Friday, December 13, 2024

ECG Blog #460 — A Wide Tachycardia ...


I was sent the ECG in Figure-1 — initially told only that it was obtained from an older man with “palpitations”.
  • The cardiology team thought the rhythm was an SVT (SupraVentricular Tachycardia) — with QRS widening as a result of aberrant conduction.


QUESTION:
  • Do YOU agree that the rhythm is consistent with an SVT, in which there is QRS widening because of aberrancy?
  • How would you treat this patient?

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).


MY Thoughts on the ECG in Figure-1:
The ECG in Figure-1 — shows a regular WCT ( = Wide-Complex Tachycardia) at ~160/minute, without clear sign of atrial activity.
  • Clinically — The 1st priority in assessing this patient would be to determine hemodynamic status! (because IF this patient was unstable with this ECG — then regardless of what the rhythm happens to be — synchronized cardioversion would become immediately indicated).
  • On the other hand — IF the patient is completely stable with this rhythm, then by definition — You have at least a “moment of time” to more thoroughly contemplate the etiology of this rhythm.

PEARL #1: As emphasized in many other blog posts (ie, ECG Blog #220 and Blog #196to name just two) — the differential diagnosis of a regular WCT rhythm without clear sign of atrial activity should be assumed to be VT (Ventricular Tachycardiauntil proven otherwise.
  • Taking all comers in an unselected adult population — statistical likelihood that a regular WCT without atrial activity will be VT is at least 80%.
  • If the patient is at least middle-aged, and especially if there is a history of underlying heart disease — then statistical likelihood that a regular WCT without atrial activity will be VT increases to ~90%. To Emphasize — This is a 90% likelihood of VT even before you look at the ECG!

  • In Today's CASE All that we initially knew was that the patient was an "older adult" — but we were not told if he had underlying heart disease. So before looking at QRS morphology — statistical odds were ~80% likelihood of VT.

PEARL #2: Assessment of the frontal plane axis and consideration of QRS morphology in the 12-lead tracing during the WCT rhythm can increase (or decrease) statistical likelihood of VT from our initial estimate of ~80% (See ADDENDUM below for user-friendly criteria I favor for this purpose).
  • Finding extreme axis deviation in the frontal plane during the WCT would strongly favor VT. 
  • To Emphasize: By “extreme” axis deviation — the QRS must be entirely negative in either lead I or lead aVF. Even a small positive deflection in either of these leads negates the reliability of this criterion. 
  • In Today's CASE The 12-lead tracing in Figure-1 does not satisfy this “extreme” axis deviation criterion — because the axis is normal (ie, The net QRS deflection is positive in both leads I and aVF — therefore the axis lies between the normal range of 0-to-90 degrees). 

Perhaps the most helpful criterion for assessing QRS morphology during a regular WCT rhythm — is whether QRS morphology resembles a typical conduction block? (ie, typical RBBB; typical LBBB — or bifascicular block with either RBBB/LAHB or RBBB/LPHB).
  • As emphasized in ECG Blog #204 — Focus on the 3 KEY leads ( = leads I,V1,V6) facilitates recognition of RBBB and LBBB within seconds. That said — whereas somewhat atypical QRS morphology does not necessarily indicate VT  — the finding of a completely typical QRS morphology for RBBB or LBBB may greatly increase the likelihood of a supraventricular rhythm.

In Today's CASE QRS morphology is very atypical for either RBBB or LBBB. As a result — the WCT rhythm in Figure-1 has to be assumed VT until proven otherwise!
  • ECG #1 is not consistent with LBBB — because while the QRS is all positive in lead V6, there is no predominant negativity in the anterior leads.
  • ECG #1 is not consistent with RBBB — because: i) Lead V1 lacks a triphasic morphology; — ii) Lateral leads I and V6 lack any terminal S wave; — and, especially because: iii) The QRS is almost all positive in all 6 chest leads (there is no more than a tiny initial q wave in leads V3,V4,V5).

PEARL #3:
 If ever there is concordance of QRS complexes in all 6 chest leads (ie, all 6 chest leads are either entirely positive or entirely negative) — this is virtually diagnostic of VT.
  • The sensitivity of this criterion not good — such that it will be rare that you will see positive or negative QRS concordance in all 6 chest leads during a regular WCT rhythm. That said, if ever you do — then you have essentially made the diagnosis of VT. 

  • In Today's CASEThose tiny initial q waves in leads V3,V4,V5 mean that positive concordance is not strictly present. That said — given how tiny these 3 precordial q waves are, I interpreted the almost all positive QRS in leads V1-thru-V6 as supportive of presumed VT (albeit not diagnostic).
  • The only exceptions that I'm aware of to the above-cited morphologic criteria for VT are: i) IF the rhythm is antidromic AVRT — in which case the impulse travels forward over an AP (Accessory Pathway) in a patient with WPW, therefore resulting in a regular WCT rhythm that resembles VT (For more on the various arrhythmias in patients with WPW — See ECG Blog #18); — ii) If the baseline ECG during sinus rhythm manifests a widened and very abnormal QRS morphology as a result of prior infarction, cardiomyopathy and/or preexisting bundle branch block; — and, iii) If there is some toxicity (such as hyperkalemia) which widens and distorts QRS morphology.
  • Conclusion: Assuming none of the above exceptions exist — the ECG in Figure-1 has to be presumed VT until proven otherwise

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CASE Conclusion:
Today's patient was hemodynamically stable in association with the ECG in Figure-1.
  • In view of this patient's hemodynamic stability — medical therapy was initially tried. There was no response to vagal maneuvers, nor to 3 doses of Adenosine. This was followed with several Amiodarone boluses — again with no response.
  • Some clinical history was obtained — which revealed that the patient has known coronary disease (S/P CABG — with ejection fraction of ~35%).

At this point — the cardiology team still suspected a supraventricular etiology for today's rhythm. That said, plans were made for synchronized cardioversion given lack of response to medical treatment. Before this could be done — the patient spontaneously converted to sinus rhythm.


Final Reflections on Today's CASE:
  • The ECG in Figure-1 strongly suggests VT. That said — clinicians often need to begin treatment before they are 100% certain of the rhythm diagnosis. In today's case — a trial of medical therapy was reasonable since the patient was hemodynamically stable.
  • It's important to appreciate that the odds that today's rhythm was VT immediately increased as soon as it was learned that the patient has significant underlying heart disease.
  • Given that multiple doses of antiarrhythmic medication were given — there should have been adequate time in this patient with known significant coronary disease — to obtain a prior ECG. This could have been insightful if a prior tracing were to show a preexisting conduction defect in sinus rhythm with the same QRS morphology as seen in Figure-1

  • While nothing is 100% — the sequence and choice of treatment options should be influenced by relative probability of the differential diagnosis.
  • Several doses of Adenosine were given in today's case. This drug is extremely effective for converting reentry SVT rhythms. It may also convert a certain number of patients with idiopathic VT. That said, by definition — today's patient does not have idiopathic VT, because he has known coronary disease. (See ECG Blog #197 — for review of idiopathic VT).
  • Although the effects of Adenosine wear off within 30-90 seconds, and most patients tolerate this drug surprisingly well — Adenosine is not benign (See ECG Blog #402). As a result — I would not have risked using Adenosine in today's case ( = my opinion) given virtual nil chance of it working.
  • That said — the fact that both vagal maneuvers and 3 doses of Adenosine failed to convert today's rhythm is yet more evidence in favor of VT.

  • IV Amiodarone (bolus and drip) — is an appropriate medication to try in today's case, given that this patient was hemodynamically stable. An advantage of this medication — is that it may be effective for both VT and SVT rhythms. As I lack full details from today's case — I do not know if it ultimately was the Amiodarone that converted today's WCT to sinus rhythm.
  • IF the decision is made for a trial of medical therapy — the provider should stay at the bedside, ready to immediately cardiovert if at any time during the treatment process the patient's hemodynamic status deteriorates.
  • Alternatively — a decision could have been made to sedate the patient and immediately cardiovert, given the 90+% likelihood of VT in this patient with known coronary disease.
  • While important to engage in thoughtful discussion about cases like this — ultimately, "Ya gotta be there" to know which therapeutic option(s) might be best, given the particulars of any given case. I offer the above as retrospective reflection to stimulate discussion on actions to consider.
  • My understanding is that the decision was made for today's patient to be formally evaluated by EP cardiology — with consideration given to ablation and/or insertion of an ICD (Implantable Cardioverter Defibrillator).
  •  
  • For more on evaluation and management of the regular WCT — See the ADDENDUM below.

 

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Acknowledgment: My appreciation for the anonymous submission of this case.

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Additional Relevant ECG Blog Posts to Today’s Case:

  • ECG Blog #185 — Reviews my System for Rhythm Interpretation — with use of the Ps, Qs & 3R Approach.
  • ECG Blog #210 — Reviews the Every-Other-Beat (or Every-Third-Beat) Method for estimation of fast heart rates — and discusses another case of a regular WCT rhythm. 

  • ECG Blog #422 and Blog #425 — Cases with Congenital Heart Disease in Adults.
  • ECG Blog #220 — Review of the approach to the regular WCT ( = Wide-Complex Tachycardia).
  • ECG Blog #196 — Another Case with a regular WCT.
  • ECG Blog #263 and Blog #283 — Blog #361 — and Blog #384 — More WCT Rhythms ...

  • ECG Blog #197 — Reviews the concept of Idiopathic VT, of which Fascicular VT is one of the 2 most common types. 
  • ECG Blog #346 — Reviews a case of LVOT VT (a less common idiopathic form of VT).

  • ECG Blog #204 — Reviews the ECG diagnosis of the Bundle Branch Blocks (RBBB/LBBB/IVCD). 
  • ECG Blog #203 — Reviews ECG diagnosis of Axis and the Hemiblocks. For review of QRS morphology with the Bifascicular Blocks (RBBB/LAHB; RBBB/LPHB) — See the Video Pearl in this blog post.

  • ECG Blog #211 — WHY does Aberrant Conduction occur?
  • ECG Blog #301 — Reviews a WCT that is SupraVentricular! (with LOTS on Aberrant Conduction).
  • ECG Blog #445 and Blog #361 — Another regular WCT rhythm ...

  • ECG Blog #323 — Review of Fascicular VT.
  • ECG Blog #38 and Blog #85 — Review of Fascicular VT.
  • ECG Blog #278 — Another case of a regular WCT rhythm in a younger adult.
  • ECG Blog #35 — Review of RVOT VT
  • ECG Blog #42 — Criteria to distinguish VT vs Aberration.

  • ECG Blog #133 and ECG Blog #151— for examples in which AV dissociation confirmed the diagnosis of VT.

  • Working through a case of a regular WCT Rhythm in this 80-something woman — See My Comment in the May 5, 2020 post on Dr. Smith’s ECG Blog. 
  • Another case of a regular WCT Rhythm in a 60-something woman — See My Comment at the bottom of the page in the April 15, 2020 post on Dr. Smith’s ECG Blog. 

  • Review of the Idiopathic VTs (ie, Fascicular VT; RVOT and LVOT VT) — See My Comment at the bottom of the page in the September 7, 2020 post on Dr. Smith’s ECG Blog.
  • Review of a different kind of VT (Pleomorphic VT) — See My Comment in the June 1, 2020 post on Dr. Smith’s ECG Blog.




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ADDENDUM (12/13/2024):
  • I've reproduced below from ECG Blog #361 — a number of helpful figures and my Audio Pearl on assessment of the regular WCT rhythm.
 


Figure-2 : My LIST #1 = Causes of a Regular WCT (Wide-Complex Tachycardia) of uncertain Etiology (ie, when there is no clear sign of sinus P waves).



Figure-3: Use of the "3-Simple Rules" for distinction between SVT vs VT.


Figure-4: Use of Lead V1 for assessing QRS morphology during a WCT rhythm.



ECG Media PEARL #13a (12:20 minutes Audio) — reviews “My Take” on assessing the regular WCT (Wide-Complex Tachycardia), when sinus P waves are absent — with tips for distinguishing between VT vs SVT with either preexisting BBB or aberrant conduction.




 







Friday, December 6, 2024

ECG Blog #459 — What did the Paramedics See?


I was sent the ECG shown in Figure-1 — told that the patient was a previously healthy 30-ish year old man who was seen by paramedics in the field for nausea and vomiting, which a little bit later was followed by CP (Chest Pain)
  • NOTE: This tracing does not satisfy STEMI criteria (ie, Sufficient ST elevation in at least 2 contiguous leads is lacking — which to qualify as a STEMI, would require ≥2 mm for leads V2,V3 in men and/or ≥1 mm for other leads).

QUESTION:
  • Despite not satisfying STEMI criteria — Were the paramedics correct to request activating the cath lab given ECG #1?

Figure-1: The initial ECG in today’s case.

MY Thoughts on the ECG in Figure-1:
In a patient with new CPECG #1 is a worrisome tracing. The rhythm is sinus tachycardia at ~100/minute — with normal intervals, normal axis, and no chamber enlargement. I’ve highlighted the worrisome ECG findings in Figure-2:
  • My “eye” was immediately captured by the 3 leads within the RED rectangle. As highlighted by the RED arrows — the T waves in leads V1,V2,V3 are all peaked and disproportionately taller-than-they-should-be in these anterior leads (in comparison with modest size of each QRS complex).
  • Normally the T wave in lead V1 is either negative, or no more than minimally positive without noticeable ST elevation (which is very different than what we see in Figure-2).
  • The hyperacute T waves in leads V2 and V3 — dwarf the QRS in these leads, with there being inappropriate (albeit <2 mm) ST elevation in lead V2. Ignoring the 3rd QRST complex in lead V3 (that is distorted by artifact) — the ST segment in lead V3 is inappropriately flat, if not slightly depressed.
  • In the context of obviously hyperacute T waves in leads V1,V2,V3 — neighboring chest leads V4,V5 also manifest taller and more-peaked-than-they-should-be T waves that are hyperacute (BLUE arrows in these leads).

In addition — the limb leads in Figure-2 are abnormal:
  • As is so often the case with acute proximal LAD OMI — lead aVL manifests ST elevation (RED arrow in this lead).
  • Reciprocal ST depression is seen in each of the inferior leads (BLUE arrows in leads II,III,aVF).

IMPRESSION: Regardless of whether or not the “millimeter-definition” for a STEMI is satisfied — in this patient with new CP — this initial ECG in today's case is diagnostic of acute proximal LAD OMI.
  • The cath lab should be immediately activated.

Figure-2: I've labeled the initial ECG in today's case.

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30 Seconds Later ...
  • In Figure-3 — What do we now see in lead V3 in this repeat ECG, done just 30 seconds later? 

Figure-3: Comparison between ECG #1 — and the repeat ECG done just 30 seconds later. What do we now see in lead V3?


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ANSWER: 
  • In Figure-3 — there is now T-QRS-D (Terminal QRS Distortion) — which is defined as the absence of both a J-wave and an S-wave in either lead V2, lead V3, and/or lead V4 (as discussed in ECG Blog #318).
  • The clinical significance of T-QRS-D — is that it is virtually diagnostic of acute OMI (ie, of acute coronary Occlusion).
  • In Figure-4 — Compare the QRST complex in lead V3 for both ECG #1 and ECG #2. Ignoring the 3rd QRS in lead V3 of ECG #1 (which is distorted by artifact) — Note that the S wave has been "lifted" above the baseline in ECG #2, which qualifies as T-QRS-D.
  • To Emphasize: Clearly, T-QRS-D is not needed in today's case to make the diagnosis of acute LAD OMI — since multiple findings described above more than suffice to justify immediate cath lab activation. But there are occasions in which ST-T wave findings may be far more subtle, for which recognition of T-QRS-D may prove to be the decisive diagnostic feature.

  • Additional NOTE: 3 ECG findings combine to suggest a proximal location for today’s acute LAD occlusion. These are i) Hyperacute T waves in the chest leads that begin in lead V1; — ii) ST elevation is seen in lead aVL; — and, iii) There is reciprocal ST depression in all 3 inferior leads.

Figure-4: T-QRS-D is now seen in ECG #2.


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4 Minutes after ECG #2 ...
  • What do we now see in Figure-5 — which compares the next serial tracing that was recorded 4 minutes after ECG #2?

Figure-5: Comparison between ECG #2 — and the next tracing recorded 4 minutes later. Has there been much change?

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ANSWER: 
In just 4 minutes — there have been a number of dynamic ST-T wave changes that we now see in Figure-5. These changes are best appreciated by lead-to-lead comparison, and include the following:
  • The most remarkable ST-T wave changes have been in the chest leads — which now show obvious ST elevation (most marked in leads V2,V3 — but also in neighboring leads V1 and V4).
  • Note further “lifting” of the J-point in lead V3 — resulting in more pronounced T-QRS-D compared to ECG #2.
  • ST-T wave changes in ECG #3 (compared to ECG #2) are more subtle in the limb leads — but clearly show a more acute appearance to the inferior lead reciprocal depression and to the hyperacute T wave in lead aVL.

=========================
2 Minutes after ECG #3 ...
  • What do we now see in Figure-6 — which compares the next tracing ( = ECG #4) recorded 2 minutes after ECG #3

Figure-6: Comparison between the chest leads from ECG #3 — and the next 12-lead ECG, that was recorded 2 minutes later. What do we now see?


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ANSWER: 
In Figure-6 — We now see a run of ventricular beats.
  • The first 3 beats in the limb leads from ECG #4 are sinus-conducted (with the RED arrow in lead II highlighting that there are upright sinus P waves with a constant and normal PR interval in this lead). Of note in ECG #4 — although the QRS complex “looks” wide in a number of leads for sinus-conducted beats — the QRS does not measure more than 0.10 second for these sinus-conducted beats (therefore not qualifying as wide).
  • Beginning with beat #4 in the limb leads of ECG #4, and continuing through to beat #8 — P waves are lost and the QRS widens, with a constantly changing QRS morphology. I interpreted beats #4-thru-8 as a 5-beat run of PMVT (PolyMorphic Ventricular Tachycardia) — which presumably was precipitated by acute ischemia from the ongoing extensive MI.
  • Ironically — there is less ST elevation in the chest leads of ECG #4 compared to ECG #3 — despite the fact that we now see a run of PMVT.

=========================

CASE Follow-Up:
Shortly after ECG #4 was obtained — the patient developed VFib. Prolonged resuscitation, including numerous defibrillation attempts failed to convert the patient to a sustainable sinus rhythm. Unfortunately — the patient could not be resuscitated, as persistent VFib ultimately deteriorated to asystole.
  • Presumably the patient died of cardiogenic shock from extensive anterior infarction.


Ischemic PMVT with Acute MI:
  • Recent decades have seen a dramatic decrease in the incidence of sustained VT deteriorating to VFib as the ultimate lethal event in patients with acute MI. Prompt treatment with reperfusion of the "culprit" artery is largely responsible for the improved prognosis with these patients.
  • That said — despite prompt treatment by paramedics on the scene in today's case — refractory VFib developed, and the patient could not be resuscitated.
  • Clues to this patient's ultimate demise include: i) Extensive myocardial damage from acute proximal LAD occlusion (presumably resulting in cardiogenic shock with asystole as the terminal rhythm); — and ii) The run of PMVT seen in Figure-4 — with occurrence of this arrhythmia in the setting of acute infarction portending an extremely poor prognosis (Bhar-Amato — Arrhythmia Electrophysio Rev 6(3): 134-139, 2017 — and — Viskin S et alCirculation 144(10): 823-839, 2021).


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Acknowledgment: My appreciation to Konstantin Тихонов (from Moscow, Russia) for the case and this tracing.
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Related ECG Blog Posts to Today’s Case:

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.

  • ECG Blog #193 — Reviews the basics for predicting the "culprit" artery (as well as reviewing why the term "STEMI" — should be replaced by "OMI" = an acute coronary Occlusion MI).
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  • CLICK HERE  for my new ECG Videos (on Rhythm interpretation — 12-lead interpretation with Case Studies for ECG diagnosis of acute OMI).
  • CLICK HERE  for my new ECG Podcasts (on ECG & Rhythm interpretation Errors — and — Errors in assessing for acute OMI).
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    • Recognizing hyperacute T waves — patterns of leads — an OMI (though not a STEMI) — See My Comment at the bottom of the page in the November 8, 2020 post on Dr. Smith's ECG Blog.
    • Recognizing ECG signs of Precordial Swirl (from acute OMI of LAD Septal Perforators— See My Comment at the bottom of the page in the March 22, 2024 post on Dr. Smith's ECG Blog. 

    • ECG Blog #294 — Reviews how to tell IF the "culprit" artery has reperfused.
    • ECG Blog #230 — Reviews how to compare serial ECGs.
    • ECG Blog #115 — Shows how dramatic ST-T changes can occur in as short as an 8-minute period.
    • ECG Blog #268 — Shows an example of reperfusion T waves.
    • ECG Blog #400 — Reviews the concept of "dynamic" ST-T wave changes.

    • ECG Blog #337 — A "NSTEMI" that was really an ongoing OMI of uncertain duration (presenting with inferior lead reperfusion T waves).