- Nonsustained: Three or more consecutive QRS complexes of uniform configuration of ventricular origin at a rate of more than 100 bpm.
- Sustained: Lasts more than 30 seconds; requires intervention for termination.
- Monomorphic ventricular tachycardia.
- Polymorphic ventricular tachycardia: Beat-to-beat variation in QRS configuration.
The magnitude of ventricular tachycardia (VT), one of the most common health problems encountered in clinical practice, can best be appreciated in terms of its various clinical manifestations, which include ventricular fibrillation (sudden cardiac death [SCD]), syncope or near syncope, and wide QRS tachycardia.
The most serious is its degeneration into ventricular fibrillation, producing cardiac arrest and SCD that accounts for 200,000 deaths a year. The second most serious clinical presentation is syncope. Although the overall prevalence of VT-related syncope is unclear, it is estimated to be frequent because inducible VT (via electrical stimulation) is the most common arrhythmia detected in patients with unexplained syncope. A high prevalence of SCD (more than 20% incidence within the ensuing 12 months) is noted in patients with syncope from cardiovascular causes, suggesting that undiagnosed VT may be an underlying cause of sudden death in patients with unexplained syncope. The third most significant clinical manifestation of VT
is a wide QRS complex tachycardia that is often hemodynamically well tolerated.
Ventricular tachycardia as a cause of morbidity and mortality is grossly underdiagnosed, potentially leading to mismanagement.
This may be particularly true when the clinical presentation is
unexplained syncope because no concomitant electrocardiographic
(ECG) documentation is available. In the case of cardiac arrest
or SCD acute myocardial infarction rather than an arrhythmic problem
is often assumed to be responsible. Most persons who have suffered
sudden death have no evidence of acute myocardial necrosis, even
though the episode often occurs in patients with underlying coronary
artery disease. Managing the underlying coronary artery disease
with no regard to treating the concomitant VT is inadequate.
When hemodynamically stable VT is recorded on the surface ECG, it is often misdiagnosed as supraventricular tachycardia (SVT) with
aberrant conduction. Any subsequent management is therefore directed
toward SVT. Although the exact logic for this line of thinking is
unclear, the main reason may be that the hemodynamic stability is associated
with the broad QRS rhythm and thus the erroneous belief that the
problem cannot be VT.
The clinical presentation of VT depends on many factors, including rate, ventricular function, presence of concomitant coronary artery
disease, the presence or absence of cardioactive drugs, and even
the patient’s posture at the time of onset. Hemodynamic
tolerance of VT can, therefore, vary considerably in different situations;
at times, it can vary in the same patient, and it is prudent not
to exclude the diagnosis of VT on the basis of hemodynamic tolerance
alone. It must be understood that approximately 80% of
the patients with sustained wide QRS tachycardia have VT. To avoid
misdiagnosis, the clinician can either use the established ECG criteria (discussed
in the next section) that distinguish VT from SVT with aberrant
conduction or simply assume the presence of VT. The assumption of
VT is more often correct; it is also safer because misdiagnosing
VT as SVT is a riskier judgment error than vice versa.
Diagnostic Approach to the Patient with Wide QRS Complex Tachycardia
The diagnosis of wide QRS complex tachycardia by ECG analysis has always been a challenge for clinicians. The differential diagnosis includes VT, SVT with aberrant conduction, and preexcited tachycardia in patients with Wolff-Parkinson-White syndrome (WPW). Figure 23–1 depicts, schematically, the reasons for normal and broad QRS complexes. Preexcited tachycardia results from antegrade activation of the ventricle via an accessory pathway in patients with WPW syndrome, which can present with atrial fibrillation, atrial flutter, atrial tachycardia, atrioventricular nodal reentry tachycardia (AVNRT), or antidromic tachycardia. Preexcited tachycardia is a rare cause of wide QRS complex tachycardia (5–8% of cases); however, the QRS pattern of preexcited QRS complex can be difficult to distinguish from VT because in both instances the QRS starts with muscle-to-muscle conduction. Electrocardiographic artifact can also mimic wide QRS complex tachycardia and be misdiagnosed as VT, leading to expensive testing and even placement of implantable cardioverter-defibrillator (ICD). Clues to the diagnosis include absence of hemodynamic deterioration, an unstable baseline, association with body movement, and ability
to march the normal QRS complexes through the artifact (“notches
sign”) at sinus R-R interval. A number of surface ECG criteria,
including the atrioventricular (AV) relationship, the QRS complex
duration, specific QRS morphology, and the QRS complex axis, have
been established to distinguish VT from SVT with aberrant conduction. These
criteria are helpful in arriving at an accurate diagnosis if they
are used in a systemic fashion.
Mechanism of wide QRS. A: Narrow QRS from simultaneous activation of the right and left ventricles. In the three types of wide QRS shown in B–D, there is sequential rather than simultaneous activation of the left and right ventricle and a variable amount of muscle-to-muscle conduction. AP, accessory pathway; AVN, atrioventricular node; BBB, bundle branch block; HB, His bundle; LB, left bundle; RB, right bundle. (Reproduced, with permission, from Akhtar M et al. Electrophysiological spectrum of wide QRS complex tachycardia. In: Zipes DP, Jalife J, editors. Cardiac Electrophysiology. From Cell to Bedside. Philadelphia: WB Saunders, 1990.)
In SVT, the arrhythmia arises in the atria or AV junction and reaches the ventricles through the AV node and His-Purkinje system.
Because the atrial arrhythmia is the primary event, either a 1:1
AV response or a varying degree ...