Ventricular Tachycardia Medication

As previously mentioned, the mainstays of treatment for clinically stable ventricular tachycardia (VT) are the various antidysrhythmic drugs.

Intravenous medications are used to suppress acute monomorphic VT. In the United States, these are limited to procainamide, lidocaine, amiodarone, and a handful of intravenous beta-adrenergic blocking agents (metoprolol, esmolol, propranolol). Bretylium is no longer available.

In patients with cardiac arrest, intravenous amiodarone is the drug of choice. Although intravenous lidocaine is effective at suppressing peri-infarction VT, it may increase the overall mortality risk. As indicated by the ACC/AHA/ESC 2006 guidelines, the use of IV procainamide is a reasonable choice for initial treatment of patients with stable sustained monomorphic VT.^[16]

Amiodarone has been shown to be superior to lidocaine or placebo in resuscitated cardiac arrest, but it has not been as well studied in stable, monomorphic VT. The ACC/AHA/ESC 2006 guidelines state that IV amiodarone is a reasonable choice in patients with sustained monomorphic VT that is hemodynamically unstable, refractory to conversion with countershock, or recurrent despite the use of procainamide or other agents.^[16] (As previously mentioned, however, mounting evidence indicates that amiodarone should not be the first-line antidysrhythmic in the treatment of stable VT, because its effects on myocardial conduction and refractoriness are gradual in onset.^{[24, 25, 26]} )

According to the ACC/AHA/ESC guidelines, if coronary revascularizaton cannot be achieved and prior MI and significant LV dysfunction are evident, the primary treatment for patients resuscitated from VF should be an implantable cardioverter defibrillator (ICD) in patients receiving chronic optimal medical therapy and those who can reasonably be expected to survive with a good functional status for more than 1 year.^[16]

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. Both drugs require careful monitoring during initiation and long-term follow-up.

Sotalol is loaded on an inpatient basis, with telemetry and electrocardiographic monitoring for bradycardia, ventricular proarrhythmia, and excessive QT prolongation. Many centers then follow sotalol patients on a quarterly basis to reassess renal function, to observe QT intervals, and to watch for new drug interactions. Amiodarone initiation requires baseline and serial liver, thyroid, and pulmonary function testing.

The ACC/AHA/ESC guidelines state that IV amiodarone or procainamide followed by VT ablation can be useful in treating patients with frequently recurring or intractable monomorphic VT.^[16]

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 associated with QT-interval prolongation, usually due to excessive potassium-channel blockade.

As stated by the ACC/AHA/ESC 2006 guidelines, removal of any offending drugs and correction of electrolyte irregularities are recommended in patients presenting with torsades de pointes.^[16] The 2006 guidelines also recommend acute and long-term pacing for patients with torsades de pointes due to heart block and symptomatic bradycardia.^[16] It is also a reasonable choice for patients who present with recurrent pause-dependent torsades de pointes.^[16]

In patients with hemodynamically significant VT/ventricular fibrillation (VF), ICDs have 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.

The ACC/AHA/ESC guidelines support the use of ablation in patients with an ICD who are receiving multiple shocks due to sustained VT that is not manageable by changing drug therapy, or who do not wish to undergo long-term drug therapy.^[16]

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

Note that the use of verapamil can precipitate VF in patients whose VT has been misidentified as PSVT with aberrancy.

Although idiopathic VTs often respond to verapamil, this agent may cause hemodynamic collapse and death when administered to VT in patients with left ventricular dysfunction.

Therefore, avoid verapamil (and all calcium-channel blockers) in any patient with wide-complex tachycardia of uncertain etiology.^[26]

Class Summary

Intravenous administration of antiarrhythmics is used for the suppression of acute ventricular tachycardia (VT). These agents alter the electrophysiologic mechanisms that are responsible for arrhythmia. Antiarrhythmics are generally used to prevent a recurrence of VT in susceptible patients.

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

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

Patients who are being monitored for drug proarrhythmia are usually admitted to the hospital during the initiation of oral antiarrhythmic medication. The patient is then monitored by telemetry and serial ECGs during 5-6 drug half-lives to be sure that the drug is well tolerated.

Procainamide (IV only, no oral version available)

Procainamide is a class Ia antiarrhythmic used for ventricular tachycardia that is refractory to defibrillation and epinephrine. This agent increases the refractory period of the atria and ventricles. Myocardial excitability is reduced by an increase in the threshold for excitation and the inhibition of ectopic pacemaker activity. It is indicated for ventricular arrhythmias such as sustained ventricular tachycardia.

Lidocaine (Xylocaine, Nervocaine, LidoPen, Duo-Trach)

This is a class IB antiarrhythmic that increases the electrical stimulation threshold of the ventricle, suppressing the automaticity of conduction through the tissue. Although lidocaine may terminate ventricular tachycardia successfully, it may increase the overall mortality in peri-infarction ventricular tachycardia.

Amiodarone (Cordarone, Pacerone)

Amiodarone is now the drug of choice in the treatment of unstable ventricular arrhythmias. Amiodarone is a class III antiarrhythmic that is indicated for hemodynamically unstable ventricular tachycardia refractory to other antiarrhythmic agents. Prehospital studies currently suggest that amiodarone is safe and efficacious for use in out-of-hospital cardiac arrest.

Sotalol (Betapace)

Sotalol is a class III antidysrhythmic that is primarily a potassium channel (IKr)–blocking drug with a weak beta-blocker effect. In the ESVEM study, survival was best in the sotalol group when sotalol was compared with 6 other drugs (not including amiodarone) in ventricular tachycardia patients. It is indicated for ventricular arrhythmias such as sustained ventricular tachycardia.

Mexiletine (Mexitil)

This agent is a class Ib antidysrhythmic that is indicated for ventricular arrhythmias such as sustained ventricular tachycardia. It is a sodium channel blocker and the closest oral analog to lidocaine. Mexiletine is generally well tolerated and is occasionally used in patients with ventricular tachycardia who respond to intravenous lidocaine. Class Ib sodium channel–blocking drugs are generally felt to be safer than Ic drugs, but no large comparative trials exist.

Metoprolol (Lopressor, Toprol XL)

Metoprolol is a selective beta1-adrenergic receptor blocker that decreases the automaticity of contractions. During IV administration, carefully monitor the patient's blood pressure, heart rate, and ECGs.

Esmolol (Brevibloc)

Esmolol is a class II antiarrhythmic that that selectively blocks beta1-receptors with little or no effect on beta2-receptor types. It has no sympathomimetic or membrane stabilizing activity. It is indicated for supraventricular tachycardia and atrial fibrillation/flutter. It can also be used to treat intraoperative and postoperative tachycardia or hypertension.

Flecainide (Tambocor)

Flecainide is a class Ic antiarrhythmic used to treat life-threatening ventricular arrhythmias. It causes a prolongation of refractory periods and decreases action potential without affecting duration. The drug blocks sodium channels, producing a dose-related decrease in intracardiac conduction in all parts of the heart, with the greatest effect on the His-Purkinje system (HV conduction). The effects of flecainide on AV nodal conduction time and intra-atrial conduction times, although present, are less pronounced than are the drug's effects on ventricular conduction velocity.

Propafenone (Rythmol)

This agent is used to treat life-threatening arrhythmias. It possibly works by reducing spontaneous automaticity and prolonging the refractory period.

Quinidine (Quinidex, Quinora, Quinalan, Cardioquin)

Quinidine is a class Ia antiarrhythmic that depresses myocardial excitability and conduction velocity. It is indicated for sustained ventricular tachycardia.

Class Summary

Electrolytes are considered to be therapeutic alternatives for refractory VT. Patients with persistent or recurrent VT following antidysrhythmic administration should be assessed for underlying electrolyte abnormalities as a cause of their refractory dysrhythmia. Some electrolyte abnormalities associated with VF include hyperkalemia, hypokalemia, and hypomagnesemia.

Magnesium sulfate, calcium chloride, and sodium bicarbonate are used in VT secondary to other medications. Magnesium sulfate acts as an antidysrhythmic agent. Sodium bicarbonate is used as an alkalinizing agent, and calcium chloride is used to treat VT caused by hyperkalemia.

Magnesium sulfate (Magnesium)

This is the drug of choice for torsade de pointes. It also may be useful to treat conventional VT, especially when hypomagnesemia is confirmed in a patient. When treating a patient with magnesium sulfate, monitor him or her for hypermagnesemia, since an overdose can cause cardiorespiratory collapse and paralysis.

Sodium bicarbonate (Neut)

Sodium bicarbonate is used only when the patient is diagnosed with bicarbonate-responsive acidosis with pH ≤7.0, hyperkalemia, or a tricyclic antidepressant or phenobarbital overdose. Routine use of sodium bicarbonate is not recommended.

Calcium chloride

This agent is useful for the treatment of hyperkalemia, hypocalcemia, or calcium channel–blocker toxicity. It moderates nerve and muscle performance by regulating action potential excitation threshold.

Class Summary

These agents augment the coronary and cerebral blood flow that is present during the low-flow state associated with CPR.

Epinephrine (Adrenalin, EpiPen, EpiPen Jr)

Epinephrine is considered to be the single most useful drug in cardiac arrest, although it has never been shown to affect mortality.

Vasopressin (Pitressin)

Vasopressin may improve vital organ blood flow, cerebral oxygen delivery, the patient's ability to be resuscitated, and the patient's neurologic recovery.