40-something male in a head-on Motor Vehicle Collision and Splenic Injury

A 40-something male presents to the stabilization room for evaluation following head on motor vehicle collision (MVC).  Pt was reported restrained driver, hit at city speeds,  with + airbag deployment.

The MVC was unquestionably caused by the other car, not by this driver.

The patient complained to EMS of chest pain and a prehospital EKG en route was concerning for STEMI.

The patient was at all times hemodynamically stable, without evidence of any profuse bleeding.

He had an ECG recorded on arrival to the ED:

Anterior and Inferior STEMI with diffuse hyperacute T-waves. 

This ECG really can't be anything else. 
Takotsubo is on the differential of anterior and inferior STE, but takotsubo just looks different (see some cases below).

This must be an occluded "wraparound" LAD (wraps around the apex to the inferior wall) and one would expect an apical wall motion abnormality, as well as probable septal, anterior, and inferior wall motion abnormalities.

But acute STEMI in this situation is not necessarily due to plaque rupture and/or thrombus.  It could be due to the trauma, and contusion of the LAD with thrombus or dissection.

Further patient history revealed that the chest pain started following the crash, and that he had no chest pain previously. Brief review of chart showed no h/o known CAD. DDx was possible aortic dissection or injury, cardiac contusion, LAD dissection, or type I MI w/ plaque rupture.

They performed a bedside ED cardiac ultrasound:

With this ECG, there must be a wall motion abnormality if the ECG and echo are done at the same time.

If you do not see a wall motion abnormality, it is because:
1.  ultrasound, or your technique or expertise, is not good enough.
2. The artery reperfused quickly enough, such that all wall motion recovered.

It is possible to have a normal echo if, immediately after the ECG:
1. The artery reperfuses and
2. The duration of ischemia was short.

This shows an apical wall motion abnormality
This is consistent with anterior/inferior MI due to wraparound LAD, and also with takotsubo.

However, this was the provider's interpretation: 

"Further bedside ultrasound of cardiac function w/o demonstration of significant WMA or impaired function."

The patient went to pan scan, with CT of chest/abd/pelvis.  It showed a splenic laceration and pelvic fracture, and also this:

Just the heart is shown from the CT of chest/abdomen/pelvis, with contrast

Shows a clear apical area without any perfusion (dark, no contrast gets to this myocardium)

Slightly different CT technique:

Again, apical area without contrast

These images further confirm the diagnosis of acute STEMI.

When the patient returned to the ED, he had another ED cardiac ultrasound:

Now there is no clear wall motion abnormality, but these can be very difficult to appreciate.

This echo was done with Speckle Tracking, Strain Echocardiography.  This was done by one of the most expert ED echocardiographers in the world:

Good contraction is measured by a large negative value.  The light green is the most negative, and this would represent the most wall contraction, and represents the lateral wall.  Red, which is the apex, has moderate contraction, so there may be a subtle apical wall motion abnormality still.

But it is very hard to appreciate with the naked eye, without speckle tracking.

At this point, another ECG should have been recorded, but was not.  It would almost certainly have shown resolution of the STEMI findings (due to spontaneous reperfusion).

Should the cath lab have been activated?  

This is a tough question.   PCI usually requires antiplatelet and antithrombotic therapy, but a persistently occluded LAD must be opened, even if such medications cannot be given.  Plain old balloon angioplasty without these meds can temporarily open the artery.

I asked our chief of cardiology, Gautam Shroff: "Plain old balloon angioplasty (POBA) requires at least one antiplatelet agent indefinitely and 2 of them for 30 days, or else it clots off.  Heparin is also needed during the cath.  For a head bleed I would sacrifice the anterior wall.  Perhaps the best approach for this case would be splenectomy (or Interventional radiology to stop the bleed?), then POBA or bare metal stent??  No good options and risk benefit has to be weighed." 

So Cardiology consultation is essential, and coordination with trauma surgery and interventional radiology.

Fortunately for this patient, as you'll see below, and unbeknownst to the providers, the artery quickly spontaneously reperfused.


FINAL ED DIAGNOSES:
1. MVC
2. Splenic laceration
3. Pelvic fracture
4. ST elevation w/ chest pain


The patient was admitted to the hospital.  He did have serial troponins:

First 3 troponins

Notice the last one shoots up, which is typical with reperfusion (artery opening, resulting in sudden troponin release).

At this point (8 hours later), the 2nd ECG was recorded:

ST Elevation is gone.  There are Q-waves in V2-V4.  The LAD has reperfused.

Formal echo was done:

Normal left ventricular cavity size.
Normal estimated left ventricular ejection fraction - 70%.
Regional wall motion abnormality- apex, distal septum and inferior segments.

This demonstrates that a bubble contrast echo, read by an expert, is superior at identifying subtle wall motion abnormalities than an ED echo.


Another 24 hours of troponins were recorded, starting at time 1504:

This was recorded another 24 hours later:

Terminal and symmetric deep T-wave inversion (reperfusion T-waves), with Q-waves (not exactly Wellens' waves, which should have R-wave preservation)

All troponins

It is really not necessary to get all these troponins, but they are interesting.

Angiogram, 5 days later:

--Culprit for the patient's "NSTEMI" (!) [comment: It is really a transient STEMI) is plaque rupture or traumatic coronary dissection in the distal LAD.  It is a wraparound LAD to the inferior wall.
--While there is residual 80-90% stenosis, there is TIMI III flow beyond
--Will initiate treatment with clopidogrel (300 mg give post-procedure), without PCI at this time, given potential inability to tolerate DAPT in the setting of splenic laceration/rupture.
--Can proceed to PCI if patient tolerates anticoagulation and develops angina prior to discharge or would plan for staged re-look angiography and PCI in 4-6 weeks.


Summary:
So this was a brief LAD occlusion, with transient STEMI.  It may have been a dissection related to the trauma, or coincidental plaque rupture, which could be triggered by the stress of the trauma.


Here are several cases of Takotsubo with ST Elevation that could mimic STEMI. 

Many takotsubo have on T-wave inversion, in which case emergent cath lab activation is not critical (though it could mimic Wellens')

Diffuse ST Elevation with Apical Ballooning: is it Takotsubo Stress Cardiomyopathy?

COPD exacerbation, what do the ECG and bedside echo show?

Takotsubo Stress Cardiomyopathy, with Echocardiogram

Two more Cases of Takotsubo Stress Cardiomyopathy

Here are some cases of myocardial contusion

Blunt Trauma in a Child

Gunshot wound to the chest with ST Elevation

A Child with Blunt Trauma -- this one has to be seen

A young peripartum woman with Chest Pain

This is written by Brooks Walsh.
https://twitter.com/BrooksWalsh

A 30 year-old woman was brought to the ED with chest pain.

It had started just after nursing her newborn, about an hour prior, and she described it as a severe non-pleuritic “pressure” radiating to the back.

She had given birth a week ago, and she had similar chest pain during her labor. She attributed the chest pain to anxiety and stress, saying "I'm just an anxious person."

A CXR and a CTA for PE were normal.

The ECGs

An initial ECG was obtained as the pain was rapidly resolving:

Minimal upsloping ST Elevation in III, with a steeply biphasic T wave, and with reciprocal ST depression in leads I and aVL.
There is also a Q-wave in III.
This strongly suggests reperfusing RCA ischemia.

There is also subtle STD in V3-V5.
(Inverted T in V2 is likely due to lead misplacement -- this is evidence by the inverted P-wave)

A second ECG was obtained 6 hours later (pain-free):

Aside from a slightly biphasic T wave in lead III, the findings from the first ECG are now resolved.

This dynamic findings, especially when correlated with the patient’s resolving symptoms, are not “non-specific.” The biphasic T wave is consistent with recent reperfusion of an occluded coronary artery supplying the inferior region. The initial STD depression in aVL and V3-V5 (later resolved)  further supports a very recent occlusion affecting this area. 

Troponins, echocardiogram

An echocardiogram showed inferobasilar hypokinesis, further supporting a diagnosis of regional ischemia, likely of the area supplied by the RCA. 

The initial troponin I was elevated at 0.75 ng/ml (99th %-ile URL = 0.04 ng/ml), and rose to 12 ng/ml six hours later. This rate and height of troponin rise strongly suggested a type 1 MI. 

Angiography

Angiography was performed after aspirin and heparin were started. 

Here’s the angiogram of the RCA:

No thrombus or plaque rupture in the RCA (or any coronary artery) was found.
However, a smooth tapering of the mid-RCA was seen, highlighted in red below:

How do we explain the MI if no sign of CAD was found? This MI wasn’t caused by a ruptured plaque of CAD - it was a coronary artery dissection of the RCA.  

Spontaneous coronary artery dissection

Dissection of a coronary artery may occur in the context of atherosclerosis, or be iatrogennic during angiography or angioplasty. In the absence of these factors it is termed spontaneous coronary artery dissection (SCAD). 

This case occurred 10+ years ago. At that time the literature suggested: 

• SCAD was rare, 
• Mostly related to pregnancy, 
• Seen on angiography as a dissection flap, and 
• Managed similarly to MI caused by CAD (ASA, BB, lytics/PCI). 

However, in the intervening years there have been marked changes in the understanding of SCAD. Many of these issues were described in a prior post by Dr. Angie Lobo (@aloboMD)

(For open-access reviews of this literature, see Saw 2016, Saw 2017, or Hayes 2018.)

See also this fascinating case:

An athletic 30-something woman with acute substernal chest pressure

Five takeaways about SCAD: 

1. SCAD isn’t rare, especially in women

Historically SCAD had been identified in < 1% of angiograms performed for ACS. However, contemporary studies find it in up to 4% of ACS, and in > 22% of ACS cases in women. A recent study found that SCAD causes almost 20% of STEMI in young women.

2. Pregnancy is not a common cause of SCAD

When ACS occurs in the peripartum period, SCAD is responsible in 43% of cases. However, pregnancy-associated spontaneous coronary dissection (PA-SCAD) is still pretty uncommon, and accounts for less than 5% of SCAD cases overall. Fibromuscular dysplasia is a much more common trigger for SCAD.

3. SCAD can have subtle angiographic features, and coronary CTA is unhelpful.

SCAD was originally thought to show a characteristic dissection flap and and false lumen(s) ion angiography. However, this “classic” pattern ( “Type 1”) only occurrs in about 25% of cases. Most SACD does not create a flap, and shows instead a long smooth narrowing of the true lumen. Type 2 is seen in almost 70% of cases. Our patient had a type 2 lesion.

Type 2 is more difficult to appreciate on angiography than type 1. The relatively poorer resolution of cardiac CTA makes it especially inappropriate to rule out SCAD. Often, intravascular ultrasound or intravascular optical coherence tomography is requeried to make the diagnosis.

4. You don’t just treat it like ACS caused by CAD 

Aggressive intervention may cause more problems than the original SCAD lesion. Guidewires for PCI may be difficult to thread through the weak, twisty arteries, and may rupture the false lumen. Heparin hasn’t been shown to help or hurt, but could theoretically promote expansion of an intramural hematoma. Fibrinolytics have been associated with devastating complications. While there isn’t good evidence that aspirin and beta-blockers help, there are few concerns about their safety, and they are generally recommended.

5. Coronary lesions often resolve without intervention, but PCI has role

Treatment of SCAD requires a different risk-benefit calculation than ACS caused by typical atherosclerotic disease, as shown by two studies form this year.

On the one hand, most SCAD lesions resolve with only conservative treatment, and PCI is not required. A study by Hassan et al. provided evidence that PCI/CABG was unnecessary for most SCAD, and should be considered for only high-risk presentations.

On the other hand , high-risk lesions appear to do well with aggressive treatment. Lobo et al. examined SCAD presenting as STEMI (unlike Hassan et al. where more than 3/4 of cases were NSTEMI). The SCAD cases in Lobo et al. were pretty sick, with mostly LM/pLAD lesions and high rates of cardiogenic shock. Despite this, there was a high rate of PCI success.
 

Outcome of our case

Once the type 2 SCAD was identified, the heparin drip was stopped. No PCI was performed, and only conservative medical therapy was pursued. No evidence of a connective-tissue disease such as FMD was found. She did well, and was ultimately discharged from her cardiologist’s care years later!

References

Lobo AS et al. Revascularization in Patients With Spontaneous Coronary Artery Dissection and ST-Segment Elevation Myocardial Infarction.  JACC 2019 Sep 10;74(10):1290-1300.

Hassan S. et al.  Natural History of Spontaneous Coronary Artery Dissection with Spontaneous Angiographic Healing.  JACC Cardiovascular Interventions 2019 Mar 25;12(6):518-527. 

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

MY Comment, by KEN GRAUER, MD (10/24/2019):

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

Superb case by Dr. Brooks Walsh regarding the entity of SCAD (Spontaneous Coronary Artery Dissection). I had no idea SCAD was so common a cause of acute STEMI in younger women, even when they are non-smokers ..

Excellent description by Dr. Walsh of the ECG findings in the 2 tracings provided in this case! KEY to assessment of these findings is appreciation of the changes between these 2 tracings. I find putting these 2 tracings together greatly facilitates interpretation (Figure-1).

Figure-1: The 2 ECGs in this case (See text).

MY Thoughts on the ECGs in Figure-1:

The patient in question was a 30-year old woman who had given birth 1 week earlier. Her chest pain was a severe, non-pleuritic “pressure” that radiated to her back. A similar episode had occurred a week earlier during labor. ECG #1 was the initial ED tracing, obtained when her chest pain was rapidly resolving (Figure-1). I’d add the following thoughts to Dr. Walsh’s comments:

• ECG #1 differs from the usual picture of acute reperfusion following RCA occlusion — in that only 1 of the 3 inferior leads ( = lead III) suggested to me a recent acute event. Leads II and III are not normal (ie, they show ST segment straightening and slight J-point depression) — but I was not at all certain about an acute event from my initial review of this tracing.
• That said — the SHAPE of the ST-T wave in lead III (showing ST segment straightening with slight elevation + sharp downslope of the T wave leading to terminal T wave inversion) is very concerning. It is the finding of a near mirror-image opposite ST-T wave picture in lead aVL + the decidedly abnormal ST segment straightening with slight depression, leading to angulation at the onset of the T wave in lead I — that should convince us of something acute until proven otherwise!
• More than just a Q wave in lead III in ECG #1 — we see an initial Q — followed by rise to a small-amplitude R wave just above the baseline — followed by an S wave. This type of fragmented QrS pattern that we see in lead III supports the possibility that the tiny q waves in the other 2 inferior leads (II and aVF) may indeed be markers of infarction.
• As per Dr. Walsh — there is subtle ST-T wave flattening with slight ST depression in leads V3-thru-V6. While important to note — I felt these changes to be nonspecific.
• Reasons why Dr. Walsh thought the T wave inversion in leads V1 and V2 was probably due to lead misplacement (placement of these leads 1 or 2 interspaces too high on the chest) — include: i) There is a prominent negative component to the P wave in leads V1 and V2; ii) There is a definite rSr’ in lead V1, and suggestion of an r’ component also in V2; and, iii) QRST morphology of lead V1 strongly resembles that in lead aVR (CLICK HERE — and look to My Comment at the bottom of the page in the November 4, 2018 SSmith Blog for more detailed discussion of how to quickly recognize too high placement of leads V1 and V2 on the chest).
• 
  
• BOTTOM LINE re ECG #1: While certain ECG features of acute MI are lacking in ECG #1 — the appearance of leads I, III and aVL — in association with subtle ST-T wave flattening with slight depression in many other leads, should clearly raise suspicion of an acute and/or recent cardiac event. Armed with new knowledge from Dr. Walsh that SCAD is surprisingly common as a cause of ACS (Acute Coronary Syndrome) among young women in the peripartum period — I will immediately include SCAD in my differential the next time I encounter a similar set of circumstances.

Comparing ECG #2 (obtained 6 hours later when the patient was pain-free) — with ECG #1:

• Lead placement looks better in leads V1 and V2. The terminal r’ is no longer seen in these leads — and although there is ST flattening, there is no longer T wave inversion in lead V2. Neither lead V1 nor V2 looks at all like lead aVR in ECG #2.
• Lead-by-lead comparison of ECGs #1 and #2 shows definite improvement. Although a q wave persists in lead III — the fragmented Q wave appearance in lead III of ECG #1 is no longer seen. Subtle J-point depression in many leads has resolved.
• NOTE: ST-T waves are still not normal in ECG #2. In addition to shallow T wave inversion in lead III — note distinct ST segment flattening in leads I, II, aVL, aVF, V2, V5 and V6. In isolation — I would interpret these ST-T wave changes we see in ECG #2 as “non-specific”. However (as per Dr. Walsh), in the context of comparison with ECG #1 — this improvement that we clearly see in ECG #2 at a time when chest pain has now totally resolved suggests dynamic ECG changes — and, in a patient with new chest discomfort — dynamic ECG changes tells us to assume an acute cardiac event until proven otherwise. This was confirmed by Echo, serum markers and cath.

Once again, our THANKS to Dr. Walsh for presenting this case!

Is this ST depression due to "lateral ischemia"?

This patient who presented with acute heart failure has a history of heart failure and atrial fibrillation:

This was interpreted as "lateral ischemia".
The patient's previous hospital admission had been predicated on this "ischemia."
What do you think?

There is atrial fibrillation with a controlled ventricular rate.  There is scooped ST depression in II, III, aVF and especially in V5, V6.

There are 4 categories of etiologies of ST depression in the context of a normal QRS:
1. Ischemia
2. Hypokalemia
3. Digoxin
4. Baseline/non-pathologic

--When the QT interval is very short, think digoxin.
--When the patient has atrial fibrillation with a controlled ventricular rate, it is not unlikely that the patient is on Digoxin for rate control.
--When the ST depression is what I call "scooped", think Digoxin.

When I suggested this as the likely etiology of the ST depression, and asked if she is on Digoxin, the resident said "That is so old school"!!

Well, it turned out she was on Digoxin, and there was no ischemia.

I showed this with no info to one of our young but very smart toxicology faculty and she instantly said "Dig", proving that this is not "old school."

Finally, it is important to remark that this is Dig effect and NOT Dig toxicity.

"Salvador Dali's mustache"
Some have likened the scooped ST depression of digoxin effect to "Salvador Dali's mustache" (for those of you who are young, Salvador Dali was the archetypal Surrealist painter).

This image comes from Life in the Fast Lane.  I'm not sure they created it.  https://litfl.com/digoxin-effect-ecg-library/

• Steve — I believe Dale Dubin first popularized the image of Salvador Dali's mustache as a representation for the "scooped" shape of Digoxin effect (Ken Grauer, MD).

Some other interesting posts on Digoxin:

Looks like a Posterior STEMI. Is it?

This one is pathognomonic of Dig toxicity.
There is an accelerated junctional rhythm
Note the ST depression has a very short QT; hence cannot be ischemia

Coved ST elevation with reciprocal ST depression: what is the diagnosis?

Here the scooped ST depression is in aVL.
Note the very short QT

ST segment depression: what is the etiology?

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

MY Comment by KEN GRAUER, MD (10/21/2019):

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

Excellent post by Dr. Smith to highlight potential causes of ST depression on ECG. While I immediately had the same initial thought about this case as Dr. Smith (ie, “Is this patient on Digoxin?” ) — I’d like to expand on his comments.

• For clarity — I’ve reproduced the 1st ECG shown in this case (Figure-1).

Figure-1: The 1st ECG shown in this case (See text).

Pertinent points regarding the interpretation of ECG #1 include:

• Descriptive Analysis of the ECG Findings: The rhythm in ECG #1 is AFib with a fairly slow ventricular response (ie, the rate dips below 60/minute in several places). All intervals are normal (as per Dr. Smith — the QTc looks short). The frontal plane axis is normal at +60 degrees. There is normal standardization — and clearly no sign of ventricular hypertrophy by voltage. Regarding Q-R-S-T Changes — there are small septal q waves (in leads aVL, V6) — transition is slightly delayed (occurs between V4-to-V5) — with the most remarkable finding being appearance of ST-T waves.
• NOTE #1: This ECG was apparently “interpreted” as showing “lateral ischemia”. This “interpretation” suggests premature closure regarding the diagnostic possibilities — so there is little wonder that the correct diagnosis was initially overlooked. We are still in the Descriptive Analysis phase, rather than “interpretation”. The way in which I would describe ST-T wave appearance in this ECG is that there are, “diffuse, nonspecific ST-T wave abnormalities” with (as per Dr. Smith) — ST segment “scooping” with a short QTc, that is most prominent in the lateral chest leads.
• NOTE #2: More than just the infero-lateral leads — virtually all leads on this tracing (except perhaps aVR and V1) show ST-T wave abnormalities (if not ST “scooping” — then nonspecific ST-T wave flattening).
• Clinical Impression: Optimal interpretation of ECG #1 should indicate that there is AFib with a fairly slow ventricular response + nonspecific ST-T wave flattening that includes ST segment “scooping” with a short QTc in several leads. Clinical Correlation is then needed to assess which one (or more) entities is (are) most likely to be responsible for this ST-T wave appearance (Figure-2).

Figure-2: Common causes of ST-T wave depression (See text). This Figure was taken from my ECG Blog #166.

Causes of ST-T Wave Depression: There are actually over 50 causes of ST-T wave changes on ECG. Although many of these causes are cardiac-related — there are also many that are not cardiac-related. Among the many non-cardiac causes of ST-T wave changes are hyperventilation; temperature extremes (excessive heat or cold exposure); anxiety or emotional stress; anemia; tachycardia; sleep deprivation; pulmonary disease; electrolyte abnormalities; central nervous system disorders; certain medications; and severe medical illness (among others). KEY Point — Many of the 50+ potential causes of ST-T wave abnormalities on ECG are non-cardiac!

• BOTTOM Line: Rather than attempting to commit to memory an exhaustive list of conditions that may predispose to ST-T wave changes — it suffices to appreciate the variety of entities that may produce changes on ECG.
• NOTE #3: In general — causes of T wave abnormalities (including T wave flattening or frank T wave inversion) are similar to potential causes of ST segment depression.

We favor remembering the short LIST of entities that we show in Figure-2. Our purpose in making this List, is to simplify your task as the interpreter. As soon as you recognize generalized ST-T wave changes on an ECG — Consider the short LIST of Potential Causes in Figure-2:

• NOTE #4: Often — more than a single cause may be operative. For example — the patient in this case had a history of heart failure and AFib — so we can presume this patient was probably taking at least a few medications. As a result — the patient might be taking Digoxin and/or a Diuretic (which might contribute to electrolyte disturbance). The patient has heart failure — so the abnormal ST-T wave changes may reflect LV “strain” (or a strain equivalent). And despite a history of recent chest pain — the ST-T wave changes we see in ECG #1 could reflect chronic ischemia. BOTTOM Line — Except for tachycardia, each of the other potential causes of ST-T wave depression in Figure-2 might be contributing in varying degree to the ECG picture we see in Figure-1.

PEARL: The Shape of the ST-T wave may suggest which one (or more) of the 6 entities in our LIST is (are) most likely to be operative in a given patient (See bottom half of Figure-2):

• Ischemia — is suggested by symmetric T inversion (RED arrow in Panel B) — especially when seen in two or more leads of a given lead group (ie, in leads II, III and aVF — or in both leads I and aVL). Ischemia may also manifest ST segment flattening or depression — but other entities may produce this same picture. However, true symmetric T wave inversion in 2 or more leads in an anatomic lead area increase the chances of ischemia (acute or chronic) as the etiology.
• Strain — from LVH, is suggested by asymmetric ST depression occurring in one (or more) of the lateral leads (less often in the inferior leads). Note the initial slow sagging of the ST segment with LV “strain” (BLACK arrow in Panel A) — with more rapid return to the baseline. “Strain” is more likely to be the cause of ST depression when ECG voltage for LVH is present. NOTE #5: On occasion, there may be Echo-verified LV enlargement with ST-T wave changes suggestive of “strain” on ECG — but without accompanying voltage. This point may be relevant to the patient in this case — as asymmetric ST-T wave depression is most marked in lateral leads in this patient with chronic heart failure (that predisposes to LV enlargement) — but who does not satisfy any ECG voltage criteria for LVH in ECG #1.
• "RV strain" — is suggested IF the picture in Panel A of Figure-2 is seen in right-sided leads (leads II,III,aVF; or V1,V2,V3) in a patient with RVH.

Use of Digoxin may affect ST-T waves in any one of 3 ways: i) There may be “scooped” ST depression in multiple leads (that simulates an inverted ice cream cone, as in Panel D of Figure-2). This is often associated with a relatively short QTc; or, ii) Digoxin “effect” may produce a "strain"-like pattern (identical to Panel A); or, iii) Despite use of an appropriate amount of Digoxin — there may be little-to-no effect on the ST-T wave.

• NOTE #6: In my experience (from correlating ECG ST-T wave appearance to serum Digoxin levels over the 3 decades that I worked closely with PharmDs at our institution) — the serum Digoxin level correlates poorly with the amount of ST-T wave scooping or depression. Thus, despite even high serum Digoxin levels — some patients fail to manifest ST-T wave abnormalities — whereas other patients show marked ST-T wave changes despite surprisingly low serum Digoxin levels.

Finally — Panel C in Figure-2 shows a non-specific ST-T wave pattern, in which the T wave and ST segment are flattened (if not slightly depressed). This pattern is called “nonspecific” — because any of the many potential causes of ST-T wave abnormalities may be operative.

BOTTOM Line (regarding ST-T wave changes in ECG #1 for this case) = Clinical correlation is needed:

• As per Dr. Smith — the “scooped” ST segment appearance in several leads (most remarkable in leads III, V5, V6) with noticeably shortened QTc make inquiring about whether the patient is on Digoxin the 1st priority.
• That said — the other entities on the LIST in Figure-2 should also be considered — as they may be contributing to the ST-T wave changes we see. Reviewing the patient’s medication list — serum electrolyte values (especially serum K+ and Mg++) — and, obtaining a prior ECG for comparison purposes would all be helpful.
• The “good news” in this case — is that the ST-T wave changes we see in Figure-1 do not look acute. In the absence of a history of worrisome, new-onset chest pain — it is highly unlikely that the ST depression in ECG #1 reflects acute ischemia.