate to toxic levels with renal dysfunction. Hemodynamic effects may be seen in patients with severe left ventricular dysfunction. Gastrointestinal side effects can also be limiting. If the drug is
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continued long-term, arthralgias and a lupus-like syndrome may develop. However, if used only for postoperative atrial arrhythmias, procainamide often can be stopped 4 6 wks after surgery. Intravenous ibutilide, a class III potassium-channel blocker, can also acutely convert atrial brillation or utter after cardiac surgery with success rates of up to 57% (31). One study showed ibutilide to be more efcacious than procainamide in conversion of short-term atrial brillation/utter (32). Ibutilide is given as a 1 mg iv loading dose over 10 mins, which can be repeated in another 10 mins. Patients should be monitored for QT prolongation and torsades de pointes. Intravenous amiodarone has been used in postoperative patients, but cost

can be inhibiting. In our experience, intravenous amiodarone is not frequently required for atrial arrhythmias in the postoperative patient, unless the following occur: hemodynamically unstable atrial brillation recurs despite cardioversion; rate control is refractory to conventional A-V nodal blocking drugs; or standard antiarrhythmic or rate-controlling drugs cannot be tolerated because of negative inotropy. Rapid oral loading, however, can usually be achieved in patients with intact gastrointestinal function. Patients remaining in atrial brillation after approximately a 24-hr trial of drug therapy typically undergo electrical cardioversion. A short-acting anesthetic (etomidate or methohexital) is administered before cardioversion. An R wave synchronized shock is delivered usually at an initial energy of 200 J for atrial brillation, but potentially at 50 100 J for atrial utter or even lower, if using biphasic waveform energy. Anteroposterior debrillation patch positions (such as right parasternal-left paraspinal) provide a better vector for atrial debrillation than the anterior-anterior positions (right parasternal-left apical) often used for ventricular debrillation. Recurrence of atrial brillation is often problematic, because the underlying conditions, such as inammation, injury, and high sympathetic tone, are ongoing. Recurrent atrial brillation may be treated with a trial of a different antiarrhythmic drug followed by repeat electrical cardioversion. Alternatively, if the arrhythmia is well tolerated, the patient may be discharged on anticoagulation and followed up for another attempt at cardioversion after recovery from surgery, often at 4 6 wks. Persistence of the arrhythmia to hospital discharge is infrequent, and even less frequently does it persist at follow-up (33). Even with a rate-control strategy alone, over 90% of patients are in sinus rhythm 2 4 wks after onset of the arrhythmia (34). Patients who maintain sinus rhythm with the aid of an antiarrhythmic drug may be discharged on that medication, which may be discontinued at the 4 6 wk follow-up visit, if there is no recurrence. Achievement and maintenance of sinus rhythm may be more difcult in patients with valvular disease, but can often be done with a reasonable expectation of success after valve surgery. However, success may be limited when the duration of atrial brillation is 13 yrs, the left
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Figure 2. Postoperative atrial brillation treatment algorithm. AF, atrial brillation; DCC, direct current cardioversion; q, every; qd, daily; LV, left ventricular; CAD, coronary artery disease; PT, prothrombin time; INR, international normalized ratio.

atrial size is 5.2 cm, or patients are older (35, 36). Anticoagulation is an important consideration for patients with atrial brillation, particularly with atrial brillation of 48 hrs in duration or with recurring episodes. Atrial brillation is known to increase the risk of stroke even for postoperative patients (1, 6). Anticoagulation is recommended, if atrial brillation persists longer than 48 hrs, particularly if cardioversion is anticipated after this time (37). Heparin may be used, but some surgeons prefer oral warfarin (target international normalized ratio, 2.0:3.0) without concomitant intravenous heparin in the immediate postoperative period. However, data supporting the benets over risks of anticoagulation in the postoperative period remain lacking.
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Ventricular Arrhythmias
Isolated premature ventricular complexes are not uncommon after surgery, often associated with electrolyte or other metabolic imbalances. However, sustained ventricular arrhythmias are uncommon with reported incidences after cardiac surgery ranging from 0.41% to 1.4% (38 40). Complex ventricular arrhythmias are associated with left ventricular dysfunction (41). Conditions associated with ventricular arrhythmias after cardiac surgery include hemodynamic instability, electrolyte abnormalities, hypoxia, hypovolemia, ischemia and infarction, acute graft closure, reperfusion after cessation of cardiopulmonary bypass, and proarrhythmia caused by inotropic and antiarrhythmic drugs.

Diagnosis. Premature ventricular complexes are usually readily identied but sometimes must be distinguished from atrial ectopy with aberrant ventricular conduction. Similarly, wide complex tachycardias may be ventricular or supraventricular tachycardia although in patients with prior infarction, the diagnosis is almost always ventricular tachycardia. If feasible, a 12-lead electrocardiogram and atrial electrograms obtained through temporary epicardial wires placed at the time of cardiac surgery can be helpful. The latter method would detect the presence of A-V dissociation, which strongly suggests ventricular tachycardia. Prognosis. The prognosis of ventricular arrhythmias is correlated with the type of arrhythmia and degree of structural heart disease. Patients with simple premature ventricular complexes postoperatively do not exhibit increased risk for developing malignant ventricular arrhythmias (41, 42). Complex ventricular arrhythmias, including both frequent premature ventricular complexes ( 30/ hr) and nonsustained ventricular tachycardia, have no impact on short-term outcome (42), but long-term outcome may be reduced if ventricular function is reduced. A study (43) of 185 patients with postoperative frequent premature ventricular complexes and nonsustained ventricular tachycardia reported no statistically signicant difference in mortality rate at an average follow-up of 3 yrs (8% compared with 5% for matched controls). However, another study (41) of 126 patients with postoperative complex ventricular ectopy reported that patients with an left ventricular ejection fraction of 40% had a 75% mortality rate and 33% incidence of sudden death at an average follow-up time of 15 months, whereas none of the patients with normal left ventricular function had sudden death. Thus, long-term outcome after complex ventricular arrhythmias occurring postoperatively appears to be related to the degree of ventricular dysfunction. Patients with sustained ventricular arrhythmias have poorer short- and longterm prognosis. A hospital mortality rate of up to 50% has been reported in patients with sustained ventricular arrhythmias after surgery and of initial survivors, up to 40% will have a recurrence. As many as 20% of these patients will die a cardiac death within 24 months (38 40). Aggressive management, potentially with an electrophysiology study and an imN139

Table 1. Rate control for postoperative atrial arrhythmias Agent Digoxin Loading Dose 0.250.5 mg iv or by mouth, then 0.25 mg every 46 hr to 1 mg in rst 24 hrs Maintenance Dose 0.1250.25 mg by mouth or iv daily Side Effects/Toxicity Anorexia, nausea; A-V block; ventricular arrhythmias; accumulates in renal failure Comments Used in CHF; vagotonic effects on the AVN; delayed onset of action; narrow therapeutic window; less effective postoperatively, paroxysmal AF with high adrenergic states Effective in heart rate control; rapid onset of action

Blockers Propranolol Metoprolol 1 mg iv every 25 mins to 0.10.2 mg/kg 5 mg iv every 5 mins to 15 mg 500 g/kg iv over 1 min 1080 mg by mouth three to four times daily 25100 mg by mouth twice a day to three times daily 50 g/kg iv for 4 mins; repeat load as required and 1 maintenance 20 50 g/kg/min every 510 mins

Bronchospasm; CHF; 2BP

Esmolol

Esmolol short acting

Calcium-channel blockers Verapamil

2BP, CHF 1 Digoxin level

Rapid onset, can be used safely in COPD and DM

2.510 mg iv over 2 mins

Diltiazem

0.25 mg/kg over 2 mins, repeat as required for 15 mins at 0.35 mg/kg

510 mg iv every 3060 mins or 40160 mg by mouth three times daily or 120480 mg per day, sustained release 515 mg/hr iv or 3090 mg by mouth four times daily or 120360 mg sustained release daily

Often well tolerated with low LVEF patients

A-V, atrioventricular; CHF, congestive heart failure; AVN, atrioventricular node; AF, atrial brillation; BP, blood pressure; COPD, chronic obstructive pulmonary disease; DM, diabetes mellitus; LVEF, left ventricular ejection fraction.

plantable cardioverter-debrillator (ICD), is often indicated, particularly in the absence of a reversible cause. Acute Treatment. Asymptomatic and hemodynamically stable premature ventricular complexes and even short runs of nonsustained ventricular tachycardia usually do not need routine acute treatment. Correction of any reversible causes of ventricular arrhythmias, as listed above, should be routine. For hemodynamically signicant or symptomatic premature ventricular complexes or nonsustained ventricular tachycardia, lidocaine has been used successfully, although without benets in morbidity or mortality (38, 44). Overdrive pacing, using either atrial or atrioventricular sequential pacing, has been used as well, although evidence of efcacy has been lacking. Sustained ventricular arrhythmias are treated in postoperative situations in a manner similar to in nonpostoperative situations (45). However, postoperative states trigger closer attention to identication and treatment of electrolyte or
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other metabolic imbalance, ischemia, infarction, graft closure, or mechanical complications of surgery. Sustained ventricular tachycardia, if hemodynamically stable, may be treated initially with intravenous antiarrhythmic medication. Lidocaine, generally the drug of rst choice, is given in a loading dosage of 11.5 mg/kg, up to a total dosage of 23 mg/kg, as needed, in two divided doses 10 15 mins apart, followed by an intravenous continuous infusion of 2 4 mg/min. The dosage should be reduced in patients who are elderly, have congestive heart failure, or have hepatic dysfunction. Procainamide, often the second line drug, is loaded intravenously at 20 50 mg/min for a total loading dosage of 15 mg/kg, followed by an infusion at 1 4 mg/min. The loading doses should be stopped early if the QRS complex widens by 50% or slowed, if hypotension develops. Dosage modications or even avoidance may be required in the presence of renal insufciency. The metabolite N-acetyl-procainamide may accumulate to toxic levels with renal failure. Bretylium is probably

less effective than the rst two agents in treating ventricular tachycardia, but can be given as 510 mg/kg iv loading dose over 10 mins, followed by 12 mg/min infusion. Postural hypotension is common. Intravenous amiodarone has also been used as a rst-line treatment for ventricular arrhythmias. A bolus of iv 150 mg is given over 10 mins, followed an initial infusion of 0.51 mg/min with tapering afterloading. Additional 150 mg iv boluses may be given over the rst few hours for recurrent hemodynamically signicant ventricular tachycardia/brillation. If possible, however, frequent boluses during the rst 24 hrs should be limited, preferably to keep the total dose under 2000 mg during the rst 24 hrs because of the risk of hepatic toxicity. Hypotension may require dose reduction or slowing of the infusion or bolus rates. High dose oral amiodarone loading can also be effective, if a patient is able to take medication orally or through a nasogastric tube. Doses up to 2400 mg could be administered in divided doses during the rst 24 hrs. In patients with left ventricCrit Care Med 2000 Vol. 28, No. 10 (Suppl.)

Table 2. Regimens for pharmacologic conversion of postoperative atrial arrhythmias Success Rate (%) 64

Drug Quinidine

Route By mouth

Dose 400 mg, then 400 mg in 4 hrs

Adverse Effects/Comments TdP, PMVT; GI; hypotension; enhanced AVN conduction; usually avoided postoperatively because of risk of proarrhythmia with diuresis/electrolyte imbalances Urinary retention; enhanced AVN conduction; AFlutter 1:1; VT; hypotension Fever; enhanced AVN conduction; accumulates in renal failure ?Avoid in CAD, LV dysfunction Avoid in CAD, LV dysfunction

Disopyramide

iv By mouth iv By mouth iv By mouth iv iv iv

2 mg/kg, then 0.4 mg/kg/hr 600 mg daily 11.5 g at 2550 mg/min 600 mg 2 mg/kg over 10 mins 300 mg 2 mg/kg over 10 mins 1 mg/kg 10 mins, 1.5 mg/kg/hr 1 hr, 0.25 mg/kg/hr 23 hrs 2 mg/kg 2 mins, 0.2 mg/kg/hr 12 hrs 2.55 mg/kg iv over 20 mins, 15 mg/kg over 24 hrs, or 1.2 g over 24 hrs 80160 mg, then 160360 mg per day 1 mg/kg, then 0.2 mg/kg 12 hrs 48 g/kg over 15 mins 1 mg over 10 mins, repeat in 10 mins as required

4885

Procainamide Propafenone Flecainide

6187 5587a 4376 90a 6590a 60 86 4193

Amiodarone

iv

Hypotension

Sotalol

By mouth iv iv iv

52a 85 3644 57

Bradycardia; hypotension; CHF; TdP

Dofetilide Ibutilide

TdP; VT; must adjust dose for renal function TdP; PMVT

TdP, torsades de pointes; PMVT, polymorphic ventricular tachycardia; GI, gastrointestinal; AVN, atrioventricular node; AFlutter, atrial utter; VT, ventricular tachycardia; CAD, coronary artery disease; LV, left ventricular; CHF, congestive heart failure. a Nonsurgical atrial arrhythmia studies.

ular dysfunction, amiodarone is often better tolerated than other antiarrhythmic agents. In patients with slower ventricular tachycardias and ventricular epicardial wires still in place, conversion using overdrive ventricular pacing may be attempted by burst pacing the ventricle at rates above the ventricular tachycardia rate. Electrical cardioversion/debrillation should be available, because acceleration of the ventricular tachycardia to ventricular brillation is possible. Electrical debrillation or cardioversion should be performed for ventricular brillation, hemodynamically compromising ventricular tachycardia, or sustained ventricular tachycardias that do not respond to antiarrhythmic medication. Generally recommended energy levels range from 200 to 360 J. Awake patients should be anesthetized with a short-acting agent, such as midazolam, etomidate, or methohexital. Initiation of emergency cardiopulmonary bypass (in the surgical intensive care unit) can be considered for patients not responding to conventional resuscitative measures. A 56% long-term survival rate
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for patients undergoing this procedure with no resultant mediastinitis and a 22% incidence of soft tissue infections has been reported (46). Long-Term Management. Patients with isolated asymptomatic premature ventricular complexes generally do not need risk stratication or long-term antiarrhythmic therapy. There is no evidence isolated premature ventricular complexes affect long-term outcome. Empirical suppression has had no benecial effect on mortality rate and may be harmful with class I antiarrhythmic drugs. Patients with normal left ventricular ejection fraction and asymptomatic nonsustained ventricular tachycardia after cardiac surgery generally have a favorable long-term prognosis and do not require electrophysiology study or an ICD. No trial has yet demonstrated the benets of ICD therapy in this population. Patients with nonsustained ventricular tachycardia, prior myocardial infarction, and left ventricular dysfunction (left ventricular ejection fraction 40%) should be considered for electrophysiologic testing with implantation of an

ICD if a sustained ventricular arrhythmia is induced. In the Multicenter Automatic Debrillator Implantation Trial (MADIT), patients with coronary artery disease, left ventricular ejection fraction 35%, nonsustained ventricular tachycardia, and inducible sustained ventricular arrhythmias not suppressible by procainamide, were randomized to prophylactic ICD implantation vs. conventional medical therapy, most of which consisted of amiodarone (47). A 54% reduction in mortality rate in the ICD arm was demonstrated. In the Multicenter Unsustained Tachycardia Trial (MUSTT) (48), patients with coronary artery disease, left ventricular ejection fraction 40%, nonsustained ventricular tachycardia, and inducible sustained ventricular tachycardia were randomized to electrophysiologic-guided therapy vs. standard therapy (angiotensin-converting enzyme inhibitors and blockers). There was a 27% reduction in arrhythmic death and cardiac arrest in the electrophysiologic-guided group compared with the no antiarrhythmic treatment group. All of this risk reduction was seen in the group that received an ICD.
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al brillation is the most common arrhythmia encountered postoperatively, although ventricular arrhythmias and bradyarrhythmias can also occur.
Applicability of these studies to nonsustained ventricular tachycardia detected in the immediate postoperative period after cardiac surgery is not well established. The Coronary Artery Bypass Graft Patch Trial (CABG-Patch) (49) showed no difference in mortality rate among patients with low ejection fraction and a positive signal-averaged electrocardiogram randomized to ICD or no ICD implantation at the time of coronary artery bypass graft surgery. These results may differ from those of the Multicenter Automatic Debrillator Implantation Trial (47) and Multicenter Unsustained Tachycardia Trial (48) because coronary artery bypass graft surgery may include risk removal by relief of ischemiaprovoked arrhythmias and because of higher operative mortality rates from ICD implantation at the time of thoracotomy for coronary artery bypass graft surgery. Mortality from ICD implantation has improved with the use of nonthoracotomy implantation methods. Patients with coronary artery bypass graft surgery within 2 months were excluded from the MADIT (47). The MUSTT (48), however, did include patients who had nonsustained ventricular tachycardia four or more days after revascularization. The postoperative monitored period is a common time to detect such arrhythmias and to provide protection to those patients at potential high risk for life-threatening ventricular arrhythmias. Thus, detection of nonsustained ventricular tachycardia during the postoperative period (even a few days after cardiac surgery) warrants proceeding with a risk stratication scheme as suggested by the MADIT (47) and the MUSTT (48). Empirical amiodarone use in patients
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rrhythmias

are

common after cardiac surgery. Atri-

with ischemic cardiomyopathy was studied in the European Myocardial Infarct Amiodarone Trial (EMIAT) (50) and Canadian Amiodarone Myocardial Infarction Arrhythmia Trial (CAMIAT) (51), which showed no improvement in overall mortality rate with empirical amiodarone use in patients after myocardial infarction with or without nonsustained ventricular arrhythmias, although benets in arrhythmic death reduction were seen. The European Myocardial Infarct Amiodarone Trial (50) excluded patients expecting imminent cardiac surgery. Management of patients with nonischemic cardiomyopathy and nonsustained ventricular tachycardia remains unclear. The Grupo de Estudio de la Sobrevida en la Insuciencia Cardiaca en Argentina (GESICA) study (52) suggested an improvement in mortality rate with empirical amiodarone in heart failure patients, but the Congestive Heart Failure Survival Trial of Antiarrhythmic Therapy (CHFSTAT) trial (53) showed no benet. The GESICA study (52) had a higher proportion of nonischemic cardiomyopathy, suggesting a possible benet from prophylactic amiodarone in this population. The CHF-STAT study (53) excluded patients within 3 months of revascularization. Ongoing multicenter trials studying the role of prophylactic amiodarone or ICD implantation in heart failure patients include the Sudden Cardiac Death in Heart Failure Trial (SCDHeFT; conventional therapy vs. amiodarone vs. ICD implantation in NYHA functional classes II and III heart failure, left ventricular ejection fraction 35%) and Debrillators in Nonischemic Cardiomyopathy Treatment Evaluation (DEFINITE; conventional therapy vs. ICD in nonischemic cardiomyopathy, left ventricular ejection fraction 35%). In patients with sustained ventricular arrhythmias, implantation of an ICD is rst-line therapy because recurrence and the long-term mortality rate is high. The Antiarrhythmics Versus Implantable Debrillators Trial (54) and other trials have demonstrated the superiority of ICD over drug therapy for patients suffering hemodynamically signicant ventricular arrhythmias. Although applicability to sustained ventricular arrhythmias suffered within the immediate postoperative period (48 hrs) is not established, in the Antiarrhythmics Versus Implantable Debrillators Trial (AVID) (54), 10% of patients in the ICD group and 12% of patients in the antiarrhythmic drug group

underwent coronary revascularization during hospitalization for the index arrhythmia. Many of these patients may warrant electrophysiologic testing and/or ICD implantation. Other therapies demonstrated to improve long-term survival should also be used in patients with ventricular dysfunction. These include -adrenergic blockers and angiotensin-converting enzyme inhibitors in the absence of contraindications or intolerance.

BRADYARRHYTHMIAS
Bradyarrhythmias are (at least transiently) common after cardiac surgery. Temporary epicardial atrial and ventricular pacing wires placed at the time of surgery usually facilitate temporary pacing. After coronary artery bypass graft surgery, permanent pacing is required for sinus node dysfunction or A-V conduction disturbances in 0.8% to 3.4% of patients. After valve operations, bradycardia usually is caused by complete or highdegree A-V block and requires permanent pacing in 2% to 4% of patients (55, 56), but may be required in up to 20% to 24% after some types of procedures, such as for calcic aortic stenosis or tricuspid valve replacement. Mitral valve repair and replacement have been associated with equal frequencies of clinically important second- or third-degree A-V block with new conduction disturbances occurring in 30.6% of patients, and complete heart block in 1.5% of patients (56). The right lateral atriotomy used in minimally invasive mitral valve operations or other transseptal superior approaches to the mitral valve can cause sinus node dysfunction with persistent symptomatic sinus bradycardia or junctional rhythms requiring permanent pacing. Permanent pacemakers are required more often after repeat valve surgeries (7.7% vs. 2.0% after initial valve surgery) (55). Other signicant risk factors include perivalvular calcication, older age, preoperative left bundle branch block, left ventricular aneurysmectomy, left main coronary artery stenosis, number of bypassed arteries, and cardiopulmonary bypass time. The frequent challenge with postoperative bradycardia is often in determining the amount of time to allow for recovery of A-V conduction or the sinus node function after surgery before implanting a permanent pacemaker. Recovery is common with long-term follow-up. Among patients who receive permanent pacing,
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only 30% to 40% of patients with sinus node dysfunction remain pacemaker dependent. The rate of recovery is less with A-V block. Among patients with complete heart block, 65% to 100% remain dependent. Our usual practice is to implant a permanent pacemaker if symptomatic complete heart block or severe sinus node dysfunction persists longer than 57 days postoperatively. If underlying intrinsic rhythm is absent or temporary pacing leads fail, permanent pacing may be performed even sooner. After orthotopic heart transplantation, sinus node dysfunction is common and leads to permanent pacemaker implantation in up to 21.1% (mean, 8%) of patients. A-V block is less common, but requires pacemaker implantation in up to 4.5% of transplant recipients. Permanent pacing is needed less after bicaval compared with biatrial transplant anastomosis (57). Bradyarrhythmias from rejection can also lead to permanent pacing. Factors predictive of bradyarrhythmias after heart transplantation include older donor age, longer donor ischemic time, and longer aortic cross-clamp time. Sinus node function after orthotopic heart transplantation often improves over longterm follow-up, but recovery might proceed over weeks to months, commonly hampering expeditious hospital discharge. The need for long-term pacing may be unpredictable, although patients with early A-V block may be more likely to require it. Chronotropic medications, such as theophylline or aminophylline, have been used for sinus bradycardia after transplantation to improve sinus node dysfunction (58) or high grade A-V block (59) and may decrease the need for permanent pacing.

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