Thursday, March 30, 2023

Is this Rhythm Puzzling to You?

My Comment by KEN GRAUER, MD (3/30/2023):
The ECG in Figure-1 was sent to me without the benefit of any history. I thought the rhythm illustrated a number of essential concepts for clinicians dedicated to Emergency Care.

  • Do YOU know what the rhythm is?

  • IF this arrhythmia is puzzling to you — READ ON!  I illustrate how to make the diagnosis within less than 15 seconds.

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

MY Initial Thoughts on the ECG in Figure-1:
As noted — I was sent today's ECG without the benefit of any history, other than knowing that the patient presented to the ED. 
  • My quick initial survey of this tracing revealed T wave inversion in lead aVL and some T waves that might be hyperacute (ie, in the inferior leads and in V1,V2,V3). That said, although this ECG is suspicious — I thought it was not at this point diagnostic of acute OMI
  • Clinically — Since this ECG is not at this point diagnostic — whether or not an acute cardiac event was in progress would appropriately be delayed until some history, a repeat ECG, and troponins could be obtained. In the meantime — I focused my attention on the "eye-catching" arrhythmia in the long lead II rhythm strip.

Time-Efficient Assessment of Today's Rhythm:
Once you ensure that the patient is hemodynamically stable — I favor the systematic Ps, Qs, 3R Approach for rhythm assessment (Are there P waves? — Is the QRS wide or narrow? — and the Rate and Regularity of the rhythm? — and whether P waves are Related to neighboring QRS complexes?):
  • To Emphasize: It does not matter in what sequence you assess the Ps, Qs & 3Rs. I favor starting with whichever of these 5 parameters are easiest to assess.
  • The QRS is narrow in all 12 leads of today's tracing. This tells us that the rhythm is supraventricular.
  • P waves are present! (RED arrows in Figure-2 highlight those P waves that we can easily identify).
  • The ventricular rhythm is not Regular! That said — there is a "pattern" to the rhythm in Figure-2 — in that there is group beating in the form of a "bigeminal" rhythm, with groups of shorter-then-longer R-R intervals (horizontal BLUE lines in Figure-2 facilitating recognition of groups with the shorter R-R interval).
  • As to the atrial and ventricular Rates — these vary in Figure-2, because of the irregularity of the rhythm, but neither the atrial nor ventricular rates appear to be excessively fast.

  • The last parameter in my systematic Ps, Qs, 3R Approach — is the 3rd "R" — which asks the question of whether atrial activity is Related to neighboring QRS complexes?

  • KEY Question: Look in Figure-2 at the RED-arrow P waves in front of each QRS complex that ends a longer R-R interval (ie, Look at the PR intervals for the RED-arrow P waves in front of beats #1357 and 9). Although greatly prolonged (to a PR interval ~0.46 second— Aren't each of these PR intervals the same? 

  • ANSWER: The fact that the PR interval in front of each of the odd-numbered beats in Figure-2 is the same tells us that these P waves are being conducted to the ventricles! (albeit with marked 1st-degree AV block).

Figure-2: I've labeled with RED arrows those P waves we can definitely identify. In addition — there is group beating (with horizontal BLUE lines facilitating recognition of groups with the shorter R-R intervals).

Is the Atrial Rhythm Regular? 
  • In Figure-2 — I highlighted with RED arrows those P waves we could be certain about. Rather than the "grouped beating" of P waves suggested by these RED arrows — Wouldn't it be much more logical for the underlying atrial rhythm to be regular? — with additional "on-time" P waves being hidden within the QRS complex of beats #2, 4, 6, 8 and 10 (PINK arrows in Figure-3)?

  • Technical NOTE (Beyond-the-Core): It is not possible to "prove" that the PINK arrows in Figure-3 truly represent P waves because: i) There is an underlying sinus arrhythmia — with slight variation in the P-P interval of the RED arrows in Figure-2; andii) There is slight variation in QRS morphology for every-other-beat in Figure-2 — which makes it impossible to tell if this change in the QRS morphology of all even-numbered beats is purely the result of aberrant conduction — or — whether there might also be some hidden deformation of the QRS of beats #2,4,6,8,10 by hidden P waves.

  • PEARL #1: Common things are common! It is far more likely for the atrial rhythm in Figure-3 to be regular (or at least almost regular — with slight variation due to sinus arrhythmia) — than for there to be the rare rhythm of atrial parasystole with 3:2 exit block. Atrial bigeminy (ie, every-other-P wave being a PACis unlikely in Figure-3 — because P wave morphology under each of the RED arrows in Figure-3 looks so similar (whereas P wave morphology usually is noticeably different with PACs).

Figure-3: I've labeled with PINK arrows the likely location of hidden "on-time" P waves. Isn't it likely that the underlying atrial rhythm is regular?

Putting IAll Together:
By the Ps, Qs, 3R Approach — we have determined the following for the rhythm in Figure-3:
  • The rhythm is supraventricular (all QRS complexes are narrow — albeit with slight variation in QRS morphology every-other-beat due to some aberrant conduction).
  • There is group beating (alternating shorter-then-longer R-R intervals).
  • The atrial rhythm is essentially regular (with slight variation in the P-P interval due to some sinus arrhythmia). That said — there are more P waves than QRS complexes — so at least some of these on-time P waves are not being conducted.
  • That said — the PR intervals for the RED-arrow P waves in front of each odd-numbered beat (ie, in front of beats #1,3,5,7,9) are equal! This proves that at least these beats are conducting.

PEARL #2: The above characteristics overwhelmingly point to AWenckebach (ie, 2nd-degree AV block, Mobitz Type I ) as the etiology of today's rhythm!
  • To Emphasize: Although my above description may seem to be in "slow motion" — I literally knew within seconds that today's rhythm was almost certain to represent some form of AV Wenckebach because: i) There is group beating (which the "trained eye" should instantly recognize)ii) The atrial rhythm is almost regular ( = sinus arrhythmia, which with use of calipers is literally established within seconds)andiii) The 1st beat in each group is conducting (witness the repeating equal PR interval in front of beats #1,3,5,7,9)andiv) There is 1st-degree AV block (It is very common for conducted beats with AV Wenckebach to manifest 1st-degree block).  

Looking CLOSER at the Rhythm:
The reason today's rhythm is challenging — is that the 1st conducted beat in each grouping has a very long PR interval. To facilitate recognition of each 3:2 Wenckebach cycle — I have chosen a different color for each P wave (Figure-4).
  • As already stated — RED-arrow P waves represent conduction of the 1st beat in each group with a long PR interval ( = 0.46 second)
  • The YELLOW-arrow P waves in each group are not conducted. (This makes sense — because these YELLOW P waves are simply not in a position where conduction is possible).

  • By the process of elimination — the BLUE-arrow P waves must therefore be conducting. That this is the case is supported by the fact that all PR intervals from a BLUE arrow until beats #2,4,6,8 and 10 are equal (albeit very long = 0.64 second). So — this is AV Wenckebach with 3:2 AV conduction (as the PR interval within each group increases from 0.46 second — to 0.64 second — until the YELLOW-arrow P waves are non-conducted).

Figure-4: Colored arrows facilitate recognition of PR interval prolongation (from RED arrow P waves that conduct with a PR interval = 0.46 second — to 0.64 second for BLUE arrow P waves) — until non-conduction of the YELLOW arrow P waves.

LADDERGRAM Illustration:
  • Doesn't the laddergram in Figure-5 clarify the mechanism of today's rhythm?

Figure-5: Laddergram illustration of today's rhythm.

  • It is extremely common to see slight variation in the P-P interval in association with either 2nd- or 3rd-degree AV block. This is known as a "ventriculophasic" sinus arrhythmia — with the theory being that the P-P interval may vary because of improved coronary perfusion, depending on whether mechanical contraction (signaled by electrical activity from a QRS) is "sandwiched" between 2 P waves.
  • Mobitz I 2nd-degree AV Block (ie, AV Wenckebach) — is very commonly associated with acute inferior infarction. IF you return for a moment to the 12-lead ECG shown in Figure-1 — I was concerned when I first saw this tracing that the T wave inversion in lead aVL — and the hypervoluminous T waves in the inferior leads and in V1,V2,V3 might be markers of a recent inferior OMI? While I did not think the initial ECG in Figure-1 was diagnostic — I felt additional information (ie, some history, repeat ECGs, troponin) was clearly indicated to clarify the clinical situation. Unfortunately — we are not privilege to the clinical outcome in today's case.
And 3 Advanced Concepts ...
  • As alluded to earlier — the 2nd beat in each group is slightly wider and slightly different in morphology from the 1st beat in each grouping. This is most probably the result of aberrant conduction by the Ashman phenomenon (ie, The slightly longer R-R interval between beats #2-3; 4-5; 6-7; and 8-9, may prolong the relative refractory period of the next beat = of beats #3,5,7,9 — which results in aberrant conduction of beats #4,6,8,10).
  • Another reason today's rhythm is challenging to interpret — is that the PR interval "increment" (ie, The amount that the PR interval is increased from 1 beat to the next within a Wenckebach cycle) — is much more than usual (ie, The PR interval increases from 0.46-to-0.64 second). While this might simply be the result of an atypical Wenckebach — it might alternatively reflect dual AV nodal pathways, each with its own degree of impaired conduction.
  • Finally — The fact that the PR interval for conducted beats in today’s tracing is very long may of itself be of clinical significance. This is because once the PR interval extends beyond ~0.30 second — the delay in ventricular contraction that occurs may result in the atria contracting against closed AV valves, with reduction in cardiac output. Thus, although Mobitz I is often a well tolerated rhythm — that may not necessarily be the case in today's tracing (especially if it did turn out that this patient had a recent inferior infarction).

For Readers Wanting More ...
For readers in search of additional practice of concepts from today's case — I refer you to My Comment in the following posts in Dr. Smith's ECG Blog:

Monday, March 27, 2023

A 40-something with 100 minutes of chest pain

I was reading ECGs on the system, and saw this one:

What do you think?

I knew that, if the patient had presented with chest discomfort, that this ECG is diagnostic of inferior posterior OMI, even though it is not a STEMI.

However, it is difficult to recognize for an interpreter who is does not have special expertise in OMI ECG diagnosis. 

We taught an AI system from PM Cardio to recognize patterns of subtle OMI 
(beware: this version of the app is not available to the public yet).  
We named the AI app the "Queen of Hearts" 
This is what the Queen said about this ECG:
"OMI with High Confidence"

ECG explanation:
--There is STE in inferior leads with reciprocal STD and T-wave inversion in aVL.  There is additional ischemic ST depression from V2-V6.  
--The STD in V2-V6 might be interpreted as subendocardial ischemia, but with the inferior STE, it is far more likely to represent posterior OMI.

Here is the history:
A 40-something male had intermittent chest discomfort until 90 minutes prior to presentation, when it became constant.  At 100 minutes, the above ECG was recorded.  

In OMI, cath lab activation is indicated.  In subendocardial ischemia, cath lab is indicated if the pain persists in spite of medical therapy (aspirin, anticoagulant, IV nitro).

The first hs troponin I returned at 245 ng/L.  This is now further confirmation of ACS.

Another ECG was recorded at 160 minutes:
There is evolution, with worsening of ischemia.
There is no doubt that this is an inferior posterior OMI.  

The patient's nitro was dialed up to 100 mcg/min but the pain persisted.

The ACC/AHA guidelines mandate less than 2 hours cath for patients with ACS with refractory pain, pulmonary edema, or electrical or hemodynamic instability.  

Angiogram at 4 hours after ECG 1 (and approximately 6 hours after pain onset):

Culprit is 100% stenosis in the mid RCA.

After PCI

Peak trop I = 39,488 ng/L

Formal contrast echo

Normal estimated left ventricular ejection fraction .

No wall motion abnormality.  (Unusual and puzzling, as there was a large focal acute MI)

Final Diagnosis: Acute MI, Non ST Elevation Myocardial Infarction.

As we have discussed before, the diagnosis of "NSTEMI" is inadequate to describe the pathology of OMI.  NSTEMI is extremely heterogenous, from a very tiny Non-OMI to a massive OMI.  

The presence or absence of ST Elevation is a poor marker with which to describe a myocardial infarction.

My Comment by KEN GRAUER, MD (2/22/2023):
Today’s case is an important one, because as per Dr. Smith (in this patient with new chest pain) — “The initial ECG is diagnostic of infero-postero OMI.” Even after the 2nd ECG showed clear signs of evolution — a total of 220 minutes passed after ECG #1 until finally cardiac cath was performed.

Attention to a few KEY factors should be all that is needed for any emergency provider to be able to recognize acute OMI based solely on the history ( = new chest pain in a 40-something man) — and — the initial ECG.
  • Given the history in today’s case — there are ST-T wave abnormalities in all leads, except perhaps lead aVR ( = in 11/12 leads!) — that need to be assumed acute until proven otherwise! These ECG findings are subtle — but they are real (See ECG #1 — which I have reproduced in Figure-1).
  • As per Dr. Smith — there is ST elevation in the inferior leads (II,III,aVF) — with reciprocal ST depression in lead aVL (Note the mirror-image opposite picture of this subtle ST elevation from lead III in lead aVL — as shown in Figure-1).
  • In support of these reciprocal changes in lead aVL — is similar subtle-but-real ST segment depression in the other high-lateral lead ( = lead I).
  • (For more on the "magic" mirror-image relationship between leads III and aVL with acute inferior OMI — See My Comment at the bottom of the page in the October 6, 2018 post in Dr. Smith's ECG Blog).

  • Also (as per Dr. Smith) — there is subtle-but-real ST depression in chest leads V2-thru-V5. In view of limb lead evidence for acute inferior OMI — the shelf-like ST depression in lead V2 is diagnostic of acute posterior OMI until proven otherwise (ie, a positive "Mirror" Test — See My Comment at the bottom of the page in the September 21, 2022 post in Dr. Smith's ECG Blog).
  • Normally — there is a small amount of gradual upsloping ST elevation in leads V2 and V3. The fact that there is J-point ST depression in lead V3 (RED arrow in this lead) — supports our suspicion of acute posterior involvement.
  • Whether the result of posterior OMI or multi-vessel disease — the flattened ST depression in leads V4-to-V6 is additional evidence of ischemia.

  • Finally: — There is subtle-but-real ST elevation in lead V1. In the context of acute inferior OMI + posterior OMI — seeing any ST elevation at all in lead V1 is not normal. This supports acute RCA occlusion as the “culprit” artery — and is indication for right-sided leads to assess for associated RV infarction (See My Comment at the bottom of the page in the July 19, 2020 post in Dr. Smith's ECG Blog).

Bottom Line KEY POINT: The diagnosis of acute OMI in today’s case is not one to be made from any single finding. Instead, in view of the history of new chest pain — it is the sum total of 11/12 leads showing subtle-but-real ECG findings that have to be taken as acute until proven otherwise.
  • Emergency care providers should be able to recognize this overall picture in Figure-1, that in this patient with new chest pain — is diagnostic of acute OMI.
  • Delay of cardiac cath by the cardiology team for 220 minutes after ECG #1 was recorded — is a mistake that should have been avoided.

Figure-1: I've labeled the initial ECG in today's case (See text).

Friday, March 24, 2023

85 year old with chest pain, STEMI negative, then normal troponin but with relatively large delta: discharge?

Written by Jesse McLaren, with comments from Smith


An 85 year old with a history of CAD presented with 3 hours of chest pain that feels like heartburn but that radiates to the left arm. Below is the ECG. What do you think?

There’s sinus bradycardia, first degree AV block, normal axis, delayed R wave progression, and normal voltages. There’s minimal concave ST elevation in III which does not meet STEMI criteria, so this ECG is "STEMI negative". But there are multiple other abnormalities that when combined are diagnostic of OMI and predictive of RCA occlusion:

  1. sinus bradycardia, which is common in RCA occlusion
  2. inferior hyperacute T waves (broad based, symmetric, tall relative to the QRS)
  3. reciprocal ST depression and T wave inversion in aVL (and I), which is highly specific for inferior OMI
  4. primary anterior ST depression, which is posterior OMI until proven otherwise


Here's the interpretation of the PMcardio AI trained in identifying OMI:


Below is the old ECG, showing the first degree AV block, delayed R wave progression and some of the precordial ST depression is old especially in the lateral leads. But the bradycardia and the infero-posterior OMI is definitely new: 


 Smith: this also has many abnormalities suggestive of ischemia: many leads have ischemic appearing ST depression


The emergency provider followed the sequential steps of the current paradigm:

1.     Use STEMI criteria to identify acute coronary occlusion: the ECG was STEMI negative

2.     Use troponin to rule out non-STEMI: two high sensitivity troponin I performed two hours apart were 4 and 16 ng/L, both in the normal range (upper limit of normal 16 in females and 26 in males).  The assay was Abbott Alinity, which is very similar to Abbott Architect high sensitivity troponin I.  See analysis below.

3.     Arrange follow up for chest pain patients who are “STEMI negative” with “normal troponin”: the patient was referred to outpatient cardiology


But 6 hours later the patient returned with recurrent chest pain: 



Again diagnostic of infero-posterior OMI, though this time it does STEMI criteria, albeit barely.  The cath lab was activated.


A repeat ECG was done on way to cath lab:



"STEMI negative" again. Hyperacute T waves are deflating, suggesting reperfusion but there is still reciprocal change in I/aVL and ST depression in V2, and the bradycardia is worse. On angiogram there was a 90% RCA occlusion. Troponin rose from 600 to 17,000 ng/L.


Discharge ECG showed resolution of bradycardia, inferior reperfusion T wave inversion, and baseline precordial ST depression.



Take home

1.     As the new ACC consensus states (citing the work of Smith/Meyers), "The application of STEMI ECG criteria on a standard 12-lead ECG alone will miss a significant minority of patients who have acute coronary occlusion. Therefore, the ECG should be closely examined for subtle changes that may represent initial ECG signs of vessel occlusion, such as hyperacute T waves...or ST-segment elevation <1 mm, particularly when combined with reciprocal ST-segment depression, as this may represent abnormal coronary blood flow and/or vessel occlusion."

2.     Using troponin for acute coronary occlusion is like relying on a rear-view mirror to navigate a car pile-up: it shows wreckage behind you that has already happened, but can’t see the road ahead and can give false reassurance when there's a head-on collision happening in real time. It’s common for acute coronary occlusion to present with troponin in the normal range, and the initial rise can’t predict the final damage. Even if the troponin on the first visit had been higher there still would have been delayed reperfusion because it would have been diagnosed as "non-STEMI"

3.     Using risk stratification tools like HEARTS or EDACS may have avoided the initial discharge, but shouldn’t be used if the ECG is already diagnostic of OMI. (See this other post: Chest pain, a ‘normal ECG’ a ‘normal trop’, and low HEART and EDACS score: discharge home? Stress test? Many errors here.) There’s also a hazard of relying on troponins that are in the normal range but above the level of detection. As this study from Dr. Smith concluded: “measurable hs-cTnI concentrations less than or equal to sex-specific URLs have important prognostic implications. Our findings underscore the importance of recognizing cTn as a continuous variable, with the higher the cTn, the higher the probability of MACE. We caution against the clinical use of the terms normal or negative among such patients.” (Clinical features and outcomes of emergency department patients with high-sensitivity cardiac Troponin I concentrations within sex-specific reference intervals.)

Smith comments on troponin:

I've done a lot of research on high sensitivity troponin, with colleagues including Fred Apple and Yader Sandoval.  We have published over 30 articles, most on high sensitivity troponin, mostly on Abbott Architect high sensitivity troponin I.  We have found that, to rule out myocardial infarction (and we mostly only studied Non-OMI), the 2-3 hour delta should be less than 3 ng/L.  This conforms with lots of other research done by the HIGH-STEACS group in Scotland and others.   In this case, the delta was 12 ng/L. 

A delta of 12 ng/L is highly likely to indicate acute MI, even if the value is below the 99th percentile.  How is that possible?  Because the 3rd or 4th troponin is highly likely to be ABOVE the 99th percentile if the 3 hour value has risen from 4 to 16 ng/L.

See this graphic from one of our papers:

The PPV is particularly low relative to the specificity because this was a very low risk population.  In a high risk situation, the PPV would be very high. 

Notice that these deltas are REGARDLESS of the initial value.  But if the initial value is very low, as in this case, a delta of 12 early in the course of chest pain is even more significant.


This patient should NEVER have been ruled out by troponin.

And the ECG findings, which are diagnostic of OMI, were also missed.

Thus, this is the protocol Fred Apple and I developed for Hennepin for the Abbott Architect:

My Comment by KEN GRAUER, MD (3/24/2023):
I like this case by Dr. McLaren — because it allows us to highlight a very important fault of the outdated STEMI paradigm that is all-too-often forgotten — namely, Being sure to obtain and clinically correlate at least 2 serial ECGs before you send the patient home! (with "clinical correlation" meaning lead-by-lead comparison of these serial ECGs — keeping in mind the presence and relative severity of CP at the time each ECG was obtained). 
  • For ease of comparison in Figure-1 — I’ve reproduced the first 3 ECGs that were done in today’s case.

In reviewing events transpired in today's case — Obtaining a 2nd ECG and clinical correlation of symptom severity with each ECG that is recorded before discharging the patient was clearly not done on this patient's 1st visit to the ED (Emergency Department). I say this because:
  • Considering that today's patient presented with new CP (Chest Pain) — the initial ECG is already diagnostic of an acute event until proven otherwise.
  • As noted by Dr. McLaren, compared to the prior tracing — there are a number of new ST-T wave changes in ECG #1.
  • There is no notation of whether CP was still present at the time ECG #1 was obtained (and if so, whether CP was increasing, remaining constant, or decreasing). Without this information — it is impossible to understand if the acute-looking ST-T wave changes in ECG #1 might indicate ongoing acute occlusion vs spontaneous reperfusion vs spontaneous reocclusion.

  • In addition to the above missteps — the Troponin Delta (ie, the increase in Troponin from 4-to-16 ng/L) that was interpreted as “negative” — is not a "normal" result (as discussed in detail by Dr. Smith). Therefore, even without the acute ECG changes seen in this case — full evaluation of this patient would be needed.

Challenging Aspects of Today's CASE:
Perhaps the most challenging aspect of today's case — is knowing HOW to interpret the initial ECG in light of obvious ECG abnormalities in the prior tracing. Addressing this issue raises the question of how to optimally compare serial tracings.

Regarding Comparison of Serial ECGs:
  • I favor picking one of the 2 tracings that you are comparing — and systematically interpreting that tracing in its entirety before you look at the 2nd tracing.
  • When comparing a current tracing with a prior ECG — we ideally should know the circumstances under which the prior tracing was done (ie, Was the patient stable and without symptoms? — or — Was the prior tracing obtained during chest pain or soon after an infarction?). Unfortunately — We do not know the circumstances under which the prior tracing in today's case was recorded.
  • Are ECG parameters in the 2 tracings you are comparing similar? (ie, Is there a change in the frontal plane axis? Is R wave progression similar? Is the heart rate and rhythm in the 2 tracings the same?). Significant change in any of these parameters may result in ST-T wave changes that are not the result of ischemia or infarction.

Comparison of the 3 Tracings in Figure-1:
The first ECG we were shown in today's case is ECG #1:
  • As per Dr. McLaren — there is marked sinus bradycardia and arrhythmia (ie, heart rate in the 40s) — with 1st-degree AV block (PR interval ~0.23 second).
  • Regarding other intervals — the QRS is narrow — and the QTc is probably normal given the slow rate. The frontal plane axis is normal (about +70 degrees). There is no chamber enlargement.

 Q-R-S-T Changes: There are artifactual undulations in the baseline of ECG #1 — but this does not prevent interpretation of this tracing. 
  • There are no significant Q waves (ie, The QS in lead V1 is not abnormal per se). A tiny-but-present initial r wave is seen in lead V2 — with this R wave progressively increasing across the precordium. Transition (where the R wave becomes taller than the S wave is deep) — is slightly delayed (to between leads V3-to-V5).
  • ST segments are straightened in multiple leads. In the inferior leads, this is associated with slight J-point ST elevation and clearly hyperacute T waves (that are disproportionately tall, "fat" at their peak — and wider than expected at their base).
  • Reciprocal changes (ie, a mirror-image opposite ST-T wave picture) — are seen in lead aVL, and to a lesser extent in lead I. Considering how tiny QRS amplitude is in these high-lateral leads — these have to be considered acute changes until proven otherwise!

  • In the Chest Leads — ST-T wave changes are equally concerning. There is ST segment coving with T wave inversion in leads V1,V2. We see a distinct straightening with downsloping of the ST segment in leads V3-thru-V6. This is followed by terminal T wave positivity in these leads — with T waves in leads V3,V4,V5 being clearly "hypervoluminous" ("fatter"-at-their-peak and wider-at-their-base than they should be — as well as disproportionately tall in leads V3,V4 considering R wave amplitude in these leads).

  • IMPRESSION of ECG #1: As per Dr. McLaren — Especially in view of the marked bradycardia, the above ECG findings are diagnostic of acute infero-postero OMI until proven otherwise! The ST segment coving in leads V1,V2 suggests possible acute RV involvement — with acute occlusion of the RCA as the presumed "culprit" artery. Given the history of new chest pain — prompt cath is clearly indicated on the basis of this initial ECG.

Comparison of ECG #1 with the Prior Tracing:
As alluded to earlier — ECG #2 is not a normal tracing. Instead — there is ST segment straightening in multiple leads, sometimes with slight ST depression. T waves look disproportionately large in a number of leads (potentially hyperacute IF the patient was having new chest pain at this time). There is ST segment coving with shallow T wave inversion in lead aVL.
  • Several differences in ECG parameters make comparison of ECG #1 with ECG #2 challenging. These include: i) The much faster heart rate in the prior tracing; andii) Little change in the frontal plane axis — but clearly increased QRS amplitude in the prior tracing.

Looking first at the Limb Leads: 
  • Although straightening of ST segments is not a new finding in ECG #1 — there should be no doubt that the subtle ST elevation in leads III and aVF is real — since if anything, there was slight ST depression in these leads on the prior tracing. Similarly, the hyperacute T wave appearance in these inferior leads is markedly increased in ECG #1.
  • Reciprocal ST-T wave depression with T wave inversion is similarly markedly accentuated in leads I and aVL of ECG #1.

In the Chest Leads:
  • Although ST segment straightening with prominent T waves was present in the prior tracing — lead-by-lead comparison suggests that the T waves in leads V3-thru-V6 in ECG #1 are relatively taller (considering QRS amplitude in each respective lead) — and definitely "fatter"-at-their-peak and wider-at-their-base (ie, more hyperacute) than they were in the prior tracing.

  • IMPRESSION: In this 85-year old patient with new chest pain — comparison of the prior tracing with ECG #1 should remove all doubt about the acuity of ECG changes on this initial tracing. Prompt cath is clearly indicated — especially in view of the worrisome bradycardia in ECG #1The patient should not have been sent home.

The Repeat ECG:
As per Dr. McLaren — the patient was unfortunately discharged from the ED — but returned 6 hours later with a recurrence of chest pain. Millimeter-based STEMI criteria are finally attained.
  • Comparison of ECG #3 with the initial ECG done 6 hours earlier — and with the "baseline" (prior) tracing, provides insight into the sequence of ECG changes correlated to patient symptoms.
  • There is now definite ST elevation in all 3 inferior leads in ECG #3 — in association with T-QRS-D (Terminal-QRS-Distortion — as the S wave in leads III and aVF has been lifted from the baselinean even greater increase in relative size of the hyperacute inferior T waves (The T waves in leads III and aVF now tower over the R waves in these leads — whereas they were approximately the same height as the R waves in ECG #1).
  • Reciprocal ST-T wave depression/T wave inversion in high-lateral leads I and aVL has increased a comparable amount to the inferior lead ST elevation.

  • In contrast — ST-T wave changes look less prominent in ECG #3 than they were on the initial tracing. The evolution of sequential ECG changes during an acute ongoing event is not always homogeneous.

Figure-1: Comparison between the initial ECG in today's case — with a prior tracing — and with the repeat ECG (done 6 hours after ECG #1).

Tuesday, March 21, 2023

Watch what happens when you teach others how to find OMI

 Submitted by Dr. Caio Aguiar from Brazil, written by Pendell Meyers

It is immensely rewarding to receive these emails, like I received from Dr. Aguiar last week:

"Last year I had a couple of lessons with you while on my internship.

I finished my residency of Emergency Medicine and I’m working at a great Emergency Department here in Brazil.

Since then, I started looking for OMI EKG findings and not just STEMI.

So, I'm a follower of your blog, and I think I have a interesting case that I attended yesterday."


"Male, 43yo, come to ED with Epigastric Pain started 3 hours ago. Risk Factors: High Cholesterol. Vitals Signs: Normal."

Here is his initial ECG:

PM Cardio standardized version below:
What do you think?

Here we have enlarged it for easier viewing, with limb leads on the left and precordial leads on the right:

Dr. Aguiar diagnosed posterolateral OMI based on hyperacute T waves and slight STE in aVL, with its reciprocal STD and reciprocal negative hyperacute T waves in II, III, aVF, as well as the STD proportionally maximal right on the border of V4/V5.

Here is PM Cardio's Queen of Hearts interpretation of the ECG. Confidently diagnoses OMI.

He contacted the interventional cardiologist who was not convinced and cancelled the cath lab, stating that he wanted to see the first troponin result.

Meyers note: In a case like this, when the cardiologist cannot see the posterior OMI, posterior leads may have shown STE, which might be more understandable for them. Remember: these findings above are included as STEMI equivalent findings in the 2022 ACC Expert Consensus Decision Pathway on ACS Patients in the ED.

The troponin I resulted at about 2-3 hours after arrival (I am not sure why it took this long), at 700 ng/L (upper reference limit 40 ng/L).

A repeat ECG at this time is below:

The repeat ECG shows more STE (but still not 1.0 mm in lead I, thus not STEMI criteria) and was finally understood by the cardiologist.

Angiogram soon after (around 4 hrs after presentation) showed multi vessel CAD, with culprit lesion total occlusion of the first obtuse marginal branch (OM1), which was stented.

No more troponins were obtained.

Unfortunately the echo was not available.


Here is his ECG several hours after reperfusion:

Resolving HATW/STE/STDmaxV1-V4, and new terminal T wave inversion in aVL, all suggesting effective reperfusion.

Learning Points:

To take optimal care of ACS patients, the initial providers who see the patient (hopefully assisted by AI soon) must be able to recognize subtle OMI findings. If only the cardiologist also had such training in this case, the 3-4 hour delay could have been avoided. If Dr. Aguiar hadn't seen it, the patient might have been labelled "NSTEMI" and forced to wait until the next day.

Speed and frequency of repeat ECGs and troponins can help distinguish some OMIs that are not yet understood.

Teaching is rewarding! Go teach some OMI findings.

My Comment by KEN GRAUER, MD (3/21/2023):
Today's case provides one more example of an acute OMI not initially recognized by the On-Call interventionist. The OMI was immediately recognized by the emergency physician who was trained by Dr. Meyers

  • Dr. Meyers' suggestion for when the interventionist does not initially recognize a posterior OMI because "there is not enough ST elevation" — is a good one: Do posterior leads.

  • To EMPHASIZE (as we have previously done in Dr. Smith's ECG Blog — as per My Comment at the bottom of the page in the September 21, 2022 post) — QRST amplitudes (and therefore the amount of ST-T wave elevation) in posterior leads is often modest at best — simply because posterior placement of leads V7,V8,V9 situates these leads in a position from which electrical activity must pass through the thick musculature of the back before being recorded on the ECG. That said — sometimes there will be ST elevation in posterior leads. This may be beneficial if it serves to convince an interventionist who otherwise was not going to cath the patient.

MY Suggestion:
It is difficult to understand why so many clinicians still have difficulty recognizing acute posterior OMI. As noted above — Even when there is posterior OMI, the amount of ST elevation that is seen in posterior leads is most often modest.
  • In contrast to posterior leads — the amplitude of ST-T wave deviations that is seen in anterior chest leads is not attenuated by the thick musculature of the back before being recorded on the ECG. As a result — the mirror-image of anterior chest leads provides a more readily visible picture of ongoing ST-T wave deviations in the posterior wall of the left ventricle.

  • I've called application of this principle the "Mirror Test". This is simply a visual aid that I've used for decades to facilitate recognition of acute posterior OMI(I've added LINKS to a series of other cases in this September 21, 2022 post that illustrate the utility of the Mirror Test)

  • As Drs. Smith and Meyers have emphasized on many occasions — ST depression that is maximal between leads V2-to-V4 in a patient with new chest pain should be assumed to be posterior OMI until proven otherwise. The shape of this ST-T wave depression indicative of posterior OMI is often quite distinctive — in that its mirror-image "looks like" an acute STEMI.

Application to Today's CASE:
The patient in today's case is a 43-year old man who presented to the ED with new symptoms (ie, Not chest pain — but epigastric pain, that can be a mimic at times for an acute cardiac event).
  • For clarity in Figure-1 — I've reproduced the initial ECG in today's case, together with the mirror-image of the chest leads to the right in this Figure.

Dr. Meyers has drawn attention to the abnormal limb lead findings in ECG #1. These include: i) Hyperacute T waves with slight ST elevation in lead aVLandii) Equally acute-looking reciprocal ST-T wave depression in each of the inferior leads.

I wanted to focus on Chest Lead findings:
  • Normally, there is gentle upsloping and slight ST elevation in leads V2,V3. Instead — the ST segment is abnormally straightened, with no more than tiny T waves in these leads. Note the distinct shelf-like ST segment in lead V2.
  • ST depression begins in lead V4 — and is maximal in leads V5 and V6.

  • Because of marked overlap of the QRS in multiple leads — I've outlined in RED the QRS complex in leads V4 and V5.

  • LOOK at the mirror-image picture of the chest leads ( = ECG #1ato the right of the initial ECG in Figure-1)Doesn't the mirror-image of the ST-T waves in leads V4,V5 look like an acute MI?

  • Limb lead findings in ECG #1 are strongly suggestive of acute high-lateral OMI.
  • Typically with isolated posterior OMI — ST depression will be maximal between leads V2-to-V4. This is not quite what we see in ECG #1. Instead — we see abnormal ST-T waves beginning with the ST-T wave flattening that begins in leads V2,V3 — with a positive Mirror Test in lead V4.
  • Significant ST depression extends out to leads V5,V6. Of note — there is also ST elevation in lead aVR.

  • IMPRESSION: I thought ECG #1 conveyed a "mixed" picture. The very acute-looking ST-T waves in the limb leads strongly suggests high-lateral OMI. The abnormally straightened ST segments in leads V2,V3 (shelf-like straightening in V2) — with positive Mirror Test in lead V4 suggests posterior OMI — which together with the hyperacute and elevated ST segment in lead aVL, is consistent with acute occlusion of a branch of the LCx. But ST depression is present in multiple leads, with ST elevation in lead aVR — a picture consistent with diffuse subendocardial ischemia from multi-vessel disease. (Alas, this is precisely what cardiac cath showed = multi-vessel disease with a "culprit" vessel in the 1st Obtuse Marginal branch of the LCx).

Figure-1: The initial ECG in today's case — with the mirror-image view of the chest leads to the right. (To improve visualization — I've digitized the original ECG using PMcardio).

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