EXTRA COPY- Should Prompt Cath be Done? (4-21.1-2029) - EXTRA COPY

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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” syndrome — 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.) and/or significant underlying 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 below).
• 
  
• BOTTOM Line: Although more information is urgently 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 — But 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 not deemed 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 feared the procedure.
• The patient's condition deteriorated — but 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. A number of weeks later on follow-up — she appeared stable on her new medical treatment regime for heart failure.

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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). Some patients have other "CP-equivalent" symptoms (ie, epigastric pain, dyspnea) —
• 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 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 will spontaneously reopen (which is why the patient's symptoms and ECG abnormalities may suddenly improve, even without treatment).
• 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 normalize — definitive treatment with PCI may be needed to prevent subsequent 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 not clear from history and serial ECGs — Cardiac cath may occasionally (not often) be needed to distinguish between a Type 1 vs Type 2 MI.

Today's ECG was called a NSTEMI (Non-ST Elevation Myocardial Infarction) — because Troponin was significantly elevated but no ECG satisfied sufficient 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. BUT — in reviewing today's case — it is still important to consider the rationale for delaying the recommendation for cardiac cath.
• 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 case a NSTEMI is potentially harmful because of the false sense of security that it gives to providers, which therefore results in significant delay until cardiac cath is finally done.
• Up to 35% of NSTEMIs are found on their delayed cath to have had acute coronary occlusion despite a lack of ST elevation (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).

PS - today's MI was called a NSTEMI because no ST elev. Practically speaking — the commonly used description of an NSTEMI is useless. Worse than that — Px often worse because "only a NSTEMI" induces a false sense of security, therefore delay (ME TO LOOK FOR REF on SSmith !!!

Features in today's initial ECG that should immediately suggest the possibility of an acute Type I MI include the following:

• XXXX  - max st dep in V2,3,4 - ST coving and sl elev. in lead III (similar to Aslangers - but not quite since no st elev. in V2

What to do if you encounter a suspicious but non-diagnostic initial ECG like Fig. 1:

• repeat ecg within 10-20 minu
• Echo at bedside (echo done days later had marked lv dysfunction - had that been done immediately - would have been enough to confirm need for acute cath
• prior ecg as soon as trop came back - should have been indication for cath

How to apply this to today's case?

• This patient refused cath with informed consent. Sometimes patients know something. I long ago learned it's best never to "force" a procedure on a patient - but although doing fairly well on follow-up - pt had resultant HF - who is to know how much myocardium might have been preserved had reperfusion treatment had been started shortly after ECG #1 done ... 

Type 2 Myocardial Infarction (Type 2 MI or T2MI) is a heart attack caused by a mismatch between oxygen supply and demand, rather than a plaque rupture (which is Type 1). It occurs when the heart muscle requires more oxygen than it receives due to stress, such as sepsis, severe anemia, tachyarrhythmias, or severe blood pressure issues. 

Key Aspects and Characteristics

• Mechanism: It is a "demand ischemia," where coronary arteries may not be acutely blocked, but cannot supply enough blood to meet high oxygen demands.
• Triggers/Causes: Common causes include sepsis (infection), operative stress, rapid arrhythmia (e.g., AFib), anemia, and extreme hypertensive/hypotensive crises.
• Patients Affected:
   Type 2 MI is very common in hospitalized patients, often affecting older patients with multiple comorbidities (like renal failure or heart disease).

go over Aslanger — OMI —  

As per many other posts — stemi criteria miss many acute occlusion MIs = OMIs — several interventions can facilitate determining if OMI was present

NSTEMI is not a helpful diagnosis ...

cath was indicated - but patient refused - although safe in hands of experienced operators, adverse effects can occur (so patient informed consent decision should be respected). I have to believe that had reperfusion been performed/cath — myocardium could have been saved - and her heart failure may not have been severe. but who 

MY REPLY:

Thanks for this follow-up — which does teach us something, namely that even though doing a cath offered potential for saving myocardium — who is to say that this patient might not be now doing equally well without having had her cath?

 

XXXXXXXXX

XXXXXX  

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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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ADDENDUM (4/XXX/2026):

• XXXX 

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From ECG Blog #258 — on ASLANGER Pattern!

https://ecg-interpretation.blogspot.com/2021/10/ecg-blog-258-mp-70-how-to-date-mi.html

Also from ECG Blog #322  

https://ecg-interpretation.blogspot.com/2022/07/ecg-blog-322-71yo-with-1-week-of-chest_26.html

I added the following to Blog #322:

NOTE: Other than the finding of ST depression in lead V2 — the initial ECG in today's case satisfies the other above-cited features of Aslanger's Pattern. 

• I can't help but wonder if the fairly deep, symmetric T wave inversion in lead III represents a reperfusion T wave from recent occlusion.

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ADDENDUM (10/28/2021) — There are elements of this case that closely resemble Aslanger's Pattern (This pattern is very nicely described by Dr. Smith in his January 4, 2021 post). 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). 

The above said — additional features to consider in today's case include: i) There is also marked LVH; and, ii) The infero-postero MI is probably at least 10 hours old, and is now showing prominent reperfusion T waves in the posterior distribution (ie, tall, peaked anterior T waves). 

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EXTRA COPY- ECG Blog #527 — What’s Going On? — EXTRA COPY

The ECG in Figure-1 — was obtained from an older man who presented for care with new CP (Chest Pain).

QUESTION: 

• Should the cath lab be activated?

Figure-1: The initial ECG in today's case.

MY Thoughts:

It is tempting on first glance at today's tracing from this patient with new CP — to be very concerned by the marked ST segment deviation. And then — I looked closer at lead I:

• PEARL #1: Compared to the other 11 leads in this tracing — the QRST complex in Lead I looks almost normal (with no more than subtle nonspecific ST-T wave flattening in this lead). My favorite Clue to the presence of Artifact as the cause of marked, bizarre complexes in many (most) other leads — is that one of the 3 standard leads looks relatively normal. And despite dramatic (and bizarre) ST-T wave deflections in the other 2 standard leads ( = leads II and III in Figure-1) — the ST-T wave in lead I looks to be relatively unaffected!

PEARL #2: As discussed in ECG Blog #201 — The distribution of the bizarre ST-T wave deflections seen in Figure-1 — precisely follows the location and relative amount of amplitude distortion predicted by Einthoven’s Triangle.

• That is — the relative amount of bizarre ST elevation is approximately equal in 2 of the 3 standard limb leads (ie, in leads II and III) — but it is not seen at all in the 3rd standard limb lead (ie, there is no artifact seen in lead I). By Einthoven's Triangle (See the picture of Einthoven's Triangle just below today’s ECG Media Pearl) — the finding of equal ST segment amplitude artifact in lead II and lead III, localizes the "culprit" extremity to the LL ( = Left Leg) electrode.
• The absence of any artifact at all in lead I is consistent with this — because, derivation of the standard bipolar limb lead I is determined by the electrical difference between the RA ( = Right Arm) and LA ( = Left Arm) electrodes, which will not be affected if the source of the artifact is the left leg.
• As I discuss in detail in my Audio Pearl below — the finding of maximal amplitude artifact in unipolar lead aVF confirms that the left leg is the “culprit” extremity. 

—  —

 

ECG Media PEARL #18 (7:45 minutes Audio) — On recognizing Artifact — and — using Einthoven’s Triangle to determine within seconds the “culprit” extremity causing the Artifact on your ECG.

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PEARL #3: Another KEY Clue to the presence of artifact — is if you are able to see undisturbed continuation of the underlying rhythm despite the artifact! Figure-2 shows how this is possible in today's case:

• There are actually 2 artifact deflections within each R-R interval in today's initial tracing (alternating BLUE and YELLOW arrows in lead aVL of Figure-2). These are seen as dual positive deflections within each R-R interval in all limb leads except lead I — and as dual negative artifact deflections within each R-R interval in the 6 chest leads.
• Focusing on the QRS complex in lead I that is unaffected by artifact — I've added a RED time-line parallel to the ECG grid line that exends through simultaneously-recorded leads II and III — with this time-line marking the beginning of the QRS complex that we can clearly see in lead I.
• I've also added a BLUE time-line that marks the end of the QRS in lead I. Thus, we can see that the QRS complex in lead I lies in between the RED and BLUE lines. This allows us to follow these RED and BLUE lines to know where to look for other "on time" partially hidden QRS complexes in simultaneously-recorded leads (and at least in lead III — we can identify a small "on time" rS complex between these 2 time-lines).
• I've added similar RED and BLUE lines to lead aVL — which suggests that very small, subtle underlying "on time" QRS deflections continue for most beats in simultaneously-recorded leads aVR and aVF.
• The presence of continuous "on time" QRS complexes is of course much easier to see in the chest leads — because the predominantly negative artifact complexes occur after the QRS, and therefore do not hide the QRS.
• 
  
• NOTE: The reason the RED and BLUE lines that I've added in Figure-2 are not "vertical" — is that this ECG is from a screen shot, in which angulation has been introduced that results in some distortion. But these colored lines are parallel to the heavy grid lines — such that the timing of complexes in simultaneously-recorded leads is accurate.

Figure-2: I've added colored time lines in simultaneously-recorded limb leads in today's initial ECG.

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The CASE Continues:

Artifact was suspected in today's case. As a result — providers took off, and then reapplied the electrode leads. They then recorded the repeat ECG that is shown below in Figure-3. Your impression?

Figure-3: I've put today's 2 tracings together to facilitate comparison. The repeat ECG (bottom tracing) was recorded after reapplication of electrode leads.

My Thoughts on Figure-3:

After repositioning the electrode leads — the artifact seen in ECG #1 has completely resolved!

• The artifact in ECG #1 was the result of PTA = Pulse-Tap Artifact (See below). 
• ECG #2 confirms that the tiny deflections seen in between the RED and BLUE time-lines in simultaneously-recorded in leads III, aVR and aVF — did indeed represent underlying "on time" QRS complexes that had been partially hidden in these leads.
• ECG #2 shows us the reason the QRS complex in lead II was so hard to see in the initial ECG — namely that after resolution of artifact in ECG #2, we see how tiny the isoelectric QRS in lead II truly is.
• We also see that the very small rS shape of the QRS that we identified in lead III of ECG #1 is comparable to the shape of the QRS in this lead after resolution of artifact.

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PTA (Pulse-Tap Artifact):

As emphasized by Samaniego et al (Emerg Med J 20:356-357, 2003) — there are 2 main sources of artifact, which are "physiologic" vs "non-physiologic" sources.

• Non-Physiologic Artifact Sources — include 60 hertz cycle interference (from AC current devices in the area) — and/or cable or electrode malfunction (ie, loose or broken wire, loose electrode lead connection, etc.).
• Physiologic Artifact Sources — include patient movement and/or voluntary or involuntary muscular activity (ie, tremor, shivering, scratching, coughing, hiccups, distressed breathing — and PTA, among others).

Pulse-Tap Artifact — is physiologic, as it is caused by electrode contact with a pulsating artery in one of the 4 extremity electrodes. Since arterial pulsations are the result of cardiac contraction — PTA occurs at a fixed interval with respect to each preceding QRS complex.

• The 1st time I saw PTA on an ECG — I did not know what this phenomenon was. Since that time — I've seen numerous cases (See ECG Blog #201 — ECG Blog #490 — with more examples of PTA from Dr. Smith's ECG Blog, as shown on my Lead Reversal-Artifact Page). 
• The "good news" is that once you become aware of PTA — you'll be able to instantly identify it by the geometric relationships it produces, as validated by Einthoven's Triangle (as I discussed above for today's case — and reinforce below in today's ADDENDUM).

PEARL #4: The above said — today's case is unique because instead of seeing a single artifact deflection related by a fixed interval to each preceding QRS complex in 2 of the 3 standard leads — we see 2 artifact deflections with each beat! (as per the alternating BLUE and YELLOW arrows in lead aVL of ECG #1 in Figure-3).

• Prior to today's case — all the examples of PTA that I had encountered only a single artifact deflection with each beat.
• However, as shown in today's case — PTA may manifest 2 separate deflections within each R-R interval. This is because the mechanical motion of the pulsating artery may contact the overlying electrode twice during each cardiac cycle ( = Once when the artery expands, as it does during systole — and a 2nd time when the artery relaxes in diastole).

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

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ADDENDUM (4/XXX/2026):

To reinforce the concepts that facilitate instant recognition of the "culprit" extremity causing PTA — I've reproduced in Figure-4 the illustration I developed for My Comment that can be found at the bottom of the page in the September 15, 2023 post in Dr. Smith's ECG Blog.

How to Recognize PTA within Seconds!

Look first at the TOP tracing in Figure-4. The bizarre deflections in multiple leads immediately suggest some form of artifact.

• We know we are looking at artifact in this TOP figure — because despite marked distortion of the QRST in leads II and III — the 3rd standard limb lead ( = lead I) is not affected by artifact!
• We know that this artifact is physiologic and related to the cardiac cycle because of the fixed distance of this artifact after each QRS complex (best seen in the long lead II rhythm strip).
• We also know this artifact is the result of a single "culprit" extremity — because it follows the rules set forth by Einthoven's Triangle.

To facilitate recognition of these Einthoven Triangle rules — I've labeled the BOTTOM tracing in Figure-4 — and have once again added the lead derivations of Einthoven's Triangle (in Figure-5 below).

• Lead I is unaffected by artifact (within the RED rectangle).
• Maximal artifact is seen in the other 2 standard limb leads ( = Leads II and III) — as well as in that augmented lead that is common to both of these maximal artifactual limb leads (in this case lead aVF, that is placed on the LL = Left Leg extremity — with these 3 leads [ = leads II,III,aVF] showing maximal artifact, as shown within the BLUE rectangles in Figure-4).
• 
  
• PEARL #5: It is by looking for that augmented lead that shows maximal artifact — that allows us to instantly identify the "culprit" extremity ( = the LL = Left Leg electrode in today's case).
• The other 2 augmented leads ( = leads aVR and aVL — within the GREEN rectangles) — show approximately half the amount of artifact, compared to the maximal artifact seen in leads II,III,aVF.
• Final confirmation that the only thing that can produce these mathematical relationships is PTA — is forthcoming from seeing a lesser amount of artifact in each of the chest leads (approximately 1/3 the amount of artifact, as shown within the YELLOW rectangles).
• 
  
• BOTTOM Line: It literally took me no more than seconds to recognize PTA in today's initial tracing because: i) Despite bizarre deflections in multiple leads — I immediately saw a normal-looking lead I; — and, ii) I saw maximal artifact in the other 2 standard limb leads ( = leads II,III) — with the fact that the augmented lead showing maximal artifact was lead aVF telling me to look at the left Foot (the LL electrode) for the source of the PTA.

Figure-4: Example of PTA excerpted from My Comment in the September 15, 2023 post in Dr. Smith's ECG Blog.

Figure-5: Using Einthoven's Triangle to determine within seconds the "culprit" extremity of the artifact on your ECG.

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Beyond-the-Core: 

I reproduce below in Figures 6, -7 and -8 — the 3-page article by Rowlands and Moore (J. Electrocardiology 40: 475-477, 2007) — which is the BEST review I’ve seen on the physiology explaining the relative size of artifact amplitude deflections when the cause of the artifact is a single extremity. These principles are illustrated above by the deflections within the colored rectangles in Figure-4.

• As noted by the equations on page 477 in the Rowlands and Moore article: i) The amplitude of the artifact is maximal in the unipolar augmented electrode of the “culprit” extremity — which is lead aVF in Figure-4; and — ii) The amplitude of the artifact in the other 2 augmented leads (ie, leads aVR and aVL) is about 1/2 the amplitude of the artifact in lead aVF (within the GREEN rectangles in Figure-4).
• Similarly — the amplitude of the artifact deflections in the 6 unipolar chest leads in Figure-4 is also significantly reduced from the maximal amplitude seen in leads II, III and aVF (within the YELLOW rectangles in each of the 6 chest leads).
• Nothing else shows fixed relation to the QRS complex in the mathematical relationships described above, in which there is equal maximal artifact deflection in 2 of the 3 limb leads (with no artifact at all in the 3rd limb lead) — in which maximal artifact in the unipolar augmented lead will be seen in the extremity electrode that shares the 2 limb leads that show maximal artifact (as according to Einthoven’s Triangle).

 

Figure-6: Page 475 from the Rowlands and Moore article referenced above (See text).

 

Figure-7: Page 476 from the Rowlands and Moore article referenced above (See text).

 

Figure-8: Page 477 from the Rowlands and Moore article referenced above (See text).