Approach to Narrow and Wide QRS Complex Tachyarrhythmias


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Approach to Narrow and Wide QRS Complex Tachyarrhythmias


I. The unstable patient (shock, acute pulmonary edema)


In a hemodynamically unstable patient with supraventricular tachyarrhythmia (shock or severe HF), always ask yourself: did the tachyarrhythmia cause the shock or did the shock cause an increase in heart rate with a secondary SVT or AF? Typically, to attribute a shock to SVT or AF, the heart rate must be >150 bpm, or>130 bpm in systolic HF. In addition, clinical features suggestive of another primary process should be sought (sepsis, acute bleed/severe anemia, tamponade, massive PE); in these cases, tachycardia is not the isolated cause of the instability, it is rather the consequence.


For example, in a patient with BP 75/50 mmHg and AF rate of 125 bpm, AF is likely secondary to the shock rather the cause of the shock.


If a tachyarrhythmia faster than 130–150 bpm is assumed to be the cause of instability, emergent DC cardioversion should be performed.


II. Initial approach to any tachycardia


When analyzing a tachycardia, start by looking at three features:



  1. Narrow QRS vs. wide QRS (≥120 ms) (choose the lead where QRS is widest)
  2. Regular vs. irregular ventricular rate
  3. Look for P waves and their relationship with QRS complexes. P waves are usually seen as notches or deflections that fall over the ST–T segments and have a consistent morphology and timing, i.e., those deflections are regularly placed and can be marched out. Try to confirm that these deflections are P waves, rather than artifacts or parts of T wave, by analyzing multiple leads. Once P waves are found, their relationship with QRS complexes is analyzed.

P waves are often best seen in lead II, which is generally parallel to the spread of atrial depolarization; and in the lead where T and QRS are smallest (opening up room to see the scattered P waves).


In wide QRS tachycardia, analyze: (i) AV dissociation, and (ii) the number of P waves compared to the number of QRS complexes. In narrow QRS tachycardia, assess the length of the RP interval.


III. Approach to narrow QRS complex tachycardias (see Figures 8.1, 8.2)

Schematic illustration of approach to narrow QRS complex tachycardias.

Figure 8.1 Approach to narrow QRS complex tachycardias.


*A narrow QRS tachycardia may occasionally be VT. If QRS is relatively narrow (~110–120 ms) but different in morphology from the baseline QRS, consider it VT or SVT with aberrancy.


**As opposed to other tachycardias, sinus tachycardia has a gradual onset and termination and does not have a fixed rate. Tachyarrhythmias typically have a sudden onset and offset and a very fixed rate, although they may have a quick warm-up at the beginning. For example, a tachycardia with a fixed rate of 122 bpm on a telemetry monitor suggests arrhythmia. The P wave of atrial tachycardia or SNRT may have a sinus P-wave morphology; the abrupt onset and the steady rate help differentiate these arrhythmias from sinus tachycardia.


***RP interval points to the interval between onset of QRS and onset of the following P wave. The P wave may be a retrograde P wave in AVNRT or AVRT. If this interval is <1/2 of the R–R interval, the tachycardia is a short RP tachycardia. A very short RP interval, i.e. < 90 ms, is diagnostic of AVNRT.


† Atrial flutter may mimic short RP tachycardia if only the flutter wave following the QRS is seen, or may mimic long RP tachycardia/atrial tachycardia if only the flutter wave preceding the QRS is seen. Atrial tachycardia with negative P waves preceding the QRS complexes in the inferior leads may, in fact, be atrial flutter. Look carefully for flutter waves to make the diagnosis.

Schematic illustration of narrow complex tachycardia, regular, rate 200 bpm.

Figure 8.2 Narrow complex tachycardia, regular, rate ~200 bpm. Differential diagnosis: AVNRT, AVRT, atrial tachycardia with 1:1 conduction, or atrial flutter with 2:1 conduction.



  1. Look for P waves: Ps are seen in leads III, aVF, and V1 (arrows).
  2. The RP interval is <1/2 R-R interval, so it is a short RP tachycardia. It is, thus, either AVNRT or AVRT. If RP interval is very short (<90 ms), and if P falls within or immediately past the QRS, looking like pseudo-S in the inferior leads or pseudo-r’ in V1, the tachycardia is AVNRT rather than AVRT. On this ECG, RP is >90 ms, and therefore either AVNRT or AVRT is possible

IV. Approach to wide QRS complex tachycardias


The differential diagnosis of a wide QRS complex tachycardia includes:



  1. VT.
  2. SVT (including AF) with aberrancy. Aberrancy signifies the occurrence of a functional RBBB, LBBB, or RBBB + LAFB during a supraventricular tachycardia, leading to a wide complex morphology simulating VT. Aberrancy occurs when the refractory period of one of the bundles or fascicles is surpassed during the tachycardia (Figure 8.3). In addition, SVT with bundle branch block can be due to a pre-existing bundle branch block, in which case the QRS morphology during the tachycardia is similar to the QRS morphology during the sinus rhythm, sometimes slightly wider.
  3. SVT (especially AF) with pre-excitation (Figure 8.4). This means that the SVT is conducted antegradely over an accessory pathway that connects one atrium to one ventricle, short-circuiting the AV node.
  4. Other diagnoses: hyperkalemia; drug toxicity (class I antiarrhythmic agents, tricyclics); ventricular pacemaker tracking an atrial arrhythmia (lack of mode switch), or pacemaker- mediated tachycardia.

A wide complex tachycardia that is very grossly irregular is AF: AF with aberrancy, AF with pre-excitation, or AF with class I antiarrhythmic drug therapy. Polymorphic VT is a distant second possibility. On the other hand, a slightly irregular rhythm, with only slight variations of the R–R interval, may be seen with VT or any SVT at its onset (the first 20 beats).


A wide complex tachycardia is not necessarily “wide” (≥120 ms), as VT or aberrancy originating high in the septum near the His bundle or the bundle branches may be 110–120 ms wide, even narrower than a wide baseline QRS. The QRS morphology during tachycardia is, however, different from the baseline QRS morphology. In particular, in patients with a wide baseline QRS, a tachycardia with a narrower QRS is VT.

Schematic illustration of explanation of how a wide QRS complex (aberrancy) may occur with SVT.

Figure 8.3 Explanation of how a wide QRS complex (aberrancy) may occur with SVT. RBBB, LBBB, or RBBB + LAFB may be seen. RBBB + LPFB is rare.

Schematic illustration of two types of SVT with pre-excitation, i.e., SVT with antegrade conduction over an accessory pathway (WPW syndrome).

Figure 8.4 There are two types of SVT with pre-excitation, i.e., SVT with antegrade conduction over an accessory pathway (WPW syndrome):



  • AF or any atrial arrhythmia with pre-excitation. The atrial waves are preferentially conducted through the fast accessory pathway, leading to a very fast ventricular rate.
  • Antidromic AVRT. The electrical stimulus spreads down through the accessory pathway then up through the AV node. The ventricles get depolarized through the pre-excited ventricle (dashed arrows), not through the His bundle, and thus have a wide QRS morphology.

Approximately 80% of wide complex tachycardias are VTs (95% in case of CAD or HF). Thus, if one is unsure of the diagnosis, it is safer to consider the arrhythmia VT than SVT and treat it as such. However, it is best to look for features characteristic of VT and establish a definitive diagnosis.


V. Features characteristic of VT, as opposed to SVT with aberrancy


A. Four features are most helpful in differentiating VT from SVT. The presence of any one VT feature is immediately diagnostic of VT



  1. The presence of AV dissociation. AV dissociation is characterized by P waves that do not have any consistent relationship with the QRS complexes. In tachycardia, AV dissociation is ~100% specific for VT. AV association, on the other hand, does not necessarily imply SVT and may be seen with VT. In fact, retrograde ventriculoatrial (VA) conduction is seen in ~25% of VTs, especially VTs slower than 170 bpm, leading to retrograde P waves that are regularly associated with the QRS complexes. This manifests as 1:1 AV association (1:1 retrograde conduction) that is indistinguishable from SVT. At times, other ratios of VA conduction may be seen (e.g., two QRS complexes with one P wave, three QRS complexes with two P waves), in which the number of QRS complexes is greater than the number of P waves, implying VT.

    Thus, VT is diagnosed if either: (i) AV dissociation is present, or (ii) QRS complexes outnumber P waves (with AV association or AV dissociation). P waves are often best seen in lead II, which is generally parallel to the spread of atrial depolarization, or leads with the smallest QRS and T wave.


  2. QRS morphology. A QRS morphology that is not consistent with a typical RBBB, LBBB, or RBBB + LAFB is characteristic of VT. In particular, a QS or Qr pattern in V4–V6 , i.e., deep Q wave in V4–V6 , is particularly suggestive of VT. In addition, in bundle branch blocks, the initial portion of the QRS complex corresponds to the quick localized depolarization at or near the septum and thus is narrow (LBBB → rS in V1 with a narrow r; RBBB → rSR’ in V1 with a narrow r). On the other hand, in VT, the electrical activity often starts away from the septum, and thus the initial QRS deflection is not narrow (Figures 8.5, 8.6, 8.7).

    Rare caveats: VT that starts in the septum has a narrower QRS than free wall VT and may simulate RBBB morphology (e.g., idiopathic left fascicular VT). Also, bundle branch reentrant VT (macroreentry down the right bundle and up the left bundle), rarely seen in dilated non-ischemic cardiomyopathy, may have a typical LBBB morphology.


  3. The onset of the tachycardia on ECG or telemetry monitor. A tachycardia that starts with a PVC and has a morphology similar to this PVC is VT. A tachycardia that starts with a wide aberrant PAC and has a morphology similar to this aberrant PAC is SVT. Also, a tachycardia that is similar in morphology to a previous PVC is VT. A tachycardia that starts with a PVC but does not have the morphology of that PVC is likely VT, but may be SVT initiated by the PVC.

    How to distinguish a PVC from an aberrant PAC? A wide QRS complex which coincidentally falls on the top of a regularly occurring sinus P wave is a PVC (the regularly occurring sinus P wave shows up as a “blip” within the PVC). PVC may also fall after the regular sinus P wave at a shorter PR distance. A PVC does not disrupt the underlying sinus/atrial rhythm, and P waves keep occurring regularly through it. On the other hand, an aberrantly conducted PAC starts after a premature and different-looking P wave that may fall within the preceding T wave and deform it. A deformation of the T wave preceding the premature complex suggests PAC.

    Schematic illustration of difference in QRS morphology between bundle branch block and VT.

    Figure 8.5 Difference in QRS morphology between bundle branch block and VT. The QRS description is in reference to lead V1.


  4. If the patient has a pre-existing RBBB or LBBB, or any intraventricular conduction delay, and the tachycardia has the exact morphology of the baseline QRS , the tachycardia is SVT.

Figures 8.5 to 8.12 illustrate these concepts.


B. Other features (again, the presence of any one feature is suggestive of VT)



  1. Brugada criteria. The Brugada criteria include four features, two of which have already been discussed: (1) AV dissociation, (2) QRS morphology inconsistent with a typical RBBB or LBBB, (3) onset of R-to-nadir of S >100 ms in any precordial lead, (4) monophasic QRS concordance in all precordial leads. The presence of any one of these is diagnostic of VT with a high sensitivity and specificity (~98%). The lack of all four is diagnostic of SVT with a high sensitivity and specificity (~98%).
    Schematic illustration of QRS morphology when VT originates in the posterior wall or the apical wall.

    Figure 8.6 QRS morphology when VT originates in the posterior wall or the apical wall.

    Schematic illustration of differences in morphology between SVT with aberrancy and VT.

    Figure 8.7 Differences in morphology between SVT with aberrancy and VT. SVT with aberrancy has a typical LBBB or RBBB morphology. Conversely, VT is suggested by:



    • LBBB with a wide initial R wave >30 ms, R-to-nadir of S >70 ms, or notched S descent in V1; or Q wave in V6.
    • RBBB with a wide R pattern in V1 instead of RSR’, R >R’ in V1, or monophasic R or QS in V6. RBBB with a left axis or with a rS pattern in V6 does not necessarily imply VT (could be RBBB + LAFB).

    While rS pattern in V6 is not typical of LBBB or RBBB, it may be seen with atypical LBBB (enlarged LV) or RBBB + LAFB. Deep Q in V6 (QS or Qr) implies VT.


    Left QRS axis may be seen with LBBB or RBBB + LAFB. Right QRS axis, on the other hand, is not typically seen with either LBBB or RBBB and usually implies VT.

    Schematic illustration of run of wide complex tachycardia on a telemetry strip.

    Figure 8.8 Run of wide complex tachycardia on a telemetry strip: is it VT or SVT?



    1. See how it starts: the first wide complex is not preceded by any premature P wave and there is no deformation of the preceding T wave. This initial complex is a PVC, and the tachycardia has a morphology similar to this initial complex: this suggests that the tachycardia is VT.
    2. Look for P waves. Some notches are visible inside the wide complex run. Try to march them out with the preceding and following sinus P waves → they do march out at the same rate as the sinus P rate, independently of the wide complex rhythm and scattered inside it. Some P waves are hidden within QRSs and cannot be seen (marked with an asterisk [*]). The two visible P waves that are dissociated from the QRS complexes imply AV dissociation, characteristic of VT.
    3. The initial upslope of the wide QRS complex is slower and less steep than the upslope of the baseline QRS. This is suggestive of VT.
    Schematic illustration of wide complex tachycardia.

    Figure 8.9 Wide complex tachycardia: VT or SVT?



    1. Look for P waves, i.e., look for scattered “blips” that: (a) have a consistent morphology and timing, and (b) can be marched out. Blips are seen in lead II (vertical arrows). These blips can be marched out (calipers) and have a consistent morphology; they are not part of the T wave, as they do not consistently fall on every T wave. They are also seen in other leads (I, V5, V6, arrows), further adding to the evidence that these are P waves, not artifacts or parts of T wave. They do not have a consistent relationship with the QRS complexes, and some of them fall inside the QRS complexes and are not seen (dashed arrows). Thus, P waves are dissociated from QRS complexes and are less numerous than QRS complexes. This is diagnostic of VT. The variable T-wave morphology is usually a hint to the presence of P waves that are dissociated from QRS/T and falling variably over some T waves.
    2. Analyse QRS morphology. QRS has a LBBB-like morphology in lead V2. However, there is a QR pattern in V5–V6, QS pattern in lead I, and right-axis deviation (QRS negative in lead I), not consistent with LBBB. Besides, QRS has excessive notching, best seen in leads V1 and V3 (horizontal arrows). Thus, this is VT.
    3. Additional findings:

      • Wide QRS complexes of different morphology are scattered within the tachycardia (stars). Those may represent fusion complexes or PVCs. Being wide, they have no diagnostic value.
      • ST-segment elevation, concordant with QRS, is seen in the anterolateral leads. This is concerning for STEMI.
    Schematic illustration of two short tachycardia runs.

    Figure 8.10 Two short tachycardia runs. The tachycardia starts after a regularly occurring sinus P wave (bar) at a shorter PR interval (the bar marches out with the arrows). This is typical of a PVC, which occurs without disrupting the timing of the underlying sinus P waves. PAC would have started with a premature P wave. Thus, the tachycardia starts with a PVC and has the same morphology as the PVC. This is VT.

    Schematic illustration of wide complex, regular tachycardia, at a rate of 135 bpm.

    Figure 8.11 Wide complex, regular tachycardia, at a rate of ~135 bpm. QRS looks narrow in some leads; this is due to the fact that part of the QRS is isoelectric in those leads. That is why QRS should be measured in the lead where it is widest. QRS is wide (~140 ms) in lead V3 in particular.



    1. QRS looks like a typical LBBB in leads I, aVL, and V1. This suggests SVT with LBBB aberrancy.
    2. P waves are seen. A negative P wave is overlying the ST–T segment and another P wave is just preceding QRS (arrows); these deflections are recognized as P waves, as opposed to being fragments of T wave, by the fact that they have a consistent morphology and can be marched out. Thus, this tachycardia is an atrial tachyarrhythmia with 2:1 AV conduction, the atrial rate being 270. The atrial rate (>240) as well as the sawtooth shape seen in leads II and aVR and the lack of isoelectric baseline make the diagnosis atrial flutter.

    Final diagnosis: Atrial flutter with 2:1 AV conduction and wide QRS due to LBBB aberrancy.

    Schematic illustration of the baseline rhythm is sinus, consisting of QRS complexes (R) preceded by sinus P waves.

    Figure 8.12 The baseline rhythm is sinus, consisting of QRS complexes (R) preceded by sinus P waves. Outside these complexes, there are premature complexes occurring in a bigeminal pattern (R1, R2, R3, R4). These could be PVCs or PACs with aberrancy. Look for P waves preceding these complexes: there is a P wave before each complex, marked #. It is an inverted, non-sinus P wave and occurs prematurely. This means that R1–R4 are PACs with aberrancy rather than PVCs. These PACs have aberrant conduction because they occur very prematurely, while the right bundle is still in its refractory period, which leads to RBBB morphology. Note that the aberrancy (QRS widening) is less pronounced when PAC is less premature. This is a form of Ashman’s phenomenon. R–R1 interval <R–R3 interval <R–R4 interval; hence, R4 is not aberrant.


    Monophasic QRS concordance in the precordial leads signifies that all QRS complexes in V1 through V6 are monophasic and pointing in the same direction, either upward or downward. In other words, these QRS complexes are either monophasic R or monophasic QS complexes. Concordance is not present if any of the six leads has a biphasic QRS (e.g., qR or RS complex).


  2. Northwest axis or right axis. The typical forms of aberrancy, LBBB, RBBB, or RBBB + LAFB, are not associated with a right axis (RBBB may be associated with a right axis when RVH coexists, as seen on the baseline ECG). On the other hand, VT most frequently originates from the ventricle with the largest mass, i.e., LV, and therefore frequently has a right axis.
  3. In patients with a wide baseline QRS (LBBB or RBBB or non-specific intraventricular conduction delay), a tachycardia that is wide but narrower than the baseline QRS is VT. Aberrancy can only widen QRS, not narrow it, whereas VT may paradoxically be narrower than the baseline rhythm. Also, a tachycardia with a bundle branch block morphology contralateral to a baseline bundle branch block is usually VT (e.g., in a patient with RBBB at baseline, a tachycardia with LBBB morphology is VT).
  4. QRS >160 ms suggests VT if the baseline QRS is narrow and in the absence of class I antiarrhythmic drug therapy.
  5. Presence of capture or fusion complexes. When an impulse originating from the sinus node conducts down the AV node and captures the ventricles, instead of allowing the VT focus to capture the ventricles, the complex that results is a capture complex squeezed within the VT. If this impulse partially captures the ventricles, while the VT focus partially captures the rest of the ventricles, the resulting complex is a fusion complex. A capture complex has the same morphology as the baseline sinus beat, while a fusion complex has a morphology intermediate between the sinus beat and VT. A fusion complex may start like the sinus-originating beat and terminate like the VT beat, or vice versa. Only when the beat squeezed in the tachycardia is narrow can one be certain that it is a capture or a fusion complex. A QRS complex that is wide but of different morphology than the tachycardia (narrower or not) may be a fusion complex in a patient with VT or a PVC in a patient with SVT or VT.
  6. In VT, the QRS complex is wide in its initial portion and has a slow initial upslope or downslope. Conversely, in SVT with aberration, QRS has a narrow initial deflection that corresponds to the septal depolarization, followed by widening of the terminal QRS portion. In addition, in VT, the impulse frequently spreads over a diseased, fibrotic myocardium and meets “bumps” on the road, creating atypical notching of the QRS complex (notching of S descent or R wave, different from bundle branch block).
  7. In aVR, VT is suggested by: (i) large or wide initial R wave, or (ii) QR pattern with a slowly downsloping Q wave >40 ms. Normally, aVR consists of a sharp and deep negative deflection, sometimes preceded or followed by a small r wave (QS, rS, or Qr pattern).

VI. Features characteristic of SVT with pre-excitation


Once a diagnosis of VT is made using the above criteria of VT vs. aberrant SVT, step back and consider the diagnosis of pre-excited SVT before closing. Since the ventricular stimulation does not spread down from the His bundle, the QRS morphology of a pre-excited SVT resembles the QRS morphology of VT, i.e., not a typical LBBB or RBBB morphology. The initial portion of QRS is slurred, but this is seen with VT as well (slow upslope) and does not help differentiate VT from pre-excited SVT. Seeing the slurred delta wave on the baseline ECG is diagnostic of pre-excitation; seeing it during tachycardia is not diagnostic and is consistent with VT as much as pre-excited SVT.


The most typical pre-excited arrhythmia is AF with pre-excitation. In this case, the wide tachycardia is irregular, implying AF rather than VT. AF with pre-excitation is diagnosed when AF has VT morphological features; or when AF is wide and polymorphic (QRS varies in height and width), bizarre looking, or very fast (>200 bpm) (Figure 8.13).

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Nov 27, 2022 | Posted by in CARDIOLOGY | Comments Off on Approach to Narrow and Wide QRS Complex Tachyarrhythmias

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