Wednesday, October 31, 2018

An elderly man with sudden cardiogenic shock, diffuse ST depressions, and STE in aVR

Written by Pendell Meyers



84 yo M with history of a “valve problem” presented for sudden onset chest pain and trouble breathing while eating lunch.

He was sitting bolt upright, diaphoretic, tachypneic, with bilateral crackles. Although his BP was 126/84, he was in acute cardiogenic shock.

Here is his initial ECG:
Sinus tach with occasional PACs. Relatively normal QRS complex with diffuse significant ST depression including leads V2-V6, I, aVL, II, III, and aVF, with ST elevation in aVR. The vector of ST depression is maximal in leads V5 and II, consistent with diffuse subendocardial ischemia. There is no evidence of any single vessel OMI (Occlusion MI). This is not consistent with posterior OMI, which would have ST depression maximal in V2-V4 usually without diffuse ST depression.

The differential for acute chest pain and cardiogenic shock without evidence of OMI on ECG includes:

(still) OMI - the ECG is not perfectly sensitive for OMI
3 Vessel disease with superimposed non-occlusive ACS
Non-occlusive ACS of any major vessel, including left main
Acute aortic stenosis or other acute severe valvular abnormality
Any other cause of acute severe supply-demand mismatch
Any combination of the above


The ECG does not differentiate the above etiologies, it simply signifies that there is severe diffuse global supply-demand mismatch, whatever the etiology.

Bedside ultrasound revealed significant LVH and an extremely bright, dense, nearly non-moving aortic valve (video not available).

He went to the cath lab semi-emergently. He was found to have severe aortic stenosis (area 0.87cm2, mean gradient 22mm Hg) as well as significant CAD:

Left main: 60% stenosis, with 90% ostial LAD and LCX stenosis, and 70% ramus intermedius stenosis
mid RCA: 50% stenosis

It seems as though the angiographers were unsure whether any of these lesions represented acute ACS or whether they were pre-existing without acute ACS.

Here are the images:
The left main ends with a trifurcation (LAD, Ramus, LCX) that shows a severe stenosis at ostia of all three vessels.

This is the "spider view" of the same lesion.

Diseased but grossly patent RCA.

The max troponin T was 2.40 ng/mL. 

The patient required urgent bioprosthetic aortic valve replacement and CABG including LIMA to LAD, SVG to ramus, and SVG to OM1.

Here is his ECG after interventions:


Learning Points:

Diffuse ST depression maximal in V4-V6 and lead II, with ST elevation in aVR, signifies diffuse subendocardial ischemia. Some etiologies of diffuse subendocardial ischemia, including unstable 3-vessel or left main ACS likely benefit from emergent revascularization, whereas other etiologies of global demand such as sepsis, hypotension, GI bleeding do not. 

Make sure you can recognize the difference between diffuse ST depression and localized ST depression maximal in V2-V4 which signifies posterior Occlusion MI. See these examples for comparison:

Posterolateral OMI resulting in VT, then R-on-T phenomenon and VF



Right Bundle Branch Block and ST Depression in V1-V3. Is that normal? And a complication.





-----------------------------------------------------------
Comment by KEN GRAUER, MD (11/1/2018):
-----------------------------------------------------------
Great job by Dr. Pendell Meyers presenting this case! I have little to add to his excellent clinical content! However, I would like to emphasize how this case provides a wonderful example of pattern recognition”. By this, I mean that when the emergency provider sees a “pattern” on ECG (as we do in ECG #in Figure-1— that you should be able to instantly know what this pattern means — and instantly know the differential diagnosis to consider.
  • Diffuse ST depression in multiple (that is, ≥7) leads, in association with ST elevation in lead aVR (and sometimes to a lesser extent, ST elevation also in lead V1) — means subendocardial ischemia.
  • The differential diagnosis for diffuse subendocardial ischemia was noted above by Dr. Meyers. I’ll mention having on occasion seen this ECG pattern in fast SVT rhythms — with resolution (or near resolution) of ST depression on conversion to sinus rhythm, with no significant coronary disease found on cath. Other, non-cardiac potentially reversible conditions (ie, severe anemia, sepsis, very sick patient) may also occasionally produce this ECG pattern. But, in an older adult with new-onset chest discomfort (as is the case here) — this ECG pattern almost always means that the patient has severe coronary disease (left-main, proximal LAD narrowing and/or advanced multi-vessel disease). MORAL: Memorize the ECG pattern shown in ECG #1 in Figure-1. Be sure to recognize this pattern as indicative of diffuse subendocardial ischemia, with need to promptly determine the cause.
Figure-1: The 2 ECGs recorded in this case (See text).
======================
Additional Interesting Observations about the ECGs in Figure-1?
I’ll preface my remarks by saying that the observations I note below do not alter clinical management. That said, they are interesting findings that the astute interpreter should pick up.
  • ECG #— As per Dr. Meyers, the underlying rhythm is sinus tachycardia with PACs. Did You Notice in the long lead V1 rhythm strip — that the T wave of each PAC (ie, beats #2,8,10,12 and 18) is different (more peaked) than the T wave of all of the other beats that are sinus conducted? I fully acknowledge that I am not certain why this is so — but it is a definite reproducible phenomenon that the astute interpreter should pick up.
Comparison between ECG #and ECG #— The important clinical finding that should be recognized is dramatic reduction in the amount of ST depression in multiple leads in ECG #2 after intervention. There is also considerably less ST elevation in lead aVR. Despite the increase in baseline artifact — there should be no doubt that successful treatment in this case correlated to reduction in the amount of ST depression.
  • Did You Notice slight change in frontal plane axis (from +75 degrees in ECG #1 — to +50 degrees in ECG #2) — and, marked change in transition and chest lead QRS morphology? Specifically, transition in the chest leads does not occur until between V3-to-V4 in ECG #1 — whereas in ECG #2, there is already a dominant R wave (as well as small q waves) by lead V2.
  • The reason for this dramatic change in chest lead QRS morphology is not apparent. Perhaps it is due to open-heart surgery, with need to alter the position of chest lead placement? Clinically, the reduction in ST depression between ECG #1 and ECG #2 is so great, that regardless of this change in QRS morphology — we are confident this improvement in ECG appearance is reflective of successful treatment. But, it is important when comparing tracings to recognize changes in frontal plane axis and chest lead morphology — because sometimes less marked differences in ST-T wave appearance may be due to these technical factors rather than a change in the severity of ischemic findings.


Saturday, October 27, 2018

Our residents are getting really good at this.

I was asked to look at this ECG in a patient with 30 minutes of acute onset of nausea and vomiting and perhaps some chest discomfort:

First ED ECG:
Here is my response:
It is VERY suspicious for acute inferior MI because of some ST Elevation and large and fat T-waves in II, III, aVF.  It is not diagnostic because of absence of ST Depression (or T-wave inversion) in aVL.  
--There are Q-waves, which suggest "old inferior MI with persistent STE" (also known as "inferior LV aneurysm") or subacute inferior MI.  
--However, symptoms for only 30 minutes, so it is not subacute.  
--On the other hand, the T-waves are too large for old MI.

I am going to guess that this is acute MI.

In our study of inferior MI, 99% had some amount of ST depression in lead aVL:
https://www.sciencedirect.com/science/article/pii/S0735675715008189


Here is the case:

A 60-something called 911 for acute onset of diaphoresis, vomiting, and also chest pain.

3 prehospital ECGs were recorded.  They were all identical.  Here is the 3rd one:
Very similar to that first ED ECG above

Here is the first ED ECG again (30 minutes of symptoms):

This was viewed by one of our fantastic 2nd year residents, BG TenBrink.  And he was very suspicious of acute MI.  They are getting very good at this!

So he showed it to one of our junior faculty, Nick Simpson.  Nick was convinced.

The patient reportedly "looked terrible and continued to drip sweat."  He had "nausea and multiple episodes of vomiting."   He was "clammy and diaphoretic for medics."  He did not receive aspirin or nitroglycerin prehospital, and "he did not endorse chest pain or shortness of breath."

In emergency department, the patient began endorsing midsternal chest pain that began while he was here in the ED. He endorsed continued nausea and diaphoresis. He denied any history of heart disease. Has not had a heart attack before.

The pain was coming and going in the ED, and another, 2nd, ECG was recorded without pain, or at least with a lot less pain, 17 minutes after the 1st ECG:
Now there is some more upward concavity in lead II. See comparisons side-by-side below.
The patient dropped his blood pressure a couple times to the mid 80's

The cath lab was activated.  Result:

RCA is a medium caliber vessel with low anterior take off.
Hazy 80% stenosis is noted in the distal vessel.

Lesion on Dist RCA: 80% stenosis 15 mm length reduced to 0%. Pre-procedure TIMI III flow was noted. Post Procedure TIMI III flow was present. Good run off was present.The lesion was diagnosed as a low risk lesion.The lesion was tubular and eccentric.The lesion showed evidence of thrombus presence, with irregular contour, mild angulation and mild tortuosity.  Lesion plaque is ruptured.

Culprit Lesion (s):
Hazy 70-80% stenosis of the dRCA

Impression:

Inferior STEMI with RCA culprit, vessel recanalization prior to angiography (i.e., spontaneous reperfusion, as indicated by ECG improvement and resolution of pain)
Successful PCI with 2.5 x 16 mm Synergy DES; excellent angiographic result

Here is an ECG the next AM:



Here are all 3 ECG together, side by side:

                First ECG                                   2nd ECG, pain free                          3rd ECG, post cath
Notice how the ST segment in lead II on the first ECG is almost straight. 
After pain resolution (2nd ECG), there is more upward concavity
3rd is after stenting and there is not much difference from ECG 2. 

The first troponin I was below the level of detection (0.010 ng/mL), as were all subsequent troponins!

Echo showed no wall motion abnormality and normal EF.

Thus, the patient ruled out for MI.

So how do we know that there actually was an acute coronary syndrome?

1. The angiogram showed a hazy lesion and ruptured plaque
2. The "gold standard" (reference standard) is ECG evolution.  If ST Elevation and/or large T-waves are due to ischemia, then when the ischemia is gone (and it always goes away at some point -- ischemia is not a chronic condition), the ST Elevation will decrease and/or T-waves become less large; if they are NOT due to ischemia, they will not change. 

Here we see the evolution: when the patient becomes pain free, the T-wave became less "fat".  The angiogram has TIMI-3 flow, corresponding to the resolving ECG.


Conclusion:

This patient was treated so fast that he had no actual infarction.  Spontaneous reperfusion certainly helped.

So this is really another case of Unstable Angina. 
Here are more cases of Unstable Angina


-----------------------------------------------------------
Comment by KEN GRAUER, MD (10/27/2018):
-----------------------------------------------------------
Superb case by Dr. Smith with prompt recognition and treatment of acute coronary syndrome resulting in rapid cardiac cath before any actual infarction occurred. The patient was lucky in that the 80% RCA “culprit lesion” spontaneously reperfused. The lesion was stented in the hope of preventing a future event.
  • I focus my comments on the ECG definition of a “normal” ST segment (Figure-1) — and on some additional fine points regarding ECG interpretation of the first 2 tracings shown in this case (Figure-2):
Figure-1: Compare the ST segment in Panel A with Panel BWhat is the difference? Is this likely to be clinically significant?  (See text).
========================-
Recognizing Subtle SSegment Changes — Consensus among expert electrocardiographers is lacking regarding the definition of a normal ST segment. Much of this relates to semantics — since minor ST-T wave abnormalities in a non-acute setting generally provide no more than a nonspecific suggestion to potential etiologies. That said — I feel it important to hone in on recognizing even minimal abnormalities because: iit is good to let others reading our interpretation be aware that we saw the abnormality in question, even if we may not have thought it clinically important for the case at hand; and, iiin an acute setting — even subtle ST-T wave abnormalities may be very important!
  • The ST-T wave in Panel A of Figure-1 is normal. Note the smooth contour at the point of transition between the end of the S wave and the beginning of the ST segment. Note an equally smooth contour at the end of the ST segment and the point where the ascending limb of the T wave begins. There is a slight normal upward concavity at this transition between the end of the ST segment, and the beginning of the T wave.
  • In contrast — Note the sharp angle in Panel B at the point where the straight (flat) ST segment ends and the ascending limb of the T wave begins (RED arrow). While admittedly “splitting hairs” — the ST-T wave in Panel B is not normal. Instead — there is nonspecific ST segment straightening (ie, with loss of that smooth transition between the end of the ST segment and the beginning of the T wave ascending limb).
  • I’ll emphasize that in a non-acute setting, “nonspecific ST segment straightening” — is a descriptive finding. It is nonspecific. It may mean nothing — especially if only seen in a single lead. Or, it may suggest some other problem (ie, electrolyte disorder) — or, it may be a nonspecific indicator of underlying coronary disease.
  • On the other hand, in an acute setting (ie, in a patient with new-onset chest pain— even subtle ECG abnormalities, especially if present in multiple leads — may be extremely important. For this reason — recognition of subtle ST-T wave changes is an essential skill for emergency providers to master.
=============================
Now look at Figure-2 — in which we compare the initial ED tracing (ECG #1obtained during chest pain — with ECG #2 obtained 17 minutes later, at a time when chest pain had greatly decreased. To facilitate discussion of the ECG abnormalities noted by Dr. Smith above — I’ve added magnified inserts (within the RED rectangles) for the first 2 complexes in leads II and aVF of ECG #1. Similar changes in the ST-T wave are seen in lead III.
  • In addition to slight-but-real J-point ST elevation — note straightening of the ST segment takeoff. The normal upward-concavity appearance of the ST segment (that we saw in Panel A of Figure-1) has been lost in each of the inferior leads of ECG #1.
  • In contrast — a more normal upward-concavity appearance for the ST segment in the inferior leads has returned in ECG #2 (as shown within the YELLOW rectangle inserts for leads II and aVF). To be clear — the ST-T waves in the inferior leads for ECG #2 are by no means normal (!) — but there clearly is less ST segment straightening — and we now clearly can see some upward concavity to the ST segment in the inferior leads.
Figure-2: Comparison between the initial ECG obtained in the ED (TOP = ECG #1) — with ECG #2 (BOTTOM) obtained 17 minutes later at a time when chest pain had markedly decreased (See text).
============================-
Additional fine points regarding the 2 serial ECGs in Figure-2:
  • Could this patient have had prior inferior infarction? After all — there are inferior Q waves that are actually quite large considering the small size of the QRS complexes in the inferior leads. We are told that the patient had “no history of prior infarction” — and, cardiac cath did not suggest any wall motion abnormality — but given presumed significant baseline RCA narrowing, with an episode of spontaneous resolution of acute occlusion — perhaps one or more similar episodes occurred in the past?
  • This is relevant — because (as emphasized earlier by Dr. Smith) — it is highly unusual with acute RCA occlusion (with inferior ST elevation) not to see reciprocal changes in lead aVL. Keep in mind that lead aVL in ECG #1 is not “normal” (ie, the ST segment is uncharacteristically flat) — but there is no ST depression. Could the reason for this be that the lead aVL “baseline” was abnormal from a prior event?
  • There is a change in lead aVL in ECG #2 — in that there is now ever-so-subtle-but-real T wave inversion. This probably is another reflection of this patient’s spontaneous reperfusion.
  • In ECG #1 — there is early transition by lead V2, with R = S in lead V1. This is not a normal appearance in lead V1, which typically shows predominant negativity. Could these findings (ie, R=S in V1 & early transition by lead V2) have similar implications as the inferior Q waves, namely reflect prior posterior infarction?
  • Finally, note in ECG #2 that the tiny QRS complex in lead V1 now manifests an rsr’ — which in conjunction with the narrow terminal s waves in leads I and V6 suggests incomplete RBBB. That said — I suspect the reason for this change in QRS appearance in lead V1 is more likely due to lead misplacement (too high) of V1 and V2 — because the P in V1 of ECG #2 is now all negative (it was biphasic in ECG #1); there is now a negative component to the P in V2 (the P wave was all positive in V2 of ECG #1) — and leads V3-thru-V6 are virtually identical in both tracings (suggesting a technical problem may be the cause of the change in V1 and V2).



Wednesday, October 24, 2018

Is this a STEMI? No, not by definition! Why not? Why is this Important?

A 40-something male presented with dyspnea and left arm numbness, and perhaps some chest tightness, for 1 1/2 hours.

Here is his triage ECG:
There is massive STE in V3-V6, and also STE in II, III, aVF.
This is all but diagnostic of STEMI, probably due to wraparound LAD

The cath lab was activated.

The patient was given sublingual nitroglycerine and his symptoms greatly improved, and another ECG was recorded:
Now there is much less ST Elevation

If you had not seen the prior ECG, you might have called this normal variant STE, or early repolarization --there are well-formed J-waves.


Because there is reciprocal ST depression in aVL, this should not be called early repol.


Suppose you had used the formula?Values: STE60V3 = 2.0, QRS V2 = 10, RAV4 = 15.5, QTc = 377 by computer
4-variable formula value = 16.2, which is very low and suggests early repol

The patient was taken to the cath lab and a Type III (wraparound) LAD with a proximal hazy area was seen. There was good flow.  This was diagnosed by IVUS (intravascular ultrasound) as a ruptured plaque.  It was stented.

A 0-hour troponin I, drawn 2 hours after symptoms onset, was below the level of detection (LoD, less than 0.010 ng/mL.

A subsequent troponin drawn 6 hours after symptom onset, remained below the LoD.

No further troponins were drawn.

Therefore, this does not meet the definition of myocardial infarction (4th Universal Definition of MI), which requires at least one troponin above the 99% reference range.  It is possible that subsequent troponins would have been elevated had they been drawn.  But maybe not.

You can see the deficiency of the definition of MI.  This was clearly severe subepicardial ischemia causing ST Elevation, but it was not of a long enough duration to result in measurable infarct.

Therefore this is "Transient ST Elevation Unstable Angina."  As there was ruptured plaque, this is NOT Prinzmetal's angina.

Why is this important?

1. First, the name (Myocardial Infarction or Not) is not important.  It is just as dangerous, as there is a ruptured plaque with thrombus (which lysed) in the proximal LAD.

2. Imagine if you had only recorded the 2nd ECG.  The patient would not have been diagnosed with acute coronary syndrome and would not have had an angiogram, would have been discharged (or perhaps had a stress test, which would be negative), and would be at great risk of another event, possibly resulting in death or heart failure.

Here are many other cases of Unstable Angina, in spite of Eugene Braunwald's Requiem for Unstable Angina.

So Unstable Angina still exists [even with high sensitivity (hs) troponins].

This was NOT high sensitivity troponin, but we know from a couple studies that, even using hs-cTnI, Unstable angina still exists:

These two slides come from my recent lecture on high sensitivity troponin:

Slide 23 in the lecture.  
Thelin et al. Eur Ht J, Acute Card Care 2014; 4(5):403-9

• Initial hs-cTnT among 478 patients presenting with chest pain as the primary symptom
• 160 (33.5%) had values below 5 ng/L
• NPV of 100% for NSTEMI (70 NSTEMI; 37 UA)
• NPV of only 94% for any ACS (includes Unstable Angina)
• Sensitivity 91% (80-95)
– Missed 10 of 107 ACS as diagnosed by angiography; 8 PCI

• Clinical judgment and pre-test probability of ACS is critical



Slide 32. 
Mokhtari et al. JACC 2016;67:1531. 
0/1 hour algorithm, with vs. w/o ECG and Gestalt


0/1 hour protocol alone (same as other 0/1 hour hs-TnT protocols)
– Rules out 65% (n = 682)
– 87% sens for ACS if one includes unstable angina as a 30 day MACE
• 0/1 hour protocol + ECG non-ischemic + Gestalt not high risk
– Gestalt risk = very low, low, or intermediate (not high risk)
– Rules out 60% (n = 625)
• 97.5% (92.9-99.5) sensitivity, 99.5% NPV (98.6-99.9).






-----------------------------------------------------------
Comment by KEN GRAUER, MD (10/24/2018):
-----------------------------------------------------------
Important teaching points are made in this post by Dr. Smith. These include: iappreciation of how problematic the definition of “acute STEMI” can be; andiiillustration of how dependence on this definition may result in overlooking acute coronary occlusion.
  • I focus my comments on some additional fine points regarding ECG interpretation of the 2 tracings shown in this case (Figure-1):
Figure-1: Comparison between the initial triage ECG in this case (TOP) — with ECG #2 (BOTTOM) obtained shortly after sublingual NTG, with much improvement in symptoms  (See text).
=========================
ECG #the initial Triage ECG (TOP— As per Dr. Smith, the dramatic ST elevation in leads V3-thru-V6, plus additional ST elevation in each of the inferior leads in a patient with new symptoms is virtually diagnostic of acute LAD occlusion. Appropriately, the cath lab was activated.
  • Lack of ST elevation in V1 and V2 suggests a mid (rather than proximal) LAD location.
  • Note baseline wander in lead aVL of ECG #1. This makes it difficult to assess for reciprocal change in this lead — since there is ST scooping with suggestion of slight depression in the first 2 complexes — but if anything, slight ST elevation in the 3rd complex in this lead. A glance at simultaneously-obtained lead aVF in ECG #1 confirms that artifact is the reason for problematic appearance of ST-T waves in the 3 beats shown in lead aVL — with bottom line, that there is no more than modest (if any) reciprocal ST depression in aVL in ECG #1.
  • Although there is no long lead rhythm strip — it is noteworthy that there is marked sinus arrhythmia in ECG #1. This finding is easy to overlook because of the lack of a long lead II … Perhaps this marked sinus arrhythmia reflects increased vagal tone? In any case, sinus arrhythmia is much less marked in ECG #2 after SL NTG with improvement of symptoms.
  • BEYOND-the-CORE: There are extremely prominent J waves in the 2 leads of ECG #1 that show the most marked ST elevation (ie, leads V4 and V5). Although still present in ECG #2 — note how much less prominent these J waves are after presumed reperfusion. We have previously discussed this phenomenon (Please see the P.S. at the bottom of the page in My Comment, from Dr. Smith’s July 11, 2018 blog post). It appears that on occasion — J waves may be induced by ischemia (thought to reflect an acute injury current from impending myocardial infarction). Whether this is the reason for the very prominent J waves in leads V4 and V5 of ECG #1 would have been more evident IF we had access to a 3rd ECG obtained a bit later showing complete resolution of these J waves.
QUESTION: Let’s follow-up with the question posed above by Dr. Smith:
  • Imagine the only ECG you are given is ECG #2 (BOTTOM tracing in Figure-1). Two troponins have come back negative. As stated, the patient is a previously healthy 40-ish year old male with dyspnea, left arm numbness and chest tightness for ~1.5 hours. Why should you resist calling this early repolarization?
ANSWER: Dr. Smith has already indicated that the presence of reciprocal ST depression in lead aVL alone tells you that ECG #2 is not a benign pattern of early repolarization. Additional ECG findings of note in ECG #2 include:
  • The amount of ST elevation in ECG #2 is maximal in leads V4 and V5. It is minimal (ie, no more than 1mm) in lead V2. This distribution of ST elevation is not the pattern expected with early repolarization.
  • The shape of the ST segment takeoff in lead aVF is straight. It is coved (ie, convex-down or “frowny” configurationin lead III. Neither of these shapes is what you expect with early repolarization.
  • Troponin does not always rise with acute occlusion IF spontaneous reperfusion occurs quickly. Two negative troponins do not exclude the possibility of short-lived acute coronary occlusion.
  • Even if you thought ECG #2 looked like early repolarization — more data would be needed because there is ST elevation in this tracing. This might include Echo obtained during symptoms (looking for wall motion abnormality) — and  serial tracings looking for dynamic change. The diagnosis of early repolarization in a patient with new symptoms should always be a diagnosis of exclusion to be made only after you rule out the possibility of an acute event.
Finally — If ECG #2 was early repolarization — we would expect some ST elevation in lead aVL. Instead (as per Dr. Smith) — there is reciprocal change in this lead. This is subtle — but it is definitely present. To assist enhancing instant recognition of the mirror-image picture “painted” by reciprocal changes — we superimpose the mirror-image of lead III above lead aVL — and the mirror-image of lead aVL above lead III (Figure-2).
  • Note that the shape of the ST-T wave of the mirror-image of lead aVL is virtually the same as the shape of the ST-T wave in upright lead III.
  • Similarly — the shape of the ST-T wave of the mirror-image of lead III is virtually the same as ST-T wave shape of upright lead aVL.
  • The finding of mirror-image reciprocal change in leads III and aVL in a patient with new symptoms is virtually diagnostic of an acute event!
Figure-2: We focus on the 6 limb leads in ECG #2 — with superimposed mirror-images of leads III and aVL shown within the BLUE rectangles  (See text).


Recommended Resources