A 79-year old man presented with palpitations and the ECG shown in Figure-1. The patient had a history of coronary disease. He was hemodynamically stable at the time this tracing was recorded.
QUESTIONS:
- How would YOU interpret the ECG shown in Figure-1?
- How certain are you of your diagnosis?
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| Figure-1: The initial ECG in today's case — obtained from a 79-year old man with palpitations. |
MY Approach to the ECG in Figure-1:
We are told that the patient whose initial ECG is shown in Figure-1 — is hemodynamically stable. By the Ps, Qs, 3R Approach (as presented in ECG Blog #185):
- There is a regular WCT ( = Wide-Complex Tachycardia) at ~190/minute, without clear sign of atrial activity.
- Although QRS morphology superficially resembles RBBB/LAHB — QRS morphology is atypical for this supraventricular bifascicular block pattern because: i) There is no triphasic rsR' in lead V1 (instead, there is a "slurred"-R wave morphology in lead V1); ii) The initial r wave in the inferior leads is tiny; and, iii) The R wave in lead I is wider-than-expected — and the S wave in this lead is much narrower-than-expected for RBBB conduction.
- Given the above noted atypical features of QRS morphology for supraventricular conduction — I estimated an even greater statistical likelihood of VT for the tracing in Figure-1 (ie, probably ~95% likelihood of VT).
- To Emphasize: A 95% likelihood of VT is not 100% likelihood. That said — Given these odds that the rhythm in Figure-1 is VT — this rhythm should be treated as VT until proven otherwise!
- As discussed in ECG Blog #197 — Fascicular VT is one of the most common forms of Idiopathic VT when this rhythm occurs in a younger adult in the absence of underlying heart disease. However, the patient in today's case is not a younger adult — and he has known coronary disease. As a result — I would treat this rhythm as an ischemic form of VT (ie, Verapamil should probably not be used).
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Advanced POINT:
Take another LOOK at the rhythm in Figure-1. Did YOU Notice the changing QRS amplitude in a number of leads?
QUESTIONS:
- What is this rhythmic changing of QRS amplitude that is seen in several leads from today's initial tracing? (See Figure-2).
- What are potential clinical implications of this phenomenon?
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| Figure-2: I've labeled Figure-1 with RED and BLUE lines to highlight the repetitive pattern of changing QRS amplitude in several leads from the initial tracing. |
Electrical Alternans:
As discussed in detail in ECG Blog #83 — the repetitive pattern of changing QRS amplitude in a number of leads in Figure-2 is consistent with electrical alternans.
- The definition of electrical alternans — is a beat-to-beat variation in any one or more parts of the ECG recording (ie, of QRS, ST-T wave or P wave size or morphology — or of the R-R interval and/or rarely the PR or QTc interval).
- PEARL #1: Although many providers assume the cyclic variation of electrical alternans must occur every-other-beat — electrical alternans may occur with some other recurring ratio (ie, 3:1, 4:1 — or as suggested by the RED and BLUE lines in Figure-2 — in a 3:2 ratio).
- There are 3 basic types of electrical alternans phenomena, related to different pathophysiologic mechanisms (ie, repolarization alternans — conduction alternans — and/or cardiac motion alternans — See ECG Blog #83).
- PEARL #2: Although electrical alternans is not a common phenomenon — it is helpful to recognize this ECG sign. This is because in the right clinical setting, the presence of electrical alternans presence may suggest: i) A significant pericardial effusion in association with pericardial tamponade; and/or, ii) A reentry mechanism for an SVT rhythm (ie, AVNRT — and especially AVRT with an accessory pathway).
- CAVEAT: Although recognition of electrical alternans in a regular wide or narrow tachycardia without sinus P waves is highly suggestive of a reentry mechanism for the rhythm — alternans may occasionally occur in association with VT (which is precisely what we suspect in today's case!).
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The CASE Continues:
Despite the presence of electrical alternans — providers on the scene suspected that the rhythm in Figure-1 was VT. They treated the patient with a loading dose of IV Amiodarone. Shortly thereafter — the ECG in Figure-3 was recorded.
QUESTIONS:
- What effect did IV Amiodarone have on the rhythm?
- HOW does the ECG in Figure-3 (obtained after IV Amiodarone loading) help you to become more certain of your diagnosis? (HINT: The answer to this question is subtle!).
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| Figure-3: ECG #2 is the repeat tracing obtained after IV loading with Amiodarone. Does this repeat ECG help you become more certain of your rhythm diagnosis? |
AV Dissociation:
I have often reviewed criteria for assessment of a regular WCT rhythm without clear sign of atrial activity — for the purpose of distinguishing between VT vs SVT with either aberrant conduction or preexisting BBB (Bundle Branch Block) — See ECG Blog #220 (among many other posts) for details.
- I've highlighted above certain morphologic features in today's tracing that are atypical for supraventricular conduction.
- In addition to morphologic criteria — one of the most sought after criteria for distinguishing between VT vs SVT rhythms — is the presence of AV Dissociation, in which an underlying regular atrial rhythm that is independent of the wide rhythm — can be identified during the WCT. When true AV dissociation is seen — it virtually proves that the wide rhythm has to be VT (See ECG Blog #133 and Blog #151 for examples of AV dissociation).
- That said — it is not common for AV dissociation to help in the diagnosis of VT. This is because those wide tachycardias for which you need help in diagnosis are the more rapid ones (ie, it is usually much easier to identify slower forms of ventricular tachycardia). The problem is that the rapid rate of fast VT rhythms usually obscures atrial activity, that tends to be hidden within QRS complexes or the ST-T wave.
- PEARL #3: In my experience — "AV dissociation" is greatly overdiagnosed! This is important because when a clinician "thinks" they see AV dissociation — there is a tendency to take this as "proof" of VT — when in fact true AV dissociation is not really there. Today's case is an exception — as true AV dissociation is present.
MY Assessment of ECG #2:
The KEY to proving that true AV dissociation is present — is to identify a regular underlying atrial rhythm. This was not possible for ECG #1 (in Figures-1 and -2) — because the rate of the wide tachycardia in the initial tracing of today's case was very fast (ie, ~190/minute).
- The rate of the wide tachycardia is significantly slower in ECG #2 (ie, ~140/minute — as seen in Figure-3, obtained following IV loading with Amiodarone).
- As alluded to above — the independent underlying atrial rhythm associated with VT may be subtle. START by identifying 2 consecutive deflections in the long lead II rhythm strip that look like underlying P waves (the 2 WHITE arrows in Figure-4). The notch that occurs just after the QRS of beat #6 (2nd WHITE arrow) — is not seen after any other QRS (except perhaps just after the QRS of beat #10) — which strongly suggests that the deflections highlighted by the 2 WHITE arrows are "real", and represent 2 consecutive sinus P waves.
- Setting calipers to the distance between these 2 WHITE arrows suggests the P-P interval.
- It's now possible to "walk out" underlying on-time sinus P waves (RED arrows) throughout virtually the entire long lead rhythm strip.
- PINK arrows explain why P waves are not seen (ie, an on-time P wave would fall within, and be buried by the QRS complex of beats #2 and 17).
- MY Impression: IV loading with Amiodarone succeeded in slowing the ventricular rate of the regular WCT rhythm from ~190/minute (in ECG #1) — to ~140/minute (in ECG #2). Other than some change in QRS amplitude — QRS morphology is very similar in all 12 leads of both tracings. The finding of a regular underlying atrial rhythm (colored arrows in Figure-4) which is totally independent of the wide tachycardia confirms AV dissociation, which proves that the rhythm is VT.
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| Figure-4: I've labeled regularly-occurring P waves in Figure-3 with colored arrows. Beat #16 represents a "capture" beat, which manifests some fusion (ie, "C" and "F" — seen in lead V1). |
Fusion and Capture Beats:
Additional confirmation that the rhythm in today's case was VT — is forthcoming from the presence of a "capture" beat, which probably manifests an element of "fusion".
- As discussed in detail in ECG Blog #128 and Blog #129 — "capture" beats occur in association with an ongoing run of VT when one or more on-time sinus P waves occur at "just-the-right-moment" that the P wave(s) is able to briefly interrupt the run of VT beats by brief "capture" of the ventricles with a sinus-conducted beats.
- "Fusion" beats occur because of simultaneous (or near-simultaneous) occurrence of supraventricuar and ventricular impulses. As a result — the supraventricular and ventricular depolarization wavefronts meet before they are able to complete their path — and the ECG appearance of the resultant fusion beat takes on characteristics of both the supraventricular and ventricular beats.
- In Figure-4 — Note how different the QRS complex of beat #16 looks in leads V1 and V2 compared to all other QRS complexes in these 2 leads. The vertical BLUE timeline extending upward from the P wave before beat #16 occurs at "just-the-right-moment" — that it is able to conduct a different-looking RBBB complex, most probably with some degree of fusion (ie, "C" and "F" in lead V1 of Figure-4).
The CASE Continues:
Unfortunately — administration of IV Amiodarone resulted in hypotension. This necessitated immediate synchronized cardioversion. Figure-5 compares the initial regular WCT rhythm with the result of synchronized cardioversion. What happened?
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| Figure-5: Comparison of the initial regular WCT rhythm with the ECG result of synchronized cardioversion. |
CASE Conclusion:
As shown in Figure-5 — synchronized cardioversion resulted in conversion of VT to sinus rhythm. Note how very different QRS morphology looks in sinus rhythm (ie, in ECG #3) — compared to QRS morphology during the initial tracing (in ECG #1). This rules out the possibility of a preexisting conduction defect as the cause of the wide tachycardia.
- No acute ST-T wave changes are seen in the post-conversion tracing ( = ECG #3).
- Cardiac cath was performed — but did not reveal any significant lesions that might benefit from revascularization.
- An ICD (Implanted Cardioverter Defibrillator) was placed — and the patient was discharged. In follow-up — the patient has been without VT recurrence.
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Acknowledgment: My appreciation to 林柏志 (from Taiwan) 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 #185 — Reviews my System for Rhythm Interpretation, using the Ps, Qs & 3R Approach.
- ECG Blog #210 — Reviews the Every-Other-Beat Method for estimation of fast heart rates — and discusses another case of a reguar WCT Rhythm.
- ECG Blog #83 — Reviews the phenomenon of Electrical Alternans.
- ECG Blog #203 — Reviews the expected QRS morphology for the Hemiblocks and Bifascicular Blocks (ie, LAHB, LPHB; RBBB/LAHB; RBBB/LPHB).
- ECG Blog #204 — Reviews the expected QRS morphology for the Bundle Branch Blocks (ie, RBBB, LBBB, IVCD).
- ECG Blog #211 — Reviews why Aberrant Conduction occurs (with illustration of those QRS morphologic features that predict aberrant conduction).
- ECG Blog #196 — Reviews another Case of a Regular WCT Rhythm.
- ECG Blog #197 — What is Idiopathic VT? — WHY do we care? Special attention to the 2 most common forms = RVOT VT and Fascicular VT.
- ECG Blog #220 — Case Study that reviews criteria for Distinction beween VT vs SVT with preexisting BBB or aberrant conduction (including Audio Pearl MP-37 — Is the Patient Hemodynamically Stable?).
- ECG Blog #38 and Blog #85 — Review of Fascicular VT.
- ECG Blog #35 — Review of RVOT VT.
- ECG Blog #42 — Comprehensive review of criteria for distinguishing VT vs Aberration.
- ECG Blog #128 and Blog #129 — Reviews the concept of Fusion Beats.
- ECG Blog #133 and Blog #151 — Reviews use of AV Dissociation to Diagnose VT.
Dear Mr Grauer. Why not IV Procainamide in VT + hearth disease suspected ?
ReplyDeletethanks
I did not say that Amiodarone was the drug of choice — only that "it was given". You could have tried IV Procainamide instead. THANKS for your comment! — :)
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