Ventricular Tachyarrhythmias

Nonsustained ventricular tachycardia


Ventricular tachycardia (VT) is defined as three or more consecutive ventricular beats occurring at a rate of 100 beats or more per minute. Nonsustained ventricular tachycardia (NSVT) ( Fig. 6.1 ) is defined as VT lasting less than 30 seconds and that does not require intervention for termination. The QRS complex morphology may be either monomorphic (e.g., uniform in a given ECG lead) or polymorphic (e.g., variable in a given lead). Polymorphic VT with a normal QT interval is most often ischemic in etiology, and that associated with a prolonged QT is referred to as torsades de pointes (TdP) and is usually nonischemic in etiology. The rate of VT ranges from 100 to 280 bpm. VT complexes are usually wide because of the slower rate of conduction through ventricular tissue compared with that occurring through Purkinje fibers. QRS duration will depend on the origin and mechanism of the VT.

Figure 6.1

Nonsustained Ventricular Tachycardia.

This lead V 1 , II, and V 5 rhythm strip shows repetitive runs of nonsustained wide QRS complex tachycardias (5-6 beats long, rate ~ 125-135 bpm) that represent nonsustained ventricular tachycardia. The second run is followed by a compensatory pause. There is AV dissociation evident in the first run on lead V 1 .

Associated Conditions

NSVT often, but not always, occurs in the presence of structural heart disease. The risk of death in patients with NSVT is disease dependent and is associated with the degree of left ventricular (LV) dysfunction. For example, if coronary artery disease (CAD) is present and if the left ventricular ejection fraction (LVEF) is reduced (< 40%), there is a substantial risk of cardiac, especially arrhythmic, death. Up to 95% of patients with dilated cardiomyopathy have NSVT, but this is of unclear prognostic significance; because of its nonsustained nature, it generally does not produce symptoms. The mechanism of NSVT varies if underlying heart disease is present and depends on the disease process, but even for CAD, the mechanism of NSVT may differ from that of sustained VT. Triggered activity or reentry mechanisms may be operative. NSVT also occurs in patients without structural heart disease. Exercise-induced, nonsustained repetitive monomorphic tachycardia is generally catecholamine-dependent. The precise incidence of catecholamine-dependent NSVT is unknown. NSVT occurring in the absence of structural heart disease may arise from the LV or right ventricular (RV) outflow tracts and is characterized by high-amplitude R waves in the inferior leads (II, III, aVF), reflecting base to apex depolarization. Idiopathic LV fascicular tachycardia may also manifest as runs of NSVT; these usually have a superior mean frontal plane QRS axis and right bundle branch block (RBBB) morphology. The QRS complexes of fascicular tachycardias are not as wide as VTs originating in ventricular tissue because ventricular depolarization proceeds, at least in part, through the Purkinje system.

Clinical Presentation and Symptoms

Most episodes of NSVT are asymptomatic; however, NSVT is not only a harbinger of sudden death in select patient populations but also may be highly symptomatic, causing palpitations, dyspnea, chest discomfort, lightheadedness or dizziness, and frank syncope. Postextrasystolic beats may be perceived as forceful “thumps” in the chest.

Approach to Management ( Algorithm 6.1 )

Unless NSVT produces symptoms or is related to CAD with LV dysfunction or other structural heart disease, the risk of death is low, and there is no need for treatment. However, new-onset NSVT may be an indication of developing structural heart disease. Investigation for specific risk factors and disease entities should be undertaken. Evaluation should initially include an ECG with specific attention to entities such as epsilon waves, QT interval, and Brugada patterns, as well as echocardiography, to assess ventricular structure and function. Other appropriate tests include Holter monitoring, event monitoring, treadmill testing, and possibly signal-averaged electrocardiography. If these tests document abnormalities consistent with significant structural heart disease, cardiac catheterization or imaging studies, such as magnetic resonance imaging (MRI), may be appropriate.

Algorithm 6.1

Nonsustained ventricular tachycardia. ARVC, Arrhythmogenic right ventricular cardiomyopathy; CM, cardiomyopathy; CPVT, catecholaminergic polymorphic ventricular tachycardia; EP, electrophysiologic study; HCM, hypertrophic cardiomyopathy; ICD, implantable cardioverter defibrillator; LVEF, left ventricular ejection fraction; MI, myocardial infarction; NSVT, nonsustained ventricular tachycardia; PM, pacemaker.

Empiric treatment of NSVT may be worse than the arrhythmia itself and should be reserved for patients who are highly symptomatic, who have high risk for sudden death, or who have a high enough NSVT burden that it contributes to a tachycardia-induced cardiomyopathy. Palpitations in NSVT are not generally a sufficient indication to plan aggressive suppressive therapy, and reassurance may be all that is needed. For symptomatic idiopathic NSVT, various therapies, including β-adrenergic blockers, class I antiarrhythmic drugs, sotalol, or amiodarone may be helpful in reducing symptoms. Radiofrequency (RF) ablation is an alternative approach if symptoms are refractory to drug therapy or if the frequency of NSVT and ectopy contribute to a tachycardia-induced cardiomyopathy (typically requiring high premature ventricular contraction [PVC] burden, such as greater than 25% of ventricular complexes or greater than 10,000 PVCs/24-hour period).

Polymorphic NSVT is not necessarily a harbinger of sustained VT. Torsades de pointes ventricular tachycardia (TdP VT) tends to occur in repetitive, nonsustained paroxysms, although sustained VT and ventricular fibrillation (VF) can occur. Structural heart disease is commonly absent. Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a cause of exercise-induced NSVT and has been associated with mutations in genes controlling intracellular calcium. These patients may respond to β-adrenergic blockers, and in high-risk patients with syncope or family history of sudden death, implantable cardioverter defibrillator (ICD) implantation may be warranted. Bidirectional VT is currently more commonly associated with this type of VT than with digitalis toxicity, which is now infrequent. LV and right ventricular outflow tract (RVOT) NSVT, as well as idiopathic LV fascicular tachycardia, may be amenable to medical therapy (β-adrenergic blockers, calcium channel blockers [especially verapamil], class I or class III antiarrhythmic drugs) or cure by catheter ablation techniques ( Table 6.1 ).

Table 6.1

Management of nonsustained monomorphic and polymorphic ventricular tachycardia

Setting Therapy Comments
Normal LV function

  • No symptoms, no heart disease: no therapy

  • Young patient with bidirectional (or polymorphic) VT that may be life-threatening (CPVT): β-adrenergic blocker

  • Symptoms of palpitations, no heart disease: β-adrenergic blocker (e.g., acebutolol, 200-800 per day)

  • Idiopathic LV fascicular tachycardia (RBBB left axis QRS morphology): verapamil

  • If LBBB (inferior axis morphology), β-adrenergic blocker is first line. Other drugs: sotalol (started in hospital), propafenone, flecainide, amiodarone.

  • RF ablation is curative for this type of VT in more than 95% if it can be initiated and mapped in the EP laboratory.

  • CAD, no symptoms: β-adrenergic blocker, no additional antiarrhythmic therapy

  • CAD with symptoms, β-adrenergic blocker, sotalol, amiodarone (started in the hospital)

  • Polymorphic NSVT

    • In the setting of the long QT with syncope, treatment is required.

    • Genotyping is available.

    • β-Adrenergic blockers are the first choice for long QT type I.

    • With syncope or family history of sudden death, LQT2, or LQT3: ICD.

  • Multiple clinical scenarios exist depending on the age of patient, heart disease, and symptoms.

  • Idiopathic VT may occur in repetitive monomorphic variety and be symptomatic.

    • Not life-threatening.

    • Is exacerbated by exercise, mental stress, and catecholamines.

  • Idiopathic polymorphic VT in the young can be potentially life-threatening.

    • Treat with β-adrenergic blocker.

    • Consider genotyping for CPVT.

  • Consider RV cardiomyopathy (dysplasia) with LBBB/noninferior axis morphology.

  • Consider ischemia.

  • The 12-lead morphology is helpful.

    • If LBBB with inferior axis, it is likely from the RV or LV/aortic cusp outflow tract in normal hearts and is ablatable.

    • If QRS is negative in I and aVL, it may be arising from the septum.

    • If it is positive in these leads, it may be arising from the free wall and may be adenosine sensitive.

    • VTs may respond to β-adrenergic blockers, verapamil, and most antiarrhythmic drugs.

  • If it is a RBBB left axis QRS pattern, it may be a reentrant idiopathic VT from the LV apical septum.

    • Thought to be due to fascicular reentry.

    • Can be cured with RF ablation.

    • Is sensitive to verapamil (only use if known to be this type of VT).

  • Even patients with normal hearts may be at slightly higher risk for CA compared with the general population, but further evaluation and therapy is not beneficial.

  • Polymorphic tachycardia may be due to ischemia or infarction and may be transient.

Ischemic cardiomyopathy

  • For LVEF ≤ 30%, more than 1 month after MI, 3 months after revascularization, ICD implantation.

  • For LVEF ≤ 35%, NYHA FC II-III, ICD implantation is recommended.

  • For LVEF ≤ 40%, EP study is recommended, and if sustained VT is induced, ICD should be implanted.

  • For NYHA FC III-IV heart failure, LVEF ≤ 35%, and QRS duration > 120 ms, cardiac resynchronization therapy is recommended.

  • Increased risk of sudden and total death.

  • Increased risk is not related to length of episodes.

  • EP testing may risk stratify.

Nonischemic cardiomyopathy

  • β-adrenergic blockers, ACE inhibitors, and other optimal therapies for heart failure

  • For LVEF ≤ 35%, NYHA FC II-III, ICD is recommended.

  • For NYHA FC III-IV heart failure, LVEF ≤ 35%, and QRS duration > 120 ms, cardiac resynchronization therapy is recommended.


  • β-adrenergic blocker, especially if symptomatic

  • Memory loop event recorders may be beneficial in correlating symptoms with arrhythmias.

  • No indication for amiodarone or other antiarrhythmic drugs if asymptomatic

  • Start amiodarone, if symptomatic, in the hospital.

  • ICD if

    • Septum > 30 mm

    • Syncope

    • NSVT

    • Family history of sudden death

    • High-risk genotype

    • If prior CA

    • Sustained VT/VF

  • Potentially indicative of a malignant, life-threatening ventricular arrhythmia.

  • EP testing of no proven benefit in this setting.


  • No specific therapy

  • Assess LV function.

  • β-Adrenergic blocker as part of the post-MI regimen

  • If continued NSVT and impaired LV function (LVEF < 0.40) after 4-6 weeks, consider ICD and suppressive antiarrhythmic therapy to slow VT rate and prevent shocks.

  • Little prognostic meaning early after MI. Predictive value increases with increasing time from MI.

  • If polymorphic, consider ischemia (or electrolyte disturbance if the QT interval is prolonged).

  • May represent a coronary reperfusion injury rhythm.


  • If noncardiac surgery planned, assess symptoms, longevity of the problem, drugs

  • If recent onset: assess LV function

  • If LVEF ≤ 0.40, and if CAD, consider EP test

  • If no CHF LVEF ≤ 0.30, ICD. If CHF and LVEF ≤ 0.35, ICD


  • No therapy

  • Has little prognostic meaning early after surgery

  • Resolves spontaneously in the great majority

  • Evaluate for underlying heart disease if risk factors are present.

  • Plan follow-up Holter monitor. If episodes continue, consider EP test. If induced VT, consider ICD if LVEF ≤ 0.40 or other criteria met (ischemic, nonischemic cardiomyopathy; discussed previously).

  • If asymptomatic, treat based on monitor results or based on EP test results.

ACE, Angiotensin-converting enzyme; CA, cardiac arrest; CABG, coronary artery bypass graft; CAD, coronary artery disease; CPVT, catecholaminergic polymorphic ventricular tachycardia; EP, electrophysiologic; FC, functional class; HCM, hypertrophic cardiomyopathy; ICD, implantable cardioverter defibrillator; LBBB, left bundle branch block; LV, left ventricular; LVEF, left ventricular ejection fraction; MI, myocardial infarction; NSVT, nonsustained ventricular tachycardia; NYHA, New York Heart Association; RBBB, right bundle branch block; RF, radiofrequency; RV, right ventricular; VT, ventricular tachycardia.

Sustained ventricular tachycardia


VT is defined as sustained ( Fig. 6.2 ) if it persists for more than 30 seconds or requires early or immediate termination (cardioversion or antitachycardia pacing) for hemodynamic instability. VT can be monomorphic (single QRS morphology in a given ECG lead) or polymorphic (multiple QRS morphologies in a given ECG lead). Monomorphic VT can be regular or irregular in rate and can display a “warm-up” phenomenon in which the tachycardia cycle length gets shorter after its onset. Multiple monomorphic morphologies can be present in a single patient at different times. Polymorphic VT is usually irregular in rate. Polymorphic VT with normal QT interval ( Fig. 6.3 ) most often occurs in the setting of myocardial ischemia or infarction. Polymorphic VT associated with long QT interval is termed TdP VT. VT rates range from 100 to 280 bpm, thereby differentiating it from accelerated ventricular rhythm. Sustained VT is a serious and potentially life-threatening problem, particularly when it coexists with structural heart disease. Hemodynamic stability depends on rate, underlying heart disease, ventricular function, ventricular activation patterns, atrioventricular (AV) relationships, and concomitant drug therapy. AV dissociation occurs in up to 60% to 70% of patients but is clearly evident on the ECG in less than 30% of patients because the rapid VT rate and the wide QRS morphology “buries” the P waves. Mimics of VT include sinus tachycardia and other supraventricular tachycardias (SVTs) with preexisting or rate-related bundle branch block (BBB) ( Fig. 6.4A and B ), hyperkalemia ( Fig. 6.5 ), antidromic AV reentrant tachycardia with antegrade activation through an accessory pathway (see Fig. 5.29 ), and artifact ( Fig. 6.6 ).

Figure 6.2

Sustained Monomorphic Ventricular Tachycardia.

This 12-lead ECG with V 1 rhythm strip shows a wide QRS complex tachycardia (rate of ~ 140 bpm) that has features of ventricular tachycardia including wide (0.16 sec) QRS complexes and atrioventricular (AV) dissociation (arrows show sinus P waves at a rate of ~ 72 bpm).

Figure 6.3

Polymorphic Ventricular Tachycardia.

This lead II rhythm stripshows polymorphic VT. This VT occurred in a patient with myocardial ischemia who did not have QT prolongation.

Figure 6.4

A) Ventricular Tachycardia Mimic: Sinus Tachycardia with Bundle Branch Block.

This 12-lead ECG with rhythm strips shows a rapid wide QRS complex tachycardia that looks like ventricular tachycardia. However, on closer inspection, there is typical right bundle branch block morphology, and there may be retrograde P waves in the terminal part of the QRS. In this case the rhythm is a supraventricular tachycardia and the wide QRS complex is due to an underlying right bundle branch block.

B) Ventricular Tachycardia Mimic: Sinus Tachycardia with Left Bundle Branch Block

This 12-lead ECG with rhythm strips shows a wide QRS complex tachycardia that looks like ventricular tachycardia. However, there is typical left bundle branch block morphology, and there are P waves before each QRS complex. The rhythm is sinus tachycardia and the wide QRS complex is due to left bundle branch block.

Figure 6.5

Ventricular Tachycardia Mimic: Hyperkalemia.

This 12-lead ECG tracing with leads V 1 , II, and V 5 rhythm strips shows a wide complex tachycardia in a patient with renal failure whose serum potassium level was >7 mmol/L. Note the very wide QRS complex and the suggestion of a sine wave pattern. With treatment of the hyperkalemia, the QRS duration decreased back to normal.

Figure 6.6

Ventricular Tachycardia Mimic: Normal Sinus Rhythm with Artifact.

This 2-lead rhythm strip shows an apparent rapid polymorphic wide complex rhythm that looks very much like ventricular tachycardia (VT). However, there is obvious noise abutting the second and third QRS complexes and last 3 QRS complexes. The QRS complexes march through the noise, most evident at the end of the rhythm strip. The noise on the baseline at the end may appear to be ventricular complexes or ventricular fibrillation, but occur immediately through and after normal QRS complexes, which would be during ventricular refractoriness. These findings are all consistent with sinus rhythm with artifact. Artifact can be misdiagnosed as VT. Distinguishing features include a lack of compensatory pause after the tachycardia and the finding that, on closer examination, the QRS complexes of the intrinsic rhythm appear to “walk through” the tachycardia (as is the case here). This may be associated with rapid movement, such as toothbrushing.

Associated Conditions

There are multiple potential mechanisms of VT. Understanding the underlying mechanism(s) is important when planning therapy, both acutely and for the long term. Monomorphic VT can be due to microreentry or macroreentry in the ventricular myocardium, usually around a scar. It can also be due to bundle branch reentry (especially in patients with dilated cardiomyopathy, in whom more than 5% of VTs are due to this mechanism). It can be due to triggered activity resulting from delayed afterdepolarizations (DADs), such as has been postulated in RVOTidiopathic VT, or early afterdepolarizations (EADs), such as in TdP. Although rarely seen nowadays, VT caused by digitalis toxicity, including bidirectional tachycardia (see Fig. 9.4 ), can also result from triggered activity.

The most common causes of sustained monomorphic VT are structural abnormalities resulting from CAD with myocardial infarction (MI), dilated cardiomyopathy, valvular heart disease, proarrhythmia caused by antiarrhythmic drug use, and arrhythmogenic right ventricular cardiomyopathy (ARVC). VT can be the cause for or the effect of ischemia and/or congestive heart failure (CHF) even if it does not cause hypotension.

Sustained monomorphic VT that occurs in the absence of structural heart disease is termed “idiopathic” VT. There are two common forms of idiopathic VT: (1) outflow tract VTs, most commonly arising from the RVOT (typically left bundle branch block [LBBB], inferior axis morphology) but also from the left ventricular outflow tract (LVOT)/aortic cusp (LBBB or RBBB morphology, inferior axis) or mitral annulus, and (2) LV fascicular tachycardia, most commonly RBBB-superior axis morphology, arising from the LV inferoapical wall due to reentry within the fascicles. However, these specific morphologies do not indicate that the tachycardia is necessarily idiopathic in origin or that it is even VT. Nonetheless, monomorphic VT should always be the suspected cause for a wide QRS complex (more than 0.12 seconds) tachycardia, particularly if the patient has structural heart disease, prior MI, or the 12-lead ECG pattern differs significantly from the baseline ECG. If the QRS complex morphology in wide complex tachycardia does not resemble classical RBBB or LBBB, it is likely VT.

Polymorphic VT is almost always life-threatening and requires emergent treatment. Long QT interval polymorphic VT (TdP) ( Fig. 6.7 ) can be due to an acquired long QT syndrome precipitated by certain drugs (e.g., class IA or III antiarrhythmic drugs) or other conditions that prolong the QT interval, such as hypokalemia and hypomagnesemia. A catecholamine-dependent form of TdP also exists. TdP is usually initiated by a long–short (“pause-dependent”) sequence that causes further prolongation of the QT interval and enhancement of the TU or U wave and increasing bizarre QRSTU complexes. The U wave in TdP is thought to reflect the magnitude of the EAD, which is the cellular basis of the arrhythmia. TdP may be due to a genetic abnormality, most commonly mutations in potassium or sodium channel–associated genes. The congenital disorder is most commonly autosomal dominant (Romano-Ward syndrome), but rare recessive forms have been described and associated with deafness (Jervell and Lange-Nielsen syndrome). Polymorphic VT with a normal QT interval is most often ischemic in etiology.

Figure 6.7

Torsades de Pointes.

This lead I, III, and V 1 rhythm strip shows sinus bradycardia with left bundle branch block and marked QT prolongation with premature ventricular contractions (R-on-T) that initiates a very rapid polymorphic ventricular tachycardia with the characteristic twisting of the QRS complex around the isoelectric baseline. Torsades des pointes literally means “twisting of the points.”

Clinical Presentation and Symptoms

VT can be well or poorly tolerated, presenting as a stable monomorphic or poorly tolerated VT presenting as hemodynamic collapse and degeneration to VF or cardiac arrest (CA). Hemodynamic stability is not a criterion for determining tachycardia origin (e.g., SVT vs. VT) because a hemodynamic state depends not only on the rate but also on the nature of the underlying cardiac disease, ventricular function, and concomitant drugs. However, in general, the faster the VT and the worse the LV function, the more poorly VT is tolerated. Very rapid VT is known as ventricular flutter; it is diagnosed if the VT rate is greater than 280 bpm or if there is no obvious isoelectric baseline of the ECG.

Approach to Management

First, it is critical to determine hemodynamic stability. If the VT is causing hemodynamic instability, urgent direct current (DC) shock is required. Assessing whether the mechanism of a wide QRS complex tachycardia is due to a ventricular or SVT is essential. Sinus tachycardia with aberrancy will not respond to a DC shock. SVT requires a different treatment pathway than VT, and ultimately the distinction between the two will be important.

Because 70% to 90% of wide QRS complex tachycardias are VT and not SVT, even with hemodynamic tolerance, the tachycardia should be treated as VT. However, if the patient is tolerating the tachycardia and SVT is strongly suspected, it is acceptable to attempt vagal maneuvers or give adenosine 6 mg intravenous (IV) followed by 12 mg IV before administering lidocaine or DC cardioversion. Adenosine may also induce ventriculoatrial conduction block, which indicates that VT is the mechanism of the tachycardia. Adenosine can terminate some RVOT idiopathic VTs. Thus tachycardia termination by adenosine is not 100% specific for the diagnosis of SVT. Although verapamil may occasionally terminate idiopathic VT, it is contraindicated in any wide QRS complex tachycardia that is of uncertain etiology or is known to be VT.

Acute Management ( Algorithm 6.2 )

Always consider emergent electric (DC) shock to stop VT. Even if the VT is tolerated, an external cardioverter defibrillator should always be close at hand and ready to be used by knowledgeable personnel because hemodynamic collapse can occur without warning or change in VT rate. The advanced cardiac life support (ACLS) protocol must be known and followed. If the sustained VT terminates spontaneously and/or recurs, an IV antiarrhythmic drug may be effective (e.g., amiodarone) in suppressing it. Cardioversion (synchronized to the QRS complex) can be performed for slower VTs if there is a distinct isoelectric interval, even if the tachycardia is well tolerated but has not responded to IV antiarrhythmic drugs. If the patient is awake, IV anesthesia should be administered promptly before cardioversion. In patients with severe hypotension (e.g., pulseless VT), a nonsynchronized DC shock should be performed, similar to defibrillation for VF. For VT without hemodynamic impairment, the initial energy to cardiovert is 50 to 100 J, delivered from a biphasic cardioverter. For those who do not tolerate the VT, an unsynchronized DC shock should be delivered at 200 J. If that is ineffective, increase to 300 J, and if that is ineffective, then deliver 360 J. If a second shock at 360 J is ineffective, additional therapy with IV drug infusions must be considered. A widely patent IV must be in place and the patient monitored carefully and continuously.

Algorithm 6.2

Sustained ventricular tachycardia—acute management. IABP, Intra-aortic balloon pump; IV, intravenous; LQT, long QT interval; MI, myocardial infarction; PM, pacemaker; VT, ventricular tachycardia.

IV antiarrhythmic drugs that can potentially convert or prevent recurrences of VT include amiodarone, lidocaine, and procainamide. Used acutely, these drugs can also prevent VT from recurring after the rhythm is converted with a DC shock. Although they may not convert the rhythm, these drugs may nonetheless still effectively suppress arrhythmias after sinus rhythm has been achieved by other means. IV amiodarone, 150 mg over 10 minutes, is the recommended antiarrhythmic drug of first choice. Lidocaine 1.5 mg/kg, repeated at a 0.5- to 1-mg/kg dose may be effective to facilitate VT termination. Procainamide 10 to 15 mg/kg given at 25 mg/min may facilitate conversion or slow the VT rate so that it can be pace terminated; however, the class I antiarrhythmic drugs can increase the energy required to cardiovert and defibrillate. Procainamide can be negatively inotropic and can precipitate hypotension. It (and its renally excreted metabolite, N-acetyl-procainamide) can cause QT interval prolongation and TdP.

If the VT rate is less than 200 bpm but recurs persistently, consider placement of a temporary transvenous pacemaker to rapidly pace the ventricles to pace terminate VT. If an ICD is already in place, antitachycardia pacing may be programmed.

If a shock is ineffective, additional drug therapy for VT includes epinephrine 1 mg IV, which may be repeated once, or vasopressin. Use epinephrine very rarely and with extreme caution if an acute infarction is suspected or if severe ischemia is present based on symptoms or ECG findings. Further drug use depends on the clinical situation (discussed later), the type of VT, the underlying cardiac diagnosis, and the LV function.

There are several important clinical situations that can have special implications regarding long-term treatment of VT. Rarely, VT is due to digitalis intoxication. This VT, which can be bidirectional, may not respond to DC shock. Digoxin antibodies are indicated, as well as correction of electrolyte disturbances, such as low potassium and magnesium. This must be done cautiously and gradually to avoid potassium-induced complete heart block, which can occur at high potassium levels in digitalis toxicity.

VT can occur after cardiac surgery. This is often transient, but if it is monomorphic and occurs after the first 24 to 48 hours or if it is associated with important LV functional impairment (LVEF ≤ 0.40), there is a high likelihood that VT may recur.

Chronic Management

In the setting of MI, transient VT episodes are not rare. Polymorphic VT with a normal QT interval may be due to ischemia. VT can also represent reperfusion injury. These VTs, although transient, especially if they occur within the first 48 hours of the MI, may indicate future arrhythmic risk if they are associated with impaired LV function (LVEF ≤ 0.40). Evaluation can include electrophysiologic (EP) testing to assess long-term implications, especially if the patient is not a candidate for revascularization. However, late (>48 hours) sustained VT generally indicates significant residual risk for sudden cardiac death, and ICD implantation is indicated for secondary prevention of sudden cardiac death.

All patients with structural heart disease and new onset of VT should undergo careful reevaluation of their underlying disease. If there is evidence of progression of CAD or valvular disease, cardiac catheterization may be needed. If the patient has a dilated cardiomyopathy, evaluation of LV function is indicated. In all cases, episodes of sustained monomorphic VT require long-term treatment when not associated with an acute event, such as drug toxicity, MI, myocardial trauma, and cardiac surgery. EP testing may be indicated in these patients. Long-term therapy usually includes ICD implantation and ablation, and/or adjunctive antiarrhythmic drug ( Table 6.2 ).

Table 6.2

Management of sustained ventricular tachycardia

Setting Therapy Comments
Acute therapy

  • Monomorphic VT well tolerated (patient awake and alert, no angina, no CHF, stable BP)

  • First line: Amiodarone 150 mg over 10 minutes followed by 1 mg/min for 6 h followed by 0.5 mg/min

    • May combine amiodarone IV with oral drug and with IV lidocaine if needed

    • Lidocaine 1.5-2 mg/kg (but only effective in < 15%)

  • Second line: Procainamide 10-15 mg/kg at 25 mg/min (or less), assessing the BP carefully

    • Procainamide can slow VT and may be effective in an additional 20% to 30%

    • Amiodarone is probably more effective than procainamide, safer, and better tolerated

  • Third line: Cardioversion after adequate anesthesia

  • Do not cardiovert while awake

  • Fourth line: Antitachycardia pacing via a temporary transvenous pacing lead

  • Assess cause and hemodynamic tolerance.

    • Guidance of therapy is dependent on the clinical status of the patient.

    • VT can always degenerate to VF even if it is at first stable.

  • IV amiodarone is emerging as first-line therapy for sustained monomorphic VT due to lack of efficacy of other drugs.

  • Procainamide has a negative inotropic effect.

  • Temporary transvenous pacing requires time and experienced personnel to accomplish.

Acute therapy, MI

  • Same as above but degree of urgency in treatment is greater

    • The length of time in VT, even if apparently tolerated, should be minimized

  • Lidocaine is associated with no improvement in mortality

  • Monomorphic VT

    • May not increase long-term mortality.

    • Can be ischemia induced but this is rare (<3% of all MIs).

    • Tends to indicate “an electrical reentry circuit” of damaged myocardium.

Acute therapy, polymorphic VT

  • Normal QT interval

  • Patient stable

  • If stable and the patient is awake (very rare):

    • If ineffective, DC shock (200 J > 300-360 J) after anesthetized

  • IV β-adrenergic blockade as tolerated

  • Assess cause and hemodynamic tolerance.

  • Rule out ischemia, infarction, electrolyte abnormality (low K + or Mg 2 + ), or adverse drug effect.

  • Assess age, underlying disease process and LV function, potential causative factors (e.g., exercise).

  • Therapy depends on the clinical status, which can always degenerate to VF even if it appears to be stable.

  • IV amiodarone may be effective, but there are no data on well-tolerated polymorphic VT.

Chronic prevention

  • No structural heart disease

  • Idiopathic VT, usually in young patient

  • Often exercise or stress induced

  • Rule out RV cardiomyopathy (dysplasia) with MRI

  • First line: β-adrenergic blocker titrated to the highest tolerated dose

  • If recurrent episodes (with moderate or severe symptoms) occur: RF catheter ablation

  • The success for LBBB inferior axis and for RBBB superior axis VT ablation is 90% to 95%

  • RF ablation is first line if patient has syncope, hemodynamic intolerance, or patient preference

  • Monomorphic VT can be highly symptomatic but is almost never “malignant” and life-threatening.

  • LBBB/inferior axis VT is usually from the outflow tract.

    • If the QRS is negative in I and aVL, suspect a septal or LV origin.

    • If it is positive in these leads, suspect a free wall origin.

    • The mechanism may be due to triggered automaticity. Highly amenable to RF ablation.

  • RBBB/superior axis VTs are likely due to reentry in the Purkinje system.

    • Are verapamil sensitive.

    • Can be successfully ablated.

  • For LBBB, noninferior axis morphology VTs, r/o ARVC.

Prior MI, ischemia can be provoked

  • If monomorphic, suspect a substrate that is due to scar, not ischemia

  • If polymorphic, suspect ischemia or infarction

  • Consider a functional stress test or coronary angiogram and revascularization if ischemic

  • ICD implantation if hemodynamically significant sustained VT/VF

  • Ablation can be successful in > 50% but with a high rate of long-term recurrence

    • Used as adjunctive therapy to ICD implantation

    • May be used to reduce recurrent ICD shocks

  • Adjunctive antiarrhythmic drugs include amiodarone or sotalol

  • May also be associated with VF.

  • Rarely, monomorphic VT is due to ischemia alone, but always suspect substrate even if episodes occur relatively soon after infarction.

    • If an antiarrhythmic drug is being used, consider the possibility of a proarrhythmic effect.

  • Most patients (> 95%) with chronic VT due to CAD will be inducible in the EP laboratory, but this does not change treatment strategy.

Only gold members can continue reading. Log In or Register to continue

Stay updated, free articles. Join our Telegram channel

Jan 30, 2019 | Posted by in CARDIOLOGY | Comments Off on Ventricular Tachyarrhythmias

Full access? Get Clinical Tree

Get Clinical Tree app for offline access