Dr.Proxy

Author: Ian S deSouza, MD, Assistant Professor, Department of Emergency Medicine, Kings County Hospital/SUNY Downstate Medical Centers
Coauthor(s): Che' Damon Ward, MD, Staff Physician, Department of Emergency Medicine, State University of New York Health Science Center at Brooklyn

Introduction

Background

Ventricular tachycardia (VT) is a tachydysrhythmia originating from a ventricular ectopic focus, characterized by a rate typically greater than 120 beats per minute with wide QRS complexes. VT may be monomorphic (originating from a single focus with identical QRS complexes) or polymorphic (may appear as an irregular rhythm, with varying QRS amplitudes and morphology). Nonsustained VT is defined as a run of tachycardia of less than 30 seconds duration; longer runs are considered sustained VT.

No absolute ECG criteria exist for establishing the presence of VT. However, several factors suggest VT, including the following:

• Rate greater than 120 beats per minute (usually 150-200)
• Wide QRS complexes (>140 ms)
• Presence of atrioventricular (AV) dissociation
• Fusion beats
• Capture beats

Other historical factors suggesting VT are prior ischemic or structural heart disease. It may exist without cardiovascular collapse but when hemodynamic compromise occurs, it may deteriorate rapidly into a more malignant dysrhythmia: ventricular fibrillation (VF). Therefore, this tachydysrhythmia must be addressed swiftly to avoid morbidity or mortality.

Pathophysiology

Ventricular tachycardia (VT) is usually a consequence of structural or ischemic heart disease, with breakdown of normal conduction patterns. Abnormal automaticity (which tends to favor ectopic foci) or activation of reentrant pathways in the myocardium can exist to generate the dysrhythmia. Electrolyte disturbances, ischemia, and sympathomimetics may increase the likelihood of VT in the susceptible myocardium.

AV dissociation, shown in the image below, is apparent in approximately half of VT episodes, and when present, it is a hallmark characteristic of VT.¹ This occurs because the sinus node is depolarizing the atria at a rate that is slower than the pathologic, faster ventricular rate. P waves can be visualized at times in between or embedded in the QRS complexes, but the P waves and QRS complexes have their own independent rates.


Fusion beats and capture beats can occur in the presence of VT depending on the refractory period of the AV node and the timing of ventricular and atrial depolarizations, respectively.

A fusion beat has a mixed morphology, due to normal AV node/His-Purkinje conduction occurring simultaneously with abnormal (wide complex QRS) ventricular depolarization. A normally conducted impulse travels from the AV node through the normal conduction pathway (a narrow QRS), and the competing impulse originates from the abnormal ectopic ventricular focus outside of the normal conduction pathway (a wide QRS). The two converge leading to a mixed (fused) QRS.A capture beat occurs when an atrial impulse arrives at the AV node at a "fortuitous" time when the AV node has just recovered from its refractory period. The timing has to be just right as the AV node is frequently in its refractory state due to depolarization caused by retrograde conduction from the rapid ventricular rhythm. When this occurs, conduction will proceed normally through the AV node/His-Purkinje system, "capturing" the ventricle and leading to a normal, narrow QRS complex. Fusion, capture beats, and AV dissociation are shown in the image below.


Retrograde conduction can also exist from the ventricles to the atria via the AV node. This is not AV dissociation and reveals itself in an ECG as a 1:1 correlation between the wide QRS complex and an inverted P wave, which follows the QRS complex. This is also seen in two different types of wide-QRS complex SUPRAventricular tachycardias, which are often confused with ventricular tachycardia: (1) antidromic AV reentrant tachycardia (AVRT) and (2) AV nodal reentrant tachycardia with aberrant conduction (AVNRT).

Antidromic AVRT may occur depending on the properties of the atrioventricular node and an accessory conduction pathway and their propensity together to develop a reentry mechanism. Forward, or anterograde, conduction through the accessory pathway may occur to depolarize the ventricles abnormally (without use of a normal HIS-Purkinje system) — this leads to a widened QRS complex. Backward, or retrograde, conduction through the AV node to the atria then occurs, which thus generates retrograde P waves, shown in the image below. AVNRT with aberrant conduction occurs when a reentrant circuit in the AV node propagates impulses both anterograde through an abnormal His-Purkinje system (thus the wide QRS) and also retrograde through the atria creating retrograde P waves. These two rhythms may be indistinguishable from VT with 1:1 ventriculoatrial conduction.
The most common cause of monomorphic sustained VT is a prior MI with ventricular myocardial scar formation. The presence of myocardial fibrosis is a substrate for slow conduction pathways and associated reentry mechanisms. Nonsustained VT and ectopy are due to abnormal automaticity mechanisms and more commonly associated with acute myocardial ischemia.

A distinctive variant of VT is torsade de pointes, with its unusual shifting-axis QRS complexes that appear (on ECG) as if the heart is rotating upon an axis. It typically occurs during sinus rhythm and in the presence of drugs or conditions that prolong the QT interval (eg, type 1A antiarrhythmics, hypomagnesemia, droperidol). The dysrhythmia may occur either in the presence or in the absence of myocardial ischemia or infarction. Torsade de pointes is shown below.

A second variant of VT is accelerated idioventricular rhythm. Sometimes termed slow ventricular tachycardia, this dysrhythmia presents with a rate of 60-100 beats per minute. It typically occurs with underlying heart disease (ischemic or structural), is transient, and only rarely is associated with hemodynamic compromise or collapse. Treatment of the dysrhythmia itself usually is not required unless significant hemodynamic impairment develops.
Due to advances in molecular biology, a number of inherited dysrhythmic disorders with a propensity toward VT have been described. Brugada syndrome, congenital long and short QT syndrome, and catecholaminergic-sensitive VT have complex inheritance patterns. Mechanistically, each disorder is characterized by imbalanced ion transport across the cardiac cellular membrane, which leads to abnormalities in cardiac repolarization, and thus increased risk of dysrhythmia. These syndromes have all been linked to sudden cardiac death. Patients with these disorders are being managed with a combination of genetic typing, antidysrhythmic medications, lifestyle modification, and implantable cardioverter-defibrillator (ICD) placement.²

Frequency

United States

Nonsustained, short runs of ventricular tachycardia are frequently observed dysrhythmias, but sustained monomorphic ventricular tachycardia is uncommon in the ED setting due to aggressive treatment of myocardial ischemia.

International

Ventricular tachycardia and coronary artery disease are common throughout most of the developed world. In developing countries, ventricular tachycardia and other heart diseases are relatively less common.

Mortality/Morbidity

• Morbidity and mortality in ventricular tachycardia arise principally from spontaneous degeneration into the more malignant ventricular defibrillation.
• Even without such degeneration, ventricular tachycardia can also produce congestive heart failure and hemodynamic compromise, with subsequent morbidity and mortality.

Sex

• Currently, most patients presenting with ventricular tachycardia are men.
• As coronary artery disease (CAD) becomes more common in women, it seems certain that the incidence of ventricular tachycardia in women will increase.

Age

• Ventricular tachycardia is unusual among pediatric patients, although when present there is associated congenital heart disease, or it occurs in the postoperative cardiac setting. Tachydysrhythmias in this population generally are PSVT.
• Ventricular tachycardia incidence rates peak in the middle decades of life, following the incidence of structural heart disease.

Clinical

History

Most patients with ventricular tachycardia (VT) present to the ED with symptoms of either ischemia or hemodynamic compromise. These may include the following:

• Chest discomfort
• Dyspnea
• Diaphoresis
• Nausea
• Palpitations
• Anxiety or feeling of "impending doom"
• Syncope and presyncope

Physical

Besides tachycardia, findings of ventricular tachycardia generally reflect the degree of hemodynamic instability.

• Signs of congestive heart failure (CHF)
  • Hypotension
  • Hypoxemia
  • Jugular venous distention
  • Rales 
• Mental status changes
  • Anxiety
  • Agitation
  • Lethargy
  • Coma 
• Subtle signs of AV dissociation
  • Irregular cannon a waves in the jugular pulse
  • Variable intensity of the first heart sound
  • Beat-to-beat changes in systolic blood pressure

Causes

Ventricular tachycardia (VT) generally is a consequence of ischemic or structural heart disease or electrolyte deficiencies (eg, hypokalemia, hypocalcemia, hypomagnesemia). It can also be triggered by the following:

• Use of sympathomimetic agents (from relatively benign caffeine to more potent agents such as methamphetamine or cocaine)
• Drugs that prolong the QT complex (eg, type 1A antidysrhythmics, droperidol and related phenothiazines) - These drugs may infrequently cause torsade de pointes.
• Rheumatologic disorders that affect the myocardium systemic such as systemic lupus erythematosus and rheumatoid arthritis
• Other structural congenital disorders such as right ventricular dysplasia and tetralogy of Fallot
• Digitalis toxicity - This can lead to biventricular tachycardia.
• Inherited channelopathies

Differential Diagnoses

Atrial Fibrillation	Hypomagnesemia
Atrial Flutter	Myocardial Infarction
Automatic External Defibrillation	Pacemaker and Automatic Internal Cardiac Defibrillator
Congestive Heart Failure and Pulmonary Edema	Premature Ventricular Contraction
Hypocalcemia	Torsade de Pointes
Hypokalemia	Ventricular Fibrillation

Other Problems to Be Considered

Supraventricular tachycardia (SVT) with aberrancy
Sudden cardiac death

Workup

Laboratory Studies

• When the patient presents with symptoms of frank hemodynamic compromise, one should defer laboratory tests until electrical cardioversion or defibrillation is performed and the patient is stabilized.
• Assess electrolyte levels of all patients with ventricular tachycardia (VT), including serum calcium, magnesium, and phosphate levels. Ionized calcium levels are preferred over total serum calcium level. Hypokalemia, hypomagnesemia, and hypocalcemia may predispose patients to either monomorphic VT or torsade de pointes.
• Obtain, when appropriate, levels of therapeutic drugs (eg, digoxin). Toxicology screens may be helpful in those cases related to recreational drug use.
• Evaluate for myocardial ischemia or infarction with serum cardiac troponin I or T levels or other cardiac markers.

Imaging Studies

• Chest radiography is indicated if symptoms suggest the possibility of congestive heart failure (CHF) or other cardiopulmonary pathology as contributing factors.

Other Tests

• ECG is the diagnostic tool of choice for confirming the presence of ventricular tachycardia (VT). Simultaneous 3-channel recordings and 12-lead tracings are more helpful than rhythm strips to analyze such dysrhythmias. 
  • Complexes of atypical morphology often are difficult to interpret. Such tachycardias can be paroxysmal supraventricular tachycardia (PSVT) with aberrant conduction. If the patient is unstable, or differentiation between VT and SVT is uncertain, treat rhythm as VT. Recall that the vast majority of patients with wide-complex regular tachycardias will have VT. 
  • ECG criteria that support VT over SVT (as described before) include AV dissociation, capture beats, fusion beats (sometimes at the initiation of the dysrhythmia), QRS duration over 140 ms. Other more subtle criteria include R or qR pattern in V₁, frontal QRS axis between 180 and 270 degrees, and positive or negative concordance across the precordial leads.³
  • ECG criteria that support SVT over VT include a right bundle branch block (RBBB) pattern when present in the native sinus rhythm, varying bundle branch block, an rsR’ pattern in V₁, or an ectopic P wave preceding the dysrhythmia.³

Remember, patients with underlying structural or ischemic heart disease are more likely to have VT than SVT. Historically, the use of adenosine to distinguish between regular wide-QRS complex SVTs and ventricular tachycardia has been discouraged due to the theoretical precipitation of ventricular fibrillation. However, a recent study has demonstrated that adenosine may be both useful and safe as a diagnostic agent in this differentiation.⁴ Adenosine through transient AV nodal blockade should terminate reentrant SVTs, which involve the AV node as a pathway (described above in Pathophysiology), but will not terminate VT.

Adenosine should NOT be used for IRREGULAR wide-QRS complex tachycardia, as this dysrhythmia may involve atrial fibrillation in presence of an accessory pathway. In this particular case, adenosine may allow conduction of rapid atrial fibrillatory impulses exclusively through an amenable accessory tract to cause very rapid, intolerable ventricular rates.

Treatment

Prehospital Care

EMTs and paramedics may be called upon to provide cardioversion/defibrillation in the field if they have sufficient training and if appropriate protocols exist.

• Rapid transport to an ED is essential.
• EMS personnel must pay adequate attention to the primary survey and address the ABCs as necessary. Beyond those steps, vascular access, supplemental oxygen, and ECG rhythm strip monitoring are all-important but should not delay rapid transport to the ED for definitive care.

Emergency Department Care

During the initial assessment, once real-time cardiac monitoring or 12-lead ECG has established ventricular tachycardia (VT) as the diagnosis, one should determine if the VT is stable or unstable as the ABCs are reassessed in the primary survey.

• Pulseless VT
  • Pulseless VT, in contrast to other unstable VT rhythms, is treated with immediate defibrillation. High-energy, unsynchronized energy should be used. The initial shock dose on a biphasic defibrillator is 150-200 J followed by an equal or higher shock dosage for subsequent shocks. If a monophasic defibrillator is used, the initial and subsequent shock dosage should be 360 J. Shock administration should be followed by immediate chest compressions, airway management with supplemental oxygen, and vascular access with administration of vasopressor agents. In cases of shock-resistant pulseless VT, one can consider use of antidysrhythmic medications.
  • Vasopressors can include epinephrine at 1 mg IV given every 3-5 minutes, or in lieu of epinephrine, vasopressin 40 U IV as a one-time dose.
  • Advanced cardiac life support (ACLS) drug therapy guidelines recommend the use of intravenous amiodarone or lidocaine as the first-line adjunctive antidysrhythmic treatment of shock-resistant pulseless VT.
• Unstable VT
  • Unstable VT is characterized by signs/symptoms of insufficient oxygen delivery to vital organs. These signs/symptoms can be chest pain, dyspnea, hypotension, or altered level of consciousness, which indicate that heart rate and contractility are not enabling adequate cardiac output.
  • In this situation, the dysrhythmia should be immediately treated with synchronized cardioversion, usually at a starting energy dose of 100 J (monophasic). Comparable biphasic recommendations are not available at this time.
  • In contrast, unstable polymorphic VT is treated with immediate defibrillation. The defibrillator may have difficulty recognizing the varying QRS complexes and therefore synchronization of shocks may not occur.
  • Antidysrhythmic therapy as outlined above for shock-resistant pulseless VT may be administered to those with shock-resistant unstable VT. 
• Stable VT
  • Stable VT denotes monomorphic VT with adequate vital end-organ perfusion. These patients do not experience signs/symptoms of hemodynamic compromise.
  • Although DC cardioversion is probably the most effective treatment of stable VT,⁵ it causes obvious discomfort and requires systemic analgesia/anxiolysis. Alternatively, stable VT can be treated with intravenous procainamide, amiodarone, or sotalol. 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.^6,7,5
  • When associated with ongoing myocardial ischemia, lidocaine is suggested as the primary antidysrhythmic medication as the mechanism is thought to be abnormal automaticity and not reentry.^3,5 In situations involving torsade de pointes, magnesium sulfate may be effective if a long QT interval is present at baseline.
  • Consider synchronized cardioversion early if medical therapy fails to stabilize the rhythm. Initial shock energy should be 100 J (monophasic), followed by higher shock energies if the response is inadequate.

Consultations

Following initial treatment and stabilization, patients with ventricular tachycardia (VT) generally should be referred to a cardiologist for admission to a monitored bed, further studies such as electrophysiologic study (EPS) with possible radiofrequency ablation, and possible automatic internal cardioverter/defibrillator (AICD) placement.
Only rarely will a patient with stable, recurrent episodes of VT have his or her dysrhythmia treated in the ED and be discharged with appropriate follow-up care. This decision must be made in consultation with a cardiologist.

Medication

The mainstays of treatment for clinically stable VT are the various antidysrhythmic drugs.
Note that use of verapamil can precipitate ventricular fibrillation (VF) in patients whose VT has been misidentified as PSVT with aberrancy. For that reason, avoid verapamil (and all calcium channel blockers) in any patient with wide-complex tachycardia of uncertain etiology.⁸

Antidysrhythmics

These agents alter the electrophysiologic mechanisms responsible for arrhythmia.

Amiodarone (Cordarone)

Newest of the antidysrhythmics used in treating VT, generally is considered a class III antidysrhythmic, yet it has pharmacologic characteristics of all 4 classes.
Now is considered a class I intervention by the American College of Cardiology's practice guidelines for managing acute MI. Drug of choice in treatment of refractory, hemodynamically unstable VT. Prehospital studies suggest amiodarone is safe for use in prehospital setting, and its adoption in the new ACLS guidelines will increasingly lead EMS authorities to adopt it as their first-line antidysrhythmic. This change already is well underway in Europe.

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

Class IB antidysrhythmics stabilize cell membranes, blunts phase 0 of the action potential, and shortens repolarization. Their net effect is to decrease firing of ectopic foci to allow a normal rhythm to reassert itself.
However, amiodarone appears to be replacing lidocaine as the drug of choice.

Procainamide (Procanbid, Pronestyl)

Class IA antidysrhythmic, slows down phase 4 (diastolic) depolarization, decreases automaticity, and slows intraventricular conduction. May be considered first-line medical therapy for treatment of stable VT.
Second-line therapy used for VT refractory to defibrillation, epinephrine, and lidocaine, it increases refractory period of atria and ventricles. Myocardial excitability is reduced by an increase in threshold for excitation and inhibition of ectopic pacemaker activity.

Sotalol (Betapace)

Class III antidysrhythmic agent, which blocks potassium channels, prolongs action potential duration (APD) and lengthens QT interval. Noncardiac selective beta-adrenergic blocker.

Electrolytes

These agents are considered therapeutic alternatives for refractory VT. Patients with persistent or recurrent VT following antidysrhythmic administration should be assessed for underlying electrolyte abnormalities as a cause for 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)

Drug of choice for torsade de pointes, it also may be useful to treat conventional VT, especially where hypomagnesemia is confirmed.
When treating with magnesium sulfate, monitor for hypermagnesemia since an overdose can cause cardiorespiratory collapse and paralysis.

Sodium bicarbonate (Neut)

Used only when patient is diagnosed with bicarbonate-responsive acidosis with pH ≤7.0, hyperkalemia, tricyclic antidepressant or phenobarbital overdose. Routine use is not recommended.

Calcium chloride

Useful to treat hyperkalemia, hypocalcemia, or calcium channel blocker toxicity, it moderates nerve and muscle performance by regulating action potential excitation threshold.

Vasopressor

These agents augment both coronary and cerebral blood flow present during low flow state associated with CPR.

Epinephrine (Adrenalin, Sus-Phrine, EpiPen)

Considered the single most useful drug in cardiac arrest, although it has never been shown to affect mortality.

Vasopressin

May improve vital organ blood flow, cerebral oxygen delivery, ability to be resuscitated, and neurologic recovery.