Saturday, May 7, 2022

ECG Blog #303 (EQC) — The Patient Fainted

Today’s tracing is another ECG “Quick Case” ( = EQC) — in which I’ll provide a more “time-efficient” account of my thought process (with goal toward expediting your interpretation within seconds rather than minutes)! Relevant links are at the bottom of the page.


Today's CASE: 
The 12-lead ECG and long lead II rhythm strip in Figure-1 — was obtained from an older woman who “suddenly fainted”. No chest pain.


  • How would YOU interpret the rhythm and the 12-lead?
  • What do you think may have happened?

Figure-1: ECG from an older woman who fainted. No chest pain.

MY Thoughts on the Initial ECG in Figure-1:

The rhythm is regular at ~50-55/minute. The QRS is wide. Looking at the long lead II rhythm strip — a P wave does precede each QRS complex with a fixed (and normal) PR interval — so there is at least some conduction.

  • In general — the best lead for identifying atrial activity is lead II. Lead II provides the extra advantage of telling us if there is or is not sinus rhythm. The P wave should always be upright in lead II if there is a sinus rhythm. The only exceptions to this general rule — is if there is dextrocardia or lead reversal.
  • That said — there are times when atrial activity is seen better in other leads. In my experience — the 2nd-best lead for viewing atrial activity is lead V1. This is followed by leads III, aVR, aVF — and then taking a quick look at the remaining 7 leads.

  • What did YOU see in lead V1?

Additional Atrial Activity:

Although it would be easy to overlook additional atrial activity if one only looked at the long lead II rhythm strip — Lead V1 clearly tells us that there are 2 equally-spaced P waves for each QRS complex (RED arrows in Figure-2).

  • The fact that these P waves in lead V1 are equally spaced (RED arrows) — tells us that the underlying sinus rhythm continues throughout the tracing. There is 2:1 AV block (ie, 2 P waves for each QRS) — which defines the rhythm as some form of 2nd-Degree AV Block.
  • Since the ventricular rate is 54/minute — the atrial rate is twice this, or 108/minute.
  • The reason the 2nd P wave may not have initially be seen in the long lead II rhythm strip — is that it was hidden within the preceding T wave (WHITE arrows in the long lead II).
  • Although the 2nd P wave within each R-R interval is easiest to recognize in lead V1 — other leads also suggest this (ie, RED & WHITE arrows in lead V5).

  • PEARL #1: Use of calipers makes it easy to confirm regularity of the underlying atrial rhythm. Thus rules out entities such as atrial bigeminy (in which every-other-P-wave is a PAC). That said — it is common to see slight variation in the P-P interval in patients with 2nd- or 3rd-degree AV block. This is called a ventriculophasic” sinus arrhythmia. Most of the time this entity can be recognized by the fact that the P-P interval that “sandwiches” a QRS complex tends to be slightly shorter than the P-P interval that does not contain a QRS complex within it (thought to be due to slightly improved circulation from the cardiac output generated by the QRS within the 2 P waves that initiates mechanical contraction).

Figure-2: I've added RED and WHITE arrows to indicate the location of regular atrial activity (See text).

What About Your Interpretation of the 12-Lead ECG?

Now that we have defined the rhythm in Figure-2 as sinus with 2nd-Degree AV Block and 2:1 AV Conduction — there remains the question of how to interpret the rest of the 12-lead ECG.

  • As stated — the QRS complex is wide (probably ~0.12 second in Figure-2). QRS morphology is consistent with complete RBBB (ie, RBBB “Equivalent” Pattern in the form of a QR in lead I — and wide terminal S waves in both leads I and V6).
  • There is also LAHB, based on the predominantly negative QRS complexes in each of the inferior leads. Therefore, there is bifascicular block ( = RBBB/LAHB).
  • There is also evidence of prior infarctions. The lack of an initial r wave in lead III (ie, Qr pattern) — is not the result of simple LAHB, and indicates prior inferior infarction at some point in time.

  • PEARL #2: It is often difficult to distinguish between LAHB with or without prior inferior infarction. This is because the initial depolarization vector with each of these entities is “opposing” — such that the initial r wave with LAHB may prevent inscription of the Q wave of inferior infarction — and — the Q wave of inferior infarction may prevent inscription of the initial positive deflection (r wave) with the hemiblock. That said, in today’s case — the CLUES that tell us that both LAHB and prior inferior infarction have occurred at some point in time are: i) The wide initial Q wave in lead III (which should not be there with simple LAHB); ii) Fragmentation of the QRS in both leads II and aVF (ie, the extra “notching” on the upslope of the S wave) — and the r’ that we see in lead III (ie, normally with simple LAHB, there is an rS pattern in all 3 inferior leads — and not a Qr as we see here).

  • PEARL #3: There has also been anteroseptal infarction at some point in time — as seen by the large Q waves in numerous chest leads. With simple RBBB — there should be a triphasic (rsR’ or rSR’) complex in lead V1. The deep, wide Q wave we see here in lead V1 tells us that there has definitely been previous anteroseptal infarction.
  • Large Q waves, as well as additional fragmentation (notching) is also seen in leads V2, V3 and V4. In addition to extensive prior anteroseptal infarction — this patient clearly has significant coronary disease (ie, fragmentation in this clinical setting suggests extensive “scar”, from infarction and/or cardiomyopathy).
  • As to assessment of ST-T wave abnormalitiesnothing looks to be acute! Instead, there is nonspecific ST-T wave flattening — with slight-but-real ST elevation in leads V2, V3, V4. 

  • PEARL #4: Note that the ST segment in lead V1 is isoelectric. Normally with simple RBBB — the ST-T wave should be “oppositely-directed” to the last QRS deflection in the 3 KEY leads (ie, Since the last deflection in lead V1 is a positive R wave — there should normally be some ST-T wave depression in lead V1 when there is simple RBBB without any complicating factors). The fact that the ST-T wave in lead V1 is isoelectric instead of being at least slightly depressed is not "normal" with RBBB.

BOTTOM LINE: In addition to 2nd-Degree AV Block with 2:1 AV conduction — there has been inferior and anteroseptal infarction at some point in time. Although there is some ST elevation in leads V2,V3,V4 (and some inappropriate ST segment flattening in lead V1) — this is minimal. Other leads show nonspecific ST-T wave flattening and shallow T inversion in V5,V6 — so none of this looks acute. Instead — the slight ST elevation may reflect a left ventricular aneursym


The CASE Continues:

ECG #2 was obtained 15 minutes after ECG #1 (See Figure-3).


  • What has happened in the 15 minutes since ECG #1?

  • Has the “degree” of AV block improved?
  •     HINT: WHY did I calculate the atrial rate in each tracing?

Figure-3: ECG #2 was obtained 15 minutes after ECG #1. What has happened during these 15 minutes?


There is no longer 2:1 AV conduction in ECG #2. Instead — there is sinus rhythm with 1:1 AV conduction (RED arrows) — and a PVC ( = beat #6).

  • I suspect that an on-time sinus P wave is hidden within the ST-T wave of beat #6 in ECG #2.
  • There has been essentially no change in QRS morphology or in ST-T wave appearance between the 2 tracings.
  • The atrial rate has slowed slightly in ECG #2 (ie, from 108/minute — to 95/minute).

PEARL #5: Often ignored is the potential effect that the atrial rate may have on AV conduction. In today’s case — it is likely that the “degree” of AV block was not “worse” in ECG #1. Instead — it may simply be that the diseased AV node (in this older patient who obviously has severe underlying heart disease) may be able to conduct 1:1 at a sinus rate of 95/minute — but when the atrial rate speeds up a little (ie, to 108/minute) — it is only able to conduct 1 out of every 2 sinus impulses to the ventricles.

  • Given the history of syncope in this older patient — and the presence of bifascicular block (RBBB/LAHB) with prior infarctions — and periods of 2:1 AV Block — a permanent pacemaker may be needed. 
  • Ongoing ECG monitoring may facilitate documenting the need for a pacemaker. 
  • Echocardiography and cardiac catheterization may be indicated looking for LV aneurysm — determining LV function — and to clarify the anatomy in the event that there may be “fixable” coronary disease that might improve the patient’s conduction system disease.

Final PEARL: We can not distinguish with certainty between the Mobitz I and Mobitz II types of 2nd-Degree AV Block when there is 2:1 AV conduction. This is because we never see 2 consecutively conducted beats in a row — which means that we never get to see whether the PR interval would increase prior to dropping a beat IF given a chance to do so (as would be typical for the Mobitz I form of 2nd-degree AV block).
  • Mobitz I is far more common than Mobitz II. That said — when the QRS complex is wide — the PR interval of conducted beats is normal — and the patient clearly has significant underlying structural heart disease (as is seen in today's case) — then the chance that the conduction defect is Mobitz II increases. That said, regardless of whether the block is Mobitz I or Mobitz II — permanent pacing may still be needed in this patient for all of the reasons mentioned earlier.


Acknowledgment: My appreciation to 유영준 (from Seoul, Korea) for making me aware of this case and allowing me to use this tracing.


Relevant ECG Blog Posts to Today's Post:
  • ECG Blog #204 — Reviews the ECG diagnosis of BBB (reviewed in the Video Pearl).
  • ECG Blog #203 — Reviews a user-friendly approach to the Hemiblocks and to Bifascicular Block.

  • ECG Blog #236 — Reviews the 3 types of 2nd-Degree AV Block.

  • ECG Blog #271 — Reviews the concept of diffuse subendocardial ischemia.
  • ECG Blog #162 — Reviews a case of LBBB with acute STEMI.
  • ECG Blog #221 — How to diagnose acute MI when there is RBBB (reviewed in the Audio Pearl).
  • ECG Blog #298 — Reviews a case of RBBB/LAHB + Post. MI.


  1. I think should always also keep isorhythmic 3rd degree with escape rhythm in differential.

    1. Thanks for your comment! The reason why I do not agree with you, is that if there was 3rd degree AV block — then there would be at least SOME variation in the PR interval.

  2. JAMA internal medicine on 2022/5/9 in the section Challenges in Clinical Electrocardiography just publish exactly the same topic about this. beta-blocker may paradoxically improve the symptom where atropin may worsen the symptoms.

  3. Thank you for your comment JJ. I did not see the JAMA article you refer to — but as you say, it is based on the same principle that Marriott taught me a number of decades ago. That is — the atrial rate may affect the ability of the AV node to conduct impulses to the ventricles.

    As to “recommending” a beta-blocker for a rhythm such as the one in today’s case — I would think this risky. While possible that by slowing the atrial rate — the overall ventricular rate might improve with a beta-blocker — the problem I see is the impossibility of knowing which way things will go … After all — the beta blocker might further reduce AV nodal conduction (in the same way that beta-blockers may convert reentry SVT rhythms).

    As to Atropine — it is limited to the emergency situation. Atropine is not benign — as it may cause excessive tachyardia — which is why its use is best limited to symptomatic patients with marked bradycardia. Atropine will be less likely to work with a lower level AV block (ie, with Mobitz II) — but it may indeed help with 2:1 block at the AV nodal level. That said — as per your comment, it is good that the clinician be aware that Atropine can sometimes worsen the degree of AV block by increasing the number of impulses that the AV node has to handle …

    Interesting points to consider! Thanks again for your comment — :)