Saturday, March 19, 2011

ECG Blog #18 — aVery Fast Tachycardia ...

QUESTION: The ECG below was obtained from a middle-aged woman with new-onset palpitations. She was otherwise not in distress, did not complain of chest pain, and had a blood pressure of 90/60 mm Hg at the time this tracing was recorded. 
  • Is she in ventricular tachycardia?
  • How might you treat her? (What medications would you not use?)

Figure 1 - Lead II rhythm strip from a middle-aged woman with palpitations. Is she in VT?

INTERPRETATION:  The rhythm is rapid and irregularly irregular.  No atrial activity is seen.  Although the QRS complex is definitely widened, the gross irregularity of the rhythm makes ventricular tachycardia unlikely.  This leaves atrial fibrillation as the probable diagnosis.  That said — the rate of the rhythm at certain points in the tracing is much faster than is usually seen with atrial fibrillation.
  • Under normal conditions with atrial fibrillation — the refractory period of the AV node does not allow more than 150-to-200 impulses/minute to be conducted to the ventricles. At certain points in Figure 1 — the R-R interval is just over one large box in duration (which corresponds to a heart rate of ~250 beats/minute). This is simply too fast for atrial impulses to be transmitted over the normal (AV nodal) conduction pathway. 
CONCLUSION:  Atrial impulses must be bypassing the AV node. The finding of atrial fibrillation at an exceedingly rapid rate (over ~220/minute) should immediately suggest the likelihood of accessory (AP) pathway conduction in a patient with WPW (Wolff-Parkinson-White) Syndrome.
  • Two additional features in favor of the rhythm in Figure 1 being WPW rather than VT are: i) variation in QRS morphology during the WCT (less likely with VT); and ii) very marked change between some R-R intervals on the tracing (some being extremely short with others being significantly longer).

WPW is a syndrome in which one or more accessory conduction pathways exist that allow an alternate route for transmission of the electrical impulse from the atria to the ventricles.  It has an approximate incidence of 2 per 1,000 individuals in the general population — just frequent enough that most emergency care providers will encounter patients with WPW-related arrhythmias from time to time.
     Conduction of the sinus impulse in patients with WPW may be via the normal (AV nodal) pathway — down the accessory tract — or it may alternate between the two.  These patients are prone to develop atrial tachyarrhythmias in which a reentry circuit is set up between the normal AV nodal pathway and the accessory tract (Figure 2).

Figure 2: Pathways of conduction of supraventricular tachyarrhythmias with WPW. Panel A represents the usual path with AVRT; Panel B with AFib (See text).

NOTE on Terminology: The older name for reentry SVT rhythms was PSVT (Paroxysmal SupraVentricular Tachycardia). At present, the more accurate and more commonly-used name = AVNRT (AV Nodal Reentry Tachycardia). When the patient has an AP (Accessory Pathway) that participates in the reentry circuit — the reentry tachycardia is then called AVRT (AtrioVentricular Reciprocating Tachycardia). As explained below — depending on the initial direction of the impulse during the reentry tachycardia (ie, going initially down the AP — or going initially down the AV Node) — AVRT will either be orthodromic or antidromic.

The following are the 4 main arrhythmias encountered in patients with WPW:
  • With AVRT — the tachyarrhythmia is almost always orthodromic (down the normal AV nodal-His-Purkinje system and back up the accessory pathway as in Panel A of Figure 2). Because conduction goes down the normal AV nodal pathway — the QRS complex is narrow during the tachycardia. AVRT is by far the most common tachyarrhythmia observed in patients with WPW.  It is usually well tolerated by the patient.
  • In contrast, with Atrial Fibrillation in WPW — the tachyarrhythmia is almost always antidromic (down the AP, with retrograde conduction back to the atria over the AV nodal pathway as in Panel B in Figure 2).  Antegrade conduction over the accessory pathway results in QRS widening during the tachycardia. Because of the short refractory period of the AP, there may be 1:1 conduction of atrial impulses during atrial fibrillation, resulting in a ventricular response that at times exceeds 250 beats/minute (Figure 1).  Such rapid rates may not be well tolerated (the ventricles may not be able to adequately contract at this rate) — and as a result the rhythm can deteriorate into ventricular fibrillation.
  • Although less commonly seen than atrial fibrillation — Atrial Flutter may also occur in patients with WPW.  As with atrial fibrillation — antegrade transmission of atrial impulses is almost always down the AP when patients with WPW develop atrial flutter.  As a result — there may be 1:1 AV conduction (so that the ventricular response may be as fast as 250-350/minute).
  • Note: In those rare (~5%) instances in which AVRT is antidromic — the QRS complex will be wide and the AVRT rhythm may be indistinguishable from VT. It may only be after conversion to sinus rhythm that "telltale" delta waves of WPW can be identified. Fortunately — the vast majority (~95%) of AVRT episodes with WPW are orthodromic (with narrow QRS).
TREATMENT: Although verapamil, diltiazem and digoxin are all effective medications for slowing the ventricular response of rapid atrial fibrillation — they are contraindicated when atrial fibrillation occurs in association with WPW.  This is because each of these drugs may accelerate conduction down the AP, and thereby exacerbate the tachyarrhythmia. 
  • Appropriate medications to consider (that slow antegrade conduction down the AP) — include amiodarone, procainamide or ibutilide.  
  • Be aware of the need to cardiovert the patient IF they decompensate.

ADDENDUM (added to Blog #18 on 2/1/2012): 
Interpret the 12-lead ECG shown in Figure 3, obtained from an older patient with palpitations. HINT: The answer is related to Figure 1 …

Figure 3: 12-lead ECG from an older patient with palpitations. Is this VT?

INTERPRETATION of FIGURE 3: There is a regular monomorphic WCT (Wide-Complex Tachycardia) seen at the exceedingly rapid rate of nearly 300/minute! (as determined by the occurrence of a QRS complex each large box). This is too fast for VT. Although this rhythm could represent ventricular flutter – it turned out to be atrial flutter at a rate of ~300/minute in a patient with WPW.
  • As was the case in Figure 1 — antegrade (forward) conduction down the AP (Accessory Pathway) is seen when atrial fibrillation or flutter occur in a patient with WPW. This leads to WCT rhythms at rates that are faster than should be seen for VT.
  • Although rare — the importance of recognizing very rapid AFib or Flutter with WPW cannot be overstated. This is because treatment with verapamil/diltiazem/digoxin are all contraindicated. Instead — one should use amiodarone/procainamide/ibutilide – with awareness of the need to immediately cardiovert the patient IF hemodynamic decompensation occurs (Further discussion of treatment recommendations in this pdf from Section 12.0 of our ACLS-2013-ePub).
- See also ECG Blog #36 and Blog #37 -


  1. Thanks Dr ken for nice explanation
    I think Amiodarone is harmful in Afib with WPW , as it has Beta blocker and Calcium channel blocker action on AV node ,which may predominate when we give to AFIB with WPW , accordingly enhance AP conduction.

    1. As Mostafa — You are entitled to your opinion. Having thoroughly research this subject, my opinion differs. I wrote this up in detail in Section 12.0 of the 5th Edition of my ACLS Pocket Brain (ACLS-2013-ePub). Here is a link to download a pdf of this entire Section. Please be sure to begin reading from Section 12.7 on ( ). Despite strong opinions by many — the actual literature is (in my strong opinion) lacking in objectivity. It is not prospective. Data is missing. There is much crossover. I summarize my impressions of available literature, and make a clinical practical suggested approach. Please review what I have written. After you have done so, if you still feel the same — then I am happy to agree to disagree with you.

  2. Dr. Grauer, in figure 3, monophasic R wave in avR shouldn't be patognomonic of VT?. Which accessory pathway could be explain it? Thank you

    1. So sorry this has taken me 4 years to respond (Somehow I never saw your question). CORRECT — The presence of WPW can explain this QRS morphology — :)

  3. Hello Marco. Thanks for your comment. If you draw a VERTICAL line up from the point on the peak of the QRS in simultaneously-obtained lead 3 — you'll see that this corresponds to the negative part of the complex in lead aVR — so the QRS in aVR is not all positive ... Fig. 3 is AFlutter in a patient with WPW — :)

  4. Dear Ken:
    Fig 3 is AFL with WPW,then we can't use AV node blocking agents like Af+WPW,right?

    1. CORRECT! The same cautions apply regarding use of antiarrhythmic medications for AFlutter as for AFib!