Saturday, August 20, 2022

ECG Blog #327 - Can You Explain this Rhythm?

The ECG in Figure-1 — is from a young woman with a several week history of intermittent “palpitations”.
  • How would YOU interpret this tracing?

Extra Credit”:
  • How would you describe atrial activity throughout the long lead II rhythm strip in Figure-1?
  • Can you explain why there are 2 different QRS morphologies in this tracing?

Figure-1: The initial ECG in today’s case — obtained from a young woman with intermittent “palpitations” in recent weeks.

MY Thoughts on the ECG in Figure-1:
There is a LOT going on in this tracing. My “thought process” for assessing the rhythm in this tracing was as follows:
  • PEARL #1: When there are multiple components to an arrhythmia (including both “easier” vs “harder”-to interpret parts)I favor beginning with those parts of the tracing that are easiest to interpret.
  • As part of this “process” — Look to see if there is an underlying rhythm? (ie, Are there any sinus-conducted beats?).

  • PEARL #2: The simple step of labeling sinus P waves can greatly facilitate determining the mechanism of the rhythm. Take another LOOK at today's tracing in Figure-2 — in which I have labeled all sinus P waves with RED arrows.

Figure-2: I’ve labeled all sinus P waves from Figure-1 with RED arrows.

Taking Another Look at ECG #1:
Now that I've labeled all P waves — Isn't it much easier to appreciate that beats #2-thru-6 in Figure-2 represent an underlying sinus rhythm? (ie, RED arrows showing fairly regular sinus P waves near the beginning of this tracing)
  • Of note — the underlying sinus rate is at least 90/minute, or a bit fast (which makes us wonder about what might be stimulating an "almost sinus tachycardia" in this patient).
  • After these first 5 sinus P waves (in front of beats #2-thru-6) — RED arrows highlight that there are 3 additional sinus P waves in the remainder of the tracing (ie, before beats #9, 15 and 16).

The 2nd QRS morphology seen in the long lead II rhythm strip — is an RS complex, in which the S wave is slightly deeper than the R wave is tall (seen for beats #1, 7-thru-15, and 17).
  • To figure out what these RS beats are — I looked first at beats #18, 12 and 14none of which are preceded by any P wave. These beats are not overly wide — BUT — If we focus our attention on simultaneously-recorded leads II and III for beat #1 — and simultaneously-recorded lead aVF for beat #7 — we see a LAHB (Left Anterior HemiBlock) morphology (within the dotted PINK rectangles for beats #1 and 7 in Figure-3).

  • IF we now look at simultaneously-recorded lead V1 for beats #10,11 — we see an all upright complex consistent with RBBB (Right Bundle Branch Block) morphology (within the dotted PINK rectangles for beats #10 and 11 in Figure-3).

  • And IF we put these findings together — RS complexes that are not overly wide and not preceded by P waves for beats #1,8,12,14 — but which manifest a RBBB/LAHB morphology — These are fascicular beats (arising from the Left Posterior HemiFascicle).

KEY Point: Although RS complexes for beats #9 and 15 are preceded by P waves — the PR interval preceding these beats is too short to conduct (ie, the PR interval preceding beats #9 and 15 is clearly shorter than the PR interval preceding sinus-conducted beats #2-thru-6). Therefore — beats #9 and 15 are also fascicular beats!
  • By extrapolation — all of the similar-looking RS complexes on this tracing ( = beats #1, 7-thru-15, and 17) must be fascicular beats. Some of these fascicular beats occur earlier-than-expected (ie, beat #7) — and some occur at a slower rate than sinus-conducted beats #2-thru-6. And then we see a salvo of 3 fascicular beats in a row (ie, beats #9,10,11) — and a couplet of 2 fascicular beats in a row (ie, beats #12,13).

  • NOTE: The hemifascicles are in the ventricles — so for practical purposes, these fascicular beats all behave functionally like ventricular beats. Those that occur earlier-than-expected act functionally like PVCs (ie, beat #7). Beats #12 and 13 are functionally like a ventricular couplet — and beats #9,10,11 like a ventricular salvo. And those fascicular beats preceded by a longer R-R interval represent fascicular "escape" beats (which considering the ventricular location of the hemifascicles — represents a slightly accelerated escape rate).

  • The final beat to mention — is beat #16. This is a normal, sinus-conducted beat — because both the preceding PR interval and QRS morphology of beat #16 is the same as the preceding PR interval and QRS morphology of sinus-conducted beats #2-thru-6.

Figure-3: Use of simultaneously-recorded leads to determine that all of the similar-looking RS complexes in the long lead II rhythm strip manifest an RBBB/LAHB morphology (albeit with minimal QRS widening). Beats #1,7-thru-15 and 17 are therefore fascicular beats arising from the left posterior hemifascicle (See text).

QUESTIONS Regarding Figure-3:

  • Did YOU see evidence of additional atrial activity?

  • IF not — Take a look at the YELLOW and WHITE arrows in Figure-4. What do these arrows that occur after the QRS of beats #7 and #9-thru-14 represent?

Figure-4: What do the YELLOW and WHITE arrows that occur after the QRS of beat #7 and beats #9-thru-14 represent? (See text).

The YELLOW and WHITE Arrows:
The YELLOW and WHITE arrows in Figure-4 represent retrograde conduction! The fascinating aspect of this retrograde conduction — is that the RP' interval is not the same for all of these arrows. Instead — the RP' interval (ie, the distance from the QRS until the point when you see the retrograde P wave) — is slightly longer for the YELLOW arrows.
  • It seems that when there is a longer preceding R-R interval before a fascicular beat (ie, as occurs before beats #12 and 14) — there is more time to “recover” — so retrograde conduction is faster (ie, producing a shorter RP’ interval = as seen by WHITE arrows).
  • In contrast — beats #7, 10, 11 and 13 occur much closer to the preceding QRS — therefore leaving less time to recover. The result is that retrograde conduction is not as efficient and takes longer (which results in the slightly longer RP' interval highlighted by the YELLOW arrows).
  • The reason there is no retrograde conduction after fascicular beats #9 and 15 — is that both of these fascicular beats are preceded by a sinus P wave with a PR interval that is too short to conduct — but which is able to render intervening AV nodal tissue refractory to retrograde conduction from a fascicular beat arising from below this level.

  • NOTE: The retrograde conduction that occurs in Figure-4 after beats #7,11,13 and 14 — presumably resets the SA Node. This results in a slight pause after these beats. The beats that follow (ie, beats #8,9,12,14 and 15) — are fascicular "escape" beats (and since the R-R interval before these beats is between 3-4 large boxes — the rate of "fascicular escape" is ~80/minute, which is accelerated).


LADDERGRAM of Today's Rhythm:

For clarity — I've drawn a laddergram to explain today's rhythm. Since fascicular beats originate from the ventricles — I've schematically drawn these beats as RED circles beginning at the bottom of the Ventricular Tier (Figure-5).

Figure-5: Laddergram illustration of today's rhythm. A fascicular beat starts the tracing ( = beat #1). We do not see how long the R-R interval preceding this 1st fascicular beat is. There follows 5 sinus-conducted beats ( = beats #2-thru-6) — after which occurs a premature fascicular beat ( = beat #7). There follows the sequence of fascicular beats we described above — with escape (beats #8,9) — the salvo (beats #9,10,11) — the couplet (beats #12,13) — more escape (beats #14,15 — with some fusion occurring for beat #15) — a normal sinus beat (beat #16) — with the rhythm strip ending with a final premature fascicular beat (beat #17).

Putting It All Together:
The young woman in today's case presented with a several week history of intermittent but symptomatic palpitations.
  • Clinically — We have an underlying "almost sinus tachycardia" — there is a somewhat accelerated fascicular escape focus, with premature fascicular beats (including a couplet and salvo). Taken together — these findings suggest something is stimulating the heart to produce this unusual rhythm.
  • Regarding the rest of the 12-lead tracing — the QTc is not prolonged — the frontal plane axis is normal — and there is no chamber enlargement by voltage criteria. That said — the one "normal beat" that we do see in leads V5,V6 (ie, beat #16) does show ST-T wave depression with a morphology consistent with LV "strain" — so despite this patient's young age and lack of voltage criteria — there may be true LVH.
  • There are no normally-conducted sinus beats in leads V1,V2,V3 — but looking at simultaneously-recorded ST-T waves in other limb leads (corresponding to sinus beats #2-thru-6) — there is some ST depression. Clearly a sustained tachycardia (or frequent premature beats) can alter ST-T waves — so we will not know the “true” ST-T wave morphology until the rate slows down and remains slow for a period of time.

  • IMPRESSION: The patient is symptomatic with an unusual arrhythmia that may explain her palpitations. Evaluation should focus on ruling out underlying heart disease (formal Echo) — complete blood count, thyroid function and electrolyte studies — chest X-ray — and a very careful History asking about anything (and everything!) that the patient ingests (ie, See ECG Blog #321 — in which a 17yo developed a sustained ventricular rhythm as a result of an unusual Chinese herb she was taking — that could have been easily overlooked if not for careful history-taking).
  • If careful evaluation and history did not reveal a cause of this patient's arrhythmia — then empiric use of a beta-blocker may help to control the ectopics. Surprisingly, especially in young adults — low doses of a beta-blocker are often all that is needed to control a symptomatic arrhythmia.

CASE Follow-Up:
This patient was initially treated with short-term Amiodarone — which controlled her arrhythmia. She was then switched over to a low-dose beta-blocker. Evaluation revealed she had primary hypothyroidism — and she was started on replacement therapy.
  • My review of literature suggested that unlike hyperthyroidism — hypothyroidism is usually not directly associated with an increase risk of tachyarrhythmias (Udovcic et alKlein & Danzi). Hypothyroidism may cause bradycardia. When severe — it may be associated with some QTc prolongation, AV conduction disturbances, reduced contractility and/or diastolic dysfunction — so arrhythmias might be seen as an indirect result of this endocrine disorder.


Acknowledgment: My appreciation to Bipin Kumar (from Koderma, India) for the case and this tracing.


Related ECG Blog Posts to Today’s Case:

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.

  • ECG Blog #185 — Reviews my Systematic Ps, Qs, 3R Approach to Rhythm Interpretation.

  • ECG Blog #188 — for Review on how to read (and draw) Laddergrams (with links to numerous illustrative laddergrams — with step-by-step explanation).

1 comment:

  1. So since hypothyroidism is typically not associated with tachyarrythmias, would this case just be considered atypical or has a severe hypothyroidism caused av/diastolic dysfunction which lead to the tachyarrythmia? Would something like levothyroxine fix the arrythmia or would this patient still likely need beta blockers?