Wednesday, July 17, 2019

A Text Message in the Middle of the night. Do you give thrombolytics?

I awoke in the morning and discovered a text with this ECG that was sent 6 hours prior by a former resident:

"60 year old with classic chest pain.  The cath lab is occupied for the next 90 minutes.  Cards says "not a STEMI".  Thinking of giving lytics."
What do you think?
What do you do?













I texted back: "Sorry for delay!  Was sleeping.  This is OMI!!  Did you give lytics?  Proximal LAD.  Great catch!"

There is 0.5 mm of ST Elevation in V3-V6.  The T-wave in V4 is far too large for the QRS.  The LAD occlusion formula would be very high due to the extremely small R-wave in V4 and QRS in V2, but without the QT I cannot calculate it exactly.

This ECG is diagnostic of LAD OMI.  Occlusion Myocardial Infarction.

I continued:

"Cards was right.  It is not a STEMI.  But the new paradigm is OMI.  And that is what is important.  ST Elevation is a very poor way to define myocardial infarction. We have a couple articles, one in press and one in review, that we hope will continue to prompt a change in that inadequate paradigm."

More about the case:

History: 60 yo woman w/ history of smoking but no other cardiac risks who presented to triage w/ CP. She had awoken in the morning w/ bilateral arm paresthesias and by evening called a nurse advice line who told her she may be having a heart attack and to go to ED to be evaluated.

While in her car she developed central chest pressure radiating to right shoulder about 20 min prior to arrival.

She was seen in triage where she had an ECG recorded at T0:
What do you think?
(The dx can be made without looking at the baseline ECG, but it is below if you want to see it)?















A baseline ECG was available and is also attached.


Now you know the diagnosis.  Acute LAD occlusion.

But the ED is a busy place:
"She was hypertensive in the 190s-200s systolic but otherwise had normal VS. The ED was very busy and there were no open rooms.

"The triage ECG was shown to a physician, I don't honestly recall if it was me or one of my partners and labs and CXR were ordered by the provide in triage.

"By the time she was roomed and I assigned myself to her care it was about 1 hr later. She remained very hypertensive and had a nursing note that said she had been too anxious to get a repeat ECG and requesting an order for Ativan.

"As I was reviewing her triage information and initial ECG another pt was roomed who appeared to be critically ill with an STEMI.

"I ordered her aspirin, NTG, fentanyl, a repeat ECG and walked into the room w/ the new STEMI pt.

"As I walked into that room that lab called w/ her initial troponin value of 1.0 (LOD < 0.03). The repeat ECG I ordered is attached here as ECG #2 and was done at T+70."

Tough to interpret

"I activated the cath lab for my 2nd pt and was not able to get to her bedside until about 30 min later. Her pain and HTN were improved but she was still having active CP. I ordered more NTG and fentanyl and obtained another repeat ECG."

(ECG 3-2 at T+100 attached here).

This is the ECG at the top


"I activated the cath lab at this point.


"Our cardiologist came back down to the ED looked at the most recent ECG and said, "That's not a STEMI".  I told him I disagreed and thought the patient needed emergent catheterization. He told me that regardless they would be unable to take her for at least 90 min b/c they were just starting the other case I had sent them.

"That's the point at which I texted you. 

"We gave heparin, started nitro gtt and was considering giving thrombolytics but our unit coordinator was able to find an accepting cardiologist at the hospital down the street in about 5 minutes. 

"She went emergently to cath (not able to figure out exact timing from my chart review) and was found to have 100% thrombotic distal LADD1 which was stented. Her troponin I there was >50 (they don't measure higher). No post cath echo yet."



The question still remains (thrombolytics?):

If there is no cath lab, are thrombolytics indicated?  If I were the treating physician, I would give thrombolytics. But that is because I am so certain that this is an LAD occlusion that there is no doubt in my mind that the benefit/risk ratio of thrombolytics favors treatment.

A careful read of all the original thrombolytic literature shows that the "criteria" for giving thrombolytics are extremely inaccurate.  Moreover, there is much recent literature showing that acute coronary occlusion frequently does not meet criteria.  In the best study to date, published last month, ST Elevation was 35% sensitive for adjudicated STEMI (51% on serial ECGs) and 21% sensitive for OMI (30% on serial ECGs).  Cardiologists were 49% sensitive for OMI. 

If I diagnose an acute Coronary occlusion, regardless of "STEMI criteria" of an artery that supplies a significant myocardial territory,  and the cath lab is not available, I will give thrombolytics if there are not any really serious contraindications.  I am not going to recommend that everyone do it because it is very dependent on ECG and other skills to be certain of the diagnosis.

Prospective validation of current quantitative electrocardiographic criteria for ST-elevation myocardial infarction


Pendell and I wrote an Editorial on this, but we cannot reproduce it here:
H. Pendell Meyers.  Stephen W. Smith.  Prospective, real-world evidence showing the gap between ST elevation myocardial infarction (STEMI) and occlusion MI (OMI)









Monday, July 15, 2019

A female in her 60s with sudden chest pressure

Written by Pendell Meyers


A female in her mid 60s with history of SVT and HTN presented with sudden onset 3/10 chest tightness while lying in bed in the early morning. She had nausea and diaphoresis with this event, as well as tightness between her scapula, and a loose bowel movement.

Here is her initial ECG at presentation to the ED at time zero (no prior available):

What do you think?









Sinus rhythm with significant downsloping STD in V1-V3, maximal in V1-V2. There is also subtle STE in V6 with large-area T-wave with straight/convex ST segment morphology. The T-waves in the inferior leads could be large if a prior ECG were available for comparison.

This ECG is diagnostic of acute MI of the posterior and lateral walls. The most common etiology of this condition is Occlusion MI (OMI) affecting these walls, most likely LCX or other artery in this territory including a diagonal or obtuse marginal, or RCA in some cases.

Because the current STEMI vs. NSTEMI paradigm greatly undermines the understanding and recognition of the STD of posterior OMI, this finding was not initially recognized.

Initial troponin returned slightly elevated at 0.02 ng/mL. This triggered a repeat ECG at t = 50 minutes:



The findings above are still present but slightly improved, however there is still active ischemia on this ECG. OMI is ongoing until proven otherwise.

It is unclear whether the patient still had symptoms at this time.

The patient was admitted to cardiology for NSTEMI. There was no bed in the cardiology unit, so the patient was boarding in the ED.

The second troponin returned at 0.13 ng/mL, prompting another repeat ECG at t = 2 hrs:
Further improvement but still not back to baseline.



CT aorta was negative for dissection.

She was started on heparin.

Trop #3 at t = 6 hrs 30 min = 0.41 ng/mL
Trop #4 at 9 hrs = 1.13 ng/mL
Trop #5 at 12 hrs = 1.17 ng/mL

Finally, a note from the admitting team states that she will be taken to cath for ongoing chest pain and rising troponins at t = 15 hrs.


Cath at t = 16 hrs:

Mid LCX 100% occlusion with TIMI 0 flow. TIMI 3 after PCI. Also noted triple vessel disease with RCA 70% and LAD mid 90%.







ECG the next day:




First five measurements were before cath, then you can see the spike as sequestered troponin in non-perfused myocardium is released after reperfusion.

Learning Points:

STD maximal in V1-V4 with a normal QRS complex (not explained by RBBB, etc) is worrisome for posterior OMI until proven otherwise. Posterior leads may be helpful, but lack of clear elevation in the posterior leads does not obviate concern for posterior OMI when the STD on the anterior leads is diagnostic.

Ongoing ischemia (by symptoms, troponin, or ECG) despite medical management is an indication for emergent cardiac catheterization.



===================================
Comment by KEN GRAUER, MD (7/15/2019):
===================================
SUPERB case discussion by Dr. Meyers regarding a tracing that I feel manifests a number of unique and important features. The patient is a woman in her 60s, who presented with new-onset chest discomfort.
  • I focus my attention on the interpretation of the initial ED tracing ( = ECG #1 in Figure-1). I've added ECG #3 to Figure-1 for comparison purposes.
Figure-1: The 1st and 3rd ECGs shown in this case (See text).

My THOUGHTS on ECG #1 The ECG findings in this initial ED tracing are subtle and easy to overlook. I've labeled some of the key findings.

Descriptive Analysis of ECG #1:
  • The rhythm is sinus at ~80/minute. The PR interval is normal. The QRS complex is not wide. Assessment of the QTc interval is a bit tricky because of the RED arrows in leads V2 and V3 (See below) — but I believe the QTc is normal. The frontal plane axis is leftward — but not enough to qualify as LAHB (left anterior hemiblock), because the QRS is not predominantly negative in lead II. I estimate the axis to be about -20 degrees. There is no chamber enlargement.
Regarding Q-R-S-T Changes:
  • Other than lead aVR, the only Q wave is seen in lead aVL. This Q in aVL is of uncertain significance.
  • Determination of Transition (where the R wave becomes taller than the S wave is deep) is difficult to discern in ECG #1 — because QRS complexes in virtually all chest leads are approximately isoelectric!
The most remarkable finding in ECG #1 relates to the ST-T wave Changes:
  • initially did not see much in the way of ST-T wave changes in the limb leads.
  • The most “eye-catching” finding is the ST depression/T wave inversion in lead V(within the RED rectangle in ECG #1). Neighboring leads V2 and V3 show ST-T wave flattening, with a lesser degree of ST depression. The T wave in V4 is almost flat, but the ST segment in this lead is not depressed.
  • The most important finding (and perhaps the easiest to overlook) — is the Selevation in lead V(within the GREEN rectangle in ECG #1). The ST segment takeoff in lead V6 is straightened (parallel to the angled BLUE line) — and the J-point clearly starts above the dotted RED baseline in this lead.
  • Returning to the limb leads for a 2nd look — the ST segment takeoff in each of the inferior leads (relative to the R wave) looks a bit straightened, and possibly fatter-at-its-peak-than-it-should-be in leads II and aVF. As per Dr. Meyers — these inferior T waves might be hyperacute — but without access to additional tracings from this patient, I would not be at all sure about whether the inferior leads manifest anything acute.
COMMENT: The clinical history (a woman in her 60s with new chest discomfort) — clearly was worrisome for an acute cardiac event. That said, I was not initially certain about acute OMI from my 1st review of ECG #1. My thoughts regarding this tracing were the following:
  • IF it would not be for the ST elevation in lead V6 — the principal finding on ECG #1 would be the ST-T wave depression in anterior (as well as right-sided) leads V1,V2,V3. Anterior ST depression and/or T wave inversion is an ECG finding that should always prompt consideration of RV “strain”, as occurs in acute PE (For more on ECG recognition of Acute P— Please see My Comment at the bottom of Dr. Smith’s April 5, 2019 Blog post). Other findings in ECG #1 that are potentially consistent with acute RV “strain” are the presence of numerous S waves (in leads I, II, III; and across all chest leadswhat could be construed as an incomplete RBBB pattern in lead V1 (with narrow terminal S waves in leads I and V6). But AGAINST acute PE as the diagnosis are: ithe History, which sounds cardiac, without hint of acute dyspnea; andiithe unusual ECG finding of ST-T wave depression being by far most remarkable in lead V1, and no more than modest in leads V2 and V3. Typically, with acute RV “strain” — leads V2, V3 and often V4 show much more marked ST-T wave abnormalities than are seen here. The most marked ST-T changes are usually not seen in V1.
  • In my opinion — the shape and relative amount of ST-T wave depression in the anterior leads is also different than what is usually seen with acute posterior involvement. Whereas the majority of acute posterior MIs are associated with acute inferior MI (which is not seen in ECG #1) — it is possible to see isolated posterior infarction with certain LCx lesions. That said, most of the time there is not that unusual ECG finding of ST-T wave depression being so much more remarkable in lead V1, than in leads V2 and V3. (For more on the ECG diagnosis of Acute Posterior M— CLICK HERE).
  • On the other hand — close inspection of the ST-T wave in lead V(within the GREEN rectanglereveals definiteacute-looking ST elevation in this lead. Rather than acute posterior MI — I believe the unusually-shaped ST-T wave depression we see in right-sided lead V1 of ECG #1 reflects a mirror-image reciprocal ST-wave change to the shape of the elevated ST segment in left-sided lead V6 (See mirror-images of leads V1 and V6 in Figure-1).
  • Many providers have been taught to obtain posterior leads” (ie, leads V7, V8 and sometimes V9when attempting to diagnose acute posterior MI. In my experience — posterior leads have never helped me, as use of the Mirror Test” (as I describe and illustrate HEREhas virtually always allowed me to recognize acute posterior MI without need to use posterior leads. That said, ECG #1 illustrates one instance in which I bet leads V7 and V8 (if they would have been done— would have further clarified the question of ST elevation in lead V6.
  • Fragmentation of the QRS complex is seen in several leads in ECG #1 (WHITE arrows in leads III, aVL and V1). The significance of recognizing fragmentation of the QRS complex — is that it suggests scar, which usually indicates prior infarction and/or cardiomyopathy. In retrospect — this fragmentation on the initial ECG provided a clue that this patient has severe multi-vessel coronary disease, as was later confirmed on cath.
  • ECG #1 also manifests U wave inversion (RED arrows in leads V2 and V3). This is not a common finding. Even when present — it is difficult to recognize, and often goes overlooked. The clinical significance of U wave inversion, is that it is a marker of severe ischemia. Suggestion of a negative U wave deflection after the T wave is less marked in subsequent ECGs done as this case progressed, and absent on the following day’s ECG after reperfusion.
BOTTOM Line: In this 60+ year old woman with new chest discomfort — the acute-looking ST elevation in lead V6 with mirror-image reciprocal ST-T wave changes in lead V1 additional ischemic changes in leads V2 and V3 — should be enough to merit acute cath.
  • Knowledge that serial troponins were increasing persistence of chest pain further supported the need for acute cath.

As I emphasized in the last Dr. Smith ECG Blog post (from July 11, 2019) — Among the best ways to enhance appreciation of subtle acute changes on an initial ECG — is by comparison with a later ECG. This should be evident from comparison of the initial ECG in this case ECG #1 in Figure-1) — with ECG #3 done 2 hours later.
  • Note in ECG #3 — that the ST elevation in lead V6 is now gone. The ST segment in this lead is also not as straight as it was in ECG #1.
  • ST-T wave changes in lead V1 do not look nearly as acute in ECG #3 as they did in ECG #1. ST-T wave changes in leads V2 and V3 are also less marked.
  • Finally — Compare T wave appearance in the inferior leads between the 2 tracings in Figure-1. The fact that the T wave in each of the inferior leads of ECG #3 is flatter supports our suspicion that early hyperacute T wave changes were present in the inferior leads of ECG #1.
  • Putting this all together — serial ECGs in this case show dynamic ST-T wave changes — which, in a patient with ongoing chest discomfort is indication for prompt cath.

Our THANKS to Dr. Meyers for presenting this case!



Thursday, July 11, 2019

A 40 year old man with chest pain since last night

Written and submitted by Ashley Mogul, with edits by Pendell Meyers and Steve Smith


A man in his 40s with recent smoking cessation but otherwise no known past medical history presented due to chest pain since the previous evening. The pain has been constant and associated with vomiting and diaphoresis. He decided to present the following day when the pain had not stopped.

Here is the presenting ECG (no prior available):
What do you think?









Relevant findings include slight STE in V1 with an upright T-wave, slightly large T-waves in V2-3 (possibly hyperacute if compared to baseline), and slight reciprocal depression in II, III, aVF, V4-V6.


Meyers: This ECG was texted to me with no clinical information, and my response was: "That looks like a very subtle LAD OMI. If clinical picture was anything compatible with ACS I would heart alert it [Ashley and I trained at Stony Brook where we call a "Heart Alert" on a situation/ECG that doesn't meet STEMI criteria but we are nevertheless worried about the need for emergent cath and emergent ACS workup] and get serial ECGs, unless I had access to an identical baseline (not likely in my opinion). Very very subtle one. What happened?"


These findings are very subtle but suspicious for LAD occlusion, as we have seen in many similar (but less difficult) cases on this blog:

A man in his sixties with chest pain at midnight with undetectable troponin







These findings were not initially recognized. Labs were sent and an initial Troponin I resulted at 2.14 ng/mL. At that time, the patient was given 324 mg ASA and sublingual NTG. Cardiology was called and the patient was taken for urgent catheterization with the time from ED arrival to cath about 1 hour and 45 minutes.

100% proximal LAD thrombotic occlusion with TIMI 0 flow was found and stented with excellent angiographic result and TIMI 3 flow. He also had non-acute CAD of the RCA (50%) and LCX (50%).

Cath images:

Before intervention.

Before intervention with arrows demonstrating the area of occlusion.

After intervention showing the site of prior occlusion.

After intervention.


ECG a few hours later:


Some leads with STD previously have now resolved. The T-wave in lead V1 is no longer upright, with terminal T-wave inversion which is likely due to reperfusion.

Echo showed akinesis of the anteroseptal and anterior walls as well as the apex with an LVEF of 45%. Troponin I elevated to 3.93 ng/mL but was not trended to peak.



Learning Points:

Not all OMI will present as STEMIs. Complete LAD occlusion can be incredibly subtle as in this case. Remember this case and the similar cases (links above) showing this patter of LAD occlusion including subtle STE with upright T-wave in V1-2 with reciprocal STD in lateral and inferior leads. When in doubt, record serial ECGs and watch out for signs of ischemia despite medical management.


===================================
Comment by KEN GRAUER, MD (7/11/2019):
===================================
Our thanks to Drs. Mogul, Meyers and Smith for this illustrative case.
  • I focus my attention on the interpretation of the initial ED tracing ( = ECG #1 in Figure-1). Although the ECG findings are challenging — I feel they should not be missed.
Figure-1: The 2 ECGs in this case (See text).


MTHOUGHTS on ECG #1  The patient is a man in his 40s with a history of smoking — who presented with new chest pain that was ongoing through much of the night, and despite associated vomiting and diaphoresis — this patient would not go to the ED until the next day when chest pain persisted.
  • This is a higher-prevalence History for acute coronary disease. By this, I mean that the onus is on us to rule out that even subtle ECG changes may be acute — rather than the other way around.
Descriptive Analysis of ECG#1:
  • The rhythm is sinus at ~85/minute. The PR, QRS and QTc intervals are normal. The frontal plane axis is normal (about +40 degrees). There is no chamber enlargement.
Regarding Q-R-S-T Changes:
  • There are Qcomplexes in leads V1 and V2. There is notching on the initial part of the downslope of the S wave in lead V2. There may be tiny q waves in lateral chest leads.
  • Transition (where the R wave becomes taller than the S wave is deep) occurs between leads V2-to-V3, which is normal. That said — R wave amplitude is minimal until lead V4 ...
The most remarkable finding in ECG #1 relates to the ST-T wave Changes:
  • Looking sequentially, first at the 6 limb leads — and then at the 6 chest leads — what immediately caught my eye was that the T wave in lead Vlooked taller-than-it-should-be (that is, disproportionate) given the lack of any r wave in this lead.
  • My eye was next “caught” by the appearance of the ST-T wave in lead V3. There is simply NO WAY that the ST-T wave in lead V3 is “normal”. A normal ST-T wave does not have a straight (ledge-like) ST segment as we see in ECG #1, that then abruptly rises to a disproportionately tall T wave (that is 1½ times the height of the R wave in this lead), and which manifests as wide of a T wave base.
  • COMMENT: I will emphasize that despite my detailed, written descriptive analysis above — it literally took me less than 5 seconds to arrive at my ST-T wave assessment — and no more than 2-3 seconds more to assess leads V2 and V3. Even without looking at anything else on this ECG — in a patient with worrisome new chest pain, the ST-T wave appearance in lead V3 the disproportionately tall T wave in neighboring lead V2 is enough (in my opinion), to say that while this may be subtle and we can’t be 100% certain — this patient merits prompt cath.
The more additional leads that we can identify in ECG #1 that show ST-T wave abnormalities — the greater the likelihood that our suspicion for an acute cardiac event (based on this history the ST-T wave appearance in leads V2 and V3is correct:
  • The ST-T wave in neighboring lead Vof ECG #1 is abnormal. It is not normal to see ≥1.5 mm of ST elevation in lead V1 — and, given the ST-T wave appearance in leads V2,V3 — there is little doubt that the ST elevation that we see in lead V1 is part of this process!
Other findings in ECG #1 are more subtle. I probably would not have thought much of them IF the ST-T wave appearance of lead V3 was not so flagrantly abnormal, with associated ST-T wave findings in neighboring leads V1 and V2 (as described above).
  • Considering the hyperacute T wave appearance in lead V3 — it is almost certain that the slight-but-real scooped ST depression and prominent T wave in lead Vis part of the process. Doesn’t the shape of the upper part of the T wave in lead V4 (if not also in V5 and V6) look a lot like the shape of the T waves in leads V3 and V2 that we now know are hyperacute?
  • ST-T wave changes in the limb leads are much less marked. But in the context of chest lead findings just described — the T wave in lead III looks hyperacute (it equals R wave height in lead III, with an extremely wide base considering this tiny R wave). Finally, while there is no ST depression in lead aVL — the ST-T wave flattening we see in this lead is not the normal response when the R wave in aVL is upright.
Taking another look at R wave progression in the chest leads:
  • Notching of the downslope of the S wave of a QS complex (as we see in lead V2 of ECG #1) — increases the likelihood that this QS complex reflects an infarction Q wave.
  • Although a predominant R wave does develop in lead V3 of ECG #1 — this R wave is barely 3 mm tall. This adds further support that the QS in leads V1,V2 (with notched S wave downslope in V2the abnormal ST-T wave changes in lead V1-thru-V4 described above are all part of the same ongoing acute process!
BOTTOM Line: While ECG #1 does not satisfy the definition of a STEMI — as per Dr. Meyers, it really looks like acute LAD OMI. And in a patient with this worrisome of a history — I don’t see how one can justify not calling a heart alert.

Additional LEARNING Points: Among the best ways to enhance appreciation of subtle acute changes — is to compare the initial ECG to one or more post-reperfusion ECGs ( = ECG #2 in Figure-1).
  • To be sure comparison of serial tracings is valid — one must always ensure that frontal plane axis, R wave progression, and QRS morphology are all comparable. And, there are slight differences in this regard when comparing ECG #1 with ECG #2. Thus, several leads (most notably leads I, III; aVR,aVL,aVF) show baseline artifact in ECG #2 that was not present previously. In addition, the frontal plane axis in ECG #2 is a little more vertical (about +75 degrees, compared to an axis of +40 degrees in ECG #1). That said, I believe that for the most part — comparison of ST-T wave appearance between these 2 tracings is valid.
  • There is a difference in QRS appearance of lead Vbetween the 2 tracings. Although impossible to prove — I suspect the return of a predominant R wave in lead V3 of ECG #2 is due to reperfusion of the LAD, rather than to any change in precordial lead placement.
  • Note after reperfusion (ie, in ECG #2) — that: ithere is now no more than trace (if any) ST elevation in lead V1; iithe T wave in lead V2 does not look nearly as disproportionate as it did before PCI; iiieven accounting for the changed QRS appearance in lead V3 — the ST-T wave in V3 of ECG #2 now looks benign; andivthe very subtle suggestion of hyperacute T wave changes in leads V4, V5, V6, as well as lead III — is no longer present in ECG #2. The ST segments in these leads also look better.
  • Final Pearl: I find it ever-so-helpful to look for those 1 or 2 leads in the initial tracing that without doubt are abnormal. Once you find such leads (such as leads V3 and V2 in ECG #1) — it becomes much easier to identify other leads that show more subtle, but clearly abnormal findings.



EXTRA Credit: Go back to ECG #2. Note the artifact in 5 of the 6 limb leads. From which extremity is the problem causing the artifact arising?


ANSWER: There is no artifact at all in lead II of ECG #2. Bipolar lead II is derived from the difference in electrical potential from the foot (F) and the right arm (RA) electrodes. But the left arm (LA) electrode is not involved in derivation of lead II. In contrast, the LA electrode is involved in derivation of both leads I and lead III (which are the leads that show the artifact). That the left arm (LAis the “culprit” extremity is supported by the fact that in the augmented leads, the amount of artifact is greatest in lead aVL, and approximately half this amount in leads aVR and aVF. CLICK HERE — for a brief article by Rowlands et al that explains these concepts in more detail.




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