Thursday, February 16, 2012

ECG Interpretation Review #38 (WCT - SVT - VT - Fascicular - RBBB Aberration - Tachycardia Algorithm)

Your patient is a 40-year-old man who presents to the emergency department with palpitations and the 12-lead ECG shown in Figure 1. No prior ECG is available. The patient had previously been healthy. He is alert and hemodynamically stable with a BP = 160/80 mmHg.  What is the rhythm?  Is this tachycardia likely to be supraventricular with RBBB aberration? How would you treat this patient?
Figure 1 – 12-lead ECG from a 40-year-old man with palpitations.  Is this tachycardia likely to be supraventricular with RBBB aberration? – NOTEEnlarge by clicking on FiguresRight-Click to open in a separate window.
INTERPRETATION:  The rhythm in Figure 1 is rapid and regular at a rate of ~200/minute. The QRS complex is monomorphic (not varying in morphology) - and - appears to be slightly (albeit not overly) wide – with an estimated duration between 0.11-0.12 second. No P waves are seen. Thus, the rhythm qualifies as a regular monomorphic WCT (Wide-Complex Tachycardia) without clear sign of atrial activity. As we have emphasized in previous blog posts (See ECG Blog #23Blog #24Blog #35) – the diagnosis of VT (Ventricular Tachycardia) must be assumed until proven otherwise.
  • VT is by far the most common cause of a regular monomorphic WCT when there is no sign of atrial activity (accounting for >80% of cases overall – and over 90% if the patient is older and has a history of documented heart disease).
  • On occasion (~5-20% of the time) – a regular WCT may be supraventricular in etiology, due either to: i) preexisting BBB (bundle branch block); or ii) aberrant conduction.
WCT: Differentiating between VT vs SVT
Distinction between VT vs SVT (SupraVentricular Tachycardia) with either preexisting BBB or aberrant conduction is often a highly challenging task (See ECG Blog #15 and Blog #33 and especially this pdf from our ACLS-2013-ePub). In many instances at the bedside – this distinction cannot be made with certainty. In others – clinical determination can only be made retrospectively when prior and post-conversion tracings become available. At times – definitive determination will not be forthcoming unless (and until) electrophysiologic study is done …
  • Clinically – the importance of distinguishing between VT vs SVT with either preexisting BBB or aberrant conduction lies with the impact this determination has on prognostic implications and the therapeutic approach. VT is a potentially life-threatening arrhythmia. In contrast – SVT is rarely life-threatening, and may often be controlled by medication without necessarily initiating cardiology referral.
  • IF in doubt – always assume a regular WCT is VT until proven otherwise. Statistically (as previously emphasized) – this will most often be the case.
  • IF the patient in a regular WCT is (or at any time becomes) unstable – treatment priorities are clear: immediately cardiovert the patient!
  • IF instead, the patient is tolerating the rhythm and is hemodynamically stable – then there is (by definition) at least a moment of time to contemplate more definitive diagnosis of the WCT rhythm before initiating treatment. It is well to remember that even patients in sustained VT may at times remain alert and hemodynamically stable for prolonged periods of time (of not only hours but days!). Therefore, as long as the patient in WCT remains hemodynamically stable – one may proceed with either: i) further diagnostic evaluation (in the hope of increasing one’s relative certainty of the etiology of the WCT rhythm); ii) initiation of medical therapy (which may include vagal maneuvers, adenosine and/or other antiarrhythmic agents); or iii) synchronized cardioversion (as soon as it becomes essential to terminate the WCT without further delay).
Further Bedside Evaluation of the Regular WCT Rhythm:  We address therapeutic aspects related to acute management of the stable WCT patient elsewhere (See Section 08.9 in this pdf from ACLS-2013-ePub). We limit comments below to those that are relevant for diagnostic assessment of the rhythm shown in Figure 1.
  • Obtaining a 12-lead ECG during the tachycardia is an essential component of the diagnostic approach. Twelve leads are needed to verify QRS width (in case part of the QRS lies on the baseline in some leads but not in others) – to fully assess for atrial activity during the tachycardia – and for assessment of morphologic clues that may strongly suggest the etiology of the WCT rhythm.
  • Obtaining additional tracings on the patient may be invaluable. This may be in the form of prior 12-lead ECGs obtained when the patient was in sinus rhythm (to see if preexisting BBB of similar morphology was present in the past) – or in the form of prior or current rhythm strips or post-conversion tracings that might be used for comparison as well as to uncover previous WCT episodes.
  • Determination that the WCT rhythm is regular (as it is in Figure 1) significantly narrows the differential diagnosis (See ECG Blog #36 for eval & mgmt. of irregular WCT rhythms).
  • Determination that the QRS complex in the 12 leads shown in Figure 1 is not overly wide (no more than 0.11-0.12 second) increases the chance that this regular WCT rhythm may be supraventricular (although the odds are still clearly much more than not that it is VT).
  • Relatively young age of the patient – previously healthy status – and hemodynamic stability all contribute to increasing the chance of SVT (though again overall odds still clearly favor VT).
  • QRS morphologic clues are consistent with a possible supraventricular etiology (See below).
QRS Morphologic Assessment:  Full description of QRS morphologic assessment during tachycardia extends beyond the scope of this ECG blog post. That said – recall of a limited number of easy-to-remember critieria may go a long way toward establishing probability of VT vs possibility of a supraventricular etiology. These easy-to-remember clues include:
  • Presence of extreme/bizarre axis deviation during the WCT strongly favors VT. Although marked LAD (Left Axis Deviation) is present in Figure 1 – the axis and appearance is not outside the limit of what might be expected with LAHB (Left Anterior HemiBlock), in that there is still some initial r wave (albeit tiny) in leads II and aVF – and the QRS is isoelectric in lead I. Therefore – the degree of LAD seen in Figure 1 is not helpful in differential diagnosis of this rhythm.
  • Presence of an entirely (or almost entirely) negative QRS in lead V6 favors VT. This is clearly not the case in Figure 1, in that a relatively tall R wave is seen in V6.
  • Presence of a monophasic R wave in lead aVR is virtually diagnostic of VT (Ref-1) – since this implies an apical origin of the WCT, which means the arrhythmia must be coming from the ventricles. The QR pattern in lead aVR of Figure 1 is nondiagnostic.
  • Presence of a delayed nadir >0.10 second (for any RS complex in any precordial lead as measured from onset of the R until deepest point of the S wave) is virtually diagnostic of VT (Ref-2). RS complexes are seen in leads V2-thru-V6 of Figure 1 – but none of these leads manifest a delayed nadir. Although this clearly does not prove SVT - it does make SVT more plausible.
  • Finally – QRS morphology is consistent with a pattern of an established conduction defect. Aberrant conduction typically manifests some form of conduction defect, since it is based on prolongation of the refractory period in one or more conduction fascicle. Most commonly – aberrant conduction manifests RBBB (Right-Bundle-Branch-Block) morphology (because the right bundle branch tends to have the longest refractory period in most individuals) – but any pattern of conduction defect may be seen (including RBBB, LBBB or hemiblock patterns). QRS morphology in Figure 1 is consistent with a pattern of bifascicular block (RBBB/LAHB) – albeit uncertainty about the presence of a small initial r wave for the RBBB pattern seen in lead V1 is a bit atypical.
BOTTOM LINE:  We are left with uncertainty about the diagnosis of the monomorphic regular WCT seen in Figure 1 – which could be either VT vs PSVT with a bifascicular block (RBBB/LAHB) pattern of aberrant conduction.
  • The important point to emphasize is that the clinician will not always know what a WCT rhythm is at the time the patient is being seen. In such cases – one has to proceed on a “best hunch” and “most likely to be safe & effective” approach.
  • Clinically – the patient in this case is stable, so that therapeutic intervention may be tried. This might include application of a vagal maneuver and/or use of adenosine as a diagnostic/therapeutic trial (See Section 06 from ACLS-2013-ePub on Using Adenosine).
  • Diagnostically – We suspect the regular WCT rhythm in Figure 1 is Fascicular VT. In this case, if vagal maneuvers/adenosine were not effective – one might cautiously attempt treatment with IV verapamil.
What is Fascicular VT?  Fascicular VT (also known as ILVT = Idiopathic Left Ventricular Tachycardia) – is a specific type of VT in which the QRS complex is relatively narrow (compared to other ischemic or structurally-related VTs) – and in which there is an RBBB pattern, usually with left axis deviation. There are 3 types of fascicular VT which are recognizable by the QRS axis they manifest during tachycardia – which depends on which fascicle is involved in the reentry (Refs 3,4,5):
  • By far the most common type is left posterior fascicular VT (~90-95% of cases) – in which the ECG shows a RBBB/LAHB pattern (consistent with that seen in Figure 1). The reason for the relatively narrow QRS and RBBB/LAHB morphology is the localized origin of the arrhythmia arising at a point in close proximity to the left posterior hemifascicle.
  • Less commonly there may be left anterior fascicular VT (RBBB pattern with a rightward axis) – and rarely an upper septal fascicular VT (RBBB pattern with a narrow QRS and a normal axis).
  • Clinical OccurrenceFascicular VT is most commonly seen in young adults (predominantly men) between the age of 15-to-40 years old. Underlying structural heart disease is usually absent. The arrhythmia is often precipitated by exercise – and symptoms commonly include palpitations, dizziness, and presyncope/syncope. As opposed to other forms of VT – sudden death is rare. However, recurrence is common.
  • Treatment Considerations – Sustained fascicular VT responds extremely well to treatment with IV verapamil (proposed role for slow inward calcium channel in genesis of the arrhythmia) – and this is the treatment of choice when the arrhythmia is recognized in the acute setting. Presumably it will also respond to IV diltiazem – though the effectiveness of oral calcium blockers for preventing recurrence is variable. Both vagal maneuvers and adenosine have been reported on occasion to convert the arrhythmia – but the response is inconsistent. Patients suspected of having fascicular VT should be referred – since recurrence of VT is common and radiofrequency catheter ablation is potentially curative.
BOTTOM LINE:  It should be emphasized that the AV nodal calcium channel blocking agents verapamil/diltiazem should never be given indiscriminately to patients with WCT in whom the diagnosis of VT is entertained as an important possibility. This is because the negative inotropic and vasodilating effects of these agents is likely to aggravate the situation if the rhythm turns out to be an ischemic or structural form of VT (which may predispose to deterioration of the rhythm to ventricular fibrillation).
  • Two exceptions to the rule that that verapamil/diltiazem do not work for VT are outflow track VTs (See ECG Blog #35) and fascicular VT, as is likely in this case. It should be emphasized the majority (~90%) of VT rhythms are structural and/or ischemic – with the biggest clue in this case that one of the less common VT forms (that may respond to adenosine or verapamil) is present, is the relatively young age of the patient and negative past medical history suggesting lack of underlying heart disease.
  • That said – IF there is any doubt about etiology – verapamil/diltiazem should not be given for WCT. Immediate synchronized cardioversion will almost always successfully convert a WCT rhythm of uncertain etiology in the acute setting – after which referral for definitive diagnosis and treatment can be made.
  • Although the regular monomorphic WCT rhythm shown in Figure 1 manifests features consistent with SVT having aberrant conduction – this diagnosis can not be made on the basis of this single 12-lead tracing. Instead – VT should be assumed until proven otherwise.
  • A main purpose of this blog post has been to describe the special form of fascicular VT and its most common ECG appearance (RBBB/LAHB pattern with minimal QRS widening). Given the overall clinical characteristics in this case – this is the likely diagnosis for the arrhythmia seen in Figure 1. In view of this – adenosine, perhaps cautiously followed by IV verapamil might be administered. Synchronized cardioversion is warranted at the first sign of decompensation. Following acute treatment – the patient should be referred.
  1. Sasaki K: A New Simple Algorithm for Diagnosing Wide QRS Complex Tachycardia- Comparison with Brugada, Vereckei and aVR Algorithms. Circulation 120:S671, 2009.
  2. Brugada P, Brugada J, Smeets ML, et al: A New Approach to the Differential Diagnosis of a Regular Tachycardia with a Wide QRS Complex. Circulation 83:1649-1659, 1991.
  3. Johnson Francis, Venugopal K, Khadar SA, et al: Idiopathic Fascicular VT. Ind Pacing and Electrophys 4:98-103, 2004.
  4. Ramprakash B, Jaishankar S, Rao HB, Narasimhan C: Ind Pacing and Electrophys 8:193-201, 2008.
  5. Srivathsan K, Lester SJ, Appleton CP, et al: VT in the Absence of Structural Heart Disease. Ind Pacing and Electrophys 5:106-121, 2005.
- Related ECG Blogs include #15 - #23 - #24 - #33 - #35 - #36 - #85.


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