ECG Blog #531 — WCT: What to Do?

I was sent the ECG in Figure-1 — with the question, "VT or SVT"?

• The sender wanted to know, "Adenosine or Amiodarone"?
• The patient was hemodynamically stable at the time the ECG in Figure-1 was recorded, so although synchronized cardioversion could be perfectly appropriate — it would seem reasonable to try medical therapy.

QUESTION:

• How would YOU interpret the ECG in Figure-1?

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

My Thoughts:

The ECG in Figure-1 shows a regular WCT (Wide-Complex Tachycardia) at ~135/minute, without clear sign of sinus P waves.

• As always when confronted with a regular WCT without clear sign of sinus P waves — the principal differential is between VT (Ventricular Tachycardia) — vs some form of SVT (SupraVentricular Tachycardia) with QRS widening from either preexisting bundle branch block or rate-related aberrant conduction.

I looked more closely at the rhythm in Figure-1:

• KEY Point #1: Statistically — at least 80-90% of regular WCT rhythms without clear sign of sinus P waves will turn out to be VT (with this figure increasing to over 90% if the patient is "older" and has underlying heart disease). This of course means that sometimes (ie, 10-20% of the time) — the WCT rhythm in front of you will be supraventricular. But it especially means that we should assume VT until proven otherwise (especially if your patient is "older" and known to have underlying heart disease). — (See ECG Blog #361 — for more on assessment of the regular WCT).
• 
  
• KEY Point #2: QRS morphology in Figure-1 is perfectly consistent with LBBB conduction (ie, Monophasic upright QRS complex in left-sided leads I and V6 — and predominantly negative QRS in lead V1, as well as in other anterior leads that all manifest a very steep S wave downslope). So, although we still need to assume VT until proven otherwise — this perfectly consistent QRS morphology for LBBB conduction clearly reduces the likelihood of VT (See ECG Blog #204 — for more on the QRS morphology of LBBB conduction).
• 
  
• KEY Point #3: There does appear to be sign of some form of atrial activity — as the narrow, pointed peak to the T waves in lead aVF looks too pointed for a naturally occurring T wave — which makes me suspicious that an underlying P wave is peaking the T wave (RED arrows in Figure-2). And if these RED arrows are P waves — they are upright, and therefore not the negative P waves of retrograde conduction that are seen with reentry SVT rhythms. Instead — these upright P waves would have a surprisingly long PR interval for this tachycardia rhythm, which suggests the Bix Rule discussed in ECG Blog #227, in which when a P wave is seen near the middle of the R-R interval, tihs often means there is 2:1 AV conduction.
• 
  
• KEY Point #4: The most commonly overlooked arrhythmia (by far!) — is AFlutter (Atrial Flutter) with 2:1 AV conduction — especially when the ventricular rate is close to 150/minute (range between 130-160/minute). As a result, the BEST way to avoid overlooking AFlutter — is to always think AFlutter until proven otherwise whenever you have a regular SVT without clear sign of sinus P waves, when the ventricular rate falls within the above rate range (See ECG Blog #287 — for review of why AFlutter is so commonly overlooked) — (And for another Step-by-Step example of my "Thought Process" for uncovering AFlutter — See my discussion in the November 12, 2019 post in Dr. Smith's ECG Blog).

Figure-2: In today's case — the lead that most made me suspect underlying atrial activity was lead aVF (RED arrows).

KEY Point #5: My "Go-To" leads when I am trying to identify subtle (partially hidden) atrial activity — are leads II, III, aVF; lead aVR; and lead V1. IF none of the above leads suggest atrial activity — then I’ll survey the remaining 7 leads as I look for atrial activity. That said, AFlutter will almost always provide ready evidence of atrial activity in one or more of my “Go To” leads.

• KEY Point #6: The BEST way to quickly find partially hidden atrial activity is to use calipers. Calipers instantly make you smarter! (and in my experience those clinicians who do not use calipers will commonly miss the diagnosis of complex rhythms).
• Since the most common conduction ratio of untreated AFlutter is 2:1 — the way in which I look for hidden flutter waves is to carefully set my calipers at precisely HALF the R-R interval of the regular SVT rhythm.

I illustrate this approach in Figure-3 — in which I've added colored arrows to 4 additional leads:

• PINK arrows in lead II highlight where I strongly suspect flutter waves are hiding.
• YELLOW arrows in leads III and aVR ( = 2 more of my "Go-To" leads) highlight even more subtle atrial activity (ie, I suspect the tiny upright deflection at the beginning of some QRS complexes in lead III is the beginning of a flutter wave — as I suspect the slow upslope of the last part of the QRS in lead aVR reveals where the 2nd negative flutter wave in this lead is hiding).
• To Emphasize: Flutter waves are very subtle in leads III and aVR — but it is the perfect regularity of 2:1 AFlutter in lead aVF with the strong suggestion of supraventricular LBBB conduction that makes me all-but-certain that the underlying rhythm in Figure-3 is 2:1 AFlutter.
• P.S.: I fully admit that I do not see flutter waves in lead I — but the YELLOW arrows clearly show where 2:1 flutter waves might be hiding.

Figure-3: It is the RED arrows in lead aVF that convinced me the underlying rhythm in today's case is AFutter with 2:1 AV conduction. Less obvious in leads II,III,aVF — I strongly suspect the colored arrows in those leads highlight where flutter waves are hiding.

 

= = = = = = = = = = = = = = 

Final Point #7: A deceptively easy but all-too-commonly-forgotten way to demonstrate hidden atrial activity is to use a Lewis Lead. Once familiar with the technique (that is described in Figure-4) — it should take no more than seconds to apply a Lewis Lead for assistance with the problematic arrhythmia you are working with.

Figure-4: How to record a Lewis Lead.

CASE Conclusion:

To return to the 2nd question I was asked by the sender of today's case:

• Since today's patient was hemodynamically stable — I thought an initial attempt at medical treatment was reasonable.
• For the reasons discussed above — I was virtually certain the rhythm in today's ECG was AFlutter with 2:1 AV conduction (If uncertain about the rhythm — a vagal maneuver could be tried to bring out flutter waves or a Lewis Lead may have made flutter waves more visible).
• While Adenosine could have been used — this drug is not effective for cardioverting AFlutter (Instead — IV Adenosine would act as a "chemical Valsalva" to slow the ventricular response, which most likely would have revealed underlying flutter waves).
• I would have instead favored IV Amiodarone — which may be effective for both VT and SVT rhythms.

Providers treated this patient with IV Amiodarone. The patient remained hemodynamically stable — and within 2 hours sinus rhythm was restored. The diagnosis of AFlutter was confirmed.

• Unfortunately — the patient was an older man with significant underlying comorbidities. He did not survive the hospitalization.

= = = = = = = = = = = = = = 

Extra Credit:

Return for a moment to the ECG in Figure-3. Did you notice the markedly coved, hyperacute-appearing ST-T waves in leads V4,V5?

• My initial concern on seeing the ST-T wave appearance in leads V4,V5 — was that whatever the etiology of the regular WCT rhythm, the "cause" of this rhythm might be an ongoing acute MI.
• That said — both QRS widening and tachycardia are notorious for affecting ST-T wave appearance (ie, In today's case — underlying flutter waves might be superimposed, thereby producing the "picture" we see in Figure-3).
• I did not think the markedly peaked ST-T waves in leads V1,V2,V3 of Figure-3 looked abnormal — as they appeared to be "proportional" given how deep the anterior S waves are. But the shape of the ST-T waves in leads V4,V5 clearly suggested the possibility of an underlying ongoing MI.
• 
  
• Bottom Line: First priority in today's patient was to determine the etiology and treat the WCT rhythm — and then repeat the ECG once converted to sinus rhythm to rule out the possibility of an ongoing infarction. This was done — and by Troponins and follow-up tracings an acute MI was ruled out (and the peaked ST coving in leads V4,V5 resolved once sinus rhythm at a controlled rate was restored). An acute infarction was not the reason for this patient's unfortunate demise. 

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Acknowledgment: My appreciation for the anonymous contribution of this case.

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Relevant ECG Blog Posts to Today’s Post: 

• See ECG Blog #185 — for review of the Systematic Ps, Qs, 3R Approach to Rhythm Interpretation.
• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• 
  
• ECG Blog #204 — Reviews a user-friendly approach to the ECG Diagnosis of conduction defects (ie, LBBB — RBBB — IVCD).
• 
  
• ECG Blog #287 — Working through the diagnosis of AFlutter (with Audio Pearls, PDF, Lewis Lead).
• The November 12, 2019 post in Dr. Smith's ECG Blog — in which I review my approach to a Regular SVT rhythm.

ECG Blog #530 — New or Old or Wellens?

I was sent the ECG in Figure-1 — but without the benefit of any history. I was asked for my opinion as to whether this tracing represented an acute STEMI? 

QUESTIONS:

• How should I answer? 
• Is this "new" or "old" Wellens?

Figure-1: The initial ECG in today's case — which was sent to me without the benefit of any history. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Answer:

Even without knowing the history — the ECG in Figure-1 is clearly of concern:

• PEARL #1: Although there is often a tendency to skip the basics, and go straight to the obvious findings (which are seen here in the inferior leads!) — I prefer to always take a brief look first at the rhythm. (For this — I favor the Ps,Qs,3R Approach for systematic rhythm interpretation = ECG Blog #185).
• To Emphasize: There is no need to spend more than a couple of seconds with this initial glance at the rhythm — and there is no need to come up with a definitive rhythm diagnosis at this point in time!
• Instead — You simply want to find out: i) What is the approximate Rate of the rhythm? (ie, Is the patient likely to be hemodynamically stable at this heart rate?); — and, ii) Is the rhythm sinus or something else?).

Is the Rhythm Sinus?

If I were charged with treating the patient in today’s case — I’d immediately go to the bedside to determine a brief history, and verify that this patient was hemodynamically stable with the rhythm shown in Figure-1. Since I was not yet provided with this information — I assumed the patient was stable enough for me to proceed with my interpretation of today’s initial ECG:

• PEARL #2: The rhythm is not sinus — because the P wave in lead II is not upright! ( = YELLOW arrows in the inferior leads in Figure-2). Assuming there is no lead reversal — the finding of a negative P wave in lead II indicates either a junctional or low atrial rhythm.
• Note that these negative P waves in lead II of Figure-2 do manifest a constant PR interval, such that they are conducting (because these P waves are Related by a fixed PR interval to neighboring QRS complexes).
• Note also that no P waves are seen throughout the long lead V1 rhythm strip at the bottom of the tracing. However, there is a negative P wave seen in simultaneously-recorded lead V3 (YELLOW arrow in that lead). Thus the reason no P wave is seen in lead V1 — is that morphology of the retrograde P wave in lead V1 must be isoelectric to the baseline.

Otherwise ... 

• The QRS complex is narrow ( = not more than half a large box in duration) — so the rhythm is supraventricular.
• The ventricular rhythm is Regular — at a Rate of ~50/minute (ie, R-R interval a tiny bit over 6 large boxes in duration).
• Bottom Line: Given lack of a visible P wave in lead V1 + the narrow QRS + the slow ventricular rate of ~50/minute — this appears to be a junctional escape rhythm.

Figure-2: Negative P waves in the inferior leads indicate this is a non-sinus rhythm. The narrow QRS, slow rate and lack of visible atrial activity in lead V1 suggest this is a junctional escape rhythm.

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The Rest of the ECG ...

In addition to the slow junctional escape rhythm — Figure-3 highlights KEY findings in the leads of most concern:

• Extremely large Q waves are seen in leads III and aVF. This is associated with a hyperacute appearance of the ST segment that manifests considerable J-point elevation with a straightened ascending ST segment takeoff. There is fairly deep terminal T wave inversion.
• The 3rd inferior lead ( = lead II) — manifests a bizarre, fragmented QRS, with similar looking but less marked ST-T wave changes.
• Reciprocal ST-T wave changes are seen in lead aVL (within the BLUE rectangle) — in the form of a straightened and depressed ST segment (that manifests gradual downsloping, but which finishes with terminal T wave positivity).
• Lead V3 is uninterpretable due to artifact ...
• Less marked but still concerning ST-T wave findings are present in 3 additional leads. These include: i) Lead I (which is similar in shape, but with less prominent reciprocal changes compared to aVL); ii) Lead V2 (which manifests ST segment straightening with loss of the normal slight ST elevation usually seen in this lead); — and, iii) Lead V6 (with a QRS and ST-T wave similar to that seen in lead II).

Putting It All Together:

I had more questions than answers after reviewing this ECG: 

• The extremely large Q waves in leads III and aVF indicate that the patient has had an inferior infarction at some point in time.
• The hyperacute-looking ST segments with ST elevation, in association with reciprocal ST depression in lead aVL — suggest an inferior MI that may be recent (or ongoing) — with the findings in leads V2 and V6 suggesting associated posterior and lateral involvement.
• The above said — the terminal T wave inversion in the inferior leads and in lead V6 + terminal T wave positivity in leads I,aVL and V2 could all represent evolving reperfusion changes of completed infarction.
• 
  
• BOTTOM Line: We need some history to proceed further with our interpretation. Along the way — finding a previous ECG for comparison should prove invaluable for determining what is "new" vs "old".

Figure-3: I've labeled the leads of most concern. 

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The CASE Continues:

I was finally able to learn a bit more about this case.

• This ECG is from a middle-aged woman with known coronary disease, having undergone stent placement following an MI about 1 year earlier.
• She presented this time with ongoing severe CP (Chest Pain) that began ~2 hours prior to the time that ECG #1 was recorded. 
• Despite the slow junctional escape rhythm — she was hemodynamically stable.

My Thoughts:

• Although with this past and present history I was still uncertain as to what was "new" vs "old" vs "new superimposed on old" — given the presence of hyperacute-looking ST-T wave changes with ST elevation and ongoing severe CP — prompt cath is needed to define the anatomy!
• 
  
• PEARL #3: The slow junctional escape rhythm in Figure-3 is an additional feature that suggests a recent and/or ongoing OMI (Occlusion-associated Myocardial Infarction) may be present ==> Prompt cath is needed!

A Previous ECG is Found ...

On searching the patient's chart — a previous ECG was found. To facilitate comparison — I've placed both tracings together in Figure-4.

QUESTIONS: 

• What do you learn from seeing this previous ECG? 
• What is the "problem" with this previous ECG?

Figure-4: Comparison of the initial ECG with a previous ECG.

ANSWERS: 

Before addressing the question as to what we learn from Figure-4 — Consider this "problem" with the previous ECG: 

• PEARL #4: All-too-often when I'm sent cases in which a previous ECG is provided for comparison — there is no indication as to what the clinical situation was at the time the prior tracing was recorded.
• For example, in Figure-4 — there are obvious marked abnormalities in the previous tracing. As a result, our approach as to how to interpret this comparison tracing that is now provided to us in Figure-4 may vary greatly depending on whether ECG #2 was recorded:
• During the acute phase of a previous OMI? 
• Immediately after this patient received her stent ~1 year earlier? 
• OR — At a routine follow-up visit after the patient had been pain-free for months?

On further review of this patient's chart — it was learned that this previous ECG was recorded around the time of her stent placement (probably shortly after stent placement in the "culprit" RCA).

• Presumably the deep Q waves in leads II,III,aVF of ECG #2 are the result of the patient's inferior MI — in which some residual ST elevation remains. In addition — there is deep symmetric T wave inversion in the inferior and lateral chest leads of this previous ECG that suggest reperfusion changes that most probably developed following stent placement.
• The overly tall T wave in lead V2 of ECG #2 — is also most probably a reperfusion change from associated posterior OMI.

KEY Point: Despite obvious abnormalities in the previous ECG — We are still able to advance our diagnosis in today's case given the clinical context that today’s patient is now presenting to the ED for acute severe CP beginning just 2 hours prior to the recording of ECG #1. My thoughts regarding Figure-4 were the following:

• The rhythm in today’s initial ECG is no longer sinus. Instead — there is a slow junctional escape rhythm at ~50/minute.
• Although the inferior Q waves are similar to those that were present in the previous ECG — there is now more ST elevation with a hyperacute appearance in each of the inferior leads (in the form of an upsloping, straightened ST segment takeoff).
• Reciprocal ST segment depression in high-lateral leads I, and especially aVL now clearly appears to be hyperacute (with ST segment straightening, prominent terminal T wave positivity, and a gently downsloping ST segment in lead aVL that reflects the mirror-image opposite picture to the ST-T wave in lead III).
• Lateral infarction is suggested by the acute ST elevation in lead V6.
• Finally — the reperfusion changes seen in the chest leads in ECG #2 have virtually resolved (ie, reduced T wave positivity in lead V2 — and resolution of T wave inversion in leads V4,V5).

Bottom Line: 

Given the presentation of new severe CP — comparison of today's initial ECG with the previous tracing suggests there is now acute reocclusion of the RCA — with need for prompt cath!

On reflection of this case — several points deserve emphasis: 

• As helpful as finding the previous tracing was in today's case — the need for prompt cath was already established by: i) The known history of coronary disease; — ii) The presentation of new severe CP just 2 hours before ECG #1 was recorded; — and, iii) The slow junctional escape rhythm in association with limb lead changes in ECG #1 that so clearly look to be hyperacute.
• An elevated Troponin would strengthen the need for prompt cath — but an increased Troponin is not needed to know that prompt cath is indicated (Remember that the initial Troponin may be normal despite acute coronary occlusion — and waiting until Troponin eventually elevated would only incur loss of more myocardium).
• An Echo at the bedside showing a localized inferior wall motion defect would strengthen the need for prompt cath — but this too is not needed to know that prompt cath is indicated (ie, We know this patient had a previous MI — so we would not be able to know if any wall motion abnormality was new or old).
• Although Wellens' Syndrome most commonly presents with ST-T wave abnormalities in the anterior chest leads (from high-grade narrowing of the LAD) — you can see the ST-T wave abnormalities of Wellens Syndrome in any coronary distribution. That said — today's patient presents with new CP — deep Q waves and hyperacute ST elevation — all of which tell us this is not Wellens' Syndrome. 
• Instead — Wellens' Syndrome manifests ST-T wave findings of reperfusion after brief coronary occlusion and before major damage occcurs — with the patient pain-free because the briefly occluded coronary vessel has now spontaneously reopened! 
• (See ECG Blog #350 and ECG Blog #453 — for review of the criteria and findings with Wellens' Syndrome).

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Acknowledgment: My appreciation for the anonymous submission of today's case with these tracings. 

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ECG Blog #529 — Should Prompt Cath be Done?

The ECG in Figure-1 was obtained from an older woman — who presented following an episode of severe epigastric pain, associated with nausea, vomiting and dyspnea. This ECG was obtained a number of hours after the episode had subsided.

QUESTIONS:

• How would YOU interpret the ECG in Figure-1?
• Should you activate the cath lab?  

Figure-1: The initial ECG in today's case — obtained from an older womman following an episode of severe epigastric pain. (To improve visualization — I've digitized the original ECG using PMcardio).

My Thoughts:

The ECG in Figure-1 shows a fairly regular sinus rhythm at ~90/minute. The PR and QRS intervals are normal — and the QTc is at most borderline prolonged. The frontal plane axis is normal at about 0 degrees. There is no chamber enlargement.

Regarding Q-R-S-T Changes:

• Q Waves: None.
• R Wave Progression: Delayed. Transition (where the R wave becomes taller than the S wave is deep) does not occur until between lead V5-to-V6. That said — at least a small R wave is present in each of the chest leads, with gradual increase in R wave size until transition occurs.

Regarding ST-T Wave Changes:

— As highlighted in Figure-2 — ST-T wave appearance is clearly of concern — with abnormal findings in almost all leads.

• ST segments in multiple leads are flat. Most remarkable is the shelf-like ST depression that is maximal in leads V2,V3,V4 (within the RED rectangle in Figure-2). 
• A lesser degree of flat ST depression is seen in the remaining chest leads (ie, in leads V1,V5,V6).
• There is terminal T wave positivity in all 6 chest leads.

In the Limb Leads:

• There is nonspecific ST-T wave flattening with slight depression in high-lateral leads I and aVL (BLUE arrows in these leads).
• In the inferior leads — leads II and aVF show nonspecific ST-T wave flattening. KEY Point: The 3rd inferior lead (which is lead III) — shows ST segment coving, with a hint of ST elevation.
• The remaining limb lead (which is lead aVR) — shows a very slight amount of ST elevation. 

My Impression: 

If today's patient had presented with the ECG in Figure-2 and a history of new-onset chest pain — then this tracing would be especially worrisome.

• Instead — this patient presented with severe epigastric pain, associated with nausea, vomiting and dyspnea. That said — in view of the fact that the symptoms reported could represent a CP (Chest Pain) “equivalent” symptom — Consideration has to be given to the possibility of an acute ongoing cardiac event.
• ST depression is seen in 8/12 leads in Figure-2 (leads I,aVL; and the 6 chest leads). Even without any more than the minimal ST elevation in lead aVR — these findings suggest DSI (Diffuse Subendocardial Ischemia). As discussed in ECG Blog #483 and ECG Blog #400 — DSI may be the result of either non-cardiac causes (ie, anemia, GI bleeding, marked hypotension, "sick" patient, etc.) — or — significant coronary disease, which could be acute.
• As suggested by the RED arrows (within the RED rectangle in Figure-2) — ST depression appears to be maximal in leads V2,V3,V4 — which strongly suggests the possibility of acute or recent posterior OMI.
• In this context — the ST segment coving with slight ST elevation in lead III could reflect associated inferior OMI in the setting of underlying multi-vessel disease (ie, similar to an Aslanger Pattern — as described in detail at the bottom of this page).
• 
  
• BOTTOM Line: Although more information is clearly needed to better define what is going on — one needs to consider the possibility of an acute occlusion infarction (ie, an "OMI") until proven otherwise.

Figure-2: I've highlighted key findings in today's ECG. 

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CASE Follow-Up:

Clinical details are unfortunately lacking in today's case. That said, from what I am aware of — the possibility of an acute MI was not considered until a serum Troponin came back markedly elevated.

• At that point — the MI was declared a NSTEMI (Non-ST Elevation Myocardial Infarction). In the absence of ST elevation — cardiac catheterization was deemed to be "not necessary".
• An Echo was not done until later. It showed an inferolateral wall motion defect with significant LV dysfunction. At this point — cardiac cath was finally recommended, but not performed because the patient refused the procedure.
• The patient's condition deteriorated — but with full informed consent, she still refused cardiac cath. Eventually, after a complicated hospital course — her condition improved and the patient was discharged from the hospital.
• The patient never underwent cardiac catheterization ( = her informed consent decision not to undergo cath). A number of weeks later on follow-up — she appeared stable on her new medical treatment regime for heart failure. We can only wonder if the heart failure resulting from this patient's extensive infarction might have been prevented had prompt cath with PCI been done.

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COMMENT:

There are lessons-to-be-learned from this case.

• It is well established that not all patients with an acute MI have CP (Chest Pain). Instead, some patients have other "CP-equivalent" symptoms (ie, epigastric pain, dyspnea) — while others have no symptoms at all (See ECG Blog #228).
• That today's patient had a recent (ongoing) MI was not appreciated until her Troponin came back markedly elevated. This possibility should have been realized as soon as her initial ECG (shown in Figure-1) was recorded. Yet a few days passed before this possibility was considered.
• Given the less typical presentation (ie, epigastric rather than chest pain) — I would interpret today's initial ECG as suspicious but non-diagnostic. The diffuse ST depression (present in 8/12 leads in Figure-2) — clearly indicates DSI (Diffuse Subendocardial Ischemia). As noted above — DSI often (but not always) indicates severe underlying coronary disease.

The situation of having to determine if a patient with a non-diagnostic initial ECG is having an acute MI is common. 

• "Time is Muscle (myocardium). If the cause of an acute MI is acute occlusion of a major coronary vessel (ie, an "OMI" = Occlusion-associated Myocardial Infarction) — then we need to appreciate that the more time that passes until the occluded vessel is reperfused (either by cardiac cath with PCI or by use of thrombolytic agents) — the greater the amount of myocardium that will be lost.
• As repeatedly shown in Dr. Smith's ECG Blog (See My Comment at the bottom of the page in the February 8, 2026 post) — the most benefit from reperfusion occurs within the first 4 hours after acute coronary occlusion (and every 2-hour delay results in up to 60% more myocardium infarcted).

There are 2 main types of acute myocardial infarction: 

• Type 1 MI's — which are caused by a ruptured plaque that results in acute occlusion of a major coronary vessel. 
• Optimal treatment of Type 1 MI's consists of reopening the acutely occluded artery (ie, reperfusion by cardiac cath with PCI — or with use of thrombolytic agents). 
• Sometimes (if not often) — the acutely occluded artery may spontaneously reopen (which is why the patient's symptoms and ECG abnormalities may suddenly improve — even before any treatment is given).
• But what spontaneously reperfuses — may just as easily spontaneously reclose (which is why with a Type I MI, even if symptoms and the ECG suddenly improve [or completely resolve] — definitive treatment with PCI may still be needed to prevent reclosure).

• Type 2 MI's — which are not the result of a ruptured plaque, but instead are due to an oxygen supply-demand mismatch (which may be seen with "high-demand" states, in which the heart requires more oxygen than it receives — as may occur with marked stress states, septicemia, severe anemia, sustained tachyarrhythmias, or shock, among other causes).
• Optimal treatment of Type 2 MI's is to find and "fix" the cause of the supply-demand mismatch (Neither PCI nor thrombolytics benefit a Type 2 MI).
• If it is not clear from history and serial ECGs — then cardiac cath may occasionally (not often) be needed to distinguish between a Type 1 vs Type 2 MI.

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Is "NSTEMI" a Useful Term?

The reason today's ECG was called a NSTEMI (Non-ST Elevation Myocardial Infarction) — is because Troponin was significantly elevated, but no ECG satisfied sufficient millimeter-based ST elevation criteria to qualify as a STEMI.

• It was on this basis (ie, that no STEMI was present) that the recommendation for acute cardiac catheterization was delayed for more than a day. As discussed above — the patient consistently refused cardiac cath — so this delay did not influence the ultimate outcome. That said — it is nevertheless important to consider WHY the recommendation for cardiac cath was so greatly delayed.
• Practically speaking — the diagnostic designation, "NSTEMI" — serves no useful purpose. On the contrary — the "default diagnosis" of calling cases such as the one in today's post a NSTEMI is not only without utility — But it is potentially harmful — because for clinicians who are "stuck" in the outdated STEMI Paradigm, declaring that an MI is a "NSTEMI" provides a false sense of security that prompt cath with PCI is not needed — and this all-too-often results in significant delay until cardiac cath is finally done (and as stated above, "Time is Muscle" = lost myocardium).
• The Clinical Reality: Up to 35% of "NSTEMIs" are found (on their delayed cath) to have had acute coronary occlusion despite a lack of ST elevation on one or more ECGs (Aslanger, Smith et al- IJC Heart & Vasculature, Vol. 30, 2020 — Chi-Sheng Hung et al- Critical Care 22:34, 2018 — Khan et al- Eur Heart J 38(41): 3082-3089, 2017 — and — Avdikos, Michas, Smith- Arch Acad Emerg Med 10(1), 2022).
• And even in those cases in which STEMI criteria are eventually met: i) Waiting for ST elevation to finally develop often results in a delay of too many hours (with loss of too much myocardium); — and, ii) As documented in many cases on Dr. Smith's ECG Blog — for many of these slow-to-develop STEMI cases, the provider still somehow ends up writing "NSTEMI" on the discharge diagnosis.

BOTTOM Line: The millimeter-based "STEMI Paradigm" is flawed — because it misses at least 25% of acute coronary occlusions (which is the group of acute MI's that we care about — because these are the MI's that benefit from prompt reperfusion by either cath with PCI or with thrombolytics). 

• We would all be better served if the outdated and misleading term, "NSTEMI" — was no longer accepted as a diagnosis.
• We would be BEST served if instead of insisting on millimeter-based ST elevation criteria before considering cath with PCI or thrombolytics — if we instead adopted those ECG and clinical clues that have been shown to predict acute coronary occlusion (ie, an acute OMI) without having to wait for sufficient ST elevation (that might never come) before doing so (See detailed discussion in my ECG Blog #337 — in the July 31, 2020 Dr. Smith post — as well as in numerous additional posts in this ECG Blog and in Dr. Smith's ECG Blog).

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What is Aslanger's Pattern?

I introduced the concept of Aslanger's Pattern in ECG Blog #258 and ECG Blog #322. The premise of Aslanger's — is that IF there is inferior MI + diffuse subendocardial ischemia — then the vector of ST elevation will shift rightward. This results in:

• ST elevation in lead III (as a result of the acute inferior MI) — but not in the other inferior leads (II, aVF) because of the rightward shift in the ST elevation vector.
• ST depression in one or more of the lateral chest leads (V4, V5, V6) with a positive or terminally positive T wave — but without ST depression in lead V2. (Marked ST depression from multi-vessel coronary disease serves to attentuate what would have been ST elevation in leads II and aVF).
• ST elevation in lead V1 that is more than any ST elevation in lead V2.
• There may be more reciprocal ST depression in lead I than in lead aVL (because of the rightward ST vector shift).
• The only leads showing significant ST elevation may be leads III, aVR and V1 (reflecting the inferior MI + subendocardial ischemia from diffuse coronary disease). 

Regarding Today's CASE:

The ECG in Figure-2 does not satisfy all of the above features of Aslanger's Pattern (ie, Instead of ST elevation in leads V1 and V2 — there is ST depression in these leads). That said — the elements of today's case that do resemble this pattern are:

• There is DSI (Diffuse Subendocardial Ischemia).
• The ST segment is coved and slightly elevated in lead III, but not in the other inferior leads.

Bottom Line: Today's patient presented with severe new-onset symptoms potentially consistent with a "CP-equivalent" syndrome. The initial serum Troponin was markedly elevated — thus confirming an acute MI. 

• ST depression is maximal in leads V2,V3,V4 — suggesting an acute posterior OMI (and acute posterior OMI is very commonly associated with acute inferior involvement).
• The diffuseness of ST depression in Figure-2 suggests severe underlying coronary disease.
• In this context, although not strictly satisfying all features of Aslanger's Pattern — I interpreted the ST coving and slight elevation in lead III as suggestive of acute inferior involvement.
• Regardless — Given the history and the markedly elevated initial Troponin — indication for prompt cath seemed apparent as soon as the initial ECG was recorded.
• An Echo was not done until later. If providers had any doubt about the need for prompt cath after seeing the ECG in Figure-2 — seeing the hypokinetic inferolateral wall motion defect on a bedside Echo could have established a definite need for prompt cath within minutes after seeing the initial ECG.
• P.S.: The history in today's case was that this patient's "CP-equivalent" symptom (severe epigastric pain) had subsided a number of hours before today's ECG was recorded. As a result — it is possible that the ECG abnormalities seen in Figure-2 may have been significantly more marked had her symptoms still been present at the time the ECG was recorded.

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Acknowledgment: My appreciation to Ahmed Marai (from Anbar, Iraq) for making me aware of this case and allowing me to use this tracing.

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ECG Blog #528 — The Patient Decided to Leave

The ECG in Figure-1 was obtained from a middle-aged patient — who presented with palpitations. The patient has known ischemic heart disease, and was hemodynamically stable with this rhythm.

QUESTIONS:

• How would you interpret the rhythm in Figure-1?
• Clinically — What would YOU do?

 

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

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My Initial Thoughts:

I found this rhythm fascinating! The "good news" — is that today's patient was hemodynamically stable with this rhythm — which tells us that we at least have a "moment in time" to contemplate what is going on. 

• As always — I favor the Ps,Qs,3Rs Approach for systematic rhythm interpretation (See ECG Blog #185 for review of the Ps,Qs,3Rs).
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• HINT #1: It does not matter in what sequence you look for P waves, QRS width, and the 3 Rs of Rate, rhythm Regularity, and whether atrial activity is (or is not) Related to neighboring QRS complexes.
• HINT #2: It sometimes helps to step back a little bit from the tracing when assessing rhythm Regularity.
• HINT #2: Using calipers will be especially helpful for interpreting the rhythm in Figure-1.

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CHALLENGE: I've labeled today's tracing below in Figure-2 — but before looking at how I labeled this — What did YOU think?

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Figure-2: I've labeled today's ECG.

Assessing the Ps, Qs, and 3Rs in Today's ECG:

My thoughts in the sequence they came to me were as follows:

• As I did not see upright P waves in front of neighboring QRS complexes — I knew the rhythm was not sinus.
• The QRS is wide (clearly more than half a large box in duration).
• The Rate of this rhythm is not overly fast (ie, with an R-R interval of ~3 large boxes in duration = about 100/minute).
• Although one might initially think the rhythm was regular — stepping back a little bit from the tracing allows us to appreciate that this rhythm is definitely not Regular. Instead — there is a "regular irregularity" — in the form of group beating (Using calipers facilitates recognizing that there are alternating shorter [RED] — then longer [BLUE] R-R intervals). 
• Looking closer at QRS complexes (especially in the inferior leads) — a sharp negative deflection follows each QRS complex in leads II,III,aVF at a fixed distance after each of the 10 beats in this tracing (YELLOW arrows). These negative deflections represent retrograde P waves with a fixed RP' interval ( = 1:1 VA conduction).
• Looking at simultaneously-recorded leads aVR,aVL,V1 — we can appreciate a small, positive pointed deflection that occurs at precisely the same instant in time as these negative deflections. This confirms that these YELLOW arrow negative deflections do in fact represent retrograde P waves (such that these P waves are Related to preceding QRS complexes by a fixed RP' interval — and this rhythm is not AFib).

My Impression of Today's Rhythm: 

To Emphasize: This is an extremely complex rhythm! What follows below goes well Beyond-the-Core!

• At this point in my assessment, given QRS widening with retrograde P waves — I suspected a ventricular rhythm with the unusual finding of group beating.
• The finding of group beating should always suggest the possibility of Wenckebach conduction (See ECG Blog #164 and Blog #457 and Blog #66, among others). It's important to realize that "Wenckebach conduction" is not limited to 2nd-degree AV block of the Mobitz I type. Instead — Wenckebach periodicity can be seen in association with SA block, with AFib, AFlutter and ATach; with retrograde conduction — and on occasion (like today's case appears to be) — with ventricular rhythms! 
• As I schematically show in Figure-3 — what can happen is that there may be a ventricular rhythm that exhibits a form of Wenckebach Exit Block out of the ventricular ectopic focus at the junction of this focus with ventricular myocardium (Credit to Dr. Harry Mond for his explanation of this fascinating and rare phenomenon — Harry's Corner of March 3, 2025).

Figure-3: Schematic of Exit Block from an ectopic ventricular focus.

Laddergram Illustration:

In Figure-4 — I schematically depict what appears to be happening with the Exit Block in today's case. 

• The lower ORANGE-shaded Tier in this laddergram represents events emanating out of the ectopic ventricular focus that I schematically drew in Figure-3.
• As can be seen in the Figure-4 laddergram — because of the Wenckebach Exit Block, only 2 out of every 3 impulses make it out of this ectopic ventricular focus (the Orange-shaded Tier) to arrive at the ventricles.
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• PEARL #1: If it were not for the Exit Block — the rate of this ectopic ventricular rhythm in today's case would be considerably faster than what it appears to be. We only see 2 out of every 3 ventricular impulses on the surface ECG. The R-R interval within which these 2 ventricular beats occur on the surface ECG equals the distance between beat #1 and beat #3 (which is ~6 large boxes in duration). As a result — the average rate of the ventricular rhythm on the surface ECG (ie, in Figure-4) is ~100/minute.
• But within the ectopic ventricular focus — 3 (not two) impulses are occurring within this R-R interval of ~6 large boxes. Thus, within the ventricular focus — an impulse is formed every 2 large boxes — and 300 ÷ 2 =150/minute. This means that if it were not for the 3:2 Wenckebach Exit Block — that the rate of the ectopic ventricular focus would be a ventricular tachycardia at 150/minute!
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• Continuing with the laddergram in Figure-4 — Once the 2-out-of-3 ventricular impulses make it out of the ectopic-ventricular junction — they depolarize the ventricular myocardium — and in today's case, also generate 1:1 retrograde conduction back to the atria (YELLOW arrows with a fixed RP' interval after each ventricular beat).

Figure-4: My proposed Laddergram of today's rhythm.

Are there Other Possibilities for Today's Rhythm?

QRS morphology in Figure-2 supports the probability that this represents a ventricular rhythm. That's because:  

• QRS morphology in this tracing does not resemble any of the usual forms of conduction block (ie, Although today's tracing is consistent with LBBB conduction in the limb leads [with an all positive QRS in leads I and aVL] — it manifests a very atypical pattern for either LBBB or RBBB conduction in the chest leads [that show a qR in lead V1, but with tall, positive QRS complexes in each of the remaining 5 chest leads]).

PEARL #2: Rarely — a supraventricular QRS morphology pattern may be seen that resembles LBBB conduction in the limb leads, but RBBB conduction in the chest leads. This pattern is known as MBBB (Masquerading Bundle Branch Block — See ECG Blog #517). 

• With regard to the rhythm in Figure-2 — although I think a ventricular rhythm with Wenckebach Exit Block out of the ventricular focus is the most likely explanation for the regular irregularity that we see in today's tracing — I can not rule out the possibility that this is a junctional rhythm with preexisting MBBB and Wenckebach conduction out of the AV Node.

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Challenge QUESTIONS: 

We come to the issues of how we might increase the certainty of our rhythm diagnosis? — and the clinical issue of How best to manage today's patient? Consider the following: 

• If you could ask this patient 1 question — What would that question be?
• If there was 1 thing you could get from review of this patient's chart — What would you look for? 

My Answers:

In addition to seeing some basic laboratory results (renal function, serum electrolytes, etc.) and learning whatever else we could about this patient:

• I'd want to know what medication(s) this patient was taking? (ie, To see if any medication might be predisposing the patient  to ventricular arrhythmias — and especially to ask if the patient is taking Digoxin [as Digoxin toxicity is notorious for causing ventricular arrhythmias and Wenckebach conduction]).
• I'd want to see a prior ECG on this patient (ie, To see if the unusual QRS morphology seen in Figure-2 was previously present during sinus rhythm).  

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The CASE Concludes:

Review of this patient's chart revealed that the patient was not taking Digoxin. However, he was being seen for psychiatric care (and he was taking Respiridone). 

• It has long been known typical antipsychotic drugs (ie, Chlorpromazine, Haloperidol, Thioridazine, etc.) increase the risk of serious, and even fatal cardiac arrhythmias. It appears that newer atypical antipsychotic drugs (including Respiridone) also significantly increase this risk (Ray et al — N Engl J Med 360(3):225-235, 2009). The mechanism is thought to be the result of blockade of potassium channels with prolongation of cardiac repolarization. Respiridone does prolong the QTc — but by itself, usually not enough to precipitate Torsades de Pointes.
• No previous ECG was found on this patient’s chart (and no indication was seen in the medical chart that the patient previously had arrhythmias).
• The patient was not cooperative — and he signed out against medical advice (It was felt that the patient was sufficiently competent mentally to do so).
• The “good news” — is the fact that this patient felt well enough that he decided to leave suggests that he was not symptomatic with this arrhythmia.
• Unfortunately — no further follow-up is available.

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Acknowledgment: My appreciation to Cardiology Notes (FB ECG site) for making allowing me to use this case.

• Special acknowledgment also to Omar Hassan Seddik (Mansoura City, Egypt) and Khaled Ash (from Damascus, Syria) for their input and for drawing my attention to this case.

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