Queen of Hearts: OMI (Output- 0.96). This is all but diagnostic of OMI.
An EKG from a year ago was available to the providers for reference at this time:
The masquerading bundle branch block pattern was therefore pre-existing, but the ischemic ST-T complexes of LAD occlusion are new.
EKG 2 was not recognized as acute LAD occlusion. The patient waited in the ED, but remained free of chest pain.
The first troponin I was sent at 22:25- 7.303 ng/mL
Smith: is this elevated troponin left over from the previous OMI, and on its way down? Or is it from a new one? Or both?
EKG 3 was recorded 2.5 hours after EKG 2:
The findings are improving, suggesting reperfusion, although there is persistent ischemic ST depression in inferior and lateral leads.
A troponin was repeated at 00:46- 7.650 ng/mL. At this point, the patient received a diagnosis of “NSTEMI”.
Smith: now we know it is climbing and due to a new superimposed infarction.
A third troponin was measured at 04:23- 12.060 ng/mL. The ED physician began to arrange for transport to a PCI center. A fourth troponin was measured at 07:09- 18.073 ng/mL.
On arrival to the PCI center EKG 4 was recorded:
Inferior and lateral ST depressions have improved since EKG 3. The R wave transition happens at V4 here as opposed to V3 like in EKG 3. V3 now shows Concordant ST elevation, although this may be a consequence of the change in precordial R wave progression, which may be a consequence of precordial electrode placement. Although the patient’s symptoms at this time are unknown, it is likely this tracing represents continued LAD territory reperfusion.
Before catheterization, a high sensitivity troponin T was drawn at 09:37- 3,669 ng/L.
Smith: For the same size infarct, troponin I has values 5-10x that of troponin T. So a troponin I of 18,000 and a troponin T of 3669 are both very high values.
Angiography was performed at 10:31, just under 13 hours after the patient’s ED presentation:
The red arrow shows a 50% distal stenosis of the left main coronary artery involving the ostium of the LAD. The green arrow in image A shows total occlusion of the proximal LAD. The blue arrow shows a 90% stenosis of the proximal RCA. The green arrow in image C shows the apical LAD filled by collaterals from the RCA.
No comment was made on the chronicity of the LAD lesion (whether CTO, subacute, or acute) but it can be reasonably estimated that the lesion had been present for some time, possibly occluding and reperfusing over the weeks leading up to the presentation, based on the patient’s story, the EKG from earlier in the week showing LAD reperfusion, and the high troponins on presentation. PCI was not performed. Instead, the patient was referred for surgical revascularization.
Smith: Alternatively, if there is chronic total LAD Occlusion (CTO), then RCA coronary syndrome would result in the same clinical and ECG syndrome, because the anterior wall would be dependent on collateral circulation from the RCA.
An echocardiogram at 13:40 showed:
Severely reduced global systolic function with an estimated EF of 10-20%
Mildly increased LV size
Akinesis of the entire septum and apex
Hypokinesis of the anterior, anterolateral, and mid posterior segments
A final troponin T was drawn at 17:23- 3,475 ng/L. The substantial increase in troponin after ED presentation suggests that immediate referral to a PCI center after the family clinic presentation earlier in the week could potentially have saved a lot of myocardium.
After angiography, The patient was transferred to a telemetry unit. At 21:02, his cardiac monitor captured this:
Two V1 rhythm strips from the telemetry unit show total AV block. A ventricular escape rhythm is apparent at first, but soon disappears leaving only P waves; there is complete ventricular standstill. This rhythm disturbance can occur in patients with severe infra-hisian conduction system disease like bifascicular block due to RBBB and LAFB because only one limb of the conduction system, in this case the left posterior fascicle, is able to propagate each supraventricular impulse through the ventricles. If that limb gives out due to ischemia or another cause, the heart becomes reliant on a ventricular escape rhythm. If the ventricular escape rhythm also gives out, the patient has cardiac arrest.
The patient received 3 x 1 mg doses of epinepherine, 1 mg of atropine, was intubated and started on a dopamine infusion. ROSC was achieved after 4 rounds of compressions. After ROSC, EKG 5 was recorded:
This was interpreted as showing ventricular tachycardia. However, the QRS morphology is nearly identical to that of EKG 4.
In fact, I believe some atrial activity can be observed, especially in the beginning of lead II where the rhythm is slowest and most irregular. While the rhythm here is difficult to discern, and is probably impossible to know with certainty, it is unlikely to represent ventricular tachycardia because of its irregularity (even though automatic VT can sometimes be irregular) and its similar morphology to previous EKGs with sinus rhythm.
Smith: this is irregularly irregular. While VT can be irregular, the vast majority of irregularly irregular rhythms are atrial fibrillation. Add to that the fact that the QRS morphology is identical to the QRS morphology in the above ECGs in sinus rhythm tells us that this is supraventricular.
The patient was transferred to the ICU on pressors, where a repeat bedside echo showed an LVEF of 10-15%. He suffered another cardiac arrest in the ICU with ROSC after another dose of epinephrine and one round of CPR. After discussion with the patient’s family, the decision was made not to resuscitate in the event of re-arrest. The patient died early the next morning.
Learning Points:
- Recognition of OMI is extremely important in patients with atypical presentations. A patient with an EKG suggestive of OMI, even with atypical symptoms, should be sent to the ED for emergent evaluation. This patient was not so far outside the "intended use population" that he did not need emergent cardiac evaluation.
- Patients with bifascicular block, especially with masquerading bundle branch block morphology, have a higher chance of developing Mobitz II and complete AV block, especially after an ischemic insult.
- PVCs and fusion beats can show signs of acute ischemia.
This shows that with Right Ventricular Hypertrophy and RBBB, the ST depression in V1-V3 can be quite deep at baseline:
And that when the LAD becomes occluded in such a patient, the ST Elevation is very subtle.
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MY Comment, by KEN GRAUER, MD (4/18/2025):
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I found today's case challenging from a clinical perspective — but very unfortunate given the patient's demise, raising the question of whether the outcome might have been different had the extent of the patient's condition been recognized sooner.
- Complicating assessment — is a lack of information at critical points in the patient's evaluation.
- I focus my comments on the EKGs that I found most challenging.
The History:
Details of the patient's past and presenting history are incomplete — but highly relevant to how I interpreted his initial ECG. From the limited information we are given — we glean the following:
- This 84-year old man with hypertension and CKD (Chronic Kidney Disease) — presented to a primary care clinic with a several week history of fatigue and lightheadedness on ambulation, with orthostatic hypotension documented at that clinic.
- The patient reported one episode of CP (Chest Pain) the week before he was seen — but additional details regarding that CP episode are uncertain. He had no CP at the time he was seen.
The Initial EKG (TOP tracing in Figure-1):
I've reproduced and labeled EKG #1 below — which is the tracing recorded at the time today's patient first presented to the primary care clinic. I did not have access to the previous EKG at the time I initially reviewed this case. My thoughts on EKG #1, considering the above history — were as follows:
- The rhythm in EKG #1 is sinus at ~65/minute.
- The QRS is very wide (about 0.15 second). Although QRS morphology superficially resembles RBBB/LAHB — there are atypical features. These include: i) A fragmented qR pattern in lead V1 (rather than a triphasic rsR' that is more typical of rbbb conduction); and, ii) Unusual morphology for rbbb conduction in left-sided limb leads (a small, fat R in lead I with minimal terminal S wave — and complete lack of any terminal S wave in aVL).
- Diffuse ST segment coving with fairly deep, symmetric T wave inversion in leads I,aVL; and across the chest leads.
- There is some ST elevation in leads V1-thru-V3 — although I thought this to be modest in amount, considering the deep, diffuse T wave inversion.
My Impression of EKG #1:
As per Hans Helseth — this initial EKG recorded at the primary care clinic is extremely abnormal.
- The above said — I thought EKG #1 and the above history (ie, no CP for the past week) were suggestive of a recent (but not acute) event — in which we were now seeing some residual ST elevation, with a predominant picture of reperfusion T waves in 8/12 leads.
- By history and EKG — my guess is that this event probably began several weeks earlier, at the time the patient began having fatigue and lightheadedness.
- Given this patient's age, and especially given orthostatic hypotension in association with his lightheadedness — I thought hospital admission for a more thorough evaluation was clearly indicated.
- PLUS: Rather than RBBB/LAHB on his initial EKG — QRS morphology resembling rbbb conduction in the chest leads but resembling lbbb conduction with marked left axis in the limb leads — suggests to me the pattern known as MBBB (Masquerading Bundle Branch Block) — which especially given this patient's age and orthostatic hypotension, would place him at high risk of sudden progression to a life-threatening conduction defect if he was sent home. Instead — Permanent pacing might be needed (See below).
- The above said, and with full awareness that sometimes, "Ya gotta be there" — I did not feel immediate activation of the cath lab was needed at this time on the basis of EKG #1 (assuming of course that this patient remained without CP, and without significant Troponin elevation or serial EKG changes).
My Thoughts on Management:The sequence of events and the severity of this patient's condition would have become evident during brief hospitalization. Non-emergent cardiac cath would probably have been part of this hospital evaluation.- I viewed it as unfortunate that this patient was sent home from the primary care clinic.
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| Figure-1: Comparison between today's initial EKG — with a prior EKG done ~1 year earlier. |
The Previous EKG (BOTTOM tracing in Figure-1):
As per Hans Helseth — a previous EKG from ~1 year earlier was found during the course of this patient's next evaluation. I include it here, together with EKG #1 to facilitate comparison — with the goal to illustrate the following:
- QRS morphology and marked QRS widening that we see in EKG #1 — is quite similar to what was already present on the prior tracing (namely, resemblance to rbbb conduction in the chest leads — but looking more like lbbb conduction with marked left axis in the limb leads — with no more than a vestige of a terminal S wave in lead I of the previous EKG).
- The q wave in lead V2 was already present in the previous EKG — suggesting that QRS abnormalities were the result of prior infarction.
- BUT — the ST segment coving, elevation and deep, symmetric T wave inversion that we see in EKG #1 was not seen in the prior tracing! So all of those changes are new!
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More on MBBB (Masquerading Bundle Branch Block):
QRS widening in the presence of sinus rhythm, in which QRS morphology is consistent with RBBB conduction in the chest leads — but LBBB conduction in the limb leads (especially with a leftward axis) — suggests the entity known as MBBB (Dhanse et al: J Cin Diagn Res, 2016). — and — Sakai et al: J Clin & Med Case Reports, 2021). I thought this to be consistent with the picture of the QRS morphology that we see in today's previous EKG. - MBBB is a special type of IVCD that although uncommon, is important to recognize because it identifies a group of patients with: i) Very severe underlying heart disease; ii) A much higher predisposition for developing complete AV block (and needing a pacemaker); and, iii) An extremely poor longterm prognosis.
- NOTE #1: Variations on this above "theme" of MBBB are common. Thus, the S wave that is typically associated with RBBB patterns in lateral chest leads V5,V6 may or may not be present. In the limb leads, rather than a strict LBBB pattern — more of an extreme LAHB (Left Anterior HemiBlock) pattern may be seen (ie, with wide and predominantly [if not totally] negative QRS complexes in the inferior leads — and with a smaller [blunted] terminal s wave in leads I and aVL).
NOTE #2: Knowing the clinical history may aid in recognition of IVCD patterns that are consistent with MBBB (ie, if the patient has a known history of severe, underlying heart disease). - Distinction from simple bifascicular block (ie, with RBBB/LAHB) — may be facilitated by seeing one or more of the following: i) More of a monomorphic upright QRS in lead V1 (which lacks the neatly defined, triphasic rsR' with taller right "rabbit ear" seen with typical RBBB); ii) Lack of a wide terminal S wave in lateral chest lead V6; iii) Seeing an all-positive (or at least predominantly positive) widened QRS in leads I and/or aVL, with no more than a tiny, narrow s wave in these leads; and/or, iv) Seeing widened, all-negative (or almost all-negative) QRS complexes in the inferior leads.
Relevance to Today's Case?
While no clear history of syncopal episodes was obtained in today's case — this elderly patient manifested other symptoms potentially consistent with severe conduction system disease — his ECG manifested marked QRS widening not due to hyperkalemia — cardiac cath demonstrated multi-vessel disease — and the patient's terminal cardiac arrest was marked by AV block, and ultimately by ventricular standstill.
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The CASE Continued:
As noted above — this 84-year old patient was not admitted to the hospital from the primary care clinic where he was first seen. Instead, he was discharged home — only to return 5 days later for severe CP that occurred during unmonitored exercise — evolving an extensive infarction and ultimately leading to the cardiac arrest that he succumbed to (details of these events discussed above by Hans Helseth).
I thought EKG #2 in today's case especially interesting and worthy of a closer look (EKG #2 being the initial tracing obtained 5 days after the primary care visit — at the time that this patient presented to his local ED).
- EKG #2 is a complicated tracing ...
- Surprisingly — the patient was not having CP at the time EKG #2 was recorded.
- The fact that no repeat ECG was done for 2.5 hours after EKG #2 indicates that KEY findings in this challenging tracing were missed ... (I wonder how EKG #2 was treated — and what happened during the 2.5 hours until EKG #3 was finally done?).
- Can You figure out what is going on in EKG #2?
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| Figure-2: Another look at EKG #2. |
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My Approach to EKG #2 (See Figure-3 below):
As I note above — this is a complicated tracing — QRS complexes are wide — the rate is fast — and multiple QRS morphologies are seen.
- As is often the case with complex arrhythmias — the simple step of labeling P waves often provides the KEY clue as to what is going on.
- We know from this patient's prior tracings — that with sinus rhythm, the QRS complex is very wide, and manifests MBBB morphology.
- Looking at the long lead II rhythm strip — the RED arrow P waves allowed me to recognize sinus tachycardia with QRS morphology similar to that seen in EKG #1. Regular sinus P waves are seen throughout this long lead II rhythm strip!
- This sinus conduction is easiest to see by focusing on the 3 consecutively-conducted sinus beats #7,8,9 in the long lead II. (The other sinus-conducted beats in this tracing are beats #2,4,11,13,15,17).
- The KEY beat — is beat #6. Note the double RED arrows that highlight the on-time sinus P wave that occurs just before the QRS of beat #6, with a PR interval that is too short to conduct beat #6! This tells us that beat #6 is a PVC (Premature Ventricular Contraction).
- Note that each of the other positive-R-wave-beats in the long lead II are smaller in size than beat #6. Note also that each of these other beats (ie, beats #3,5,10,12,14,16,18) are preceded by a P wave.
- What makes this tracing so difficult to interpret is the underlying tachycardia — that makes it hard to determine if the PR interval preceding beats #3,5,10,12,14,16,18 is a little bit shorter than the PR interval before the sinus-conducted beats. But all of these other beats look to be intermediate in QRS morphology between sinus-conducted beats and beat #6 that we know is a PVC. This is best seen for the sequence of beat #4 (which is sinus-conducted) — beat #6 (which we know is the "pure" PVC) — and beat #5 (which manifests a QRS and a T wave of intermediate morphology between the QRST morphology of beats #4 and #6). This tells us that beat #5 is a fusion beat (F).
- Each of the other positive-R-wave-beats are also fusion beats. The reason for the variation in QRS morphology of beats #3,5,10,12,14,16,18 — is the result of different degrees of fusion.
- PEARL: Look at the appearance of fusion beat #12 in simultaneously-recorded leads V1 and V2. As per the GREEN arrows in these 2 leads — the ST-T waves of beat #12 in leads V1,V2 are diagnostic of acute LAD OMI. Thus EKG #2 — provides an excellent example of how the ST-T wave of ventricular beats (in this case, of a fusion beat) may sometimes be more diagnostic of acute OMI than sinus-conducted beats.
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| Figure-3: I've labeled EKG #2. |
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