Saturday, February 4, 2012

ECG Interpretation Review #36: (WCT - VT - A Fib - Irregular VT - WPW - Wide Tachycardia)

One of the most challenging tasks faced by emergency care providers is assessment and management of the patient with a stable WCT (Wide-Complex Tachycardia). When the QRS complex is wide – the rhythm is regular – and no P waves are seen – then VT (Ventricular Tachycardia) is the presumed diagnosis (Figure 1).
Figure 1Regular WCT without definite atrial activity. VT should be presumed until proven otherwise. (All Figures in this Blog are reproduced from ACLS-2013-ePub)NOTEEnlarge by clicking on FiguresRight-Click to open in a separate window.
In patients with underlying heart disease – VT is far more common than SVT (SupraVentricular Tachycardia) with either preexisting bundle branch block or aberrant conduction. For this reason, and because VT is potentially life-threatening – VT should always be presumed as the cause of a regular WCT until proven otherwise (See ECG Blog #23 for review of the approach to a regular WCT).
  • NOTE: Some patients tolerate VT surprisingly well. Such patients may remain awake and alert for hours (or longer) despite being in persistent VT. Therefore – finding that your patient is alert with normal (or even increased) blood pressure in no way rules out the possibility that the rhythm is sustained VT.
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Diagnosis of WCT rhythms becomes especially challenging when the rhythm is irregular and definable atrial activity is not seen during the tachycardia. Four examples of this are shown below in Figures 1, 2, 3, and 4. Imagine the patient is hemodynamically stable in each case, and that you are forced to make a diagnosis without the benefit of a 12-lead ECG obtained during the tachycardia. Match the rhythms shown in Figures 2-thru-5 to the following answer choices:
     a) Ventricular tachycardia.
     b) Atrial fibrillation with bundle branch block.
     c) Atrial fibrillation with WPW.
     d) Torsades de pointes.
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4 Irregular WCT Rhythms: Match the 4 irregular WCT rhythms below (in Figures 2-thru-5) to one of the above 4 answer choices:
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Figure 2Irregular WCT without atrial activity. NOTEEnlarge by clicking on FiguresRight-Click to open in a separate window.
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Figure 3 – An initial sinus beat or two – then an irregular WCT without atrial activity.
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Figure 4Irregular WCT without atrial activity.
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Figure 5 – Three initial sinus beats – then an irregular WCT without atrial activity. The tracing concludes with 2 sinus beats.
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GENERAL NOTE:  Although definitive diagnosis of each of these 4 rhythms is difficult given the lack of prior tracings and absence of a 12-lead ECG obtained during tachycardia – one should still be able to establish a high-probability diagnosis for each rhythm strip. Being able to do so will often be important clinically – when there may not be sufficient time to obtain more history – compare with prior tracings – and get a 12-lead during tachycardia. Optimal treatment choices vary tremendously depending on what the irregular WCT is likely to be.
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ANSWER to Figure 2:  Although subtle - the rhythm in Figure 2 is in fact irregularly irregular. The QRS is wide. An occasional undulation in the baseline is seen – but there are no definite P waves. We therefore strongly suspect atrial fibrillation (AFib) as the diagnosis – here with a rapid ventricular response.
  • Although VT is not always a perfectly regular rhythm – it usually does not vary from one beat to the next as seen here. This is the finding that strongly suggests AFib as the diagnosis. That said – this example highlights the point that when AFib is rapid – variability in the R-R interval between one beat and the next may be minimal (and at times require use of calipers for confirmation).
  • We say that the ventricular response of AFib in this example is “rapid” – because R-R intervals in Figure 2 are between 2-to-3 large boxes in duration (closer to the former). Thus, heart rate is in the range of 120-130/minute.
  • QRS morphology in this right-sided lead V1 is consistent with LBBB (Left Bundle Branch Block). This was confirmed by the 12-lead tracing shown below, obtained from this patient at the time of the lead V1 rhythm strip (Fig. 2-ANS).
Figure 2Irregular WCT without atrial activity. 
The type of bundle branch block is diagnosed by assessment of QRS morphology in the 3 KEY leads = Leads I,V1,V6 (See ECG Blog #3 - Blog #11 - and Blog #13). The monophasic upright QRS in left-sided leads I,V6 of Fig. 2-ANS – in association with the predominantly negative QRS in right-sided lead V1 is consistent with the diagnosis of typical LBBB.
  • Confirmation that the irregular WCT in Figure 2 is in fact AFib with QRS widening from preexisting bundle branch block was forthcoming from comparison with a prior 12-lead ECG on this patient that showed similar irregularity with identical QRS morphology due to this patient’s chronic LBBB.
Figure 2-ANS: – 12-lead ECG from the patient’s whose lead V1 rhythm strip was shown in Figure 2.  The rhythm is rapid AFib. QRS widening is due to LBBB.
Clinical Note: As opposed to RBBB (Right Bundle Branch Block) – patients with chronic LBBB almost invariably have significant underlying heart disease. Thus, a very common clinical scenario predisposing to the rhythm seen in Figure 2 is heart failure (resulting from loss of the atrial kick) due to new-onset AFib with a rapid ventricular response in a patient with underlying LBBB.
  • Treatment of new-onset rapid AFib entails (whenever possible) correction of precipitating causes (such as heart failure) – andslowing the ventricular response with AV nodal blocking drugs (verapamil-diltiazem-β-blockers-digoxin).
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ANSWER to Figure 3:  The 1st and 3rd beats in Figure 3 appear to be sinus conducted. We suspect the 2nd complex is a fusion beat manifesting a QRS morphology intermediate between the two sinus beats and the initial part of the irregular WCT that follows.
  • A useful classification of WCT rhythms separates them into those that are monomorphic (with similar QRS morphology during the tachycardia) vs those that are polymorphic (in which QRS morphology varies).
Figure 3 – An initial sinus beat or two – then an irregular WCT without atrial activity.
Beginning with the 4th beat in Figure 3 – a very rapid irregular WCT without atrial activity is seen. QRS morphology varies almost from beat-to-beat. This is polymorphic VT.
  • Torsades de Pointes – is defined as polymorphic VT that occurs in association with a long QT interval on baseline ECG. The very rapid irregular WCT seen in Figure 3 clearly manifests the shifting QRS polarity around the baseline (“twisting of the points”) that is characteristic of Torsades. However, whether the QT of the sinus beats seen in Figure 3 is prolonged – is suspected but not at all clear from the indistinct boundaries of the terminal part of the T wave …
  • Technically: Identification of polymorphic VT in the absence of QT prolongation is simply termed, “polymorphic VT”. As opposed to the multifactorial etiology of Torsades (drug-induced, electrolyte depletion, CNS disturbance or other underlying disorder that may predispose to QT lengthening) – polymorphic VT without QT lengthening most often has an ischemic etiology.
  • Clinically: Torsades de Pointes (= polymorphic VT with long QT) – responds extremely well to IV Magnesium. Although IV magnesium is also indicated as initial treatment of polymorphic VT with a normal QT – it is clearly less likely to respond than when the QT interval is prolonged. Instead – antiarrhythmic drugs such as amiodarone or β–blockers may be needed for treatment.
Definitive diagnosis of the irregular WCT seen in Figure 3 is forthcoming from an expanded look at this rhythm (Figure 3-ANS).
    Figure 3-ANS: – Expansion of the rhythm seen in Figure 3. This is Torsades de Pointes.
    The easiest way to look at the lead II rhythm strip shown in Fig. 3-ANS – is to step back a bit from the tracing. Doing so allows full appreciation of the characteristic alternating polarity of QRS complexes around the baseline during the irregular WCT.
    • Note in the magnified view of the first few beats (Fig. 3-ANS-2) that the QT interval is in fact prolonged (ie, more than half the R-R interval) – confirming that the example of polymorphic VT in Figure 3 is indeed Torsades (See Basic Concepts #2 beginning with Figure-9 for brief review on assessing the QT interval).
    Figure 3-ANS-2: Magnification of the first few beats of Fig-3-ANS. The baseline QT interval is prolonged; it comprises more than half the R-R interval for each of the first 2 sinus beats.

    NOTE: Electricity may be needed. That is – IF the patient in polymorphic VT is (or at any time becomes) hemodynamically unstable – immediate shock is indicated. Because of the continuously variable nature of the QRS complex during the tachycardia – synchronized cardioversion will usually not be possible. As a result – unsynchronized shock (ie, defibrillation) is recommended if the patient is unstable.

    • Polymorphic VT often recurs – especially if an uncorrected predisposing cause is present. Repeated shock may be needed while efforts are made to determine and correct any underlying causes.
    • Recognition of a prolonged QT on baseline ECG of such patients suggests a likely contribution from drug- or electrolyte-induced QT prolongation. Hopefully – IV Magnesium will reverse the disorder and prevent subsequent episodes. Efforts addressed at treating ischemia may be helpful in treating polymorphic VT when the QT is normal.
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    ANSWER to Figure 4:  The QRS complex is monophasic, albeit with some variation in the height of the QRS. The rhythm is irregularly irregular with marked variability in the R-R interval from one beat to the next. No atrial activity is seen. Although the QRS is clearly widened – the gross irregularity of the rhythm makes VT unlikely. This leaves atrial fibrillation (AFib) as the probable diagnosis (See ECG Blog #18).
    Figure 4Irregular WCT without atrial activity.
    The KEY point in interpreting this rhythm is appreciation of the exceedingly rapid ventricular response – which is far faster than that usually seen with atrial fibrillation.
    • Under normal conditions with AFib – 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 4 – the R-R interval is just over one large box in duration (which corresponds to a heart rate of ~250/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 AFib at an exceedingly rapid rate (over ~220/minute) should immediately suggest the likelihood of accessory (AP) pathway conduction in a patient with WPW (Wolff-Parksinson-White) syndrome (See ECG Blog #18 for review of tachyarrhythmias with WPW).
    • The example of AFib seen in Figure 4 can easily be distinguished from the much more common variety of rapid AFib that conducts over the normal AV nodal pathway by the rate. Suspect AFib with WPW whenever you encounter an excessively rapid and irregular WCT (>220/minute in parts of the tracing) without evidence of atrial activity.
    • Clinically: The importance of distinguishing the common form of rapid AFib seen in Figure 2 from the excessively rapid form due to WPW (Figure 4) – lies with recommendations for treatment. The usual AV nodal blocking drugs recommended for controlling the ventricular response of rapid AFib are contraindicated when AFib occurs in association with WPW. Thus – verapamil, diltiazem, digoxin (and possibly β–blockers) may all potentially accelerate forward conduction down the AP, thereby further increasing the rate of this already exceedingly rapid rhythm and predisposing to deterioration to ventricular fibrillation.
    • Recommended treatment of very rapid AFib that occurs in association with WPW includes amiodarone, procainamide, and ibutilide. Immediate cardioversion is indicated if hemodynamic decompensation occurs at any time during the treatment process.
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    ANSWER to Figure 5:  The initial 3 beats are sinus in this V1 rhythm strip. Then follows a rapid irregular WCT. This represents a run of monomorphic VT, albeit with more irregularity in the rhythm than is usually seen in VT.
    • Reasons in support of a ventricular etiology for the run of WCT seen in Figure 5 include abrupt onset of QRS widening with a QRS complex that is completely different in morphology than seen for the sinus conducted beats.
    • Presence of a post-ectopic pause following the run (less commonly seen following SVT).
    • Lack of a premature P wave preceding the run of WCT.
    • High statistical likelihood that a WCT such as is seen in Figure 5 is VT rather than SVT with preexisting bundle branch block or aberrant conduction.
    Figure 5 – Three initial sinus beats – then an irregular WCT without atrial activity – followed by 2 sinus beats at the end of the tracing.
    PEARL: We added this last example (Figure 5) as a contrast to the regular WCT in Figure 1 to emphasize the point that VT is not always completely regular.
    • Most of the time – any irregularity seen with VT will be minimal.
    • On occasion – there may either be a “warm-up” or “cool-down” phenomenon – in which the initial few beats of the VT run will either gradually speed up or slow down until a fairly regular R-R interval is established. A “cool-down” period is seen in Figure 5 (manifest by slowing of the VT rate after the first few beats).
    • The irregular WCT in Figure 5 is not AFib with WPW.  As opposed to Figure 4 – Figure 5 begins and ends with sinus-conducted beats. In between is a monomorphic WCT of very different morphology without atrial activity. This is VT.
    • The irregular WCT in Figure 5 is not Torsades because it is not polymorphic. Instead we see a run of monomorphic WCT consistent with conventional VT.
    Clinically: The importance of identifying the irregular WCT seen in Figure 5 as VT lies with recommendations for treatment. Favored antiararhythmic options for monomorphic VT include amiodarone – procainamide – sotalol. This is very different than the recommended treatment for Torsades or AFib with QRS widening from aberrant conduction or WPW.
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     See ECG Blog #18, Blog #23, Blog #24 and Blog #37 
      See also these pdfs excerpted from our ACLS-2013-ePub on Known VT  Torsades de Points  Very rapid AFib with WPW  
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    4 comments:

    1. Thanks for the post, it's pretty helpful.

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    2. My pleasure Javier. Please stayed tuned for the corresponding issue on treatment of irregular WCTs - which should appear as Issue #5 within the next few days in my ACLS COMMENTs column (https://www.kg-ekgpress.com/acls_comments/ ). Your specific comments/questions will be welcome! - : ) Ken (ekgpress@mac.com)

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    3. in the first tracing posted here, rhythm strip of lead II, complex #11 is of different morphology, or rather - of different amplitude. How to explain this?

      I know that fusion beats can occur with both SVT with wide complexes and VT. However it seems not to be premature compared to the other complexes. Do you know if this was SVT with abberancy or VT? Can one make the assumption that this is SVT with abberancy from this finding alone, as it may indicate some type of increased block, eg LAFB or LPFB in the setting of an already widened QRS?

      Nossen

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    4. Nossen - EXCELLENT observation on your part that QRS morphology in Figure 1 does change. On close inspection - not only is QRS morphology of beat #11 slightly different (taller with deeper ST depression) - but there is slight (less marked than for beat #11, but nevertheless definitely present) variation in QRS morphology for many of the other beats on this tracing .... albeit I don't think the variation enough to say this is "polymorphic VT" ... That said - as you note, beat #11 is not premature. It also looks like there may (?) be retrograde 1:1 VA conduction (note the notch in the ST segment for virtually all complexes except beat #11) - though this doesn't necessarily prove any specific etiology. That said - we are still left with the finding of a regular WCT without normal atrial activity that has to be presumed VT for Figure 1 until proven otherwise. I don't think beat #11 is a fusion beat - because it is not early, and I don't see another QRS focus that it is fusing with ... Having a 12-lead tracing during this tachycardia - plus a prior 12-lead on the patient obtained during sinus rhythm may be very helpful. In summary - one has to assume VT, and even though QRS variation is not as marked as is usual for polymorphic VT - I would expect this WCT to "act" like polymorphic VT (ie, synchronized cardioversion may be more difficult - and I'd have a low threshold for rapidly increasing energy, and if not responsive shifting to unsynchronized shock if the rhythm was resistant to treatment). THANKS again for your excellent comment! - Ken (ekgpress@mac.com)

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