A 70-something woman with syncope and a wide complex

This case was written by Andy Lichtenheld (https://twitter.com/ALichtenheld), a really smart 2nd year resident here at our Emergency Medicine program at Hennepin County Medical Center.  

Here is some shameless promotion of our residency, which was started in 1972 and which we think is second to none:


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Case

A 70-something woman with a history of CAD arrived by EMS after a syncopal episode. She had been in her usual state of health when she suddenly became lightheaded and collapsed. She regained consciousness prior to EMS arrival and arrived in the ED confused but gradually clearing. She had no chest discomfort, shortness of breath, arm pain, jaw pain or any other symptoms.

An initial ECG was recorded:
What do you think?





















The computer has identified it as sinus with a Mobitz I AV block with a LBBB.   

However, both the rhythm and QRST appear to be more complicated.  

Rhythm: Regular P-waves can be seen throughout the rhythm strip. Without using calipers and without using more thought than necessary in an emergency, it is hard to say whether this is first or second degree AV block with conduction to a left bundle branch block, or if it is third degree (complete) heart block with an escape from the right ventricle.  Beats 3 and 5 are PVCs.   

Smith: After scrutinizing at leisure, I do think it is complete heart block with an RV escape, but it is complicated.


What else?

There is excessively discordant ST elevation in V1 & V2.  ST/S ratio in V1 is 5/15 = 33%.

There is excessively discordant ST elevation in aVR.  The ST/S ratio is 3/8 = 37%.

There is also excessively discordant ST depression in lead I (ST/R ratio = 100%) and V4 (ST/R ratio = ~60%).

If you accept, as Dr. Smith does, that the Smith Modified Sgarbossa criteria can be used not only in LBBB, but also in ventricular escape rhythms, then any one of these findings meets those criteria.  The STE in V1 as well as the STD in I and V4 are particularly specific for occlusion.

Furthermore, there is an abnormal amount of STD in V5 and V6 (ST/R ratio almost 20%).

Smith Modified Sgarbossa Criteria for LBBB and Ventricular Paced Rhythms

Rule 1: (80-90% sensitive, 95% specific for occlusion)
Any one of:
1. 1 mm concordant STE in any one lead
2. 1 mm concordant STD in any one of V1-V3
3. At least 1 mm discordant STE that is ≥25% of the preceding S-wave in at least one lead

Rule 2: (Only 64% sensitive, but 98% specific for occlusion)
Any one lead with proportionally discordant STE or STD of at least 30% of the preceding R- or S-wave

Smith comment

One more finding!!   PVCs!!!!   The 5th beat is a PVC and has an RBBB morphology (large R-wave in aVR with wide S-wave in V5).  This implies a PVC originating in the left ventricle.  RBBB morphology PVCs should never have an ST segment that is concordant to the QRS, as it is here in lead aVR.  This is diagnostic for STEMI.

See these cases:



Case continued

A previous ECG was obtained:
There is a preexisting LBBB with proportionally normal discordant ST elevation, which makes the ST changes in the new EKG obvious by comparison.

This also suggests that the rhythm in the first ECG is supraventricular, because the QRS morphology is LBBB.  However, if you look closely at V5 and V6 in the first ECG, both have a very narrow peak compared to this old ECG which is much more typical LBBB.

Smith comment: I am still not completely certain as to whether the first ECG is supraventricular with left bundle branch block, or with RV escape.  But it does not matter: the patient has a coronary occlusion until proven otherwise.  She needs immediate pacer pad placement and angiography/PCI.

Case Continued

The clinicians caring for the patient were concerned about an acute coronary occlusion. The cardiologist was in hospital and was paged to the resuscitation area. Over the course of the following few minutes, the patient gradually recovered to her normal mental status. She remained normotensive and entirely asymptomatic. 

As the cardiologist arrived, a change in the QRS morphology was noted on the monitor and a repeat ECG was obtained:
What is your interpretation?









Now there is definitely complete heart block with a ventricular escape:
--The predominant QRS morphology is now RBBB + LAFB with interposed PVC's, which indicates a dominant escape focus now in the left posterior fascicle.
--The ST elevation in V1 and V2 with reciprocal ST depression are now obvious.  It is RBBB morphology with ST elevation concordant to the R-wave, similar to the PVC mentioned above.  This does not happen without ischemia.
--There is marked ST depression in lead II which is then attenuated in aVF and then entirely absent in lead III.  

Smith comment: What is the infarct artery???  With STE in V1 and aVR, one might think this is LAD or left main. Such a conclusion would be consistent with the diffuse ST depression.  

The ST axis is exactly towards aVR, which is what you expect with diffuse subendocardial ischemia (ST depression vector towards I and II, with a reciprocal ST elevation vector towards aVR).  However, the ST elevation is so much more pronounced than the ST depression.  

Is there something else going on??

Andy Lichtenheld wrote: "This is also consistent with inferior and large RV MI due to proximal RCA occlusion."


Case continued:

The initial troponin I returned elevated at 4.5 ng/mL.

She was taken to the cath lab where a 90% proximal RCA lesion, proximal to the RV marginal branch, was stented and a temporary pacemaker was placed.

The next day echo showed very poor LV function with an inferior wall motion abnormality.

Smith comment: 

So Dr. Lichtenheld was correct.  It was an inferior + right ventricular (RV) STEMI.

This pattern of ST elevation and depression is often due to LAD or left main.

I can't fully explain why there was no ST elevation in the inferior leads, especially lead III.

See this case: 

Septal STEMI with ST elevation in V1 and V4R, and reciprocal ST depression in V5, V6



More on ECG in inferior and RV MI:
http://hqmeded-ecg.blogspot.com/2014/03/the-ecg-told-whole-story-but-no-one.html


Here are comments from Ken Grauer:

ECG Interpretation


Fascinating case, about which we’ll probably never know the mechanism of the rhythms for certain. I’ll make a few speculations. I suspect that ECG #1 was not complete AV block — because of the clear irregularity of the ventricular response. In most cases with complete AV block — the ventricular response will be more regular. We see this in ECG #3, in which there clearly IS complete AV block. Returning to ECG #1 — the atrial rhythm is NOT regular. Initially P waves are buried within the ST segment of the first few beats. If you follow out atrial deflections carefully with calipers — the P-P interval varies in a difficult-to-predict manner in some parts of the parts of the tracing. This can happen with atrial infarction, though we really do not see P wave ST segment deviation … QRS morphology in ECG #1 I believe is consistent with LBBB (albeit with lots of fragmentation) — with beats #3 and #5 being PVCs. As per Dr. Smith — the situation is extremely complex. I suspect there may be atypical Wenckebach (PR intervals increasing to quite long toward the end of the tracing) — though R-R interval periodicity is clearly atypical. What IS apparent (as per Dr. Smith) — is that ST-T wave morphology that we see in ECG #1 is abnormal regardless of the etiology of the QRS complex. This ST-T wave abnormality in ECG #1 was confirmed when the baseline LBBB tracing was obtained. NOTE — The first 2 beats in ECG #2 conduct with a NARROW QRS complex — which suggests that this patient’s “baseline” ECG had a rate-related LBBB! I believe that theory is confirmed in ECG #3, which as per Dr. Smith now definitely DOES show complete AV block — with regular escape rhythm and now clearly much more regular atrial activity than we saw in ECG #1. I believe we may have an AV nodal (junctional) escape rhythm in ECG #3 — as the escape rate is ~50/minute, and QRS morphology looks VERY supraventricular given well definite RBBB-morphology in anterior leads and sharp/narrow initial deflections in lateral leads with wide terminal S waves. The heart rate is slower — so the rate-related LBBB has now resolved. We are left with a pattern of marked ST elevation in V1,V2,V3 — with maximal ST elevation in lead V1. As astutely pointed out by Dr. Lichtenheld — this pattern is consistent with isolated acute RV infarction! Of note — virtually all other leads on ECG #3 show significant scooped ST depression (actually a “mirror-image” shape opposite to the coved ST elevation in V1,V2,V3 — so my thought is that in addition to acute RV infarction — there was diffuse subendocardial ischemia. Note however, that there IS suggestion of ST coving in lead III on ECG #3, as well as relatively LESS ST depression in lead aVF — so perhaps the reason we did not see ST elevation in the inferior leads, is that this was essentially cancelled out by the diffuse subendocardial ischemia ST depression seen in virtually all other leads except V1,2,3? Finally — If we go back to ECG #1 (when there was rate-related BBB) — we actually DO see the same type of ST segment deviations that we see in ECG #3 — with the difference being that these ST deviations in ECG #1 were partially masked by the underlying rate-related LBBB. That is, marked ST coving in lead III, ST elevation in V1,2,3 — and dramatic ST depression (beyond the amount expected for LBBB) in all other leads. GREAT case! Thanks for presenting!

A 30-something woman with chest pain and h/o pulmonary hypertension due to chronic pulmonary emboli

A 30-something woman with known history of pulmonary hypertension due to chronic pulmonary emboli presented with 12 hours of substernal chest pain.

Here was her ED ECG:
What do you think?























This precordial T-wave inversion is typical of right ventricular hypertrophy (RVH).  However, most other features of RVH are not present.  There is an incomplete RBBB, which does support RVH.  But there is no right axis deviation (axis is however borderline at 83 degrees, nearly vertical.  There is no large R-wave in V1.  However, these findings are not sensitive enough for RVH to rule it out.

The T-wave morphology, along with the known history of pulmonary hypertension, should alert you to look for a previous ECG.

I saw this and thought immediately that this was probably her baseline EKG.  We looked for old ones, and indeed previous ECGs were identical.

The patient ruled out for both PE and MI while in the ED, and could be discharged.  This was her baseline ECG.  Our diagnosis was gastroesophageal reflux.



Here are a couple other cases of RVH:

55 year old woman with chest pain and precordial T-wave Inversions

This one does have right axis deviation and a large R-wave in V1






A 50-something male with Dyspnea
This one also has right axis deviation and a large R-wave in V1

A 50-something with h/o coronary bypass has chest pain and a ventricular paced rhythm

A 50-something male with h/o CAD and CABG, and dual chamber pacemaker due to sick sinus syndrome, called 911 for onset of acute chest pain 2 hours prior.

Here was the prehospital ECG:

There is sinus rhythm with very long PR interval (about 300 ms).

There is a wide QRS [(nonspecific intraventricular conduction delay (IVCD)]

Neither RBBB nor LBBB

There is some ST elevation discordant to deep wide S-waves in III and aVF, and V3 and V4, appears baseline.

There is some reciprocal ST depression in aVL, but this is normal when there is ST elevation in III that is likely to be due to LBBB, LVH, IVCD, or WPW (in this case, it appears to be due to IVCD)

V1 has some ST elevation, and V2 has absence of expected discordant ST elevation, with a very flat ST segment.

This is all non-diagnostic.

The medics brought the patient to the critical care area, as they were suspicious of acute MI.

The pain started at rest, was constant, sharp in the sternum and radiating to the jaw and left arm and into the upper back, associated with diaphoresis but no SOB. No history of venous thromboembolism.  It was not relieved with nitroglycerin at home, but decreases from 9/10 to 7/10 after EMS gave NTG.  He stated it felt like a prior MI. 

Here is the first ED ECG, at time zero:
There is a wandering baseline in the limb leads.
Nevertheless, there is a suggestion of proportionally excessively discordant ST elevation in inferior leads, with proportionally excessively discordant reciprocal ST depression in aVL.

There is also almost excessively discordant ST elevation in precordial leads, but due to wandering baseline, it is hard to say whether it reaches 25% of the preceding S-wave.

Lots of change since the prehospital ECG! 

The prehospital ECG has normal conduction without ischemic ST elevation.
The ED ECG now has a ventricular paced rhythm (VPR).
The ED ECG now has new ST Elevation.
Is all this new ST elevation only due to VPR.
No!


Smith modified Sgarbossa criteria (for use in LBBB and in VPR):

Rule 1 (80-90% sensitive, 95% specific)
Any one of:
1. 1 mm concordant STE in any one lead.
2. 1 mm concordant STD in any one of leads V1-V3
3. At least 1 mm discordant STE that is greater than or equal to 25% of preceding S-wave in at least one lead.

Rule 2 (Only 64% sensitive, but 98% specific, for occlusion):

Any single lead with proportionally excessively discordant STE or STD of at least 30% of preceding S- or R-wave.

Lead aVL seems to have STD that is at least 30% of preceding R-wave.

Smith modified Sgarbossa criteria are being studied now in the PERFECT  study (Paced ECG Requiring Fast Emergent Coronary Therapy).  Preliminary Results are encouraging that they work in ventricular paced rhythm as well (not surprisingly).  See abstract and references below.
___________________

Case continued

The physicians were worried about this, and 16 minutes later recorded this ECG:
Now there is clearly excessively discordant STE in III and aVF, with excessive STD in aVL.
Notice there is also quite a bit of ST elevation in V1; is this due to RV MI?

The cath lab was activated.

It was a very interesting angiogram.

There was a known chronically occluded proximal RCA, proximal to the RV marginal branch supplying the RV.
The RCA distal to this was known to be supplied by a CABG graft to the posterolateral branch of the RCA (on the posterior wall!), such that flow to the RCA was retrograde.
This posterolateral branch (not the graft itself) was occluded such that that branch could no longer supply the inferior wall and the RV.
Therefore, it caused inferior and RV STEMI.

It was opened and stented with good results.

Full angiogram report:
1. Left main: patent stent.
2. LAD: 70% stenosis in the mid segment at the take-off of a diminutive D1 (angiographically unchanged from previous angiography in 9/2017), then >90% stenosis after D2 (D2 has a 2.0-2.5 mm caliber). The distal LAD is supplied by a patent LIMA.
3. LCX: chronically occluded. The OM is supplied by a patent vein graft.

4. RCA: known chronic occlusion, therefore not studied. The RPLA is supplied by a patent vein graft. Antegrade flow into the RPLA is good, however, retrogradely the RPLA is occluded with contrast hang-up indicative of a thrombotic occlusion. Hence the flow to the RPDA is compromised.


Here is the post intervention ECG:
Atrial, but not ventricular, pacing.
STE resolved
T-wave inversion (reperfusion T-waves) in inferior leads.
Reciprocally upright T-wave in aVL

Lateral T-wave inversion.
Was there indeed ischemia in the myocardial territory under V3-V6?


The patient went into a paced rhythm, and so had a paced ECG recorded about the same time post cath as the above ECG:
Post cath with some ventricular paced beats and some native beats with atrial pacing.
V1-V3 and the first complexes of V4-V6 have ventricular paced beats.
In the paced beats:
There is new STE in V2 with a large upright T-wave, suggesting that the first paced ECG, with isoelectric ST segment in V2, was due to posterior MI.
There is less STE in V3-V6, and some T-wave inversion, suggesting that there was ischemia in this territory as well, that is now resolved.
I'm not sure exactly how to correlate the angiogram with the findings in V3-V6.



Learning Point:

Modified Sgarbossa Criteria are very useful in Ventricular Paced Rhythm


Smith modified Sgarbossa criteria:

-->
Validation in LBBB: 

Meyers HP.  Limkakeng AT.  Jaffa EJ.  Patel A. Theiling BJ. Rezaie SR. Stewart T. Zhuang C.  Pera VK. Smith SW.  Validation of the Modified Sgarbossa Rule for Diagnosis of STEMI in the Presence of Left Bundle Branch Block. American Heart Journal170(6):1255-1264; December 2015.

Derivation in LBBB:

--> Smith SW.  Dodd KW.  Dvorak D.  Henry TD.  Pearce LA.  Diagnosis of Acute Myocardial Infarction in the Presence of Left Bundle Branch Block using the ST Elevation to S-Wave Ratio in a Modified Sgarbossa Rule.  Annals of Emergency Medicine 2012; 60(12):766-776.

STEMI in Ventricular Paced Rhythm

We have some preliminary results of the PERFECT study, presented today at the Society for Academic Emergency Medicine.

The short version: They work!!

Here is the long version

Paced Electrocardiogram Requiring Fast Emergent Coronary Therapy (PERFECT) Study 


ClinicalTrials.gov Identifier:

Dodd KW.  Zvosec DL.  Elm K.  Hart M.  Karim R.  Lurie K.  Smith SW.  Performance Characteristics of the Modified Sgarbossa Criteria for Diagnosis of Acute Coronary Occlusion in Emergency Department Patients with Ventricular Paced Rhythm and Symptoms of Acute Coronary Syndrome.  Academic Emergency Medicine 2017; 24(S1):S36. Abstract 82.

Background: The ECG diagnosis of acute coronary occlusion (ACO) in the setting of ventricular paced rhythm (VPR) is purported to be impossible. However, VPR has a similar ECG morphology to LBBB. The validated Smith-modified Sgarbossa criteria (MSC) have high sensitivity (Sens) and specificity (Spec) for ACO in LBBB. MSC consist of ≥ 1 of the following in ≥ 1 lead: concordant ST Elevation (STE) ≥ 1 mm, concordant ST depression ≥ 1 mm in V1-V3, or ST/S ratio < -0.25 (in leads with ≥ 1 mm STE). We hypothesized that the MSC will have higher Sens for diagnosis of ACO in VPR when compared to the original Sgarbossa criteria. We report preliminary findings of the Paced Electrocardiogram Requiring Fast Emergency Coronary Therapy (PERFECT) study (#NCT02765477).

Methods: The PERFECT study is a retrospective, multicenter, international investigation of ED patients from 1/2008 - 12/2016 with VPR on the ECG and symptoms suggestive of acute coronary syndrome (e.g. chest pain or shortness of breath). Data from four sites are presented. Acute myocardial infarction (AMI) was defined by the Third Universal Definition of AMI. A blinded cardiologist adjudicated ACO, defined as thrombolysis in myocardial infarction score 0 or 1 on coronary angiography; a pre-defined subgroup of ACO patients with peak cardiac troponin (cTn) >100 times the 99% upper reference limit (URL) of the cTn assay was also analyzed. Another blinded physician measured all ECGs. Statistics were by Mann Whitney U, Chi-square, and McNemar’s test.
Results: The ACO and No-AMI groups consisted of 15 and 79 encounters, respectively. For the ACO and No-AMI groups, median age was 78 [IQR 72-82] vs. 70 [61-75] and 13 (86%) vs. 48 (61%) patients were male. The median peak cTn ratio (cTn/URL) was 260 [33-663] and 0.5 [0-1.3] for ACO vs. no-AMI. The Sens and Spec for the MSC and the original Sgarbossa criteria were 67% (95%CI 39-87) vs. 46% (22-72; p = 0.25) and 99% (92-100) vs. 99% (92-100; p = 0.5). In pre-defined subgroup analysis of ACO patients with peak cTn >100 times the URL (n = 10), the Sens was 90% (54-100) for the MSC vs. 60% (27-86) for original Sgarbossa criteria (p = 0.25).
Conclusions: ACO in VPR is an uncommon condition. The MSC showed good Sens for diagnosis of ACO in the presence of VPR, especially among patients with high peak cTn, and Spec was excellent. These methods and results are consistent with studies that have used the MSC to diagnose ACO in LBBB.











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