Tuesday, July 19, 2011

ECG Interpretation Review - #24 (Wide Tachycardia - WCT - VT vs SVT vs Flutter)

The lead II rhythm strip shown below was obtained from a patient admitted to the Emergency Department. Interpret the rhythm. How certain are you of your answer?  What would you do?
  • Scenario #1:  The patient is unresponsive with a BP = 60 palpable.
  • Scenario #2:  The patient is alert and asymptomatic.  BP = 120/80 mmHg.

Figure 1 – Lead II rhythm strip showing tachycardia. What to do?

INTERPRETATION:  The rhythm is fast and fairly (but not completely) regular. The QRS looks to be wide (ie, more than half a large box) and there are no definite P waves.  Thus, this appears to be a WCT (Wide Complex Tachycardia) of uncertain etiology.  As to the question of What To Do? the answer depends on the clinical scenario. 
  • IF the patient is unstable (Scenario #1) immediately cardiovert.  Regardless of whether the rhythm is VT or SVT with bundle branch block or aberrant conduction — hemodynamic instability is an indication for immediate cardioversion.  
  • On the other hand — IF the patient is stable (Scenario #2) then by definition, you have at least some time to contemplate treatment (while you work to determine the rhythm). We would obtain more history (previous episodes of WCT?) look for prior tracings on the patient (either on telemetry or from the patient’s chart) and get a 12‑lead ECG during tachycardia (Figure 2)

The 12-lead ECG during tachycardia is shown below (Figure 2):

Figure 2 – 12-lead ECG obtained during tachycardia. Does this help with your answer?  

12-Lead Analysis:  The rhythm is rapid and looks to be regular (albeit with occasional minor variation in the R-R interval).  The rate is ~150/minute (the R-R is ~2 large boxes in duration).
  • The QRS is wide (clearly more than half a large box in leads II,III,V3,V4).  That said — overall QRS morphology looks to be supraventricular (in the form of LAHB with LVH and “strain”).
  • “Normal atrial activity” is absent in Figure 2 (RED arrow showing no upright P in lead II)
Beyond-the-Core:  One wonders if the RED arrow and negative deflections before the QRS in the inferior leads might represent some form of atrial activity … (Figure 3):

Figure 3 – Short vertical lines have been added to Figure 2 highlighting what might represent underlying atrial activity (See Figure 4).

IMPRESSION (What to do?): This case illustrates the importance of the clinical situation in the approach to this patient.  Whereas immediate cardioversion would be indicated if the rhythm in Figure 1 was associated with hemodynamic instability — additional diagnostic assessment would be appropriate IF the patient is stable (Scenario #2).  Clearly — sometimes “ya just gotta be there” to know which approach is best for an individual patient.  Our Hunch (based on Figures 1,2,3) — is that the rhythm is supraventricular.
  • Slight QRS widening (~0.1-0.2 msec) may be seen with both LVH (it takes longer to get through a thicker ventricle) and with LAHB (conduction is delayed through the left hemifascicle).  Thus — QRS widening (as seen in Figure 2) may occur IF there is both LVH and LAHB. 

To PROVE Our Hunch:
  • Find a prior ECG on this patient.  See IF QRS morphology in the past (during sinus rhythm) is the same as on the Figure 2 12-lead obtained during tachycardia (which shows LAHB; LVH with strain). 
  • Get more History (prior episodes of WCT that look like Figure 2? ) 
  • Consider a vagal maneuver or “chemical Valsalva” (ie, administration of IV adenosine, which may produce similar effect as carotid massage). 
  • Treatment will clearly be more effective IF we can be sure of the diagnosis — BUT — IF at any time during the process the patient becomes unstable — Be ready to immediately cardiovert! 
Chemical Valsalva in the form of an IV bolus of adenosine was attempted.  The result is shown below (Figure 4).

Figure 4 – Result of “chemical Valsalva”. What does this prove?

Result of “Chemical Valsalva”:  Administration of IV adenosine results in reduced AV conduction with slowing of the ventricular response (RED arrow).  This reveals underlying flutter activity at an atrial rate of ~300/minute (sawtooth flutter waves occurring approximately each large box).  
  • Retrospective review of the 12-lead ECG during tachycardia suggests that the negative deflections previously noted in the inferior leads (and to a lesser extent in lead aVR) were in fact flutter waves (short vertical RED lines in Figure 3).

KEY Points in this Case:
The 2 scenarios proposed in this case illustrate how to clinically work though assessment and management of a patient with WCT of uncertain etiology.

  • Always presume VT until proven otherwise.  Immediate cardioversion is indicated if the patient is unstable.  BUT — IF the patient is stable, there is at least some time to work through the diagnosis.
  • Treatment will be much more effective (and you as clinician will be more confident) — IF you are able to determine what the WCT actually is.  In this case — Knowing that the rhythm in Figure 1 is atrial flutter with 2:1 AV conduction and QRS widening from LVH/LAHB allows us to treat the patient with IV diltiazem (bolus and drip) — whereas diltiazem would be contraindicated if the rhythm was an ischemic form of VT.
  • BOTTOM Line: You will not always know the etiology of a tachycardia at the time you first encounter the patient.  No matter — as you can still proceed with an appropriate clinical approach as outlined above.  
  - See also ECG Blog #23


  1. Is this not LBBB than calling it LAFB??? QRS seem to be 3mm wide and the morphology fits...

    1. QRS width and morphology is in a "gray zone". Precise answer really requires review after conversion to sinus rhythm. That said, the QRS "looks supraventricular". While one can debate if QRS width is 0.11 vs 0.12 ... the width of the monophasic R wave in lateral leads is not overly wide; the initial r in V1,2,3 is larger than is usual in lbbb; and the QRS just "looks" supraventricular. Remember that BOTH LAHB and LVH may slightly widen the QRS — and that is my strong hunch of what we have here — :)

    2. I guess that comes with experience, little tough for me at this stage.. Thank you doctor...

  2. Why is Diltiazem contrindicated in VT???

    1. Hi. THANKS for your question. Please realize that I wrote this post in 2011 — and that your excellent question is only coming to me 12 years later. Since 2011 when I wrote this — our appreciation of how IV Diltiazem (and/or IV Verapamil) are actually drugs of choice and very effective for treatment of Fascicular VT (See ECG Blog #38, written the following year in 2012 — https://tinyurl.com/KG-Blog-212 ) — as well as many other blog posts on Fascicular VT that I have since presented (you can search for Fascicular VT to find these). The mechanism for Verapamil/Diltiazem's efficacy with Fascicular VT is reviewed in Blog #212. Thanks again for your question (You'll note that I CHANGED what I wrote in this 2011 blog — to say that you shouldn't use Diltiazem for an ischemic form of VT — for which Dilitiazem might precipitate VFib.