Basic considerations
Wide QRS tachycardias represent either VT or SVT with aberrant conduction.
VT and SVT represent vastly different clinical situations as far as etiology, extent of underlying cardiac disease, treatment, and prognosis.
The following discussion applies to hemodynamically stable patients; unstable patients should have emergent electrocardioversion.
Brugada’s criteria
In 1991, Brugada published a landmark paper on this problem, and his algorithm will be followed here (Brugada P, et al., A New Approach to the Differential Diagnosis of a Regular Tachycardia with a Wide QRS Complex. Circulation, Vol. 83, No. 5, May 1991).
Brugada’s criteria is based on the standard 12-lead ECG, but additional leads and techniques may aide in diagnosis.
Application of Brugada’s criteria (see tree diagram)
The presence and duration of an RS complex in the precordial leads
Any initial R wave followed by an S wave in the precordial leads qualifies for analysis.
Lack of an RS in any precordial lead is highly specific for VT.
An RS interval (defined as the interval between the onset of the R wave and the nadir of the S wave in any precordial lead) greater than 100 msec is highly specific for VT.
AV dissociation
The presence of AV dissociation is highly specific for VT.
AV dissociation can be detected on the standard ECG in about 20% of VT.
Methods for detection of AV dissociation
Examination of the patient may reveal irregular cannon A waves, in the neck veins caused by coincidental simultaneous atrial and ventricular systole.
Standard ECG leads II, III, aVF, and V2 are best for detecting P waves.
Moving one of the chest leads to the V3R position may reveal P waves.
An S5 or “Lewis’ leads” is obtained by placing the right arm lead in the second right interspace and the left arm lead in the suprasternal notch with the ECG machine set to Lead I.
A transesophogeal or intraatrial lead may be necessary to make a definitive diagnosis
Another evidence of AV dissociation is the presence of occasional narrow complex beats in the midst of a wide complex tachycardia. These so-called “capture beats” result from AV nodal transmission of a fortuitously timed supraventricular beat that “captures” the ventricle.
The morphology of the QRS complexes in V1–V2 and V6 (see table)
The first determination is whether the QRS morphology in the precordial leads is a RBBB or a LBBB
If the QRS complexes in V1–V2 and V6 both meet criteria for VT (see diagram), VT is confirmed.
If there is discordance between the criteria for VT in V1–V2 and V6, SVT is strongly implicated. (Day 8-01) (Day 8-02) (Day 8-03) (Day 8-04) (Day 8-05) (Day 8-06) (Day 8-07) (Day 8-08) (Day 8-09) (Day 8-10) (Day 8-11)
DAY 8-01
DAY 8-02
DAY 8-03
DAY 8-04
DAY 8-05
DAY 8-06
DAY 8-07
DAY 8-08
DAY 8-09
DAY 8-10
DAY 8-11
Sample Tracings
ECG 1
ECG 2
ECG 3
ECG 4
ECG 5
ECG 6
ECG 7
ECG 8
ECG 9
ECG 10
ECG 11
ECG 12
ECG 13
ECG 14
ECG 15
ECG 16
ECG 17
ECG 18
ECG 19
ECG 20
The Differential Diagnosis of Wide-QRS Tachycardias
ECG 1
Atrial rate:
Ventricular rate: 165
Rhythm: Ventricular tachycardia
P wave:
PR interval:
QRS complex:
Axis: -90°
Duration: 200 msec
Voltage:
Morphology:
ST segment:
T wave:
QT interval: 350 msec
U wave:
Diagnosis: This is a wide complex tachycardia with perhaps a QS complex in V1. In any case, the RS interval is >100 msec confirming the diagnosis of ventricular tachycardia.
ECG 2
Atrial rate:
Ventricular rate: 145
Rhythm: Ventricular tachycardia
P wave:
PR interval:
QRS complex:
Axis: -45°
Duration: 180 msec
Voltage:
Morphology:
ST segment:
T wave:
QT interval: 380 msec
U wave:
Diagnosis: This is a wide complex tachycardia that has RS complexes in the precordial leads. The RS interval in V4 is >100 msec, confirming the diagnosis of ventricular tachycardia.
ECG 3
Atrial rate: 220
Ventricular rate: 220
Rhythm: Atrial flutter with 1:1 AV conduction
P wave:
PR interval:
QRS complex:
Axis: 180°
Duration: 125 msec, RBBB
Voltage: Normal
Morphology: Normal
ST segment:
T wave:
QT interval: 200 msec
U wave:
Diagnosis: This is a wide complex tachycardia with RS complexes in the precordial leads. None of the RS intervals exceeds 100 msec. There is no evidence of AV dissociation. The presence of an RSR’ configuration in V1 strongly favors a supraventricular rhythm. The administration of intravenous adenosine subsequently proved that this was atrial flutter with 1:1 AV conduction and RBBB.
ECG 4
Atrial rate: 270
Ventricular rate: 135
Rhythm: Atrial flutter with 2:1 AV block
P wave:
PR interval:
QRS complex:
Axis: 75°
Duration: 160 msec, LBBB
Voltage:
Morphology:
ST segment: