ECG Blog #521 — Inferior MI? — Anything else?

The ECG in Figure-1 was obtained from a middle-aged man with a long history of smoking — who presents with severe new-onset CP (Chest Pain).

• The patient reports having 2 episodes of severe CP — each of which spontaneously resolved. He then presented to the ED (Emergency Department) several hours after the 2nd episode (ie, He was not having CP at the time ECG #1 was recorded).
• The initial Troponin level was negative for acute infarction.

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 middle-aged man with CP — but who was asymptomatic at the time this ECG was recorded. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on Today's ECG:

The ECG in Figure-1 shows a regular sinus rhythm at ~80/minute. Intervals (PR, QRS, QTc) and the axis are normal. There is no chamber enlargement.

Regarding Q-R-S-T Changes:

• Q Waves: There are q waves in the lateral leads (ie, leads I,aVL; and leads V4,V5,V6). These have the appearance of normal septal q waves — in that all of these q waves are narrow and small in size.
• R Wave Progression: Normal (ie, R wave amplitude progessively increases as we move across the chest leads — with transition occurring normally between leads V2-to-V4).

Regarding ST-T Wave Changes:

• In this patient with new CP — My "eye" was immediately drawn to the "scooped" ST depression in lead V2 (within the RED rectangle in Figure-2). 
• This ST depression continues in neighboring leads V3,V4 (RED arrows in these chest leads) — but has largely resolved by lead V5.
• 
  
• ST-T wave changes in the inferior leads are more difficult to evaluate (See below).

Figure-2: I've labeled the ECG in today's case.

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ANSWERS: Putting It All Together . . .

There are a number of reasons why assessment of today's case is challenging. Unfortunately, we lack many details and only have limited follow-up. That said, my purpose in presenting this case — is that the following points can still be made from the brief history we are given, and from today's initial ECG:

• The history of several episodes of new-onset and severe CP in this middle-aged man with a longterm history of smoking immediately place him in a higher-risk group for having an acute cardiac event. Awareness of this clinical situation should lower our threshold for accepting ST-T wave findings as abnormal.
• Availability of a prior ECG for comparison would have made it much easier to determine if the ST-T wave changes that we see in ECG #1 are acute.
• Repeating the ECG within 10-20 minutes of the initial tracing is advisable when symptoms are new and there is uncertainty about whether ST-T wave findings are acute — as diagnostic "dynamic" ST-T wave changes may sometimes be seen within minutes (See ECG Blog #115 — and ECG Blog #459). 
• Obtaining a bedside Echo may sometimes be diagnostic if it shows a localized wall motion abnormality. (While Echo may be diagnostic if positive — a normal Echo does not rule out an acute event if the patient is not having CP at the time the Echo is done).
• The initial normal hs-Troponin in today's case in no way rules out an acute cardiac event (See ECG Blog #508). In addition to infarct size, whether or not Troponin will be elevated depends on how long the "culprit" artery is occluded for — which we do not know in today's case. But if the duration of time that the "culprit" artery is occluded is very brief — there may not be any Troponin elevation at all (and on occasion — the first 2 Troponin values may come back normal despite the patient going on to develop a STEMI).

Consider the following additional points:

• The patient was not having CP at the time ECG #1 was recorded. This suggests that spontaneous resolution of acute coronary occlusion may have occurred — in which case acute ST-T wave abnormalities that were present during CP may signficantly improve (and even resolve).
• That said — there normally should be slight, gently upsloping ST elevation in leads V2 and V3. This is why in a patient with new CP — the finding of ST depression that is maximal in leads V2,V3,V4 (as is seen in ECG #1) — is diagnostic of acute posterior MI until proven otherwise! (See ECG Blog #351 — and ECG Blog #298, among many others).
• NOTE: Because of a common blood supply to the inferior and posterior walls of the left ventricle — I always look for acute inferior lead changes whenever I suspect acute posterior OMI. Unfortunately, the inconsistent ST-T wave appearance in the inferior leads of ECG #1 makes it all-but-impossible to assess the inferior leads (ie, Whereas complex B within the BLUE rectangle suggests a straightened, hyperacute ST segment with terminal T wave inversion — complexes A and C do not look acute).

BOTTOM Line: Maximal ST depression in leads V2,V3,V4 in this patient with a history of new CP suggests acute posterior OMI until proven otherwise. Knowing that this patient's CP had completely resolved at the time ECG #1 was recorded may account for relatively modest ST-T wave changes in the remaining leads.

• Ideally — the cath lab would be activated on seeing ECG #1.
• If the interventionist was reluctant to catheterize the patient at this point — then the following actions might serve to expedite acceptance to perform this procedure: i) Repeating the ECG within 10-20 minutes — and if this initial repeat tracing failed to show dynamic changes — follow-up with a few more repeat tracings within the hour; — ii) Immediately repeating the ECG if at any time the patient's CP returns; — iii) Searching for a prior ECG on this patient (that most probably would confirm that the ST depression in leads V2,V3,V4 is acute); — iv) Performing bedside Echo, looking for a localized wall motion abnormality; — and, v) Looking for any elevation in the 2nd Troponin value (which in a patient with new worrisome symptoms is indication for prompt cath — even when ECG changes are less than diagnostic).

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CASE Follow-Up: 

My follow-up is limited — but the results that I have reinforce the above clinical points:

• The repeat Troponin was elevated at ~60 (I'm not sure of units or norms — but a value of 60 is clearly elevated).
• A repeat ECG done many hours later seemed to show less acute changes compared to ECG #1.
• Bedside Echo done the next day showed a wall motion abnormality localized to lateral and posterolateral segments.
• Cardiac cath done the next day confirmed the LCx (Left Circumflex) as the "culprit" artery (I do not know about additional cardiac cath findings).

Lessons to Be Learned:

• Waiting for ST elevation before activating the cath lab misses a substantial percentage of acute coronary occlusions. Acute posterior OMI is most easily recognized in a patient with new CP by maximal ST depression in leads V2,V3,V4 — which is much easier to recognize and more reliable than than trying to assess the dampened amplitudes obtained with posterior leads (See ECG Blog #80). Posterior OMI is the best example of how we can make a presumptive diagnosis of acute coronary occlusion without insisting on ST elevation
• The diagnosis of acute OMI could have been made significantly earlier in today's case.
• Delay in diagnosis (and therefore in reperfusion treatment of acute coronary occlusion) comes at a price. The most benefit from reperfusion occurs within the first 4 hours after acute coronary occlusion (Every 2-hour delay results in 60% more myocardium infarcted). Documentation of these Lessons-to-be-Learned is forthcoming in these 3 posts from Dr. Smith's ECG Blog ( = the February 8, 2026 post — the January 15, 2026 post — and the October 23, 2025 post — with My Comment appearing at the bottom of the page in each of these posts).

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Acknowledgment: My appreciation to Hisham Alshamekh (from Egypt) for the case and this tracing.

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ADDENDUM (3/7/2026): 

For more regarding the concept and ECG interpretation of OMIs (that do not satisfy millimeter-based STEMI criteria):

• Check out ECG Blog #337 — that reviews a case with focus on distinction between a "NSTEMI" vs an OMI.
• Consider the 2 Audio Pearls at the bottom of this page.
• Consider Figure-3 — which reviews some ECG findings to look for when you suspect an acute OMI in a patient who does not satisfy the millimeter-based STEMI criteria that I review below this Figure.

Figure-3: ECG findings to look for when your patient with new-onset cardiac symptoms does not manifest STEMI-criteria ST elevation on ECG.
= = = = =
KEY Note #1: Insistence in satisfying millimeter-based STEMI criteria before considering prompt cath with PCI (or thrombolytic therapy when access to 24/7 cath-capability is not available) — will miss at least 1/3 of all acute coronary occlusions. In a patient with new CP — attention to the ECG findings in Figure-3 may allow you to identify these patients with an acute OMI despite lacking STEMI criteria.
= = = = =
KEY Note #2: Loss of potentially viable myocardium is actually much greater than that implied in Key Note #1 — because even for patients in whom a "STEMI" is eventually recognized — by waiting until millimeter-based criteria are finally satisfied, the needed reperfusion therapy (PCI or thrombolytic therapy) is all-too-often delayed (often by many hours!). Time is critical! — as the greatest amount of potential myocardial-saving benefit occurs when reperfusion therapy is provided within the first few hours! (with the self-fulfilling prophecy that the outdated and inferior "STEMI-paradigm" gets perpetuated in the literature — because data will be recorded saying PCI was delivered "within minutes" of STEMI elevation [neglecting the clinical reality that OMI-criteria will often have been present hours earlier! ] ).
= = = = =
Note #3: See ECG Blog #318 — for clarification of T-QRS-D (Terminal QRS Distortion = my 2nd bullet in Figure-4).

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How a "STEMI" is Defined:

I've excerpted the following Akbar and Mountfort's citation in StatPearls, 2024 — of ECG Guidelines for defining a "STEMI" from the AHA (American Heart Association), ACC (American College of Cardiology), ESC (European Society of Cardiology), and the WHF (World Heart Federation):

• New ST-segment elevation of ≥1 mm at the J point in 2 contiguous leads (except in leads V2 and V3).
• 
  
• In leads V2 and V3:
• ST elevation ≥2 mm for men >40 years of age.
• ST elevation ≥2.5 for men ≤40 years of age.
• ST elevation ≥1.5 mm for women.

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—  —

ECG Media PEARL #10 (10 minutes Audio) — reviews the concept of why the term “OMI” ( = Occlusion-based MI) should replace the more familiar term STEMI — and, reviews the basics on how to predict the "culprit" artery.

—  —

ECG Media PEARL #11 (6 minutes Audio) — Reviews how to tell IF the “culprit” (ie, acutely occluded) artery has reperfused, using clinical and ECG criteria.

ECG Blog #520 — How Certain are You?

You are asked to interpret the ECG in Figure-1. Which of the following choices provides the best answer?

• A) AFib with a rapid ventricular response.
• B) SVT with RBBB aberration.
• C) The rhythm could be VT.
• D) The rhythm is VT. 

Figure-1: Which of the above choices is the best answer?
= = = = = = =
[ Abbreviations: AFib (Atrial Fibrillation) — SVT (SupraVentricular Tachycardia) — RBBB (Right Bundle Branch Block) — VT (Ventricular Tachycardia)].

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MY Approach to Today's Tracing:

As much as we always want at least a brief history (including at least the age of the patient — and the reason why the ECG was recorded) — we are not provided with one. Nevertheless, there is enough information to select the right answer.

• Take another LOOK at today's tracing in Figure-2. For clarity — I've numbered the beats in the long lead II rhythm strip.

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

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MY Thoughts:

By the P's, Q's, 3R Approach (See ECG Blog #185) — the rhythm in Figure-2 is a regular WCT (Wide-Complex Tachycardia):

• The overall rhythm appears to be Regular. This is best assessed in simultaneously recorded leads I and III, in which it is easier to see the consistency in the R-R interval (and more difficult to appreciate in lead II — where there is more artifact distortion).
• The Rate of the rhythm is slightly more than 150/minute (ie, with an R-R interval of slightly less than 2 large boxes in duration).
• The QRS is wide (at least 3 small boxes in duration — therefore ≥0.12 second).
• 
  
• Are there P waves?

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What Can We Already Rule Out?

• The fact that the R-R interval in Figure-2 is regular effectively rules out AFib (and if we can confirm that P waves are truly present — this would definitively rule out AFib).

What We Know:

• The rhythm in Figure-2 is a regular WCT (Wide Complex Tachycardia).
• The rate of the rhythm is slightly more than 150/minute. 
• There is no clear sign of sinus P waves (ie, There is no consistent upright P wave with constant PR interval preceding each QRS complex in the long lead II rhythm strip).
• The above said — a number of small upright deflections in the baseline do appear to be present throughout the long lead II. These could be P waves.
• PEARL #1: Assuming today's patient is an adult — by far, the most common cause of a regular WCT rhythm without clear sign of sinus P waves is VT. Therefore — We need to assume VT until proven otherwise!

PEARL #2: We can go 1 step further in our differential diagnosis by looking at QRS morphology. 

• Although the predominantly upright QRS complex in lead V1, in association with wide terminal S waves in lateral lead V6 could be consistent with RBBB conduction — you should virtually never see an all negative QRS complex in lead I with a supraventricular rhythm. 
• Based on QRS morphology then — this strongly suggests that the rhythm in Figure-2 is VT (which means we can effectively rule out SVT with RBBB aberration). 

QUESTION:

• But — Are we 100% certain that today's rhythm is VT?

  

My Next Thoughts:

At this point in my interpretation — I would estimate the statistical likelihood that the rhythm in today’s case is VT at over 95%! (based on the fact that sinus P waves are absent in this regular WCT rhythm — and the finding that QRS morphology in lead I is all negative). That said — I prefer to increase the accuracy of my interpreatation as much as possible — and — there is a way in today's case that we can increase the statistical likelihood of VT to 100%

• To Emphasize: IF we were at the bedside with this patient — the 1st thing we would do is determine if the patient is hemodynamically stable! That's because if the patient is not stable with this rhythm — then it would no longer matter what the rhythm is, because synchronized cardioversion would then be immediately indicated.
• But assuming that this patient is hemodynamically stable — this gives us a moment in time to quickly look a little closer.
• 
  
• Please NOTE: I have described my above thoughts in slow motion. With practice and experience — You should be able to arrive at this point in the process in no more than 10-to-15 seconds!

The Next Step: So — Are there P waves in Today’s ECG?

Take another LOOK at the ECG in Figure-2.

• Is there an EASY way to determine with certainty whether P waves are (or are not) present in today’s ECG?

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ANSWER: Are there P waves in Today’s ECG?

The KEY to optimizing the accuracy of our interpretation — is to determine IF underlying regular sinus P waves are present!

• PEARL #3: As I have often emphasized in this ECG Blog — the simple step of labeling P waves is incredibly helpful for determining the presence and nature of underlying atrial activity.
• In Figure-3 — I’ve labeled with RED arrows those small upright deflections in the long lead II rhythm strip that look like they may represent P waves.
• If these RED arrows in Figure-3 are in fact highlighting the presence of regular underlying P waves — Does this suggest what the P-P interval might be?
• 
  
• PEARL #4: If we can demonstrate that the small upright deflections in Figure-3 remain consistently regular throughout the long lead II — this would prove that these small upright deflections do represent an underlying rhythm of regular atrial activity. 
• To do this — I look to see what the shortest distance between 2 consecutive RED arrows appears to be. Doesn't it look like this shortest distance repeats between the 4th and 5th RED arrows — and between the 7th and 8th RED arrows?

Figure-3: I've highlighted with RED arrows the small upright deflections in the long lead II rhythm strip that I can clearly see.

PEARL #5: To determine within seconds if an underlying rhythm of regular P waves may be present in the long lead II — You have to use calipers!

• To Emphasize: I am not encouraging the use of calipers if your patient is unstable. A hemodynamically unstable patient in a WCT rhythm should be immediately cardioverted!
• But IF the patient whose rhythm is shown in Figure-3 is hemodynamically stable — it takes no more than seconds using calipers to "walk out" the rhythm that I've highlighted with colored arrows in Figure-4.

Figure-4: I've added WHITE and PINK arrows to Figure-3.

Breaking Down Figure-4: 

All that I've done to get from Figure-3 to Figure-4 — is to set my calipers to the P-P interval suggested by the distance between the 4th and 5th RED arrows in Figure-4 (which equals the distance between the 7th and 8th RED arrows) — and then to "walk out" this presumed P-P interval with your calipers throughout the remainder of the long lead II.

• Although on-time regular wide QRS complexes prevent us from seeing P waves under the WHITE arrows that I've added to Figure-4 — a definite underlying upright deflection can clearly be seen peaking out from the tail end of the QRS of beats #7 and 28 (ie, under each of the 2 PINK arrows).
• This tells us that the colored arrows in Figure-4 represent an underlying rhythm of regular P waves occurring at an atrial rate of ~90/minute!

PEARL #6: The P waves represented by the colored arrows in Figure-4 are unrelated to neighboring QRS complexes. This tells us there is complete AV dissociation occurring throughout the long lead II rhythm strip — which proves that the rhythm is VT!

• In my experience — AV dissociation is very much overdiagnosed! This is because of the tendency to assume there is AV dissociation whenever clinicians see any suggestion of underlying baseline deflections. In my decades of following up on regular WCT rhythms — most cases of WCT rhythms labeled as showing "AV dissociation" do not truly represent this finding.
• It is because true AV dissociation proves that a WCT rhythm is VT — that I feel it best to avoid the diagnosis of AV dissociation unless you can clearly demonstrate the presence of underlying regular P waves throughout a significant portion of the rhythm. Doing so can only be done by use of calipers.
• Unfortunately — the clinical reality is that it is rare to see AV dissociation in faster WCT rhythms. This is because when a WCT occurs at a faster rate — the wide QRS complexes (and accompanying often large-sized ST-T waves) are highly efficient at concealing underlying on-time P waves that are hidden within.
• 
  
• BOTTOM Line: The colored arrows seen in Figure-4 are convincing of AV dissociation — because they consistently occur thoughout the long lead II rhythm strip. This proves beyond doubt that today's WCT rhythm is VT!

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NOTE: For readers wanting more regarding the concepts and clinical use of AV dissociation for assessing the etiology of a regular WCT rhythm — Review of ECG Blog #335 should prove insightful.

• Additional examples of "My Take" on assessing the regular WCT rhythm can be found in ECG Blog #196 — Blog #220 — Blog #263 — and Blog #283 — among many others.

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Today's CASE Continues:

The patient in today's case is a middle-aged man with a history of hypertrophic cardiomyopathy. He was seen for new palpitations that occurred in association with today's presenting rhythm.

• Paramedics on the scene cardioverted the patient. This worked momentarily to restore a normal rhythm — but soon after the WCT rhythm returned.
• IV Amiodarone was started. The patient quickly improved — and vital signs stabilized. 
• At this time — the repeat ECG shown at the bottom of Figure-5 was recorded. 

QUESTIONS:

• How do you interpret the rhythm in the repeat ECG?
• Does ECG #2 support our diagnosis of VT in the initial tracing?

 

Figure-5: The repeat ECG recorded after starting IV Amiodarone. The initial ECG is shown on top (with RED arrows highlighting AV dissociation from the underlying regular sinus P waves). 

The Rhythm in ECG #2:

The repeat ECG ( = the tracing at the bottom of Figure-5) — shows a bigeminal rhythm, in which every-other-beat is a PVC.

• Once again — the KEYs to interpreting the repeat tracing are to: i) Label the P waves in ECG #2; — and, ii) Determine if the P waves in ECG #2 are related to neighboring QRS complexes?

Note the following:

• Regular P waves are seen in the repeat ECG throughout the long lead II rhythm strip ( = RED arrows in the bottom tracing in Figure-6). The rate of these P waves in the repeat tracing is slightly slower than it was in ECG #1.
• Normal sinus rhythm conduction is seen in ECG #2 for all odd-numbered beats — as determined by the fixed PR interval before beats #1,3,5,7,9,11,13,15,17.
• All even-numbered beats in ECG #2 are PVCs. The fact that on-time sinus P waves continue throughout the long lead II rhythm strip in this repeat tracing proves that beats #2,4,6,8,10,12,14,16 are PVCs — as is shown in the laddergram in Figure-7 ( = the only way for on-time sinus P waves to continue uninterrupted in Figure-7 — is for the even-numbered beats to originate from the ventricles, with retrograde conduction of these PVCs not reaching all the way back to the atria).
• Finally — Note that QRS morphology of the premature wide beats in ECG #2 is identical to QRS morphology in each of the 12 leads of the initial ECG (thereby confirming our diagnosis of VT for ECG #1).

Figure-6: I've labeled P waves in the repeat ECG.

 

Figure-7: Laddergram of the repeat ECG.

CASE Conclusion:

• The paramedic team transported the patient to the hospital. Referral was made to EP cardiology for consideration of an ICD (Implantable Cardioverter-Defibrillator).

 

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Acknowledgment: My appreciation to Konstantin Тихонов (from Moscow, Russia) for the case and this tracing.

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ECG Blog #519 — LV "Strain" or Acute MI?

The ECG in Figure-1 was obtained from a patient who presented to the ED (Emergency Department) with typical CP (Chest Pain).

QUESTIONS:

• Given this brief history — How would you interpret this ECG?
• What is in your differential diagnosis?

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

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MY Thoughts on this CASE:

The history in this patient who presented to the ED with typical CP is clearly worrisome — and immediately places this patient in a higher-risk group for having an acute cardiac event. This places the "burden of proof" on us as providers to rule out an acute event — rather than the other way around (ie, We need to assume the abnormal findings on this ECG represent an acute MI until we can prove otherwise!).

Looking at today’s initial ECG in Figure-1:

• The rhythm in ECG #1 is sinus at ~80/minute. All intervals (PR,QRS,QTc) and the axis are normal.
• There are deep S waves in anterior leads V2 and V3. This may represent LVH (Left Ventricular Hypertrophy).
• The principal concern in this patient with new CP are the tall T waves with ST elevation in leads V2 and V3.
• 
  
• PEARL #1: When LVH is manifest on ECG by the presence of deep anterior S waves — then LV "strain" from LVH (and not from acute infarction) may manifest as anterior ST segment elevation!

Consider the ECG in Figure-2 — which I’ve taken from ECG Blog #461:

• The BLUE arrows in Figure-2 clearly highlight significant ST elevation. However, this ST elevation is not the result of acute infarction. Instead — this patient turned out to have marked LVH without any evidence for acute ischemia or infarction (Note the very deep S waves in leads V2,V3).
• Note within the RED insert in Figure-2 how the mirror-image of the ST-T elevation in these anterior leads — looks exactly like the typical ECG picture that we are used to seeing when LV “strain” is present in the lateral chest leads.

Figure-2: Tracing from my ECG Blog #461 — in which anterior ST elevation was not because of acute MI, but instead was solely the result of LV "strain" in a patient with marked LVH!

Take another LOOK at today’s initial ECG — that I’ve reproduced in Figure-3. Keep in mind that this patient presented to the ED for new CP.

• As noted earlier — there are deep S waves in leads V2,V3. 

QUESTIONS:

• Is the ST elevation and the tall T waves that we see in these anterior leads the result of LV “strain” — or — Does it seem like these ST-T wave changes may be more than what we might expect from simple LVH?
• 
  
• In view of this patient’s CP — Is there anything we can do? (ie, to help distinguish if the anterior lead ST-T wave changes in Figure-1 are the result of LV “strain? — or acute ischemia? — or, of both LV “strain” + acute ischemia?).

Figure-3: Today’s initial ECG — that I’ve reproduced from Figure-1.

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Confession: When I first saw today’s case — I was not at all certain regarding my impression for distinguishing between LV “strain” vs acute ischemia with infarction.

• Instead — I saw features consistent with LVH (ie, the deep S waves in leads V2,V3) — and — features consistent with acute ischemic ST elevation.

For clarity in Figure-4 — I’ve labeled ECG findings prompting my concern:

• PEARL #2: The concept of “proportionality” is KEY. While fully aware from clinical examples such as the case I illustrate above in Figure-2 — T wave amplitude in leads V2,V3 in Figure-3 "looks" disproportionately increased (both of these T waves rising ~10 mm above the baseline). The base of these T waves also “looks” wider-than-I-would-expect from simple LVH.
• To Emphasize: I have no numerical numbers for telling me the “accepted size” of T waves that would be consistent with LV “strain” from LVH. Instead — I rely on “pattern recognition” that my “eye” instantly recognizes from the experience of seeing countless cases. Even then — I was still not certain of my suspicion from pattern recognition alone. 
• That said — In support of my suspicion that the T waves in leads V2,V3 are hyperacute (and potentially indicative of acute ongoing infarction) — was the following: i) The clinical setting (Today’s patient presented with new CP); — ii) Neighboring leads V1 and V4 show subtle-but-real ST segment straighteing (slanted RED lines in these leads in Figure-4); — and, iii) Subtle ST segment flattening (if not slight ST depression) is seen in lateral lead V6 (BLUE arrow in this lead) — potentially consistent with an early Precordial "Swirl" pattern (See ECG Blog #380 — for review of Precordial Swirl).
• 
  
• P.S.: Limb lead findings in ECG #1 did show some ST segment flattening — but I interpreted this as nondiagnostic. However, the above noted chest lead findings were enough to significantly increase my index of suspicion.

Figure-4: I've labeled the initial ECG.

PEARL #3: The clinical reality is that we will not always be able to confirm our clinical suspicion as to whether or not a patient's symptoms are indicative of acute ongoing infarction from a single initial ECG. Fortunately — there are some simple, routine actions that will often very quickly provide a definitive answer. Among these actions are the following:

• i) Check Troponin. In 2026 — Patients presenting to an emergency facility for new CP will almost automatically have a serum Troponin assay immediately drawn. Initial results are often forthcoming within 1 hour in an active ED. Any degree of Troponin elevation in a patient with new worrisome symptoms is significant (and may of itself be indication for prompt cath — even with a nondiagnostic ECG). 
• KEY Point: Although any elevation of Troponin is significant in a patient with new worrisome CP — Keep in mind that an initial normal hs-Troponin does not rule out acute infarction! (See Pearls #3,4,5 in ECG Blog #392 — for more on the fine points regarding use of serum Troponin levels).
• 
  
• ii) Look for a prior ECG on your patient. Perhaps the fastest and easiest way to determine if seemingly nondiagnostic ECG findings are "new" (therefore indicative of a new acute change until proven otherwise) — is to compare the initial ECG with a baseline tracing on the patient.
• iii) Do bedside Echo — looking for a localized wall motion abnormality. Interpreting bedside Echo for a wall motion abnormality can be tricky — and requires a skilled operator. But if your patient with new CP manifests a localized wall motion abnormality — this is highly suggestive of acute ongoing infarction. (NOTE: If the Echo is normal — but your patient was not have CP at the time the Echo was done — then this does not rule out acute infarction).
• 
  
• iv) Repeat the ECG within a short period of time (I favor repeating the ECG in a patient like the one in today's case within 10-to-20 minutes!). It is often surprising how quickly (and dramaticallly) a non-diagnostic initial ECG may change within a very few minutes!

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The Repeat ECG ...

Providers on the case "read my mind". They were suspicious of an ongoing acute event from the history and initial ECG — but could not at that point convince the interventionist.

• A prior tracing was not readily available for comparison.
• Providers repeated the ECG within 15 minutes.

To facilitate comparison in Figure-5 — I've put the initial ECG next to the repeat ECG done just 15 minutes later.

• To no one's surprise — Cardiac catheterization was immediately arranged on seeing the repeat ECG.

 

Figure-5: Comparison between today's 2 ECGs.

PEARL #4: Clinicians sometimes wait much longer than is needed to repeat an initial non-diagnostic ECG. Especially when CP is ongoing — the dynamic ST-T wave changes that are obvious in Figure-5 occurred within 15 minutes!

• There is no need to wait longer than this to repeat the initial ECG.
• And if you are still concerned by the history — but the 1st repeat ECG remains non-diagnostic — Have a low threshold to continue repeating frequent ECGs until such time that you can feel comfortable with a definitive diagnosis. 

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CASE Conclusion:

• Unfortunately — I do not have further follow-up on this case.
• That said — the cause of the serial ECGs in Figure-5 is virtually certain to be acute proximal LAD occlusion.

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Acknowledgment: My appreciation to Tayfun Anil Demir (from Antalya, Turkey) for the case and this tracing.

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ECG Blog #518 — A WCT with Low Urine Output ...

The ECG in Figure-1 was obtained from a previously healthy middle-aged man — who presented to the ED (Emergency Department) with acute shortness of breath. The patient complained of malaise — but no chest pain or other bodily pain. He has had difficulty urinating.

QUESTIONS:

• How would you interpret the ECG in Figure-1?
• What are your first clinical considerations?

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

MY Thoughts on the Rhythm in Figure-1:

Our 1st clinical consideration given the ECG shown in Figure-1 — is to ensure that this patient is hemodynamically stable.

• Determination of hemodynamic stability is not readily apparent from the brief history we are given (ie, Today’s patient is short of breath — but not in pain; The heart rate is ~130/minute, but we do not know the patient’s blood pressure).
• Sometimes, “Ya just gotta be there” — in order to determine if the patient is sufficiently stable to allow a moment to more closely assess the rhythm.

Let’s assume that this patient is hemodynamically stable! 

By the P's, Q's, 3R Approach (See ECG Blog #185) — the rhythm in Figure-1 is a regular WCT (Wide-Complex Tachycardia):

• The rhythm itself is Regular.
• The QRS is obviously wide (at least 4 small boxes in duration ==> ≥0.16 second — which is very wide).
• The Rate of the ventricular rhythm is ~130/minute.
• P waves are absent (which means that the 5th Parameter = Are P waves Related to neighboring QRS complexes? — is to be answered with a “No” —). 

As is often emphasized in this ECG Blog — We need to assume VT until proven otherwise whenever we see a regular WCT rhythm without clear sign of P waves.

• This leads us to our next STEPs in assessing a regular WCT without P waves: i) LOOK at QRS morphology. We want to determine if QRS morphology during the WCT rhythm provides further clue to the etiology of the rhythm (ie, A QRS morphology not consistent with any known form of conduction defect would strengthen our assumption of VT).
• At the same time: ii) We want to look at ST-T waves during the WCT rhythm to see if this suggests acute ischemia or other abnormality.

Take another LOOK at QRS and ST-T wave morphology in Figure-1.

• Consider that this patient has recently felt ill (malaise) — and has had trouble urinating ...

Figure-1: Take another LOOK at the ECG in Figure-1 ...

Taking Another LOOK: 

As noted above — the rhythm in Figure-1 is a regular WCT at ~130/minute, without clear sign of P waves.

• QRS morphology for the ECG in Figure-1 is consistent with LBBB conduction (ie, Monophasic R wave in leads I and V6 — with predominantly negative QRS in the anterior leads).
• BUT — Aren't T waves in many of the leads tall and peaked (if not pointed)?
• Not only are positive T waves peaked (and quite pointed in leads II,III,aVF; and V3,V4,V5) — but the negative T waves in leads I and aVL are also pointed at their deepest part! (See this Eiffel Tower effect for pointed positive and negative T waves below in Figure-2).
• 
  
• And — WHY is the QRS so wide? (can be seen to be at least 4 small boxes in duration in leads like V3,V4 ==> 0.16 second).

Figure-2: Note the Eiffel Tower effect of both positive and negative T waves in many of the leads in today's ECG.

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CASE Follow-Up:

The above observations were appreciated by emergency providers:

• Based on this acutely ill patient's description of "difficulty urinating" — a foley catheter was inserted, and resulted in an output of 1,500 cc of urine within minutes.
• Based on a presumptive diagnosis of acute renal insufficiency — several empiric IV Calcium doses were given (before serum K+ levels returned). Within minutes — the QRS complex narrowed as the rhythm slowed and the patient stabilized (Unfortunately — I was unable to obtain those follow-up tracings).
• Lab results returned: Serum K+ = 8.7 mEq/L.
• The patient went for emergency dialysis and did well.

COMMENT:

• I'll refer the reader to my ECG Blog #516 — in which I detail empiric use of IV Calcium (formulations and dosing — with emphasis on the minimal downside from giving empiric IV Ca++ when the clinical situation is suggestive and the ECG shows a worrisome "too fast or too slow" arrhythmia).
• Also in ECG Blog #516 — I reviewed the challenges of assessing the rhythm when serum K+ is markedly elevated.
• More on hyperkalemia in ECG Blog #275 (including the textbook sequence of ECG changes with hyperK+ — with emphasis on why not all patients "read" the textbook).
• With yet one more hyperK case of another regular WCT in ECG Blog #244 — in which the cath lab was activated (reviewing how common Brugada-1 patterns may be seen with hyperK).
• And — More on "decreased urine output and acute kidney injury" in this review article by Chenitz and Lane-Fall (Anesthesiol Clin 30(3):513-526, 2012).
• 
  
• "Take-Home" Message: Among the many potential ECG presentations of hyperkalemia is a regular WCT rhythm that looks like VT. Sometimes one or more empiric doses of IV Calcium is indicated (even before the serum K+ level returns from the laboratory). In such situations — empiric IV Calcium may be lifesaving!

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Acknowledgment: My appreciation to Hamid Himat (from Bratislava, Slovakia) — for allowing me to use this case and these tracings.

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