WORKUP	Section 5 of 11
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Lab Studies:

• Include electrolyte levels in an acute evaluation.

• Consider serum and urine toxicology screens for cocaine metabolites and tricyclic antidepressants in accordance with the clinical history.

• Check cardiac enzyme levels if clinical symptoms or signs of ischemia are present.

• In some patients with spontaneous polymorphic VT, genetic studies may be appropriate. Commercial genotyping studies have been available in the United States since FDA approval in 2004. Spontaneous polymorphic VT may be related to genetic mutations affecting ion channels, as occurs in long QT syndrome, Brugada syndrome, and idiopathic VF. Finally, some patients with drug-induced ventricular arrhythmias have underlying genetic and channel defects.

Imaging Studies:

• Following conversion to sinus rhythm, chest radiographs, multiple gated acquisition (MUGA) scans, and echocardiography may establish the presence of ventricular dysfunction and structural heart disease. These considerations are paramount in defining further treatment in any patient with VT.

• Ultrafast cardiac computed tomography (CT) scans and gated cardiac magnetic resonance imaging (MRI) technologies are evolving quickly but have not yet supplanted echo and nuclear imaging for quantification of ventricular function.

• Although gated cardiac MRI has been proposed for evaluation of right ventricular dysplasia, the diagnostic yield of this test has yet to be clearly defined. Right ventricular angiography may still be the criterion standard imaging study.

• Coronary angiography may be useful in establishing the presence of coronary artery obstruction.

Other Tests:

• Signal-averaged ECG is a noninvasive test that often produces abnormal results in patients with VT related to prior infarct or right ventricular dysplasia. Quantification of T-wave alternans has also been proposed as a noninvasive risk stratifier for sudden death risk.

• Electrocardiography is the criterion standard for diagnosis of VT. If no pacing device is present, the challenge is to discriminate between VT and aberrantly conducted SVT. Brugada et al (1991) have developed the best diagnostic criteria. Specific findings for VT include the absence of RS complexes in the precordial ECG leads (V1-V6), RS duration greater than 100 milliseconds in any precordial lead, and ventriculoatrial dissociation.

• Patients with tachyarrhythmias may present with syncope. The ECG should be screened carefully for myocardial infarction, conduction abnormalities, QT-interval prolongation or shortening, precordial T-wave inversions, ventricular preexcitation, and ventricular hypertrophy.

• Patients with pacemakers represent a special challenge because they can present with wide complex tachycardia (WCT) that is secondary to rapid ventricular pacing.

• Possibilities include tracking of an atrial tachyarrhythmia in a dual-mode, dual-pacing, dual-sensing (DDD) or an atrial-triggered, ventricular-inhibited (VDD) device; endless loop tachycardia; inappropriate rate responsive pacing due to sensor problems or incorrect sensor programming; and overt pacemaker failure (runaway pacer).

• The most common problem involves the patient whose device is tracking atrial fibrillation or flutter. In the absence of a mode-switching algorithm, a VDD or DDD pacer will respond by pacing the ventricle at the programmed upper rate limit of the device. Application of a magnet to the pacer generator may terminate endless loop tachycardia or drop the paced rate enough to allow diagnosis of the underlying atrial tachyarrhythmia.

• Occasionally, patients with structural heart disease present with recurrent syncope or palpitations. In this setting, an arrhythmic cause of syncope may be sought. Options include Holter monitoring, which has a low yield, or event recording. The goal is to document the patient's rhythm during symptoms. If this is not practical, a provocative electrophysiologic study (EPS) can be performed.

Procedures:

• Diagnostic EPS requires placement of electrode catheters in the ventricle, followed by programmed ventricular stimulation using progressive pacing protocols. Premature ventricular beats are induced following conditioning pacing drives, in an attempt to induce reentrant arrhythmia. In patients with symptoms suggestive of VT, this kind of provocative testing is often used to assess whether the ventricles can sustain a reentrant tachyarrhythmia. Diagnostic yield of EPS is highest in patients with reentrant VT circuits.

• EPS is particularly relevant to patients felt to be at high risk for sudden death due to significant underlying structural heart disease. EPS may be useful in demonstrating whether the substrate for sustained VT is present in a patient presenting with syncope or ischemic, nonsustained VT. In patients with recurrent symptoms related to VT, programmed electrical stimulation (PES) can generally reproduce clinically relevant VT circuits.

• Occasionally, screening for sustained VT is appropriate in asymptomatic patients. In the Multicenter Automatic Defibrillator Implantation (MADIT) and Multicenter UnSustained Tachycardia Trials (MUSTT), EPS was used to assess sudden death risk in patients with ischemic cardiomyopathy and nonsustained VT. Patients with inducible sustained VT had better outcomes with implantable cardioverter-defibrillator (ICD) implantation than with conventional rhythm management.

• If right ventricle dysplasia is being considered, many laboratories perform right ventricular angiography as a part of the EPS. Diagnostic abnormalities include right ventricular dilation, dyskinesis, and aneurysms.

Histologic Findings: As noted above, most reentrant VTs are related to myocardial scarring from ischemic or dilated cardiomyopathy. Fibrotic replacement of myocytes and interweaving of scar tissue with functional myocytes is common along slow conduction zones of VT circuits.

	TREATMENT	Section 6 of 11
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Medical Care: The acute management strategy depends upon the immediate hemodynamic consequences of the arrhythmia. VT associated with loss of consciousness or hypotension is a medical emergency requiring immediate cardioversion. In a normally sized adult, this is typically accomplished with a 200-to 360-J monophasic shock or a clinically equivalent biphasic energy dose.

When the hemodynamic status is stable, the patient is well perfused, and no evidence for coronary ischemia or infarction is present, then a trial of intravenous medication may be considered. If left ventricular function is impaired, amiodarone, then lidocaine, are favored over procainamide because of the latter drug's potential for exacerbating congestive heart failure. If medical therapy is unsuccessful, synchronized cardioversion (50-200 J monophasic) following sedation is appropriate.

If runs of polymorphic VT are observed punctuated by sinus rhythm with QT prolongation, then attempts should be made to correct torsades with magnesium, isoproterenol, and/or pacing. Phenytoin and lidocaine may also help by shortening the QT interval in this setting, but procainamide is contraindicated because of its QT prolonging effects. Efforts should be made to correct hypokalemia and withdraw any chronic medications associated with QT-interval prolongation.

Occasionally, patients present with wide QRS complex tachycardia of unknown mechanism. In the absence of pacing, the differential diagnosis includes VT and aberrantly conducted SVT. If hemodynamic compromise is present or if any doubt exists about the rhythm diagnosis, the safest strategy is to treat the undiagnosed rhythm as VT. If the clinical situation permits, a 12-lead ECG should be obtained prior to conversion of the rhythm. The ECG criteria of Brugada et al (1991) may be useful in differentiating the arrhythmia mechanism.

Rarely, patients present with repetitive runs of nonsustained VT, as in Image 3. Prolonged exposure to this (or any other) tachycardia may cause a tachycardia-induced cardiomyopathy, which typically improves with medical or ablative therapy of the VT.

Chronic management strategies may include medications, ICD implantation, and catheter-based ablation. Combinations of these therapies are typically used when structural heart disease is present.

Because VT patients with structurally normal hearts have a low risk of sudden death, ICDs are unnecessary in this setting. These patients are therefore treated with medications or ablation.

• Antiarrhythmic drug trials have been disappointing. Placebo-controlled arrhythmia prevention trials often show that antiarrhythmics increase sudden death mortality, particularly with the use of Vaughn Williams Class I antiarrhythmics.

• These medications work by slowing propagation and reducing tissue excitability through sodium channel blockade. The class III antiarrhythmics prolong repolarization through potassium channel blockade.

• The ESVEM (Electrophysiologic Study Versus Electrocardiographic Monitoring) study of VT/VF patients demonstrated the superiority of sotalol over several type I antiarrhythmic drugs, but the trial did not include a placebo control group.

• Amiodarone is a complex antiarrhythmic drug that deserves special mention. It is generally listed as a class III drug but has measurable class I, II, and IV effects. Although the complex kinetics of this drug did not allow inclusion in ESVEM, the Cardiac Arrest in Seattle: Conventional versus Amiodarone Drug Evaluation (CASCADE) trial suggested that amiodarone was superior to conventional antiarrhythmics (a mix of class I drugs) for secondary arrhythmia prophylaxis (ie, prior VT/VF). Based in large part upon the results of ESVEM and CASCADE, current clinical practice favors class III antiarrhythmics.

• Amiodarone has also been studied as primary arrhythmia prophylaxis in the postinfarct setting, but it had no impact on overall mortality rates.

• Unlike class I antiarrhythmics, amiodarone appears to be safe in patients with left ventricular dysfunction.

• In the setting of congestive heart failure, the best proven antiarrhythmic drug strategies appear to be the use of angiotensin-converting enzyme (ACE) inhibitors and chronic beta-receptor–blocking agents.

• The ICD has changed the face of ventricular arrhythmia management. Like pacemakers, these devices can be implanted transvenously quickly in a low-risk procedure.

• Once installed, the ICD can detect ventricular tachyarrhythmias and terminate them with defibrillation shocks or antitachycardia pacing algorithms. These devices can also function as backup pacemakers in patients with bradyarrhythmias.

• The advent of transvenous ICD technology triggered several trials comparing the ICD to conventional antiarrhythmic therapies.

• In patients with prior VT/VF, ICD therapy was compared to the best available antiarrhythmic drugs, amiodarone, and sotalol.

• The Antiarrhythmics Versus Implantable Defibrillators (AVID) study; the Canadian Implantable Defibrillator Study (CIDS); and the Cardiac Arrest Study, Hamburg (CASH) demonstrated better survival in patients randomized to ICD therapy. The survival difference was significant in AVID, of borderline statistical significance in CIDS (P<0.06), and of no statistical difference in CASH. A meta-analysis of the 3 trials suggested a 28% reduction in the relative risk of death related to ICD implantation in this clinical setting (Connolly, 2000).

• Primary prevention of sudden death has been a difficult problem for cardiologists due to the difficulties of accurate risk stratification.

• The Multicenter UnSustained Tachycardia Trial (MUSTT) and Multicenter Autonomic Defibrillator Implantation Trial (MADIT) studied high-risk patients who had never had VF or sustained VT.

• In these studies, patients with ischemic cardiomyopathy, ejection fractions greater than 35-40%, and nonsustained VT were taken to EPS.

• Patients with inducible sustained VT were randomized between conventional antiarrhythmic therapy and prophylactic ICD implantation.

• In each study, ICD patients had better survival than patients receiving antiarrhythmic drugs.

Surgical Care: In the 1980s, ventricular arrhythmia surgery was explored at several centers, using excision and cryoablation of infarct zones to prevent recurrent VT. The high mortality rates of these procedures and the success of the ICD led to a decline in open surgical procedures for VT. Catheter ablation of VT remains an option for patients with recurrent ICD shocks or non-ICD patients with preserved ventricular function. Ablation is used to treat symptomatic VT, rather than to reduce sudden death risk.

• Reentrant VT requires a slow conduction zone, and this is usually located along the border of a scarred zone of myocardium.

• The small physical size of the slow conduction zone makes it an ideal target for focal ablation procedures.

• Cell disruption can be achieved using radiofrequency energy or cryoablation via transvenous catheters during closed-chest procedures.

• Because patients with ischemic VT often have multiple reentrant circuits, ablation is typically used as an adjunct to ICD therapy.

• If VT arises from an automatic focus, the focus can be targeted for ablation.

• In patients with structurally normal hearts, the most common form of VT arises from the right ventricular outflow tract (RVOT). The typical outflow tract ectopic beat shows a positive QRS axis in the inferior leads. Abnormal or triggered automaticity is the most likely mechanism, and focal ablation is curative in these patients. Ablation cure rates are typically greater than 90% in this setting.

• Reentrant tachycardia occasionally arises from the RVOT in patients with right ventricular dysplasia and repaired tetralogy of Fallot patients. The tachycardia mechanism can usually be determined during EPS, and these circuits are commonly amenable to catheter ablation.

Consultations: Cardiac electrophysiology is a subspecialty devoted to the diagnosis and management of cardiac arrhythmias. Patients with VT should be referred to general cardiologists or electrophysiologists for specialized care.

Diet: Patients with ischemic VT may benefit from low-cholesterol and/or low-salt diets. Patients with idiopathic VT may notice a reduction in symptoms when stimulants, such as caffeine, are avoided.

Activity: VT may be precipitated by increased sympathetic tone during strenuous physical exertion. One goal of successful VT management is to allow the patient to return to an active lifestyle through medications, ICD implantation, and/or ablation therapy.

	MEDICATION	Section 7 of 11
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Intravenous medications are used to suppress acute VT. In the United States, these are limited to amiodarone, lidocaine, procainamide, and a handful of intravenous beta-adrenergic blocking agents (metoprolol, esmolol, propranolol). Bretylium is no longer available. In patients with acute VT or VF, intravenous amiodarone is the drug of choice. Although intravenous lidocaine is effective at suppressing peri-infarction VT, it may increase the overall mortality risk. In the ARREST (Amiodarone in the Out-of-Hospital Resuscitation of Refractory Sustained Ventricular Tachyarrhythmias) study, intravenous amiodarone was superior to placebo in patients with out-of-hospital cardiac arrest. In the ALIVE (Amiodarone versus Lidocaine in Prehospital Refractory Ventricular Fibrillation Evaluation) study, intravenous amiodarone was superior to lidocaine in a similar patient group.

In patients with idiopathic VT (associated with structurally normal hearts), medications are often avoided entirely through the use of curative catheter-based ablation.

Oral medications are used to chronically suppress recurrent VT. As noted earlier in this article, current evidence favors class III antiarrhythmic drugs over class I drugs. No large studies compare the currently available class III drugs, amiodarone, and sotalol. When VT is observed in a patient receiving an antiarrhythmic drug, discrimination must be made between VT recurrence and drug-induced ventricular proarrhythmia. The most common form of proarrhythmia is torsades de pointes (see Torsade de Pointes), associated with QT-interval prolongation, usually due to excessive potassium channel blockade.

In patients with hemodynamically significant VT/VF, ICD implantation has superseded medication as primary therapy. Because ICDs treat, rather than prevent, ventricular arrhythmias, as many as 50% of ICD patients require therapy with antiarrhythmic drugs to reduce the potential for ICD shocks. Once an ICD has been implanted, adjunctive drug and catheter ablation therapies can be used to reduce the number of ICD discharges.

Drug Category: Antiarrhythmics -- Intravenous administration is used for suppression of acute VT. Agents alter the electrophysiologic mechanisms responsible for arrhythmia. Medications are generally used to prevent recurrence of VT in susceptible patients.

Careful attention must be paid to drug pharmacokinetics due to relatively narrow therapeutic windows involved.

Most antiarrhythmic drugs may actually cause ventricular arrhythmias, and risks generally increase with serum drug levels.

To monitor for drug proarrhythmia, patients are often admitted to the hospital during initiation of oral antiarrhythmic medication.

Drug Name	Lidocaine (Xylocaine, Nervocaine, LidoPen, Duo-Trach) -- Class IB antiarrhythmic that increases electrical stimulation threshold of the ventricle, suppressing automaticity of conduction through the tissue. Although lidocaine may terminate VT successfully, it may increase the overall mortality in peri-infarction VT. Evidence for effectiveness is considered "Indeterminate" in the 2000 American Heart Association Emergency Cardiovascular Care guidelines.
Adult Dose	1-1.5 mg/kg IV push, followed by 0.5-0.75 mg/kg IV push to a maximum of 3 mg/kg Continuous 1–4 mg/min infusion should be started after arrhythmia is suppressed
Pediatric Dose	Endotracheal, intraosseous, and IV loading dose: 1 mg/kg, may repeat twice at 10- to 15-min intervals if necessary; follow with continuous IV infusion of 20-50 mcg/kg/min
Contraindications	Documented hypersensitivity to amide-type local anesthetics; avoid in Adams-Stokes syndrome and Wolf-Parkinson-White syndrome; avoid in severe sinoatrial, atrioventricular (AV), or intraventricular block if artificial pacemaker not in place
Interactions	Coadministration with cimetidine or beta-blockers, increases toxicity of lidocaine; coadministration with procainamide and tocainide may result in additive cardiodepressant action; may increase effects of succinylcholine
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Do not use a drug solution that contains preservatives; caution in heart failure, hepatic disease, hypoxia, hypovolemia or shock, respiratory-depression, and bradycardia; elderly patients may be at increased risk for CNS and cardiac adverse effects due to increased half-life or decreased clearance of the drug; high plasma concentrations can cause seizures, heart block, and AV conduction abnormalities; has been associated with malignant hyperthermia

Drug Name	Procainamide (Procanbid, Pronestyl) -- A Class IIB level therapy used for VT refractory to defibrillation and epinephrine. Increases refractory period of atria and ventricles. Myocardial excitability is reduced by increase in threshold for excitation and inhibition of ectopic pacemaker activity.
Adult Dose	20-30 mg/min continuous IV infusion until arrhythmia suppressed, patient becomes hypotensive, QRS widens 50% above baseline, or maximum dose of 17 mg/kg is administered; once arrhythmia is suppressed, may be infused at rate of 1-4 mg/min continuously Long-acting formulation: 1000 mg PO bid; adjust dose based on levels of procainamide and NAPA
Pediatric Dose	Not established; suggested dosage is 15-50 mg/kg/d PO divided q3-6h to maximum 4 g/d Alternatively, 20-30 mg/kg/d IM divided q4-6h to maximum 4 g/d or 3-6 mg/kg per dose IV infused over 5 min Maintenance: 20-80 mcg/kg/min IV by continuous infusion; not to exceed 100 mcg per dose or 2 g/d
Contraindications	Complete heart block or second- or third-degree heart block, if pacemaker not in place; torsade de pointes; documented hypersensitivity; systemic lupus erythematosus
Interactions	Can expect increased levels of procainamide metabolite NAPA in patients taking cimetidine, ranitidine, beta-blockers, amiodarone, trimethoprim, and quinidine; procainamide may increase effect of skeletal muscle relaxants, quinidine, lidocaine, and neuromuscular blockers; ofloxacin inhibits tubular secretion of procainamide and may increase bioavailability; when taken concurrently with sparfloxacin, may increase risk of cardiotoxicity
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Monitor for hypotension; plasma concentrations of procainamide and active metabolite, NAPA, may increase in renal failure; high or toxic concentrations may induce AV block or abnormal automaticity; caution in complete AV block, digitalis intoxication, organic heart disease, renal disease, and hepatic insufficiency

Drug Name	Amiodarone (Cordarone, Pacerone) -- Now the drug of choice in treatment of unstable ventricular arrhythmias. Currently considered a Class IIb intervention by the American Heart Association 2000 Emergency Cardiovascular Care Guidelines. Prehospital studies currently suggest that amiodarone is safe and efficacious for use in out-of-hospital cardiac arrest. Often used for life-threatening ventricular arrhythmias in patients who have relative contraindications to its use.
Adult Dose	150 mg IV infused over 10 min, follow with 1 mg/min constant infusion for 6 h, then maintenance infusion at 0.5 mg/min Oral dosing generally 400 mg/d following load
Pediatric Dose	Not established; weight-based dosing suggested; consider for refractory ventricular arrhythmias in children
Contraindications	Documented hypersensitivity; sinus node dysfunction; atrioventricular conduction disorders; underlying hepatic, pulmonary, or thyroid disease
Interactions	Increases effect and blood levels of theophylline, quinidine, procainamide, phenytoin, methotrexate, flecainide, digoxin, cyclosporine, beta-blockers, and anticoagulants; cardiotoxicity of amiodarone is increased by ritonavir, sparfloxacin, and disopyramide; coadministration with calcium channel blockers may cause an additive effect and decrease myocardial contractility further; cimetidine may increase amiodarone levels
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Hypotension, bradycardia, and AV block may occur; hypotension is most common adverse effect during intravenous administration; acute life-threatening pulmonary or hepatic toxicity may complicate acute or chronic use of this drug; elevation of serum hepatic enzymes and/or TSH requires that patients be monitored carefully during amiodarone therapy; rarely, irreversible blindness from optic neuritis is observed with chronic use

Drug Name	Sotalol (Betapace) -- Primarily a potassium channel (IKr)–blocking drug, with weak beta-blocker effect. In ESVEM study, sotalol was compared with 6 other drugs (not including amiodarone) in VT patients. Survival was best in the sotalol group.
Adult Dose	80-120 mg PO q12h initially; occasionally, doses as high as 240 mg q12h are used with careful monitoring for toxicity
Pediatric Dose	Not established; weight-based dosing recommended; can be considered for refractory ventricular arrhythmias in pediatric population
Contraindications	Documented hypersensitivity; complete AV block; intraventricular conduction defects; patients taking ritonavir or sparfloxacin
Interactions	Increases effect and blood levels of theophylline, quinidine, procainamide, phenytoin, methotrexate, flecainide, digoxin, cyclosporine, beta-blockers, and anticoagulants; cardiotoxicity of amiodarone is increased by ritonavir, sparfloxacin, and disopyramide; coadministration with calcium channel blockers may cause an additive effect and decrease myocardial contractility further; cimetidine may increase amiodarone levels
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Risk of proarrhythmia increases with dose; monitor for QT prolongation, dyspnea, fatigue, depression, bradycardia, and syncope due to torsade de pointes

Drug Name	Mexiletine (Mexitil) -- A class Ib sodium channel blocker, and the closest oral analog to lidocaine. Generally well tolerated and occasionally used in patients with VT responding to intravenous lidocaine. Class Ib sodium channel–blocking drugs generally felt to be safer than Ic drugs, but no large comparative trials exist.
Adult Dose	150 mg PO q8h initially; may increase to 300-450 PO q8h
Pediatric Dose	Not established; weight-based dosing recommended; consider for refractory ventricular arrhythmias
Contraindications	Documented hypersensitivity; mexiletine may exacerbate congestive heart failure or hypotension; clearance is reduced in hepatic failure
Interactions	Medications that decrease mexiletine levels include aluminum-magnesium hydroxide compounds, atropine, narcotics, hydantoins, rifampin, and urinary acidifiers; metoclopramide and urinary alkalinizers may increase mexiletine levels; cimetidine can either increase or decrease mexiletine levels; medications whose levels are increased by mexiletine include caffeine and theophylline
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Second- or third-degree AV block (without a pacemaker) is a contraindication; can be used cautiously in patients who have pacemakers and second- or third- degree block; in those with first-degree AV blocks, sinus node dysfunction, intraventricular conduction abnormalities, hypotension, or congestive heart failure, consultation with a cardiologist is recommended before using this medication; liver injury reported, particularly in conjunction with congestive heart failure or cardiac ischemia; monitor liver enzymes; rarely, leukopenia or agranulocytosis has been observed; CBC should be monitored; convulsions have occurred in about 0.2% of patients on this medication, caution is indicated if history of seizures is present; avoid other drugs that significantly modify the pH of urine

Drug Name	Acebutolol (Sectral) -- Selective hydrophilic beta-blocking drug with mild intrinsic sympathomimetic activity. Approved by the FDA for use in treating patients with hypertension and ventricular arrhythmias.
Adult Dose	400 mg PO qd initially administered as 200 mg bid, titrate to 600-1200 mg/d for clinical response
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; cardiogenic shock; bradycardia or heart block; sinus node dysfunction; AV conduction abnormalities
Interactions	Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effect; cardiotoxicity of sotalol may increase when administered concurrently with sparfloxacin, astemizole, calcium channel blockers, quinidine, flecainide, and contraceptives; toxicity of sotalol increases when administered concurrently with digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, and catecholamine-depleting agents
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Beta-adrenergic blockade may decrease signs and symptoms of acute hypoglycemia and clinical signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; withdraw drug slowly and monitor patient closely; caution in hypokalemia, peripheral vascular disease, hypomagnesemia, congestive heart failure, and congestive heart failure

Drug Name	Atenolol (Tenormin) -- Selectively blocks beta1-receptors, with little or no effect on beta2 types.
Adult Dose	50 mg PO qd; increase to 100 mg/d, if necessary
Pediatric Dose	1-2 mg/kg/dose PO qd
Contraindications	Documented hypersensitivity; congestive heart failure; pulmonary edema; cardiogenic shock; AV conduction abnormalities; heart block (without a pacemaker)
Interactions	Coadministration with aluminum salts, barbiturates, calcium salts, cholestyramine, NSAIDs, penicillins, and rifampin may decrease effects; haloperidol, hydralazine, loop diuretics, and MAOIs may increase toxicity of atenolol
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Beta-adrenergic blockade may reduce symptoms of acute hypoglycemia and mask signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism and cause thyroid storm; monitor patients closely and withdraw drug slowly; during an IV, carefully monitor BP, heart rate, and ECG

Drug Name	Metoprolol (Toprol XL, Lopressor) -- Selective beta1-adrenergic receptor blocker that decreases automaticity of contractions. During IV administration, carefully monitor blood pressure, heart rate, and ECG.
Adult Dose	100 mg/d PO qd or divided bid/tid initially and increase at 1-wk interval prn to a total of 450 mg/d if necessary
Pediatric Dose	1-5 mg/kg/24h PO divided bid
Contraindications	Documented hypersensitivity; uncompensated congestive heart failure; bradycardia; asthma; cardiogenic shock; AV conduction abnormalities
Interactions	Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels of metoprolol, possibly resulting in decreased pharmacologic effects; toxicity of metoprolol may increase with coadministration of sparfloxacin, phenothiazines, astemizole, calcium channel blockers, quinidine, flecainide, and contraceptives; metoprolol may increase toxicity of digoxin, flecainide, clonidine, epinephrine, nifedipine, prazosin, verapamil, and lidocaine
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Beta-adrenergic blockade may reduce signs and symptoms of acute hypoglycemia and may decrease clinical signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; monitor patient closely and withdraw the drug slowly; during IV administration, carefully monitor blood pressure, heart rate, and ECG

Drug Name	Flecainide (Tambocor) -- Treats life-threatening ventricular arrhythmias. Causes a prolongation of refractory periods and decreases action potential without affecting duration. Blocks sodium channels, producing a dose-related decrease in intracardiac conduction in all parts of the heart, with greatest effect on the His-Purkinje system (HV conduction). Effects on AV nodal conduction time and intra-atrial conduction times, although present, are less pronounced than on ventricular conduction velocity.
Adult Dose	100 mg PO bid q12h; increase q4d to a maximum of 400 mg/d
Pediatric Dose	3-6 mg/kg/d or 100-150 mg/m2/d divided PO tid to 11 mg/kg/d or 200 mg/m2/d
Contraindications	Documented hypersensitivity; third-degree AV block; myocardial depression
Interactions	Amiodarone, cimetidine, and digoxin may increase plasma concentrations of flecainide; beta-adrenergic blockers, verapamil, and disopyramide may have additive inotropic effects when administered with flecainide; ritonavir may increase cardiotoxicity of flecainide
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Caution in renal or hepatic impairment

Drug Name	Propafenone (Rythmol) -- Treats life-threatening arrhythmias. Possibly works by reducing spontaneous automaticity and prolonging the refractory period.
Adult Dose	150 mg PO q8h and increase at 3- to 4-d intervals up to 300 mg q8h
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; bronchospastic disorders; conduction disorders; bradycardia; uncontrolled heart failure
Interactions	Decreases serum levels of rifampin; cimetidine, quinidine, warfarin, and beta-blockers may increase serum levels of propafenone
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Should only be used for life-threatening arrhythmias; caution in patients with congestive heart failure, myocardial infarction, or hepatic or renal dysfunction

Drug Name	Quinidine (Quinidex, Quinora, Quinalan, Cardioquin) -- Depresses myocardial excitability and conduction velocity.
Adult Dose	200 mg IV q2-3h for 5-8 doses with subsequent daily increases until sinus rhythm is restored or adverse effects occur; not to exceed 3-4 g/d in any regimen Quinidine gluconate: 324 mg PO tid; adjust based on quinidine levels
Pediatric Dose	30 mg/kg/d PO in 5 divided doses
Contraindications	Documented hypersensitivity; complete AV block or intraventricular conduction defects; presently taking ritonavir or sparfloxacin
Interactions	Phenytoin, rifampin, and phenobarbital may decrease quinidine concentrations; toxicity of quinidine is increased when taken with ritonavir, sparfloxacin, beta-blockers, amiodarone, verapamil, cimetidine, alkalinizing agents, or nondepolarizing and depolarizing muscle relaxants; may enhance effect of anticoagulants
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Caution in G-6-PD deficiency and those with a tendency to develop granulocytopenia; avoid use in myocardial depression, hepatic or renal insufficiency, and myasthenia gravis

	FOLLOW-UP	Section 8 of 11
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Further Inpatient Care:

• Initiation of antiarrhythmic medications may require telemetry monitoring for drug-induced proarrhythmia. Monitor patients starting class Ia drugs and class III drugs for QTc prolongation and torsade de pointes until steady-state drug levels (5 or more clearance half-lives) have been reached. A notable exception is amiodarone administration, which may require months to achieve steady state. Drug loading of amiodarone necessarily is completed on an outpatient basis.

• Class Ic antiarrhythmics are associated with drug-induced VT and rate-related conduction slowing. Many centers commit their patients to telemetry monitoring and predischarge exercise testing during initiation of Ic agents. Sinus bradycardia and sinus node dysfunction are often exacerbated by antiarrhythmic drugs.

• The possibility of drug-specific noncardiac adverse effects requires special vigilance. These effects are drug-specific (visual disturbances with flecainide, joint pains with procainamide) and emphasize the need for physicians to be familiar with these medications.

Further Outpatient Care:

• Patients receiving chronic antiarrhythmic therapy should be observed regularly for proarrhythmia and adverse effects. Adverse reactions may be observed at any time during the course of drug therapy.

• Chronic procainamide administration may be associated with a lupus syndrome. Life-threatening pulmonary and hepatic toxicities are well known in patients receiving amiodarone.

• Patients should be questioned carefully about recurrent palpitations and syncope.

• Patients with ICDs require regular outpatient device follow-up to allow monitoring of battery and transvenous lead status. Although the battery lifetime is somewhat predictable, lead fracture and failure may occur at any time. In addition, efficacy of the device should be rechecked following initiation of medications that may increase the ventricular defibrillation threshold. This is typically accomplished with an outpatient noninvasive programmed stimulation study (NIPS) carried out through the implanted device.

• Lead problems can generally be diagnosed in clinic and occasionally require lead revision or replacement.

In/Out Patient Meds:

• Because most patients with VT have an underlying cardiomyopathy, continued therapy of congestive heart failure and coronary artery disease remains important.

• Outpatient medication choices depend upon the degree of ventricular dysfunction, comorbid disease such as asthma, and the presence or absence of an ICD.

Prognosis:

• Prognosis varies with the specific cardiac process but is predicted best by left ventricular function. In patients with ischemic cardiomyopathy and nonsustained VT, sudden death mortality rates approach 30% in 2 years. In patients with idiopathic VT, the prognosis is excellent and the major risk is due to poorly timed syncopal spells. A few exceptions exist to the above rule. Patients with long QT syndrome, right ventricular dysplasia, and hypertrophic cardiomyopathy may be at increased risk of sudden death despite relatively preserved left ventricular function. These possibilities should be considered in any patient with a strong family history of premature sudden death.

Patient Education:

• For excellent patient education resources, visit eMedicine's Heart Center, Cholesterol Center, and Public Health Center. Also, see eMedicine's patient education articles Heart Rhythm Disorders, Coronary Heart Disease, Chest Pain, Heart Attack, Cardiopulmonary Resuscitation (CPR), Supraventricular Tachycardia, and Palpitations.

	MISCELLANEOUS	Section 9 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography

Medical/Legal Pitfalls:

• Confusion with SVT

• Occasionally, patients present with hemodynamically stable VT.

• Hemodynamic stability does not help discriminate VT from SVT.

• Hemodynamic deterioration and death have been reported from inappropriate use of verapamil in this setting.

• Confusion with paced rhythms

• Occasionally, patients present with rapid rhythms generated by permanent pacemakers. The most common cause is tracking of atrial tachyarrhythmias, such as atrial flutter or fibrillation. The pacemaker will typically pace around the programmed maximum tracking limit, which is often set at 120-140 beats per minute in older patients.

• If a pacemaker programmer is not available, a magnet placed over the pacer generator will deactivate atrial sensing temporarily and allow diagnosis of the atrial arrhythmia.

• Missed diagnoses

• Patients with sudden death may present with syncope first.

• In a syncopal patient, the ECG should be screened carefully for myocardial infarction, conduction abnormalities, QT-interval prolongation, precordial T-wave inversions, ventricular preexcitation, and ventricular hypertrophy.

• Patients treated chronically with antiarrhythmic drugs require careful follow-up to minimize the risk of proarrhythmia and other adverse effects

Special Concerns:

• In patients with VT related to genetic abnormalities, family screening is essential. When a patient is identified with long QT syndrome, short QT syndrome, hypertrophic cardiomyopathy, or right ventricular dysplasia, family screening should be contemplated. This usually can be accomplished with a history and physical examination, combined with noninvasive testing (ECG, echocardiogram, treadmill testing).

	PICTURES	Section 10 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography

Caption: Picture 1. This is a rapid monomorphic ventricular tachycardia (VT), 280 beats per minute, associated with hemodynamic collapse. This tracing was obtained from a patient with severe ischemic cardiomyopathy during an electrophysiologic (EP) study. The rhythm later converted to sinus with a single external shock. This patient had an atrial rate of 72 beats per minute (measured with intracardiac electrodes, not shown). Although ventriculoatrial dissociation (faster V rate than A rate) is diagnostic of VT, the surface ECG findings are only present approximately 20% of the time. In this tracing, the ventricular rate is simply too fast for P waves to be observed. VT with cycle lengths from 200-240 ms is often termed ventricular flutter.
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Caption: Picture 2. This is a slow monomorphic ventricular tachycardia (VT), 121 beats per minute, from a patient with an old inferior wall myocardial infarction and well-preserved left ventricular function (ejection fraction [EF] 55%). He presented with symptoms of palpitation and neck fullness. Note the ventriculoatrial dissociation, most obvious in V2 and V3. Slower VT rates and preserved left ventricular (LV) function are associated with a better long-term prognosis.
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Caption: Picture 3. Repetitive monomorphic ventricular tachycardia (VT) from an asymptomatic 45-year-old female wind surfer. This patient has a structurally normal heart. This ECG pattern is typical for a form of idiopathic VT arising from the right ventricular outflow tract. Unlike ischemic VTs, this form of VT is often provoked by exercise and suppressed by beta blockade or verapamil. The prognosis for these patients is good, with the following 2 exceptions: (1) occasionally, this form of VT is associated with right ventricular dysplasia, which is associated with sudden death, and (2) occasionally, patients with incessant VT develop congestive heart failure due to tachycardia-induced cardiomyopathy. The cardiomyopathy generally resolves when the tachycardia is treated.
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Caption: Picture 4. At first glance, this tracing suggests rapid, polymorphic ventricular tachycardia (VT). This is actually sinus rhythm with a premature atrial complex and superimposed lead motion artifact. The hidden sinus beats can be observed by using calipers to march backwards from the final 2 QRS complexes. This artifact can be generated easily with rapid arm motion (eg, brushing teeth) during telemetry monitoring.
Picture Type: ECG

Caption: Picture 5. Torsade de pointes. This is a polymorphic ventricular tachycardia (VT) associated with resting QT-interval prolongation. In this case, it was caused by the potassium channel blocker, sotalol. This rhythm is also observed in families with mutations affecting certain cardiac ion channels.
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Caption: Picture 6. Preexcited atrial fibrillation. This patient has an accessory atrioventricular connection. Atrial fibrillation has been induced. Conduction over the accessory pathway results in a wide QRS complex, mimicking ventricular tachycardia (VT).
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Caption: Picture 7. Curative ablation of ventricular tachycardia (VT) This patient has VT in the setting of an ischemic cardiomyopathy. His VT was induced in the electrophysiology laboratory, and a special catheter was placed upon a critical area of slow conduction within the VT circuit. Modified electrocautery energy (RF) is applied to the tissue through the catheter tip, and VT terminates when the critical tissue is destroyed.
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Caption: Picture 8. Ventricular pacing at 120 beats per minute Newer pacemakers often use bipolar pacing. If the smaller pacing stimulus artifact is overlooked, an erroneous diagnosis of ventricular tachycardia (VT) may result. Because leads are most commonly placed in the right ventricular apex, paced beats will have left bundle branch block (LBBB) morphology with an inferior axis. Causes of rapid pacing include (1) tracking of an atrial tachycardia in DDD mode, (2) rapid pacing due to rate response being activated, and (3) endless loop tachycardia. Application of a magnet to the pacemaker will disable sensing and allow further diagnosis.
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Picture Type: ECG

Caption: Picture 9. Supraventricular tachycardia (SVT) with aberrancy This is a patient with a structurally normal heart who has a normal resting ECG. This rhythm is an orthodromic reciprocating tachycardia with a rate-related left bundle branch block. Note the relatively narrow RS intervals in the precordial leads.
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Caption: Picture 10. Termination of ventricular tachycardia (VT) with overdrive pacing. This patient has a reentrant VT, which is terminated automatically by pacing from an implantable cardioverter-defibrillator (ICD).
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Picture Type: ECG

	BIBLIOGRAPHY	Section 11 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography

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