ECG Interpretation: ECG Blog #428 — How Much to Do at Age 92?

I was sent the tracing in Figure-1 — with the following information:

92-year old patient with a history of "known arrhythmia" and hypertension.
The patient was asymptomatic at the time ECG #1 was obtained — with the ECG presumably being recorded because an irregular rhythm was heard on auscultation.

QUESTIONS:

How would YOU interpret the rhythm in Figure-1?
How much should we do for this 92-year old patient?
Extra Credit: Which arm or leg is most responsible for the artifact seen in today's initial ECG?

Figure-1: The initial ECG in today's case.

Answer to EXTRA Credit Question:

To begin with the answer to the Extra Credit Question — I suspect the cause of the abnormal baseline deflections seen in Figure-1 is muscle tremor artifact (See Bouthillet T — ACLS Med Training, Dec, 2015). A quick LOOK at the patient would confirm this — but I unfortunately do not have any information about the patient's appearance.

NOTE: The abnormal baseline deflections in Figure-1 are maximal in leads I,III and aVL — modest in lead aVF — and minimal in lead II, as well as being minimal in the 6 chest leads. Therefore — the "culprit" extremity most responsible for the artifact in today's tracing is the LA (Left Arm).
As discussed in detail in ECG Blog #255 — We can identify the "culprit" extremity because the relative size of the artifact deflections in Figure-1 manifest the relative dimensions expected when a single extremity is primarily responsible for a certain type of artifact.
PEARL #1: That one extremity is primarily responsible for a certain type of artifact — can be quickly recognized by the finding of approximately equal artifact amplitude in 2 of the 3 standard limb leads (ie, in leads I and III for Figure-1) — and, minimally or not seen at all in the 3rd standard limb lead (ie, artifact is minimal in lead II).
By Einthoven’s Triangle (See ECG Blog #255) — the finding of equal artifact amplitude in Lead I and Lead III, localizes the “culprit” extremity to the LA ( = Left Arm) electrode.
The greatly reduced artifact amplitude in lead II is consistent with this — because, derivation of the standard bipolar limb lead II is determined by the electrical difference between the RA ( = Right Arm) and LL ( = Left Leg) electrodes, which are not affected if the source of the artifact is the left arm.
SHORTCUT (To find the "culprit" extremity in seconds!): When 2 of the standard limb leads show approximately equal maximal artifact amplitude — and the 3rd standard limb lead shows minimal or no artifact — then whichever augmented lead shows maximal amplitude indicates the "culprit" extremity (which in Figure-1 is Lead aVL = which means that the LA is the "culprit" extremity).

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Back to Today's CASE:

How would YOU interpret the rhythm in Figure-1?
How much should we do for this 92-year old patient?

Figure-1 (Repeated): The initial ECG in today's case.

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MY Initial Thoughts:

From an arrhythmia standpoint — I found the rhythm in today's case to be fascinating.

That said — this patient is elderly and asymptomatic, which raises the questions as to, How much evaluation? — and — What clinical management would be optimal?

We are told in the brief information given — that today's patient has a history of a "known arrhythmia". Thus, the 1st issue that comes to mind in today's case is — What is the arrhythmia that this patient is "known" to have?

By far — the most common cause of an irregularly rhythm in an asymptomatic elderly patient is AFib (Atrial Fibrillation).
IF this patient had AFib — then determination of the need for rate control and/or informed consent by the patient (and/or by the family, if the patient is no longer mentally competent) regarding the pros and cons of anticoagulation — would be indicated.
The above said — I was not made aware of additional specifics of this patient's medical history — and, the rhythm in today's case is not AFib.

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HOW to Interpret Today's Rhythm:

The "good news" — is that the elderly patient in today's case is asymptomatic. This means that we have at least a moment of time to try to figure out the rhythm in Figure-1. My initial observations include the following:

The rhythm is obviously irregular.
There are 2 different QRS morphologies. These are: i) Beats #1-thru-4; beat #11; and beats #15,16 — all of which are at most, boderline prolonged, with an rS configuration in the long lead II rhythm strip; and, ii) The remaining 10 beats — all of which are of normal QRS duration, and manifest an RS configuration in the long lead rhythm strip.
The first 4 beats are regular at a rate of ~95-100/minute — and, they are not preceded by P waves. These first 4 beats manifest marked LAD (Left Axis Deviation) — being positive in lead I — but virtually all negative in simultaneously-recorded leads II and III.
Beats #11 and #15,16 manifest an incomplete RBBB morphology (ie, with a nearly equiphasic R=S for beat #11 in lead V1 — and, with wide, terminal S wave for beats #15,16 in lead V6). This combination of incomplete RBBB + LAHB morphology for beats #1-thru-4; beat #11; and beats #15,16 — suggests that these 7 QRS complexes are all fascicular beats that arise from the LPH (Left Posterior Hemifascicle).
NOTE: Since fascicular beats are ventricular beats — this means that the first 4 beats in Figure-1 constitute a short run of NSVT (Non-Sustained Ventricular Tachycardia), albeit an NSVT at the modest rate of ~95-100/minute.
The remaining 10 beats in Figure-1 manifest a narrow QRS complex in all 12 leads — and, are therefore supraventricular.

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QUESTION:

In Figure-1 — Is the underlying rhythm sinus?
HINT: Is there a predominant P wave morphology?

ANSWER: The easiest way to tell if an underlying sinus rhythm is present — is to LOOK for: i) A predominant P wave morphology (ie, in which the P wave in lead II is upright with a constant PR interval); and, ii) A consistent R-R interval before the predominant P wave morphology.

As can be seen in Figure-2 — it appears that both of these features are present in today’s rhythm.

Figure-2: I've labeled sinus P waves with RED arrows.

NOTE in Figure-2 — The underlying rhythm is sinus!

RED arrows in Figure-2 highlight what appear to be similar-looking upright P waves in the long lead II rhythm strip. At least before beats #6, 7 and 9 — the preceding R-R interval is very similar, suggesting these 3 P waves represent normal sinus-conducted beats.

Now that we have identified that, with the exception of fascicular beats #1-4; 11; 15,16 — the underlying rhythm in today's tracing is sinus — We can focus our attention on the remaining beats in today’s tracing:

Beats #5; 8; 12; 13; and 17 — all occur earlier-than-expected — are all preceded by a P wave with a P wave morphology that is different from that of the RED arrow P waves — yet all manifest the same supraventricular QRS morphology as the 3 sinus-conducted beats ( = beats #6,7,9).
These 5 beats ( = beats #5,8,12,13,17) — are therefore PACs (Premature Atrial Contractions).

Putting It All Together:

I summarize in Figure-3 — what we have thus far determined for today’s arrhythmia:

There are 2 distinct QRS morphologies in today’s rhythm.
Beats #1,2,3,4 — beat #11 — and beats #15,16 — represent the first QRS morphology, in which there is slight QRS widening with a pattern consistent with incomplete RBBB/LAHB conduction. Based on the regularity of beats #1-thru-4, and the absence of sinus P waves in front of these 4 beats — these must be fascicular beats from the LPH.
Since QRS morphology of beats #11,15,16 is so very similar to that of beats #1,2,3,4 in the long lead II rhythm strip — all of the beats marked by a RED circle in Figure-3 are fascicular beats.
The finding of 4 consecutive beats of ventricular etiology at an accelerated rate — means that beats #1-thru-4 represents a 4-beat run of NSVT.
YELLOW arrows highlight a negative deflection occurring just after the QRS of these first 4 beats. Because no such negative deflection follows the QRS of the other 3 fascicular beats (each of which is preceded by a RED arrow sinus P wave) — we know that the 4 YELLOW arrows in Figure-3 must represent 1:1 VA conduction (ie, retrograde P waves) that follow these first 4 fascicular beats.

Figure-3: Further labeling of today's tracing.

Additional Findings in Today's Rhythm:

As noted earlier — the underlying rhythm in today's tracing is sinus, since there is a predominant P wave morphology in the form of similar-looking upright P waves with constant PR interval in front of beats #6,7; 9,10; 14 (RED arrow P waves in front of these beats in the long lead II rhythm strip).

PEARL #2: Seemingly on-time RED arrow P waves also appear in front of fascicular beats #11,15,16 — but with a shorter PR interval. This observation provides further support that beats #11,15,16 are of ventricular etiology (ie, The shorter PR interval of these on-time RED arrow P waves represents transient AV dissociation).
PEARL #3: Did YOU notice the slightly smaller S wave amplitude of fascicular beat #11? The reason for this — is that beat #11 is a fusion beat (ie, the RED arrow P wave in front of beat #11 partially conducts — resulting in "fusion" between fascicular beat morphology and the RS morphology of supraventricular beats). As per ECG Blog #128 — identification of fusion beats in this setting proves a ventricular etiology.
Finally in Figure-3 — I've selected different colors to represent the different P wave morphologies of the 5 PACs (colored P wave arrows before beats #5,8,12,13,17).

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LADDERGRAM Illustration:

For clarity — I offer my proposed laddergram in Figure-4.

RED arrows represent sinus P waves. Slight variation in the P-P interval is the result of sinus arrhythmia.
The first 4 beats represent a 4-beat run of fascicular NSVT. Dotted lines extending from these first 4 fascicular beats represent conduction back to the atria (resulting in the YELLOW arrow retrograde P waves).
The different colored circles within the Atrial Tier — represent PACs arising from different sites within the atria.
I've drawn the laddergram to reflect that I suspect each of the later 3 fascicular beats ( = beats #11,15,16) are fusion beats — though it is admittedly difficult to detect significant difference in QRS morphology between fascicular beats #15,16 vs QRS morphology of the pure fascicular beats #1-thru-4.

Figure-4: Laddergram illustration of today's rhythm.

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CASE Conclusion: Clinical Implications ...

There is no specific "classification" that fits all aspects of today's rhythm. The occurrence of so many PACs of different P wave morphologies brings to mind features of MAT (Multifocal Atrial Tachycardia) — but there are too many consecutive P waves of similar origin to be consistent with the concept of "true" MAT, in which P wave morphology and the PR interval varies from one-beat-to-the-next (ie, We see too many consecutive on-time RED arrow sinus P waves).

PEARL #4: As discussed in ECG Blog #366 — Rather than strict definition of "MAT" — many patients manifest variations along the spectrum of MAT, in which there may be multiple P wave morphologies sandwiched between periods of fairly normal on-time sinus P wave activity. Such is the case in today's rhythm.
Clinically: Even when "pure" MAT is not present — rhythms with multiple PACs of multiple morphologies often "behave" in similar fashion to MAT in that: i) Severe pulmonary disease and/or "sick" patient with multisystem comorbidities (ie, acid-base and/or electrolyte abnormalities; shock; multi-system failure) are often the cause; and, ii) The BEST treatment is to "find and fix" the underlying cause (as per ECG Blog #366).
As to the rest of the 12-lead ECG in today's case — supraventricular complexes (ie, beats #10,12,13 in leads V1,2 + beats #14 and 17 in leads V5,V6) — show increased voltage consistent with LVH — and ST-T wave changes consistent with LV "strain" — but this does not appear to be acute.
Finally: Today's rhythm further defies classification — because it includes frequent ventricular beats with a 4-beat run of fascicular NSVT.

MY Suggestion for Management:

Since today's patient is 92 and asymptomatic — We do not want to "do too much to him". Simply stated — "It is hard to make an asymptomatic patient feel better!"

The above said — it is good to appreciate that even though today's arrhythmia does not fit the full definition of "MAT" — this rhythm does behave clinically in similar fashion as does MAT. Therefore — We should look for simple potentially "fixable" exacerbating factors, such as electrolyte imbalance (ie, Check serum K+ and Mg++ levels, as well as other electrolytes) — hypoxemia (Check O2 saturation levels) — heart failure, sleep apnea, dehydration, etc.
If nothing "easily fixable" turns up abnormal — it may be that this 92-year old man has been in this rhythm for years! In that case — we may want to leave him alone.

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Acknowledgment: My appreciation to Chun-Hung Chen = 陳俊宏 (from Taichung City, Taiwan) 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 — Reviews the Ps, Qs, 3R Approach to Rhythm Interpretation.
ECG Blog #188 — Reviews how to read and draw Laddergrams (with LINKS to more than 80 laddergram cases — many with step-by-step sequential illustration).
ECG Blog #128 and ECG Blog #129 — on Fusion beats.
ECG Blog #366 — MAT explained.
ECG Blog #199 — More on MAT.
ECG Blog #65 — for an example of MAT in a patient with chronic pulmonary disease (plus more on the differential diagnosis of MAT).
ECG Blog #200 — on Wandering Atrial Pacemaker.

I link to 2 additional illustrative Cases taken from Dr. Smith’s ECG Blog. For each of these posts — Please scroll down to the bottom of the page to see My Comment. These cases provide insight to assessment for MAT:

The January 5, 2020 post in Dr. Smith’s ECG Blog — for an example of MAT.
The September 30, 2019 post in Dr. Smith’s ECG Blog — for an example of “MAT”, but without the tachycardia ...