RISK FACTORS : HYPERLIPIDEMIA, HYPERTENSION, CIGARETTE SMOKING
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.
o Amiodarone has also been studied as primary arrhythmia prophylaxis in the postinfarct setting, but it had no impact on overall mortality rates.
o 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.
o In these studies, patients with ischemic cardiomyopathy, ejection fractions greater than 35-40%, and nonsustained VT were taken to EPS.
o Patients with inducible sustained VT were randomized between conventional antiarrhythmic therapy and prophylactic ICD implantation.
o 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.
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.
DRUG THERAPY : 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.
1. 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.
- LIDOCAINE
- PROCAINAMIDE
- AMIODARONE
- SOTALOL
- MEXILETINE
- ACEBUTOLOL
- ATENOLOL
- METOPROLOL
- FLECAINIDE
- PROPAFENONE
- ANTIDIGOXIN ANTIBODIES IF DIGOXIN TOXIC
- DRUGS TO CORRECT ELECTROLYTE IMBALANCE LIKE POTASIUM FOR HYPOKALEMIA