Medication Summary
The mainstays of treatment for clinically stable ventricular tachycardia (VT) are the various antiarrhythmic drugs. In the United Sates, the intravenous (IV) antiarrhythmic drugs available for suppression of acute monomorphic VT are limited to procainamide, lidocaine, and amiodarone, along with the beta-adrenergic blocking agents metoprolol, esmolol, and propranolol. Bretylium is no longer available.
In view of the relatively narrow therapeutic windows with these agents, careful attention must be paid to drug pharmacokinetics. Most antiarrhythmic drugs may actually cause ventricular arrhythmias, and risks generally increase with rising serum drug levels.
IV administration of antiarrhythmics is used for the suppression of acute VT. These agents alter the electrophysiologic mechanisms that are responsible for the arrhythmia. Amiodarone is the drug of choice for acute VT refractory to cardioversion shock. After recovery, oral medications are used for long-term suppression of recurrent VT. Current evidence favors class III antiarrhythmic drugs over class I drugs.
Antiarrhythmics, Class IA
Class Summary
Class IA antiarrhythmics increase the refractory periods of the atria and ventricles. Myocardial excitability is reduced by an increase in threshold for excitation and inhibition of ectopic pacemaker activity.
Procainamide (Procanbid, Pronestyl, Pronestyl [SR])
Procainamide is a class IA antiarrhythmic used for VT that is refractory to defibrillation and epinephrine. It is indicated for ventricular arrhythmias such as sustained VT. Procainamide is available only in IV form and is rarely used, because of hypotension and proarrhythmia risk. However, procainamide still maintains a specific niche as the drug of choice for management of stable preexcited atrial fibrillation. Its use is contraindicated by the presence of QT prolongation or congestive heart failure.
Quinidine (Quinidex, Quinora, Quinalan, Cardioquin)
Quinidine is a class IA antiarrhythmic that depresses myocardial excitability and conduction velocity. It is indicated for sustained VT but is rarely used, because of proarrhythmia risk. It still maintains a specific niche for VT suppression in specific patients with Brugada syndrome.
Antiarrhythmics, Class IB
Class Summary
Class IB antiarrhythmics suppress automaticity of conduction tissue by increasing the electrical stimulation threshold of the ventricle and His-Purkinje system and inhibiting spontaneous depolarization of the ventricles during diastole through a direct action on the tissues. These antiarrhythmics block both initiation and conduction of nerve impulses by decreasing the neuronal membrane’s permeability to sodium ions, thereby inhibiting depolarization, with resultant blockade of conduction.
Lidocaine (Xylocaine, Nervocaine, LidoPen, Duo-Trach)
Lidocaine is an IV class IB antiarrhythmic that increases the electrical stimulation threshold of the ventricle, suppressing the automaticity of conduction through the tissue. Although lidocaine may terminate VT successfully, it may increase the overall mortality in peri-infarction VT. It can only be given IV. Its use for VT has declined as a consequence of trials showing IV amiodarone to be superior.
Mexiletine (Mexitil)
Mexiletine is a class IB antiarrhythmic that is indicated for ventricular arrhythmias such as sustained VT. It is a sodium-channel blocker and the closest oral analogue to lidocaine. Mexiletine is generally well tolerated and is occasionally used in patients with VT who respond to IV lidocaine. Class IB sodium channel–blocking drugs are generally felt to be safer than IC drugs, but no large comparative trials exist. This drug is still occasionally used for outpatient VT suppression.
Antiarrhythmics, Class IC
Class Summary
Class IC antiarrhythmics slow conduction in cardiac tissue by altering the transport of ion across membranes, thus causing slight prolongation of refractory periods and decreasing the rate of rise of action potential without affecting its duration. These agents are typically avoided in the presence of coronary artery disease.
Flecainide (Tambocor)
Flecainide is a class IC antiarrhythmic approved for treatment of life-threatening ventricular arrhythmias. It 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 atrioventricular (AV) nodal conduction time and intra-atrial conduction times, though present, are less pronounced than are the drug's effects on ventricular conduction velocity.
Flecainide carries a US Food and Drug Administration (FDA) black box warning regarding increased mortality when the drug is used in ischemic cardiomyopathy patients. Consequently, the use of flecainide is avoided in patients with structural heart disease. This drug is used almost exclusively for suppression of atrial arrhythmias in the structurally normal heart.
Propafenone (Rythmol)
Propafenone is similar in function to flecainide and carries a similar black box warning. It is almost exclusively used for suppression of atrial arrhythmias in the structurally normal heart.
Antiarrhythmics, Class III
Class Summary
Class III antiarrhythmics prolong the action potential duration. Some agents in this class inhibit adrenergic stimulation (alpha- and beta-blocking properties); affect sodium, potassium, and calcium channels; and prolong the action potential and refractory period in myocardial tissue. These effects result in decreased AV conduction and sinus node function.
Amiodarone (Cordarone, Pacerone, Nexterone)
Amiodarone is the drug of choice for the treatment of hemodynamically unstable VT that is 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 antiarrhythmic that is primarily a potassium channel (IKr)-blocking drug with a weak beta-blocking effect. It is indicated for ventricular arrhythmias such as sustained VT. Because sotalol is renally cleared, renal function must be monitored.
Beta Blockers, Beta1-Selective
Class Summary
At low doses, cardioselective beta blockers block response to beta1-adrenergic stimulation and have little or no effect on beta2 receptors.
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 electrocardiograms (ECGs). Long-term use of metoprolol has been shown to reduce
Electrolytes
Class Summary
Electrolytes are considered therapeutic alternatives for refractory VT. Patients with persistent or recurrent VT after administration of antiarrhythmic drugs should be assessed for underlying electrolyte abnormalities as a cause of their refractory dysrhythmia. Electrolyte abnormalities that may be 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 antiarrhythmic agent. Sodium bicarbonate is used as an alkalinizing agent, and calcium chloride is used to treat VT caused by hyperkalemia.
Magnesium sulfate (MgSO4)
Magnesium sulfate is the agent of choice for torsades de pointes. It also may be useful for treating conventional VT, especially in patients with confirmed hypomagnesemia. Patients treated with magnesium sulfate require monitoring for hypermagnesemia; an overdose can cause cardiorespiratory collapse and paralysis.
Calcium chloride
Calcium chloride is useful for the treatment of hyperkalemia, hypocalcemia, or calcium-channel blocker toxicity. It moderates nerve and muscle performance by regulating the action potential excitation threshold.
Alkalinizing Agents
Class Summary
Alkalinizing agents act as a buffer against acidosis by raising blood pH.
Sodium bicarbonate
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.
Alpha-/Beta-Adrenergic Agonists
Class Summary
Alpha-/beta-adrenergic agents augment the coronary and cerebral blood flow that is present during the low-flow state associated with hemodynamic compromise from VT.
Epinephrine (Adrenalin)
Epinephrine is considered to be the single most useful drug in cardiac arrest, although it has never been shown to enhance long-term survival or functional recovery. Epinephrine stimulates alpha, beta1, and beta2 receptors, resulting in relaxation of smooth muscle, cardiac stimulation, and dilation of muscle vasculature.
Vasopressin-Related
Class Summary
Vasopressin is a vasoconstrictor without inotropic or chronotropic effects.
Vasopressin (ADH, Pitressin)
Vasopressin may improve vital organ blood flow, cerebral oxygen delivery, resuscitability, and neurologic recovery.
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This electrocardiogram (ECG) shows rapid monomorphic ventricular tachycardia (VT), 280 beats/min, associated with hemodynamic collapse. The tracing was obtained from a patient with severe ischemic cardiomyopathy during an electrophysiologic study. A single external shock subsequently converted VT to sinus rhythm. The patient had an atrial rate of 72 beats/min (measured with intracardiac electrodes; not shown). Although ventriculoatrial dissociation (faster V rate than A rate) is diagnostic of VT, surface ECG findings (dissociated P waves, fusion or capture beats) are present in only about 20% of cases. In this tracing, the ventricular rate is simply too fast for P waves to be observed. VT at 240-300 beats/min is often termed ventricular flutter.
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This electrocardiogram shows slow monomorphic ventricular tachycardia (VT), 121 beats/min, from a patient with an old inferior wall myocardial infarction and well-preserved left ventricular (LV) function (ejection fraction, 55%). The patient presented with symptoms of palpitation and neck fullness. Note the ventriculoatrial dissociation, which is most obvious in leads V2 and V3. Slower VT rates and preserved LV function are associated with better long-term prognosis.
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At first glance, this tracing suggests rapid polymorphic ventricular tachycardia. It is actually sinus rhythm with premature atrial complex and a superimposed lead motion artifact. Hidden sinus beats can be observed by using calipers to march backward from the final two QRS complexes. This artifact can be generated easily with rapid arm motion (eg, brushing teeth) during telemetry monitoring.
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Torsade de pointes. Image A: This is polymorphic ventricular tachycardia associated with resting QT-interval prolongation. In this case, it was caused by the class III antiarrhythmic agent sotalol. This rhythm is also observed in families with mutations affecting certain cardiac ion channels. Image B: Torsade de pointes, a form of ventricular tachycardia. Courtesy of Science Source/BSIP.
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Preexcited atrial fibrillation. The patient has an accessory atrioventricular connection. Atrial fibrillation has been induced. Conduction over an accessory pathway results in a wide QRS complex, mimicking ventricular tachycardia.
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Curative ablation of ventricular tachycardia (VT). The patient had VT in the setting of ischemic cardiomyopathy. VT was induced in an electrophysiology laboratory, and an ablation catheter was placed at the critical zone of slow conduction within the VT circuit. Radiofrequency (RF) energy was applied to tissue through the catheter tip, and VT was terminated when the critical conducting tissue was destroyed.
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Ventricular pacing at 120 beats/min. Newer pacemakers use bipolar pacing. If a smaller pacing stimulus artifact is overlooked, an erroneous diagnosis of ventricular tachycardia may result. Because leads are most commonly placed in the right ventricular apex, paced beats will have a left bundle-branch block morphology with inferior axis. Causes of rapid pacing include (1) tracking of atrial tachycardia in DDD mode, (2) rapid pacing due to the rate response being activated, and (3) endless loop tachycardia. Application of a magnet to the pacemaker will disable sensing and allow further diagnosis. Sometimes “pacing spike detection” must be programmed “ON” in the electrocardiographic system to make the spike apparent.
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Supraventricular tachycardia with aberrancy. This tracing is from a patient with a structurally normal heart who has a normal resting electrocardiogram. This rhythm is orthodromic reciprocating tachycardia with rate-related left bundle-branch block. Note the relatively narrow RS intervals in the precordial leads.
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Termination of ventricular tachycardia (VT) with overdrive pacing. This patient has reentrant VT, which is terminated automatically by pacing from an implantable cardioverter-defibrillator.
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Posteroanterior view of a right ventricular endocardial activation map during ventricular tachycardia in a patient with a previous septal myocardial infarction. The earliest activation is recorded in red, and late activation as blue to magenta. Fragmented low-amplitude diastolic local electrograms were recorded adjacent to the earliest (red) breakout area, and local ablation in this scarred zone (red dots) resulted in termination and noninducibility of this previously incessant arrhythmia.
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This tracing depicts monomorphic ventricular tachycardia.
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This image demonstrates polymorphic ventricular tachycardia.
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This electrocardiogram is from a 32-year-old woman with recent-onset heart failure and syncope.
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This electrocardiogram is from a 48-year-old man with wide-complex tachycardia during a treadmill stress test. Any wide-complex tachycardia tracing should raise the possibility of ventricular tachycardia, but closer scrutiny confirms left bundle-branch block conduction of a supraventricular rhythm. By Brugada criteria, RS complexes are apparent in the precordium (V2-V4), and the interval from R-wave onset to the deepest part of the S wave is shorter than 100 ms in each of these leads. Ventriculoatrial dissociation is not seen. Vereckei criteria are based solely upon lead aVR, which shows no R wave, an initial q wave width shorter than 40 ms, and no initial notching in the q wave. The last Vereckei criterion examines the slope of the initial 40 ms of the QRS versus the terminal 40 ms of the QRS complex in lead aVR. In this case, the initial downward deflection in lead aVR is steeper than the terminal upward deflection, yielding Vi/Vt ratio above 1. All of these criteria are consistent with an aberrantly conducted supraventricular tachycardia. Gradual rate changes during this patient's treadmill study (not shown here) were consistent with a sinus tachycardia mechanism.
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The electrocardiogram shows a form of idiopathic ventricular tachycardia (VT) seen in the absence of structural heart disease. This rhythm arises from the left ventricular septum and often responds to verapamil. Upon superficial examination, it appears to be supraventricular tachycardia with bifascicular conduction block. Closer examination of lead V1 shows narrowing of fourth QRS complex, consistent with fusion between the wide QRS complex and the conducted atrial beat, confirming atrioventricular dissociation and a VT mechanism.
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A wide QRS complex tachycardia is evident on this electrocardiogram from a 64-year-old man with history of previous myocardial infarction (MI) and syncope. In patients with a prior MI, the most common mechanism of wide QRS complex tachycardia is ventricular tachycardia.
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This tracing depicts atrioventricular dissociation.
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Fusion beats, capture beats, and atrioventricular dissociation can be seen on this electrocardiogram.
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Note the retrograde P waves in this electrocardiogram.
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Retrograde P waves are also observed in this electrocardiogram.
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This electrocardiogram reveals torsade de pointes.
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Hematoxylin and eosin stain; intermediate power of a healed myocardial infarct. Note the areas of fibrosis (pale pink) dissecting between the myocytes (red).
Tables
| Recommendation | Class |
|---|---|
| Resting 12-lead electrocardiography (ECG) in all patients | Class I |
12-lead ambulatory ECG to evaluate QT-interval changes or ST changes |
Class I |
| Cardiac event recorders when symptoms are sporadic to rule out transient arrhythmias | Class I |
Implantable loop recorders when symptoms are sporadic and suspected to be related to arrhythmias and when a symptom–rhythm correlation cannot be established by conventional diagnostic techniques |
Class I |
Exercise stress testing in adult patients who have an intermediate or greater probability of having coronary artery disease (CAD) to provoke ischemic changes or ventricular arrhythmia (VA) |
Class I |
| Exercise stress testing in patients with known or suspected exercise-induced VA | Class I |
| Echocardiography in all patients | Class I |
Pharmacologic stress testing plus imaging modality study to detect silent ischemia in patients with VAs who have an intermediate probability of having CAD and are physically unable to perform a symptom-limited exercise test |
Class I |
Cardiac magnetic resonance imaging (cMRI) or computed tomography (CT) scanning in patients with VAs when echocardiography does not provide accurate assessment of left- and right-ventricular function and/or evaluation of structural changes |
Class IIa |
Electrophysiologic study in patients with CAD with remote myocardial infarction with symptoms suggestive of ventricular tachyarrhythmias, including palpitations, presyncope, and syncope. |
Class I |
Coronary angiography to establish or exclude significant obstructive CAD in patients with life-threatening VAs or in survivors of sudden cardiac death, who have an intermediate or greater probability of having CAD by age and symptoms |
Class IIa |
