The ECG shown in Figure-1 — was obtained from an older man with “CP” (Chest Pain) for the past 2 days. BP = 80/50 mm/Hg. Adenosine 6 mg IV was tried without response.
QUESTIONS:
- How would YOU interpret this ECG?
- Your thoughts regarding optimal management?
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| Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio). |
MY Initial Thoughts on Today's ECG:
The ECG in Figure-1 — shows what I initially thought was a regular WCT (Wide-Complex Tachycardia) at ~180/minute, without clear sign of of atrial activity.
- My initial thoughts were that statistically — knowing nothing more than that this older man is presenting in a WCT rhythm that looks regular, and that lacks clear sign of atrial activity — the chance that the rhythm in Figure-1 is VT (Ventricular Tachycardia) is at least 80%.
- Looking closer at the ECG in Figure-1 — QRS morphology does not resemble any known form of conduction defect because: i) Although the all positive QRS complex in lead V1 could represent some form of RBBB (Right Bundle Branch Block) — the amorphous shape of this V1 complex (ie, without any hint of the expected triphasic configuration that is typical for RBBB conduction) — this amorphous shape of the QRS in lead V1 favors VT (within the BLUE rectangle in Figure-2); — ii) The almost all negative QRS in lead I suggests a marked right axis much more consistent with VT (within the RED rectangle in Figure-2); — iii) Abrupt transition from the predominant positivity seen from lead-V1-until-lead-V5 — to sudden development of predominant negativity in lead V6 strongly favors VT (within the other BLUE rectangle); — and, iv) The initial deflection of the QRS in multiple leads is slow (especially for the overly wide small initial r waves in leads I and V6) — with slow initial depolarization of the QRS in multiple leads suggesting origin in the ventricles (ie, away from the conduction system — therefore most likely to be VT).
- Putting this All Together (ie, considering older age of this patient and complete lack of resemblance to any known form of conduction defect) — I now estimated statistical likelihood of VT at over 90%.
- Given 90+% likelihood that the rhythm in Figure-2 is VT — We need to assume VT until proven otherwise (and treat the patient accordingly!).
- As noted above — 1 dose of Adenosine was tried without success. That said — this would not be a patient for whom I would try Adenosine because: i) Although Adenosine may successfully convert some forms of idiopathic VT (ie, VT in a patient who does not have underlying heart disease — as discussed in ECG Blog #197) — Adenosine is not effective for treating ischemic VT — which this older patient with markedly abnormal QRS morphology almost certainly has; ii) Adenosine is not a completely benign medication (See ECG Blog #402 for pros and cons of using Adenosine); and, iii) This patient is symptomatic. He also appears to be hemodynamically unstable (ie, The patient has had CP for 2 days — the rate of the initial rhythm in Figure-2 is rapid — and the patient's BP at the time this rhythm was recorded = 80/50 mm Hg.).
- Instead — immediate cardioversion is indicated! Given that this patient is symptomatic (as well as hemodynamically unstable) — it no longer matters whether this rhythm is of supraventricular etiology or VT because regardless — immediate cardioversion is clearly indicated.
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PEARL #1: I will emphasize that although it may seem that my above step-by-step discussion of how I assessed ECG #1 is complex — the total time it took me to arrive at the greater than 90% likelihood of VT was less than 10 seconds. With practice — this becomes easy to do. But for those wanting a "simpler" approach" — Consider the following (which I review below in my ADDENDUM):
- This patient is in a wide, "ugly-looking" and seemingly regular tachycardia without P waves.
- As per Figures-5, -6, and -7 below in the ADDENDUM — there is marked right axis — the QRS is almost all negative in lead V6 — and the amorphous upright QRS in lead V1 does not look anything like a typical RBBB pattern, which characteristically manifests a triphasic (rSR' complex) in lead V1.
- And — the patient is older — has been having CP — and is hypotensive (80/50 mm Hg). Therefore, this rhythm has to be assumed VT until proven otherwise — and — in need of immediate cardioversion (regardless of what the rhythm turns out to be).
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| Figure-2: I've labeled the KEY leads that "caught" my eye (See text). |
CONFESSION: I initially thought the WCT rhythm in Figure-2 was regular. It turns out that today's initial rhythm is not regular (This is perhaps best seen in lead V3 — which suggests an almost alternating regularity between an ever-so-slightly longer vs a slightly shorter R-R interval).
- As opposed to polymorphic VT that by definition is irregularly irregular — monomorphic VT is usually a fairly (if not completely) regular rhythm (See ECG Blog #231 for the various forms of VT).
- Most of the time when a monomorphic WCT rhythm is not regular — the rhythm will be of supraventricular etiology with either preexisting bundle branch block or a rate-related form of aberrant conduction.
- PEARL #2: The above said — there are 2 common exceptions to the generality that monomorphic VT is usually a regular rhythm. These exceptions are IF: i) There is a "warm-up" period of slower and gradually accelerating ventricular beats before the VT becomes regularized; — or, ii) There is a "cool-down" period in which after the regular run of VT, the rate of the VT progressively slows until the VT run finally resolves (these concepts thoroughly illustrated and explained in ECG Blog #417).
- PEARL #3: Aside from a "warm-up" and/or "cool-down" period just before or just after a run of regular monomorphic VT — On occasion, monomorphic VT may simply manifest a variable R-R interval (Oreto et al — Am Heart J 124(6):1506-11, 1992). Potential reasons for R-R interval variability with monomorphic VT include: i) The presence of 2 VT reentry circuits that share the same exit pathway; or, ii) Variation in conduction velocity over the reentry circuit.
- Bottom Line — Most of the time (but not always) — monomorphic VT will be regular. But if a run of wide beats without P waves is not regular, this finding alone does not necessarily rule out the possibility of VT.
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The CASE Continues:
Following 1 dose of Adenosine — synchronized cardioversion was applied. The result is shown in Figure-3.
QUESTION:
- How would YOU interpret the post-cardioversion ECG?
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| Figure-3: The repeat ECG recorded after synchronized cardioversion of the rhythm in Figure-2. (To improve visualization — I've digitized the original ECG using PMcardio). |
The Post-Cardioversion ECG in Figure-3:
Although the presence of much artifact in Figure-3 makes assessment more difficult — this post-cardioversion tracing is interpretable:
- The "good news" — is that sinus rhythm has been restored, as noted by the presence of upright P waves with fixed and normal PR interval in lead II.
- All intervals (PR-QRS-QTc) and the frontal plane axis are normal. There is no chamber enlargement.
- There is low voltage in all 6 of the limb leads (More on this momentarily).
- There is a Q wave in lead III.
- R wave progression is not normal. Instead — the R wave is already predominant (R>S wave) in lead V1. As reviewed in ECG Blog #81 — the finding of a Tall R Wave in Lead V1 should prompt consideration of 6 potential entities (More on the likely cause of the Tall R in V1 in today's case momentarily).
Regarding ST-T Wave Changes (See Figure-4):
- Although there is much artifact-related variation in ST-T wave morphology — all 3 of the inferior leads (within the RED rectangles in leads II,III,aVF) show hyperacute ST elevation, in which T waves in these leads dwarf the tiny QRS complexes.
- That this inferior lead ST elevation is "real" and acute — is confirmed by the mirror-image opposite picture of hypervoluminous T wave inversion in high-lateral leads I and aVL (as per the BLUE arrows in these leads).
- My "eye" was immediately captured by the marked ST depression in leads V1,V2 (within the RED rectangle) — with these first 2 chest leads showing disproportionately tall (predominant) R waves.
- Finally — lateral chest lead V6 shows coved ST elevation (within the BLUE rectangle in this lead).
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Putting It All Together:
Keeping in mind that today's patient was just cardioverted out of sustained VT — We need to contemplate WHY might this patient have been in VT?
- PEARL #4: As alluded to above — the finding of a Tall R Wave in Lead V1 should prompt consideration of the following LIST of the 6 most common Causes: i) WPW; ii) RBBB; iii) RVH; iv) Posterior MI; v) HCM (Hypertrophic CardioMyopathy); and, vi) Normal variant — as a diagnosis of exclusion (See ECG Blog #81 for more on this issue).
- Working through the above LIST — the narrow QRS complex rules out WPW and RBBB — there are no findings suggestive of chamber enlargement — an Echo would rule out HCM — and ECG #2 is clearly not a normal variant. This leaves posterior MI as the most likely cause of the Tall R in Lead V1 of ECG #2.
- PEARL #5: A LIST of causes of low voltage is reviewed in ECG Blog #272 — of which reduced cardiac output as a result of myocardial "stunning" in association with a large acute MI is the important consideration in today's case.
- BOTTOM Line: The ECG in Figure-4 shows an extensive infero-postero-lateral STEMI. The early transition in the chest leads (ie, with predominant R wave already in lead V1) — is the mirror-image equivalent of a Q wave, and is consistent with posterior infarction. If the dramatically reduced limb lead voltage is a new finding — it most likely represents reduced cardiac output from extensive infarction. Prompt cath is clearly indicated. Unfortunately — further follow-up in today's case is not available.
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| Figure-4: I've labeled KEY findings in the post-conversion ECG. |
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Acknowledgment: My appreciation to Rajeesh R Pillai (from Kollam, India) for the case and these tracings.
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ADDENDUM (8/23/2024):
- I've reproduced below from ECG Blog #196 — a number of helpful figures and my Audio Pearl on assessment of the regular WCT rhythm.
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| Figure-5 : 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). |
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| Figure-6: Use of the "3-Simple Rules" for distinction between SVT vs VT. |
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| Figure-7: 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 to distinguish between VT vs SVT with either preexisting BBB or aberrant conduction.
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Additional Relevant ECG Blog Posts to Today’s Case:
- ECG Blog #185 — Reviews my System for Rhythm Interpretation, using the Ps, Qs & 3R Approach.
- ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
- 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 #220 — Review of the approach to the regular WCT ( = Wide-Complex Tachycardia).
- ECG Blog #196 — Another Case with a regular WCT rhythm.
- ECG Blog #263 and Blog #283 — and Blog #361 — 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, the Hemiblocks — and the Bifascicular Blocks.
- ECG Blog #211 — WHY does Aberrant Conduction occur?
- ECG Blog #42 — Review of criteria to distinguish between VT vs Aberration.
- 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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- ECG Blog #193 — Reviews the basics for predicting the "culprit" artery (as well as reviewing why the term "STEMI" — should be replaced by "OMI" = Occlusion-based MI).
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- CLICK HERE — for my 6 new ECG Videos (on Rhythm interpretation — 12-lead interpretation with Case Studies for ECG diagnosis of acute OMI).
- CLICK HERE — for my 2 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.
- ECG Blog #351 — Blog #285 — Blog 246 — Blog #80 — for examples of acute posterior OMI.
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