Tuesday, June 28, 2022

ECG Blog #316 — What & When was the "Culprit"?

The ECG in Figure-1 — was obtained from an older man who presented to the ED (Emergency Department) with new-onset symptoms that began within the past 1-2 hours. The patient had a long history of smoking — but no prior history of heart disease.

  • How would YOU interpret the ECG in Figure-1?
  • Can you identify the “culprit”?
  • Extra Credit: Why is there no ST elevation in lead aVL?

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

MY Thoughts on ECG #1:
The rhythm is sinus tachycardia at ~110/minute. The QRS complex is wide with morphology consistent with complete RBBB (ie, QR pattern in lead V1; wide terminal S waves in leads I and aVL).

  • There are wide and deep Q waves in each of the inferior leads — and in leads V1-thru-V6. In fact — the QRS complex is tiny with complete loss of R wave in the most lateral chest lead ( = lead V6).
  • There is marked ST elevation in no less than 9/12 leads in this tracing!

The ECG is diagnostic of a huge ongoing STEMI — that by history, most probably began ~1-2 hours earlier.

  • ST elevation is most marked in leads V2-thru-V6 — though it is also present in the inferior leads. This suggests either acute proximal LAD (Left Anterior Descending) coronary artery occlusion orLMain (Left Main) occlusion.

  • With diffuse ST elevation in no less than 9/12 leads — Why is there no ST elevation in lead aVL?

I suspect that the reason there is no ST elevation in lead aVL — is that there is a "cancellation" effect.
  • Although lead aVL is often thought of as a "high lateral" lead — MRI studies suggest that its perspective actually views the anterior-medial wall of the left ventricle (Bayes de Luna — Circulation 114:1755-1760, 2006). As a result, most of the time with a proximal LAD occlusion — there will be ST elevation in lead aVL. There will also usually be reciprocal ST depression in the inferior leads.
  • On the other hand — there may be anatomic "wraparound" of the LAD (such that the LAD is a longer vessel that extends beyond the anterior wall to also supply the inferior wall of the left ventricle). If there is acute occlusion of a "wraparound" LAD — then in addition to anterior lead ST elevation, there may also be ST elevation in the inferior leads (with reciprocal ST depression in lead aVL).

  • When there is both proximal LAD occlusion + anatomic "wraparound" — there may be extensive anterior and also inferior infarction, with resultant cancellation of some forces (consistent with the picture seen in Figure-1, in which there is ST elevation in chest leads and in inferior leads — but with a flat ST-T wave in lead aVL).

CASE Follow-Up:
In today's case — the severity of the situation was immediately recognized — and the patient was promptly transferred to a treatment center. Troponin was markedly elevated. Unfortunately, despite treatment — the patient died within 1-2 hours of presentation. 
  • Echo with Doppler documented blood flow across the interventricular septum — indicative of VSR (Ventricular Septal Rupture).

About VSR (Ventricular Septal Rupture):
I found the concise Review of VSR by Mubarik and Iqbal insightful in today's case (NIH StatPearls Publishing — April, 2022). Below some highlights:

  • VSR is an uncommon presentation of acute MI. Whereas the incidence of this complication used to be ~2% — this has decreased to a fraction of 1% of acute MIs because of improved treatment and revascularization of acute MI.
  • The prognosis of acute VSR depends on the site in the septum and the size of the rupture. If the acute infarct is smaller with prompt reperfusion and stable hemodynamics — then stabilization of the patient may be possible, with the goal of enabling successful surgical closure.
  • In contrast — the condition is likely to rapidly prove fatal when septal rupture results from a very large infarction that quickly leads to cardiogenic shock. This is presumably what occurred in today’s case. Development of bifascicular block with large Q waves in 9/12 leads (covering the inferior and antero-lateral walls) — document the extensive myocardial damage in today’s case. Acute biventricular volume overload from the septal rupture, added to an already compromised cardiac output from the huge infarction is unlikely to be treatable.

  • NOTE: Whereas surgical repair of VSR offers the only realistic chance for survival — immediate surgery is far more challenging than when surgery is delayed several days. This is because of the difficulty trying to distinguish between healthy and newly infarcted tissue — with inability of newly infarcted myocardium to hold sutures.

Take another LOOK at the initial ECG in today's case (Figure-2). Considering the History — namely, that this older man presented to the ED within 2 hours after symptom onset — and then died 1-2 hours later after arrival in the hospital (with Echo Doppler confirming acute VSR) — Do YOU think it more likely that the "culprit" artery was:
  • An acute proximal LAD occlusion? 
  • Acute LMain occlusion? 
  • Something else?

Figure-2: Another LOOK at the initial ECG in today's case.

The “Culprit” Artery in Today’s Case?
I do not know a definitive answer to the above question. The patient died before cardiac catheterization could be done — and no post-mortem examination was performed. That said — my thoughts are the following:
  • Emergency providers rarely encounter patients with acute LMain occlusion. The reason for this is simple — Most such patients die quickly, usually before they reach the hospital.
  • At the time the initial ECG in Figure-2 was recorded (which according to the information available, was 1-2 hours after symptom onset) — there are already extremely large Q waves in 9/12 leads (as well as RBBB and marked ST elevation in 9/12 leads). Yet despite this — the patient survived another 1-2 hours after arrival in the hospital. IF the "culprit" was the LMain coronary artery — I would not expect the patient to survive this long with the extensive damage suggested by his initial ECG.

  • MY Thought: Instead of LMain occlusion — I feel ( = my opinion) that a much more logical sequence of events in today's case is that there was acute proximal LAD occlusion — which because of the extensive damage that this already caused (evidenced by the RBBB and extremely large Q waves in inferior and anterolateral leads) — resulted in the uncommon complication of acute VSR (Ventricular Septal Rupture), after which the patient promptly decompensated.

WHAT then are the ECG Findings of Acute LMain Occlusion?
The final question raised by today's case, is what the ECG signs of acute LMain occlusion are?
  • In a word — You can see almost anything!
  • Dr. Stephen Smith reviewed his data and experience regarding this issue in the August 9, 2019 post in Dr. Smith's ECG Blog. 
  • In my attempt to simplify the answer to this question — I summarize Dr. Smith's findings in Figure-3.

Figure-3: Reasons for the varied ECG presentation of acute LMain occlusion — excerpted from Dr. Smith’s 8/9/2019 post (See text).


Acknowledgment: My appreciation to Kianseng Ng and Yap Wan Teng (from Malaysia) for the case and this tracing.




Relevant ECG Blog Posts

  • ECG Blog #193 Reviews a case with a dominant LCx as the "culprit" artery (with ECG AUDIO Pearl on the concept of "OMI" and on Predicting the "Culprit" Artery).

  • ECG Blog #184  That magical inverse relationship between leads III and aVL.
  • ECG Blog #167 — More on that "magical" lead III-aVL relationship.
  • ECG Blog #183 — deWinter-like T waves.

  • ECG Blog #56 — Posterior MI; Mirror Test.
  • ECG Blog #80 — What’s the Culprit Artery? + the Mirror Test
  • ECG Blog #82 — What’s the Culprit Artery?
  • ECG Blog #162 — What’s the Culprit Artery?
  • ECG Blog #193 What's the Culprit Artery?
  • ECG Blog #222What's the Culprit Artery?


Friday, June 24, 2022

ECG Blog #315 — Bradycardia and Abdominal Pain

The ECG in Figure-1 — was obtained from a 65-year old woman who presented to the ED (Emergency Department) for abdominal pain. No chest pain. She was hemodynamically stable at the time the ECG in Figure-1 was recorded.
  • How would YOU interpret the ECG in Figure-1?
  • What is the rhythm?

Figure-1: 12-lead ECG and long lead II rhythm strip obtained from a 65-year old woman with abdominal pain. What is the rhythm?

NOTE: The ECG in today's case was reproduced from a smart phone photo. As a result — the tracing is angled and slightly distorted. That said — the advantage of transmitting smart phone tracings is that within seconds — consultation from anywhere in the world with an internet connection becomes possible.
  • Despite some distortion — accurate interpretation of the rhythm in Figure-1 still is possible!
  • Please Also NOTE: Recording of the long lead II rhythm strip from this smart phone photo was not entirely simultaneous with the 12-lead ECG above it. This adds to the challenge of interpreting this tracing — since we lose the ability to directly compare changes in QRS morphology for each beat in the rhythm strip — to morphology changes in the 12-lead. Are YOU up to the challenge?

MY Approach to the ECG in Figure-1:
As always — I favor beginning with the long lead rhythm strip at the bottom of the tracing before concentrating on the 12-lead. My systematic approach to every arrhythmia that I encounter is encompassed by the memory aid, "Watch Your Ps, Qs and the 3Rs" (See ECG Blog #185):
  • The overall rhythm is slow. The rhythm is not regular. That said — there does appear to be a "pattern" to the rhythm, in that there are coupled beats that are spaced at a similar distance to the preceding QRS complex (ie, the coupling interval of beats #2, 5 and 8 in the long lead rhythm strip looks to be equal).
  • Realizing that there is some distortion of this tracing — many of the R-R intervals appear to repeat! That is — the R-R interval between beats #2-3; 5-6 and 8-9 looks to be the same! (ie, just under 6 large boxes in duration).
  • The slightly longer R-R intervals that are seen between beats #3-4; 6-7; 9-10 and 10-11 also appear to be equal! (ie, about 7 large boxes in duration). This repetition of intervals is not due to chance!

Continuing with the Ps, Qs & 3Rs:
  • The QRS complex of the underlying rhythm is narrow. That is — the 1st beat in each grouping (ie, beats #1, 3, 4, 6, 7, 9, 10 and 11) is narrow and not preceded by any P wave! Each of these beats must therefore be a junctional "escape" beat (at a junctional escape rate here, set at an appropriate junctional rate of between 40-60/minute).

  • I next looked for P waves. There are some P waves on this tracing! For clarity in Figure-2 — I have added colored arrows to highlight the P waves that I believe to be present.

Figure-2: There are some P waves on this tracing! (See text).

PEARL #1: How to Find P Waves ...
The KEY to interpreting today's rhythm lies with identifying the P waves that are present. This is challenging! — because most of the P waves on this tracing are partially (or totally) hidden within preceding T waves.
  • Begin by identifying those deflections that you know represent P waves (RED arrows).
  • At this point I thought to myself: "IF there was an underlying regular sinus rhythm — what would the P-P interval have to be?" I contemplated my answer based on knowing that the 2 RED arrows in Figure-2 definitely represented 2 P waves.
  • Working backward from the 2nd RED arrow — it is clear that there is no P wave within the R-R interval between beats #8-9. Looking carefully at each of the T waves for beats #1, 4, 6, 7 and 10 — I thought the T wave of beat #7 looked different (ie, with a smaller peak — as suggested by the PINK arrow).
  • IF this PINK arrow is truly highlighting a partially hidden P wave — then the P-P interval in this tracing could be the distance between this PINK arrow — and the RED arrow that occurs just after beat #9.
  • IF this was true — then the remaining P waves in Figure-2 might be hiding (and slightly deforming) the T waves of beats #1, 4, 6 and 10 (as highlighted by the WHITE arrows).

PEARL #2: It is Essential to Use Calipers!
As I have emphasized on multiple occasions in this ECG Blog — many complex rhythms defy interpretation unless you use calipers.
  • Accounting for the slight distortion we have noted in the rhythm strip, as well as for some degree of sinus arrhythmia (that so often accompanies sinus bradycardia) — it literally took me no more than seconds to postulate the probable location of underlying sinus P waves that I highlight with the colored arrows in Figure-2. I simply could not have identified these P waves without calipers.

PEARL #3: It Helps When You Know What You Are Looking For!
Solving complex arrhythmias is similar to solving a mystery in a detective story. Most of the time — there are a limited number of possibilities. In today's case — the "pattern" of the rhythm is bradycardia with intermittent coupled beats (ie, there is an intermittent bigeminal rhythm).
  • As discussed in ECG Blog #243 — the differential diagnosis for a bigeminal rhythm is limited. Once you are aware of the possibilities for a bigeminal rhythm (that I summarize in Figure-3) — recognition of the slow rate with junctional escape at the end of each of the longer R-R intervals in Figure-2 — should immediately suggest "escape-capture" as the most likely mechanism. None of the other entities in Figure-3 make sense. Therefore — I immediately suspected (and looked for) an escape-capture mechanism for today's rhythm.

Figure-3: Causes of a Bigeminal Rhythm (See text).

A picture is worth 1,000 words! It's easiest to illustrate the mechanism in today's case with a laddergram (Figure-4).

Figure-4: Since the QRS complex of beats #1,3,4,6,7,9,10,11 is narrow and not preceded by any P wave — we established that these are junctional "escape" beats, here with an appropriate junctional "escape" rate in the low 40s (ie, with an R-R interval between successive junctional beats of ~7 large boxes). Because the sinus bradycardia rate is even slower than the junctional rate — most beats on this tracing are junctional except for the on-time P waves that occur before beats #2, 5 and 8 (which occur at a point in the cardiac cycle in which they are able to "capture" the ventricles).

Final Observations:
As noted earlier — recording of the long lead II rhythm strip in today's tracing was not entirely simultaneous with the 12-lead ECG above it.
  • PEARL #4: There are numerous ECG recording systems in use across the world. The one in use for today's tracing was different than the recording systems that I am accustomed to. The first 3 beats in the long lead II rhythm strip are recorded simultaneous with the recording of the 3 beats seen leads I, II and III of the 12-lead ECG. 
  • The 12-lead ECG then shows the appearance of these first 3 beats in the long lead rhythm strip in each of the 3 remaining lead groupings (ie, in leads aVR,aVL,aVF — in leads V1,V2,V3 — and finally in leads V4,V5,V6).
  • For example — the 2nd beat in lead V1 manifests an RBBB pattern. This corresponds to beat #2 in the long lead rhythm strip.
  • Note that this beat #2 in the long lead II rhythm strip — corresponds to the 2nd beat that is recorded in the lead grouping that shows leads I, II and III. The wide terminal S wave in lead I for this beat #2 is consistent with RBBB conduction.
  • Finally — Note that QRS morphology for this beat #2 shows a very deep S wave in lead I — and a qR in leads II and III — which is consistent with LPHB conduction.

  • PEARL #5: Each of the coupled beats in the long lead II rhythm strip (ie, beats #2, 5 and 8) look similar — in that they are each slightly wider than beats #1,3,4,6,7,9,10,11 (because they have a terminal S wave). Since QRS morphology of beats #5 and 8 looks identical to that of beat #2 in the long lead rhythm strip — all 3 of these beats must be conducting with RBBB/LPHB aberrancy!
  • It is completely understandable that these conducted "capture" beats (ie, beats #2,5,8) might conduct with aberration — since they each occur early in the cycle, at a time when these P waves may fall within the relative refractory period.

The primary problem in today's case is marked sinus bradycardia. Perhaps this is simply a result of increased vasovagal tone brought about as a pain response to this patient's abdominal discomfort?
  • Since the rate of this patient's sinus bradycardia is slower than her junctional "escape" rate — the principal rhythm that we see is junctional escape.
  • There is no evidence of any AV block in Figure-4 — because the P waves occurring right after the QRS complexes of beats #3, 6, 9 and 10 all occur so early in the cycle, that they would not be expected to conduct. And when on-time P waves occur just a little bit later in the cycle — they do conduct (ie, "capture" the ventricles) with a reasonable PR interval.
  • Because sinus bradycardia is often the 1st rhythm disturbance seen with SSS (Sick Sinus Syndrome) — clinical correlation will be needed to determine IF the marked sinus bradycardia in today's case is simply a vasovagal response to pain — or something more significant (ie, drug or electrolyte effect, sleep apnea, hypothyroidism, SSS, etc.).

Acknowlegment: My thanks to Rafi Mohd (from Jammu-Kashmir, India) for allowing me to use this tracing and clinical case.


Relevant ECG Blogs to Today's Audio Pearl:

  • ECG Blog #185 — Reviews the Ps, Qs & 3R Approach to Systematic Rhythm Interpretation. 
  • ECG Blog #188 — Reviews how to understand (and how to drawLaddergrams! 

  • ECG Blog #256 Escape-Capture Bigeminy (with junctional escape and "capture" from retrograde conduction — with AUDIO Pearls on "Escape-Capture" and on "Sick Sinus Syndrome" plus Step-by-Step Laddergram).
  • ECG Blog #163 — Escape-Capture Bigeminy (with sinus bradycardia and resultant junctional escape — and possibly also with SA block).

  • ECG Blog #239 — Reviews the concept of Echo Beats, and its clinical applications (showing an unusual bigeminal rhythm case of AV Wenckebach over dual AV nodal pathways, terminated by Echo beats).
  • ECG Blog #232 — For review of a bigeminal rhythm due to subtle 3:2 AV Wenckebach. (NOTEThe Audio Pearl in this post is devoted to the concept of Bigeminal Rhythms)
  • ECG Blog #243 — For review of a bigeminal rhythm due to AFlutter with dual-level Wenckebach conduction out of the AV node.
  • ECG Blog #252 — For review of a bigeminal rhythm due to atrial trigeminy with blocked PACs
  • ECG Blog #206 — For review of a fascinating case of a bigeminal rhythm due to 3:2 AV Wenckebach with alternating Hemiblock.

  • ECG Blog #70 — Reviews the Ashman Phenomenon (as a reason for aberrant conduction)

Monday, June 20, 2022

ECG Blog #314 — A 79yo with Palpitations

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.

  • How would YOU interpret the ECG shown in Figure-1?
  • How certain are you of your diagnosis?

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.

Y Impression:
We were told that the patient in today's case was a 79-year old man with known coronary disease. This means that even before looking at the ECG in Figure-1statistical odds that a regular WCT rhythm without clear sign of atrial activity will turn out to be VT are greater than 90% when the patient is an older adult who has underlying heart disease. 
  • 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!

Fascicular VT:
Because of the resemblance of QRS morphology to a bifascicular block pattern (ie, to RBBB with LAHB) — the rhythm in Figure-1 is known as Fascicular VT. 
  • As discussed in ECG Blog #197Fascicular 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).

Advanced POINT:
Take another LOOK at the rhythm in Figure-1. Did YOU Notice the changing QRS amplitude in a number of leads?

  • 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?

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!).

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. 

  • 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!).

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/minuteas 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.

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?

Figure-5: Comparison of the initial regular WCT rhythm with the ECG result of synchronized cardioversion.

CASE Conclusion:
As shown in Figure-5synchronized 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.


Acknowledgment: My appreciation to 林柏志 (from Taiwan) for the case and this tracing.


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.

Thursday, June 16, 2022

ECG Blog #313 — Acute Post-Partum MI?

The ECG in Figure-1 — was obtained from a 40-year old woman 10 days after a normal vaginal delivery. She presented to the ED (Emergency Department) with a history of progressive dyspnea over the previous 3 days.

  • In view of this history — How would YOU interpret the ECG in Figure-1?
  • Many staff physicians were concerned about an acute MI. Do YOU agree?

Figure-1: Initial ECG from a woman 10 days post-partum — who presented to the ED with progressive dyspnea. (To improve visualization — I've digitized the original ECG using PMcardio).

My THOUGHTS on the ECG in Figure-1:
The rhythm is sinus tachycardia at ~110/minute. The PR interval is normal. The QRS complex is narrow — but the QTc appears to be prolonged (although this is more difficult to assess given the tachycardia). No chamber enlargement. 

Additional relevant ECG findings include:
  • Overall low voltage (especially in the chest leads).
  • Incomplete RBBB (ie, rSR' pattern in lead V1 — with normal QRS duration and narrow terminal s waves in leads I and V6).
  • An indeterminate frontal plane Axis (ie, nearly isoelectric complexes in most limb leads).
  • An S1Q3T3 pattern is present!

Regarding Q-R-S-T Changes:

  • There is a Q wave in lead III — as well as small q waves in leads I, II, aVF.
  • Regarding R Wave Progression — a tiny initial r wave (positive deflection) is seen in lead V1 — consistent with the incomplete RBBB pattern noted above. An rSr' pattern persists in lead V2 — but the fact that the P wave is positive in both leads V1 and V2 indicates that these rSr' patterns in leads V1,V2 are "real" (ie, they are not due to chest lead misplacement). 
  • QRS complexes remain extremely small across the chest leads — with nearly isoelectric QRS complexes in leads V3-thru-V6. There is persistence of S waves across all chest leads (with a significant S wave still present in lateral lead V6).
  • ST segments are coved — with a hint of ST elevation in a number of leads (ie, leads III, aVR, V1, V2). Perhaps the most remarkable finding is the deep (considering the small R wave amplitude) and symmetric T wave inversion that is seen in the inferior leads — and — in leads V1-thru-V6.



The History is KEY in today’s case: Rather than an acute cardiac event — the history of progressive dyspnea 10 days post-partum in a younger woman should immediately suggest the following entities: i) Post-Partum Cardiomyopathy; ii) Takotsubo Cardiomyopathy; and, iii) Acute PE (Pulmonary Embolism). 

  • Even before results from bedside Echo were seen — the ECG in Figure-1 should strongly suggest acute PE as the presumed diagnosis until proven otherwise.



The ECG Diagnosis of Acute PE:

As I've discussed on prior ECG Blog posts (See ECG Blog #233) — the ECG is far from optimal as an investigative tool for the diagnosis of acute PE. That said — there are times when the ECG, in conjunction with the clinical history — can be extremely helpful in suggesting the diagnosis even before additional testing can be accomplished. The ECG in Figure-1 provides an excellent example of this situation.

  • PEARL #1: The ECG is unlikely to identify patients with smaller PEs. Do not expect to see anything on the ECG of these patients (This may be a "blessing in disguise" — as the longterm benefit of anticoagulating such patients is debatable). Sensitivity of the ECG for suggesting the possibility of acute PE is clearly better with large (especially submassive) PEs.


PEARL #2: One of the problems with using the ECG as a diagnostic tool for detecting acute PE — is that there is no single ECG finding definitive for this diagnosis. Instead, acute PE may be suggested by a combination of several supportive ECG findings that occur in association with the right clinical scenario (ie, recent onset of unexplained dyspnea, syncope and/or shock — especially in a patient predisposed or with a prior history of venous thromboembolism).

  • The clinical setting of today's case serves as a "perfect set-up" for development of acute PE (ie, an otherwise healthy, adult woman who presents with progressive dyspnea during the first 2 weeks post-partum).

  • For clarity — I summarize the KEY ECG findings to look for when considering the diagnosis of acute PE in Figure-2. These ECG findings are expanded on in the ADDENDUM below (See Figure-3 and Figure-4 — and the attached Audio Pearl).


Figure-2: ECG findings associated with acute PE. There is no single ECG finding that is diagnostic of acute PE. Instead, the diagnosis may be suggested by the presence of at least several of these ECG findings when they occur in the “right” clinical setting (See text).


WHAT are the ECG Findings in Today's Case?

I list below those positive and negative ECG findings from Figure-2 — as they are relevant to today's case:

  • Sinus Tachycardia — While not absolutely essential for the diagnosis, a rapid heart rate (usually to at least 90/minute) is a common and expected finding in patients with hemodynamically significant acute PE. The heart rate in Figure-1 is over 100/minute.

  • Acute RV “Strain” — Awareness of ECG evidence of RV (Right VentricularStrain is one of the most important ECG indicators of acute hemodynamically significant PE. Unfortunately, this sign remains all-to-often unappreciated and misinterpreted as coronary ischemia (as it was in today's case). RV “strain” manifests as ST depression and/or T wave inversion that typically occurs in anterior leads (V1,2,3) — and/or — in inferior leads (II,III,aVF). Abnormal ST-T wave changes consistent with acute PE are seen in both of these lead areas in Figure-1 (and these changes extend out to the lateral chest leads = until lead V5!).

  • S1-Q3-T3 — Whereas the diagnostic value of this pattern is minimal at best when seen as an isolated finding — a definite S1Q3T3 pattern can be extremely helpful IF seen in association with other ECG evidence of acute PE. Such is the case in Figure-1.

  • There is no RAA.
  • There is an indeterminate frontal plane axis (ie, nearly isoelectric QRS complexes in most limb leads).
  • An incomplete RBBB pattern is present (ie, Narrow QRS with rSr' in leads V1,V2 — with a terminal narrow s wave in lateral leads I and V6).
  • There is no tall R wave in lead V1.
  • Persistent Precordial S Waves — Poor R wave progression with persistence of S waves across the chest leads (through to lead V6) — is another ECG sign seen here that is consistent with new or chronic pulmonary disease.
  • ST Elevation in Lead aVR and/or Lead III — Among the unappreciated benefits of lead aVR in ECG interpretation, is awareness that acute right heart “strain” (as seen with large acute PE) may often produce ST elevation in right-sided lead aVR. Although subtle — there is at least a hint of ST elevation in the 3 "right-sided" leads in Figure-1 (ie, in leads III, aVR, V1).
  • Atrial fibrillation is not present.


PEARL #3: Boey et al (Singapore Med J 56:533-537, 2015) — make the point that in addition to the ECG findings noted in Figure-2more extensive and severe PE has been associated with: i) Low QRS voltage; ii) Pseudo-infarction patterns (ie, Q waves in leads III, aVF); and/or, iii) ST segment changes that extend to leftsided chest leads (ie, leads V4,V5,V6).

  • NOTE: All 3 of these ECG findings that have been associated with more severe PE are present in today's case!

Putting It All Together: The one unifying diagosis that explains all of the ECG findings noted above in Figure-1, in this 40-year old post-partum woman who presented to the ED with progressive dyspnea (but no mention of chest discomfort) — is acute PE.

  • The "beauty" of the initial ECG in today's case — is that it expedited an accurate presumptive diagnosis of extensive acute PE within minutes!


The patient was hypotensive on arrival in the ED. Stat Echo in the ED revealed a compressed left ventricle — septal flattening with paradoxical movement — and a grossly dilated right ventricle. These Echo findings ruled out Takotsubo and Post-Partum Cardiomyopathy — and confirmed the diagnosis of massive acute PE.

  • The patient was immediately treated with Streptokinase — which fortunately resulted in significant improvement.
  • Subsequent CT Angiography of the Chest confirmed extensive bilateral PE.
  • The patient continued to improve — and she was soon discharged from the hospital in stable condition on oral anticoagulation.


Acknowledgment: My appreciation to Dr. Rasheed (from Sana'a, Yemen) for making me aware of this case and allowing me to use this tracing.



Related ECG Blog Posts to Today’s Case: 

  • 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).

  • 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”

  • ECG Blog #209 — Reviews the ECG diagnosis of Wellens’ Syndrome (What it is — and what it is not! ).
  • ECG Blog #59 — Reviews the causes of Giant T Wave Inversion.



ADDENDUM (6/16/2022): 

I've excerpted below in Figure-3 and Figure-4 — several pages from my ECG-2014-ePub — that summarize the ECG findings of acute PE (Pulmonary Embolus) — as well as an Audio Pearl relevant to today's topic.


Figure-3: Summary of KEY findings in the ECG diagnosis of acute PE.

Figure-4: Summary (Continued) of KEY findings in the ECG diagnosis of acute PE.

Today’s ECG Media PEARL #49 (7:40 minutes Audio) — Reviews the ECG finding of Anterior T Wave Inversion (with emphasis on not overlooking acute PE as the cause!).

  • NOTE #2: Among the topics discussed in this Audio Pearl are the ECG findings with acute PE (See Figure-3 and Figure-4 in the ADDENDUM below) — Wellens' Syndrome (reviewed in ECG Blog #209) — and — Giant T Wave Syndrome (reviewed in ECG Blog #59).