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.
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.
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 ).
|Normal LV function|
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 ).
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.
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.
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.
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 ).
|Acute therapy |
|Acute therapy, MI|
|Acute therapy, polymorphic VT |
|Chronic prevention |
|Prior MI, ischemia can be provoked|