Sudden Chest pain and SOB with a Wide Complex Tachycardia

This case was contributed by a medic who wishes to remain anonymous (his comments are in red).

This was a 60 something male who called for sudden onset of severe chest pain and dyspnea. No medical history or medications. 

Upon arrival he was in extremis with altered mentation, cyanosis and diaphoresis . We were unable to get an initial ECG due to diaphoresis but the pulse ox showed a sat of 53 and a rate of 170 without palpable radial pulse. 

Initial ECG:

There is a wide complex tachycardia at a rate of 148.
What is it?

Smith Interpretation:

It is fast and the patient is in extremis, so electricity is the appropriate treatment.  If the patient were only moderately ill, you could try adenosine.

Do you think adenosine would work?

I think it would.  This has a fairly convincing LBBB pattern, with rapid depolarization of the first part of the QRS in V1-V3.  

Aside: One person commented that there is concordance in precordial leads (all QRS in the same direction without an RS-waves).  This is an excellent observation, however not quite true!  There is not really concordance: there is an rS in right precordial leads, just as in LBBB. True concordance would not have that (small) r-wave, which is best seen in V3.

However, the LBBB is not entirely convincing: look at inferior leads, which have a notch in the downstroke of the S-wave.  Thus, the depolarization is NOT as fast as it is in precordial leads, and leads one to think that this is possibly VT.  

So the differential is:

1. VT vs. 

2. SVT (flutter, AVNRT, AVRT) with LBBB and a "fragmented QRS." 

If this is LBBB with a fragmented QRS, it is similar to, but not identical to, Chapman's sign (notch on the ascending limb of the R-wave in I, aVL, or V6 in LBBB) or Cabrera's sign (notch greater than 50 ms on the ascending limb of the S-wave in one of V3-V5 in LBBB).

A sudden (paroxysmal) regular tachycardia (without P-waves) that looks like LBBB is likely to be supraventricular with "aberrancy" (the "aberrant" conduction being due to LBBB).

If so, it will usually be responsive to adenosine. If not, it will be safe in VT.  So if the patient is not in extremis, adenosine is a fine alternative to electricity.

Fragmented QRS is defined as: The RSR′ pattern includes various morphologies of the QRS interval (QRS duration less than 120 ms) with or without the Q wave. It was defined by the presence of an additional R wave (R′) or notching near the nadir of the S wave, or the presence of 2 or more R′-waves (fragmentation) in 2 contiguous leads, corresponding to a major coronary artery territory. 

[Mithilesh K. Das, et al. Significance of a Fragmented QRS Complex Versus a Q-wave in Patients with  Coronary Artery Disease.  Circulation. 2006;113:2495-2501.]

Case continued

Combi pads we're applied and showed a wide complex rhythm and synchronization was attemped, but the monitor repeatedly synced to the area in-between the QRS complexes (presumably due to the T wave?).  So we proceeded with unsynchronized cardioversion (same as defibrillation) at 100 J [probably should have been defib doses (200J) in hindsight]. 

This was recorded after unsynchronized cardioversion:

Notice that there are now P-waves (sinus tach at a rate of 112).
The QRS morphology is the same (LBBB).  
The fragmented QRS in inferior leads is still present.  
This QRS fragmentation is probably the result of an old inferior MI.

This proves that the tachycardia, which responded to electricity, was indeed supraventricular.  It could have been atrial flutter, but since there is no suggestion of flutter waves on that first ECG, it is probably due to AVNRT or orthodromic AVRT.

Somewhat later, the heart rate is decreasing.

No significant change

I work in a very rural area so we transport by ground for about 30-40 min to meet air transport. 

After cardioversion the patient improved but still had a wide complex rhythm at 120-150. Aspirin, Amiodarone and high flow oxygen were started. CPAP was initiated and serial 12 leads were recorded, a POC chem 3 showed normal K, Na and Hemoglobin.

The patient improved and was sent by air to the hospital as a STEMI alert.   He ultimately was not Cathed and spent a few days in the ICU and was discharged with a diagnosis of new onset CHF and hypertension.  After the call we were pretty sure the initial rhythm was Ventricular Tachycardia (VT), but we, as well medical control, are not sure what the ongoing rhythm was. 

We also weren't sure about the monitor not syncing and if unsynchronized shocks we're the best action (though I'm not sure what else we could have done without being able to change leads)?

Comment:

Excellent management.  It did not matter that the medics thought it was VT.  Electricity works fine, and when a patient is in extremis, they do not even remember the shock.

As for using automated synchronization, it occasionally is hazardous because the machine cannot find the appropriate point to synchronize, as here.  Thus, it was appropriate to change to defibrillation in this case.

Beware Automated Synchronization for Cardioversion!

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Comment by KEN GRAUER, MD (8/5/2018):

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Excellent discussion by Dr. Smith about this illustrative case regarding a regular WCT (= Wide-Complex Tachycardia) rhythm. My thought process essentially mirrors that of Dr. Smith — to which I will add the following points. For ease of discussion — I’ve put the first 2 of the 3 ECGs shown in this case together in Figure-1.

Figure-1: Initial ECG at Time = 0 — followed by the post-conversion tracing 25 minutes later (See text).

ECG #1 (@T=0, TOP tracing in Figure-1) — My preference is to always begin my assessment by describing what we see in context with the clinical situation. In ECG #1 — there is a regular WCT @ ~150/minute without clear sign of sinus P waves in a patient who is hemodynamically unstable. As per Dr. Smith, since this patient is unstable — it does not matter what the tachycardia rhythm is since regardless, immediate “electricity” is indicated. If “synch” isn’t possible — unsynchronized shock is the intervention of choice.

• Even though electricity is immediately indicated — it is worthwhile to contemplate the Differential Diagnosis of a Regular WCT without clear sign of sinus P waves: i) Always think VT until proven otherwise (since studies show >80% of all regular WCTs without clear sign of sinus P waves turn out to be VT — and, VT is the “worst” thing this could be); ii) SVT with preexisting BBB (Bundle Branch Block or IVCD); iii) SVT with Aberrant Conduction; or, iv) A “WPW-related” SVT.
• Since >80% of WCTs without sinus P waves turn out to be VT — our thinking should be that we must prove the rhythm is not VT, rather than the other way around. That said, if your patient is stable — then even if you believe the rhythm is VT, this does not mean that you need to immediate cardiovert. Sometimes, medication may be tried first. That was not the case here — since this patient was unstable, and needed immediate electricity!
• That said, as per Dr. Smith — ECG #1 looks like it may be supraventricular! That’s because QRS morphology does resemble LBBB-morphology — and, because the initial depolarization vector in many leads is rapid (straight initial deflection within the RED ovals in Figure-1). When the rhythm is VT, with the impulse originating from the ventricles and away from the conduction system — the initial depolarization vector tends to be much slower! NOTE: There is much artifact in ECG #1. Given the tenuous clinical condition of this unstable patient, this is totally understandable! But, it’s important to recognize that because of this artifact, ECG assessment is much more challenging.
• Beyond-the-Core: Although QRS morphology in ECG #1 resembles a LBBB pattern — it is not quite typical for LBBB because: i) We lack a monophasic (ie, all upright) QRS complex in lateral leads I and V6; ii) There appears to be an initial Q wave in lateral lead aVL; and, iii) There is marked fragmentation of the QRS complex in many leads. Because of marked LVH that is so often present in patients with LBBB — many tracings with LBBB do not show an all positive R wave until lateral chest lead V7 or V8. In addition, some patients with LBBB may intermittently develop right axis deviation in the frontal plane, thought to be due to a greater degree of “relative block” in the posterior compared to anterior hemifascicle. That said, the very narrow initial depolarizations in so many leads in ECG #1 (within the RED ovals) — plus, the very steep (straight) S wave downslope in anterior chest leads both strongly favor the likelihood of a supraventricular etiology. NOTE: As per Dr. Smith, there is NOT global negativity of the QRS in all chest leads in ECG #1 — because the QRS is not all negative in all 6 leads! (instead, a small and narrow initial r wave seems to be present in virtually each of these 6 leads!).
• As per Dr. Smith — Adenosine would have been an excellent initial drug to try IF this patient would have been hemodynamically stable at the time ECG #1 was recorded. My preference is not to use Adenosine when I am virtually sure the rhythm is VT (even though adverse effects will usually not occur, even if the rhythm is VT) — but in view of the above morphologic characteristics, I would be ~90% comfortable that the WCT rhythm in ECG #1 was supraventricular. NOTE: This means that we cannot be 100% certain that the rhythm in ECG #1 is supraventricular from this single initial tracing alone! It’s important to realize that we often have to initiate treatment based on our “best educated guess” before we know for certain what a given rhythm is.
• As per Dr. Smith — ECG #2 proves our suspicion of a supraventricular rhythm for ECG #1 was correct — because for the most part, QRS morphology is the same after conversion to sinus rhythm as it was during the WCT (the only exception being that the QRS complex is now clearly predominantly negative in the post-conversion tracing).
• Semantic POINT: I would not call the reason for QRS widening in ECG #1 “aberrancy”. That’s because ECG #2 shows there was preexisting BBB! My preference is to reserve the term, “aberrant conduction” for those cases in which QRS widening occurs during the tachycardia because the faster heart rate reduces recovery time in one or more of the conduction fascicles, and therefore results in QRS widening during (but not after) the tachycardia.
• Sinus rhythm has been restored in ECG #2 (RED arrows). Note that at least in some of the QRS complexes in lead aVL (within the BLUE rectangle) — that there is ST segment coving with slight elevation. As a result — I’d be concerned about the possibility of acute or recent OMI as the cause of the tachycardia. I’ll emphasize that other than the straight “shelf” ST segment flattening in lead V6 — that we really do not see other indication in ECG #2 of recent OMI in the post-conversion tracing — so what we see here in aVL may well turn out to be nothing. But the point to be made is that by always maintaining a high index of suspicion (until proven otherwise) — you are much less likely to miss subtle but important diagnoses.

OMI Can be Diagnosed by "Pseudonormalization of ST Segments"

This post was written by Tarissa Lai, one of our outstanding EM residents at Hennepin County Medical 
Center, with comments by Steve Smith and Dan Lee.

Case

A 30 something y.o. female with HTN, HLD, diabetes, ESRD on dialysis is brought in by EMS with 
sudden onset, left -sided chest pain for the past four hours.

This is her pre-hospital ECG:

 This is her first ECG in the ED:

What do you think?

I interpreted this as normal sinus rhythm with LVH, but no significantly peaked T waves concerning 
for hyperkalemia. I did not appreciate any significant ST elevation.

However, the prehospital ECG is more worrisome: the T-wave inversion in V5 and V6 is preceded
by ST Elevation. In LVH, T-wave inversion in leads V5 and V6 should be preceded by ST depression, or
at least by an isoelectric ST segment. These look like ischemic ST segments and T-waves.

More Clinical history:

I first met her on an overnight shift while she was sleeping in a hallway bed. She was a difficult 
historian as she kept answering in one word replies before falling back asleep. The patient had gone 
to dialysis that day without any significant change in her regimen. While she was in her bed at home, 
she had sudden onset of left sided chest pain that radiated to her shoulder.  The pain
was pleuritic, without nausea or diaphoresis. The nitro she took in the ambulance did not help. 
Her physical exam was remarkable for a young woman sleeping comfortably in bed, whose chest pain
was easily reproducible with palpation.

Although her comfortable appearance with pleuritic and reproducible chest pain were reassuring, some 
components of her story were concerning, including the sudden left sided chest pain and radiation to 
her shoulder. Given her risk factors (HTN, HLD, ESRD from diabetes) I decided to obtain a broad 
cardiac workup for the patient: serial ECGs, labs, serial troponins, CXR and bedside cardiac ultrasound. 
She also received an additional nitro in the ED after receiving aspirin and nitro via EMS.

This is the patient's old ECG from ~2 months prior:

There is ST elevation that is most notable in V1, V2 and aVR with ST depression that is most obvious 
in the inferior leads and V6. I interpreted these as findings consistent with "secondary" ST-T abnormalities due to
her known LVH.
When comparing the old and new ECGs, there is:
New relative ST depression in V1-V3 and
New relative ST Elevation in: II, III, aVF and in V5 and V6.
When I say "relative," I mean relative to the previous ECG, which is the baseline, chronic, non-ischemic ECG.

Here is the Point of Care Cardiac Ultrasound (POCUS), short axis:

This shows the anterior wall (top) and septum contracting perfectly, but the postero-lateral walls not contracting.

Parasternal Long Axis View

There is a posterolateral wall motion abnormality. This appears to be new, as her last formal 
echocardiogram 2 years ago was relatively normal.

All of this is consistent with an acute postero-lateral MI. [New relative ST elevation in V5 and V6 (lateral
wall), new relative ST depression in V1-V3 (posterior wall) and new relative ST Elevation in II, III, aVF
(inferior wall).

At this time, her initial troponin came back at 103.2 ng/mL (103,000 ng/L, extremely high!!),
and her K was 4.6 mEq/L.

While the patient was known to have mild troponin elevations in the past, this was clearly diagnostic of acute MI.

Given the WMA on her echo, a repeat ECG was obtained with posterior lead placement:

There is now STE in V7, V8 and V9, which is consistent with a posterior MI.
The decreased voltage noted in the first couple ECGs is even more obvious now.
There is now also ST depression in V2 and V3 (previously only relative)

On closer evaluation of her old ECG compared to the ones from today, you can see what might
be called "ST Segment Pseudonormalization." Her previous ST elevation in V1-V3 is now gone,
and the voltage from her LVH is decreasing with each successive ECG. This would make sense in
the setting of an acute posterior MI, which can present with precordial ST depression.

V1-V3 side by side:

NEW OLD  

The patient was emergently taken to the cath lab and found to have severe multi-vessel disease with 
high thrombus burden, and the culprit lesion was a 100% thrombotic occlusion in the proximal
left circumflex.

Diagnostic angiogram:

Post PCI of the circumflex artery. She had an uncrossable lesion in the LAD with an estimated 99% 
occlusion. Arrowheads represent some of the remaining thrombotic lesions.

Troponin peaked around 325 ng/mL (massive). Pertinent results of the formal Transthoracic Echo:

-Moderately severe concentric left ventricular hypertrophy.
-Severely decreased left ventricular systolic function with an estimated EF of 22%.
-Akinesis of the apical septal, apical inferior, and apical segments
-Hypokinesis of the basal to mid anterolateral and basal to mid inferolateral segments. (Basal
Inferolateral = Posterior)

Learning Points:
1. Pseudonormalization of STE and/or STD, as in this patient with LVH, but also in LBBB and other
etiologies of chronic ST shift, should raise concern for OMI (Occlusion Myocardial Infarction).
2. Likewise, ST shift from a previous ECG (relative ST elevation or depression) is equivalent to STE or STD.
3. Ultrasounds can be very helpful in guiding your diagnostic pathway: location of WMA on US led 
to obtaining posterior leads.
4. Clinical presentation is important, but so is history. Have a higher suspicion for true pathology in 
anyone with significant comorbidities such as ESRD from diabetes, even if they are young and 
appear “not sick” on presentation.
5. Refractory Chest pain with a clearly positive troponin, without an alternative explanation, is an indication
for emergent cath lab activation regardless of ECG or bedside echo findings.

Comments by Dan

This case was particularly interesting for several reasons. First, the patient is such a young woman to have an occlusion MI (OMI), the likely difference being her significant risk factors. If she had no risk factors, it is doubtful that she would have developed such extensive coronary artery disease as we see on the angiogram. 

Because the troponins were so high, the clinicians did not need to rely on other diagnostics, including posterior leads and ultrasound, to confirm OMI and salvage what myocardium could be saved after hours of constant chest pain before the patient presented.  However, this additional information was supportive.

Note that by current guidelines, this patient had a NSTEMI, but it would hard to argue that her condition would not have worsened if she was left to 'next day cath'.  I took part in her ICU care and she was extubated and stable to transfer to a stepdown unit after a few days. Her repeat ECHO showed an improving EF of 37%. Patients like her are the reason we are advocating for a change in the ACS paradigm from STEMI to OMI. 

Her first EKG in isolation has no hard findings that are diagnostic for an acute coronary occlusion. The importance of having a baseline EKG for comparison cannot be understated. The old EKG shows LVH by Sokolow-Lyon and Cornell criteria but much of that voltage is resolved in the new EKG, which is commonly seen in acute occlusion superimposed onto LVH. For some reason (with debatable physiology), coronary occlusion often causes decrease in the high voltage of LVH on the EKG. Thus it is difficult to study occlusions, particularly subtle occlusions, in the context of LVH. Armstrong et al attempted to study it but may have included too many 'obvious' cases - the criteria from that paper would certainly have missed this case.

There is an interesting finding in this EKG which is the positive notching of the latter portion of the QRS complex, upright in I, II, aVL and downward notching in III, aVF.  

I believe these represent the equivalent of Q-waves, or infarcted myocardium, of the posterior (inferobasal, lateral) wall. They appear in the latter part of the QRS complex because the posterior/basal wall is the last part of the ventricle to depolarize. The notching is not seen in the precordial leads because as it is traditionally taught, a tall R wave in V1 represents the 'upside down' Q wave in posterior infarction.  Thus, if you have LVH in which baseline precordial voltages are already predominantly negative, a posterior infarction should 'cancel out' some of that voltage and possibly diminish the voltage evidence of LVH on the EKG. Note that this is completely different from 'terminal QRS distortion'. 

This paper by Nui et al describes this finding (the "Delayed Activation Wave") in left circumflex occlusions but (I believe mistakenly) compares it to terminal QRS distortion. This finding is not new, and is analogous to Cabrera's and Chapman's sign.  As a Q-wave equivalent, this notching would be expected to persist in subsequent EKGs, as seen in the patient's follow up EKG 6 days later: