Thursday, May 6, 2021

ECG Blog #221 (ECG MP-38) — Do You Need to Pull the Patient's Chart?

You are assigned to do “ECG Review” for the day — which means that you need to review all of the ECGs obtained in your busy Emergency Care Center — to ensure that nothing was overlooked.


The only information you are told about the patient whose ECG is shown in Figure-1 — is that it came from an 83-year-old woman.


  • HOW would you interpret this 12-lead ECG?
  • Is this a case for which you need to pull the patient’s chart?
  • HOW LIKELY is it that a recent cardiac event may have occurred?


Figure-1: ECG obtained from an 83-year-old woman. No history provided (See text).





NOTE #1: Some readers may prefer at this point to listen to the 11:30 minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to review to My Thoughts on this tracing (that appear below ECG MP-38).


Today’s ECG Media PEARL #38 (11:30 minutes Audio)  Reviews the ECG Diagnosis of Acute MI when there is BBB.

  • I summarize the information in this Audio Pearl in Figures-2-3 and -4 in the Addendum below. CLICK HERE to download a 6-page pdf of this information.




NOTE: For those who want a user-friendly video review illustrating how to diagnose the Bundle Branch Blocks in less than 5 seconds — I am repeating from ECG Blog #204, my ECG Media Pearl #22 (13:15 minutes Video).

  • CLICK HERE — to download a 12-page pdf (from my ECG-2014-ePub) that summarizes the ECG diagnosis of BBB.


ECG Media Pearl #22 (13:15 minutes Video) — on ECG Diagnosis of the Bundle Branch Blocks.




MY Approach to this Tracing:

As always — I favor a Systematic Approach for every ECG I encounter (This Systematic Approach reviewed in ECG Blog #205). My descriptive analysis of the ECG shown in Figure-1 is as follows:

  • Rate & Rhythm: The rhythm is fairly (but not completely) regular at a rate just under 50/minute. Although small in amplitude, upright P waves are seen in lead II, with a constant PR interval — therefore the rhythm is sinus bradycardia.


Regarding Intervals:

  • The PR interval appears to be upper normal (ie, not clearly more than 1 large box in duration — therefore not clearly >0.20 second).
  • The QRS complex is wide. Interval duration should be assessed in whichever lead the onset and offset of the interval can be clearly seen — and in which the interval appears to be longest. QRS duration extends over 3 little boxes ( 0.12 second) in lead V1, which is wide.
  • PEARL #1: Regardless of whatever system you favor for interpretation of 12-lead tracings — it’s important to assess intervals at an early point in the process. This is because IF the QRS complex is wide — then criteria for assessing the QTc, Axis, Chamber Enlargement and Ischemia/Infarction will all change! Therefore, as soon as you recognize QRS widening — STOP — and Figure Out WHY the QRS is Wide before going further in your assessment!


WHY is the QRS Complex Wide?

As discussed in my ECG Media Pearl #22 (above) — once you confirm that the rhythm is supraventricular — the reason for QRS widening can be most time-efficiently determined by focusing attention on the KEYleads (ie, leads I, V1 and V6).

  • Lead V1: Normally — lead V1 is predominantly negative. This is because predominant electrical activity is normally directed away from this right-sided lead, and toward the larger left ventricle. Therefore — the finding of a predominantly positive QRS complex, in the form of the QR complex seen in lead V1 of Figure-1 — is not a “normal” finding. And when this predominantly upright QRS complex in lead V1 is wide and assoicated with wide terminal S waves in lateral leads I and V6 — then criteria for RBBB (Right Bundle Branch Block) have been satisfied. This is the case in Figure-1. Although S waves in both leads I and V6 are not overly deep — these terminal S waves are wide (ie, at least 1 little box, therefore ≥0.04 second in duration)and, therefore confirming the diagnosis of RBBB.
  • PEARL #2: When RBBB is “typical” — the QRS complex in lead V1 will manifest an rsR’ pattern in which the initial r wave is small and thin — the S wave that follows this initial small r wave descends below the baseline — and, the terminal R’ is tall and thin (producing a taller right “rabbit ear”). Loss of the initial  positive r-wave deflection in lead V1, so as to result in the QR pattern seen in Figure-1 (with a wide and deep Q wave, that is followed by a tall R wave) strongly suggests that septal infarction has taken place at some point in time.


Returning to our Systematic Approach:

Now that we’ve determined the reason for QRS widening (which is complete RBBB) — We can return to our Systematic Approach for assessment of the remaining parameters:.

  • QTc: The remaining interval to assess is the QTc. Bundle branch block per se may prolong the QTc. That said — the longest QT that I measure in Figure-1 looks to be ~480 msec, which considering the bradycardia and conduction defect is probably not prolonged. (Visually — the QT interval is decidedly less than half the R-R interval — although the value of this measurement is decidedly less when the ventricular rate is so slow).


AXIS — The “meaning” of axis is altered in RBBB. This is because of the zig-zag direction of electrical activity due to this conduction defect. That is — the initial left-to-right vector of septal depolarization is preserved (since the conduction defect with RBBB is on the right side of the septum) — which is followed by depolarization of the unblocked LV (during which time the wave of depolarization travels back to the left— and finally, return rightward, as the “blocked” RV is the last part of the heart to depolarize. 

  • Clinically — the only thing we care about regarding the axis with RBBB is whether there is: i) RBBB +LAHB; ii) RBBB + LPHB; oriii) RBBB without any hemiblock. In Figure-1, neither LAHB nor LPHB are present (LAHB is not present since the QRS in lead II is not predominantly negative — and — LPHB is not present since there is no deep S wave in lead I). Therefore — there is RBBB without any hemiblock.


Chamber Enlargement: There is no RAA, LAA or RVH. There is LVH

  • Criteria for atrial abnormality are unaffected by bundle branch block. However, because RBBB and LBBB alter the sequence of both ventricular depolarization and ventricular repolarization — voltage criteria and ST-T wave changes of LV or RV “strain” will be more difficult to identify.
  • That said — because the LV depolarizes unopposed with RBBB (since depolarization of the much smaller right ventricle is delayed by this conduction defect) — the effect of RBBB on ECG diagnosis of LVH may not be marked. How much of an effect RBBB may have on ECG diagnosis of LVH may be difficult to predict. So, realizing that data and definitive answers are lacking — the significantly increased voltage that we see in Figure-1 for the R wave in lead aVL (ie, ~15 mm), in association with the nonspecific ST-T wave flattening that we see in this lead (a "strain" equivalent?) suggests at least probable LVH.


 Regarding Q-R-S-T Changes:

  • Q Waves — are seen in leads I and V1. The Q wave in lead aVL is both deeper and wider than expected for a normal septal q wave — so it could reflect prior lateral infarction. As noted previously — the very large Q wave in lead V1 suggests prior septal infarction.
  • R Wave Progression — is less relevant in this tracing, since RBBB by definition results in a predominant R wave in lead V1.



PEARL #3: There are primary ST-T Wave Changes in multiple leads. As discussed in my ECG Media Pearl #22 (above) and also in ECG Blog #204 — the normal response of ST-T waves in the 3 KEY leads with BBB is to be oppositely directed to the last QRS deflection.


Looking first at the KEY leads — the ST-T waves in leads I, V1 and V6 are all clearly abnormal. 

  • In both of the lateral leads ( = leads and V6) — the ST segment is abnormally coved, and the T wave is symmetrically inverted (instead of showing a normal upward-sloping ST segment with upright T wave — as illustrated below in Figure-2 of the Addendum).
  • In lead V1 — the ST segment appears to be slightly elevated, and the T wave is clearly upright (whereas the expected response with RBBB is for there to be some ST-T wave depression in lead V1 — as shown in Figure-2).


Looking next at neighboring leads:

  • Lead V2 shows a similar upright T wave as is seen in lead V1. Normally, with simple RBBB — there should be ST-T wave depression in at least several anterior leads.
  • The remaining chest leads ( = leads V3, V4, V5 and V6) all show abnormal ST segment coving and fairly deep, symmetric T wave inversion that is clearly abnormal.
  • Similar ST segment coving and fairly deep, symmetric T wave inversion is seen in each of the inferior leads ( = leads II, III, aVF).


Putting It All Together:

The ECG in Figure-1 shows the following abnormalities:

  • Fairly marked sinus bradycardia.
  • RBBB
  • Probable LVH
  • A deeper-than-expected Q wave in lead aVL of uncertain significance (possibly indicative of prior lateral infarction).
  • QR pattern in lead V1 — with a deep and very wide initial Q wave in this patient with RBBB (strongly suggesting prior septal infarction at some point in time).
  • Clearly abnormal ST-T wave abnormalities in no less than 10 of 12 leads — which in this 83-year-old woman strongly suggests ischemia if not recent infarction (possibly very recent).
  • BOTTOM LINE: The only way to determine if the above abnormalities are new — recent — or old — is to pull this patient's chart and possibly contact this patient (depending on what information and additional ECGs are found in the chart).



Related ECG Blog Posts to Today’s Case: 

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation (outlined in Figures-2 and -3, and the subject of Audio Pearl MP-23 in Blog #205)
  • ECG Blog #204 — Reviews the ECG diagnosis of the Bundle Branch Blocks (RBBB/LBBB/IVCD). 
  • ECG Blog #203 — Reviews ECG diagnosis of Axis and the Hemiblocks. For review of QRS morphology with the Bifascicular Blocks (RBBB/LAHB; RBBB/LPHB) — See the video ECG Media Pearl #21 in this blog post.


ADDENDUM (5/5/2021):

I've reproduced in Figures-2-3 and -4 below the 6-page section from my ECG-2014-ePub on ECG Diagnosis of Acute MI when there is Bundle Branch Block.

  • CLICK HERE to download a 6-page pdf of the information in these Figures.

Figure-2: Pages 1,2: The ST Opposition Rule — You can see Q waves with RBBB!



Figure-3: Pages 3,4: Diagnosis of MI with LBBB (Smith-Sgarbossa) — Case Examples.



Figure-4: Pages 5,6: Several Case Examples (Cont.).

Sunday, May 2, 2021

ECG Blog #220 (ECG MP-37) — VT or Aberrancy?

The long lead II rhythm strip shown in Figure-1 was obtained from an 51-year-old man who presented to the ED (Emergency Department) with "palpitations" that began 1 hour earlier.

  • HOW would you interpret this tracing?
  • Clinically — What would YOU do?

Figure-1: Long lead II rhythm strip, obtained from an 51-year-old man with palpitations (See text).





NOTE #1: Some readers may prefer at this point to listen to the 6:00 minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to review to My Thoughts on this tracing (that appear below ECG MP-37).



Today’s ECG Media PEARL #37 (6:00 minutes Audio) — Reviews how to determine IF Your Patient with an Arrhythmia is Hemodynamically Stable!



MY Approach to the Rhythm in Figure-1:

We are provided with only very limited clinical information — namely, that the patient is a 51-year-old man who presented to the ED with "palpitations" of 1-hour duration. Clearly, we need to find out more about what is going on ...

  • The 1st Thing to do — is to LOOK at the patient! The KEY Question to answer is to determine IF the patient is hemodynamically stable! 
  • The above 6-minute Audio PEARL ( = ECG MP-37addresses this issue in detail. In essence — "Ya gotta be there!" in order to determine if the patient is hemodynamically stable (ie, without significant symptoms such as chest pain, shortness of breath, hypotension, mental status changes — as a direct result of the fast rate).
  • The importance of assessing for hemodynamic stability, even before deciding on the rhythm diagnosis — is that IF the patient is not hemodynamically stable with the rhythm shown in Figure-1 — then it no longer matters whether this rhythm is VT (Ventricular Tachycardia)  or an SVT (SupraVentricular Tachycardia)  or something else — since regardless, immediate synchronized cardioversion will be indicated!
  • On the other hand — IF the patient is hemodynamically stable with the rhythm in Figure-1, then by definition there is at least a moment-in-time for you to assess the rhythm diagnosis.


For the purpose of discussion — Let's assume that this patient is and remains hemodynamically stable!


  • QUESTION: IF this patient is hemodynamically stable — Does this rule out the possibility that the rhythm is VT?





  • Definitely not! Although many patients with sustained VT promptly lose consciousness — a surprising number of patients in sustained VT remain alert and relatively asymptomatic for not only minutes — but sometimes for hours or longer (I am aware of a significant number of cases of sustained VT lasting over a day).
  • PEARL #1: The fact that a patient is alert, with a normal (or even increased) blood pressure and no more than minimal symptoms — does not rule out the possibility of VT.




  ( assuming the patient remains hemodynamically stable)?




Since the patient is hemodynamically stable — it's time to assess the rhythm in Figure-1. I favor the Ps, Qs & 3R Approach (Reviewed in ECG Blog 185).

  • P waves are absent on this single lead monitoring strip.
  • The QRS is wide. Although the QRS complex does not look to be excessively wide — it clearly takes up at least 60% of 1 large box (shown in PURPLE in Figure-2) — which means that QRS duration is ≥0.12 second.
  • Regularity: The rhythm is regular.
  • Rate: The rate is rapid. Figure-2 illustrates use of the Every-Third-Beat Method for rapid estimation of heart rate (this method discussed in full in ECG Blog #210). It takes a little less than 5 large boxes (BLACK numbers in Figure-2) — to record 3 beats (RED numbers). Therefore — 1/3 of the rate is a bit faster than 300 ÷ 5 = 60-65/minute X 3 ~190-195/minute as the ventricular rate.
  • Related: Since P waves are absent — there is no "relation" between P waves and the QRS.
  • Therefore — We have described the rhythm in Figure-2 as a regular WCT ( = Wide-Complex Tachycardia) at ~190/minute, without clear sign of atrial activity.


Figure-2: I've labeled Figure-1 to illustrate estimation of heart rate (by the "every-third-beat" Method) — and — assessment of QRS duration (the solid PURPLE box showing that onset and offset of the QRS measures at least 0.12 second).



  • What is the differential diagnosis of the regular WCT rhythm in Figure-2?
  • What can we do to increase the accuracy of our diagnosis?


I favor considering the following 10 entities in the Differential Diagnosis of a Regular WCT rhythm, in which P waves are absent:

  • VT (Ventricular Tachycardia).
  • VT
  • VT
  • VT
  • VT
  • VT
  • VT
  • VT
  • An SVT (SupraVentricular Tachycardia) with either preexisting BBB (Bundle Branch Block) or Aberrant Conduction.
  • Something else ... (ie, WPW, hyperkalemia).




KEY POINTS Regarding the Above Differential Diagnosis:

  • My reason for repeating VT no less than 8 times before listing another possibility — is to emphasize that statistical odds that a regular WCT rhythm without clear sign of atrial activity will turn out to be VT begin at ~80%. As per ECG Blog #196 — these odds increase to ≥90% if the patient is of a "certain age" (ie, middle-aged and beyond) and has underlying heart disease. As a result — Assume VT until proven otherwise! 
  • PEARL #2: When assessing a hemodynamically stable patient in a regular WCT rhythm without P waves — our "mindset" should be that we need to prove that the rhythm is not VT, rather than the other way around.


Regarding the Next Thing To Do:

  • Since we are told that this patient remains hemodynamically stable — the next thing to do is obtain a 12-lead ECG during the tachycardia (Figure-3):


Figure-3: 12-lead ECG obtained from an 51-year-old man with palpitations (See text).




Reasons for Getting a 12-Lead During the Tachycardia:

As alluded to in ECG Blog #196 — there are a number of reasons for obtaining a 12-lead ECG duringthe wide tachycardia:

  • Getting a 12-lead allows for assessment of QRS morphology. This 12-lead tracing may prove to be diagnostic of either VT or a supraventricular etiology (See Figure-6 and Figure-7 in the ADDENDUM below).
  • Getting a 12-lead provides us with 11 additional leads to look for atrial activity. This may reveal "telltale" flutter waves with 2:1 AV conduction — or, it may uncover previously hidden regular sinus P waves that are totally dissociated from neighboring QRS complexes, thereby proving that the rhythm is VT.
  • IF there is any doubt about QRS duration — assessing the QRS complex in all 12 leads should resolve the problem. Sometimes, a part of the QRS lies on the baseline in one or more lead — and, if this happens in the one lead you are monitoring — it may make the QRS appear much narrower than it really is.
  • Assessing frontal plane axis during a regular WCT rhythm is EASY to do and, may be diagnostic. IF there is "extreme" axis deviation (as determined by the finding of an all negative QRS in either lead I or in lead aVF— this strongly suggests that the rhythm is VT.
  • Sometimes, definitive diagnosis of a regular WCT rhythm will not be possible during the tachycardia. However, in some of these cases — comparing the 12-lead ECG obtained during tachycardia with a follow-up ECG obtained after conversion to sinus rhythm may allow retrospective diagnosis of the WCT rhythm.
  • PEARL #3: In general — aberrant conduction is most likely to resemble some form of conduction defect (of either bundle branch block and/or a hemiblock pattern). In contrast — VT is more likely to manifest a less well defined QRS morphology that looks different from known forms of conduction block (this concept discussed in more detail in ECG Blog #211). Exceptions exist (!) — but appreciation of this general concept goes a long way toward understanding what to look for when assessing a 12-lead tracing obtained during a regular WCT rhythm.
  • PEARL #4: Finding a prior 12-lead ECG on the patient, at a time when they were in sinus rhythm — may prove invaluable. Especially in older patients with significant underlying heart disease — "baseline" QRS morphology may look very abnormal. But IF QRS morphology in all leads during the WCT rhythm looks identical to QRS morphology on a baseline tracing when the patient was in sinus rhythm — you have proven a supraventricular etiology!
  • PEARL #5: A notable exception in which RBBB-type morphology may be seen with VT, is when there is a Fascicular VT. In such cases of this form of idiopathic VT — the impulse arises from a site in the ventricles in close proximity to either the left anterior or posterior hemifascicles. The result is a regular WCT rhythm that resembles RBBB with either LAHB or LPHB (ie, it may be difficult to distinguish between fascicular VT vs SVT with aberrant conduction from a single 12-lead tracing). The QRS complex is usually not greatly prolonged with fascicular VT (most often between 0.11-to-0.14 second). Awareness of this entity is important because despite its ventricular origin — the drug of choice for initial treatment is IV Verapamil (For more on Fascicular VT — See ECG Blog #197).


  • Do you think that the 12-lead ECG shown in Figure-3 makes it more or less likely that this regular WCT rhythm is VT?



My THOUGHTS on the 12-Lead shown in Figure-3:

What follows includes basic and more advanced thoughts on the 12-lead ECG obtained during the regular WCT rhythm:

  • Although assessment of all 12 leads in Figure-3 confirms QRS widening — the QRS does not appear to be markedly widened.
  • There is no sign of atrial activity in any of the leads.
  • Although the frontal plane axis in Figure-3 is markedly leftward — the fact that the QRS complex in the inferior leads is not entirely negative reduces the diagnostic value of this ECG finding for suggesting VT (ie, there is a tiny-but-present initial r wave in each of the inferior leads) — See Simple Rule #1 in Figure-6 of the Addendum below.
  • The QRS complex in lead V6 of Figure-3 is predominantly (but not entirely) negative. As per Simple Rule #2 in Figure-6 of the Addendum below — this favors VT, but is not nearly as convincingly as it would be IF the QRS in lead V6 was entirely negative.
  • Overall QRS morphology in Figure-3 resembles RBBB (Right Bundle Branch Block) conduction — in that there is an rsr' complex in lead V1, with wide terminal S waves in lateral leads I and V6. That said — there are atypical features for RBBB conduction, including: i) The QRS complex in lead V1 is tiny, and lacks a tall, terminal R' wave (See Figure-7 of the Addendum below)andii) The r wave in lead V6 is tiny, with R wave amplitude decreasing (instead of increasing) as one moves laterally from lead V4 to lead V6.
  • The markedly leftward frontal plane axis in Figure-3 resembles LAHB (Left Anterior HemiBlock) morphology— but the r wave in the inferior leads is atypical for LAHB in being smaller in all 3 inferior leads than is usually seen with supraventricular conduction.

Putting It All Together: Assessment of the 12-lead ECG in Figure-3 during the tachycardia reveals a regular WCT rhythm at ~190/minute, without clear sign of atrial activity.

  • Statistically — We started with a ≥80% likelihood that the rhythm was VT. As per PEARL #2 — Remember that we need to prove that the rhythm is not VT, rather than the other way around.
  • Assessment of QRS morphology in Figure-3 superficially suggests bifascicular block (RBBB/LAHB). That said — the atypical features described above and lack of more marked QRS widening if anything, are in favor of a diagnosis of Fascicular VT. While impossible to rule out an SVT with either preexisting RBBB/LAHB or aberrant conduction — I'd estimate the likelihood that this rhythm is fascicular VT as approaching 90%.
  • Finding a prior ECG on this patient could be diagnostic of SVT with a preexisting conduction defect — IF QRS morphology on a prior tracing during sinus rhythm showed identical QRS morphology as was seen during the WCT rhythm in Figure-3. In the absence of a prior ECG — VT should be assumed, and the patient treated accordingly.
  • As discussed in ECG Blog #197 — therapeutic options for this patient might include IV Adenosine — IV Verapamiland/or Synchronized Cardioversion. It turns out that Adenosine was tried, but was unsuccessful. Synchronized cardioversion with 100 joules resulted in the 2 rhythms shown in Figure-4.



Figure-4: Lead II rhythm strips obtained during the WCT rhythm (Panel A) — and immediately after synchronized cardioversion with 100 joules (the RED arrow shows the point where cardioversion was applied). Panel B — was obtained moments after cardioversion.



MY THOUGHTS on the Rhythm Strips in Figure-4:

Synchronized cardioversion was successful in producing a supraventricular rhythm.

  • In Panel A — within less than 3 seconds synchronized cardioversion, we see conversion to a supraventricular rhythm with 3 narrow QRS complexes (albeit the first 2 of these 3 narrow beats are followed by PVCs).
  • A little while later in Panel B — we see 5 supraventricular beats, albeit with marked bradycardia and an irregular rhythm. It is difficult to tell whether or not a low amplitude sinus P wave might be present before the first 3 narrow QRS beats. But the KEY finding in the Panel B rhythm — is the 2nd beat, which is almost certain to be a PVC, since it is wide, very different in morphology from the narrow, supraventricular beats, and not preceded by any P wave. 
  • Isn't QRS morphology of this PVC ( = the 2nd beat in Panel B of Figure-4) very similar to QRS morphology in Panel A during the run of VT before cardioversion? 
  • PEARL #6: The finding of a PVC after cardioversion with very similar QRS morphology as was seen during the WCT further supports our assumption that the wide tachycardia was indeed VT.



The marked bradycardia in Panel B was treated with Atropine. The result is shown in Figure-5.

  • Sinus rhythm at a regular and normal rate of 60-65/minute has returned in Figure-5 (albeit upright sinus P waves in lead II are extremely small in amplitude).
  • Fairly large Q waves are seen in each of the inferior leads. This suggests prior inferior infarction.
  • There is voltage for LVH (S in V2 + R in V5 ≥35 mm; R in V6 ≥18 mm).
  • Nonspecific ST-T wave changes are seen — although these do not appear to be acute.
  • Impression: This follow-up 12-lead ECG in Figure-5, obtained shortly after synchronized cardioversion suggests that this patient probably has underlying heart disease (ie, a prior inferior MI; LVH) — and that his coronary disease may have served as the substrate for the episode of VT. That said — at least there are no acute changes on this post-cardioversion ECG.


Figure-5: Following treatment with Atropine — the patient stabilized, and this 12-lead ECG was obtained.



Related ECG Blog Posts to Today’s Case: 

  • ECG Blog #185 — Reviews my System for Rhythm Interpretation, using the Ps, Qs & 3R Approach.
  • ECG Blog #210 — Reviews the Every-Other-Beat (or Every-Third-Beat) Method for estimation of fast heart rates — and discusses another case of a regular WCT rhythm.
  • ECG Blog #196 — Reviews another Case with a Regular WCT Rhythm. 
  • ECG Blog #197 — Reviews the concept of Idiopathic VT, of which Fascicular VT is one of the 2 most common types. 
  • ECG Blog #204 — Reviews the ECG diagnosis of the Bundle Branch Blocks (RBBB/LBBB/IVCD). 
  • ECG Blog #203 — Reviews ECG diagnosis of Axis and the Hemiblocks. For review of QRS morphology with the Bifascicular Blocks (RBBB/LAHB; RBBB/LPHB) — See the video ECG Media Pearl #21 in this blog post.
  • ECG Blog #211 — WHY does Aberrant Conduction occur?



ADDENDUM (5/1/2021):

I've reproduced below from ECG Blog #196 — 2 helpful figures for assessment of the regular WCT rhythm: 


Figure-6: Use of the "3 Simple Rules" for distinction between SVT vs VT (taken from ECG Blog #196).


Figure-7: Use of lead V1 for assessing QRS morphology during a WCT rhythm (taken from ECG Blog #196).