ECG Blog #328 — What Happened After the Fall?

The ECG in Figure-1 — was obtained from a middle-aged man with a long history of alcoholic liver disease, who was admitted following a fall. He was acutely ill at the time this ECG was recorded.

QUESTIONS:

• How would YOU interpret the ECG in Figure-1?
• Clinically — What might account for the changes you see?

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

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NOTE: There are a number of reasons why interpretation of today's rhythm turned out to be especially challenging. These include:

• There is artifact.
• P waves are small — and they are not seen in most leads.
• The QRS complex in lead II is tiny — because QRS morphology in leads I and III is almost oppositely directed (This makes it difficult to distinguish between P waves vs QRS complexes vs T waves in the single long lead II rhythm strip).
• The underlying rhythm is not obvious.
• There is more than 1 QRS morphology.

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MY Thoughts on the ECG in Figure-1:

I thought the KEY for interpreting today's rhythm was to first identify atrial activity. As I allude to above — this initial task was complicated by the small size of P waves — and the difficulty distinguishing between P waves vs QRS complexes vs T waves in the long lead II rhythm strip.

• There are 2 QRS complexes that look different from the other 14 beats ( = beats #1 and 13). The QRS for these 2 beats appears to be very wide — is not preceded by a P wave — and at least for beat #13, this beat occurs early (See Figure-2 — which highlights these 2 beats that look different in all simultaneously-recorded leads). Presumably — beats #1 and 13 are PVCs (Premature Ventricular Contractions).
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• Because electrical activity for the PVC which is beat #1 is oppositely directed in lead I (which is predominantly negative) compared to lead III (which is all positive) — QRS morphology for this PVC in intervening lead II is almost a null vector. I have illustrated this "almost null-vector" for the QRS of these 2 PVCs in the long lead II rhythm strip by means of vertical BLUE timelines placed at the beginning and end of these 2 PVCs in Figure-2.

Figure-2: I've placed vertical BLUE timelines at the onset and offset of the QRS for beats #1 and 13, which are PVCs (See text).

Identifying the P Waves:

I count today's tracing as among the most difficult I have encountered for identifying atrial activity. I approached this task in steps:

• STEP-1: I find it easiest to begin by quick overview of the entire long lead rhythm strip — with the goal of trying to identify at least 2 deflections in-a-row that look like sinus P waves. 
• STEP-2: IF there is an underlying sinus rhythm — then once I identify 2 definite P waves (and determine the P-P interval between them) — it should become much easier to know where to look for additional sinus P waves.
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• PEARL #1: The use of calipers is essential for "solving" today's rhythm. It is simply impossible to accurately assess relative P-P and R-R intervals in a complex tracing like this one unless you use calipers.
• PEARL #2: Contrary to what many clinician think — Using calipers speeds up your interpretation! This is because once you set your calipers to a given P-P or R-R interval — it takes no more than seconds to "walk through" that interval in other parts of the tracing.
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• Applying these principles in Figure-3 — I've highlighted with RED arrows the 2 deflections that I thought looked most like sinus P waves. NOTE: If these 2 RED arrows in Figure-3 are indeed sinus P waves — then the PR interval preceding beats #7 and 8 is not equal (which immediately suggests that there may be AV dissociation).
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• Realizing that the P-P interval of an underlying sinus rhythm will not always be exactly the same for every beat (ie, there may be a sinus arrhythmia) — I used the P-P interval suggested by the distance between these 2 RED arrows in Figure-3 — and thought the "extra" deflection seen at the onset of the preceding 2 QRS complexes (PINK arrows) most probably represented the 2 preceding sinus P waves.

Figure-3: Starting with the 2 consecutive deflections that I thought looked most like sinus P waves (RED arrows) — I used this P-P interval to look backward — which suggested that the "extra" deflection at the onset of the QRS of beats #5 and 6 (PINK arrows) represented the preceding 2 P waves.

Walking Out Additional P Waves:

Encouraged by what seems to truly be 4 sinus P waves in a row (with approximately the same P-P interval between these P waves) — I continued working my way backward with calipers set at this similar P-P interval (PINK arrows in Figure-4).

• Although the deflections highlighted by PINK arrows in Figure-4 are admittedly not as definitive for pointing out P waves as they are for the RED arrows — there are subtle indications of an "extra something" that occurs with similar P-P interval spacing between deflections.

Figure-4: Working my way backward with calipers set at a similar P-P interval — I thought additional sinus P waves were probably present under the PINK arrows.

The Underlying Rhythm Is Sinus!

Although subtle — I felt that I was able to march out fairly regular sinus P waves throughout the entire long lead II rhythm strip (additional ARROWS that I added to the rhythm strip in Figure-5).

• Obviously — No sign of atrial activity can be seen between the artifactual "dip" in the baseline between beats #8-9. But IF we continue advancing calipers from just before beat #8 onward (applying a similar P-P interval that I've used up until this point) — a slight "something" is seen under each of the next 8 PINK arrows in Figure-5. While fully acknowledging that this extra "something" is subtle (ie, no more than slight deformation of a T wave — or a "pseudo-r wave" at the onset of the QRS for beats #15,16) — I think it highly unlikely that these "extra" deflections are all due to chance.
• NOTE: I used a WHITE arrow for the tiny deflection coinciding with the end of the QRS complex of the 1st PVC (which is beat #1) — because I can not prove this deflection is a P wave. But this extra little deflection does occur on time at a similar P-P interval spacing prior to the 1st RED arrow.
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• BOTTOM LINE: Nothing is perfect. That said — the colored arrows I have placed in Figure-5 are spaced at a similar (albeit not exactly equal) P-P interval duration from each other. I strongly suspect that these arrows represent an underlying sinus mechanism (ie, sinus arrhythmia) in today's tracing.

Figure-5: Working my way forward from where I left off in Figure-4 — I feel the colored arrows represent an underlying fairly regular sinus rhythm throughout the entire rhythm strip.

Are P Waves Related to Neighboring QRS Complexes?

Now that we have identified an underlying sinus rhythm in Figure-5 — We need to determine IF any of these P waves are related to neighboring QRS complexes?

• We have already identified beats #1 and 13 as PVCs.
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• QRS morphology for the remaining 14 beats in the long lead II rhythm strip is very similar — and the R-R interval (except for the PVCs) is surprisingly regular. Thus, although QRS morphology changes with each 3-lead grouping — it appears that beats #2-thru-12; and #14-16 are all arising from the same site.
• The QRS complex for these 14 beats is wide. While more difficult to appreciate this for beats #2,3,4 in lead III — and for beats #5-8 in lead aVF — there is no doubt that the QRS complex for beats #2-12; and #14-16 in the chest leads is wide.
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• FOCUS Attention on the QRS complex for each of these 14 beats (ie, beats #2-thru-12; and #14-16). Looking at the nearest colored arrow in Figure-5 to each of these 14 beats — Isn't the relationship between each QRS and each of these colored arrows constantly changing? This suggests there is complete AV dissociation! (ie, all P waves are unrelated to neighboring QRS complexes!).
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• Since the QRS complex of beats #2-12 and #14-16 is wide and completely dissociated from neighboring P waves — I suspect that these 14 beats  represent an accelerated ventricular rhythm. That said — I fully acknowledge that I can not rule out the possibility of an accelerated junctional rhythm with preexisting RBBB/LAHB (although judging by QRS morphology — I feel this would be less likely).

My Proposed LADDERGRAM:

To clarify my proposed interpretation of the rhythm in today's case — I've drawn a Laddergram in Figure-6.

Figure-6: My laddergram illustration of today's rhythm. None of the regular sinus P waves in the Atrial Tier are able to be conducted to the ventricles. Thus, there is complete AV dissociation — which I propose is resulting from an accelerated ventricular rhythm (RED circles arising from the Ventricular Tier) — and from 2 PVCs (beats #1 and 13) arising from another site in the ventricles.

PEARL #3: Regardless of the site of the rhythm for beats #2-12 and #14-16 — the rate of the ventricular response in Figure-6 is almost the same as the rate of the sinus P waves (ie, the rate of both the ventricular response and the rate of sinus P waves is ~90-to-100/minute). This proximity of the rate for these 2 independent pacemakers qualifies the rhythm as isorhythmic AV dissociation. 

• As discussed in ECG Blog #195 — the phenomenon of isorhythmic AV dissociation could account for the slight variation that we see in P-P and R-R intervals. With this phenomenon, despite independent beating of the SA node and escape pacemaker — there is often a "back-and-forth" relationship between P waves and neighboring QRS complexes. Although my reading of the literature fails to provide a definitive mechanism for this phenomenon — both pacemakers appear to be subject to slightly differing influences involving autonomic reflexes and vagal tone (with resultant slight ongoing variation in the P-P and R-R intervals).

PEARL #4: Although there is complete AV dissociation in today's rhythm (because none of the P waves in the long lead rhythm strip are conducted to the ventricles) — this rhythm does not qualify as complete AV block. As emphasized in ECG Blog #195 — this is because none of the P waves (RED arrows in Figure-6) have a chance to conduct.

• The rate of the ventricular response (at ~90-100/minute) — is simply too fast to allow P waves the opportunity to occur during a time when the PR interval would be both long enough to allow conduction to the ventricles — and, at a time when P waves are not occurring simultaneous with the QRS complex or within the ST segment during the absolute refractory period.
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• BOTTOM LINE Regarding Today's Rhythm: There may or may not be some degree of AV block. We simply can not tell from the 16-beat rhythm strip provided in today's case. What we can say — is that there is a fairly rapid underlying sinus rhythm with complete AV dissociation due to near identical sinus and ventricular rates + 2 PVCs. The escape pacemaker — is most likely an accelerated ventricular rhythm.

FINAL Step: What About the Rest of Today's ECG?

Now that we've interpreted the rhythm in today's tracing — we need to return to the rest of the 12-lead ECG (which for clarity — I've reproduced in Figure-7). The remarkable findings are: i) ST segment coving in all 6 chest leads; ii) Marked J-point ST depression in these chest leads (that attains 2-3 mm in leads V3-thru-V5); and, iii) Deep, symmetric T wave inversion in all 6 chest leads — that is clearly beyond that expected with simple RBBB.

• Regardless of whether beats #2-12 and #14-16 represent an accelerated ventricular escape focus or junctional tachycardia with RBBB/LAHB — these ST-T wave changes are markedly abnormal, and indicative of some acute process.
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• Regarding the Differential Diagnosis that immediately comes to mind considering today's abnormal rhythm and the dramatic ST-T wave changes seen in the chest leads — I think of: i) Acute ischemia/infarction; ii) Massic acute PE (Pulmonary Embolism); and, iii) Acute fat embolism. 
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• Given the History ( = an acutely-ill patient with alcoholic liver disease — admitted for a recent fall) — I favored either acute PE or acute fat embolism as the more likely precipitating event.

 

Figure-7: I've reproduced Figure-2 — so that we can focus on assessment of the ST-T waves in today's tracing (See text).

CASE Follow-Up:

Our follow-up of today's case is unfortunately limited — but I learned that this patient died several hours later, after the ECG in Figure-7 was recorded. 

• Although I know little of the specific nature of this patient's fall that prompted hospital admission — I thought his rapid demise in association with today's ECG was most consistent with either acute PE or fat embolism as the precipitating cause.
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• Increasing attention has focused on massive acute PE in recent years as a cause of sudden death or rapid patient demise in patient's presenting with shock or acute dyspnea. This diagnosis should especially be thought of when the initial ECG shows anterior (or diffuse) chest lead T wave inversion and/or ST depression similar to that seen in Figure-7. (See ECG Blog #313 — for more on the ECG diagnosis of acute PE).
• Much less attention has focused on the entity of fat embolism — which may cause similar unexpected and rapid demise. This syndrome most often follows orthopedic trauma — and is characterized by systemic dissemination of fat emboli throughout the systemic circulation. In many instances — the diagnosis of fat embolism is only established during autopsy. (See Kwiatt & Seamon: Int J Crit Illn Inj Sci 3(1):64-68, 2013 — and — Adeyinka & Pierre: NIH StatPearls, 2022 — for more on fat embolism syndrome).

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Acknowledgment: My appreciation to Bipin Kumar (from Koderma, India) 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.
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• ECG Blog #185 — Reviews my Systematic Ps, Qs, 3R Approach to Rhythm Interpretation.
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• ECG Blog #188 — for Review on how to read (and draw) Laddergrams (with links to numerous illustrative laddergrams — with step-by-step explanation).