ECG Blog #547 — What Happened When?

 The ECG in Figure-1 was obtained from a mid-30s man — who presented with CP (Chest Pain) that began ~1 hour earlier.

• The patient had previously been well. He had some risk factors — but no known history of heart disease.
• He reports a similar episode about a week earlier. He did not seek care at that time — because the episode resolved spontaneously. 

QUESTIONS:

• In view of the above history — How would YOU interpret the ECG in Figure-1?
• What happened when?
• What is the “culprit” artery?

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

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My Thoughts on Today’s CASE:

The challenge in this case is not to diagnose that there is an ongoing acute MI, since that is obvious. Instead — the objective is to figure out what may have happened when?

• The rhythm in Figure-1 is sinus at the relatively fast rate of ~95/minute.
• QRS duration looks to be at the upper limit of normal. The QTc is no more than borderline prolonged. There is no clear sign of chamber enlargement.

The remainder of this tracing is markedly abnormal. I’ve labeled the principal findings in Figure-2: 

• The most “eyecatching” findings are in anterior leads V1,V2,V3 (within the RED rectangle in Figure-2).
• Deep QS complexes are seen in these first 3 anterior leads (YELLOW arrows in leads V1,V2,V3).
• The T waves in leads V2,V3 are hyperacute — in that they are huge (taller than the S waves are deep in these leads) — with symmetric rise-and-fall, with a “fattened” peak and widened base. We instantly know that the cath lab needs to be activated! That said — I found it impossible to identify the J-point defining the amount of ST elevation, because the ascending limb of these hyperacute T waves is so smooth (I suspect there is at least 2-3 mm of ST elevation — but can’t prove this on the basis of this initial tracing).
• PEARL: T waves do not have to be as tall as they are here in order for them to be "hyperacute". There admittedly is some subjectivity in defining one or more ST-T waves as 'hyperacute". I generally classify ST-T waves in this way when, in a patient with acute symptoms — ST-T waves exceed "expectations" (ie, When there are one or more acutely angled or straightened ST segment takeoffs — with a "fatter"-than-expected peak and/or wider-than-expected T wave base).
• With experience — You'll know when an ST-T wave is "hyperacute".
• 
  
• It’s insightful to recognize that the ST-T wave in lead V1 is clearly abnormal! The coved shape that we see here, with ≥1 mm J-point ST elevation — is not normal in lead V1 (and this abnormal appearance provides an important clue regarding the “culprit” artery).
• In contrast to the hyperacute anterior T waves in Figure-2 — is the scooped ST depression in lateral chest leads V5,V6 (BLUE arrows in these leads).
• I interpreted lead V4 as a “transition” lead — in that it shows an “intermediate” pattern with less hyperacuity than its neighboring anterior leads, and less ST depression than its neighboring lateral chest leads.

There are comparable ST-T wave abnormalities in the limb leads:

• There is marked reciprocal ST depression in the inferior leads (BLUE arrows in leads II,III,aVF).
• Lead aVL is especially abnormal — with a deep and wide Q wave indenting a fragmented QRS, followed by an obvious hyperacute ST-T wave (showing ST segment straightening, ≥1 mm of J-point ST elevation with “fattened” T wave peak and widened T wave base).
• The other high-lateral lead ( = lead I ) shows less marked, but still hyperacute ST-T wave changes.
• NOTE: I am not as strict when defining neighboring leads as "hyperacute". For example, by itself — I might not classify lead I as being "hyperacute". But in the context of this patient with new CP — in association with such obvious hyperacuity elsewhere, especially in neighboring lead aVL — the "fatter"-than-expected peak and wide base of the lead I T wave qualifies by my subjective definition as being "hyperacute".

Figure-2: I've labeled today's ECG. What do you see?

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Putting It All Together:

Despite the younger age and seemingly benign prior history of today’s 30-ish year old man — determining the “culprit” artery, as well as “What happened when?” does not change the obvious need for prompt cath as soon as this can be accomplished. Virtually all leads on this tracing show marked ST-T wave abnormalities! 

• Q waves have been documented to develop in as short a time period as 1-2 hours. That said — it would seem unlikely for Q waves as large as we see in leads V1,V2,V3 (and in fragmented lead aVL) to develop over the 1 hour that this patient has had symptoms. I therefore suspected that some event had occurred prior to this patient's onset of CP (that only began 1 hour before he came to the hospital).
• The patient acknowledges "a similar episode about a week earlier" — so perhaps he had an initial event at that time.
• "Silent" MI (in which an acute MI occurs in the absence of CP) is a real entity (See ECG Blog #228). That said — "true" Silent MI is less common among previously healthy younger adults. As a result — it would be worthwhile to revisit the History — since sometimes patients overlook past symptoms unless specifically asked to, "Think back over recents days to weeks as to whether at any time you had chest discomfort or other symptoms that concerned you for a period of hours or a day or two".
• For as much as the very deep QS complexes in Figure-2 do not seem acute — the huge hyperacute T waves in leads V2,V3, with marked ST-T wave abnormalities in virtually all other leads clearly do look acute — and strongly suggest acute proximal LAD (Left Anterior Descending) occlusion (The abnormally coved ST elevation in lead V1 + hyperacute leads V2,V3 + scooped ST depression in leads V5,V6 — strongly suggest a Precordial Swirl pattern — as described in ECG Blog #380).

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The CASE Continues:

On seeing this patient's initial ECG — providers promptly activated the cath lab.

Cath Findings = multi-vessel disease:

• Left-dominant coronary system.
• 100% proximal LAD occlusion.
• 80% distal LCx stenosis.
• 95% left PDA stenosis.
• PCI was successfully performed in the proximal LAD, the distal LCx (Left Circumflex), and the left PDA (Posterior Descending Artery).
• Post-procedure ejection fraction was surprisingly preserved!

Final Thoughts:

Despite the patient's younger adult age and seemingly benign past medical history — cardiac cath revealed severe multi-vessel disease with acute proximal LAD occlusion as the cause of his acute event.

• Presumably the patient had an acute extensive anterior infarction superimposed on previous anterior infarction.
• The "good news" is that despite severe underlying coronary disease — this patient did survive, and left ventricular function following PCI was relatively preserved. 
• Discharge management clearly needs focus on risk factor reduction, consideration of preventive and maintenance medication (ie, antiplatelet therapy, statin, beta-blocker, ACE-inhibitor or ARB, etc.) — with need for good compliance with close clinical follow-up.

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Acknowledgment: My appreciation for the anonymous contribution of today's case. 

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ECG Blog #546 — Which Beat is Key?

 

I was sent this tracing ...

• The patient whose ECG is shown in Figure-1 is a man in his 60s with CKD (Chronic Kidney Disease) — who presented with "dizziness".

QUESTIONS:

It is immediately understandable why this patient may have dizziness — as the cardiac rhythm is obviously abnormal. 

• How to begin to assess this rhythm?
• HINT: Which one beat is KEY for our understanding of the etiology of the rhythm?

• And — What might be causing this rhythm?

Figure-1: I was sent this tracing — knowing only that it was from a man in his 60s with CKD. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts:

I fully acknowledge that it took me a moment to know how to proceed for assessing this rhythm. That's because the rhythm is clearly irregular with a number of different elements.

• PEARL #1: When you encounter a rhythm with multiple different elements (some of which are clearly more complex than others) — Start with the EASIER part(s)!
• Save those parts of the tracing that are more challenging to interpret for later ...

I was initially uncertain as to what I was seeing in Figure-1.

• I focused my attention on the long lead II rhythm strip. I highlight in Figure-2 the one beat that caught my "eye".

Figure-2: The KEY to today's rhythm is beat #2.

The KEY to Today's Rhythm ...

Beat #2 is the KEY to today's rhythm.

• Beat #2 is a sinus-conducted beat (RED arrow in the long lead II rhythm strip showing an upright sinus P wave with normal PR interval preceding this beat). I've highlighted this beat #2 within a RED rectangle in the picture of lead II from the 12-lead tracing.
• 
  
• PEARL #2: The reason beat #2 is so essential to understanding today's rhythm — is that this is the only beat that shows us what a "normal T wave" looks like!

QUESTION:

• Does PEARL #2 explain why the ST-T waves of beats #1,3,4,6,8,9 and 11 look different than the ST-T wave of beat #2?
• HINT: Check out Figure-3 ...

Figure-3: What is suggested by the YELLOW arrows?

ANSWER:

Beat #2 is the only sinus-conducted beat in this tracing.

• All beats in Figure-3 (with the exception of beat #10) manifest a narrow QRS complex. This confirms that all of these narrow beats are supraventricular. Since no P wave precedes beats #1,3,6,8,9 and 11 — these must be junctional escape beats.
• 
  
• PEARL #3 (Advanced concept!): Although the shape of the junctional escape beats looks similar to the shape of sinus-conducted beat #2 — the escape beats following each of the short pauses in the long lead II rhythm strip ( = beats #1,3,6,8,9,11) all appear to be slightly taller than the one sinus-conducted beat #2.
• On occasion in complex arrhythmias — it may be difficult to tell if one or more beats are sinus conducted vs escape beats from the AV Node. Awareness of a slight difference in appearance in the QRS complex of escape beats in such a tracing may provide a subtle clue as to whether or not these beats are being conducted. (An example of this advanced concept in which awareness of a slightly different QRS shape immediately tells you which beats are "escape" vs conducted beats — is seen in ECG Blog #63).

PEARL #4: The most plausible reason for the negative deflections that are highlighted by YELLOW arrows in the long lead II rhythm strip of Figure-3 — is that these negative deflections are the result of retrograde P waves that arise from the junctional escape beats.

• Note that the RP' interval (ie, the distance from the R wave of beats #1,3,6,8,9,11 in Figure-3 — until the negative deflection that follows) is the same!
• Note also that another QRS complex follows the retrograde P waves of beats #3, 6, 8 and 9 to produce beats #4,7, and 10. These beats #4,7 and 10 are called "Echo" beats (because rather than conducting down to the ventricles, the atrial impulses prior to these beats "turned around" and were directed back to the atria).

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Laddergram Illustration:

Today's rhythm is admittedly complex. That said — it offers a superb example of how drawing a laddergram serves to facilitate our understanding the mechanism of an "escape-capture" rhythm in which "capture" is the result of retrograde P waves that produce "echo" beats.

• I guarantee that this complex mechanism will become clearer by following my sequential derivation of today's laddergram — beginning with the legend in Figure-4.

Figure-4: As discussed above — beat #2 is the only sinus-conducted beat in today's tracing (as it is the only beat that is preceded by an upright P wave in this long lead II rhythm strip).

Figure-5: The next step in drawing today's laddergram — is to fill in the Ventricular Tier. I do this by drawing in near-vertical RED arrows to represent rapid conduction through the ventricles of narrow beats #1,3,4,5,6,7,8,9, and 11 (I'll explain beat #10 momentarily).
The large BLUE arrows in this figure schematically show that I timed each of the RED arrows in the Ventricular Tier to the occurrence of these beats in the rhythm strip.

Figure-6: As discussed in my explanation before beginning to draw this laddergram — We know that beats #1,3,6,8,9,11 are all junctional "escape" beats, because each of these beats follows a similar duration short pause, and none of these beats are preceded by P waves. I represent the AV Nodal origin of these escape beats by RED circles placed within the AV Nodal Tier.

Figure-7: I next represent the timing retrograde P waves by dotted BLUE lines that schematically show conduction back to the atria.

Figure-8: Conduction through the AV Node is slower than conduction through the atria. I schematically show this by the angled dotted BLUE lines that I've added in Figure-8 to represent retrograde conduction back to the atria from each of the junctional escape beats. This leaves me with having to explain how beats #4,5,7 and 10 come about! (which I do in Figure-9). 

Figure-9: The most plausible way to explain beats #4,7 and 10 — is that these must be "echo" beats, in which the retrograde impulse arising from junctional beats #3,6 and 9, turns around to produce forward conduction of beats #4,7,10. But this now leaves me having to explain how beat #5 comes about! (which I do in Figure-10).

Figure-10: Beat #5 must be another "echo" beat. And the only way I can explain how this might come about — is if during the forward path of conduction through the AV node on the way to produce beat #4 — there once again is retrograde conduction back to the atria (dotted BLUE line in this Figure-10).

Figure-11: The solid BLUE line that I've now added in this Figure-11 completes the laddergram. Thus, this figure shows the presence of 2 successive "echo" beats ( = beats #4 and 5).
Note in this Figure-11 that retrograde conduction back to the atria, followed by forward conduction to produce another QRS complex does not always occur. The reason why it sometimes does, and sometimes does not occur is not clear.

Figure-12: This is the completed laddergram. All that remains is to explain why the QRS of beat #10 is wide? (which I do in today's Figure-13 by going back to the original 12-lead tracing).

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Putting It All Together: 

Whenever we encounter a complex arrhythmia — it's important to always go back to the clinical situation and the original 12-lead tracing.

• The only history we were provided with for today's patient — is that this man in his 60s presented with "dizziness" — and that he has a history of CKD (Chronic Kidney Disease).
• Armed with awareness that hyperkalemia is notorious for producing unusual arrhythmias that are often featured by bradycardia and unusual forms of AV conduction disturbances — checking the serum K+ level is essential in today's case.
• Although subtle — I thought a number of chest lead T waves to be more peaked than expected, leading me to suspect some degree of hyperkalemia as a contributing factor. (Unfortunately — I was unable to find out the serum K+ level in today's case).
• Attention to the ST segments in leads V3,V4,V5 (within the BLUE rectangle in Figure-13) — suggests ST segment straightening and some ST depression. Perhaps this represents a recent or acute posterior OMI that may be responsible for the bradycardia with junctional escape beats? (Unfortunately — I was unable to obtain follow-up regarding this possibility in today's case).
• Finally — If we look in Figure-13 at the simultaneously-recorded chest leads for beat #10 — it becomes apparent that this beat is conducted with RBBB aberration (rsR' for beat #10 in lead V1 — with a wide terminal S wave in lead V6 for beat #10). This explains why beat #10 in the long lead II rhythm strip looks different and is slightly wider than other beats in this tracing. 
• It also explains why beat #7 in the long lead II rhythm strip is shorter than other beats in this tracing (Beat #7 is being conducted with incomplete RBBB aberration — as suggested by the rSr' morphology of beat #7 in simultaneously-recorded lead V1).  

Figure-13: Returning to today's original 12-lead tracing (See text).

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Acknowledgment: My appreciation to 林柏志 (from Taiwan) and M Shah (from Srinagar, India) — for allowing me to use this case and this tracing.
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ECG Blog #545 — Is the Rhythm VT?

The ECG in Figure-1 was obtained from a 60-something year old man — who presented with a history of recurrent palpitations over the past several years. He was hemodynamically stable with this rhythm.

• Prior to the onset of these episodes of palpitations — the patient had been healthy without medical problems.

• Of note — the patient recently developed ankle edema with progressively increasing dyspnea on exertion.

QUESTIONS:

• How would you interpret the rhythm in Figure-1? 
• What clinical entity is suggested by the above history?

  

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

My Thoughts on Today's CASE:

As frequently reviewed on this ECG Blog — I favor the Ps,Qs,3R Approach for assessment of tachycardias (See ECG Blog #185 — for review of this system).

• The rhythm in Figure-1 is Regular at a Rate of ~150/minute.
• The QRS is wide (ie, ≥0.12 second).

Regarding the 4th and 5th parameters of the Ps, Qs and 3Rs:

• P waves are absent — which by definition means there is no Relation between P waves with neighboring QRS complexes (since there are no P waves).

Impression: The ECG in Figure-1 shows a regular WCT (Wide-Complex Tachycardia) at ~150/minute.  

• Statistically in an adult of a certain age — We start with the reality that 80-90% of regular WCT rhythms without sinus P waves will turn out to be VT. Therefore — Assume VT until proven otherwise. Treat the patient accordingly.
• That said, since this patient is hemodynamically stable — You have at least a moment in time to look closer at the rhythm for features that might increase (or decrease) your diagnostic likelihood of an 80-90% chance that the rhythm is VT.

As illustrated in last week's ECG Blog #544 — Among the most time-efficient and helpful ECG features that I look for are the following:  

• The frontal plane axis during the WCT rhythm. 
• Other potential signs of atrial activity.
• QRS morphology.

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Looking Closer at Figure-1 ...

In today's case — neither the frontal plane axis nor searching for signs of atrial activity help to provide an answer:

• Although the frontal plane axis during the WCT rhythm is markedly leftward — the axis does not satisfy my definition of an "extreme" axis (because the QRS is not entirely negative in either lead I or lead aVF). Instead — a small-but-definitely-present upright initial positive deflection (r wave) is present in lead aVF. As a result — assessment of the frontal plane axis is not sufficiently discriminating to be helpful.
• I see no clear indication of atrial activity in Figure-1. This feature is therefore of no assistance for determining the etiology of today's rhythm.

QRS Morphology during the WCT:

This leaves us with assessing QRS morphology in our hope to increase statistical likelihood beyond the 80-90% likelihood that we start with by simply knowing that today's rhythm is a regular WCT without clear sign of sinus P waves.

• As emphasized in ECG Blog #211 — the chance that a WCT rhythm will turn out to be supraventricular will significantly increase IF — we can demonstrate that QRS morphology is typical for one of the known forms of conduction block (ie, RBBB, LBBB, LAHB or LPHB; or RBBB with one of these hemiblocks).

PEARL #1: The entity of fascicular VT marks an exception to the general rule that when a regular WCT resembles a bifascicular block — that the rhythm is likely to be supraventricular. The reason for this — is that by definition, “fascicular VT” will resemble one of the hemiblock forms (ie, either RBBB/LAHB or RBBB/LPHB). 

• The KEY to recognizing that a regular WCT rhythm that bears a certain resemblance to an rbbb conduction pattern (with either marked left or right axis deviation) is unlikely to represent a supraventricular rhythm — is that there are some features that are atypical for rbbb conduction with either LAHB or LPHB.
• To Emphasize: QRS morphology is not a perfect science. Even in the best of hands — nothing is perfect (ie, It is always possible that prior scarring from cardiomyopathy or previous infarction will result in a markedly abnormal baseline tracing during sinus rhythm).
• This leaves us with the clinical reality that much of the time — we'll need to begin our treatment of a regular WCT before we know for certain what the etiology of the rhythm is. That said — I find it helpful to be aware of the relative probability for VT vs some type of SVT rhythm before I contemplate therapeutic options for treatment.

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Take another LOOK at today’s initial ECG:

I've reproduced today's initial ECG in Figure-2. 

• Does QRS morphology during the WCT rhythm in Figure-2 look like one of the known forms of conduction block?

  

Figure-2: I've reproduced today's initial ECG. 

Answer:

YES — Today's initial ECG that is shown in Figure-2 does resemble the RBBB/LAHB form of bifascicular block. That said, as I suggest below in Figure-3 — there are some atypical features:

• PEARL #2: Although the possibility of rbbb conduction is suggested by the all upright QRS in lead V1 — a triphasic rsR' morphology is lacking (ie, in which there is an s wave that descends below the baseline with a terminal taller right "rabbit ear" R’ wave in lead V1). 
• As discussed in detail in ECG Blog #211 — whereas not all patients with RBBB necessarily manifest a classic triphasic rsR' morphology — the finding of an entirely upright monophasic R wave that we see in lead V1 of Figure-3 could be either the result of supraventricular rbbb conduction or this could be VT. Therefore — the resemblance that we see in lead V1 to rbbb conduction is not helpful in distinguishing between SVT vs VT.
• PEARL #3: The other characteristic feature of rbbb conduction is the presence of a wide terminal s wave in lateral leads I and V6. And although in Figure-3 we do see a terminal s wave in both leads I and V6 (the YELLOW arrows in these leads) — this terminal s wave is narrow in lead I and tiny in lead V6.
• PEARL #4: The typical appearance of lahb conduction — is for there to be rS waves (with predominant negativity) in each of the inferior leads. And although there are initial r waves in leads II,III,aVF — these initial r waves are extremely small in leads II and aVF (YELLOW arrows in these leads) — which is not the typical picture for QRS morphology with lahb conduction.
• PEARL #5: The initial vector of depolarization tends to be fast with supraventricular conduction (because electrical activity once it reaches the ventricles — begins within the His-Purkinje system). In contrast — the slope of the initial depolarization vector tends to be slower with VT (because electrical activity begins away from the conduction system — from within ventricular myocardium). 
• Instead of a more vertical upslope — the R wave in lead I rises at a slower rate than I'd expect with supraventricular conduction (BLUE arrow in this lead).
• PEARL #6: An insensitive, but highly specific morphologic feature to be aware of when assessing a WCT rhythm — is that IF there is either global positivity or global negativity in all 6 chest leads (ie, Leads V1-thru-V6 being either all positive or all negative) — then the etiology of the rhythm is almost certain to be VT.
• There would be global positivity in leads V1-thru-V6 in Figure-3 — if it were not for tiny intermittent s waves in lead V2; and in leads V4,V5,V6. These tiny s waves reduce specificity of this finding for VT (albeit the nearly all positive chest lead QRS morphology remains highly suspicious for VT).

Bottom Line: While fully acknowledging that QRS morphology is not definitive for either VT or a supraventricular etiology in today's initial ECG — the above atypical features made me strongly suspect left posterior fascicular VT as the diagnosis.

Figure-3: I've labeled key features regarding QRS morphology.

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The CASE Continues:

The patient was treated for presumed VT with IV Amiodarone, but without success. Electrical cardioversion was applied, which transientlly converted the rhythm — only to result in recurrence of the regular WCT moments later. 

• The patient's condition deteriorated requiring intubation.
• Persistence of the regular WCT led to marked hypotension with cardiogenic shock.
• Finally — overdrive pacing successfully converted the WCT. The resultant rhythm is shown in the bottom tracing in Figure-4.

QUESTIONS:

• Does the repeat ECG recorded after successful overdrive pacing shed light on the etiology of today's initial ECG?
• Going back to the history that we were given at the beginning of today's case (ie, that this 60-something patient had been having recurrent palpitations over a period of years — with recent development of ankle edema and increasing dyspnea on exertion) — What clinical entity is suggested?

Figure-4: Comparison between today's initial ECG — and the repeat ECG recorded after successful overdrive pacing.

CASE Conclusion:

The "good news" is that this patient improved greatly after overdrive pacing successfully converted the WCT rhythm.

• The repeat ECG in Figure-4 — shows restoration of sinus rhythm. The remarkable finding is that QRS morphology in sinus rhythm is almost identical during the WCT and during sinus rhythm.
• ECG #2 shows a sinus rhythm at a rate just over 60/minute.
• There is bifascicular block (RBBB/LAHB).
• There is LVH (R wave in lead aVL ≥12 mm; R wave >18 mm in lead V6).
• ST-T waves do not look acute (The inverted T waves in the inferior leads are not necessarily abnormal given the predominantly negative QRS complexes in these leads — and chest lead ST-T wave changes are most likely secondary to the RBBB and to LVH).

• PEARL #8: Cases like today keep us humble! Despite strong suggestion from QRS morphology that today's WCT rhythm was fascicular VT — the finding of nearly identical QRS morphology in the repeat ECG after overdrive pacing tells us that the rhythm in ECG #1 was a reentrant SVT rhythm (and not fascicular VT). 
• This highlights the importance of being aware that "atypical" QRS morphology during a regular WCT rhythm may occasionally be the result of a markedly abnormal baseine ECG (and not VT).

PEARL #9: The patient's history of frequent episodes of recurrent palpitations over a period of years (ie, with recent development of ankle edema and worsening dyspnea on exertion) suggests development of TICM (Tachycardia-Induced CardioMyopathy). Over time, this so depressed LV function as to result in progressively increasing heart failure (See Nerheim et al: — Circulation 110(3):247-252, 2004 — and — Huizar et al: JACC 73(18):2328-2344, 2019 — for more on TICM).

• Although TICM typically takes weeks (or longer) to develop after exposure to a persistent tachyarrhythmia — it's important to be aware that TICM may develop in as little as 3 days!
• Fortunately — the depressed LV function that occurs with TICM is usually reversible after rate control is achieved (ideally with conversion to sinus rhythm). Return to normal LV function may be surprisingly fast (within days to a few weeks).  A majority of patients recover within 6 months.
• Unfortunately, if the tachyarrhythmia recurs — deterioration of LV function tends to be rapid. As a result — longterm monitoring of the patient's heart rate is essential.

Final Disposition: Today's patient was referred to EP Cardiology. EP study revealed the etiology of today's WCT rhythm to be recurrent AVNRT with dual AV nodal pathways. Ablation of the extra pathway resulted in "cure" of the patient's arrhythmia.

• Normal LV function returned soon after resolution of the arrhythmia. This rapid response to treatment proved that the patient's heart failure was indeed the result of TICM.

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Acknowledgment: My appreciation to Mohammed Elsisi (from Benha City, Egypt) — for allowing me to use this case and this tracing.

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For Additional Review:

• See ECG Blog #489 — for insightful review of another case that illustrates my approach to a patient with suspected fascicular VT.

 

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