ECG Blog #542 — Why is the Rhythm Irregular?

The ECG in Figure-1 was obtained from a man in his 60s — who is aware of his "irregular heart beat".

Relevant history:  

• The patient is overall healthy — with the exception of some "kidney issues" for which he periodically has "low potassium" and sees a nephrologist.
• The patient notes that his "skipped beats" tend to increase when he is lying down — and generally go away when he stands up.

 

QUESTIONS:

• How to interpret the rhythm in Figure-1?
• What is your differential diagnosis for the irregularity?
• How does the 12-lead ECG help in diagnosing the rhythm?

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

ANSWER:

By the Ps, Qs, 3R Approach to systematic rhythm interpretation (See ECG Blog #185) — I note the following:

• The QRS is narrow everywhere. This tells us that the rhythm is supraventricular.
• The Rate is controlled, averaging ~60/minute — but the rhythm is not Regular. Instead, there is a bigeminal rhythm (ie, Every-other-beat occurs early — such that we see a repetitive pattern with groups of 2 beats followed by a short pause). See ECG Blog #232 for more on the types of bigeminal rhythms.
• P waves are present. These P waves precede each of the 9 beats in the long lead II (as per the RED arrows in the long lead II rhythm strip in Figure-2).
• These P waves are "Related" to neighboring QRS complexes — because the PR interval before each QRS complex is constant (as well as being normal = not more than 1 large box in duration).

Figure-2: I've added RED arrows to highlight regularly occurring P waves that precede each QRS with a constant (conducting) PR interval.

Our Differential Diagnosis:

We've arrived at a relatively common situation in that there is a bigeminal rhythm — in which all QRS complexes are preceded by P waves that appear to be conducting because they have a constant PR interval. At this point — my diagnostic considerations were the following:

• Atrial bigeminy (in which every other beat is a PAC). I thought this to be unlikely — because as I look at all 12 leads in the simultaneously-recorded ECG above the long lead II rhythm strip — P wave morphology looks to be identical for the early beats ( = beats #1,3,5,7,9) — and for the normal sinus-conducted beats ( = beats #2,4,6,8). Because PACs arise from a different place in the atria — P wave morphology of PACs should differ from the P wave morphology of normal sinus-conducted P waves (and it does not in Figure-2).
• Atrial trigeminy with blocked PACs (ie, in which every 3rd beat is a non-conducted PAC). This is also unlikely, because as I look at all 12 leads in the ECG above the long lead II — the T waves of beats #1,3,5,7,9 do not manifest any notching or extra peaking that would alert to hidden, non-conducted P waves.
• 2nd-degree AV block of the Mobitz I Type (which is the same thing as AV Wenckebach) is not present because: i) The  PR interval is not increasing within each of the 2-beat groups; — and, ii) The P-P interval is not regular (or at least almost regular) — as it should be if AV block was present.
• 2nd-degree AV block of the Mobitz II Type is not present. This is because the P-P interval is not regular (or at least almost regular) — as it should be if there was some form of AV block.
• Sinus arrhythmia is also unlikely. This is because the rhythm in Figure-2 represents a fixed pattern of group beating, in which the duration of each of the longer, and each of the shorter R-R intervals is remarkably consistent. In contrast — the duration of R-R interval variation is generally longer with sinus arrhythmia, and manifests much more variability than what we see in Figure-2.
• 
  
• SA (SinoAtrial) block . . .

Conclusion: Having ruled out my top 5 diagnostic considerations that I list above — We are left with the last consideration on my list = SA Block!

• The reason I put SA block last on my list — is that true SA block is the least common of the above entities that I encounter. That said — it "fits best" for the characteristics of today's ECG.
• My proposed laddergram in Figure-3 illustrates what appears to be the mechanism of this patient's SA block. 

Figure-3: My proposed laddergram for today's rhythm.

Laddergram Illustration:

I review how to read laddergrams (as well as presenting a primer for how to draw them) — with numerous examples of laddergrams in ECG Blog #188.

• As I illustrate in Blog #188 — it's EASY to read laddergrams that have already been drawn for you. All the laddergram does — is follow the electrical impulse as it records the cardiac rhythm, showing the path of electrical activity as the electrical impulse makes its way through the Atria — then through the AV Node — and finally through the Ventricles.
• In today's case, since the mechanism of the rhythm is SA Block — the problem arises from within the SA Node.

We show this schematically in Figure-3:

• Beginning with beat #2 — We see that only 2 out of every 3 SA nodal impulses ( = the RED circles at the very top of the laddergram) — are able to make it through the SA Node to arrive in the Atria.
• Keeping in mind that time is recorded horizontally on a laddergram — We can see that once an impulse arrives in the atria, that conduction speeds up. We schematically depict this by drawing the RED lines that pass through the Atrial Tier vertically (representing fast conduction through specialized atrial fibers).
• Conduction then slows down as the electrical impulse exits the atria and passes through the AV Nodal Tier (with this slowing down of conduction accounting for the slight increase in angulation of the RED lines within the AV Nodal Tier).
• On arrival in the ventricles — conduction now speeds up due to fast conduction through specialized His-Purkinje fibers (resulting in less angulation of the RED lines within the Ventricular Tier).

Return for a moment to the SA Nodal Tier at the top of the laddergram: 

• Note the increase in angulation between the 1st and 2nd RED circles in each group — with the 3rd RED circle being blocked — after which the sequence begins again. This represents Wenckebach conduction! (ie, There is 3:2 SA block of the Wenckebach Type).
• For more on SA Block — See the ADDENDUM below! 

Clinical Correlation in Today's CASE:

Going back to the brief history presented at the beginning of this case — We were told that today's patient has a history of hypokalemia — and that he noticed a tendency for his "skipped beats" to increase when lying down, and to go away when standing up.

• In my experience of having looked for true examples of SA block over decades — the phenomenon of SA block is not common in the general population.
• At times I've observed incidental SA block, seemingly without clinical consequence (almost like a normal variant).
• At other times, this rhythm is clearly pathologic — accompanying inferior infarction with 2nd-degree AV block of the Wenckebach (Mobitz I) Type — or — as a component of the arrhythmias seen with SSS (Sick Sinus Syndrome).
• In today's case — I suspect that this patient's periodic hypokalemia was at least contributing to development of his SA block, if not frankly causative.
• Holter monitoring showed this patient's SA block to be without hemodynamic consequence, although persistent through much of the day and night that the Holter was done. I lack the follow-up to know if the rhythm resolved once serum K+ normalized.
• Otherwise — selected patients with cardiac arrhythmias have been known to observe a change in the frequency of certain rhythm disorders depending on body posture (Grauer et al — Fam Prac Recert 12(9):32, 1990). This effect is highly individualized — with literature on the subject scarce, and the mechanism uncertain. Theories include variation in vagal tone, which tends to increase when resting supine. Other theories involve changes in intrathoracic pressure occurring with changes in body position — and/or increased "stretch" on cardiac tissue seemingly being more likely when supine.
• Bottom Line: It's hard to know what to do with a history that the patient notes of a change in arrhythmia frequency depending on body position — other than to accept that in some selected patients, there is evidence that arrhythmias may increase or decrease depending on body position. 

==================================

Acknowledgment: My appreciation to Stewart (from Los Angeles, USA) — for allowing me to use this case and this tracing.

================================== 

 

ADDENDUM:

Figure-4: Essentials of SA Block (Modified from Grauer: ACLS-2013-ePub).

============================

Related ECG Blog Posts to Today’s Case: 

• ECG Blog #312 and ECG Blog #488 — for additional examples of SA block. 
• ECG Blog #147 — Reviews a case showing blocked PACs. 
• ECG Blog #57 — Reviews a case showing atrial bigeminy with blocked PACs.

ECG Blog #541 — Obvious MI; WHAT is the Culprit?

The ECG in Figure-1 was obtained from a patient with chest pain.

• NOTE: The challenge in today's case is not to recognize that prompt cath is needed — because that is obvious.

• The challenge is to determine the culprit artery?

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

Why Care about the "Culprit" Artery?

In addition to the intellectual challenge of trying to predict the "culprit" artery from the initial ECG of a patient with chest pain — there are times when awareness of the likely "culprit" artery is clinically invaluable.

• We are aware of cases in which recognizing the culprit artery on ECG has clued the angiographer into looking especially closely during cath at a specific coronary artery for a subtle but important acute occlusion that might not otherwise be obvious (this being particularly relevant for subtle occlusion of the 1st or 2nd LAD Diagonal branch of the LAD that may not always be obvious on initial inspection).
• Another example for which awareness of the culprit artery may prove invaluble — involves distinction between the RCA (Right Coronary Artery) vs the LCx (Left Circumflex). This is because management decisions may be impacted depending on whether or not RV involvement is likely, which is common when there is a proximal RCA culprit (and extremely rare when the LCx is the culprit artery).
• Knowing there is significant acute RV involvement mandates careful attention to volume hemodynamics (ie, emphasis on prompt cath with PCI, avoidance of sublingual NTG, cautious fluid management of likely hypovolemia) — See Shams and Parks: StatPearls, 2026 and ECG Blog #190 for more on RV MI.

Today's Initial ECG:

I initially thought the "culprit" artery for the obvious acute STEMI in Figure-1 had to be the LCx because: 

• i) Q waves with dramatic hyperacute ST elevation are seen in both high-lateral leads ( = leads I and aVL); 
• ii) Equally marked reciprocal ST depression is present in all 3 inferior leads ( = leads II,III,aVF); — and, 
• iii) A lesser degree of hyperacute ST elevation is also seen in lateral chest leads V5,V6 (and to a lesser extent in antero-lateral leads V3,V4 — which show subtle ST segment straightening, with disproportionately increased size of the overly "bulky" ST-T waves in these leads).

================================== 

The CASE Continues:

The obvious acute STEMI was immediately recognized — and the cath lab was activated.

• This patient's course was complicated. During angioplasty — sustained VT (Ventricular Tachycardia) occurred and the patient arrested. Multiple shocks were required during the extended resuscitation effort. 
• Finally, after successfully opening the acutely occluded RCA — the patient stabilized.
• There was no occlusion in the LCx.

The repeat ECG after successful PCI of the RCA is shown in Figure-2 — placed below the initial ECG.

QUESTIONS:

Take another LOOK at today's initial ECG in Figure-2. Compare it to the repeat ECG recorded after successful PCI of the RCA.

• In today's case — Can YOU explain the cath findings of acute RCA occlusion in the face of a non-occluded LCx?
• Is the repeat ECG consistent with these cath findings?
• 
  
• What clues to identifying the correct "culprit" vessel did I miss in my above description of the findings in ECG #1?

Figure-2: Comparison between today's initial ECG — and the repeat ECG recorded after successful PCI of the RCA.

================================== 

What did the post-PCI ECG show?

In Figure-3 — I highlight findings in the post-PCI ECG consistent with reperfusion following an acute inferior STEMI:

• Large Q waves are seen in each of the inferior leads (YELLOW arrows in leads II,III,aVF).
• The amount of residual ST elevation in the inferior leads is modest in ECG #2 — and there is inferior lead T wave inversion consistent with post-PCI reperfusion.
• Remarkably absent in ECG #2 — are the Q waves that were present in the high-lateral leads in ECG #1 (RED arrows in leads I,aVL).
• The hyperacute ST-T wave changes that had previously been seen in the anterolateral chest leads of ECG #1 — are no longer present in ECG #2. Instead — chest lead T waves are tiny with, if anything — slight J-point ST depression.

Figure-3: I highlight key findings in the post-PCI ECG.

==================================

The Answer:

The reason I mistakenly thought that the "culprit" artery in today's case was the LCx — is that I did not initially recognize LA-LL Lead Reversal!

• In my experience — the most easily overlooked lead reversal is the failure to recognize when the LA (Left Arm) and LL (Left Leg) electrodes are interchanged (See ECG Blog #375 — for another example of this).

What Happens with LA-LL Lead Reversal?

My favorite on-line “Quick GO-TO” reference for the most common types of lead misplacement comes from LITFL ( = Life-In-The-Fast-Lane). I have used the superb web page they post in their web site on this subject for years. It’s EASY to find — Simply put in, “LITFL Lead Reversal” in the Search bar — and the link comes up instantly.

• This LITFL web page describes the 7 most common lead reversals. There are other possibilities (ie, in which there may be misplacement of multiple leads) — but these are less common and much more difficult to predict from a single ECG.
• 
  
• By far (!) — the most common lead reversal is mix-up of the LA (Left Arm) and RA (Right Arm) electrodes. This lead reversal is usually EASY to spot — because it typically produces global negativity of the P wave, QRS and T wave in lead I — which is something that is virtually never normally seen (See ECG Blog #264 — for an example of LA-RA lead reversal).
• 
  
• In contrast — it is EASY to overlook LA-LL reversal — because the ECG picture seen with this type of lead reversal does not immediately stand out as physiologically “off”. For clarity in Figure-4 — I’ve reproduced with slight modification the illustration from LITFL on LA-LL reversal.

Figure-4: LA-LL Lead Reversal (adapted from LITFL).

==================================

The "Tip-Off" to LA-LL Reversal:

As suggested in Figure-4 under the "Quick Guide" to spotting LA-LL Reversal — it is the relative size of the P wave in lead I compared to the size of the P wave in lead II that provides the KEY clue.

• PEARL #1: Because the overall direction of travel by the electrical impulse with sinus rhythm (as the impulse passes from the SA Node to the AV Node) — is most closely oriented toward the location of lead II (lead II being located at +60 degrees in the frontal plane) — the P wave with normal sinus rhythm should not only be positive in lead II — but also larger in lead II than in lead I (which is oriented at 0 degrees in the frontal plane).
• PEARL #2: As stated a moment ago — it is often EASY to overlook LA-LL reversal because the changes in QRST morphology that this lead reversal produce often do not look "off" enough to arose suspicion of some form of lead misplacement. This is especially true if P wave size in the limb leads is relatively small — as it is in today's case.
• In addition, if instead of sinus rhythm an ectopic atrial rhythm is present — then it is possible that an upright P wave in lead II might not necessarily be larger in size than the upright P waves in other limb leads.

What today's ECG should look like ...

Take a look in Figure-5 below — at ECG #1 and ECG #1a, in which I have reproduced today's initial ECG — and compare it to what today's initial ECG would have looked like if the LA and LL electrodes would have been correctly placed.

• Note in Figure-5 that QRST morphology with LA-LL reversal does not change the appearance of complexes in the chest leads — because misplacement of the LA and LL electrodes has nothing to do with the appearance of complexes in the 6 unipolar chest leads.
• Note also in ECG #1 — the overall low amplitude of P waves in each of the 12 leads. As a result — I still interpreted the rhythm in today's initial tracing as sinus, because even though the P wave in lead II is tiny — this tiny P wave in lead II is upright.
• That said — I did notice that the amount of ST elevation in high-lateral leads I and aVL seemed excessive (I rarely see this much ST elevation in leads I and aVL). However, this excessive ST elevation in leads I and aVL did not prompt me to consider LA-LL reversal — because I attributed these changes to acute occlusion of a dominant LCx vessel (with this also accounting for the hyperacute ST-T wave appearance in leads V3-thru-V6 in ECG #1).

Now look at the schematic bottom tracing in Figure 5.

• After accounting for the changes expected when there is LA-LL reversal — Doesn't the limb lead appearance in ECG #1a now look like a large inferior STEMI?

Figure-5: Comparison of the initial tracing in today's case ( = ECG #1) — with what the initial 12-lead ECG would have looked like ( = ECG #1a) after correction to account for LA-LL Lead Reversal.

==================================

Taking another LOOK at the post-PCI ECG:

I conclude today's case with Figure-6 that combines ECG #1a (which is what today's initial tracing would have looked like had the LA and LL electrodes been correctly placed) — with the repeat ECG that was recorded following successful PCI to the "culprit" RCA.

Concluding Question:

• Does the evolution of QRST changes between the 2 serial ECGs in Figure-6 now make sense?

Figure-6: Comparison between what today's initial ECG would have looked like (if LA and LL electrodes had been correctly placed) — with the repeat ECG following successful PCI to the "culprit" RCA.

==================================

CASE Conclusion:

We now see a completely logical conclusion to today's case — with the evolutionary ECG changes in Figure-6 that one would expect following successful PCI reperfusion of the "culprit" RCA.

• ECG #1a — shows the occurrence of ongoing extensive acute inferior infarction, with developing Q waves and marked hyperacute ST elevation in leads II,III,aVF — and with equally marked reciprocal ST depression in high-lateral leads I and aVL.
• Hyperacute (ie, disproportionately "bulky") ST-T waves in chest leads V3-thru-V6 — reflect acute lateral involvement. It is not uncommon to see this in association with acute occlusion of a dominant RCA, in which posterolateral branches wrap around the LV to supply the posterolateral wall (albeit acute lateral wall ST-T wave changes are usually limited to leads V5,V6).
• ECG #1a is also consistent with posterior involvement — because lead V2 lacks the usual slight amount of upward sloping ST elevation that is normally seen with posterior OMI in this lead (ie, I suspect that the ST depression usually seen in leads V2, V3 with posterior OMI — was attenuated by hyperacute changes occurring elsewhere). 
• For example, the slightly coved ST elevation in lead V1 in association with acute RCA occlusion — may be indication of acute RV involvement. Attenuation of anterior lead ST depression by right-sided ST elevation from RV MI may also account for the lack of frank ST depression in lead V2 (although right-sided leads would be needed for confirmation of RV MI).

Following successful PCI of the RCA — the expected evolutionary ST-T wave changes are now seen:

• ECG #2 — shows progression to larger infarction Q waves in each of the inferior leads. The "good news" — is that this is accompanied by deflation of the marked ST-T wave deviations that were seen in the initial tracing:
• Minimal residual ST elevation persists in the inferior leads, that now manifest reperfusion T waves in leads II,III,aVF.
• The prominant reciprocal ST depression that had been seen in leads I and aVL has almost completely resolved.
• The hyperacute ST-T waves previously seen in leads V3-thru-V6 are no longer present.
• The ST segment in lead V1 remains coved — but the subtle ST elevation is no longer seen.

==================================

Acknowledgment: My appreciation to Op. Sanooj (from Calicut, India) — for allowing me to use this case and this tracing.

================================== 

 

ADDENDUM:

I have added this Tab on Technical "Misadventures" — to the Menu at the top of every page in this ECG Blog:

— Where to find this LINK in the Top Menu! —  

All-too-often lead reversals, unsuspected artifact, and other "technical misadventures" go unrecognized — with resultant erroneous diagnostic and therapeutic implications. 

• In the hope of facilitating recognition of these cases — I am developing an ongoing listing on this page with LINKS to examples that I’ve published in this ECG Blog, as well as in Dr. Smith’s ECG Blog where I frequently write commentaries.

ECG Blog #540 — Does it "Fit" the Clinical?

The ECG in Figure-1 was recorded from a 60-ish year old woman who presented via EMS (Emergency Medical Services) to a rural hospital for sudden onset of confusion and seizure activity.

• The patient became agitated and combative during transport. She was non-responsive on arrival in the ED (Emergency Department).
• The patient's medical history was unknown at the time she was seen.

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 a 60-ish year old woman who presented with confusion and seizure activity. (To improve visualization — I've digitized the original ECG using PMcardio).

The ECG in Figure-1:

This patient's initial ECG is clearly abnormal:

• The rhythm is sinus tachycardia at a rate of ~130/minute.
• The QRS is narrow and the PR interval is normal.
• While fully acknowledging the difficulty estimating the QTc with marked tachycardia — the QTc is at most "borderline" (Our on-line QTc calculator suggests that the QTc is less than 450 msec.).
• Otherwise — the frontal plane axis is normal, and there is no chamber enlargement.

Regarding Q-R-S-T Wave Changes:

• Q Waves: Considering small size of the QRS in lead aVL — the Q wave in this lead is large in size (deep and wide). In view of the even smaller size of the QRS in lead I — the tiny Q wave in this lead is also likely to be significant.
• R Wave Progression: There is loss of R wave between leads V1 and V2. Although a reasonably sized R wave returns in lead V3 — transition (when the R wave becomes taller than the S wave is deep) is delayed until between leads V5-to-V6.

The above said, the most concerning findings in today's initial ECG are highlighted in Figure-2 (in the 4 leads within the GREEN rectangles). 

• Hyperacute ST elevation is clearly seen in both high-lateral leads ( = leads I and aVL). There is reciprocal ST depression in lead III. 
• In support of this reciprocal change in lead III — ST segment straightening and a lesser degree of ST depression is seen in the other 2 inferior leads ( = leads II and aVF).

In the Chest Leads: 

• Lead V2 is noteworthy because of its slightly elevated and disproportionately enlarged ST-T wave (being both "fatter"-at-its-peak and wider-at-its-base than expected given modest size of the S wave in this V2 lead).
• The picture in this lead V2 stands out in stark contrast to the complete lack of ST-T wave abnormality in the 4 chest leads that follow.

My Impression of ECG #1:

I initially saw today's initial ECG before knowing the history. 

• As suggested by the schematic image that appears above the ECG in Figure-2 — I immediately thought ECG #1 was diagnostic of the South African Flag Sign (See below for review of this important ECG finding). 

Figure-2: Today's ECG "fits" criteria for the South African Flag Sign!

The South African Flag Sign:

The clinical importance of recognizing the South African Flag Sign — is that in a patient with new Chest Pain — this ECG finding strongly suggests acute occlusion of the 1st or 2nd Diagonal Branch of the LAD (Left Anterior Descending) coronary artery. As per the schematic image above the ECG in Figure-2 — the South African Flag Sign is present when there is: 

• i) ST elevation in leads I, aVL and V2; 
• ii) Reciprocal ST depression in lead III (ST depression is also often seen to a lesser degree in neighboring inferior leads II and aVF);
• iii) No ST elevation in any chest lead except for lead V2.

I previously reviewed the South African Flag sign in ECG Blog #320 (See Pearl #1 in that Blog #320 post) — as well as in My Comment at the bottom of the page in the January 18, 2025 post in Dr.Smith's ECG Blog.

• PEARL #1: Sometimes acute proximal LAD occlusion will initially look like an acute occlusion limited to the 1st or 2nd Diagonal Branch. This is because early on — ST elevation may only be seen lead V2, and not yet in leads V1,V3,V4. A tincture of time (and serial ECGs) will usually clarify the situation.
• PEARL #2: The clinical significance of being aware of a Diagonal Branch "culprit" — is that: i) Since only 1 chest lead shows ST elevation (ie, lead V2) — this pattern will not “fit” the definition of a STEMI, because only 1 chest lead shows ST elevation (and by definition, to satisfy criteria for an anterior STEMI — 2 contiguous chest leads must show ST elevation); — and, ii) Recognizing the S. African Flag Sign alerts the angiographer where to look for the “culprit” artery. We have seen cases in which a capable angiographer initially missed the cath finding of Diagonal Branch occlusion — BUT — seeing this ECG pattern conveyed the need for another LOOK at the cath film, with focus on the expected area for Diagonal Branch takeoff then revealing subtle-but-complete occlusion in one of the Diagonals. 

The History Doesn't "Fit" ...

The problem with today's case — is that the history does not "fit" with the ECG picture that strongly suggests acute occlusion of the 1st or 2nd Diagonal Branch of the LAD.

• Today's patient had no chest pain. Instead — this 60-ish year old woman presented with neurologic symptoms, and arrived at the hospital in a non-responsive state.
• While possible for there to be a "silent" MI (ie, in which chest pain is absent) — the clinical presentation of today's case is contrary to what one would expect for an acute cardiac event. Could something else be going on?

=================================

The CASE Continues:

Given the atypical history for an acute MI (especially in view of this patient's non-responsive state on arrival at the hospital) — the cardiologist on call appropriately opted to explore other etiologies before deciding on where best to transfer this patient (as the capability for cardiac catheterization and/or acute stroke management was not available at the rural hospital where this patient was brought to).

• Complicating assessment — an initial Troponin value was moderately elevated!
• The patient was transferred to a facility with cardiac catheterization and acute stroke management capability.
• Initial imaging suggested a necrotic ring-enhancing mass with significant surrounding edema that was thought to represent a brain tumor.

Figure-3 shows the follow-up ECG that was recorded ~4 hours after ECG #1.

• How do you interpret this repeat tracing? 

Figure-3: Comparison between the follow-up ECG recorded ~4 hours after the initial tracing.

Interpretation of ECG #2:

Compared to ECG #1 — the repeat ECG in Figure-3 shows the following:

• Some slowing of the sinus tachycardia (from ~130/minute — down to a rate of ~110/minute).
• Deflation of virtually all hyperacute ST-T wave changes that had been seen 4 hours earlier.

CASE Conclusion:

• The repeat Troponin was essentially unchanged from its initial value (showing similar moderate elevation).
• Cardiac Cath was performed — and showed completely normal coronary arteries — with an abnormal wall motion abnormality typical for Takotsubo (Stress) Cardiomyopathy.
• Further brain imaging suggested that rather than a brain tumor — the patient's neurologic injury was the result of necrotic transformation from a stroke. Given that the patient's neurologic condition returned to near normal — her longterm prognosis was promising.

Lesson-to-be-Learned:

• As discussed on a number of occasions in this ECG Blog — CNS Catastrophes (from CNS bleeds, stroke, tumor, trauma, undifferentiated coma, etc.) — are notorious for producing some of the most bizarre-looking ECGs that are prone to simulate acute infarction (See ECG Blog #299, among others).
• Today's case illustrates just how close the pseudoinfarction pattern from a "CNS catastrophe" may be! (For all the world — Today's initial ECG suggested acute 1st or 2nd Diagonal occlusion).
• Despite the alarming, seemingly acute ST-T wave changes in today's initial ECG — the clinical scenario did not "fit" for an acute MI. While fully aware that some acute MI patients may not necessarily present with chest pain — it was this "disconnect" between the initial ECG and the patient's history that clued to on call cardiologist into the need to explore other potential diagnoses.
• For other examples in which the unexpected clinical presentation suggested that acute-looking ECG changes represented a pseudoinfarction pattern (and not acute infarction) — Check out the February 20, 2025 post in Dr. Smith's ECG Blog (with My Comment at the bottom of the page in that post).
• A common denominator between these CNS catastrophes and the pseudoinfarction patterns they produce on ECG — is greatly increased endogenous catecholamines! This helps to explain the common finding of Takotsubo Cardiomyopathy (Stress Cardiomyopathy) that so often accompanies these conditions. It also explains many of the abnormal ECG findings, as well as the moderately elevated but non-rising Troponin value (See ECG Blog #456 — for review of the ECG findings in Takotsubo Cardiomyopathy).

==================================  

Acknowledgment: My appreciation to Paul Carr and Nataliya Szozda (from Toronto, Canada) for contributing this case.

==================================