Ventricular Arrhythmias and Defibrillators

and Conor D. Barrett¹

(1)

Harvard Medical School Cardiac Arrhythmia Service, Cardiology Division, Department of Medicine, Massachusetts General Hospital, Boston, MA, USA

Introduction

Distinguishing Wide QRS Complex Tachycardias

Classification of Ventricular Arrhythmias

Implantable Cardioverter-Defibrillators

Quick Review

References

Abstract

Ventricular tachyarrhythmias have heterogeneous etiologies, clinical consequences, and treatment strategies. Distinguishing ventricular tachyarrhythmias from supraventricular tachycardia (SVT) with aberrancy clinically and on the surface electrocardiogram can be challenging, yet has substantial therapeutic implications. A wide body of randomized clinical trial data has emerged addressing the efficacy of implantable cardioverter defibrillators (ICDs) for the prevention of sudden cardiac death. In this chapter we discuss these issues as well as consensus guideline recommendations for the implantation of ICDs.

Abbreviations

AAD

Antiarrhythmic drugs

ACC

American College of Cardiology

AHA

American Heart Association

CABG

Coronary artery bypass grafting

EPS

Electrophysiology study

HRS

Heart Rhythm Society

ICD

Implantable cardioverter defibrillator

LVEF

Left ventricular ejection fraction

Myocardial infarction

NSVT

Nonsustained ventricular tachycardia

NYHA

New York Heart Association

SVT

Supraventricular tachycardia

Ventricular fibrillation

Ventricular tachycardia

Introduction

Distinguishing Wide QRS Complex Tachycardias

History: A prior history of structural or coronary heart disease favors ventricular tachycardia (VT).

Clinical exam: Neither hemodynamic stability nor physical exam findings are of sufficient specificity to be relied upon in order to distinguish between wide QRS complex tachycardia etiologies.

Jugular venous exam may reveal cannon “a” waves due to atrioventricular dissociation in patients with VT.
A third heart sound may favor VT but is not specific enough to diagnose VT.

Differential diagnosis:

Ventricular tachycardia
Supraventricular tachycardia with aberrancy
Preexcitation
Other causes: adverse medication reactions (e.g., digitalis toxicity [specifically associated with bidirectional VT], class Ic agents), ventricular pacing with atrial arrhythmia, metabolic derangement (e.g., hyperkalemia)

The 12-lead ECG may be useful to identify VT from SVT with aberrancy and should be obtained if the patient is hemodynamically stable.

Discrimination of VT from SVT with aberrancy :

Helpful factors are detailed in Table 24-1
Atrioventricular dissociation is characteristic of VT, however given the high prevalence of atrial fibrillation, the absence of evident atrioventricular dissociation does not exclude VT. In some patients with intact VA conduction VTs may have a 1:1 VA relationship, so a 1:1 relationship can not be relied upon to exclude VT and diagnose SVT.
Additional factors favoring VT [2]:
- QRS duration > 160 ms
- Right superior QRS axis (−90^o to ±180^o)

Table 24-1

Stepwise algorithm for discriminating VT from SVT with aberrant conduction [1]

	Sensitivity for VT	Specificity for VT
1. Absence of RS complex in all precordial leads (negative precordial concordance)	0.21	1.0
2. R to S interval > 100 ms in any precordial lead	0.66	0.98
3. AV dissociation	0.82	0.98
4. Morphology criteria for VT in V1-2 and V6	0.99	0.97
Overall algorithm	0.97	0.99

Figure 24-1

The rs interval is defined as the duration spanning the onset of the r wave and the trough of the s wave. A qs wave is depicted without any demonstrable r wave

Classification of Ventricular Arrhythmias

Table 24-2

Classification of ventricular arrhythmias

Arrhythmia	Associated features
Post-infarction ventricular tachycardia (Fig. 24-2)	Mechanism often reentry around scar
	Typically monomorphic unless associated with active ischemia
	Associated wall motion abnormalities and left ventricular dysfunction on imaging
Idiopathic ventricular tachycardia
Outflow tract tachycardias (Fig. 24-3)	cyclic adenosine monophosphate mediated delayed afterdepolarizations, triggered activity
	Inferior axis, often left bundle branch block morphology during tachycardia but right bundle branch block morphology may be seen from VT from the left ventricular outflow tract
	More common in women, can be exacerbated with exercise and in pregnancy
	Adenosine, calcium channel blocker, or beta-blocker sensitive
	Treatable with meds or catheter ablation
	Benign prognosis
Fascicular tachycardias (Fig. 24-4)	Reentry involving Purkinje tissue
	Commonest forms are of a right bundle branch block, left anterior fascicular block or left posterior fascicular block pattern during tachycardia
	More common in men
	Verapamil sensitive
	Treatable with verapamil or catheter ablation
	Benign prognosis
Ventricular tachycardia and congenital heart disease	Reentry often involving surgical patch, suture lines, or scar
Ventricular tachycardia and congenital heart disease	May be amenable to ablation but ICDs often favored given structural disease
Other ventricular tachycardias
Bundle branch reentrant ventricular tachycardia	Reentry involving the bundle branch fascicles
	Typical left or right bundle branch block pattern
	Associated with structural heart disease (e.g., dilated cardiomyopathy)
	Poor response to pharmacologic therapy; catheter ablation is first-line therapy; ICDs appropriate as typically unstable
Arrhythmogenic right ventricular cardiomyopathy	Reentry around areas of fibrofatty tissue
	Commonly LBBB pattern
	Baseline ECG
	May be essentially normal in some
	1st degree atrioventricular block
	Epsilon wave (early after depolarization)
	T wave inversion V_1–3
	Right bundle branch block or incomplete right bundle branch block, or prolonged S wave upstroke (>55 ms) in V_1–3 in absence of right bundle branch block
	More common in young men, progressive disorder
	Associated with desmosomal mutations; genetic testing may be useful
	Typically exercise induced ventricular arrhythmias
	Sotalol useful, avoidance of competitive sports, ICD in high-risk patients
Ventricular tachycardia in nonischemic cardiomyopathy	Reentry around deep myocardial scar or fibrosis
Polymorphic ventricular tachycardia and fibrillation (Fig. 24-5)	Reentry, automaticity, or triggered activity
	Torsades de Pointes represents “twisting of the points” in context of a long QTc interval