ECG Blog #551 — Are there any "Normal" Beats?

I was sent the ECG in Figure-1 — told only that it was from a middle-aged man who presented for acute CP (Chest Pain). 

QUESTIONS:

• What is going on?
• How to approach interpreting this ECG?
• What is the rhythm?

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

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My Approach:

As always (assuming your patient is stable and not in need of immediately cardioversion) — I favor a systematic approach, beginning with a quick look at the rhythm ==> "Watch your Ps,Qs, and the 3Rs" (as reviewed in ECG Blog #185).

• I vary which of these 5 KEY parameters I look at first — depending on particularities of the rhythm (and depending on which of these 5 parameters are easiest to recognize).
• In today's case, as I looked at the long lead II rhythm strip — I was struck by the almost beat-to-beat variability in QRS morphology. That said — many of the beats look to be narrow, suggesting the underlying rhythm is supraventricular.
• P waves are present!

PEARL #1: The simple step of labeling P waves is often surprisingly helpful in figuring out what is going on. I have done this in Figure-2 (RED arrows highlighting those P waves that I can definitely identify).

• What do we learn from Figure-2?

Figure-2: I've labeled those P waves that I can definitely identify.

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What We Learn from Figure-2:

• The underlying rhythm in today's tracing appears to be sinus — as upright P waves with a constant and normal PR interval are seen in front of beats #1,3,4,6,8,11,13 and 15.
• I look for 2 sinus-conducted beats in a row — since if the underlying atrial rhythm is regular, seeing 2 sinus-conducted beats in a row will suggest what the P-P interval is (We see this for beats #3 and 4). The R-R interval between beats #3 and 4 is just over 3 large boxes — suggesting the presence of an underlying sinus rhythm at ~90/minute.
• NOTE: Although we do not clearly see P waves throughout the entire tracing in Figure-2 — the constant P-P interval between consecutive RED arrow P waves that we do definitely see suggests that there probably is a regular underlying P wave rhythm. 

PEARL #2: By far, the most time-effective way to interpret today's complex tracing — is to use calipers! Simply stated — I could not have determined today's rhythm with any degree of certainty without using calipers. And, by using calipers — it took me literally no more than 5 seconds to establish the conclusions that become obvious on viewing the long lead II rhythm strip that I've labeled in Figure-3:

• The underlying atrial rhythm is regular. 
• In addition to the RED arrow P waves that we definitely see — the PINK arrows in Figure-3 highlight "on time" sinus P waves that partially deform some part of the QRS.
• Even though we do not see any deformation of beat #10 — it makes sense that another "on time" sinus P wave is hidden entirely within this beat ( = the WHITE arrow drawn over beat #10).
• 
  
• PEARL #3: The PR interval for all of the "on time" PINK arrow P waves is too short to conduct normally. This establishes the presence of intermittent AV dissociation — and this proves that beats #2,5,7,14 and 16 must all be ventricular beats.
• The reason for slight variation in QRS morphology for these ventricular beats is that there is some degree of fusion between sinus-conducted P waves and the ventricular beats that follow so soon thereafter that they interrupt conduction of sinus-initiated impulses through the ventricles (See ECG Blog #128 — for more on fusion beats).
• Fusion is unlikely for beat #10 — because the "on time" WHITE arrow P wave occurs too late to be able to enter the ventricles in time to conduct. The fact that the WHITE arrow P wave arrives in the ventricles too late to conduct provides insight as to what PVCs will look like in lead II — and therefore also what PVCs will look like in simultaneously-recorded leads V1,V2,V3. 

Figure-3: Using calipers — I’ve added PINK arrows and a WHITE arrow where I expect "on time" P waves to be partially or totally hiding throughout today’s long lead II rhythm strip.

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Focus for a moment on these 4 simultaneously-recorded leads ( = leads V1,V2,V3 — and lead II in the long lead rhythm strip) For clarity — I facilitate doing this in Figure-4. 

• It should now be obvious from Figure-4 — that beat #11 looks different than the 3 other beats in leads V1,V2,V3, and in the long lead II. This is because the only normal sinus-conducted impulse among these 4 beats is this beat #11.
• Beats #9,10 and 12 are ventricular (presumably with some degree of fusion for beats #9 and 12). 

Figure-4: Focus on the 4 simultaneously-recorded leads V1,V2,V3; and on the long lead II for the purpose of highlighting QRST morphology of beats #9,10,11,12).

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Putting It All Together:

Now that we know from Figure-4 that beat #11 in the long lead II rhythm strip manifests the QRST morphology of a normal sinus-conducted beat — We can go back to Figure-3 to figure out which of the 16 beats in today's ECG are sinus conducted without partial fusion from ventricular beats:

• Beats #1,3,4,6,8,11,13 and 15 are all purely sinus-conducted.
• 
  
• PEARL #4: Assessment of ST-T wave morphology for the presence of acute ischemic changes is best done from assessment of normally conducted sinus beats.

In Figure-5 — I have selected simultaneously-conducted sinus beats in each of the 4 major lead groups (within the 4 dotted BLUE rectangles).

Figure-5: Within each of the 4 dotted BLUE rectangles — are simultaneously recorded sinus beats from each of the 4 lead groups.

To facilitate visualization of QRST morphology in each of the 4 lead groups — I have modified Figure-5 by shading out the other beats in Figure-6.

• Isn't it now much easier to appreciate marked acute ST elevation in the anterior leads? ( = beat #11 as it is seen in leads V1,V2,V3 in Figure-6)?
• Completing the pattern of Precordial Swirl that is diagnostic of acute proximal LAD occlusion (See ECG Blog #380 — for more on Precordial Swirl) — is ST depression in lateral chest leads V5,V6 (beat #13). 
• Normal sinus-conducted beats #3 and #6 reveal large Q waves with slight ST elevation in inferior leads III and aVF — and ST depression in leads I,II,aVL. There is also some ST elevation in lead aVR.

Figure-6: To facilitate visualization of acute ST-T wave changes in each of the 12 leads for sinus-conducted beats — I've shaded out other beats on this tracing.

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CASE Conclusion:

Unfortunately — I lack follow-up and the results of cardiac catheterization. Nevertheless, given the history of new CP — I feel confident in concluding the following from today's initial ECG that I have once again reproduced in Figure-7.

• The underlying rhythm in Figure-7 is sinus.
• The reason for the frequently changed QRS morphology in the long lead II rhythm strip is superimposed AIVR (Accelerated IdioVentricular Rhythm) at a rate of ~115/minute. As reviewed in ECG Blog #108 — in the setting of an acute evolving OMI, AIVR is often a "reperfusion" arrhythmia that is usually short-lived, and which usually does not require specific antiarrhythmic treatment. Instead, prompt cath with PCI is needed to prevent reocclusion of the "culprit" artery.
• The reason today's ECG is so challenging to interpret — is the frequent occurrence of fusion beats that results in constantly changing QRS morphology.
• Shading out these fusion beats (as was done in Figure-6) facilitates recognition of acute proximal LAD occlusion (Precordial "Swirl" pattern — with hyperacute anterior lead ST elevation and flattened ST depression in leads V5,V6 — as described in ECG Blog #380).
• The large inferior Q waves + ST depression in leads I,II,aVL,V5,V6 in association with ST elevation in lead aVR suggests that there may be multi-vessel disease (and/or prior inferior infarction) vs extensive LAD occlusion with "wraparound". But the message is clear ==> acute proximal LAD occlusion with immediate need for cardiac cath with PCI.

Figure-7: Today's ECG with "on time" P waves labeled. 

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

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ECG Blog #550 — Guess the Clinical Setting

The ECG in Figure-1 was obtained from a middle-aged man who presented with CP (Chest Pain). I was asked for my thoughts on the rhythm.

QUESTIONS:

• What is the rhythm?
• How certain are you of your answer?
• What is the probable cause of this rhythm?

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

My Approach to Today's Tracing: 

We are at a distinct disadvantage in Figure-1 for determining the rhythm. This is because we only see 9 beats, and because we lack a long lead rhythm strip. Nevertheless, a number of deductions can confidently be made.

• PEARL #1: LIfe is easier — IF we simply number the beats (as I have done in Figure-2). Doing so allows us to talk intelligently with colleagues about what is going on (as well as making it easier for us to appreciate relationships between P waves and neighboring QRS complexes).

Take Another Look in Figure-2:

• HINT:  Look first at the chest leads ...

Figure-2: I've numbered the beats in today's tracing.

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What We See in Figure-2:

P waves are present in front of beats 7,8,9 (RED arrows in Figure-3):

• The P wave in front of beat #7 is clearly too short to be normally conducted to the ventricles. Thus, at least for this one beat #7 — there is AV dissociation (which simply means that the P wave in front of beat #7 is not completely conducting this QRS complex).

Figure-3: RED arrows highlight the presence of sinus P waves.

PEARL #2: Recognizing that the PR interval in front of beat #7 is too short to be a normal sinus-conducted beat is the KEY clue to today's rhythm — as it tells us that beat #7 must be a ventricular escape beat!

• In contrast — the QRS complex in front of beats #8 and 9 is narrow, very different-looking than the QRS of beats #7,8,9 — and, the PR interval in front of beats #8 and 9 is constant and long enough to be sinus-conducted (I measure the PR interval in front of beats #7,8 to be ≥0.13-0.14 — and the PR interval might be longer if we were to see P waves in lead II).
• This tells us that beats #5 and 6 must be ventricular escape beats at the slightly accelerated rate of ~55/minute (the R-R interval between beats #5-6 and 6-7 being between 5-to-6 large boxes). 
• 
  
• PEARL #3: If we focus our attention on lead V3 — Doesn't the QRST complex of beat 7 look slightly different than the QRST of beats #5 and 6? (At least in lead V3 — the QRS and T wave of beat #7 are a little less tall than for beats #5 and 6). This tells us that beat #7 is a fusion beat, and proves that beats #5 and 6 are ventricular in origin (See ECG Blog #128 — for more on fusion beats).
• NOTE: It makes sense that beat #7 is a fusion beat — because the PR interval in front of this beat is just a little bit shorter than the PR interval of the sinus-conducting P waves in front of beats #8 and 9 (as we'll see momentarily in the Laddergram in Figure-5).

PEARL #4: That beats #5 and 6 are ventricular escape beats — is supported by another look at QRST morphology of beats #1-thru-4 in the limb leads:

• Note in lead I — that the QRS complex begins with a very deep and wide Q wave! We virtually never see such a deep and wide initial negative deflection in left-sided lead I with normal sinus conduction. Thus, this initial deep and wide Q wave in lead I strongly suggests a ventricular etiology for the 4 beats in this lead.
• PEARL #5: Note the subtle-but-real negative deflection at the end of the QRS in each of the 3 inferior leads (YELLOW arrows in Figure-4 highlighting this negative deflection in lead III — but with a similar terminal negative deflection also being seen in leads II and aVF). This terminal negative notch most likely reflects retrograde conduction of the P wave from ventricular beats #1,2,3,4.
• I suspect retrograde conduction continues in the chest leads, and is seen after beats #5 and 6 — until slight acceleration of the underlying sinus P wave rhythm allows the RED arrow P waves in front of beats #8 and 9 to recapture the ventricles with sinus-conducted beats #8 and 9 (See the laddergram below in Figure-5). 

Figure-4: YELLOW arrows suggest retrograde conduction of P waves following ventricular escape beats.

Figure-5: Laddergram suggesting the mechanism of today’s rhythm.

My Impression: I suspect the rhythm in Figure-5 begins with 7 beats of AIVR (Accelerated IdioVentricular Rhythm) at ~55-60/minute — and ends with 2 sinus-capture beats ( = beats #8 and 9).

• The first 6 ventricular beats manifest retrograde P waves (dotted RED lines in the laddergram that are headed back to the atria).
• Slight acceleration of the rate of sinus impulses allows the RED arrow P waves to recapture the ventricles with beats #8 and 9.
• The overly short PR interval and intermediate shape of the QRS complex and of the T wave for beat #7 — suggests this is a fusion beat. Early arrival of this 1st RED arrow P wave in the ventricles prevents retrograde conduction of ventricular beat #7 — which therefore makes it possible for the 2nd RED arrow P wave to “capture” the ventricles with a sinus-conducted beat.

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Putting It All Together:

• Today’s patient presented with CP.
• The underlying rhythm in the initial ECG appears to be sinus bradycardia and arrhythmia that is intermittently interrupted by AIVR at a rate of ~55-60/minute.
• 
  
• PEARL #6: The combination of AIVR in a patient who presents to the ED for CP — is commonly seen during the evolution of an acute OMI ( = Occlusion-based Myocardial Infarction). As a result — We need to go back and Take Another LOOK at the initial ECG in today's case, looking to see if there might be subtle ECG clues of a recent OMI (keeping in mind that acute ST-T wave changes of an OMI may be difficult to recognize in the presence of a ventricular rhythm such as AIVR).

PEARL #7: When AIVR is seen in association with an evolving OMI (as is especially likely when the patient presents with CP, as in today's case) — it often represents a reperfusion arrhythmia (See ECG Blog #108 — for the basics regarding AIVR).

• As a result — correlating each serial ECG with the presence and severity of CP becomes especially important for understanding the sequence of events (and for determining whether the "culprit" artery is likely to be open or closed at the time a given ECG is recorded). 
• In today's case — We would want to find out IF this patient's CP had decreased (or resolved) at the time the initial ECG was recorded. If symptoms are less at the time of this initial ECG before any treatment has been administered — this would suggest that there has been spontaneous reperfusion of the "culprit" artery (in which case ECG signs of acute infarction may be especially subtle!).

In Figure-6 — I've reproduced today's initial ECG.

• Take another LOOK at this initial ECG — with special attention looking for subtle signs of recent infarction.

Figure-6: I've reproduced today's initial ECG.

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Subtle ECG Signs of Recent Infarction:

Despite the presence of AIVR (and the likelihood of sponaneous reperfusion) — I thought there are subtle ECG signs of recent infarction in today's initial ECG (See labeled Figure-7 below):

• I focused first on the 2 sinus-conducted beats — since assessment of ST-T waves for acute changes is more reliable when seen in normally conducted beats than it is when looking at ventricular beats ( = beats #8 and 9 — within the RED rectangle in Figure-7).
• The amount of ST elevation in lead V2 for beats #8,9 looks to be disproportionately increased given modest depth of the S wave in these sinus-conducted beats.
• The ST segment takeoff in lead V3 looks to be straightened for sinus-conducted beats #8,9.
• There is ST segment straightening with slight depression in lateral chest lead V6 (BLUE arrow in this lead).   

To Emphasize: Acute ST-T wave changes can sometimes be seen in ventricular beats. It's just that these changes tend to be subtle and more difficult to recognize than when acute changes are seen in normally conducted beats:

• In the limb leads (which show 4 consecutive ventricular beats) — the overly "bulky" and depressed ST-T waves in each of the inferior leads looks disproportionate and "off" for what I'd expect given modest QRS amplitude in leads II,III,aVF (RED arrows in these leads).
• Given this inferior lead ST-T wave appearance — the elevated and overly large upright T waves in leads I and aVL manifest the mirror-image opposite picture of what we see in the inferior leads (BLUE arrows in leads I and aVL).
• In the chest leads — the ST-T wave in lead V2 looks to be disproportionately large, with an angled and overly elevated J-point for the ventricular beats. Especially in leads V4,V5,V6 — the T waves look disproportionately large given the tiny size of the QRS in these lateral chest leads (RED arrows in the above noted chest leads for ventricular beats #5,6,7).

Impression: The above noted subtle signs in multiple leads of Figure-7 in this patient with CP and intermittent AIVR are suggestive of a Precordial "Swirl" pattern from recent acute LAD occlusion (See ECG Blog #380 — for review of Precordial Swirl).

• To Emphasize: The above ECG findings are subtle! But especially IF this patient's CP was less (or resolved) at the time the ECG in Figure-7 was recorded — we are expecting less obvious ECG signs than what would probably have been seen if severe CP was still present.

Figure-7: I've labeled a series of subtle ST-T wave abnormalities present in Figure-6 that suggest there has been a recent OMI.

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The CASE Concludes:

Providers were appropriately concerned by this patient's history of new CP in association in association with today's initial ECG.

• Cardiac cath was performed in a timely manner — and revealed acute proximal LAD occlusion, amenable to PCI. 
• A repeat ECG done the next day after successful PCI is shown below in Figure-8.

QUESTIONS:

• How do you interpret the repeat ECG in Figure-8?
• How do beats #8 and 9 in ECG #2 compare with beats #8 and 9 in Figure-7?
• Why might the voltage be so low in Figure-8?

Figure-8: Repeat ECG done the day after successful PCI.

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ANSWERS:

AIVR has resolved — with reestablishment of a sinus rhythm in the repeat ECG recorded after successful PCI (RED arrows showing sinus bradycardia at ~55/minute throughout the tracing in Figure-9).

• Note that all 5 sinus-conducted beats in the chest leads of this repeat ECG look identical to sinus-conducted beats #8 and 9 in today's initial ECG.
• Note that the QRS in Figure-9 is now narrow in all beats — whereas the QRS was wide for the ventricular beats in Figure-6. The wide initial Q wave in lead I that tipped us off in the initial ECG to the presence of AIVR is no longer present.
• There is poor R wave progression in the chest leads of Figure-6 (a QS is present in leads V1,V2 — and transition to a predominant R wave never occurs). This is consistent with this patient's recent anterior MI.
• This post-PCI tracing is also remarkable for diffuse low voltage (No R wave exceeding 5 mm in the limb leads — with overall reduced QRS amplitude also in the chest leads). As highlighted in other cases on this ECG Blog — the finding of low voltage in a patient with recent infarction may be a sign of myocardial "stunning", with reduced cardiac output (See ECG Blog #272 — for more on the causes of low voltage).

Figure-9: I've labeled sinus P waves in the repeat ECG.

Final Thoughts:  

Common things are common. Recognition of AIVR in a patient who presents with CP is an important clue to the likelihood of recent infarction. This should prompt:

• Attention to the details of the patient's history — with efforts to closely correlate the presence and relative severity of CP to the timing of each ECG. Recognition of AIVR at a time when the patient's CP has decreased or resolved is an important clue that spontaneous reperfusion may have occurred.
• ECG signs of recent infarction may be especially subtle following spontaneous reperfusion — as was probably the case for today's initial ECG.
• The ECG signs of recent infarction in Figure-7 are admittedly subtle! That said — these subtle signs become much easier to recognize when you know that the combination of CP and AIVR is commonly seen following recent infarction (and when you know that ECG clues may be very subtle if the patient's CP has decreased or resolved at the time the initial ECG was recorded).

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Acknowledgment: My appreciation to Ali Ibrahim (from Tikrit, Iraq) for allowing me to use this case and these tracings. 

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ECG Blog #549 — No Chest Pain

The ECG in Figure-1 is from a middle aged woman who presented with palpitations and dizziness of 2 hours duration. No chest pain. BP ~120/70 mm Hg.

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

QUESTIONS: 

• How would you interpret the ECG in Figure-1?
• Do the wide beats represent NSVT (Non-Sustained Ventricular Tachycardia) — or aberrant conduction?
• How certain are you of your answer? 
• What would you do?
• Does this ECG show anything else?

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DISCLAIMER:

My follow-up of the above case is unfortunately limited. That said — What counts is your approach to this arrhythmia. 

• This matches the clinical reality that we so often encounter — that is, seeing a patient for whom we need to initiate management before we know for certain what the diagnosis is.

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I've numbered the beats in Figure-2.

Take Another LOOK at this ECG ...

• What are the hints in this tracing that either point to the likelihood of VT? — vs suggesting that the wide beats are aberrantly conducted?

Figure-2: I've numbered the beats in today's tracing.

MY APPROACH:

The simple step of numbering the beats is surprisingly helpful!

• Numbering the beats instantly allows better appreciation of the relationship between the elements of a complex tracing.
• It also allows you to intelligently discuss the case with others (Since otherwise, valuable time will inevitably be lost trying to figure out which beat(s) is being discussed).
• NOTE: We lack a long lead rhythm strip in today's case. If I was seeing this patient in real time — I would immediately record a period of ongoing monitoring in a long lead II, since otherwise there is no way to know for sure IF the frequent changes in QRS shape that we see in the 12-lead tracing are the result of a single QRS morphology or multiple QRS morphologies arising from multiple sites in the ventricles.

My Observations:

The "good news" — is that although today's patient is symptomatic (ie, with palpitations and dizzyness) — she appears to be at least relatively hemodynamically stable (ie, without chest pain — in association with a BP = 120/70 mm Hg). This leaves us with at least a moment of time to try to determine — What is the underlying rhythm?

• To answer this question — I focused my attention on the narrow beats in Figure-2. These are beats #7,8,9; 11,12,13; 15,16,17; and 23,24,25.
• Note that no P waves are seen anywhere in Figure-2 (ie, Although we see multiple small undulations in the baseline — We do not see any with a consistent enough shape to verify as truly being P waves).
• Note also that the overall heart rate of the narrow beats in this tracing is fast — with a constantly changing R-R interval that is less than 3 large boxes in duration ( ==> the average ventricular rate is over 100/minute). 
• Impression: The underlying rhythm in today's tracing, as suggested by the irregularly irregular narrow QRS complexes without convincing indication of true P waves in Figure-2 — appears to be AFib (Atrial Fibrillation), here with a rapid ventricular response.

I next focused my attention on the wide beats:   

• Note that despite the underlying rhythm of AFib — the coupling interval of wide beats in this tracing remains the same! (ie, The distance from the narrow beat that precedes wide beats #10,14,18,26 is constant — as highlighted below by the 4 "C's" in Figure-3). 
• Given that the underlying rhythm in today's tracing is AFib — Shouldn't we expect the coupling interval to be as irregular as the underlying rhythm? (In contrast, with premature ventricular beats — the reentry mechanism that is most often operative with a single ventricular focus typically results in a constant coupling interval). 
• In addition — a post-ectopic pause (labeled "P") occurs after the 2 short runs of wide beats in Figure-3 (and a post-ectopic pause is clearly more likely to be seen after a run of ventricular beats compared to aberrantly conducted beats when the rhythm is AFib — since a run of wide beats with aberration tends to maintain a similar degree of irregularity as the underlying AFib).
• Finally — QRS morphology for the wide beats in Figure-3 is atypical for LBBB conduction, in that a predominantly positive QRS complex is already seen by lead V3, whereas normally — transition in the chest leads (ie, the point where the R wave becomes taller than the S wave is deep) does not occur until lead V5 or V6 when there is LBBB conduction.
• NOTE: QRS widening in Figure-3 does not manifest the Ashman phenomenon. This is because with the Ashman phenomenon — QRS widening from aberrant conduction follows a longer pause that predisposes to subsequent aberrant conduction by lengthening the subsequent relative refractory period. This is not what we see before beats #10,14,18 — which are not preceded by a relatively longer pause (See ECG Blog #70 and ECG Blog #71 — for review of the Ashman phenomenon).   

Clinical Impression:

• From a statistical viewpoint with rapid AFib — Intermittent QRS widening from aberrant conduction occurs much more commonly than ventricular ectopy. That said — the combination of constant coupling intervals, post-ectopic pauses after runs of wide beats, and a QRS morphology for the wide beats that is atypical for LBBB conduction — all favor ventricular ectopy as the cause of intermittent QRS widening.
• If the wide beats are of ventricular etiology — then the runs of 6 and then 5 consecutive wide beats ( = beats #1-thru-6 — and then #18-thru-22) constitute runs of NSVT. That said — since we do not see what happened before beat #1 in Figure-3 — We have no idea as to how long the 1st run of wide beats really lasts? 
• P.S.: QRS morphology during the runs of wide beats suggest that this is RVOT VT (Right Ventricular Outflow Track VT) — because QRS morphology resembles lbbb conduction in the chest leads in association with a rightward frontal plane axis (See ECG Blog #525 — for more on RVOT VT).

Figure-3: I’ve labeled findings suggestive of ventricular ectopy.

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What is the Cause of NSVT in today’s Case?

After assessment of a complex rhythm — it’s important to Take Another LOOK at the 12-lead ECG in search of potential clues that might explain the cause of the rhythm.

• In the absence of more information (and a prior ECG) — We do not know if the AFib in today’s case is new or old? Presumably (given the patient's new symptoms of palpitations and dizzyness) — the runs of NSVT are most likely new.

QUESTION:

• Do you see any potential clues in Figure-3  — as to what might be causing the runs of NSVT?
• HINT: Look closely at ST-T waves in the chest leads.

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A Hint suggesting the Cause …

I highlight in Figure-4 — a hint to the cause of the runs of NSVT.

• For assessment of ST-T wave morphology — it’s best to focus attention on the normally conducted ( = narrow) beats.
• ST-T waves in narrow beats #7,8,9; 11,12,13; and 15 — show nonspecific ST-T wave flattening.
• However, in the chest leads — there appears to be maximal ST depression in leads V3,V4,V5 (BLUE arrows in these leads).

Impression: Common things are common. 

• As is often emphasized on this ECG Blog — the finding of maximal ST depression in leads V2, V3 and/or V4 in patient with new symptoms may be the result of posterior OMI.
• And — an acute MI makes for a common setting that may precipitate runs of NSVT.
• Clearly — We can not prove that the precipitating cause of these runs of wide beats is an acute OMI, but our index of suspicion has to be raised (ie, with need to follow this patient with serial Troponins and repeat ECGs to see if this maximal ST depression in leads V3,V4,V5 persists once the rate of this patient's rapid AFib is controlled).

Figure-4: BLUE arrows highlight maximal ST depression in leads V3,V4,V5.

The CASE Concludes ...

Unfortunately my follow-up is limited beyond learning that sinus rhythm was restored with administration of IV Amiodarone — and maintained with beta-blockers without return of the runs of wide beats. 

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

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