Wednesday, August 10, 2022

ECG Blog #325 — A 50s Woman with Chest Pain


HOW would you interpret the ECG in Figure-1 — IF told that this middle-aged woman was having chest discomfort?
  • Should you activate the cath lab?

Figure-1: ECG obtained from a middle-aged woman with chest discomfort.


MY Thoughts on the ECG in Figure-1:
The rhythm is sinus at ~90/minute. All intervals (PR, QRS, QTc) and the frontal plane axis are normal. There is no chamber enlargement. 

Regarding Q-R-S-T Changes:

  • There are no Q waves.
  • R wave progression is normal. Transition (where the R wave becomes taller than the S wave is deep) — occurs normally between leads V3-to-V4. 


Regarding ST-T Wave Changes:
There is subtle-but-real ST elevation in lead aVL. The reason this is difficult to recognize — is that QRS amplitude in lead aVL is tiny. But the shape of the ST segment is unmistakeably coved and elevated above the baseline (Figure-2).

  • The other lead showing ST elevation in Figure-1 is lead aVR.
  • Otherwise — there is subtle-but-real ST depression in no less than 8/12 leads (ie, leads I,II,III,aVF; and in V3-thru-V6)
  • The amount of ST depression appears to be greatest in the inferior leads (II,III,aVF) — which clearly show straightening of the ST segment, as well as depression.

  • NOTE: Although there is no ST elevation in lead V2 — there is normally slight ST elevation in this lead. Therefore — the fact that the J-point is not at all elevated in lead V2 may indicate that there has been some depression from the usually slightly elevated ST-T wave baseline.


Figure-2: Magnified view of lead aVL from ECG #1 — showing that the ST segment is elevated in this lead.


Putting It All Together:
I've previously reviewed optimal use of lead aVL for predicting the "culprit" artery when there is ST elevation in this lead (See ECG Blog #324).
  • When ST elevation is isolated to lead aVL — acute LCx (Left Circumflex) occlusion becomes a prime suspect as the "culprit" artery (especially involving occlusion of the 1st obtuse marginal branch).
  • Alternatively — this could represent acute occlusion of the 1st or 2nd Diagonal, although this would seem less likely given the lack of ST elevation in lead V2. That said — the patient in ECG Blog #324 had ST elevation isolated to lead aVL (without any ST elevation in lead V2) — so exceptions do exist.
  • Acute occlusion of the LAD would not be expected from seeing the ECG in Figure-1 — because there is no ST elevation in any of the chest leads.
  • OR — "something else" may be going on (ie, prior infarction, an anatomic variant, an unusual pattern of collateral circulation).

What About the ST Depression in 8/12 Leads?
Recognition of the ECG pattern in which there is diffuse ST segment depression (usually present in at least 7-8 leads+ ST elevation in lead aVR (and sometimes in lead V1) — should immediately suggest the following Differential Diagnosis:
  • Severe Coronary Disease (due to LMain, proximal LAD, and/or severe 2- or 3-vessel disease) — which in the right clinical context may indicate ACS (Acute Coronary Syndrome).
  • Subendocardial Ischemia from some other cause (ie, sustained tachyarrhythmia; cardiac arrest; shock/profound hypotension; GI bleeding; anemia; "sick patient", etc.).

  • To Emphasize: This pattern of diffuse subendocardial ischemia does not suggest acute coronary occlusion (ie, it is not the pattern of an acute MI) — but rather ischemia due to the above differential diagnosis!

BOTTOM Line: The history we were given — is that this middle-aged woman was having chest discomfort in association with the ECG shown in Figure-1. While possible that the subtle ST elevation isolated to lead aVL might represent acute occlusion of the LCx — this initial ECG is not definitive.
  • What is definite — is that in this middle-aged patient with new chest pain, the presence of ST segment straightening, with at least some ST depression in 8/12 leads + ST elevation in lead aVR — should be interpreted as subendocardial ischemia until proven otherwise.

  • Additional investigation is indicated in today's patient to rule out an acute cardiac event (ie, repeat ECGs, serial troponins, Echo during chest pain — looking for a localized wall motion abnormality).
  • Even if troponins are negative and no frank criteria for a STEMI are seen on follow-up ECGs — IF chest pain persists — then cardiac cath would be indicated to clarify the anatomy (See ECG Blog #193regarding the importance of recognizing OMI when STEMI criteria are lacking on ECG).


CASE Follow-Up:
Today's tracing was sent to me. I subsequently learned additional details about this case:
  • The patient was a previously healthy, middle-aged woman without significant cardiac risk factors. She was initially seen in the ED for exertional chest pain and dyspnea that occurred several months prior to the ECG shown in Figure-1. Evaluation in the ED revealed ECGs similar to today's tracing — with normal serial troponins and no wall motion abnormality on Echo. No cardiac cath was recommended at that time.
  • The patient overall did well for a period of several months — but then had another episode of exertional chest pain and dyspnea. Once again — troponin was negative and Echo showed no wall motion abnormality. The patient's symptoms resolved — and the ECG shown in Figure-1 was obtained at that time. Because of the recurrence of symptoms, and the diffuse ST depression on ECG — the decision was made to perform cardiac catheterization to clarify the anatomy. 
  • The result of cardiac cath is shown in Figure-3.

QUESTION:
  • Can you explain the cardiac cath findings shown in Figure-3 — on the basis of this patient's history and the ECG in Figure-1?

Figure-3: Cardiac cath films on today's patient — showing a high-grade stenosis of the mid-RCA (Right Coronary Artery). There was no significant disease elsewhere. Right Panel: PCI (Percutaneous Coronary Intervention) successfully restored flow.


MY Thoughts on this CASE:
I did not expect to see single-vessel disease in the RCA. This would not be expected to produce the subtle ST elevation isolated to lead aVL. When diffuse ST depression is the result of ischemia — it usually is indication of either multi-vessel disease — or LMain or a proximal LAD lesion.
  • Troponins were negative — and Echo failed to reveal a localized wall motion abnormality on the 2 occasions that the patient was evaluated.
  • Perhaps the patient had an inferior MI in the past? (ie, that spontaneously reperfused, but retained the high-grade mid-RCA stenosis that was seen on cath?).
  • OR — Perhaps the high-grade mid-RCA lesion reduced coronary flow enough to produce the exertional angina episodes — but the Echo studies was not obtained during chest pain (ie, Echo is only valid for ruling out an acute cardiac event IF there is no wall motion abnormality and the Echo is obtained during an episode of chest pain).

  • BOTTOM Line: Although I cannot fully explain the cath results of today's patient in light of the history and ECG findings — the correct decision was made. This patient had exertional chest pain with an abnormal ECG that strongly suggested coronary disease. When troponins and Echo studies were unrevealing — cardiac cath was needed to define the anatomy.

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Acknowledgment: My appreciation to Nelson Nersisyan (from Yerevan, Armenia) 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 — illustrates use of the Mirror Test to facilitate recognition of acute Posterior MI. This blog post reviews the basics for predicting the "Culprit" Artery.

  • ECG Blog #320 — Reviews the typical ECG picture for recognizing the 1st or 2nd Diagonal as the "culprit" artery (ie, the "South African Flag" Sign).
  • ECG Blog #324 — for another example of isolated ST elevation in lead aVL (here due to acute OMI of the 1st Diagonal).

  • ECG Blog #285 — for another example of acute Posterior MI (with positive Mirror Test).
  • ECG Blog #246 — for another example of acute Posterior MI (with positive Mirror Test).
  • ECG Blog #80 — reviews prediction of the "culprit" artery (and provides another case illustrating the Mirror Test for diagnosis of acute Posterior MI).

  • ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL (featured in Audio Pearl #2 in this blog post)
  • ECG Blog #167 — another case of the "magical" mirror-image opposite relationship between lead III and lead aVL that confirmed acute OMI.


  • ECG Blog #228 — Reviews the concept of "Silent" MI (including an Audio Pearl on this topic).

  • ECG Blog #271 — Reviews determination of the ST segment baseline (with discussion of the entity of diffuse Subendocardial Ischemia).

  • ECG Blog #266 — Reviews distinction between Posterior MI vs deWinter T waves (with anterior terminal T wave positivity reflrecting "Reperfusion" T-waves).

  • ECG Blog #258 — How to "Date" an Infarction based on the initial ECG.



Saturday, August 6, 2022

ECG Blog #324 — Only 1 Lead ...


The patient whose ECG is shown in Figure-1 — is an elderly woman, who was admitted for acute abdominal pain. CT scan revealed splenic infarction. She also complained of an atypical type of chest pain.
  • How would YOU interpret her ECG in Figure-1?
  • Should you activate the cath lab?

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


MY Thoughts on the ECG in Figure-1:
Although there is no long lead rhythm strip — it should be apparent that the rhythm is irregularly irregular — and that there are no P waves. The rhythm is AFib with an overall controlled ventricular response. There is 1 PVC (seen in simultaneously-recorded leads V4,5,6). Continuing with my Systematic Approach (as per ECG Blog #205):
  • The QRS is narrow. The QTc is at most no more than minimally prolonged. The frontal plane axis is slightly leftward — but not enough to qualify as LAHB (ie, the QRS in lead II is not predominantly negative).
  • Assuming normal standardization — there is no chamber enlargement.

Regarding Q-R-S-T Changes:
  • Other than the Qr complex in lead V1 (which by itself, is not significant) — there are no Q waves.
  • R Wave Progression is normal (with progressive increase in R wave amplitude — leading to normal transition between leads V3-to-V4).

The KEY findings relate to the ST-T Waves:
  • 1 mm of coved ST elevation is present in high-lateral lead aVL. Given modest height of the R wave in this lead — this finding is significant! There appears to be subtle-but-real beginning T wave inversion in this lead.
  • Otherwise — there is significant ST depression no less than 8/12 leads (ie, in leads II,III,aVF; and in V2-thru-V6).
  • There is ST elevation in lead aVR.

Putting It All Together:
Today's case presented a challenging clinical picture. On the one hand — this elderly woman presented with acute abdominal pain, and was found to have a splenic infarction. On the other hand — she did have chest pain, although this did not seem to be her primary complaint.
  • This patient's ECG showed AFib (which presumably was not new) — and suggested the following considerations: i) Diffuse Subendocardial Ischemia (with ST depression in 8/12 leads + ST elevation in lead aVR); ii) Acute MI (with isolated ST elevation in lead aVL); and/or, iii) A combination of i) and ii).

PEARL #1: As emphasized in ECG Blog #271 — Recognition of the above ECG pattern, in which there is diffuse ST segment depression (usually present in at least 7-8 leads+ ST elevation in lead aVR (and sometimes also in lead V1) — should immediately suggest the following Differential Diagnosis:
  • Severe Coronary Disease (due to LMain, proximal LAD, and/or severe 2- or 3-vessel disease) — which in the right clinical context may indicate ACS (Acute Coronary Syndrome).
  • Subendocardial Ischemia from another Cause (ie, sustained tachyarrhythmia; cardiac arrest; shock/profound hypotension; GI bleeding; anemia; "sick" patient, etc.).
To EMPHASIZE: The pattern of diffuse Subendocardial Ischemia by itself does not suggest acute coronary occlusion (ie, it is not the pattern of an acute MI) — but rather ischemia due to the above differential diagnosis!


PEARL #2: Complicating our differential diagnosis of the likely cause of the ECG findings in Figure-1 — is the isolated ST elevation in lead aVL. By way of review — I've reproduced in Figure-2, the Table published in ECG Blog #320 — in which I summarize optimal use of lead aVL for predicting the "culprit" artery.
  • According to Figure-2 — the finding of isolated ST elevation in lead aVL (without ST elevation in any other chest leads) — suggests LCx occlusion (especially of the 1st Obtuse Marginal Branch of the LCx).

Figure-2: Optimal use of lead aVL for predicting the "culprit" artery in acute OMI.


PEARL #3: As helpful as the general rules reviewed in ECG Blog #193 are for predicting the "culprit" artery in acute OMI ( = Occlusion-based MI) — these rules are not perfect. Potential confounding factors include anatomic variations — unusual patterns of collateralization (especially after prior infarction) — multi-vessel disease — and/or — other factors that may affect ST-T wave appearances (ie, drugs, electrolyte disorders, chamber enlargement, conduction defects — among others).
  • KEY Point: Much more important in Figure-1 than precise identification of the "culprit" artery — is recognition that in a patient with chest pain, prompt cath is indicated to clarify the anatomy.

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CASE Follow-Up:
Suspicion from the ECG in Figure-1 that an acute OMI was actively evolving — was confirmed by return of a markedly elevated troponin.
  • Echo revealed an ejection fraction of ~25% — and — wall motion abnormalities localized to the mid-inferoseptal and apical-septal areas.
  • Cardiac Cath was performed — and revealed that the "culprit" artery was a large 1st Diagonal Branch of the LAD (RED arrow in Figure-3). This was successfully reperfused. There was minimal disease in the LCx. The RCA was a hypoplastic vessel with ~80% narrowing that was not felt to be a "culprit" in this patient's ongoing infarction.

Figure-3: Cardiac Catheterization (Left coronary angiogram — RAO caudal view) — showing high-grade stenosis of a very large 1st Diagonal Branch off of the LAD (See text).


Final Concepts:
I recently reviewed the typical ECG picture for recognizing acute OMI in a 1st or 2nd Diagonal Branch of the LAD (See ECG Blog #320):
  • Look for the "South African Flag" Sign — in which the leads showing maximal ST-T wave deviation take the form of the horizontal "Y" of the South African Flag (Figure-4). 

  • Note in Figure-4 — that there is significant ST elevation in leads I, aVL and V2 — but not in other chest leads.
  • Completing the horizontal "Y" of the South African Flag — maximal ST depression is seen in lead III. 

Figure-4: The pattern of maximal ST-T wave deviation with acute occlusion of the 1st or 2nd Diagonal Branch of the LAD — corresponds to the the arrangement of GREEN coloring in the horizontal "Y" of the South African Flag (This ECG is taken from the case presented in ECG Blog #320).


PEARL #4: The unique aspects of today's case relate to the ECG finding in high-lateral lead aVL of isolated ST elevation limited to this single lead (with exception of lead aVR — that manifests ST elevation as a reciprocal change).
  • KEY Point: It is important to recognize that acute OMI may occasionally present with ST elevation only in lead aVL!

  • Whereas most of the time with acute occlusion of the 1st or 2nd Diagonal, there will be ST elevation in lead V2 (but not in other chest leads)No chest lead in today's case showed ST elevation.

  • Instead, despite ST elevation limited to lead aVL — the area of infarction in today's case corresponded to the distribution of the occluded large 1st Diagonal Branch. This corroborates the Advanced Point brought out in ECG Blog #320 — namely, that MRI anatomic correlations support the concept that lead aVL provides an electrical perspective of ongoing events in the mid-anterior wall more than from a "high-lateral" viewpoint.

  • Finally — the diffuse ST depression in 8/12 leads (with modest ST elevation in lead aVR) suggest a component of diffuse subendocardial ischemia — most probably reflective of severe 2-vessel disease (ie, the ~80% narrowing of the hypoplastic RCA) occurring in the setting of extensive myocardial injury (marked by greatly increased troponin) that resulted from acute occlusion of the very large 1st Diagonal Branch.

P.S.: It remains uncertain as to whether the patient's AFib exerted a causative or contributing role in the splenic infarction and/or acute occlusion of the 1st Diagonal. Coronary thromboembolism is a potential complication of AFib — but available evidence suggests this is not a common event (El-Shetry et al Br  Hosp Med, 2021).



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Acknowledgment: My appreciation to Nelson Nersisyan (from Yerevan, Armenia) 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 — illustrates use of the Mirror Test to facilitate recognition of acute Posterior MI. This blog post reviews the basics for predicting the "Culprit" Artery.

  • ECG Blog #320 — Reviews the typical ECG picture for recognizing the 1st or 2nd Diagonal as the "culprit" artery (ie, the "South African Flag" Sign).

  • ECG Blog #285 — for another example of acute Posterior MI (with positive Mirror Test).
  • ECG Blog #246 — for another example of acute Posterior MI (with positive Mirror Test).
  • ECG Blog #80 — reviews prediction of the "culprit" artery (and provides another case illustrating the Mirror Test for diagnosis of acute Posterior MI).

  • ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL (featured in Audio Pearl #2 in this blog post)
  • ECG Blog #167 — another case of the "magical" mirror-image opposite relationship between lead III and lead aVL that confirmed acute OMI.


  • ECG Blog #271 — Reviews determination of the ST segment baseline (with discussion of the entity of diffuse Subendocardial Ischemia).

  • ECG Blog #266 — Reviews distinction between Posterior MI vs deWinter T waves (with anterior terminal T wave positivity reflecting "Reperfusion" T-waves).

  • ECG Blog #258 — How to "Date" an Infarction based on the initial ECG.




Sunday, July 31, 2022

ECG Blog #323 — WCT with RBBB Morphology


The ECG in Figure-1 — was obtained from a man in his 50s, who presented to the ED (Emergency Department) with "palpitations".
  • How would YOU interpret the ECG in Figure-1?
  • Doesn't this look like RBBB (Right Bundle Branch Block)?

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:
There is an obviously fast tachycardia in Figure-1. Usually I begin by assessing the rhythm in the long lead II rhythm strip that appears at the bottom of the tracing. Unfortunately — small amplitude of the artifact-laden, nearly isoelectric QRS complex in lead II renders such assessment problematic. That said — virtually every other lead provides the overview that follows. Using the Ps, Qs, 3R Approach (See ECG Blog #185):
  • The rhythm in ECG #1 is fast and Regular. I estimate the Rate to be ~210/minute.
  • I see no sign of atrial activity (ie, No P waves)
  • The QRS complex during the tachycardia is wide (I measure ~0.12 second = 3 little boxes in duration).

IMPRESSION: The above parameters lead to description of the rhythm in Figure-1 as being a regular WCT ( = Wide-Complex Tachycardia) at ~210/minute, without clear sign of atrial activity.

  • As emphasized in many of my prior ECG Blogs (especially in ECG Blog #220) — the finding of a regular WCT rhythm without clear sign of atrial activity should always be assumed to be VT until proven otherwise (statistical odds ~90% when such individuals are older adults with underlying heart disease).

PEARL #1: 90% is not 100%! Although we need to assume VT for any regular WCT rhythm without P waves until proven otherwise — sometimes the rhythm will be supraventricular!
  • Assessment of QRS morphology helps greatly to narrow down the likelihood that a given WCT rhythm is either VT or an SVT (SupraVentricular Tachycardia) with preexisting BBB (Bundle Branch Block) or aberrant conduction (See ECG Blog #196 for details).

  • The chances of a WCT rhythm being supraventricular are greatly increased IF — QRS morphology is consistent with one of the known forms of conduction block (ie, RBBB; LBBB; LAHB or LPHB; or RBBB with one of the hemiblocks).


Take another LOOK at the ECG in Figure-1:
  • Doesn't QRS morphology look like RBBB conduction?
  • Is the rhythm in this tracing VT?or SVT with RBBB conduction?

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


ECG #1: Is this VT? or SVT with RBBB Conduction?
As emphasized in Pearl #1 — the chance that a regular WCT rhythm will turn out to be supraventricular is increased IF — QRS morphology is consistent with some known form of conduction defect.
  • As emphasized in ECG Blog #204 — the 3 KEY leads for rapid determination of BBB are right-sided lead V1 — and the 2 left-sided leads I and V6. I've enclosed a QRS complex from each of these 3 leads within a RED rectangle in Figure-2. QRS morphology is perfectly consistent with RBBB conduction because: i) There is an rsR' complex in lead V1 (with an s wave that descends below the baseline — and a taller right "rabbit ear" R' wave); and, ii) There are upright R waves with wide terminal S waves in lateral leads I and V6.


PEARL #2: The other (more subtle) factor I favor for assisting in determination of the likelihood that a regular WCT rhythm is VT — is whether any of the other 9 leads show findings that look atypical for a particular conduction defect.
  • None of the "rules" for assessing QRS morphology when assessing a regular WCT rhythm are perfect. Exceptions always exist. For example — QRS morphology may be dramatically altered in a "baseline" ECG in patients who have significant underlying heart disease. In such cases — QRS morphology will not look "typical" when heart rate increases.
  • That said — I've enclosed within a BLUE rectangle in Figure-2, a representative QRS complex in 5 leads that looks unusual for "typical" RBBB conduction. Specifically — i) The QRS in lead II looks bizarre. It's tiny amplitude, biphasic shape looks "out-of-place" between the RS complex in lead I and the rSR' complex in lead III; and, ii) QRS morphology in chest leads V2,V3,V4 and V5 also looks highly unusual for RBBB conduction — because of multiphasic (overly fragmented) complexes that look "out-of-place" following the highly characteristic rsR' complex in lead V1.

BOTTOM Line: While impossible to rule out an SVT with RBBB conduction for the regular WCT rhythm in Figure-2 — the unusual appearance of the above 5 leads suggests that this rhythm is VT.
  • Since QRS morphology in the 3 KEY leads (I,V1,V6) resembles RBBB conduction — a Fascicular VT should be presumed until proven otherwise. 

  • PEARL #3: As discussed in ECG Blog #197 — Fascicular VT is one of the 2 most common forms of Idiopathic VT, which is the term used to describe the approximately 10% of all VT rhythms in which the patient has VT in the absence of underlying structural heart disease. Recognition of Fascicular VT is therefore very relevant clinically — because the course, prognosis and treatment of this arrhythmia is different from that of ischemic or scar-related VT, that makes up the other 90% of VT rhythms.

  • NOTE: By way of a reminder — I've reproduced below in the ADDENDUM the Summary Sheet and Audio Pearl on Idiopathic VT from Blog #197.


CASE Follow-Up: 
The initial ECG in today's case was recognized as Fascicular VT — and treated accordingly. Since the patient was hemodynamically stable — 5 mg of IV Verapamil was given. The result of this treatment is shown in ECG #2 (See Figure-3).


Figure-3: Comparison of the initial ECG — with the post-conversion tracing, obtained after giving 5 mg IV Verapamil. (To improve visualization — I've digitized the original ECG using PMcardio).



Case CONCLUSION:
Prompt conversion to sinus rhythm is the typical response of Fascicular VT to IV Verapamil in a patient with no underlying heart disease.
  • EP study confirmed that the patient had a left posterior fascicular VT. This was successfully ablated.


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Acknowledgment: My appreciation to Mubarak Al-Hatemi (from Qatar) for the case and this tracing.

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ADDENDUM (7/31/2022):

I summarize KEY features regarding Idiopathic VT in Figure-4.


Figure-4: Review of KEY features regarding Idiopathic VT (See text).



Today’s ECG Media PEARL #14 (8 minutes Audio) — What is Idiopathic VT? — WHY do we care? Special attention to the 2 most common forms = RVOT (Right Ventricular Outflow Track) VT and Fascicular VT. 

 

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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).
  • ECG Blog #196 — Reviews another Case with a Regular WCT Rhythm

  • 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 #197 — Review of Fascicular VT (including Audio Pearl and Summary sheet on Idiopathic VT).
  • ECG Blog #301 — Reviews a WCT that is SupraVentricular! (with LOTS on Aberrant Conduction).

  • 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 — Comprehensive review of criteria for distinguishing VT vs Aberration.





Tuesday, July 26, 2022

ECG Blog #322 — 71yo with 1 Week of Chest Pain



The ECG in Figure-1 — is from a 71-year old man who presented to the ED (Emergency Department) with a 1-week history of recurrent severe chest and throat painNo prior tracing available.
  • In view of this history — How would YOU interpret the ECG in Figure-1?
  • Is there AV block?


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


MY Thoughts on the ECG in Figure-1:
I favor beginning with the long lead II rhythm strip.
  • The rhythm in the long lead II rhythm strip is clearly irregular. That said — a majority of beats on this tracing are sinus-conducted, with an upright P wave with constant PR interval in lead II (RED arrows in Figure-2).
  • Sinus P waves are not regular. Instead — every 3rd P wave occurs early (BLUE arrows). The early-occurring P waves are seen to notch their preceding T wave (for the P waves before beats #4 and 7). The premature P wave before beat #10 occurs a little later in the cycle — such that it is more clearly separated from the preceding T wave. 
  • Since every 3rd beat is a PAC (Premature Atrial Contraction) — the rhythm is atrial trigeminy.

  • PEARL #1: Most of the time with the AV blocks — the atrial rhythm will be regular (or at most, no more than slightly irregular when there is sinus arrhythmia). The fact that in Figure-2 — the rhythm in the long lead II rhythm strip is clearly not regular immediately tells us that this rhythm is unlikely to represent 2nd- or 3rd-degree AV block.

Figure-2: I've labeled the P waves from Figure-1 with colored arrows (See text).


Continuing with My Assessment of ECG #1:
The rhythm in Figure-2 is atrial trigeminy. Regarding Intervals — the PR interval and the QTc are both normal. But the QRS complex is wide (I measure 3 little boxes = 0.12 second in duration in a number of leads).
  • QRS morphology is consistent with complete RBBB (Right Bundle Branch Block) because: i) There is an rSR' complex in right-sided lead V1andii) There are wide terminal S waves in left-sided leads I and V6.
  • There is no chamber enlargement.

Regarding Q-R-S-T Changes:
  • Small and narrow Q waves of uncertain significance are seen in leads V5,V6. It is difficult to determine if there is or is not a small q wave in lead III.
  • The question of R wave progression is unimportant given the presence of complete RBBB.

ST-T Wave Abnormalities:
The most remarkable findings in ECG #1 relate to ST-T Wave Changes. Abnormal ST-T wave findings are seen in virtually every lead in this tracing. Some of these are subtle — others less so. But it is important to recognize the totality of these abnormal findings in today's patient who presents with a 1-week history of recurrent chest and throat pain.
  • PEARL #2: Normally with RBBB — there should be at least some ST-T wave depression in lead V1. Although the T wave in this lead is inverted (as it should be) — the shape of the ST segment in lead V1 is slightly coved, and the ST segment is not at all depressed (it actually looks to be slightly elevated). This is not normal!

  • PEARL #3: When there is ST-T wave depression in lead V1 with RBBB — the relative amount of ST depression should be maximal in lead V1. ST depression should then decrease as one moves from lead V1-to V2-to V3 — IF — the reason for the ST depression is purely the conduction defect. This is not what we see in Figure-2 — in which the relative amount of J-point ST depression becomes maximal in leads V3 and V4.
  • Note that the shape of the depressed ST segment in leads V2 and V3 is coved instead of downsloping. Together with the increasing amount of J-point ST depression — this is an ischemic response.

  • There is 1-1.5 mm of abnormal (straightened) ST depression in lateral chest leads V5 and V6. Note the terminal T wave positivity.
  • Similar ST segment straightening with slight depression and terminal T wave positivity is seen in high-lateral leads I and aVL.
  • Nonspecific ST-T wave flattening with slight depression is seen in lead II — and without ST depression in lead aVF.
  • Lead III is interesting — in that the ST segment is distinctly coved, albeit no more than minimally elevated — with symmetric T wave inversion.
  • Finally — there is significant ST elevation in lead aVR.

Putting IAll Together: 
There is a lot going on with this tracing. The rhythm is atrial trigeminy. There is RBBB — and ST-T wave abnormalities consistent with ischemia in virtually all 12 leads.
  • The finding of ST depression in no less than 8/12 leads (I,II,aVL; V2-thru-V6) — with significant ST elevation in lead aVR suggests diffuse subendocardial ischemia. When due to a cardiac cause — this often indicates severe coronary disease (ie, LMain or proximal LAD stenosis — or multivessel disease).
  • Support of the likelihood of multivessel disease is forthcoming from resemblance of ECG #1 to many of the features of Aslanger's Pattern (See below).
  • The history of recurrent severe symptoms of 1-week duration in today's case — in association with the above ECG findings suggests the likelihood that an event (infarction) occurred during this past week.
 
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PEARL #4: There are elements in today's case that closely resemble Aslanger's Pattern (This pattern is very nicely described by Dr. Smith in his January 4, 2021 post). The premise of Aslanger's — is that IF there is inferior MI + diffuse subendocardial ischemia — then the vector of ST elevation will shift rightward. This results in:

  • ST elevation in lead III (as a result of the acute inferior MI) — but not in the other inferior leads (II, aVF) because of the rightward shift in the ST elevation vector.
  • ST depression in one or more of the lateral chest leads (V4,V5,V6) with a positive or terminally positive T wave — but without ST depression in lead V2. (Marked ST depression from multi-vessel coronary disease serves to attentuate what would have been ST elevation in leads II and aVF).
  • ST elevation in lead V1 that is more than any ST elevation in lead V2.
  • There may be more reciprocal ST depression in lead I than in lead aVL (because of the rightward ST vector shift).
  • The only leads showing significant ST elevation may be leads III, aVR and V1 (reflecting the inferior MI + subendocardial ischemia from diffuse coronary disease). 

NOTE: Other than the finding of ST depression in lead V2 — the initial ECG in today's case satisfies the other above-cited features of Aslanger's Pattern
  • I can't help but wonder if the fairly deep, symmetric T wave inversion in lead III represents a reperfusion T wave from recent occlusion.

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CASE Follow-Up:
Initial troponin was slightly elevated. The ECG was repeated ~2 hours after the initial tracing (Figure-3). Unfortunately — additional details of this case are lacking.
  • How would you interpret the repeat ECG in Figure-3?

Figure-3: Comparison of the initial ECG — with the repeat ECG done ~2 hours later. Unfortunately — clinical details are lacking regarding the nature of the patient's symptoms during this 2-hour time period
 

Comparison of the 2 ECGs in Today's Case:
The rhythm in ECG #2 is similar to that in the initial ECG ( = sinus rhythm with PACs). Overall QRS morphology is also similar in the 2 tracings.
  • There is less ST segment depression in leads V2-thru-V5 of ECG #2 compared to the initial tracing.
  • In lead III — there is now a definite Q wave and slight-but-real ST elevation. There is no longer any T wave inversion.
  • The flat ST depression with terminal T wave positivity that was seen in high-lateral leads I and aVL of ECG #1 — has been replaced by mirror-image opposite T wave inversion (opposite in shape, compared to the ST elevation in lead III). There is no longer terminal T wave positivity.

MY Impression of ECG #2:
I wish we had more follow-up information on this case. I suspect the following:
  • The new ST elevation in lead III — with reciprocal (mirror-image opposite) ST depression in leads I and aVL — to me suggest reocclusion of the RCA (Right Coronary Artery). Remember that with Aslanger's Pattern — ST elevation of inferior infarction may only be seen in lead III.
  • Clear reduction in the amount of ST depression in leads V2-thru-V5 — that occurs in association with signs of RCA reocclusion — suggests to me that ECG #2 may represent the phenomenon of "pseudo-normalization", in which the ECG looks "improved" because previously depressed ST segments are on their way toward ST elevation.


ADDENDUM (7/26/2022):
I have just received additional follow-up on this case. Cardiac cath was done — and revealed total occlusion of the LCx. The RCA was hypoplastic and showed 80% stenosis. The LMain was patent — and there was insignificant disease in the LAD. Ejection fraction ~42%. Successful PCI was performed (Figure-4).

Figure-4: Cardiac Cath — showing total occlusion of the LCx (LEFT). Successful PCI restoring flow to the LCx (RIGHT).




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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 #204 — Reviews a user-friendly approach for diagnosis of the Bundle Branch Blocks.

  • ECG Blog #186 — and ECG Blog #236 — for review on the basics of 2nd-degree AV Block.

  • ECG Blog #258 — Reviews the concept on how to "date" an infarction (and also introduces the concept of Aslanger's Pattern).
  • ECG Blog #271 — and ECG Blog #250 — Review the concept of diffuse subendocardial ischemia.
  • ECG Blog #142 — Presents another case for discussion on how to "date" an infarction.

  • ECG Blog #193 — illustrates use of the Mirror Test to facilitate recognition of acute Posterior MI. This blog post reviews the basics for predicting the "culprit artery". NOTE: Figure-5 in the Addendum of this blog post illustrates the essentials for identifying an isolated posterior MI.

  • ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL (featured in Audio Pearl #2 in this blog post).
  • ECG Blog #80 — reviews prediction of the "culprit" artery (and provides another case illustrating the Mirror Test for diagnosis of acute Posterior MI).