Sunday, May 31, 2020

A Young Woman with Regular Narrow Complex Tachy at both 160 and 240

A young woman presented with palpitations, chest pressure, SOB and weakness.

She had a rapid rate and BP of 140 systolic.  She was in no distress.

Her prehospital ECGs showed SVT at 2 different rates: 160 and 240 (approx)

On arrival, this was the first ECG:
Narrow complex regular at 160.
Not sinus.
There is no suggestion of atrial flutter.
So this is paroxysmal SVT.

She was given 6 mg of IV adenosine, after which she converted to sinus for 2 beats, then had several PACs, then went back into SVT at a rate of 240.

Here is her ECG:
Same as above, but with a rate of 240.


What is going on? What do we do?

To understand SVT, it is necessary to understand how it initiates and propagates:


Pathophysiology 
(From the EmRap compendium chapter written by Pendell Meyers and Steve Smith)
  • "Made possible by “dual AV nodal physiology,” in which the AV node is thought to contain 2 pathways that separate briefly and reunite inside the AV node, both conducting from the atria to the bundle of His.
  • "The “fast pathway” exhibits faster conduction but a longer refractory period than the “slow pathway.”
  • "In sinus rhythm, each AP propagates simultaneously down the dual AV nodal pathways without the opportunity for reentry, since the 2 pathways block each other at the point of re-unification.
  • "The normal time between beats ensures that both pathways are available for the next AP.
  • "However, a properly timed premature atrial beat may arrive early at the AV node, at a time when the fast pathway is still refractory but the slow pathway is fully repolarized and able to accept the oncoming AP.
  • "The AP then proceeds anterogradely down the slow pathway only, during which the fast pathway completes its repolarization.
  • "The AP arriving at the reunification point is then able to access the fast pathway, continuing retrogradely up the fast pathway and subsequently anterogradely down the slow pathway, sending APs to both the atria and ventricles.
  • "This creates a regular tachycardia with retrograde P-waves that may occur before, during, or after the QRS complex."
  • In SVT caused by an accessory pathway, the pathophysiology is similar except that the second conducting limb is the bypass tract, not another limb in the AV node.

Why 2 different rates?
  • Suppose there are BOTH 2 pathways in the AV node (which conduct at different speeds) AND an accessory pathway (3 total pathways)?
  • Then it could use either AV nodal pathway do descend (at different rates), and the accessory pathway for as the ascending pathway.

Important point: Adenosine or verapamil does not cause the slower rhythm to accelerate into the faster rhythm.  A PAC can initiate SVT down either limb of the AV node, it seems this is random.  So the rhythm can randomly re-initiate at either rate.

What do we do about it?

Because this is narrow complex, its antegrade propagation must be traversing the AV node.  The temporary blockage by adenosine confirms this.

Management: One suggestion that was offered was to use electrical cardioversion, since adenosine "did not work."  However, adenosine did work.  But it only lasts for seconds.  Then the dysrhythmia was re-initiated (in this case by PACs, which are the basic reason that SVT gets initiated, as above).

Cardioversion will not work!  We need to either:
1) prevent re-initiation of the dysrhythmia, by preventing PACs, OR
2) persistently block the AV node transmission with a drug that has a relatively long duration of action (adenosine only does so transiently)

There are 2 primary medication classes for this purpose:

1) Ca channel blockade, with verapamil or diltiazem.  Verapamil was the standard treatment in the early 80s, before adenosine. It has a slightly greater chance of hypotension than adenosine (3.5% incidence in one large study)

2) Beta blockade, which will both inhibit PACs and slow AV nodal conduction.


Clinical Course
We decided to use verapamil to block the AV node persistently.  Verapamil is a powerful negative inotrope, so it should never be used when there is poor LV function.   We did a bedside ultrasound which confirmed excellent contractility.

We gave 5 mg verapamil over 2 minutes.

There was temporary success, but then more PACs, and SVT re-started, this time at a rate of 240.

It would stop and start, randomly at either 160 or 240, always initiated by a PAC.

We gave another 5 mg, without much success.

After this, we turned to beta blockade.  It may be hazardous to administer both Verapamil and beta blockade, due to to the possibility of profound negative chronotropy and inotropy.  Therefore, we decided on esmolol, which has a short half life and could be turned off if there were adverse effects.

We gave 500 mcg/kg of esmolol and started a 50 mcg/kg/min drip.

This is the result:
Sinus with many PACs
So the esmolol is primarily slowing AV nodal conduction and has not stopped the PACs


Shortly thereafter, a subsequent ECG and all rhythm strips showed sinus rhythm with no PACs.  The esmolol worked.

As she tested positive for COVID, no EP study was done.  She was discharged on a beta blocker.


More pathophysiology

Here is one likely anatomy for our patient today.  For the other, see "Alternative Explanation" below, and Ken's commentary.

However, in our patient today the direction of conduction would be OPPOSITE from this diagram.  It goes down one of the AV node pathways, and UP the accessory pathway:
This schematic comes from this blog post:

Wide Complex Tachycardia in a 20 something.

As stated above, the AV node can have 2 pathways and this is the anatomic substrate for AVNRT. 
But here there is also an accessory pathway, for a total of 3 pathways.

The tachycardia has two different rates because A and B have different conduction speeds.  

In contrast to the case today, the previous case was wide complex because it went down the bypass tract (causing pre-excitation and a wide complexand up through the AV node (antidromic).

Previous case: the conduction back up through the AV node can go through either limb within the AV node.  One is fast and one is slow, and they have differing refractory periods.  The rate of the tachycardia depends on which AV node limb it ascends through.

Today's case: there is orthodromic conduction.  The rate is dependent on which limb of the AV node is conducting.
Alternative explanation: no accessory pathway.
It is possible also that there is NOT an accessory pathway, but rather only 2 pathways within the AV node.  If so, then in one case, the impulse goes down the slow pathway and up the fast pathway (resulting in a very fast rate), and in the other, it goes down the slow pathway and up the fast pathway (resulting in a less fast rate).

The rate depends on the time that it takes the impulse to make a complete circuit through the AV node. For the two rates to be different, the rate of conduction would have to be different depending on the direction of the impulse.  This is possible.

Procainamide and amiodarone were also suggested by some as management.  However, they have very limited success in refractory SVT, especially SVT that involves AV nodal conduction.  This article studied their effect in pediatrics:
https://www.ahajournals.org/doi/full/10.1161/CIRCEP.109.901629




===================================
MY Comment by KEN GRAUER, MD (5/30/2020):
===================================
Fascinating case presented by Dr. Smith (!) — about this young woman who presented with palpitations and sequential reentry SVT rhythms — initially at a ventricular rate of ~160/minute — and then following administration of 6mg IV adenosine, another reentry SVT at a much faster rate of ~240/minute. HOW could this happen?
  • For clarity — I have put together the 3 ECGs from today’s case in Figure-1.
  • Dr. Smith has reviewed (above) the pathophysiology of dual AV nodal pathways responsible for sustaining reentry SVT rhythms. I focus My Comment on additional insights to be gained from this case.

Figure-1: The 3 ECGs shown in today’s case (See text).



ADENOSINE is NOT Always Benign: Adenosine’s reputation as a superb, rapid-acting agent for treatment of reentry SVT rhythms is well established. The drug acts immediately — with a half-life of less than 10 seconds. As a result — any adverse effects that may be produced will almost always be short-lived (typically resolving within 30-to-90 seconds).
  • Common adverse effects (that are to be expected) following IV adenosine include: i) chest pain; ii) cough (from transient bronchospasm); iii) cutaneous vasodilatation (transient skin flushing); iv) metallic taste; vtransient nausea, sweating, nervousness, numbness, lightheadedness and a sense of “impending doom”; andvi) transient bradycardia that may be marked (and which may even cause a brief period of asystole).
  • Adenosine may shorten the refractory period of atrial tissue — which could initiate AFib in a predisposed individual. For this reason — Adenosine should be used with caution in patients with known WPW, given theoretic possibility of inducing AFib (which could have significant consequence in a patient with accessory pathways).
  • Adenosine may cause a reflex increase in sympathetic tone and circulating catecholamines. This may lead to increase in heart rate; atrial or ventricular ectopy; and/or enhanced conduction over accessory pathways (Mallet ML: Emerg Med J 21:408-410, 2004).
  • In addition to AFib — Mallet describes other Proarrhythmic effects of adenosine (in which administration of this drug may cause another arrhythmia). These proarrhythmic effects include: i) PVCs and/or non-sustained VT (including on occasion polymorphic VT and Torsades de Pointes, especially when this arrhythmia is pause-dependent); ii) Induction of other atrial arrhythmias, including ATach and AFlutter; iii) Enhanced AV conduction of established AFlutter (from 2:1 to 1:1 AV conduction); andiv) Acceleration of the ventricular response to a reentry SVT. This latter effect is the probable explanation for the paradoxical increase in ventricular rate that occurred in this case, with sequential SVT rhythms showing an increase from 160/minute to 240/minute after administration of 6 mg of IV adenosine (Figure-1). As shown by Curtis et al (J Am Coll Cardiol 30[7]1778-84, 1997) — the dual AV nodal pathways referred to by Dr. Smith (above) may manifest different sensitivities to IV adenosine. This property could have facilitated a switching of orthodromic (forward) conduction from the slow to the fast AV nodal pathway at the time the heart rate increased to 240/minute (ECG #2 in Figure-1).

BOTTOM LINE Regarding Use of Adenosine: Adenosine is a great drug — especially in an emergency setting! It works fast. It is highly effective for reentry SVT rhythms (both AVNRT and AVRT!). In addition:
  • Adenosine may serve as a “chemical Valsalva” — in which Adenosine is given as a diagnostic/therapeutic trial for a narrow tachycardia (SVT rhythm) of uncertain etiology. Presumably adenosine will convert the rhythm if it is a reentry SVT. If not — it will hopefully slow the rhythm enough (transiently) to allow a definitive diagnosis to be made (just like Valsalva ... ).
  • Adenosine can be a valuable agent to be used as a “therapeutic trial” for a regular, monomorphic WCT of uncertain etiology — in which the drug may convert the rhythm if the WCT is either an adenosine-sensitive form of idiopathic VT or a reentry SVT rhythm. And, in the event adenosine does nothing — adverse effects are generally short-lived and well tolerated by most patients.
  • BUT — Because adenosine is not benign — the drug should not be used in cases in which it is unlikely to work (ie, when the patient has polymorphic VT or Torsades; or for known VT of ischemic etiology) — and, it should definitely not be used for WPW with rapid AFib.

Some Additional Observations about Figure-1: As per Dr. Smith — the initial ECG in the ED ( = ECG #1) showed a regular SVT rhythm at ~160/minutewithout clear sign of atrial activity. After 6 mg of IV adenosine — the rate of the regular SVT increased to 240/minute ( = ECG #2).

PEARL: It can be very helpful to look for sign of retrograde atrial activity during a regular SVT rhythm — as this may provide an important clue to the mechanism of the SVT rhythm. I discuss and illustrate this key concept in detail in My Comment at the bottom of the March 6, 2020 post in Dr. Smith’s ECG Blog. In brief:
  • With the usual ( = “slow-fast”) form of AVNRT — the RP’ interval during the SVT is typically very short (ie, with the retrograde P wave either hidden within the QRS complex, or distorting the terminal part of the QRS). This is because with the “slow-fast” form of AVNRT — the reentry circuit is relatively smaller, being completely contained within the AV node (therefore, little distance to travel retrograde — which results in a short RP’ interval).
  • In contrast, with AVRT — the RP’ interval during the SVT tends to be longer (with the retrograde P wave most often occurring near the middle of the ST-T wave). This is because the reentry circuit is longer, since it involves an AP (Accessory Pathway) which lies outside of the AV node (therefore, a longer distance for atrial activity to travel retrograde — which results in a longer RP’ interval).
  • Unfortunately — there is much baseline artifact in both ECG #1 and ECG #2. As a result — it was exceedingly difficult to look for signs of atrial activity That said — I agree with Dr. Smith that neither sinus P waves nor 2:1 flutter waves seemed to be present in either ECG #1 or ECG #2.
  • I do not see any sign of retrograde atrial activity in ECG #1.
  • However — do see a distinct positive notch (pseudo-r’ ) in lead V1 of ECG #2 (RED arrow pointing to this r’ notch within the RED circle in ECG #2). I believe this r’ notch in lead V1 is real — because it was not present in lead V1 in either ECG #1 or ECG #3. Therefore — this r’ notch in lead V1 is almost certain to represent retrograde atrial activity during ECG #2.

My THEORY (Beyond-the-Core): The fact that we see this retrograde P wave in ECG #2 but not ECG #1 suggests that orthodromic conduction has switched from one AV nodal pathway to the other.
  • The fact that this r’ notch in lead V1 of ECG #2 manifests a short RP’ interval — suggests to me that retrograde conduction is contained within the AV node (since I’d expect a longer RP’ interval if there was concealed retrograde conduction over an AP).
  • I suspect the reason we did not see any retrograde P wave in ECG #1 — was that ECG #1 conducted down the slower AV nodal pathway (therefore the slower rate = 160/minute) — but back up the faster AV nodal pathway (such that the RP’ interval was shorter, and the retrograde P wave in ECG #1 was entirely hidden within the QRS complex!).
  • This is the opposite of what I suspect happened with ECG #2 — which conducted down the faster AV nodal pathway (therefore the faster rate = 240/minute) — but then back up the slower AV nodal pathway. This resulted in a slightly longer RP’ interval — that was long enough for the retrograde P wave to emerge from beyond the QRS to porduce a pseudo-r' in lead V1.
  • Therefore — I thought it more likely that there was no participation of any AP in the reentry circuit (ie, No AVRT) — but instead, that the SVT rhythms in ECG #1 and ECG #2 were both AVNRT, with the reentry circuit being totally contained within the AV Node. (That said — I fully acknowledge that I could be wrong, and I cannot exclude the possibility of participation by an accessory pathway).

Finally — About ECG #3: We need to remember from Dr. Smith’s presentation that ECG #3 was obtained after two 5 mg doses of verapamil — and after esmolol loading + infusion — and — that the ECG shortly thereafter showed conversion to normal sinus rhythm ( = presumed success in maintaining conversion to sinus rhythm following administration of the ß-blocker).
  • Take a look at the long lead II rhythm strip in ECG #3. The rhythm is irregularly irregular — and except for the P wave preceding beat #2, atrial deflections in the long lead II rhythm strip are of extremely small amplitude.
  • Wouldn’t it be EASY if you only saw the long lead II rhythm strip of ECG #3, to think this was AFib with a rapid ventricular response? NOTE: Nowhere on this long lead II rhythm strip do we see 2 similar atrial deflections in a row.
  • Confession: I was not initially sure what the rhythm in ECG #3 was after looking at this long lead II rhythm strip. It was only after looking at the other 11 leads on this tracing that I was able to confirm that there were definite P waves. P waves are seen best in lead V1, albeit P wave morphology clearly changes from one-beat-to-the-next in this lead (the PURPLE, GREEN and PINK arrows in lead V1). Using the concept of simultaneous-leads — the thin, vertical PURPLE line that begins under the P wave in lead V1 confirms that the tiny upright deflection in front of beat #14 in the long lead II rhythm strip is indeed a P wave.

MORAL of the STORY: Always remember that, “12 Leads are Better than One”. In the case of ECG #3— looking at the simultaneously-recorded leads above the long lead II rhythm strip is instrumental in confirming that this irregularly irregular rhythm is not AFib.
  • Technically (since the rhythm in ECG #3 is completely irregular, and P wave morphology does change from one beat to the next) — the rhythm in ECG #3 might best be defined as MAT (Multifocal Atrial Tachycardia).
  • That said, practically speaking — I think of the rhythm in ECG #3 rather as a “rhythm in transition” — in this patient who shortly before ECG #3 was in a reentry SVT at 240/minute — for which she received several antiarrhythmic drugs — and then soon after ECG #3, was found to be in normal sinus rhythm without any PACs at all.

Our THANKS to Dr. Smith for presenting this insightful case.



Tuesday, May 26, 2020

A middle-aged male with chest pain

A 40-something male presented with chest pressure.

Here is his triage ECG:
What do you think?


















The triage physician suspected that this was a false positive due to benign normal variant ST Elevation (Often called "Early Repolarization," though many are trying to get away from that terminology for this morphology)

When I saw the ECG I immediately thought that this was not STEMI.

I applied the Early Repol/LAD occlusion formula.
See this post for explanation and references:

12 Example Cases of Use of 3- and 4-variable formulas to differentiate normal STE from subtle LAD occlusion


Remember it can only be applied when NONE of these are present:
1. Presence of a straight or convex ST segment in just ONE of V2-V6
2. STE of at least 5 mm in one lead of V2-V4
3. ANY ST depression in ANY lead, reciprocal or not
4. Any T-wave inversion
5. Any Q-wave in V2-V4
6. Any terminal QRS distortion (absence of both an S-wave and J-wave (notch) in either V2 or V3
If any of these are present, it is NOT normal variant, and so the formula should not be applied.


ST Elevation at 60 ms after the J-point in lead V3 = 4 mm
R-wave amplitude in V4 = 20 mm
QRS amplitude in V2 = 10 mm
Computerized QTc was 365 ms (this is the feature of this ECG which is most potent -- it is a very short QTc for acute MI.  In our series of subtle LAD occlusions, the mean QTc was 420 ms, vs. 390 for normal variant STE) 

Formula value = 16.36 (most accurate cutpoint is 18.2; a value below 17.0 is 97% sensitive and a value above 19.0 is 97% specific.

I generally give this warning:  
--Use the formula to help you make the diagnosis of LAD occlusion when you did not suspect it.  
--Do NOT use the formula to dissuade you from the diagnosis of LAD occlusion.

I was already convinced by looking at the ECG that this was a false positive, so the formula value reassured me.

Then I went to look for a previous ECG:

And found one:
Not exactly the same, but pretty close


History revealed that the symptoms had been going on constantly all day, so an initial troponin would be positive if this was a true positive ST elevation.

The first trop returned undetectable, as did the 2nd trop.

We discharged the patient with "atypical chest pain."
___________________________

Ken wrote below about all the features that make this unlikely to be an acute MI.
However, what he wrote are features specific to acute MI, but not sensitive.  These features do NOT make acute MI unlikely by themselves, they make is less likely.

In our series of 355 consecutive LAD occlusions, 143 had none of the features that Ken discusses:

LAD occlusions were excluded from the study if they had any of the following:
1. Presence of a straight or convex ST segment in just ONE of V2-V6. (There must be concavity)
2. STE of at least 5 mm in one lead of V2-V4
3. ANY ST depression in ANY lead, reciprocal or not
4. Any T-wave inversion
5. Any Q-wave in V2-V4
6. Any terminal QRS distortion (absence of both an S-wave and J-wave (notch) in either V2 or V3


So when you apply the formula, it must be ONLY to ECGs that have NONE of the above.

If they have any ONE of the above, then you must assume that it is LAD occlusion because normal variant STE in V2-V4 has NONE of them.

Finally, we looked at degree of upward concavity in V2-V4 and it did not add ANY additional value to the multivariable formula.  It does have univariate value, but does not help at all if you are already using the formula, which is far better.  In other words, unless there is a straight or convex ST segment, in which case you must assume it is not normal, the SHAPE of the ST Segment has no further added value over the formula, except insofar as it makes you recognize normal variant more easily.



===================================
MY Comment by KEN GRAUER, MD (5/26/2020):
===================================
While contemplating My Comment for this case — I decided to concentrate on ST segment elevation SHAPE. So, I looked through previous cases I commented on for Dr. Smith’s ECG Blog — and I came across My Comment in the June 7, 2019 post, in which the points I’m about to make on today’s case are virtually identical to what I wrote in that 2019 case. Clearly, this is an “ECG Theme” that repeats itself.
  • For clarity — I again show the initial ECG in the ED for today’s case (Figure-1).

Dr. Smith gave “the Answer” to today’s case above — namely, that the ECG in Figure-1 is unlikely to indicate acute coronary syndrome.
  • QUESTION: In addition to a very low (totally normal) value in Dr. Smith’s Formula — WHAT are the ECG findings that suggested to me that ECG #1 was less likely to indicate acute OMI?

Figure-1: The initial ECG in the ED for today’s case (See text).



My THOUGHTS on ECG #1: There is a significant amount of artifact, especially in the limb leads.
  • PEARL #1 — While the amount of artifact in this tracing is not enough to prevent accurate interpretation of this ECG — knowing how to quickly determine which extremity is the cause of the artifact (due to tremor, a faulty lead connection/inadequate skin contact, etc.) is helpful, because this may expedite correction, which may be important when artifact does impede interpretation. In ECG #1 — baseline artifact is most prominent in leads I, II and aVR in the limb leads, with significantly less baseline disturbance in the chest leads. This suggests that the right arm is most likely the source of this artifact. (NOTE: For a quick primer on how to recognize which extremity is the cause of artifact — Please SEE the 1st bullet in Observation #2 in My Comment for the September 27, 2019 post in Dr. Smith’s ECG blog).

Returning to my Descriptive Analysis of ECG #1:
  • The rhythm in ECG #1 is sinus at ~60/minute. All intervals (PR/QRS/QTc) are normal. The frontal plane axis is normal at about +15 degrees. There is no chamber enlargement.

Regarding Q-R-S-T Changes:
  • There are narrow septal Q waves in leads I and aVL.
  • Transition (ie, R Wave Progression) occurs early — as the R wave becomes taller than the S wave is deep as soon as between leads V1-to-V2.
  • Regarding ST-T Wave Changes — The limb leads look fairly unremarkable. Although difficult to be certain due to the baseline artifact — there appears to be slight, concave-up ST elevation in leads I and aVL (and possibly also in lead II— without any reciprocal ST depression in the inferior leads. The ST-T wave in lead III is flat. This does not look acute.
  • There is definite J-point ST elevation in each of the chest leads. The amount of ST elevation is minimal in V6 — and maximal in leads V1, V2, V3 (up to 2-3 mm). The shape of ST elevation seen is consistently concave-up (similar to the shape of the gently curved RED lines in these leads — seen in Figure-2).
  • There is prominent J-point notching in leads V4, V5, V6 (BLUE arrows).

Figure-2: I’ve labeled key ECG findings seen in ECG #1 (See text).



Clinical IMPRESSION: WHY I thought the above findings in ECG #1 were less likely to be acute:
  • DISCLAIMER: No set of ECG features is perfect for ruling out acute OMI on the basis of a single ECG. Clearly, additional assessment will often be needed in the patient who presents with new symptoms — which is the situation for today's case (ie, the 40-something man in today's case did present with "chest pressure" which apparently was new). As a result — additional evaluation would be advised (ie, more history; comparison with a baseline ECG; serial tracings; stat Echo; troponin, etc.) — before comfort could be attained that no acute ischemic event is ongoing. THAT SAID — I thought the sum total of ECG findings in today’s case suggested that acute cath lab activation would not be indicated on the basis of this initial ECG! 
  • NOTE: My rationale below is based on qualitative findings. I did not use Dr. Smith's multivariate formula in my decision-making process.

PEARL #2 — ECG Findings that reduce the likelihood of an acute process in ECG #1 include the following:
  • Lack of any reciprocal ST depression! While true that a significant percentage of acute anterior MIs do not manifest reciprocal ST depression in the inferior leads (especially when there is mid-to-distal rather than proximal LAD occlusion) — the ST elevation seen in ECG #1 begins in lead V1! As a result — I would normally expect to see at least some reciprocal inferior lead ST depression if there was acute proximal LAD OMI.
  • The shape of the ST elevation that we see in the chest leads is uniformly concave-up (similar to the shape of the gently curved RED lines in these leads). While this upward-concavity (ie, smiley”-configuration) shape by itself does not rule out the possibility of acute ischemia — this type of ST segment shaping is often seen in repolarization variants. In contrast — straightening of the ST segment and/or ST segment coving (ie, frowny”-configuration) shape is much more commonly associated with acute ischemic heart disease.
  • There is prominent J-point notching in leads V4, V5, V6 (BLUE arrows). Especially when seen in multiple leads in association with benign-appearing (ie, concave-up) ST elevation — this type of J-point notching often occurs with repolarization variants.
  • The 2 q waves noted in this tracing are small and narrow — and, they are seen in lateral leads I and aVL. Normal “septal” q waves (attributable to the normal left-to-right initial vector of septal activation) may commonly be seen in any of the lateral leads (I, aVL; V4,V5,V6) — so the appearance of these q waves that are seen in ECG #1 is perfectly consistent with these being normal “septal” q waves.
  • A normal (if not relatively short) QTc interval. I estimate the QTc to be ~370 msec — which clearly is on the shorter side of the normal QTc range. In contrast — acute MI is often associated with QTc prolongation.
  • Prominent R wave forces in the chest leads. Acute anterior OMI often manifests reduced anterior R wave amplitude. The opposite is present here — as the R wave becomes tall and predominates as early as in lead V2.
  • Finally — There is a lack of localization! Counting the slight ST elevation in leads I, II and aVL — no less than 9 out of 12 leads in ECG #1 manifest ST elevation. Acute ischemic heart disease is far more likely to localize — instead of manifesting a consistent concave-up shape for the ST-T waves that we see here in 9 of the 12 leads in this tracing.

BOTTOM Line: I’ll repeat my “disclaimer” that I wrote above:
  • DISCLAIMER: No set of ECG features is perfect for ruling out acute OMI on the basis of a single ECG. Additional assessment may be needed before full comfort can be attained that no acute ischemic event is ongoing. Even if the ECG is unremarkable — sometimes cardiac cath will still be indicated to rule out an acute process. THAT SAID — I thought the overall picture, based on the combination of findings in ECG #1 was less likely to represent acute ischemic heart disease.
  • For additional practice in applying these concepts — Please CHECK OUT the June 7, 2019 post on Dr. Smith’s ECG Blog.

Our THANKS to Dr. Smith for presenting this case.


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