A dialysis patient with nonspecific symptoms and pseudonormalization of ST segments

This is a case written by Dan Lee (One of our fantastic Hennepin Residents, class of 2020)
edits by Smith

A 60 something-year-old man with a history of ESRD, LVH and prior CABG presented after an episode of hypotension during his hemodialysis, run followed by a syncopal episode which caused his run to be terminated early.  His other symptoms on presentation were general lethargy and mild shortness of breath.  No chest pain.  His vitals were initially normal.

We will start with his baseline EKG:

There is voltage suggestive of LVH.  There are appropriate repolarization changes secondary to the LVH, including 1-2mm of ST elevation in V2 and V3. 

This is his presenting EKG (T= 26min):

What do you think?





















 Presenting EKG (T= 26min):

Compared to the baseline EKG which looks fairly typical of normal LVH, this presenting EKG has what we call “pseudonormalization” of the ST segments in V2 and V3 - the ST elevation that was once present at baseline is now "normalizing", to the point where there is virtually no elevation in V3.  Hence, the term "pseudonormalization", because it is not really normal - LVH should have repolarization changes seen in the baseline EKG.  Thus, there is relative ST depression.  It is analogous to a normal EKG having ST depression in V2 and V3, which would be abnormal and concerning for posterior MI in the right clinical context.  But because of LVH, this is masked in this patient.  There is also ST depression in the inferior leads - this was present on the old EKG, but there is also NEW ST depression in aVL.

Closer look at V2 and V3 side by side:

Furthermore, in both V2 and V3, the ST segment has flattened, resulting in more concavity of the ST-T complex.  Normally, concavity in ST segments suggests absence of anterior ischemia (though concavity by itself is not reassuring - see this study).  But in this case, the concavity is actually more concerning because now we are worried about posterior MI.  Given the inverted voltage from the posterior myocardium that we see on a normal EKG, deepening concavity would be analogous to elevating convexity in the posterior myocardium.

Same image above with V3 inverted and flipped on its axis to better visualize the posterior ST segment:

This is inverted: it is as if you were looking from the posterior wall.
The baseline is on the left, and now it looks as if the ST segment is rising, with less downsloping.

The patient's initial troponin I was 2.0 ng/mL (99% reference level = 0.030 ng/mL.  With his ESRD, he does have an elevated baseline troponin at  ~0.40 ng/mL.  His ED cardiac ultrasound (which is not at all ideal for detecting wall motion abnormalities, and is also very operator dependent for this finding) was significant for depressed global EF.  His prior EF from an ECHO 6 months prior indicated 35% LVEF.

What would you do in this scenario?

I think a good start would be a posterior EKG and a high quality contrast echocardiogram read by an expert.  Unfortunately, neither were done in this case.

This was the patient's second EKG in the ED, 3 hours after the first (T= 217min):

Deeper and more downsloping ST in V5 and V6
There is also pseudonormalization of the previously inverted T-wave in aVL

The patient's symptoms were attributed to probable  hypovolemia secondary to poor oral intake and to a UTI, but given his troponin elevation he was admitted on a heparin drip and serial troponins due to his high risk history.

His inpatient clinicians did not think that an urgent angiogram was warranted given that he was chest pain free, his EKG appeared nondiagnostic, and serial troponins were not elevating beyond 2 ug/L.

Later on during the night of his admission he had a short episode of chest pain that resolved with sublingual nitroglycerin. 

Around midnight, the patient became more hypotensive with systolic BP in the 60s, and was complaining of feeling nauseous and "sick to his stomach".

He had another EKG recorded at this time (T = 487 min):

More subtle flattening of ST segment in V2 and V3.

Around 4AM, the patient had worsening dyspnea and hypoxia with continued hypotension.

He became confused and had another EKG done (T = 899 min):

Even more pseudonormalization.  V2 hardly has any ST elevation now.  
Overall voltage is decreased as well. 
Just as importantly, the pseudonormalized T-wave in aVL is now larger, with deeper reciprocal T-wave inversion in inferior leads

Shortly after this EKG, his HR dropped into the 40's and he subsequently had a PEA arrest requiring 1 round of chest compressions, followed by ROSC.  He was taken to the cath lab at that time (T = 1024 min).

He was found to have a 100% occlusion of the proximal anastomotic portion of a prior SVG from the aorta to the OM1 which in turn had a vein graft to the distal RCA. There was initially TIMI 0 flow .  The lesion was intervened on with balloon angioplasty and had subsequent TIMI 3 flow.  It was thought to be an in stent restenosis and thrombosis from a DES placed in the same region 6 months prior.

His troponin I peaked at 97 ng/mL (very large MI!). 

His follow up ECHO the next day revealed an EF of 24% and a posterior wall motion abnormality.  Fortunately, he was extubated several days later in the ICU with intact baseline mental status and was discharged shortly thereafter to subacute rehab.

---------
Acute myocardial infarction in patients with dialysis

Patients on dialysis have a well studied history of underdiagnosis and undertreatment for acute myocardial infarction.  This is paradoxical given the absurdly high 2 year mortality rate of 70% after a MI in dialysis patients.

This study from Herzog et al (from our own Hennepin County Medical Center) included patients from a national registry and compared 3049 patients on dialysis admitted and eventually found to have acute MI compared with 534,395 patients not on dialysis admitted with an eventual diagnosis of acute MI. Of these groups, only 22% of dialysis patients had an admission diagnosis consistent with acute MI while 43.8% of nondialysis patients had the correct admission diagnosis of acute MI.  Dialysis patients had double the rate of cardiac arrest (11% vs 5%), were less likely to receive reperfusion therapy when eligible (47% vs. 75%), and had an increased odds ratio of death compared to nondialysis patients 1.5 (95% CI 1.3-1.7).

Why is this?  One reason for underdiagnosis might be that only 44% of these dialysis patients presented with chest pain while over 68% of those not on dialysis had chest pain on presentation.  Another reason may be that the EKG is more difficult to interpret in patients with dialysis due to baseline abnormalities, including LVH.  In this study of dialysis patients with severe CAD, 77% had an abnormal resting EKG and the most common abnormality was LVH.  

Herzog et al. comment on this latter study:  “There is a lower index of clinical suspicion and a higher level of inaccuracy for initial diagnosis of acute coronary syndromes in dialysis patients with AMI because twice as many patients were incorrectly diagnosed on admission.  Further diagnostic confusion may have resulted from the greater prevalence of hypertension and likely attendant hypertensive heart disease and uninterpretable ST depression in the dialysis cohort.”

What can we learn?

1. Occlusion Myocardial Infarction  (OMI) often does not present with diagnostic ST elevation, or even any STE, especially in dialysis patients.

2. Pseudonormalization of ST segments, and also of T-waves, may be a useful sign to help detect OMI in the setting of LVH.

3. Patients on dialysis often do not have chest pain in the setting of acute MI.  Have a high index of suspicion for MI in these patients and advocate for them.

3. Think about, and use, emergent contrast echocardiography more liberally.

-----------------------------------------------------------

Comment by KEN GRAUER, MD (10/1/2018):

-----------------------------------------------------------

Excellent case presentation by Dr. Dan Lee — with superb insight into the subtleties (and true “art”) of clinical electrocardiography. THANK YOU Dr. Lee! In the interest of enhancing several important concepts in clinical ECG interpretation — I focus my comments on a number of points not elicited in the above presentation.

• Essential to the clinical deductions made in this case was access to a prior baseline tracing on this patient. This critical point is often overlooked. Even when available — without meticulous lead-by-lead comparison — subtle ECG changes are easy to miss ...
• For clarity, I have put the first 3 ECGs shown in this case together in Figure-1:

My approach to comparing a current tracing with a prior one — is to begin by completely interpreting one of the 2 tracings. ONLY THEN — do I begin lead-to-lead comparison to assess which differences might be clinically relevant.

• For optimal comparison — it is essential to ensure that you are “comparing apples with apples — and not with oranges”. By this I mean, that not only ST-T wave appearance needs to be assessed — but also QRS appearance (relative size of R and S waves, as well as total voltage) — R wave progression (Does transition occur at the same point in the chest leads of both tracings?) — and frontal plane axis (Is there a difference in axis between the 2 tracings?).
• NOTE: Much of the time, there will be at least some differences in QRS appearance, transition and/or frontal plane axis. This does not mean that lead-to-lead comparison cannot be done — but rather: i) that the interpreter BE aware that precise comparison of ST-T wave appearance is not the entire story — and, that it may not be completely reflective of whether or not true ST-T wave changes have occurred vs a difference in ST-T wave appearance as the result of a shift in axis or electrode lead placement, or the patient now being supine compared to a previous inclined position; and, ii) that the interpreter needs to “factor in” whatever axis or QRS changes have occurred in their assessment as to whether ST-T wave changes are (or are not) likely to be significant. Herein lies the “ART” of electrocardiography.

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

Take another look at this patient’s baseline tracing (= TOP ECG in Figure-1). How would YOU interpret this tracing?

• Is there evidence of possible prior infarction?
• How likely is it that this patient has LVH? (ie, Is it more than 50-60% likely?).
• In there ECG evidence of possible ongoing ischemia? (ie, What IF this “baseline tracing” was the only ECG you had — and it was obtained from a patient describing new chest discomfort? In this case — Could any of the changes be acute?).

Figure-1: The first 3 ECGs shown in this case (See text).

ANSWER: The rhythm in the baseline tracing is sinus at ~75/minute. The PR, and QRS intervals look normal normal. The QTc looks to be slightly prolonged. The axis is normal (about +50 degrees). Q waves are present in each of the 3 inferior leads. This may reflect prior inferior infarction. A small (probably septal) q wave is present in V6. Regarding chamber enlargement — the unusually pointed P wave in lead V2 is consistent with RAA (Right Atrial Abnormality). Artifact prevents assessment of the P wave in lead V1 for LAA (Left Atrial Abnormality). There is dramatic increase in QRS voltage in multiple chest leads (with overlap of QRS and S waves in leads V3,V5,V6).

• ST-T wave changes in lateral chest leads are clearly consistent with LV “strain” — which together with the clinical history + dramatic increase in QRS amplitude makes the likelihood of true chamber LVH >98%.
• In addition — there is J-point depression in leads V5,V6 with ST segment coving in these leads. T wave inversion in lead V5 is clearly more symmetric than is usually seen with just LV “strain”. ST segment coving with slight, symmetric T wave inversion is also seen in leads I and aVL — and inferior leads clearly show ST-T wave flattening.
• IMPRESSION: I’d interpret this tracing as consistent with LVH and/or “strain” and/or ischemia. I’d suspect that these changes are probably not acute, but rather consistent with longstanding hypertension + renal failure — BUT — it’s important to be aware that: i) Clinical Correlation is needed in order to assess the ECG findings we see on this baseline tracing; and, ii) More than just LVH appears on this baseline tracing.
• NOTE: For those wanting review of ECG assessment for LAA, RAA and LVH (with “strain” and/or ischemia) — CLICK HERE (for LVH) — AND HERE (for RAA/LAA).

=========================
Drs. Lee and Smith have highlighted the important subtle differences in ST-T waves during sequential tracings in this case (especially evident with the superb blow-ups of leads V2,V3 in their presentation above).

QUESTION: While I completely agree with the assessment by Drs. Lee and Smith, that there appear to be dynamic ST-T wave changes that are ongoing in this case in association with clinical symptoms — Take ANOTHER LOOK at the Baseline ECG and ECG #1 in the ED, as shown in Figure-1:

• Are we truly comparing “apples with apples” when we look at these 2 tracings?
• Now take another look at ECG #2 (Bottom tracing in Figure-1) — and compare it with ECG #1 in this Figure. Your Comment?

ANSWER: Clearly, there are differences in axis, QRS amplitude, and R wave progression between the Baseline ECG and ECG #1:

• Note the predominant negativity of the QRS complex in lead III of ECG #1 and the much smaller QRS in aVF ( = some axis shift has clearly occurred since the baseline tracing). In addition, lateral chest lead R waves are clearly less tall, and transition occurs later in ECG #1.
• NOTE: I completely agree with Drs. Lee and Smith that despite these differences in axis, amplitude and transition — the subtle changes of “pseudonormalization” are most probably real. My point is simply to highlight the importance of taking these differences in axis, amplitude and transition into account — and to realize that in some cases, such differences will make it much more difficult to assess the clinical significance of ST-T wave changes.
• Finally — Note that axis, QRS amplitude and transition in ECG #2 all look more like they did in the Baseline ECG. Yet despite this — inferior T waves are now all clearly inverted in ECG #2 (compared to the baseline ECG) — the ST coving and shallow T inversion in leads I and aVL have been replaced by flatter ST segments and upright T waves — and, the subtle ST-T wave “pseudonormalization” changes are still present in many of the chest leads. This supports the notion that there have been ongoing dynamic ST-T wave changes in this patient with clear indication for cardiac catheterization.

A 65 year old with chest pain, ECG recorded at 50 mm/sec

This case was sent by Peter Hammarlund, from Stockholm, Sweden:

Hi Steve,

What would you say about this ECG?

A 65 yo smoking man with a prior MI 15 years ago who lives in Stockholm, but who was in southern Sweden on vacation. There was no other known previous illness. 

He suddenly experienced central chest pressure, 9/10, without radiation, but with associated nausea. 5/10 after sublingual NTG.

This prehospital ECG was sent to the Hospital and I was on the night shift and reviewed the ECG. What do you say?

This is recorded at 50 mm/sec on the left (12-lead), and 12.5 mm per sec on the right (for rhythm).
That's the way they do it in Sweden.
For an image that may be easier to interpret, I have horizontally compressed the ECGs at the bottom.

Peter,

Good to hear from you!

LAD occlusion.  Could be a D1 occlusion.

V2 with hyperacute T-wave

II, III, aVF with STD

Tell me!

Steve

Peter:

"But you were of course right, Steve!

I saw this and I immediately recognized the hyperacute T wave in V2 and the reciprocal ST segment changes in the inferior leads as well as the subtle STD in the lateral leads." 

"The ECG was highly suspicious for LAD occlusion (however, a couple of years ago before I started reading your blog I probably wouldn’t have picked this up)." 

"Our cath lab is currently only available during office hours so I had to decide if the patient was in need of immediate coronary angiography and in that case he would have to be transported to Lund University Hospital (30 minutes by ambulance). Since I know that these patients sometimes are difficult ”to sell” and the ambulance wasn’t far from our ED, I called the paramedics and told them to transport to our ER (with highest priority) for a rapid evaluation and probably an immediate transfer to Lund." 

"When the patient arrived ~10 minutes later a new ECG was obtained about 35 minutes after the first:" 

This again is recorded at 50 mm/sec on the left, and 12.5 mm per sec on the right.
For an image that may be easier to interpret, I have horizontally compressed the ECGs at the bottom.

Peter: "Now there are T waves of hyperacute appearance in both V2 and V3, with some new STE in V3."  

"The patient wasn’t in apparent distress, but stated that he was having continuous chest pressure (5/10). I performed a rapid bedside echo where I saw an RWMA in the apical-septal region. Within 10 minutes from arrival in our ED I called the cardiologist on call in Lund who accepted the patient and activated their cath lab." 

"The patient was immediately transported to Lund. A subtotal occlusion in mid-LAD (99% stenosis with TIMI-2 flow) was opened and stented. Hs-TnT rose from 44 to ~450 ng/L. The patient had a great outcome with EF in the lower normal range and hypokinesis of the apico-septal wall on formal echo. He was discharged two days later." 

"What I found interesting is that both the 3- and 4-variable formula predicts this to be BER (I get 22.80 and 18.02 on the 1st ECG, respectively; the latter being quite close to the "STEMI” cut-off). I usually rely on my visual impression so I must admit that I don’t use the formulas that often." 

"However, I guess the formulas are not applicable in this case because of the STD? Exactly correct, Peter!    To my understanding the exclusion criteria were a sum of 1 mm STD in the inferior leads (I’m not sure that he fulfills that criteria) or STD in the lateral leads (any STD?).  I don’t recall reading any millimeter cut-off defining significant STD in the lateral leads) so I guess this case would have been excluded in your studies? (At least based on the lateral STD)." 

Yes!! ANY ST depression in precordial leads is an exclusion and the first ECG has STD in V4 and V5.  Normal variant ST elevation is never associated with ST depression on other precordial leads; thus, the STE in V2 must be ischemic until proven otherwise.

"I guess this case is a reminder that one should pay attention to hyperacute T waves and be aware that the formulas shouldn’t be used (or at least should be used with great caution) if the patient fulfills one of the exclusion criterias. Also, echo is super useful in these borderline cases, as you’ve mentioned several times on your blog!" 

Here I have compressed ECG 1 horizontally so it looks more like a 25 mm/second ECG:

Here is ECG 2 compressed horizontally:

Learning points:

1. Recognise hyperacute T-waves
2. ST Elevation in precordial leads is not normal variant (early repol) if there is any ST depression in precordial leads
3. ECGs that are recorded at "paper" speed that is different from what one is accustomed to can be very difficult to read.

-----------------------------------------------------------

Comment by KEN GRAUER, MD (9/26/2018):

-----------------------------------------------------------

As an American physician — I had not in the past been exposed to ECG formats other than those used in the United States. Now that I’m actively participating in multiple internet ECG forums with a large international audience — I’ve become well aware that other countries do some things differently ...

• NOTE: In addition to recording the ECGs shown in this case at 50mm/second speed (instead of at 25mm/second, as is standard in the U.S.) — the Cabrera Format was used (Figure-1). In this recording format — the vertical limb lead display begins with lead aVL (within the small BLUE rectangles) — and, reversed polarity is used for lead aVR (= -aVR, as shown within the small PURPLE rectangles). For additional details regarding the Cabrera Format that is used in certain other countries — CLICK HERE—

Figure-1: Side-to-side comparison of the 2 ECGs included in this case. Note that the Cabrera Format was used. Note also that instead of the original ECGs presented by Dr. Hammerlund, I show the 2 tracings that Dr. Smith compressed horizontally, so that their morphologic appearance looks more like a 25mm/second ECG (See text).

CONFESSION: I have difficulty interpreting 12-lead ECGs that have been recorded at 50mm/second speed. I believe the reason for this is interesting:

• Although I teach and religiously employ in my own interpretation a Systematic Approach to ECG interpretation — engrained in my brain from the past 45+ years of regular exposure to countless ECGs are the data from pattern recognition of all tracings that I have ever seen. This is the experiential process that allows near instant recognition by experienced interpreters of the most important ECG findings for almost any tracing.
• All of this “data” in my brain is invalidated the moment I am shown a tracing recorded at 50mm/second speed. Other clinicians may be far better than me at making the transition from a 25mm/second tracing to one recorded at 50mm/second — but no matter how hard I try, I find myself in the uncomfortable position of no longer being able to draw on my “internal data bank” of what looks to be normal vs abnormal. Instead, I feel like a novice interpreter once again … (This is why I so greatly appreciate Dr. Smith’s compression of the 2 tracings in this case — as shown in Figure-1).

Comment on Figure-1: There are subtle abnormalities in multiple leads in both tracings — with progression of findings, at least in leads V1, V2 and V3 in ECG #2 obtained 35 minutes later.

• As per Drs. Hammarlund and Smith — the principal initial finding in ECG #1, obtained from this 65yo man with severe new-onset chest pain is the hyperacute ST-T wave (taller and fatter-than-it-should-be) in lead V2 — that occurs in association with subtle inferior and lateral chest lead ST depression.
• I would add that lead V1 in ECG #1 also looks distinctly abnormal. The ST segment takeoff in this lead is straight, with slight J-point ST elevation and a coved shape to the ST segment. This is not the usual ST-T wave appearance in lead V1.
• As astutely picked up by Dr. Hammarlund — there has been progression in the amount of ST elevation and the hyperacute appearance for leads V2 and V3 in ECG #2.
• I would add that there has also been progression in the amount of ST elevation and the hyperacute appearance of the ST-T wave in lead V1 in ECG #2. And, without change in the relative size of the R wave-to-S-wave in lead V4 between ECG #1 and #2 — the T wave is now relatively taller in this 2nd tracing (it is now almost 2/3 the height of the R wave in this lead).
• NOTE: Although the T wave in lead III of ECG #2 is now clearly inverted — the significance of this change is difficult to assess given slight variation in the frontal plane axis (the QRS complex in lead III is now predominantly negative — whereas it was predominantly positive in ECG #1). However, since QRS morphology in all chest leads for both tracings is virtually unchanged — there is no doubt that the above noted progressive ST-T wave findings in this patient with new chest pain are real and significant!

Our THANKS to Drs. Hammarlund and Smith for presentation of this superb case!

Tachycardia and ST Elevation.

This Case was sent from Anonymous.

A middle-aged patient was sent to the ED with tachycardia. He denied any sensation of palpitations, but his heart rate was consistently 150 bpm. The other vitals were normal. He had JVD and swollen legs, but clear lungs and a normal room air oxygen saturation.

He denied all typical and atypical ischemic symptoms. He noted, however, that he had had marked fatigue starting about 5 days ago, but that he was actually feeling much better today.

The initial ECG:

The rhythm appeared to be atrial flutter, but also concerning were the ST segment elevations in I, aVL, V2, and V3, as well as ST depression in the reciprocal inferior leads.

But atrial flutter can alter the baseline such that there is only apparent STE or STD (see example cases below) 

Is this:

1) true STEMI (acute or subacute)?

2) PseudoSTEMI due to the underlying atrial flutter wave?

3) PseudoSTEMI due to old MI (persistent STE after previous anterior MI, also known as LV aneurysm morphology?

The physician's thoughts: This pattern is concerning for anterior wall OMI, specifically a proximal LAD lesion. There are Q waves in V1-V3, suggesting an old anterior MI, but the T waves in V2 and V3 are fairly tall, suggesting some degree of acute ischemia. Also, there are no T wave inversions which would suggest a subacute, evolved, or reperfused MI.

The patient, with an easy smile, again denied any symptoms.

Atrial flutter can mimic the ECG signs of an MI. (For example, see this case, this case, this case, these erroneous computer interpretations, and this case report.)

K. Wang makes this comment: "A great case. It's important, as you did, to point out, that atrial flutter waves can cause findings suggestive of STEMI. In this tracing, the answer is in the lead aVL. There, the beginning of the ST segment is higher than the top of the flutter wave in front of the QRS, proving that the ST segment is indeed elevated."

To clarify the ECG, the emergency physician administered IV metoprolol to slow the ventricular response. However, the patient became borderline hypotensive after this (although still completely symptom-free). A bedside echo was performed:

There is akinesis of the anterior wall, best seen on the parasternal short axis (PSSA) view.

So there is a myocardial infarction.

But is it old or new?

There is no evidence of aneurysm formation on this echo (the myocardial wall is not thin); therefore, it appears to be acute or subacute.

The cardiac catheterization team was activated. The blood pressure dropped precipitously while in the lab preparing for the angio, and the patient was electrically cardioverted. An occlusion of the proximal LAD was then found and intervened on.

The troponin obtained in the ED was almost 10 ng/mL, suggesting a subacute occlusion.

This was recorded next AM:

There are QS-waves with continued ST Elevation with large upright T-waves in V2 and V3

Smith comment:

Is this the so-called “left ventricular aneurysm” pattern? --LV aneurysm can be distinguished by the size of the T-wave, specifically the T/QRS ratio:

--LV aneurysm has a relatively small T-wave, often with some slight (shallow) inversion.

--Acute MI has a large upright T-wave, but may be inverted if reperfused (shallow in the case of Wellens' pattern A; deep in patthern B, which is a later evolution). However, Wellens' waves are preceded by R-waves, not by QS-waves.

LV aneurysm rule: One should especially suspect LV aneurysm, and use the rule, when there are QS-waves in any of V1-V4. A QS-wave means a single negative deflection, without any R-wave or with only a tiny r-wave.

Here is the rule:

If there is one lead of V1-V4 with a T/QRS ratio greater than 0.36, then it is acute MI. If less then 0.36, it is either subacute (over 6 hours) or old.(see references 1, 2). In this case, the T/QRS ratio is largest in V3 at 5/9 = 0.55.

If this were the presenting ECG, you would not want to say that those QS-waves are due to old MI with persistent ST Elevation (LV aneurysm morphology).

But now we are post-reperfusion, so what does the ECG tell us?

That there is persistent ischemia in spite of reperfusion.

This is a bad prognostic sign. The STE and hyperacute T-waves at this point could be either persistent ischemic or re-occlusion. If there had been intervening resolution on the ECG, it would represent re-occlusion. But in this case it was persistently elevated ST segments and hyperacute T-waves. This is typical of "no reflow," which is a result plugging of downstream small vessels by platelet-fibrin aggregates. Read about it here:

Clinical value of 12-lead electrocardiogram after successful reperfusion therapy for acute myocardial infarction (Lancet 1997)

[Alternative explanation for persistently upright T-waves: post-infarction pericarditis (which happens in transmural MI)].

T/QRS ratio to differentiate anterior STEMI from anterior LV aneurysm:

1. Validation (Klein, Shroff, Smith): Electrocardiographic criteria to differentiate acute anterior ST-elevation myocardial infarction from left ventricular aneurysm

2. Derivation (Smith): T/QRS ratio best distinguishes ventricular aneurysm from anterior myocardial infarction

Case by Anonymous, continued

My personal M and M session:

If there is a similar “next time,” I may change my approach.

First, I deferred the echo too long. My initial reasoning was that this was just a rhythm problem, and that checking the Ejection Fraction at a rate of 150 was unreliable, and would be falsely low. Had I done the echo before the metoprolol, I likely would have felt more justified in considering cardioversion first!

Second, in retrospect, cardioversion would have been better than medications, both because his hemodynamics were precarious, and because it would have clarified the ECG interpretation. I delayed cardioversion because the patient looked “too good” for electrical therapy. Furthermore, the patient was likely in atrial flutter for greater than 48 hours, theoretically raising the risk of post-conversion CVA.

But sometimes ST changes will disappear with conversion of atrial flutter to NSR, and urgent angiography can be avoided. Or, in this case, the true ST segment changes will be revealed, and appropriate timing of angiography can be determined.

Smith comment:

I agree. Electrically cardiovert, then re-assess.

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

My Comment, by KEN GRAUER, MD (9/24/2018):

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

Excellent case for discussion. I’ll focus my comments on the 2 ECGs in this case, which for clarity I have put together in Figure-1. I’ll verbalize the thought process in my assessment, which led me to conclusions that mirror those detailed by Dr. Smith.

 

Figure-1: Comparison of the 2 tracings in this case. TOP — Initial ECG in the ED, obtained from this middle-aged patient with tachycardia. BOTTOM — ECG #2, obtained the following morning after cardioversion and cardiac catheterization (See text).

• ECG #1 — shows a regular SVT (= SupraVentricular Tachycardia) with a narrow QRS complex, and a ventricular rate of ~150/minute. Sinus P waves are absent.
• PEARL #1: It is helpful to keep in mind the differential diagnosis of a regular SVT rhythm in which sinus P waves are not clearly evident. For practical purposes, when the ventricular response is this fast, the differential diagnosis consists of 4 entities: i) Sinus tachycardia (which could still be present, if sinus P waves were hidden within the preceding ST-T wave); ii) Reentry SVT (such as AVNRT or AVRT); iii) Atrial Flutter with 2:1 AV conduction; and, iv) Atrial Tachycardia with 2:1 AV conduction. Awareness of this short differential list greatly facilitates clinical decision-making.
• The rhythm in ECG #1 is not sinus tachycardia. We know this is — because although there is atrial activity, the P wave in lead II is negative (slanted RED arrows). Unless there is lead misplacement or dextrocardia — a negative P wave in lead II excludes the possibility of a sinus mechanism.
• PEARL #2: In my experience, AFlutter is by far the most commonly overlooked arrhythmia. The best way to avoid missing the diagnosis of AFlutter is to, “Think AFlutter until proven otherwise” — whenever you encounter a regular SVT at a rate close to ~150/minute, in which sinus P waves are not evident. If you regularly look for AFlutter in such cases — then you are far less likely to overlook it (See ECG Blog #40).
• PEARL #3: You can virtually prove that the rhythm in ECG #1 is AFlutter even before slowing the rate by using CALIPERS. Set your calipers to exactly HALF the R-R interval — and see if you can precisely march out 2:1 AV conduction. If so — See in how many leads you are able to do so. We illustrate application of this technique in Figure-1. The non-sinus negative deflection before the QRS in lead II (slanted RED arrow) is perfectly equidistant from a similar-looking negative deflection right after the QRS (slanted PINK line).
• The best leads to look for flutter waves with typical AFlutter are most often the inferior leads + leads aVR and V1 — and clear evidence of 2:1 AV conduction is seen in all these leads in this example (slanted PURPLE lines). Flutter waves are actually also seen in most of the remaining leads. Some cases of AFlutter only show flutter waves in 1 or 2 leads — but the more leads you clearly see 2:1 conduction in — the more confident of your diagnosis you can be without necessarily needing to slow the rate. NOTE: Reasons ECG #1 is unlikely to be ATach, are that this rhythm is much less common in a non-EP setting than AFlutter — and, that with 2:1 conduction, this would entail an atrial rate ~300/minute, which is clearly above the atrial rate usually seen with ATach.

As emphasized by Dr. Smith — AFlutter can alter the ECG baseline, making it extremely difficult to assess for acute ST-T wave changes. This is especially true when “typical” AFlutter is present, in which there are large amplitude flutter waves in the inferior leads, as well as in other leads. For this reason, I was not initially certain that the tall T waves with apparent ST elevation in the anterior leads of ECG #1 was indicative of an acute event. And, even though there are QS complexes in leads V1,V2 — with no more than tiny initial r waves in V3,V4 of ECG #1— these QRS morphologic changes do not always persist on repeat ECG under more controlled conditions after the rate has slowed.

• PEARL #4: No matter how you might try to imagine “interference” from flutter waves affecting ST-T wave appearance in the anterior leads of ECG #1 — there is ≥2mm of ST segment elevation in lead aVL (LIGHT GREEN arrows, seen within the GREEN rectangle) that can not be explained away by flutter waves distorting the ST segment. That’s because we see NOTHING resembling flutter waves occurring at half-the-R-R interval distance away from the ST elevation in lead aVL (DARK GREEN arrows in this lead). In my experience — Lead aVL is often a “magical lead” for providing the support needed to convince me that suspected ST elevation in equivocal cases is real.
• Clinically — the case presented here is perfectly consistent with probable “silent MI” occurring about 5 days earlier (when this patient noted marked “fatigue”) — with persistent tachycardia and the likely large anterior STEMI accounting for gradual progression of right-sided heart failure (JVD, swollen legs noted). I took this as further support of my suspicion of recent acute STEMI.

PEARL #5: The best way to hone your Clinical ECG Interpretation skills — is to follow up on those cases about which you initially had questions on. Comparison of the initial ECG with ECG #2, obtained the next morning — provides us with an excellent opportunity to do this (Figure-1).

• Note with reestablishment of sinus P waves in ECG #2 — that the double negative deflections in lead II (as well as in other leads) have disappeared.
• Note in lead aVL similar shape and amount of ST elevation as we suspected from assessment of ECG #1 during AFlutter. Same is true (albeit to a lesser amount) in lead I.
• Note the presence of “mirror image” reciprocal ST depression in each of the inferior leads in ECG #2. This was present in ECG #1 — though it was much more difficult to be certain this ST depression was real and not just superposition from AFlutter in the initial ECG.
• Note similar QS complexes and poor R wave progression with persistent anterior ST elevation after conversion to sinus rhythm.

 

Our THANKS to Dr. Smith for presentation of this highly insightful case!