What ECG characteristic is consistent with ventricular tachycardia?

SVT-VT Discrimination

The combination of ventricular rate and duration serves as an implicit SVT-VT discriminator and suffices in many patients,25,27 but patients in whom SVTs and VTs overlap in rate require an explicit discrimination process in which a sequence of sensed EGMs that satisfies rate and duration criteria for VT/VF are classified as either SVT or VT/VF.Discriminators are individual algorithm components or “building blocks” that provide a partial or complete rhythm classification for a subset of rhythms. Individual discriminators may be considered in relation to the EGMs analyzed [ventricular only or both atrial and ventricular], the rhythm that they identify [e.g., AF, sinus tachycardia, VT], or the type of EGM information analyzed [intervals versus morphology].25,27eTable 41.5 summarizes the most commonly used individual discriminators.Discrimination algorithms integrate complementary component discriminators to classify tachycardias as VT/VF or SVT [eFigs. 41.13 to 41.15].

EFIGURE 41.14. Correct classification of rapidly conducted atrial fibrillation [AF] by ventricular EGM morphology. The atrial EGM, right ventricular sensing EGM, and dual-chamber marker channel are shown. Most intervals are classified in the ventricular fibrillation [VF] zone [FS], which is programmed to less than 320 milliseconds. The “AF” designation at right of the marker channel [red box] indicates that the rhythm is classified as AF. The basis for this classification is shown in thelower panel, which compares the morphology of shock [high-voltage] EGMs during tachycardia [solid lines] with those of a template stored during baseline sinus rhythm [dotted line]. Match percentages of 70% or greater between the two EGMs are considered sufficiently close that the rhythm is classified as “supraventricular.” It is designated as AF based on the atrial rhythm.

ETABLE 41.5. SVT-VT Discriminators Used in ICDs

AEGM, atrial electrogram;AF, atrial fibrillation;AV, atrioventricular;SVT, supraventricular tachycardia;VEGM, ventricular electrogram;VF, ventricular fibrillation;VT, ventricular tachycardia.

Pathophysiology

Premature ventricular complexes [PVCs] are often the events that lead to ventricular tachycardia. These premature beats may occur as a result of either a change in automaticity or a conduction defect.

As a premature ventricular beat often propagates by traveling through ventricular muscle, conduction is delayed and the QRS complex on the electrocardiogram is wide Goldberger [1999]. For an example, see //www.ecglibrary.com/ventricular tachycardiaavd1.html. The pattern may also be one of bigeminy, a premature beat for every normal beat [see //www.ecglibrary.com/bigem.html], or trigeminy, wherein every third beat is a premature beat. As the premature beat originates in the ventricle, it is not associated with a P wave preceding it Spooner and Rosen [2001].

Sustained monomorphic ventricular tachycardia sometimes appears as a narrow QRS complex on the electrocardiogram if the sinus node generates a wave front that results in depolarization of the ventricles prior to the effect of the premature ventricular beat, essentially canceling the spread of the premature beat. This is called a capture beat. Sometimes, a combination of a narrow QRS complex and a wide QRS complex occurs. This hybrid QRS complex is called a fusion beat.

Polymorphic ventricular tachycardia has a unique pattern on the ECG and is considered with respect to torsades de pointes

Genetic predispositions are a risk factor for ventricular tachycardia. As ion channel activity is the basis for the electrophysiological properties of the heart, inherited channelopathies play a role in arrhythmia susceptibility. Displayed below is an action potential in the myocardium with contributions of ion currents to its various phases.

The relative magnitudes of the various ionic fluxes, as they apply to the cell, are shown by the size of the arrows above the action potential; ↑, a depolarizing current; ↓, a repolarizing current. Predominate channel subtype activities for Ca++ and K+ channels are shown above the respective arrows [T = transient calcium, L = long-lasting calcium, Kr = rapid potassium, Ks = slow potassium, Kur = ultra-rapid potassium, Kir = inwardly rectifying potassium].

An increase in the conductance of the sodium channel can lead to long QT intervals on the electrocardiogram and torsades de pointes [polymorphic ventricular tachycardia]. A decrease in sodium channel opening can lead to the Brugada syndrome and greater risk of ventricular tachycardia. Polymorphic ventricular tachycardia is also associated with a mutation of the ryanodine receptor Ca++ channel, co-localized near T tubules, where L-type Ca++ channels also contribute to an increase in Ca++ current and thereby contribute to a risk of ventricular tachycardia. A decrease in function of Ks and Kr potassium channels can also predispose to long QT-associated arrhythmias. These channel mutations may be present but not manifest themselves unless there is a precipitating cause, such as a drug that prolongs the QT interval, an electrolyte imbalance, or high catecholamine levels.

Inherited cardiomyopathies also increase the risk of ventricular tachycardias. Right ventricular dysplasia and mutations of one of several proteins in the sarcoplasmic reticulum increase the risk of ventricular tachycardia.

Stress can increase the risk of ventricular tachycardia.

Differentiation Between Ventricular and Supraventricular Tachycardia

Although fusion and capture beats and AV dissociation provide the strongest electrocardiographic evidence for differentiation of VT from SVT with aberrant conduction, these features are not always present. Other clues characterizing supraventricular arrhythmia with aberrancy include [1] consistent onset of the tachycardia with a premature P wave; [2] very short RP interval [0.1 second], which often requires an esophageal recording or invasive electrophysiologic study [EPS] to visualize the P waves; [3] QRS configuration the same as that occurring from known supraventricular conduction at similar rates; [4] P wave and QRS rate and rhythm linked to suggest that ventricular activation depends on atrial discharge [e.g., P-P interval changes preceding and therefore causing subsequent R-R intervals]; and [5] slowing or termination of the tachycardia by vagal maneuvers, although vagal maneuvers can terminate right ventricular outflow tract VTs.

Analysis of specific QRS contours can also be helpful in the diagnosis of VT and localization of its site of origin. For example, QRS contours suggesting VT include left axis deviation in the frontal plane and a QRS duration exceeding 140 milliseconds with normal duration during sinus rhythm. In precordial leads with an RS pattern, the duration of the onset of the R to the nadir of the S exceeding 100 milliseconds suggests VT as the diagnosis. During VT with an RBBB appearance, [1] the QRS complex is monophasic or biphasic in V1, with an initial deflection different from that of the sinus-initiated QRS complex; [2] the amplitude of the R wave in V1 exceeds that of R′; and [3] a small R and large S wave or a QS pattern in V6 may be present. With a VT having an LBBB contour, [1] the axis can be rightward, with negative deflections deeper in V1 than in V6; [2] a broad prolonged [>40 msec] R wave can be noted in V1; and [3] a small Q–large R wave or QS pattern in V6 can exist. A QRS complex that is similar in V1 through V6, either all negative or all positive, favors a ventricular origin, as does the presence of a 2 : 1 VA block. [An upright QRS complex in V1 through V6 can also occur as a result of conduction over a left-sided accessory pathway.] Supraventricular beats with aberration often have a triphasic RSR′ pattern in V1, an initial vector of the abnormal complex similar to that of the normally conducted beats, and a wide QRS complex that terminates a short cycle length after a long cycle [long-short cycle sequence].

During atrial fibrillation [AF], fixed coupling, short coupling intervals, a long pause after the abnormal beat, and runs of bigeminy rather than a consecutive series of abnormal complexes all favor a ventricular origin of the premature complex rather than a supraventricular origin with aberration. A grossly irregular, wide-QRS tachycardia with ventricular rates exceeding 200 beats/min should suggest AF with conduction over an accessory pathway [seeFig. 37.22].

Focal Purkinje Ventricular Tachycardia

Idiopathic focal VTs can arise from the Purkinje system in either ventricle and can present as PVCs, accelerated idioventricular rhythm, or VT. Focal Purkinje VTs arising from the left Purkinje network exhibit an RBBB pattern with either left- or right-axis deviation and can be difficult to distinguish from fascicular VT. In contrast to the reentrant idiopathic fascicular VT, focal Purkinje VTs are most likely related to abnormal automaticity. These VTs are sensitive to autonomic tone and frequently display chronotropic properties. Focal Purkinje VTs are typically induced by exercise and catecholamines and slowed or terminated by beta-blockers [and hence classified as “propranolol-sensitive” VTs] and lidocaine. Unlike fascicular VT, focal Purkinje VTs are not responsive to verapamil and cannot be induced or terminated by programmed electrical stimulation. In addition, these VTs are transiently suppressed by adenosine and with overdrive pacing.11

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.

Surface Electrocardiogram

VTs from the papillary muscles have an RBBB pattern [see Fig. 29.10 and Fig. 29.11]. The QRS width is significantly greater in papillary muscle arrhythmias compared with idiopathic left verapamil-sensitive VTs [150 ± 15 vs. 127 ± 11 ms].25 Papillary muscle VT often exhibits multiple QRS morphologies, with subtle changes seen spontaneously or during ablation. These subtle morphologic changes are thought to be from preferential conduction to different exit sites or multiple regions of origins within the complex structure of the papillary muscles [see Fig. 29.10].22

Subtle ECG differences can help differentiate papillary muscle VT from fascicular VT.25,26 Papillary muscle VT usually has a wider QRS; it does not have Purkinje potentials preceding the QRS during VT; and if present, Purkinje potentials will be late in sinus rhythm compared with pre-QRS with fascicular VTs. The V1 morphology of posterior papillary muscle VTs typically has a qR morphology or R compared with an rsR′ for fascicular VTs, and will notably have an absence of Q waves in leads I and aVL.25

CLASSIFICATION

Ventricular tachycardia [VT] is usually associated with structural heart disease, with coronary artery disease and cardiomyopathy being the most common causes. However, about 10% of patients who present with VT have no obvious structural heart disease [idiopathic VT].1 Absence of structural heart disease is usually suggested if the ECG [except in Brugada syndrome and long-QT syndrome], echocardiogram, and coronary arteriogram collectively are normal.2 Nevertheless, structural abnormalities can be identified by magnetic resonance [MR] imaging, even if all other test results are normal. In addition, focal dysautonomia in the form of localized sympathetic denervation has been reported in patients with VT and no other obvious structural heart disease.

Several distinct types of idiopathic VT have been recognized and classified with respect to the origin of VT [right ventricle [RV] VT versus left ventricle [LV] VT], VT morphology [left bundle branch block [LBBB] versus right bundle branch block [RBBB] pattern], response to exercise testing, response to pharmacological agents [adenosine-sensitive VT versus verapamil-sensitive VT versus propranolol-sensitive VT], and behavior of VT [repetitive salvos versus sustained].

Ventricular Tachycardia

Ventricular tachycardia presents a challenge in terms of applications of catheter ablation techniques. The extremely variable site of tachycardia origin and the diffuse nature of the arrhythmia circuit make localizing successful sites for energy application difficult. Initial ablation therapy in ventricular tachycardia was undertaken in patients with recurrent ventricular tachycardia and structurally normal hearts [idiopathic ventricular tachycardia]. Catheter mapping and ablation have abolished recurrent ventricular tachycardia successfully with a remarkably low recurrence rate. However, only a small portion of patients have idiopathic ventricular tachycardia with sustained recurrent ventricular tachycardia. Other candidates for radiofrequency ablation are patients with nonischemic cardiomyopathy and bundle-branch reentry tachycardia. In these patients, ablation of the right bundle may eliminate the ventricular tachycardia.

Patients with coronary artery disease represent most patients with recurrent ventricular tachycardia. Patients with sustained hemodynamically stable ventricular tachycardia and relatively well-maintained LV function seem to be the best candidates for mapping and ablation procedures. Another relative contraindication to ablative therapy is the induction of multiple ventricular tachycardia morphologies during initial EPS.