Wide complex tachycardias

Causes of wide complex tachycardias

A narrow QRS complex (120 milliseconds or less) requires rapid, highly synchronous electrical activation of the right and left ventricles, 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 can be fixed and present at all heart rates, and they can 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). ^,

Wide complex tachycardia (WCT) is defined as a rhythm with a rate of more than 100 beats/min and a QRS duration more than 120 milliseconds ( Fig. 25.1 ). Several arrhythmias can manifest as WCTs ( Table 25.1 ); the most common is ventricular tachycardia (VT), which accounts for 80% of all cases of WCT. SVT with aberrancy accounts for 15% to 20% of WCTs. Supraventricular tachycardias (SVTs) with bystander preexcitation and atrioventricular reentrant tachycardia (AVRT) account for 1% to 6% of WCTs.

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 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 valuable information.

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 the presence and severity of hemodynamic instability 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 or subaxillary region.

An important objective of the physical examination in the stable patient is to attempt to document the presence of atrioventricular (AV) dissociation. The presence of AV dissociation strongly suggests VT, although its absence is less helpful. AV dissociation, when 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 intermittent simultaneous atrial and ventricular contraction. Cannon A waves must be distinguished from the continuous and regular prominent A waves seen during some SVTs, which 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 contribution to LV filling, stroke volume, and cardiac output. Moreover, variability in the occurrence and intensity of heart sounds (especially S ₁ ) can also be observed and is heard more frequently when the rate of the tachycardia is slower.

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 slowing and block of AV nodal (AVN) conduction; the arrhythmia itself, however, is unaffected. AVRNT and AVRT will either terminate or remain unaltered with carotid sinus massage. VTs are generally unaffected by carotid sinus massage, although this maneuver can potentially slow the atrial rate and, in some cases, expose AV dissociation. Some VTs, such as idiopathic VT from the right ventricular (RV) outflow tract, can infrequently terminate in response to carotid sinus massage.

Laboratory testing

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; however, correction of abnormalities of electrolytes is not sufficient for therapy. Hyperkalemia can cause a wide QRS complex rhythm, usually with a slow rate, with loss of a detectable P wave (the putative sinoventricular rhythm; eFig. 25.1 ) 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.

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 IV administration of drugs used for the treatment of SVT (verapamil, diltiazem, 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: RBBB-like pattern (QRS polarity is predominantly positive in leads V ₁ and V ₂ ) or left bundle branch block (LBBB)-like pattern (QRS polarity is predominantly negative in leads V ₁ and V ₂ ). 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 has further implications for evaluating several other features on the ECG, including the QRS axis, the QRS duration, and the QRS morphology ( Table 25.2 , Fig. 25.2 ).

Atrioventricular dissociation

AV dissociation is characterized by atrial activity (P waves) that is completely independent of ventricular activity (QRS complexes). The atrial rate is usually slower than the ventricular rate ( eFig. 25.2 ). A regular R-R interval in the presence of AF would most likely be AV dissociated.

The presence of AV dissociation is strongly suggestive of VT, although it can also be observed during subatrial SVT, such as junctional ectopic tachycardia and nodofascicular reentrant tachycardia. The absence of AV dissociation, however, is not as helpful in the differential diagnosis of WCT. AV dissociation is absent in a large subset of VTs (especially those at a slower rate); in fact, approximately 30% of VTs have 1:1 retrograde ventriculoatrial (VA) conduction ( Fig. 25.2 ) and an additional 15% to 20% have second-degree (2:1 or Wenckebach) VA block ( eFig. 25.3 ). Even when AV dissociation is present but during VT, it may not be obvious on the surface ECG because of rapid ventricular rates.

Several ECG findings are helpful in establishing the presence of AV dissociation, including the presence of dissociated P waves, fusion beats, or capture beats.

Dissociated P waves

When the P waves can be clearly seen and the atrial rate is unrelated to and slower than the ventricular rate, AV dissociation consistent with VT is present ( Fig. 25.3 ). An atrial rate faster than the ventricular rate is more often seen with SVTs having AV conduction block. However, during a WCT, the P waves are often difficult to identify; they can be superimposed on the ST segment or T wave (resulting in altered morphology). Sometimes, the T waves and initial or terminal portions of the QRS complex can resemble atrial activity and be mistaken for P waves. If the P waves are not obvious on the ECG, several alternative leads or modalities can help in their identification, including a modified chest lead placement (Lewis leads), an esophageal lead (using an electrode wire or nasogastric tube), right atrial recording (obtained by an electrode catheter in the right atrium), carotid sinus pressure (to slow VA conduction and therefore change the atrial rate in the case of VT), or invasive electrophysiological testing.

Fusion beats

Ventricular fusion occurs when a ventricular ectopic beat and a supraventricular beat (conducted via the AVN and HPS) simultaneously activate the ventricular myocardium. The resulting QRS complex has a morphology intermediate between the appearance of a sinus QRS complex and that of a purely ventricular complex. Intermittent fusion beats during a WCT are diagnostic of AV dissociation and therefore of VT ( Fig. 25.3 ). However, it is also possible for PVCs during SVT with aberration to produce fusion beats, which would erroneously be interpreted as evidence of AV dissociation and VT.

Capture beats

A capture beat (once called “Dressler beat”) is a normal QRS complex, identical to the sinus QRS complex, occurring during the VT at a rate faster than the VT. The term capture beat indicates that the normal conduction system has momentarily captured control of ventricular activation from the VT focus ( Fig. 25.3 ). Fusion and capture beats are more commonly seen when the tachycardia rate is slower. These beats do not alter the rate of the VT, although a change in the preceding and subsequent RR intervals is frequently observed.