ECG Blog #445 — VT or LBBB?

The ECG in Figure-1 was obtained from an 80-year old woman — who presented to the ED (Emergency Department) — with a several hour history of "palpitations" and CP (Chest Pain). She was hemodynamically stable at the time ECG #1 was recorded.

QUESTIONS:

The ECG in Figure-1 was seen by a number of physicians — the majority of whom thought the rhythm was some form of SVT (SupraVentricular Tachycardia) with LBBB (Left Bundle Branch Block) aberration.

• Do YOU Agree with the interpretation of the majority of physicians who said that the rhythm in ECG #1 was SVT with LBBB aberration?
• How certain are you of your answer?
• 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 Today's CASE:

The ECG in Figure-1 — shows a regular WCT (Wide-Complex Tachycardia) rhythm at a rate just under 150/minute, with no clear sign of sinus P waves.

• Although QRS morphology — is consistent with LBBB conduction in the limb leads of Figure-1 (ie, monophasic, all-upright R wave in lateral leads I and aVL) — QRS morphology is not as expected in the chest leads, because we never see a predominant R wave in lateral lead V6. Instead — a similar rS morphology is seen in all 6 chest leads, in which the initial upright deflection (r wave) is surprisingly wide already by lead V4. 
• NOTE: The deep S waves in leads V1,V2 in ECG #1 suggest the likelihood of underlying LVH. One reason why LBBB conduction in a patient with marked LVH may not evolve to a predominant (if not all positive) R wave by lead V6 — is that leftward and posterior forces of marked LVH with LBBB may delay transition to predominant positivity in the chest leads until more posteriorly oriented chest leads, such as V7 or V8.

MY Impression of ECG #1: As emphasized often in this ECG Blog (See today's ADDENDUM below) — statistical odds that a regular WCT rhythm without clear sign of sinus P waves will turn out to be VT begin at 80% likelihood. 

• The older age of today's patient and somewhat atypical QRS morphology for LBBB conduction — move this statistical likelihood up to ~90%.
• While 90% is not equal to 100% — the message regarding the ECG in Figure-1 is clear: Assume VT until proven otherwise! Treat the patient accordingly.
• PEARL #1: Stated a different way — Rather than having to prove that ECG #1 is VT — We need to prove that this rhythm is not VT. Until we do — Assume VT until proven otherwise (and treat the patient accordingly).

Additional Points regarding ECG #1: 

Is there truly no sign of atrial activity in this initial tracing?

• Although there are small-amplitude undulations in the baseline in today's initial tracing — these undulations are present in all 6 limb leads, whereas "true" atrial activity will generally appear more prominently in some leads compared to others (and true atrial activity should not persist throughout the entire baseline — as we see in leads I, aVR and aVL).
• The undulations that we see in the limb leads of Figure-1 — are not consistent in shape, as I would expect them to be if this truly represented atrial activity.
• Finally — although the rate of almost 150/minute in ECG #1 should suggest the possibility of underlying AFlutter with 2:1 AV conduction — 2:1 atrial activity does not work out! (See Figure-2):

Figure-2: I've added RED lines to Figure-1 to show that 2:1 atrial activity does not work out! (See text).

PEARL #2: The way in which I look for flutter waves is to carefully set my calipers at precisely HALF the R-R interval of the tachycardia (since IF the rhythm is AFlutter — then the atrial rate should be twice the ventricular rate if there is 2:1 AV conduction). 

• My "GO TO" leads that I favor for identifying less obvious atrial activity are leads II, III, aVF; aVR; and V1. IF none of these 5 leads suggest atrial activity — then I’ll survey the remaining 7 leads. That said, AFlutter will almost always provide ready evidence of atrial activity in one or more of my “Go To” leads.
• In Figure-2 — I've placed RED lines above those points in leads II, III and aVR that I thought might possibly indicate underlying atrial activity. But notice that the distance between these RED lines is not constant, as it would need to be IF there was underlying flutter with a precisely regular P-P interval. Therefore — the rhythm in ECG #1 is not AFlutter! (See ECG Blog #287 — if interested in more on ECG recognition of AFlutter).

How Would You Treat this Patient?

As is often emphasized in this ECG Blog — "Sometimes ya just gotta be there!" That said — I'll offer the following thoughts:

• The rhythm in ECG #1 is a regular WCT rhythm at ~150/minute, without clear sign of sinus P waves. As noted above, given the older age of this patient and the somewhat atypical QRS morphology for lbbb conduction — I would estimate statistical likelihood that the rhythm is VT at ~90%. Therefore — Assume VT, and treat accordingly!
• We are told that this patient was "hemodynamically stable" — but, given that this older woman is complaining of chest pain — I would not want to leave this patient in this rhythm (that is probably VT) for an extended period of time before moving to synchronized cardioversion.
• I would not try Adenosine — because the rhythm is most likely ischemic VT, and: i) Although Adenosine may convert some forms of idiopathic VT (ie, in which the patient is a younger adult without underlying heart disease) — Adenosine is unlikely to convert ischemic VT; and, ii) Adenosine is not completely benign (For more on the pros and cons of Adenosine — See the ADDENDUM in ECG Blog #393).
• Depending on your level of comfort in this particular case (ie, "Sometimes ya just gotta be there!" ) — IV Amiodarone might be tried, with the provider being ready to cardiovert at the 1st sign of decompensation.

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The CASE Continues:

The patient spontaneously converted to the repeat ECG that is shown below in Figure-3. This spontaneous conversion occurred before any antiarrhythmic medication was given.

• The patient was placed on a "Rule-Out MI" protocol — but the CP she was having disappeared almost immediately after she spontaneously converted to the rhythm shown in ECG #2.
• IV Amiodarone was started in the hope of preventing recurrence of the WCT that the patient presented with.

QUESTIONS:

• How would YOU interpret the repeat ECG shown in Figure-3?
• Is the rhythm in ECG #2 now sinus?
• Does the ECG in Figure-3 alter your opinion in any way as to what the initial rhythm in Figure-1 was?
• Is the patient having an acute MI?

Figure-3: I have put together the initial ECG — with the repeat ECG obtained after spontaneous conversion. (To improve visualization — I've digitized the original ECG using PMcardio).

ANSWERS:

Looking at ECG #2 — the rate of the rhythm has slowed and the QRS complex has narrowed compared to what it was in ECG #1. That said — Did YOU Notice that no upright P wave is present in lead II of ECG #2? (BLUE arrow in lead II of Figure-4).

• PEARL #3: The lack of a clearly upright P wave in lead II in the presence of upright P waves in leads I and aVL (RED arrow in Figure-4) — is most often due to 1 of 2 causes: i) A low atrial rhythm; — or, ii) A "technical misadventure". 
• The most common type of lead reversal is mixup of the LA (Left Arm) and RA (Right Arm) electrodes. This is not present in ECG #2 because the P wave and QRS complex are both positive in lead I, and the QRS is negative in lead aVR (See ECG Blog #264 — for more on LA-RA reversal).
• 
  
• The 2nd most common type of lead reversal in my experience, is mixup of the LA-LL (Left Arm - Left Leg) electrodes (See ECG Blog #375 — for more on LA-LL reversal).
• The "good news" — is that regardless of whether there is a low atrial rhythm in ECG #2 — or, whether the rhythm is sinus, but with LA-LL lead reversal — the patient is no longer in a WCT. Instead — the patient has spontaneously converted to a supraventricular rhythm at a much more controlled heart rate (and without suggestion of acute ST-T wave changes in this repeat ECG).

Figure-4: I've added colored arrows to ECG #4 to highlight the lack of an upright P wave in lead II of the post-conversion tracing.

IF there was LA-LL Reversal — What would ECG #2 Look Like?

Lead placement was not checked after recording the post-conversion tracing — and I was not provided with any more tracings from this case. As a result — We'll never know if the post-conversion tracing represents a low atrial rhythm or sinus rhythm with LA-LL reversal.

• As discussed and illustrated in ECG Blog #375 — LA-LL lead reversal will result in the ECG changes shown in Figure-5.

Figure-5: The effect of LA-LL reversal on an ECG.

Correcting for LA-LL Reversal:

We can correct for the predicted changes of LA-LL lead reversal. Doing so allows us to predict what the post-conversion ECG would have looked like if the reason for the lack of an upright P wave in lead II of ECG #2 was LA-LL reversal.

• I show in ECG #2a (Bottom tracing in Figure-5) — what the post-conversion ECG would have looked like if the reason for lack of an upright P wave in lead II was LA-LL reversal.
• 
  
• Note in ECG #2a — that an upright sinus P wave is now seen in lead II (as would be expected if the post-conversion rhythm is sinus).

So — Assuming that there was LA-LL lead reversal in ECG #2 — that we have now "corrected for" in ECG #2a — I show in Figure-6 what comparison of today's initial tracing ( = ECG #1, in which there was the regular WCT rhythm) would look like — compared to the post-conversion tracing corrected for presumed LA-LL lead reversal.

Figure-6: What ECG #2 would have looked like if the reason for the lack of an upright P wave in lead II was LA-LL reversal.

PEARL #4: The reason for me highlighting the likelihood of LA-LL reversal in the post-conversion tracing of today's case — is that we will often not be certain as to the etiology of a regular WCT at the time that we need to begin treatment.

• In such cases — it may only be after return to sinus rhythm, that by comparison of the WCT with the post-conversion tracing, can we retrospectively determine whether the WCT was VT (See ECG Blog #422 and ECG Blog #263).
• In today's case — the corrected post-conversion tracing ( = ECG #2a) shows sinus rhythm and no preexisting bundle branch block. While this does not rule out the possibility of rate-related aberrant conduction — the unusual QRS morphology that I described above still suggests (in my opinion) — a ~90% probability that the regular WCT in ECG #1 was VT.

CASE Conclusion:

Given the rapid rate of the regular WCT rhythm in today's case in this symptomatic older woman — additional evaluation to assist in optimal management was indicated.

• Echo was done — and was found to be unremarkable (with normal LV function). 
• Troponin — was negative for acute infarction. 
• Cardiac cath — showed no significant coronary disease.
• The patient was offered EP (ElectroPhysiologic) study — but she refused, since she "was feeling well". She was discharged from the hospital on Amiodarone.

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Acknowledgment: My appreciation to Jean Max Figueiredo (from Nova Iguaçu, Brazil) for the case and this tracing.

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ADDENDUM (8/29/2024):

• I've reproduced below from ECG Blog #196 — a number of helpful figures and my Audio Pearl on assessment of the regular WCT rhythm.

Figure-7 : 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-8: Use of the "3-Simple Rules" for distinction between SVT vs VT.

Figure-9: 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.

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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 #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).
• e Regular WCT (Wide-Complex Tachycardia).
• ECG Blog #196 — Reviews another Case with a regular WCT rhythm.
• 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 #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.

 

ECG Blog #444 — CP and Aberrant SVT?

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?

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%.

BOTTOM Line: Although I would not yet be 100% of the etiology of today’s initial rhythm — what is certain, is that immediate treatment is needed!

• 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).

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?

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).

Regarding Q-R-S-T Changes: 

• 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).

In the Chest 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.

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.

 

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).

Figure-6: Use of the "3-Simple Rules" for distinction between SVT vs VT.

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.

ECG Blog #443 — A 40s Man with CP and Dyspnea

The ECG in Figure-1 was obtained from a man in his 40s — who presented to the ED (Emergency Department) because of CP (Chest Pain) and shortness of breath.

QUESTIONS:

• In view of the above history — How would YOU interpret the ECG in Figure-1?
• Based on the history and the patient's initial ECG — the cath lab was activated. Do you agree?

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

MY Thoughts on this CASE:

Not being there — I am unaware of physical exam parameters (blood pressure, respiratory rate; oxygen saturation; heart and lung auscultation, etc.). What we can comment on, given the brief history of new CP and dyspnea — is the initial ECG shown in Figure-1. I see the following:

• There is sinus tachycardia (upright P wave with fixed PR interval in lead II) — at the rapid rate of ~130/minute.
• Regarding intervals — the PR interval is normal — the QRS is of normal duration. Given the rapid rate — it is hard to say much about the QTc.
• There is RAD (Right Axis Deviation) — in that that QRS is slightly more negative than positive in lead I ( = estimated frontal plane axis about +100 degrees).

Regarding chamber enlargement — LVH is not present. Although frank criteria for RVH (Right Ventricular Hypertrophy) are not present — there are a number of ECG findings consistent (if not suggestive) of acute RV "Strain" (See Figure-2). 

• PEARL #1: Before going further — We need to consider the possibility of acute PE (Pulmonary Embolism)! Acute PE remains one of the most commonly overlooked diagnoses. As per links that I provide below — IF the diagnosis of acute PE is not thought of, this entity will be missed! (See ECG Blog #435 — ECG Blog #313 — as well as My Comment at the bottom of the page in the June 17, 2024 post in Dr. Smith's ECG Blog).

I review the ECG diagnosis of acute RV "strain" and acute PE in the ADDENDUM below (See Figures-7, -8, -9). For now — Let's continue with ECG signs consistent with and suggestive of acute RV "Strain".

• Sinus Tachycardia and RAD — as already noted above.
• PEARL #2: In the absence of associated heart failure (cardiogenic shock) — sinus tachycardia is not a common finding in acute MI. As a result — the finding of sinus tachycardia in today's patient, who presents with both CP and shortness of breath (especially to as rapid a heart rate as the ~130/minute seen here) — should immediately prompt consideration of something other than acute coronary occlusion.
• 
  
• Although criteria for RAA (Right Atrial Abnormality) are not strictly satisfied (P wave amplitude in lead II does not attain 2.5 mm in amplitude) — the P wave in lead II is more peaked and pointed than it usually is (within the RED oval in Figure-2). In the context of a suggestive clinical history and other ECG signs of acute RV "strain" — I interpret more-than-expected inferior lead P wave peaking as suggestive of RAA, therefore another supportive (albeit subtle) indication of RV "strain" (See ECG Blog #75 — for more regarding ECG criteria for RAA).
• 
  
• S1Q3T3 — Whereas the diagnostic value of this pattern is limited when seen as an isolated finding — a definite S1Q3T3 pattern (as seen in Figure-2) — is very helpful in today's case, given association with other ECG evidence pointing to the possibility of acute PE. 
• 
  
• PEARL #3: ST-T wave findings of acute RV "Strain" — are most often seen in the form of anterior T wave inversion (and/or anterior ST depression). The other ECG area to look for RV "strain" — is in the inferior leads, though it is less common in my experience to only see RV "strain" inferiorly without also seeing ST-T wave changes anteriorly.
• As a result — I admittedly, was initially deterred from the diagnosis of acute PE because of the lack of anterior T wave inversion in ECG #1. That said — ST-T wave changes of acute RV "strain" are present in each of the inferior leads (BLUE arrows in leads II,III,aVF in Figure-2).
• 
  
• PEARL #4: Instead of anterior lead T wave inversion — there is some ST elevation in leads V1 and V2, with ST segment straightening in lead V3. On occasion — such anterior lead ST elevation (instead of T wave inversion) can be seen with acute PE (Zhan et al — Ann Noninvasive Electrocardiol 19(6):543-551, 2014 — and — Omar HR — Eur Heart J: Acute Cardiovascu Care (5(8): 579-586, 2016). 
• Right-sided leads such as leads III, aVR and V1 — face the anterior region of the RV. If the RV is enlarged — then leads V2 and V3 may also face the anterior region of the RV — and — if there is severe transmural ichemia of the RV, any of these leads may show ST elevation (as is seen in leads aVR and V1,V2 in Figure-2).

PEARL #5: The KEY for being able to suspect acute PE from the ECG — is when you see a constellation of ECG findings potentially consistent with this diagnosis (as listed below in the ADDENDUM in Figure-7) — in a patient with a suggestive history. 

• Today’s patient presented to the ED not only with chest pain — but also with shortness of breath, therefore with a history potentially consistent with the diagnosis. 
• Easily attainable bedside findings that further support the diagnosis of acute PE include a low oxygen saturation — and — an increased respiratory rate. To emphasize — Count the respiratory rate yourself! (Reading the respiratory rate off of nursing notes is not necessarily accurate in my experience — so spending 15-20 seconds simply looking at the patient breathing and counting breaths is well worth this short amount of your time).
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• ECG Signs (in addition to those already mentioned above) — that are consistent with acute PE in today’s tracing (as per the Table in Figure-7) include: i) Poor R wave progression, with persistence of S waves through to lead V6; and, ii) The rSr' morphology seen in lead V1, which in association with the narrow terminal s waves in lateral leads I and V6 — is consistent with a IRBBB proxy (See labeled Figure-2 below).

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

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QUESTION: 

Although today’s initial ECG is potentially consistent with acute PE — I would not be 100% convinced of this diagnosis from the tracing shown in Figure-2 alone.

• What could be done at the bedside within no more than a few minutes to verify the diagnosis of acute PE?

ANSWER:

• A POC (Point-Of-Care) ECHO — will sometimes be diagnostic of acute PE. When it is — this may greatly expedite clinical decision-making for anticoagulation and/or thrombolysis.
• The sensitivity of POC Echo is not perfect. That said — the specificity of Echo for acute PE can be excellent IF certain echocardiographic findings are present. This is especially true for larger, more hemodynamically significant PEs — with prognostic insight provided depending on the degree of impairment of RV function (On and Park — Korean J Intern Med: 38(4);456-470, 2023 and Hritani et al — Cleveland Clin J Med 85(110: 826-828, 2018).

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The ECHO on Today's Patient:

In Figure-3 — I've labeled the 4-chamber view from the Echo on today's patient. In Figure-4 — I've included the video recording of this view. What do you think?

Figure-3: Still picture of the Echo 4-chamber view.

Figure-4: Video recording of this 4-chamber view. I include a slow-motion section to facilitate recognition of the diagnostic Echo sign described below.

Figures-3 and -4 on Today's Echo:

For orientation — the 4 chambers are shown in Figure-3:

• The RV (Right Ventricle) is clearly dilated, and appears to be even larger than the LV. As a result of RV overload — the IVS (InterVentricular Septum) is shifted toward the left side of the heart. In a patient with a suggestive history and ECG findings consistent with acute PE — seeing this degree of RV dilation on Echo strong favors acute PE as the diagnosis. That said — seeing RV dilation on Echo does not distinguish between acute vs chronic causes of RV "strain".
• 
  
• PEARL #6: In contrast to the finding of RV dilation (that could be a longstanding condition) — the McConnell Sign is a dynamic echocardiographic finding that is specific for conditions causing acute RV "strain", such as acute PE. 
• 
  
• A McConnell Sign is said to be present when 2 echocardiographic findings are seen: i) There is RV free wall akinesis (seen as per the YELLOW arrow in Figure-3 — as an outward movement of the RV free wall as a result of increased pressure in the dilated RV chamber); and, ii) The RV apex manifests hypercontractility, as a result of being "tethered" to the LV (RED arrow moving inward). This sign is positive in the video recording shown in Figure-4 — in which the RV apex has been described as "a trampoline bouncing up and down while the rest of the RV remains still."
• 
  
• References on Echo for PE Diagnosis: Oh and Park - Korean J Intern Med 38(4):456-470, 2023 — and — Hritani et al - Cleveland Clin J Med 85(11):826-828, 2018 — and — IF you want an excellent 5-minute video review on recognition of the McConnell Sign on Echo — WATCH_this_VIDEO by Dr. Christopher Voscopoulos.

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Diagnostic CTPA on Today's Patient:

Final confirmation of acute PE in today's case was obtained by CTPA ( = Pulmonary Angiography in Figure-5). 

• Excellent review of diagnostic testing for acute PE (Moore et al — Cardiovasc Diagn Ther 8(3):225-243, 2018).
• For a 10-minute video review on reading Pulmonary CT Scan — WATCH_this_VIDEO by Dr. Jake Gibbons.

Figure-5: CTPA view in today's case — showing large clot burden in the right and left main pulmonary arteries.

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CASE Follow-Up:

The "good news" in today's case — is that the patient received thrombolytics, and ultimately did well. That said — the diagnosis of acute PE was delayed for a number of hours, because providers were initially more concerned about an acute MI. As a result — diagnostic Echo was not performed until after cardiac cath was found to be normal.

• PEARL #7: Echo at the bedside is a fast test that takes only minutes! In today's case — the Echo could have been done while waiting for cath facilties to get ready. Had this been done — the dramatic RV dilation and positive McConnell Sign seen in Figures-3 and -4 — would have allowed immediate confirmation of acute PE that could have avoided any need for cardiac cath, thereby expediting initiation of thrombolytic therapy.

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Repeat ECG After Thrombolytic Therapy:

I found it of interest to compare the follow-up ECG obtained after successful thrombolytic therapy (Figure-6).

• Sinus tachycardia has resolved.
• Right axis deviation in ECG #2 is much less (predominant positivity of the R wave in lead I has returned).
• RV "strain" is no longer evident (resolution of ST depression in the inferior leads).
• Right-sided ST elevation that had been present in leads aVR, V1,V2 of ECG #1 — is no longer seen in the repeat tracing.
• S waves no longer persist through to lead V6.

Figure-6: Comparison between the initial ECG in today's case — with the repeat ECG obtained following thrombolytic therapy.

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Acknowledgment: My appreciation to Magnus Nossen (from Fredrikstad, Norway) for the case and these tracings.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #313 and ECG Blog #435 — Review cases on the ECG diagnosis of acute PE.
• ECG Blog #233 — Reviews a case of Acute PE (with discussion of ECG criteria for this diagnosis).
• ECG Blog #119 — Reviews a case of Acute PE (and ECG criteria for this diagnosis).
• My Comment at the bottom of the page in the June 17, 2024 post in Dr. Smith's ECG Blog (regarding a case similar to today's ECG Blog).
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• ECG Blog #234 — Reviews ECG criteria for the diagnosis of RVH and RV "Strain".
• ECG Blog #77 — Another review of ECG criteria for the diagnosis of RVH and RV “Strain”. 

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ADDENDUM #1 (8/16/2024): 

I've included below some review material regarding the ECG diagnosis of acute PE (Pulmonary Embolus) and RV "strain".

Figure-7: ECG Findings associated with acute PE (from ECG Blog #435).

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PEARL #8: The "Note" under the S1Q3T3 finding in Figure-7 — refers to data from Kosuge et al (Am J Cardiol 99(6): 817-821, 2007 — and the March 4, 2023 post in Dr. Smith's ECG Blog) — that state that when there is T wave inversion in the chest leads, if T waves are also inverted in leads III and V1 — then acute PE is far more likely than acute coronary disease (See the Addendum ECG in Figure-10 below).

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Figure-8: Summary of KEY findings in the ECG diagnosis of acute PE (from my ECG-2014-ePub).

Figure-9: Summary (Continued) of KEY findings in the ECG diagnosis of acute PE.

 

ADDENDUM #2 (8/17/2024): 

My thanks to Konstantin Tikhonov (from Moscow, Russia) — who sent me the following illustrative ECG and case the very next day after I posted this ECG Blog #443.

• The patient whose ECG is shown in Figure-10 — had progressively increasing dyspnea over a 10 day period.
• Considering the ECG findings shown above in Figure-7 (with attention to PEARL #8) — How many ECG findings of acute PE can you identify?

Figure-10: Addendum ECG (My thanks to Konstantin Tikhonov for sending me this case). 

ANSWER:

The ECG in Figure-10 shows the following findings in favor of acute PE:

• Sinus tachycardia.
• S1Q3T3.
• Persistent precordial S waves (through to lead V6).
• Acute RV "strain" (here in the form of deep, symmetric chest lead T wave inversion that is maximal in leads V2,V3,V4 — and as per PEARL #8, shows T wave inversion in lead V1 and lead III, as well as in lead aVF).

Follow-Up: Pulmonary CT scan confirmed an acute submassive PE.