EXTRA COPY — ECG Blog #539: Does SVT cause Hypotension? — EXTRA COPY

The ECG in Figure-1 was obtained from a young adult woman — with a history of recurrent SVT. She was hypotensive with this most recent episode.

QUESTIONS:

• How would you interpret the ECG in Figure-1?
• Does this tracing "fit" with this patient's history?
• Extra Credit: Is there evidence of underlying atrial activity?

Figure-1: The initial ECG in today's case — obtained from a young adult woman with a history of recurrent SVT. (To improve visualization — I've digitized the original ECG using PMcardio).

Review of some Clinical Concepts:

The ECG in Figure-1 shows a regular WCT (Wide-Complex Tachycardia) at ~180-190/minute.

• Although in a number of limb leads the QRS does not seem wide — it "looks" wide in most of the chest leads, and measures 0.11-0.12 second in leads V1,V2.
• PEARL #1: I've seen different answers for what constitutes "QRS widening" in an adult. I favor the following 2 guidelines: i) For measuring QRS duration — Use that lead in which you can clearly determine the onset and offset of the QRS complex — and in which the QRS is longest; — and, ii) Because some cases of fascicular VT may only measure 0.11 second in duration — I consider the QRS to be "wide" if in any lead the QRS clearly measures ≥0.11 second in duration.
• PEARL #2: Just because a given diagnosis is written in a patient's chart — does not necessarily mean that diagnosis is correct (unless you also find firm objective evidence in that patient's chart to support the diagnosis!). We need to remain open to other possibilities.
• PEARL #3: It is still all-too-commonly believed that the cause of the overwhelming majority of regular WCT rhythms in younger adults is some form of SVT (SupraVentricular Tachycardia) — in which QRS widening is explained by either preexisting BBB (Bundle Branch Block) or aberrant conduction. However, as was shown in ECG Blog #489 — Blog #38 — and Blog #464, among others — the idiopathic VTs (which occur in patients without underlying heart disease) are much more common in younger adults than is currently appreciated (More on the idiopathic VTs below in today's ADDENDUM).

PEARL #4: Today's patient was hypotensive in association with the rhythm in Figure-1. Although it is clearly more common for a patient in VT to be hypotensive (than for a patient in an SVT rhythm) — a patient's BP (blood pressure) is not an infallible predictor for distinguishing between VT vs SVT (See ECG Blog #220 — Blog #38 — and Blog #297). For example:

• We've seen a number of patients in sustained VT remain hemodynamically stable not only for hours — but for days!
• In contrast, most otherwise healthy younger adults who present in a sustained SVT rhythm — will remain stable for long periods of time.
• Bottom Line: The fact that today's patient was hypotensive in association with the rhythm in Figure-1 is not reliably predictive of this rhythm's etiology. That said — it is indication of the need for prompt effective therapy (ie, having a lower threshold to proceed with synchronized cardioversion).

The ECG in Figure-1:

As already noted — the rhythm in Figure-1 is a regular WCT at a rate of ~180-190/minute. With regard to atrial activity — there is no consistent sign of upright sinus P waves in lead II, or in any other lead. That said — the negative notching in the terminal portion of the QRS in leads II and aVF suggests there are 1:1 retrograde P waves (YELLOW arrows in Figure-2).

• PEARL #5: Even if the negative notching highlighted by YELLOW arrows in Figure-2 does represent 1:1 retrograde P waves — this does not help in our differentiation of the rhythm because both VT and reentry SVT rhythms may manifest 1:1 VA conduction.

Figure-2: YELLOW arrows highlight what appears to be 1:1 retrograde P waves.

What about QRS Morphology?

Up until this point — We've highlighted this young woman's history, namely of recurrent SVT, with today's episode thought to represent just one more recurrence. That said, because the QRS in Figure-1 is wide — We need to consider the possibility of VT.

• PEARL #6: Aberrant conduction most often presents as rate-related QRS widening that manifests a QRS morphology that resembles some form of known conduction defect (ie, either RBBB, LBBB, LAHB, LPHB, or RBBB with a hemiblock). This is because the refractory periods of the various conduction fascicles are not the same. In most patients — the refractory period of the right bundle branch tends to be the longest, which is why RBBB conduction is the most common form of rate-related aberrancy. But any conduction pattern may be possible with rate-related aberrancy (See ECG Blog #211 — for more on the WHY of aberrant conduction).
• PEARL #7: As discussed below in the ADDENDUM to today's post — fascicular VT is one of the most common forms of idiopathic VT. Because of its origin near the left anterior or the left posterior hemifascicle — QRS morphology with fascicular VT resembles either RBBB/LAHB or RBBB/LPHB conduction. That said — my favorite clue that a WCT rhythm may turn out to be fascicular VT — is that there are some atypical ECG features of RBBB/hemiblock conduction!

NOTE: As shown in Figure-3 — QRS morphology is not typical for RBBB with either left anterior or posterior hemiblock.

• Instead of the expected triphasic rsR' complex in lead V1 (with taller right "rabbit ear" and a distinct S wave that descends below the baseline) — a qR pattern is seen in this lead. While SVT rhythms do not always show "typical" QRS morphology — it's important to appreciate that atypical conduction features may be a hint of a ventricular etiology (See Figure-9 in the ADDENDUM below).
• Typical RBBB conduction should manifest a wide terminal S wave in left-sided leads I and V6. While we do see a wide terminal S wave in lead I — this feature is missing in lead V6 (ie, the deep S wave in lead V6 in Figure-3 is narrow and followed by a small positive deflection = an RSr' in lead V6).
• With RBBB conduction — left-sided lead I typically manifests predominant positivity prior to the wide terminal S wave. However, the R wave in lead I in Figure-3 is relatively small.
• QRS morphology in leads II and III is not typical for either LAHB or LPHB conduction (ie, leads II and III lack the predominant positivity of LPHB — and the rSr' pattern in lead III is not the expected rS pattern typical of LAHB conduction).

BOTTOM Line: While the above subtle morphologic features do not rule out the possibility of an SVT rhythm for today's tracing — they should increase our suspicion that the rhythm in Figure-3 may represent fascicular VT.

• PEARL #8: Assessment of QRS morphology on the surface ECG is not definitive for distinguishing between SVT vs VT. Sometimes the only way to determine the true etiology of a regular WCT rhythm is by EP testing. That said — especially given the history in today's case of recurrent episodes — these atypical morphologic features made me highly suspicious that the rhythm in Figure-3 was probably fascicular VT.

PEARL #9: As has been emphasized on many posts in this ECG Blog — the treatment of choice for a hemodynamically stable patient in fascicular VT is IV Verapamil (or IV Diltiazem).

• Although Adenosine may convert some cases of fascicular VT — it is much less effective than IV Verapamil in this group of patients.
• IV Verapamil or IV Diltiazem should not be given to patients with ischemic VT (ie, in patients with underlying structural heart disease). This is because the negatively inotropic and vasodilating effects of these drugs may lead to hemodynamic decompensation. However, these drugs are safe in patients with idiopathic VT who do not have underlying heart disease.
• The extra advantage of using IV Verapamil to treat an otherwise healthy younger adult with suspected fascicular VT — is that this drug is likely to be effective regardless of whether the rhythm is fascicular VT or a reentry SVT rhythm!
• The above said, since today's patient was hypotensive in association with the rhythm in Figure-1 — the treatment of choice is synchronized cardioversion.

Figure-3: QRS morphology in today's tracing is not typical for RBBB/hemiblock conduction.

One More Clue to Today's Rhythm!

Take another LOOK at today's rhythm in Figure-4.

• Could the slanted RED lines in Figure-4 represent atrial activity?

Figure-4: What do the slanted RED lines indicate?

Answer:

Overall — there is very little artifact in Figure-4. As a result — I was struck by the consistent disturbance in the baseline in lead II that has to be "real" (ie, slanted RED lines in Figure-4) — with similar disturbance of the baseline in lead lead aVF (slanted BLUE lines) — albeit not in the other inferior lead ( = lead III), and not in other leads.

• I wondered IF the slanted RED lines in lead II might represent underlying AV dissociation?

To explore this possibility — I've isolated and enlarged in Figure-5 the 15 beats that we were seeing in Figure-4.

Figure-5: A closer look at the 15 beats in lead II.

As suggested earlier in Figure-2 — YELLOW arrows pointing to the terminal negative notching in Figure-6 highlight retrograde P waves. 

• But did YOU previously notice when you first examined this tracing, that this negative terminal notching is not present after beats #3 and 10? Why might this be so?

Figure-6: Retrograde P waves are not seen after beats #3 and 10.

Calipers are needed to answer this question.

• I thought the 2 consecutive RED arrows in Figure-7 looked to be highlighting 2 consecutive sinus P waves (ie, upright in this lead II rhythm strip).
• Setting my calipers to the P-P interval between these 2 consecutive RED arrows — I then looked for additional deflections likely to represent more sinus P waves, keeping in mind that slight variation in this P-P interval would be possible if there was an underlying sinus arrhythmia. This led me to the deflections highlighted by the PINK arrows in Figure-7.
• This left me to postulate the likely presence of "on time" sinus P waves directly over the QRS of beats #3 and 10 (the 2 WHITE arrows).
• NOTE: Beats #3 and 10 are the only QRS complexes in Figure-7 that lack retrograde conduction (ie, No YELLOW arrow is seen at the end of the QRS of beats #3 and 10).

Figure-7: Using calipers allows us to identify the likely presence of an underlying sinus rhythm (ie, AV dissociation).

My Proposed Laddergram:

Normally — I would never expect to see the simultaneous presence of AV dissociation from an underlying sinus rhythm in a patient with VT that produces 1:1 VA conduction. That said — this is what appears to be happening.

• I drew my proposed laddergram in Figure-8 — as my attempt to explain how these findings might reasonably account for the failure of retrograde conduction for only 2 out of 15 QRS complexes in this tracing.
• It is because the 2 "on time" underlying sinus P waves highlighted by the WHITE arrows in Figure-8 occur at precisely the time when ventricular beats #3 and #10 are conducting retrograde through the AV Node — that completion of retrograde conduction is rendered impossible by downward conduction from these 2 "on time" WHITE arrow P waves.
• PEARL #10 (Beyond-the-Core): This failure of retrograde conduction from ventricular beats #3 and 10 proves that today's rhythm is VT (and not SVT with aberrant conduction) even more convincingly than the finding of AV dissociation — because the reentry circuit of a supraventricular reentry rhythm could not be maintained if retrograde conduction was intermittent.
• Editorial Comment (Beyond-the-Cord): I don't believe I have ever encountered the sequence of events portrayed in Figure-8. That said — the "beauty" of this rare occurrence is that: i) It provides a wonderful example of the concept known as "concealed" conduction — in which we are able to predict an electrophysiologic happening (in this case, failure of retrograde conduction after ventricular beats #3 and 10) despite not seeing the reason why this is happening on the surface ECG; — and, ii) It absolutely proves that today's ECG (and presumably most, if not all of the recurrent arrhythmia episodes this young woman has had) were the result of fascicular VT, and not of a reentry SVT.

Figure-8: My proposed laddergram.

CASE Conclusion:

I subsequently learned that this patient's recurrent ED visits for "palpitations" in association with a regular WCT rhythm (similar to the rhythm shown in today's case) — were resistent on several occasions to initial treatment with Adenosine, but responsive to IV Verapamil.

• Now that the correct diagnosis of fascicular VT has been made — the patient was referred for EP study, most probably to be followed by ablation that hopefully will be curative.
• In the interim (awaiting scheduling for her EP appointment) — I'd consider oral Verapamil in hope of minimizing (eliminating) episodes.

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Acknowledgment: My appreciation to Hamdallah Naser (from AL-Najaf, Iraq) — for allowing me to use this case and this tracing.

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ADDENDUM:

I've added below relevant materials in support of today's diagnosis. 

Figure-9: QRS morphology in lead V1 suggestive of either aberrant conduction vs VT (Figure 08.25-1, excerpted from my ACLS Pocket Brain-2013).

Figure-10: Review of KEY features regarding Idiopathic VT (See text).

—  —

ECG Media PEARL #14 (8 minute Audio): What is Idiopathic VT? — with special attention to the 2 most common forms = RVOT (Right Ventricular Outflow Track) VT and Fascicular VT. 

EXTRA COPY — ECG Blog #536 — Why 2 Morphologies? — EXTRA COPY

The ECG in Figure-1 was sent to me for my thoughts. Initially I had no clinical information.

QUESTIONS:

• What is the rhythm?  
• Why are there 2 different QRS morphologies?
• What is the likely underlying cause of this rhythm?

Figure-1: The initial ECG in today's case — initially sent to me without clinical information. (To improve visualization — I've digitized the original ECG using PMcardio).

My Thoughts:

The overall rhythm in Figure-1 appears to be regular with obvious QRS widening — and a ventricular rate of just under 100/minute (ie, with an R-R interval just over 3 large boxes in duration).

• There are 2 different QRS morphologies.
• Although the R-R interval varies slightly — I attributed this to uncertainty regarding where the QRS begins in some leads.
• P waves are absent. The only suggestion of atrial activity that I saw is possible retrograde P waves in some chest leads.

PEARL #1: This tracing emphasizes the important concept that, "12 leads are Better than One" — because if you only looked at leads I and V1 (and/or at leads V2,V3,V4) — it would be easy to think the rhythm was simply AIVR (Accelerated IdioVentricular Rhythm). 

• Instead, as shown in Figure-2 — there clearly is an alternating QRS morphology that is seen every-other-beat.

Figure-2: For clarity — I've numbered the beats in the limb leads. 

What is Going On?

Based on what I saw in Figure-2 — I thought the following:

• There is a regular wide QRS rhythm at ~95/minute — but without clear sign of atrial activity. QRS morphology is not consistent with any known form of conduction block — so this most likelly represents a ventricular rhythm.
• Many leads strongly suggest that QRS morphology alternates every-other beat — but without explanation as to why this may be so (ie, There are no P waves that may be conducting — and no significant variation in R-R intervals that might be producing a rate-related effect).
• BOTTOM Line: I was left with the conclusion that the rhythm in Figure-2 most likely represents the rare arrhythmia known as BiDirectional VT.

Semantics:

I've previously reviewed the concept of "AIVR" (Accelerated IdioVentricular Rhythm) — which is a slower form of "VT" (See ECG Blog #108).

• Technically, AIVR is not "VT" — because the ventricular rate is not ≥100/minute. But the ventricular rhythm known as AIVR clearly is faster than the usual ventricular "escape" rate, which normally is between 20-40/minute ==> the designation preferred by many is that AIVR represents a form of "slow VT".
• As emphasized in Blog #108 — the importance of recognizing AIVR depends on the clinical setting in which it occurs (ie, AIVR often occurs as a reperfusion arrhythmia in patients who have had a recent MI).
• PEARL #2: Whenever I see AIVR — I carefully consider the possibility that the patient may have had a recent MI that could have passed undetected.

What is BiDirectional VT?

I presented a case of bidirectional VT in ECG Blog #436:

• As discussed in ECG Blog #231 — bidirectional VT is a special form of VT, in which there is beat-to-beat alternation of the QRS axis. This unique and very uncommon form of VT is distinguished from PMVT (PolyMorphic VT) and from pleomorphic VT — because a consistent pattern of alternating QRS morphology is seen every-other-beat throughout the VT episode.
• Typically with bidirectional VT — there are alternating longer-then-shorter R-R intervals that correspond to the alternating QRS morphology. That said — as was seen with the case I presented in ECG Blog #436 (as well as with today's case) — QRS widening with uncertainty in some leads as to where the onset of the QRS begins may render it difficult to distinguish subtle alternation in R-R interval duration from what otherwise appears to be a fairly regular ventricular rhythm.
• Technically — this raises the question as to whether today's rhythm might simply represent AIVR with alternating exit sites accounting for the alternating QRS morphology (as I allude to in my discussion of ECG Blog #231). While fully acknowledging these theoretical considerations — My impression of today's rhythm remains unchanged = the most likely explanation for the rhythm in Figure-1 is bidirectional VT.

PEARL #3: There are a limited number of causes of bidirectional VT. As reviewed by Almarzuqi et al (Vasc Health Risk Mgmt 18:397-406, 2022) — Potential Causes of Bidirectional VT include:

• Digitalis toxicity.
• CPVT (Catecholaminergic PolyMorphic VT).
• Acute myocardial ischemia.
• Familial hypokalemic periodic paralysis.
• Cardiac Sarcoidosis.
• Primary Cardiac Tumors and/or Cardiac Metastasis.
• Andersen-Tawil Syndrome ( = Long QT Syndrome, Type 7).
• Acute Myocarditis.
• Certain drug overdoses (Aconitine poisoning, severe caffeine poisoning).

PEARL #4: Given how rare bidirectional VT is — the 1st thing to do when contemplating this diagnosis is to consider whether the patient might have one of the above-listed potential causes of this rhythm.

• In years past — Digitalis toxicity used to be the most common cause of bidirectional VT. This no longer appears to be true — given the overall reduced use of Digoxin (and in those cases in which Digoxin is still prescribed — toxicity is much less common nowadays because dosing of this drug is so much less than it used to be). 
• With the exception of myocardial ischemia and myocarditis — the other entities listed as potential causes of bidirectional VT are rare (which explains why bidirectional VT is rare).
• To Emphasize: In my experience — bidirectional VT is not a common manifestation of myocardial ischemia. But the PEARL is that ischemia/infarction should always be considered whenever you contemplate a diagnosis of bidirectional VT.
• Clinically: The BEST treatment of bidirectional VT — is to identify the causative condition in the hope that there may be effective treatment of that condition.

Follow-Up in Today's CASE:

It turns out that today's patient was a previously healthy middle-aged woman — who presented to the ED (Emergency Department) with new-onset CP (Chest Pain). The patient's condition rapidly deteriorated with resultant cardiac arrest.

• A complicated course followed, fortunately with successful ROSC (Return Of Spontaneous Circulation) — and, at the earliest opportunity cardiac catheterization was performed.

QUESTION:

• What do you think cardiac cath showed?  

HINT #1: To facilitate assessment of QRST morphology for the 2 "families" of QRS complexes — in Figure-3, I've enclosed beat #3 and beat #6 within the BLUE and RED dotted rectangles. 

Figure-3: To facilitate assessment of QRST morphology — I've enclosed beats #3 and #6 within BLUE and RED dotted rectangles.

HINT #2: To facilitate concentration on ST-T wave morphology even more for the 2 "families" of QRS complexes — I've shaded out the remaining beats in the limb leads.

Figure-4: I've shaded out the remaining limb lead beats.

Answer:

Today's rhythm is bidirectional VT. This means that there are no normally conducted QRS complexes — but instead, all beats on today's tracing are ventricular in etiology.

• PEARL #5: Most acute OMI (Occlusion-based MI) tracings identified by ECG will be diagnosed on the basis of ST-T wave morphology changes in sinus-conducted beats. Assessment of ST-T wave morphology in PVCs is usually not a reliable indicator of an acute event.
• That said — On occasion, the shape of ST-T wave elevation or depression in one or more PVCs may be diagnostic of acute infarction. This is precisely what we for the PVCs in ECG Blog #359.
• NOTE: For an example of a case in which assessment of the normal (sinus-conducted) beats was not definitive for acute OMI — such that the diagnosis of acute infarction was only made by recognizing the abnormal ST-T wave morphology of several PVCs — See My Comment at the bottom of the October 8, 2018 post in Dr. Smith's ECG Blog.

Applying the advanced concept from PEARL #5 to today's tracing — the shape of ST-T wave morphology in Figure-5 is clearly disproportionate and "off" from what we'd expect for both QRS families. Specifically:

• The QRS family of odd beats in Figure-5 (illustrated by beat #3) — shows inappropriate ST elevation in the inferior leads with reciprocal ST depression in lead aVL (the RED and BLUE arrows in these leads).
• More subtle, but still evident — the QRS family of even beats (illustrated by beat #6) — shows inappropriate ST elevation in each of the inferior leads (which is especially apparent in lead II given tiny size of the QRS in this lead).
• Both families of QRS complexes show a disproportionately increased amount of ST depression in the mid-chest leads of Figure-5 — with the BLUE arrows in leads V2,V3,V4,V5 of the even-numbered beats highlighting the obvious abnormality of this finding by the marked amount of horizontal (ledge-like) ST depression.

CASE Conclusion: 

Today's ECG illustrates a case of bidirectional VT that developed as a result of acute infero-postero OMI. This was confirmed on cardiac catheterization that showed multi-vessel disease with acute total occlusion of the LCx (Left Circumflex) coronary artery.

Figure-5: Both families of QRS complexes suggest that the cause of this bidirectional VT is acute infero-postero OMI. 

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Acknowledgment: My appreciation to Fardeen Baray and Hameedullah Ahmadzai (from Kabul, Afghanistan) for the case and these tracings.

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EXTRA COPY — ECG Blog #535: A "Fluttering" ECG - EXTRA COPY

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

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Figure-2: XXXXX 

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Acknowledgment: My appreciation to Cardiology Notes (FB ECG site) for allowing me to use this tracing — and to Ahmed Marai (from Anbar, Iraq) for drawing my attention to this case.

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From Ahmed:

Hello Dr. Grauer — I came across this ECG on facebook, which belongs to to a 50-year-old male, hypertensive and diabetic, recorded while he underwent a routine check up.

This is the link to the poster

https://m.facebook.com/story.php?story_fbid=pfbid0wAJTSLDFuYExamcgrFy3RaR1DzcE6xbef7jf77Pdzy8htmBamYTTG5EJNSM2H13zl&id=61563573262961

This is my interpretation:

A 12 lead ECG, unlabelled calibration and speed, but it looks standard.

Ventricular rate: around 62-66 bpm

Rhythm: regular narrow complex rhythm

Axis: within normal range

No obvious P waves, however, there are regular waves between the QRS complexes, which run at around 273bpm, it appears in all the 12 leads and looks much taller in the chest leads compared to the limb leads.

Regarding QRS complex, it is narrow, with very subtle irregularity. In the chest leads, the QRS is dominantly positive (no obvious S waves), and has high voltage in V2-V5.

 

No obvious ST-T changes, and the QT intervals cannot be determined accurately.

Clinical impression: The regular waves seen between the QRS complexes are probably flutter waves, it runs at around 273bpm, and since ventricles beat at around 66bpm, then it is probably AFlu with 4:1 AV conduction. However, these flutter waves are atypically tall in the chest leads.

The high voltage of R waves in chest leads, is suggestive of possible LVH, the history of hypertension may support the possibility of LVH. The S waves are are not obvious in chest leads, but they are possibly present but are cancelled on the paper by the tall flutter waves. 

However, artifact should be suspected and excluded.

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My thoughts: At the beginning I thought this is an obvious atrial flutter with 4:1 av conduction, however, when I noticed the size of flutter waves in the chest leads, I thought this is unusual. 

I saw many people in the comments say, Artifact !! 

If this was an artifact coming from one limb, then one of these leads ( I, II or III ) should be spared. If the artifact is coming from 2 limbs, then it should be chaotic and not regular like this one.

If this was an artifact, then it is probably coming from the patient torso, maybe the patient was dancing while recording the ECG. This may explain why these waves are taller in the chest leads compared to the limb leads, as they are closer to the torso. Excited to hear your ideas on this ECG — Ahmed

MY REPLY:

Hi. I basically AGREE with you!

I’ve attached what I wrote on the FB site.

I also wrote to Cardiology Notes, asking them for follow-up! (They have great cases — but often don’t tells us what happened unless specifically asked!

: ) Ken

P.S. Another clue should be looked for — which is whether the DISTANCE between the closest deflection and the QRS is equal !!! Be SURE to use your calipers when looking for this. Usually (although not always) — IF the ventricular rhythm is regular — then the distance between the closest deflection and the QRS should be THE SAME! If it is not — and if the R-R interval remains constant — then this implies that NONE of the deflections are conducting!

But in this case — there is a very slight-but-real difference in the “PR” interval across lead II ==> IF the R-R interval would stay precisely equal, then if this was Aflutter — it implies complete AV block (which is possible but not common).

So — We wonder if this patient has a tremor, or perhaps something going on in his chest …

CARDIOLOGY NOTES (on Facebook !!! )

Hello Prof Ken. It was ARTIFACT! The patient is diagnosed with drug-induced Parkinsonism !!!!

EXTRA COPY — ECG Blog #537 — What is the Rhythm? — EXTRA COPY

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

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Figure-2: XXXX

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Figure-3: XXXX

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Figure-4: XXXX

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Figure-5: XXXX

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Acknowledgment: My appreciation to Bashiruddin Sayeem  (from Chittagong, Bangladesh) for the case and this tracing.

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THE CASE: Dear sir, this is an EKG of a 60 years old diabetic lady presenting with SOB. Is this LVH with strain, LAHB, RBBB?

MY REPLY:

Hello Bashiruddin — This is AIVR (or "or slow VT") at ~120/minute!

 

The KEY is to look at the long lead II — and RED arrows show 2 places were we KNOW there are 2 consecutive P waves (which are upright in this long lead II, therefore 2 consecutive sinus P waves. Now set your calipers at this P-P interval (between 2 consecutive RED arrows — and the PINK arrows show partial deflections that we SEE, which we KNOW must be underlying "on time" sinus P waves. The WHITE arrows then show you where additional "on time" sinus P waves lie — telling us there is an underlying sinus tach.

 

Thus there is AV dissociation — with beat #17 being a CAPTURE beat — and beats #6,7 and 16 being FUSION beats — all of which proves that the underlying rhythm is an isorhythmic AV dissociation by "usurpation" by an AIVR at 120/minute that is slightly faster than the underlying sinus tach! (The upright R wave in V1 is not "RBBB" — but indication of the ventricular focus!)

 

Note that the QRS IS actually wide (The tracing is slanted — but the WHITE line that I drew parallel to the heavy grid line shows that what looks like "narrow" beats in the long lead II are actually WIDE (because there is an initial small, upright r wave before the deep S waves)

 

Within the dotted BLUE rectangle we see the capture beat — that shows marked LVH with very deep, symmetric (ischemic) T wave inversion in leads V5,V6 — and also in lead aVF. That said, I don't acute ST elevation in the leads in which I am able to assess — so from what I can see, probably no acute STEMI ...

 

Now this 60 yo woman presented with SOB — so the KEY is to find out WHY she is SOB (ie, heart failure, pneumonia) — and then to treat that — and possibly (hopefully) the underlying "slow VT" will resolve!

 

This would be a SUPERB CASE for an ECG Blog! May I have your permission to use this case! I will acknowledge you as I have in the past (See attached). Let me know what happens! BEST — :) Ken

 

Bashiruddin REPLY:

Thank you sir Please feel free to use it in your ECG Blog.