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

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

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 during VT and the significant shift in the frontal plane axis in VT versus NSR. B, VT with an RBBB pattern and long RS interval. Note the superior (“northwest”) frontal plane axis during VT. C, VT with a left bundle branch block (LBBB) pattern, long RS interval, and 1:1 ventriculoatrial conduction. Retrograde P waves (red arrows) are visible following the QRSs during VT. D, VT with LBBB pattern and negative concordance. Note that the second QRS (blue arrows) is a fusion between the sinus beat and the VT beat.

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