Causes of Wide Complex Tachycardias

A narrow QRS complex requires rapid, highly synchronous electrical activation of the right ventricular (RV) and left ventricular (LV) myocardium, which can only be achieved through the specialized, rapidly conducting His-Purkinje system (HPS). A wide QRS complex implies less synchronous ventricular activation of longer duration, which can be due to intraventricular conduction disturbances (IVCDs), or ventricular activation not mediated by the His bundle (HB) but by a bypass tract (BT; preexcitation) or from a site within a ventricle (ventricular arrhythmias). IVCDs may be fixed and present at all heart rates, or they may be intermittent and related to either tachycardia or bradycardia. IVCDs can be caused by structural abnormalities in the HPS or ventricular myocardium or by functional refractoriness in a portion of the conduction system (i.e., aberrant ventricular conduction).¹

Wide QRS complex tachycardia (WCT) is a rhythm with a rate of more than 100 beats/min and a QRS duration of more than 120 milliseconds. Several arrhythmias can manifest as WCTs (Table 21-1); the most common is ventricular tachycardia (VT), which accounts for 80% of all cases of WCT. Supraventricular tachycardia (SVT) with aberrancy accounts for 15% to 20% of WCTs. SVTs with bystander preexcitation and antidromic atrioventricular reentrant tachycardia (AVRT) account for 1% to 6% of WCTs.

TABLE 21-1 Causes of Wide QRS Complex Tachycardia

AT = atrial tachycardia; AVNRT = atrioventricular nodal reentrant tachycardia; AVRT = atrioventricular reentrant tachycardia; BBB = bundle branch block; BT = bypass tract; SVT = supraventricular tachycardia; VT = ventricular tachycardia.

In the stable patient who will undergo a more detailed assessment, the goal of evaluation should include determination of the cause of the WCT (particularly distinguishing between VT and SVT). Accurate diagnosis of the WCT requires information obtained from the history, physical examination, response to certain maneuvers, and careful inspection of the electrocardiogram (ECG), including rhythm strips and 12-lead tracings. Comparison of the ECG during the tachycardia with that recorded during sinus rhythm, if available, can also provide useful information.²

Clinical History

Physical Examination

Most of the elements of the physical examination, including the blood pressure and heart rate, are of importance primarily in determining how severe the patient’s hemodynamic instability is and thus how urgently a therapeutic intervention is required. In patients with significant hemodynamic compromise, a thorough diagnostic evaluation should be postponed until acute management has been addressed. In this setting, emergency cardioversion is the treatment of choice and does not require knowledge of the mechanism of the arrhythmia.

Evidence of underlying cardiovascular disease should be sought, including the sequelae of peripheral vascular disease or stroke. A healed sternal incision is obvious evidence of previous cardiothoracic surgery. A pacemaker or defibrillator, if present, can typically be palpated in the left or, less commonly, right pectoral area below the clavicle, although some older devices are found in the anterior abdominal wall.

An important objective of the physical examination in the stable patient is to attempt to document the presence of atrioventricular (AV) dissociation. AV dissociation is present, although not always evident, in approximately 20% to 50% of patients with VT, but it is very rarely seen in SVT. Thus, the presence of AV dissociation strongly suggests VT, although its absence is less helpful. AV dissociation, if present, is typically diagnosed on ECG; however, it can produce a number of characteristic findings on physical examination. Intermittent cannon A waves may be observed on examination of the jugular pulsation in the neck, and they reflect simultaneous atrial and ventricular contraction; contraction of the right atrium (RA) against a closed tricuspid valve produces a transient increase in RA and jugular venous pressure. Cannon A waves must be distinguished from the continuous and regular prominent A waves seen during some SVTs. Such prominent waves result from simultaneous atrial and ventricular contraction occurring with every beat. Additionally, highly inconsistent fluctuations in the blood pressure can occur because of the variability in the degree of left atrial (LA) contribution to LV filling, stroke volume, and cardiac output. Moreover, variability in the occurrence and intensity of heart sounds (especially S₁) can also be observed and is heard more frequently when the rate of the tachycardia is slower.²

The response to carotid sinus massage can suggest the cause of the WCT. The heart rate during sinus tachycardia and automatic atrial tachycardia (AT) will gradually slow with carotid sinus massage and then accelerate on release. The ventricular rate during AT and atrial flutter (AFL) can transiently slow with carotid sinus massage because of increased atrioventricular node (AVN) blockade. The arrhythmia itself, however, is unaffected. Atrioventricular reentrant nodal tachycardia (AVRNT) and AVRT will either terminate or remain unaltered with carotid sinus massage. VTs are generally unaffected by carotid sinus massage, although this maneuver may slow the atrial rate and, in some cases, expose AV dissociation. Some VTs, such as idiopathic outflow tract VT, can rarely terminate in response to carotid sinus massage.

Laboratory Tests

The plasma potassium and magnesium concentrations should be measured as part of the laboratory evaluation. Hypokalemia and hypomagnesemia can predispose to the development of ventricular tachyarrhythmias. Hyperkalemia can cause a wide QRS complex rhythm, usually with a slow rate, with loss of a detectable P wave (the so-called sinoventricular rhythm; Fig. 21-1) or abnormalities of AVN conduction. In patients taking digoxin, quinidine, or procainamide, plasma concentrations of these drugs should be measured to assist in evaluating possible drug toxicity.

FIGURE 21-1 Wide QRS complex rhythm caused by hyperkalemia. No P waves are visible.

Pharmacological Intervention

The administration of certain drugs can be useful for diagnostic, as opposed to therapeutic, purposes. Termination of the arrhythmia with lidocaine suggests, but does not prove, that VT is the mechanism. Infrequently an SVT, especially AVRT, can terminate with lidocaine. On the other hand, termination of the tachycardia with procainamide or amiodarone does not distinguish between VT and SVT. Termination of the arrhythmia with digoxin, verapamil, diltiazem, or adenosine strongly implies SVT. However, VT can also occasionally terminate after the administration of these drugs.

Unless the cause for the WCT is definitely established, however, verapamil, diltiazem, and probably adenosine should not be administered, because they have been reported to cause severe hemodynamic deterioration in patients with VT and can even provoke ventricular fibrillation (VF) and cardiac arrest. Direct current (DC) cardioversion in unstable patients and intravenous procainamide or amiodarone in hemodynamically stable patients are the appropriate management approach.²

Ventricular Tachycardia Versus Aberrantly Conducted Supraventricular Tachycardia

Because the diagnosis of a WCT cannot always be made with complete certainty, the unknown rhythm should be presumed to be VT in the absence of contrary evidence. This conclusion is appropriate both because VT accounts for up to 80% of cases of WCT, and because making this assumption guards against inappropriate and potentially dangerous therapy. As noted, the intravenous administration of drugs used for the treatment of SVT (verapamil, adenosine, or beta blockers) can cause severe hemodynamic deterioration in patients with VT and can even provoke VF and cardiac arrest. Therefore, these drugs should not be used when the diagnosis is uncertain.

In general, most WCTs can be classified as having one of two patterns: a right bundle branch block (RBBB)–like pattern (QRS polarity is predominantly positive in leads V₁ and V₂) or a left bundle branch block (LBBB)–like pattern (QRS polarity is predominantly negative in leads V₁ and V₂). The determination that the WCT has an RBBB-like pattern or an LBBB-like pattern does not, by itself, assist in making a diagnosis; however, this assessment should be made initially because it is useful in evaluating several other features on the ECG, including the QRS axis, the QRS duration, and the QRS morphology (Table 21-2).

TABLE 21-2 Electrocardiographic Criteria Favoring Ventricular Tachycardia

Rate

The rate of the WCT is of limited value in distinguishing VT from SVT because there is wide overlap in the distribution of heart rates for SVT and VT. When the rate is around 150 beats/min, AFL with 2:1 AV conduction and aberrancy should be considered.

Regularity

Regularity of the WCT is not helpful in distinguishing VT from SVT because both are regular. However, VT is often associated with slight irregularity of the RR intervals, QRS morphology, and ST-T waves. Although marked irregularity strongly suggests atrial fibrillation (AF), VTs can be particularly irregular within the first 30 seconds of onset and in patients treated with antiarrhythmic drugs.

QRS Duration

In general, a wider QRS duration favors VT. In the setting of RBBB-like WCT, a QRS duration more than 140 milliseconds suggests VT, whereas for LBBB-like WCT, a QRS duration more than 160 milliseconds suggests VT. In an analysis of several studies, a QRS duration more than 160 milliseconds overall was a strong predictor of VT (likelihood ratio > 20:1). On the other hand, a QRS duration less than 140 milliseconds is not helpful for excluding VT, because VT can sometimes be associated with a relatively narrow QRS complex.

A QRS duration more than 160 milliseconds is not helpful in identifying VT in several settings, including preexisting bundle branch block (BBB), although it is uncommon for the QRS to be wider than 160 milliseconds in this situation, preexcited SVT, and the presence of drugs capable of slowing intraventricular conduction (e.g., class IA and IC drugs). Of note, a QRS complex that is narrower during WCT than during normal sinus rhythm (NSR) suggests VT. However, this is rare, occurring in less than 1% of VTs.²

Rarely (4% in one series), VT can have a relatively narrow QRS duration (<120 to 140 milliseconds). This can be observed in VTs of septal origin or those with early penetration into the His-Purkinje system (HPS), as occurs with fascicular (verapamil-sensitive) VT.

A recent report found that the QRS onset-to-peak time (also termed “R wave peak time” or “intrinsicoid deflection”) in lead II (measured from the beginning of the QRS to the first change of the polarity, independent of whether the QRS deflection is positive or negative) was significantly wider in VT compared with SVT with aberrancy, and a cutoff value of 50 milliseconds or greater identified VT with high sensitivity, specificity, and positive predictive values (93%, 99%, and 98%, respectively). However, this criterion has not been tested prospectively or validated in patients with preexisting conduction system disease, antiarrhythmic drug therapy, electrolyte imbalance, prior MI, and preexcited tachycardias. Additionally, certain types of VTs such as fascicular VT, bundle branch reentrant (BBR) VT, and septal myocardial VT, can have a shorter QRS onset-to-peak time because of their origin within or in close proximity to the His-Purkinje network.^1,3

QRS Axis

Generally, the more leftward the axis, the greater the likelihood of VT. A significant axis shift (>40 degrees) between the baseline NSR and WCT is suggestive of VT (Fig. 21-2A). A right superior (“northwest”) axis (axis from –90 degrees to ±180 degrees) is rare in SVT and strongly suggests VT (see Fig. 21-2B).²

FIGURE 21-2 Surface ECG of four different patients illustrating ECG morphology during normal sinus rhythm (NSR) versus ventricular tachycardia (VT). A, VT with right bundle branch block (RBBB) pattern, positive concordance, and long RS interval. Note the monophasic R in lead V₁

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