Friday, October 28, 2022

I'm so sorry when medics get abused for activating the cath lab

Cortland Ashbrook from Spokane County, Washington, sent this message:

Hey doctor Smith, I wondered if you’d give me your opinion on these ECG tracings I took as a paramedic in the field?


The call was an elderly gentleman who was at home when he experienced a sudden onset of vague chest discomfort along with nausea, and left arm aching. It started while walking, and began to decrease at rest but never fully resolved. It was central and constant. He has a pacemaker for an unknown arrhythmia reason, and has a hx of a PE but is not anti-coagulated currently. I believed this met modified Sgarbossa in II, III and aVF with excessive discordance as well as reciprocal in aVL.

Initial presentation was oddly benign. He had a gradual onset of nausea, left elbow aching and a vague indescribable feeling in his chest. The nausea and elbow aching resolved with rest, and he stated the “off feeling “ in his chest was a 0-1 during transport, and even at onset was no more than a 2/10. No diaphoresis at any point, and he appeared in no distress. Both the patient and his wife attributed it to spicy food a couple hours prior, and I had to talk him in to being transported.

The ER physician was pretty rudeto me for calling an activation, but wouldn’t educate me on what I may have been misinterpreting. I’m an avid reader of your blog, and wanted your valued opinion on this.

Here are the ECGs:

Here I use the PMCardio app (from Powerful Medical) to clean and digitize the image:
There is a paced rhythm, with wide QRS.
In inferior leads, the QRS is so distorted by the massive ST Elevation that it is even hard to distinguish from the ST-T!
Lead II has massive excessively discordant STE and III and aVF have massively concordant STE.
Leads V5 and V6 have huge proportionally excessively discordant STE.

This is obviously diagnostic of inferior and lateral Occlusion Myocardial Infarction.
The location of the infarct is clear, but that does not necessarily tell you what artery it is.

Learn about the Smith-Modified Sgarbossa Criteria for Diagnosis of OMI Paced Rhythm:

Dodd, Meyers, Smith, et al.  Annals of Emergency Medicine 2021.  Electrocardiographic diagnosis of acute coronary Occlusion Myocardial Infarction in ventricular paced rhythm using the modified Sgarbossa criteria.

Cortland recorded another ECG:

Again, the PM Cardio App is used to improve the image:
There is again obvious OMI, with hugely excessively discordant STE in lateral leads and of course also in inferior leads (with excessively discordant reciprocal ST depression in aVL).

Diagnosis: Obvious Inferior and lateral Occlusion MI.

Smith Response: Cortland, you were absolutely right. There is no doubt about these 2 EKGs: they are due to acute coronary occlusion. These are not even CLOSE to being subtle!! Unfortunately, many or most physicians, including EM and cardiology, do not know this and too many also are too arrogant to learn from a paramedic. Great job!! You should get followup on the case.

Cortland: Thank you so much for your reply! I just got the follow up that he had a near complete very proximal LAD occlusion, and a complete PDA occlusion. He went into cardiogenic shock and is intubated in the cardiac ICU. Not the culprit artery I was expecting but potentially a wraparound LAD?

Smith: You should try to educate him/her

Cortland: I tried to mention the findings and the sensitivity of modified Sgarbossa but he brushed me off. I really appreciate you getting back to me!

MY Comment by KEN GRAUER, MD (10/23/2020):
Today's tracing is similar to many others that we've published on Dr. Smith's ECG Blog — namely, an EMS pacer tracing obtained in the field from an elderly patient with new chest pain — which despite concern by medics in the field, was discounted by the physician charged with initial care of the patient. 
  • For clarity — I've chosen the 2nd tracing in today's case to comment on, since it had less artifact. To improve visualization — I've digitized the original ECG using PMcardio (Figure-1).

My approach to this case was similar to that described in My Comment — at the bottom of the page in the October 3, 2018 post in Dr. Smith's ECG Blog:
  • Even before looking at the ECG — today's patient is in a "high prevalence" population for acute coronary disease because he is elderly, obviously has underlying heart disease (after all, he has a permanent pacer) — and he was bothered by new-onset chest pain severe enough that he summoned the EMS team to his home.
  • Modified-Smith-Sgarbossa Criteria provide objective criteria for assessing patients with LBBB and/or pacemaker tracings for acute coronary disease. That said — I favor beginning with a qualitative approach, which has served me well over a period of decades. Doing so — my immediate conclusion was identical to that of Dr. Smith — namely, that there is no doubt that today's ECG indicates acute coronary occlusion until proven otherwise.

Figure-1: The 2nd ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

Abnormal Findings in ECG #2:
The rhythm in ECG #2 is challenging to assess — because the QRS is wide and slightly irregular — there are no discernable P waves — and there is much artifact. Despite the absence of pacer spikes — this presumably is a paced rhythm.
  • The main premise of my qualitative approach — is to be suspicious of an acute cardiac event when you see ST-T wave findings that shouldn't be there. Admittedly — this may be challenging to assess with pacer tracings because of the many variations in QRS morphology that may be seen given different types and different placements of the various cardiac pacemakers. Despite this — it will sometimes be quite obvious (as in today's case) that the ST-T wave deviations seen in a number of leads just should not be there.

  • I've drawn horizontal dotted-RED lines in multiple leads to clarify the ST segment baseline. RED arrows in these leads point to the change in angulation of the ST segment, which indicates the amount of ST elevation in these leads. The amount of ST elevation in multiple leads is clearly excessive, given relative size of the QRS complex in these leads. In addition — ST-T waves are clearly hyperacute (ie, hypervoluminous) in many leads with respect to proportionality with QRS amplitude.

  • NOTE: The size of QRS amplitudes is limited in many prehospital ECG recorders. For example — the reason for the horizontal ending to the QRS at its lowest point in leads V2, V4 and V5 (horizontal dotted BLUE lines in these leads) — is that S wave depth was limited to 10 mm. This makes it difficult to apply the rule of "proportionality" in these leads (because we don't know how deep the S waves really are). But QRS amplitude was not limited in the limb leads or in lead V6 — and there should be no doubt about the acuity of ST segment deviations in these leads!

BOTTOM Line: Despite the fact that ECG #2 is a paced tracing — the diagnosis of acute OMI is not in doubt. 

Tuesday, October 25, 2022

Back to basics: what is this rhythm? What are your options for treating this patient?

Written by Bobby Nicholson MD, with edits by Meyers, Smith, Grauer

A woman in her early 40s presented to the emergency department for evaluation of palpitations.  She reported that she has been experiencing this since she was diagnosed with COVID a little over 1 week ago. She reported a prior history of SVT and has previously performed vagal maneuvers at home with symptom resolution.  She reports that she is now unable to vagal out of her palpitations and is having shortness of breath and dull chest pain. Her initial EKG is below.

We see a regular tachycardia with a narrow QRS complex and no evidence of OMI or subendocardial ischemia. The differential of a regular narrow QRS tachycardia is sinus tachycardia, SVT, and atrial flutter with regular conduction. There are no P waves preceding the QRS complexes, and no clear flutter waves. SVT is by far the most likely rhythm in this case. 

There are retrograde P waves seen immediately after the QRS complex in most leads. They are inverted in lead II, for example.

She was treated with 6mg adenosine rapid IV push. The following EKG was obtained after administration of adenosine.

Now the patient is in sinus tachycardia. Unfortunately, shortly after this EKG was obtained, the patient returned to SVT.


Same as initial ECG.

Smith: should we give adenosine again?

Smith: No!  Adenosine worked.  It converted the rhythm.  But adenosine only lasts for seconds, and if the dysrhythmia recurs, then the adenosine is gone.

We need to do one or both of two things:

1. Prevent the initiation of the dysrhythmia -- this can be done with a beta blocker by prenenting PACS

2. Have a long acting AV nodal blocker -- this can be done with a longer acting AV nodal blocker: both a beta blocker or calcium channel blocker.  

Metoprolol  (beta blocker) thus does BOTH

1. Prevents the PAC that initiates SVT
2. Blocks the AV node to prevent propagation.

Diltiazem and Verapamil (Calcium channel blockers) block AV conduction        

  • Metoprolol
  • 5 mg IV q 5 minutes x 3 (max 15 mg), then 25-50 mg orally.
  • Verapamil
    • Dosed at 2.5-5 mg IV over 2 min (over 3 min in elderly patients).
    • A follow-up dose of 5-10 mg (0.15 mg/kg) IV is administered 15-30 min later if the SVT persists and no adverse reaction occurs. The maximum dose is 20-30 mg.
    • This may be followed by an infusion of 0.005 mg/kg/min.
  • Diltiazem
    • Dosed at 0.25 mg/kg IV over 2 min.
    • A subsequent dose of 0.35 mg/kg IV is administered if no response is seen and no significant drug-induced adverse event occurs

She remained hemodynamically stable and was treated with 10 mg of IV diltiazem. The following EKG was obtained


After treatment with diltiazem, the patient remained in normal sinus rhythm with a rate persistently in the 80s and 90s.

Given recurring SVT without obvious resolution of its cause, she was admitted for further observation and did not have any recurrence. She had an echocardiogram which was normal. She was prescribed oral diltiazem to prevent recurrence and was discharged.


MY Comment, by KEN GRAUER, MD (10/25/2022):


Today’s blog post reviews the important topic of how to approach the patient who presents with palpitations from an SVT (SupraVentricular Tachycardia) rhythm. I focus my comments on a number of additional points aimed at supplementing the above excellent discussion by Drs. Nicholson and Meyers.
  • Today’s patient is a 43-year old woman with a history of intermittent “SVT” that in the past has responded to vagal maneuvers that she performed on herself at home.

Some General Thoughts on SVTs:
I’ve previously reviewed in detail an approach to the regular SVT (Please see My Comment — at the bottom of the page in the March 6, 2020 post in Dr. Smith’s ECG Blog). Relevant points from that discussion that relate to today’s case include the following:
  • Knowing that today’s patient had a history of intermittent SVT” does not tell us the specific rhythm involved. Even experienced providers make the mistake of using the term, “SVT” as a specific diagnosis — when in fact this generic term includes all arrhythmias in which the rate is “tachycardic” (ie, ≥100 in an adult). This includes sinus tachycardia, atrial fibrillation or flutter, MAT, and others. Causes and treatments for these various forms of “SVT” may differ.
  • The above said — the fact that today’s patient describes success with home vagal maneuvers strongly suggests that we are dealing with some type of reentry SVT rhythm.

  • For optimal initial and longterm care of today’s patient — additional features in the History to inquire about include the following: i) How long this patient has had SVT? — How often she gets it? — and — How long it takes vagal maneuvers to work?; ii) Are there any specific precipitating factors? (ie, dehydration, periods of increased stress or anxiety, stimulants such as caffeine, alcohol, recreational drugs, etc.); iii) How often has she had to go to the ED for her SVT?; andiv) Previous treatments tried?

Diagnosis of Today’s Rhythm:
I favor a systematic approach to rhythm interpretation — in which the memory aid, “Watch your Ps, Qs and 3Rs” reminds me of the 5 KEY parameters to assess (CLICK HERE — if interested in more on this Ps, Qs, 3R approach).
  • For clarity in Figure-1 — I’ve reproduced and labeled the initial ECG in today’s case, with the follow-up 12-lead after administration of 6 mg IV Adenosine.

  • Applying the Ps, Qs, 3R Approach to ECG #1 — there is a regular SVT ( = narrow QRS) rhythm at a rate of ~140/minutewithout sign of sinus P waves. 

  • PEARL: It’s important to keep in mind the importance of the rate of a regular SVT rhythm — since since entities such as sinus tachycardia (with sinus P waves hidden within preceding T waves) and atrial flutter (with 2:1 AV conduction) become become far less likely when the rate of a regular SVT exceeds ~170/minute
  • In contrast, a regular SVT rhythm at a rate between ~130-160/minute (as in today’s case) — includes a differential diagnosis of i) Sinus tachycardia; ii) AFlutter (Atrial Flutter); iii) ATach (Atrial Tachycardia); and/oriv) A “reentry SVT rhythm (with AVNRT and orthodromic AVRT being the most common forms of this).

Compare QRS morphology for the 2 ECGs shown in Figure-1. With attention to the RED arrows in ECG #1 — What is the difference in QRS morphology between these 2 tracings?
  • Clinically — What is the significance of this difference?

Figure-1: The first 2 ECGs in today’s case. What is the clinical significance of the RED arrows in ECG #1?

Those RED Arrows in ECG #1:
The RED arrows in Figure-1 highlight 7 leads in ECG #1 that show retrograde atrial activity during the tachycardia.
  • PEARL: The clinical significance of identifying retrograde atrial conduction during a regular SVT rhythm (such as the one in today’s case) — is that it confirms the diagnosis of a reentry SVT rhythm! Sinus tachycardia, AFlutter and ATach do not do this. 
  • To Emphasize — It is not common to see clear evidence of retrograde conduction in as many leads as shown by the RED arrows in ECG #1. The reason I highlight this finding — is that knowing how to look for retrograde atrial activity is helpful when its presence is far more subtle. This is because once we can confirm the diagnosis of a reentry SVT — we know what optimal treatment in the ED will be if our initial dose of Adenosine is ineffective (ie, repeat Adenosine and/or Diltiazem, Verapamil or a ß-Blocker).

How to Confirm Retrograde Conduction:
Retrograde conduction produces a negative P wave that appears after the QRS in the inferior leads. This is because the retrograde impulse is traveling away from the direction of lead II, which is positively oriented at +60 degrees.
  • As a result, when looking for retrograde atrial activity — I first focus my attention on the very last part of the QRS in the inferior leads (II,III,aVF) — looking for a negative notch or deflection in one or more of these leads. The wide, “pseudo-S wave” seen in each of the inferior leads in ECG #1 is distinctly unusual, especially given the absence of RBBB conduction. Proof that this truly represents retrograde atrial conduction in ECG #1 — is forthcoming by comparison of these leads in ECG #2, in which this negative “pseudo-S wave” deflection in the inferior leads after conversion to sinus rhythm is much narrower.

  • After the inferior leads — I look next at right-sided leads aVR and V1 — which commonly show retrograde conduction as a short positive “pseudo-r’ deflection” (RED arrows in leads aVR and V1 in ECG #1). Note that this pseudo-r’ deflection is no longer present in ECG #2 after conversion to sinus rhythm.
  • Sometimes lead aVL shows retrograde conduction as a positive deflection after the QRS (as seen in ECG #1). 
  • In my experience — it is less common to see retrograde conduction in other leads.

  • HINT: The way to get good at recognizing retrograde conduction during regular SVT rhythms — is to routinely go back and compare deflections that you thought looked suspicious during the tachycardia — with QRS morphology in those same leads after conversion to sinus rhythm. BOTTOM Line: It’s nice to be able to definitively diagnose that the cause of the regular SVT rhythm in front of you is a reentry SVT. Identifying retrograde atrial conduction during a regular SVT rhythm allows you to do so.
  • CAVEAT: The opposite is not necessarily true — because some cases of AVNRT manifest such a short RP’ interval, that the retrograde P wave is hidden within the terminal part of the QRS (and therefore not visible on ECG).

PEARL: The RP’ interval (ie, distance of the retrograde P wave from the preceding R wave) — can provide a clue to the mechanism of the reentry SVT. For example — very short RP’ intervals (in which the retrograde P wave notches the terminal portion of the QRS complex) — suggest that the reentry circuit is contained within the AV node. In contrast — longer RP’ intervals (in which the retrograde P wave notches a portion of the ST segment) suggest that an AP (Accessory Pathway) which is located “further away” (ie, outside of the AV node) may be participating in the reentry circuit.
  • The RED arrows in today’s case suggest a fairly short RP’ interval — that is more consistent with AVNRT.
  • For more on the concept of retrograde conduction during a regular SVT rhythm — Please see My Comment at the bottom of the page in the March 6, 2020 post of Dr. Smith’s ECG Blog.

Some Final Thoughts on Today’s Case:
It is not at all surprising that the reentry SVT rhythm in today’s case recurred shortly after IV Adenosine (ie, the half-life of IV Adenosine is less than 10 seconds!). As a result — it should be expected that a longer-acting agent may need to be added to maintain sinus rhythm (as was done with Diltiazem in today’s case). Among considerations that arise following hospital discharge of today’s patient are the following:
  • Awareness that in a younger adult without underlying heart disease (ie, unremarkable Echo) — a reentry SVT is a non-life-threatening and usually fairly benign rhythm disturbance. As a result — the main indication for treatment is to control symptoms. How best to do this depends on answers to the series of questions in the History that I suggested above (under Some General Thoughts on SVTs).
  • There is no need to immediately refer today’s patient to EP for ablation. Although treatment of reentry SVTs by ablation is highly effective, with an excellent safety record when done in a center with quality results — there remains potential for a small-but-real incidence of complications with this procedure. Patients should be offered a choice for a trial of medication vs ablation for this non-life-threatening arrhythmia. Clearly, EP ablation becomes indicated in patients with frequent refractory SVT recurrences — but not necessarily before.
  • The “best” treatment of recurrent reentry SVT is to find and fix a precipitating cause, when one is present. I’ve had pregnant patients who only got their reentry SVTs during their pregnancy. I’ve had other patients who would have frequent SVT recurrences during periods of intense stress/anxiety — with their reentry SVT episodes controlled when these precipitants were controlled. Excess caffeine or OTC sympathomimetics are other potential precipitants that may be easily controlled once identified.
  • Commonly used medications to suppress recurrent reentry SVT episodes include Diltiazem, Verapamil or a ß-Blocker. These medications do not necessarily need to be used continually on an indefinite basis. Life circumstances change. My patient with stress-induced SVT did well for months at a time when her stress was controlled. She stopped her daily Diltiazem during lower-stress periods — and then resumed daily Diltiazem when life stressors resurged.
  • For patients with infrequent recurrences that are easily controlled with AV nodal blocking agents — use of “prn medication” (ie, with permission for home use by the patient of a dose of Diltiazem, Verapamil, or a ß-Blocker) at the time of a recurrence, and then going into a quiet room — may resolve the SVT within 30-120 minutes, thereby avoiding an ED visit.

  • BOTTOM Line: Longterm management of the patient with a reentry SVT should be individualized for the life circumstances of the patient at hand. 

Sunday, October 23, 2022

30 yo woman with trapezius pain. HEART Pathway = 0. Computer "Normal" ECG. Reality: ECG is Diagnostic of LAD Occlusion.

This is a repost of this amazing case: 

Echocardiography, even (or especially) with Speckle Tracking, can get you in trouble. The ECG told the story.

A completely healthy 30-something year old woman with no cardiac risk factors had sudden onset of bilateral trapezius pain that radiated around to her throat.  It resolved after about 5 minutes, but then recurred and was sustained for over an hour.  She called 911.

EMS recorded these prehospital ECGs:

Time 0:

In V2-V4, there is ST elevation that does not meet STEMI "criteria," of 1.5 mm at the J-point, relative to the PQ junction.  But there are also unusually Large T-waves

Time = 13 min
T-wave in V2 is now taller and fatter, the ST segment is more straight.
T-wave in V3 is no taller, but it is fatter due to a straighter ST segment
These are hyperacute T-waves that are DIAGNOSTIC of LAD Occlusion.

Time = 24 min
S-wave depth is diminishing

These prehospital ECGs were lost and not seen.

The patient arrived in the ED.

The pain completely resolved after nitroglycerine 

Moments later, the this ECG was recorded in the ED when she had been pain free for moments only:
Computer read: Normal ECG.
However, T-waves are still unusually hyperacute; the computer almost never sees this.
The T-wave in V2 is smaller.  QTc is 444 ms.
How about using the 4-variable formula?
STE 60 V3 = 1.5 mm, R-wave amplitude V4 = 15 mm, QRSV2 = 8.5
Formula value is 19.38, which indicates LAD occlusion 
(Most accurate cutpoint is 18.2 -- value > 18.2 has high probability of LAD Occlusion).

This patient has a non-diagnostic ECG by most rules.  

However, with attention to subtleties, especially when compared with the unseen prehospital ECGs, it is diagnostic of LAD occlusion with probable spontaneous reperfusion.

The first troponin was below the level of detection (LoD).

If you use something like the HEART score:
1. H  History: She has atypical pain (trapezius) (score = 0)
2. E  EKG: a negative ECG (score = 0)
3. A  Age: = 0
4. R  Risk factors = 0
5. T:  Troponin = 0 [first troponin (contemporary, not high sensitivity) was less than the level of detection). 
Total HEART score = 0.  Risk of 30-day adverse events is less than 1.7%.   Some might send her home.

But maybe she has an acute LAD occlusion that will get even worse. 

The providers did a bedside echo and even used speckle tracking to look for strain:

hyperacute T-waves standard echo nstemi vid 3 from Stephen Smith on Vimeo.

I think maybe there is an anterior wall motion abnormality, but this is very difficult.  They read it as normal.

Here are a couple shots with strain, or "speckle tracking" on ED Echo:

hyperacute T-waves speckle 1 x4 from Stephen Smith on Vimeo.

hyperacute T-waves speckle 2 x4 from Stephen Smith on Vimeo.

To, me these look like anterior wall motion abnormality, but I showed them to one of our ultrasound fellows who is very interested in this.

She said:

This is a tough one. I see what you mean, initially when I looked at the image, I also thought there was an anterior wall motion abnormality.  But then on closer inspection, I suspect that maybe the anterior wall is just not being tracked well. In systole, you can see the anterior wall come down and outside of the area that is being tracked (more so than the other tracked walls). Even though the strain values are a little off in the graph (so is the posterior wall) it is still a value range (about -18) that would be considered non-ischemic by the cardiology literature, I believe.  I have been wrong before though! So it is possible that I am misinterpreting the clip. If it were me, I would get values at the level of the mitral valve, papillary muscles, and apex (all in PSS axis). Also, narrowing the area being tracked helps the walls get recognized much better.

As I wrote, the first troponin was below the Level of Detection.

She remained pain free, and was admitted without further serial ECGs.  

When in doubt, one should always get serial ECGs.  Bedside echo is not enough.

At time = 240 minutes (4 hours), the second troponin returned at 1.15 ng/mL.  That prompted recording of this ECG:
Back to normal for this patient.  This demonstrates that all ST elevation of the previous ECGs was ischemic, not normal.  She was having a transient STEMI, briefly.

It is very lucky that she spontaneously reperfused her LAD.  It did not progress to full STEMI with loss of the anterior wall, as in this case.

Also, persistence of a pain free state does not guarantee an open artery.  See this case.

A formal contrast echo was done at this point:
Normal estimated left ventricular ejection fraction, 65%.
Regional wall motion abnormality-distal septum and apex.

She was treated medically for NonSTEMI, pending next day cath, which showed  ulcerated plaque and a 60% thrombotic stenosis in the LAD distal to the first diagonal.  

It was stented.

Learning Points:
1. Always get serial ECGs when there is any doubt about what is going on.
2. Use the 4-variable formula!!

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

3. Always find and look at prehospital ECGs.  They give extremely valuable information.
4. Hyperacute T-waves remain for some time after reperfusion of an artery.  I always say that "you get hyperacute T-waves both 'on the way up' (before ST segment elevation) and 'on the way down' (as ST elevation is resolving).
5. Wall motion abnormalities are very hard to see, even with advanced Speckle Tracking technology.  They require a great bubble contrast exam and expert interpretation.
6.  This case does not demonstrate it, but a wall motion abnormality may disappear after spontaneous reperfusion (see this case).
7. Patients with transient occlusion may manifest only transient STEMI on ECG.  Subsequent troponins may be all negative and subsequent formal echo may be normal.  See this case
8. Risk scores + EKG and troponin should not be considered negative unless there are 2 troponins.
9. Risk scores should not be used at all in the setting of a diagnostic EKG.  These are DIAGNOSTIC of LAD OCCLUSION.


MY Comment by KEN GRAUER, MD (10/23/2020):
There are a number of important lessons worthy of repeating from today's repost of our case from March 28, 2017. As per Dr. Smith:
  • Always search for and find prehospital ECGs. These will often provide invaluable information.
  • Serial ECGs correlated to the presence (and severity) of chest pain — often reveal the status of the "culprit" artery (ie, occluded, reopened, reoccluded).
  • Hyperacute T waves may maintain their appearance for a period of time after reperfusion of the culprit artery.
  • Some patients are lucky — in that the culprit artery may spontaneously reperfuse — and then remain open until definitive diagnosis and treatment can be instituted. Other patients are not so lucky.
  • If spontaneous reperfusion occurs rapidly — serial troponins may be no more minimally elevated (if elevated at all). Echo may be normal (especially if the patient no longer has chest pain).

I found review of the 3 serial pre-hospital ECGs in this case to be especially insightful as to how lead-by-lead comparison often "tells the tale" — by confirmation of dynamic ST-T wave changes.
  • KEY Point: Subtle serial ECG changes may be EASY to overlook unless careful lead-by-lead comparison is performed.
  • Be sure to verify QRS morphology in both the limb leads and chest leads when performing lead-by-lead comparison. This allows you to ensure that neither frontal plane axis shifts nor variation in chest lead electrode placement are influencing ST-T wave appearance in the tracings you are comparing.

For clarity — I've taken the chest leads from the 3 pre-hospital tracings in this case, and placed them side-by-side in Figure-1. The reason I omitted the limb leads — is that I did not appreciate any significant ST-T wave change in the limb leads from these 3 tracings. In contrast — There are subtle-but-real changes in ST-T wave appearance in many of the chest leads.

Take Another LOOK at the serial chest leads in Figure-1What are the dynamic ST-T wave changes that you see?
  • HINT: When contemplating whether T wave size is increased from one tracing to the next — be SURE to compare relative size of the R wave in each lead you are looking at!

Figure-1: Comparison of the chest leads in the 3 serial ECGs performed by the EMS team prior to hospital arrival. What are the ST-T wave changes that you see?

MY Thoughts on the 3 Pre-Hospital ECGs:
T waves are tall and peaked in the chest leads from each of these 3 pre-hospital tracings shown in Figure-1.
  • Especially in lead V3 of ECG #1 — the T wave is already huge (>10 mm), and outsizes the R wave in this lead.

ECG #2 (Time = 13 minutes):
  • Beginning with lead V3 — the T wave is not quite as tall as it was in lead V3 of ECG #1. But this is most probably because the R wave in lead V3 of ECG #2 is relatively smaller. The R wave in lead V3 now only measures 7 mm — whereas the R wave was much taller in lead V3 of ECG #1. Relatively Speaking — the T wave is taller in ECG #2, because it is now almost twice the height of the R wave in this lead!
  • Even more important than this relative increase in T wave height — is the increase in "volume" of the T wave in lead V3 of ECG #2. Note how much "fatter-at-its-peak" and "wider-at-its-base" the T wave now is.
  • I thought all 6 chest leads in ECG #2 show a relative increase in both size and volume of their T waves, compared to T waves in the chest leads of ECG #1.

ECG #3 (Time = 24 minutes):
The difference in ST-T wave appearance between chest leads in ECG #2 and ECG #3 is more subtle — but still present!
  • Isn't the T wave in Lead V2 of ECG #3 more voluminous (ie, with a wider base— than it was in ECG #2?
  • Considering further decrease in R wave amplitude — Isn't the T wave in lead V3 of ECG #3 relatively taller and more voluminous than it was in ECG #2?
  • In lead V4 of ECG #3 — the T wave is taller than the R wave for each of the 3 QRS complexes that are shown. In contrast — the R wave is slightly taller than the T wave for each of the 3 complexes in lead V4 of ECG #2.

To Emphasize — The changes I describe above in ST-T wave appearance between ECG #2 and ECG #3 are extremely subtle. If I didn't have ECG #1 as my starting point — I would not have attributed clinical significance to the subtle changes between ECG #2 and ECG #3.

  • BUT — Given that we do have all 3 serial pre-hospital tracings as a basis for comparison — I think the trend that we see from one tracing to the next is real — and clearly suggests dynamic ST-T wave change (which in this patient with new cardiac symptoms — indicates an acute ongoing process until proven otherwise).
  • Take Home POINT: It would be EASY to overlook these dynamic ST-T wave changes if one was not meticulous in their lead-by-lead comparison.

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