ECG Blog #368 — Why So Fast?

I start today’s case with the ECG shown in Figure-1 — obtained from a 30-something year old man, who presented with palpitations.

• How would YOU interpret the ECG in Figure-1?
• Treatment?
• What is unusual about this arrhythmia?

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NOTE: The ECG in Figure-1 has been recorded at the usual 25mm/second speed — but with the Cabrera format (Please see my Editorial Note near the top of the page in ECG Blog #365 for review of the basics of this recording system).

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Figure-1: The initial ECG in today’s case. What is the rhythm? NOTE: This tracing was recorded at the standard 25 mm/sec. speed — but using the Cabrera format.  (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-1:

The rhythm in Figure-1 is regular and extremely rapid. QRS width is best assessed in leads V1,V2,V3 — which show a wide QRS (ie, ≥0.12 second in duration). Atrial activity is not seen.

• Accurate estimation of the heart rate in Figure-1 provides an important clue to the etiology of today’s rhythm. To do this — I like to look for a part of the QRS complex (in this case — the peak of the R wave) that starts on a heavy line. Doing so suggests that the R-R interval of this exceedingly rapid arrhythmia is just a tiny amount over 1 large box — which corresponds to a ventricular rate just under 300/minute (ie, between 290-300/minute).
• Morphology of the wide QRS in ECG #1 — is strongly suggestive of RBBB conduction because: i) There is a very typical triphasic (rSR’) complex in lead V1 — in which the initial r wave is slender — the S wave descends below the baseline — and there is a single, taller “right rabbit ear” (R’ deflection); and, ii) There are wide, terminal S waves in both of the key lateral leads ( = leads I and V6).

PEARL #1: An additional (less well known) feature of QRS morphology in today’s initial tracing that favors aberrant conduction — is the finding of the mirror-image opposite morphology for the QRS in lead I and/or lead V6 — compared to the rSR’ complex just described for lead V1. That is, in lead V6 of ECG #1 — we a qRS complex (ie, a definite initial Q wave — followed by a slender R wave — finishing in a wide, terminal S wave). 

• While impossible to completely rule out fascicular VT —  the very typical rSR’ and qRS morphologies seen in leads V1 and V6, respectively — overwhelmingly suggests a supraventricular etiology for the rhythm in Figure-1.

PEARL #2: In association with the RBBB morphology suggested in leads V1 and V6 — QRS morphology in limb leads I, II and III is perfectly consistent with LPHB (Left Posterior HemiBlock) conduction (ie, predominant negativity of wide terminal S wave in lead I — with a qR pattern in leads II and III). 

• This finding of completely typical QRS morphology for bifascicular block conduction (ie, RBBB/LPHB) — is yet one more feature of QRS morphology suggesting a supraventricular etiology (and not fascicular VT) for the rhythm in Figure-1.

Putting It All Together:  — The Rhythm in Figure-1

What we have just described is the following:

• A regular WCT ( = Wide-Complex Tachycardia) at a rate very close to 300/minute — without clear sign of atrial activity.
• QRS morphology that almost certainly indicates a supraventricular etiology.

Among the fast Supraventricular Rhythms:

• This is not AFib — because the rhythm is regular.
• It is also unlikely to be a reentry SVT rhythm (such as AVNRT or AVRT) — because these rhythms typically do not go this much faster than 240/minute.
• VT is highly unlikely because QRS morphology (as per Pearls #1 and #2) is so consistent with a supraventricular etiology.
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• By the process of elimination — this leaves AFlutter with 1:1 AV conduction as the most likely etiology of the rhythm in Figure-1.

PEARL #3: Atrial Flutter with 1:1 AV conduction is rare! By far — the most common AV conduction ratio with untreated AFlutter is 2:1. Since the rate of atrial activity with flutter in adults is most often very close to 300/minute (ie, usual range for atrial activity ~250-350/minute) — AFlutter with 2:1 AV conduction typically results in a regular ventricular rate of ~140-160/minute.

• The reason 1:1 AV conduction with AFlutter is rare — is the "built-in" refractory period of the AV node, which serves to "protect" the patient from attaining excessively fast ventricular rates (ie, over 250/minute) that may be hemodynamically compromising because they do not allow adequate time for ventricular filling.
• Therefore — IF ever you see AFlutter with an excessively rapid ventricular rate (ie, over 250/minute) — LOOK for a reason WHY this may be so. The most common reason for 1:1 AV conduction with AFlutter is the presence of an AP (Accessory Pathway) in a patient with WPW (Antegrade conduction over the AP is faster than over the normal AV nodal pathway). Other reasons that might account for 1:1 AV conduction with AFlutter include use of a 1A or 1C antiarrhythmic agent — or hyperthyroidism (ie, these being 2 conditions that may also facilitate acceleration of AV conduction by either enhancing sympathetic tone — or by pharmacologic reduction of the AV node refractory period) — See Nigussie et al (Cureus 12(6): e8739, 2020) and Murthy et al (BMJ Case Rep, 2013).

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Today's CASE Continues:

Follow-up on today's patient is unfortunately limited (ie, No EP study was done). There was a known history of hyperthyroidism, with the patient on medication for this condition. Therefore — 1:1 AV conduction of AFlutter may have been facilitated by hyperthyroidism. There was no history or current indication of WPW.

• Today's patient was symptomatic in association with the rhythm shown in Figure-1, which I have repeated in the TOP panel of Figure-2. He was treated with IV Metoprolol — with the result of this treatment shown in the BOTTOM panel below.
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• How would YOU interpret ECG #2 in Figure-2?

Figure-2: ECG #2 shows the result of treatment with IV Metoprolol. (To improve visualization — I've digitized the original ECG using PMcardio).

ANSWER:

Treatment of the exceedingly rapid (ie, 1:1 AV conduction) pattern of AFlutter seen in ECG #1 — resulted in considerable slowing of the rhythm, as seen in ECG #2:

• The rhythm in ECG #2 — is a regular tachycardia at a rate just under 150/minute (ie, about half as fast as the rhythm in ECG #1).
• QRS morphology in ECG #2 clearly looks supraventricular — with now, only minimal QRS widening and incomplete RBBB conduction (ie, rSr' pattern in lead V1 — with narrow, terminal s waves in lateral leads I and V6). The bifascicular conduction pattern of complete RBBB/LPHB, that was seen in ECG #1 — has now resolved.
• Atrial activity in the form of 2:1 AV conduction (best seen in lead V1) is now clearly seen.
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• IMPRESSION: The rhythm in ECG #2 now shows AFlutter with 2:1 AV conduction — with the ventricular rate being half the rate that was seen in ECG #1. Therefore — the IV Metoprolol succeed in reducing the rate of AV conduction of flutter from 1:1 (in ECG #1) — to 2:1 (in ECG #2).
• Resolution of the bifascicular block with the slower ventricular rate suggests that QRS widening in ECG #1 was the result of rate-related aberrant conduction.

Today's CASE Concludes:

Although the ventricular rate in ECG #2 was reduced in half following administration of IV Metoprolol — the patient remained in AFlutter with the rapid ventricular response of ~140-145/minute. Cardiac CT was obtained to rule out atrial thrombus — after which synchronized cardioversion was performed — resulting in ECG #3, as shown in Figure-3.

• What do you see in Figure-3?

Figure-3: ECG #3 shows the result of synchronized cardioversion. (To improve visualization — I've digitized the original ECG using PMcardio).

ANSWER:

Atrial flutter is an extremely responsive arrhythmia to synchronized cardioversion — with ECG #3 showing successful conversion to sinus rhythm. Note the change in P wave appearance (best seen in the limb leads) — with clear return of sinus P waves (ie, upright in lead II of ECG #3).

• Judicious use of ß-blockers and control of hyperthyroidism were the post-cardioversion treatment measures undertaken.
• The patient was referred for ablation of his AFlutter.

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Acknowledgment: My appreciation to Magnus Nossen (from Fredrikstad, Norway) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• ECG Blog #185 — Review of the Ps, Qs, 3R Approach for systematic rhythm interpretation.
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• ECG Blog #215 — Reviews the Cabrera Format (and explores potential advantages of this more logical anatomical sequencing).
• ECG Blog #114 — Reviews another case using the Cabrera format (from Romania)
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• ECG Blog #229 — reviews distinction between AFlutter vs ATach (and WHY AFlutter is so commonly overlooked).  
• ECG Blog #287 — More on AFlutter.
• ECG Blog #220 — reviews my LIST #1: = Causes of a Regular WCT.
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• The November 12, 2019 post in Dr. Smith's ECG Blog — in which I review my approach to a Regular SVT rhythm.
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• ECG Blog #196 — Reviews "My Take" on assessing the regular WCT (Wide-Complex Tachycardia) — with tips of distinguishing between VT vs SVT with either preexisting BBB or aberrant conduction.
• ECG Blog #211 — Reviews WHY some early beats and some SVT rhythms are conducted with Aberration (and why the most common form of aberrant conduction manifests RBBB morphology).
• ECG Blog #197 — Reviews the common forms of Idiopathic VT (including Fascicular VT). 
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• ECG Blog #18 and ECG Blog #37 — regarding very rapid rhythms with WPW.

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ADDENDUM (3/13/2023):

I've presented this material before — but it bears repeating for reference. These concepts should be automatic for assessment of the patient who presents with a regular SVT rhythm.

—  —

ECG Media PEARL #64 (10:50 minutes Audio) — Reviews my LIST #2: Common Causes of a Regular SVT Rhythm.

—  —

ECG Media PEARL #45 (10:00 minutes Audio) — Why is Atrial FIutter so commonly overlooked?

• For those wanting a more advanced review regarding AFlutter — Check Out this article by García-Cosío F et al (Clinical Approach to ATach and AFlutter, Rev Esp Cardiol 65(4):363-375, 2012).