Saturday, May 27, 2023

ECG Blog #381 — Why was the Troponin Normal?

The ECG in Figure-1 was obtained from a 60-ish year old man with a history of coronary disease (including prior CABG) — who presented to the ED (Emergency Department) with new CP (Chest Pain) of 3 hours duration, diaphoresis and nausea/vomiting. 
  • The patient was hypotensive at the time his initial ECG in Figure-1 was obtained.

The decision was made not to immediately perform cardiac cath — because there is no ST elevation in Figure-1 — and because the initial troponin was negative.
  • Do YOU agree with the decision not to cath at this time?
  • How would you interpret ECG #1

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

MY Initial Thoughts on Today's CASE:
The clinical scenario presented in today's case is extremely concerning:
  • The patient has a known history of coronary disease.
  • His symptoms of CP are new! These symptoms are associated with diaphoresis, naursea/vomiting — and of special concern, hypotension! Even before looking at the initial ECG — the clinical scenario suggests probable need for prompt cath until proven otherwise!

Interpretation of ECG #1:
Normal sinus rhythm at ~80-85/minute is seen in Figure-1. The PR interval is normal — but the QRS is wide, with QRS morphology consistent with RBBB (Right Bundle Branch Block) and LAHB (Left Anterior HemiBlock). There is no chamber enlargement. 

Regarding Q-R-S-T Changes:
  • There is a Q wave in leads aVL that is "significant" — given its width relative to the R wave in this lead. This may represent high-lateral infarction at some point in time. No other Q waves are present (ie, There is a tiny initial r wave in lead V1).
  • R wave progression — is irrelevant, given the RBBB. 

Regarding ST-T wave Changes:
  • The most "eye-catching" abnormalities are in leads V3 and V4 — both of which show definitely abnormal ST depression. The QRS complex is tiny (as well as fragmented) in lead V3 — with disproportionate J-point ST depression, followed by a coved, downsloping ST segment with an abnormally biphasic terminal T wave. The shelf-like ST depression in lead V4 is never normal, nor is the terminal T wave positivity seen in this lead. The S wave in lead V4 is also fragmented (ie, a sign of prior "scar" and/or infarction).
  • Abnormal ST depression continues in leads V5 and V6, each with prominent (? hyperacute) T waves. The QRST appearance of these 2 lateral chest leads looks very similar to the QRST appearance in each of the inferior leads (albeit there is less J-point depression in the inferior leads).
  • There is ST segment coving and T wave inversion in lead aVL.
  • There is significant ST elevation in lead aVR.
  • Finally, in lead V1 — the ST-T wave depression is expected with RBBB — but the subtle-but-real ST elevation in this lead is not expected with simple RBBB.

Putting It All Together:
Missing from this presentation at this time — is a prior (baseline) ECG on this patient who has a known history of significant coronary disease. As a result — I was not initially sure what was "new" vs "old". That said:
  • There is bifascicular block (RBBB/LAHB) — which if new, would be an extremely worrisome sign.
  • Multiple leads show abnormal ST segment straightening, with ST depression. This ST depression appears to be maximal in leads V3-to-V5 — which could reflect acute posterior OMI (Occlusion-based Myocardial Infarction) — most probably with multi-vessel disease (ie, diffuse subendocardial ischemia suggested by the ST depression with ST elevation in aVR>V1).
  • This patient has new CPand — he is hypotensive.

  • BOTTOM Line: The normal initial troponin — and lack of ST elevation are not reasons for not performing cardiac catheterization. Acute posterior OMI results in ST depression, not ST elevation (with this ST depression typically maximal in leads V2-to-V4). Troponin rise is sometimes delayed. Even if acute coronary occlusion is not present in today's case — the findings of diffuse subendocardial ischemia in a patient with bifascicular block and known coronary disease — who presents with new CP and hypotension — constitute clear indication for immediate cath lab activation at this point in the case.


The CASE Continues:
Another ECG was obtained 54 minutes after ECG #1. Unfortunately — I do not have information on the patient's symptoms and hemodynamics at the time ECG #2 was recorded.

For ease of comparison in Figure-2 — I've put these 2 ECGs together.
  • How would you interpret ECG #2 in light of the initial tracing done 54 minutes earlier?

Figure-2: Comparison between the initial and repeat ECGs.

MY Thoughts on the Repeat ECG:
QRS morphology in the repeat ECG is virtually the same as in the initial tracing — which means that lead-by-lead comparison for subtle differences in ST-T wave morphology will be valid.
  • There are now Q waves in leads V1 and V2 of ECG #2 — that were not previously present.
  • There is more ST elevation in leads aVR and V1.
  • There is more ST depression in virtually all leads compared to what was present in ECG #1.

  • Impression: ECG signs of diffuse subendocardial ischemia have clearly increased. Coronary reperfusion is urgently needed.

The Baseline ECG was Found:
A prior ECG on today's patient, done ~9 months earlier — was found. For ease of comparison in Figure-3 — I've put this baseline tracing together with the initial ECG in today's case. 
  • What do we learn from the baseline ECG? 

Figure-3: Comparison between the initial ECG in today's case — with a prior tracing recorded ~9 months earlier. What does this baseline ECG tell us?

MY Thoughts on the Baseline ECG:
Although I lack information regarding when the baseline ECG was obtained with respect to this patient's bypass surgery — 9 months earlier, the QRS was narrow without evidence of any conduction defect. With the exception of minimal, nonspecific inferior lead ST-T wave flattening — ECG #3 is essentially a normal tracing!
  • Impression: The baseline tracing confirms that all of the above-described findings in ECG #1 are acute!


CASE Conclusion:
A final 12-lead ECG was obtained on today's patient — which for ease of comparison in Figure-4, I have put together with ECG #2.
  • Unfortunately — I do not have information on the sequence of treatment interventions, nor on correlation between patient symptoms, hemodynamics and specific timing with each of these serial ECGs.

  • At some point ~1-2 hours after the initial ECG — the patient developed runs of VT, leading to cardiac arrest. He could not be resuscitated.

There are lessons to be learned from this case. I include the final 12-lead that was done in Figure-4 — as I found it instructive to compare this last tracing with ECG #2 done 52 minutes earlier.
  • How would you interpret ECG #4?

Figure-4: Comparison between the last ECG and ECG #2.

MY Thoughts on the Final ECG:
I am not certain what the rhythm in ECG #4 is.
  • We see runs of rapid beats that I initially thought represented an irregular VT. However, the long lead II rhythm strip at the bottom of the tracing shows these runs to be punctuated by a number of pauses (ie, between beats #3-4; 5-6; 7-8; and 15-16) — and that an upright sinus P wave is clearly seen to be present at the end of each pause before beats #1, 4, 6, 8 and 16.
  • Looking at each of the 18 beats in this long lead rhythm strip — the QRS morphology of sinus beats #1,4,6,8,16 is similar to QRS morphology of the rapid, irregular beats that follow these sinus-conducted beats in virtually each of the simultaneously-recorded leads of the 12-lead tracing (with possible exception of beats #14,15) — which makes me wonder if the rhythm in the long lead II is sinus with multiple successive PACs (perhaps a short run of AFib from beats #9-thru-15?) — vs — sinus rhythm with very frequent PVCs manifesting a QRS morphology very similar to the morphology of sinus beats.

  • What is certain — is the continued marked ST depression in the mid-chest leads, consistent with an ongoing, extensive infarction in this patient with severe symptoms and hypotension.


Acknowledgment: My appreciation to 張三毛 = JJ (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 — Review of the Ps, Qs, 3R Approach for systematic rhythm interpretation.

  • ECG Blog #271 — Reviews the concept of diffuse Subendocardial Ischemia.

  • ECG Blog #316 — The patient died. Was the LMain coronary artery the "culprit"?

Additional 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 #374Acute LMain Occlusion.

  • 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 — as well as the importance of the term, "OMI" ( Occlusion-based MI) as an improvement from the outdated STEMI paradigm.

  • ECG Blog #56 — Posterior MI; Mirror Test.
  • ECG Blog #80 — What's the Culprit Artery (and 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 #222 — What's the Culprit Artery? 

  • ECG Blog #367 — for another example of acute LCx OMI

  • ECG Blog #294 — How to tell IF the "culprit" artery has reperfused.
  • ECG Blog #194 — AIVR as a sign that the "culprit" artery has reperfused.

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

  • The importance of the new OMI (vs the old STEMI) Paradigm — See My Comment in the July 31, 2020 post in Dr. Smith's ECG Blog.

  • ECG Blog #260 and ECG Blog #292 — Reviews when a T wave is hyperacute — and the concept of "dynamicST-T wave changes
  • ECG Blog #230 — How to compare serial ECGs.

  • ECG Blog #337 — an OMI misdiagnosed as an NSTEMI ...

  • 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 #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.

Saturday, May 20, 2023

ECG Blog #380 — What is "Swirl"?

The ECG in Figure-1 — was obtained from an older woman with persistent CP (Chest Pain) over the previous day. Her symptoms lessened after Nitroglycerin — so the decision was made not to activate the cath lab. Do YOU agree with this decision?

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

MY Thoughts on the ECG in Figure-1:
In a patient with CP that had been persistent over the previous day (until Nitroglycerin was given) — the initial ECG shown in Figure-1 is extremely worrisome. 
  • The rhythm is sinus. Intervals (PR, QRS and the QTc) and the frontal plane axis are normal.
  • Voltage for LVH is satisfied — at least by Peguero Criteria (Sum of deepest S in any chest lead + S in V4 ≥23 mm in a woman — as discussed in ECG Blog #73).

Regarding Q-R-S-T Wave Changes: 
  • Q Waves — None are seen. 
  • R Wave Progression — Transition (where the R wave becomes taller than the S wave is deep) is slightly delayed, occurring between leads V4-to-V5. That said — R wave amplitude is of reasonable size in all anterior leads (with slight reduction in R wave size from V2-to-V3 probably the result of lead placement).

The most significant abnormalities relate to ST-T Wave Changes:
  • In the Limb Leads — There is nonspecific ST-T wave flattening, with slight ST depression in multiple leads (ie, in leads I,II,III,aVF).
  • In the Chest Leads — Assessment for ST elevation in the anterior leads is especially challenging in ECG #1. This is because there is normally a small amount of upward-sloping ST elevation in leads V2 and V3. That said — in a patient with CP, the amount of ST elevation in leads V2 and V3 looks excessive to me, in association with ST-T waves that look potentially hyperacute. Thus, despite satisfying voltage criteria for LVH — considering the depth of the S waves in leads V2,V3 — the ST-T waves in these leads still look a little bit taller, fatter-at-their-peak and wider-at-their-base than I would expect them to be.
  • Support that the ST-T waves in leads V2,V3 are likely to be abnormal — is forthcoming from the appearance of the ST-T wave in lead V1. In the absence of a deep S wave in lead V1 — it is uncommon to see ST elevation in this lead. It is simply not normal to see a full 1 mm of ST elevation in lead V1 (as we do in Figure-1) — especially in view of the ST segment straightening that is present in this lead.

  • PEARL #1: The above noted findings in leads V1,V2,V3 are subtle! It is for this reason that I'll emphasize that the one lead in ECG #1 that indisputably manifests an abnormal ST-T wave is lead V6. In a patient with new and persistent CP — it is never normal to see the amount of flat ST depression that is present in lead V6. Abnormal ST segment flattening and depression is also seen in neighboring lead V5, but not nearly as marked as in lead V6. 
  • KEY Point: It is the fact that I know the flat ST depression in lead V6 is abnormal in a patient with persistent CP — that tells me the ST-T waves in leads V1,2,3 also have to be assumed abnormal until proven otherwise!

BOTTOM Line: The patient in today's case is an older woman who presents with a 1-day history of new and persistent CP. Her initial ECG should be interpreted as highly suggestive of acute proximal LAD occlusion until proven otherwise.
  • NEW Concept: In a patient with CP — the ECG findings of anterior lead ST elevation, in association with lateral chest lead ST depression — is consistent with the pattern of Precordial "Swirl" (that I discuss below).

Continuation of Today's CASE:
A prior ECG on today's patient (done ~5 years earlier) was found — and is shown in comparison with the initial ECG in Figure-2
  • Does this previous tracing strengthen our impression about this patient's initial ECG? 

Figure-2: Comparison of the initial ECG in today's case — with a prior ECG done ~5 years earlier. What do we learn from reviewing this previous ECG?

Comparison of ECG #1 and ECG #2:
IF there was any doubt about whether the ECG findings in today's tracing (ie, in ECG #1) are acute — it should have vanished the moment the prior ECG in Figure-2 was found!
  • NOTE: It's important to correlate ongoing circumstances at the time that a prior tracing was done (ie, Was the patient stable and asymptomatic — or were they having chest pain, an exacerbation of heart failure, or some other ongoing process at the time the prior ECG was recorded?). This point is particularly relevant regarding ECG #2 — because sinus tachycardia is seen on this earlier ECG. In addition — there were more prominent anteroseptal forces on this earlier tracing (ie, in the form of an R wave = S wave in lead V1, with similar-looking equiphasic QRS complexes in leads V2-thru-V5).
  • The above said — there previously was no indication of any ST elevation, or of any potentially hyperacute ST-T waves in the anterior leads of ECG #2 — nor was the distinct, flat ST depression in lead V6 present in this prior ECG! These differences between the 2 tracings in Figure-1 strongly support our suspicion that the ST-T wave changes in ECG #1 have to be interpreted as acute until proven otherwise!


What is Precordial Swirl?
In the October 15, 2022 post of Dr. Smith's ECG Blog — Drs. Smith and Meyers introduce the colorfully descriptive term known as Precordial Swirl — as an intriguing ECG sign that facilitates recognition of a unique ECG pattern strongly suggestive of a very proximal site of acute LAD occlusion (usually proximal to the 1st septal perforator) — with resultant septal ischemia, in addition to anterior wall and apical involvement.

PEARL #2: In the setting of acute LAD OMI (Occlusion-based MI ) — the pattern of Precordial Swirl is recognized by the finding of ST elevation in leads V1 and aVR — and — reciprocal ST depression in leads V5 and V6.
  • When considering Precordial Swirl — I like to focus on the ST-T wave appearance in leads V1 and V6.
  • Although 1-2 mm of upsloping ST elevation is commonly (and normally) seen in anterior leads V2 and V3 — most of the time we do not see ST elevation in lead V1 (or if we do — it is minimal!). Therefore — I become immediately suspicious of "Precordial Swirl" whenever there is suggestion of LAD OMI — and — in addition, lead V1 looks different than expected!

  • NOTE: Sometimes recognition that lead V1 looks "different-than-expected" — is only forthcoming after realizing that lead V2 is clearly abnormal.

In Figure-3 — I've selected 6 sets of V1,V2 leads from the series of tracings shown by Drs. Smith and Meyers in their October 15, 2022 post on Precordial Swirl.
  • Although admittedly subtle — the ST segment coving with slight but disproportionate ST elevation in lead V1 of A, B and C in Figure-3 is clearly an abnormal appearance for the ST segment in lead V1. In association with neighboring chest leads suggestive of acute LAD OMI — this picture should raise suspicion of Precordial Swirl.
  • Example F in Figure-3 is more subtle — because the S wave in lead V1 is deeper. That said — this coved shape of ST elevation in lead V1 of F should still raise suspicion in a patient with new symptoms.
  • The ST-T wave segment in lead V1 of example D — closely resembles the "shape" of LV strain in an anterior lead from a patient with LVH. However, the S wave in example D — is not at all deep in either lead V1 or V2 — which in a patient with chest pain should strongly suggest the possibility of Precordial Swirl.
  • The ST-T wave shape in lead V1 of example E also appears to be subtly abnormal. Support that this finding is real — is forthcoming from our impression that the T wave in neighboring lead V2 looks more peaked than expected — which in a patient with new symptoms, should strengthen our suspicion of a disproportionately positive T wave in lead V1.

Figure-3: Selected sets of V1,V2 leads from the examples of Precordial Swirl provided in the October 15, 2022 post in Dr. Smith's ECG Blog.

NOTE: It's EASY to get fooled by LVH! This is because LV "strain" with LVH is sometimes more manifest in anterior rather than lateral chest leads — in which case there may be anterior lead ST elevation (ie, the reciprocal of lateral lead ST-T wave depression). The history and associated deep anterior S waves (ie, the reciprocal of tall lateral lead R waves) will suggest LVH rather than Precordial Swirl (See ECG Blog #254 and My Comment at the bottom of the page in the February 6, 2020 and June 20, 2020 posts in Dr. Smith's ECG Blog).
  • For additional examples that illustrate this concept of "proportionality" (regarding relative size of ST-T wave deviations compared to QRS amplitude in the respective lead) — Check out the additional examples of LVH that mimic Precordial Swirl which are provided in the October 15, 2022 post in Dr. Smith's ECG Blog.

Precordial Swirl Appearance in Lead V6:
The final component for diagnosing Precordial Swirl — is to see reciprocal ST depression at least in lead V6 (if not also in lead V5):
  • Once I've decided that the tracing I am looking at is not an example of LVH that mimics Precordial Swirl — I focus my attention on the shape of the ST-T wave in lead V6.

  • I've reviewed my approach to the ECG diagnosis of LVH ofte(See ECG Blog #245 — among many other posts). In Figure-4 — I've reproduced from the above cited June 20, 2020 post my schematic illustration of the ST-T wave appearance that may be seen in one or more lateral leads for demonstrating LV "strain".

PEARL #3: In general, the shape of ST-T wave depression in lead V6 with Precordial Swirl does not look like either C or D in Figure-4. Instead — the depressed ST segment tends to be flatter. Therefore — THINK Precordial Swirl in a patient with new symptoms IF you see: 
  • Other signs suggestive of acute LAD OMI.
  • The ST-T wave in lead V1 looking "different-than-expected". 
  • A relatively flattened appearance to the depressed ST segment in at least lead V6 (if not also in lead V5).

Figure-4: Schematic illustration and description of LV "strain" on ECG.

CASE Follow-Up:
Cardiac cath was performed on today's patient — and complete proximal LAD occlusion was found.
  • In Figure-5 — I compare the post-PCI ECG with the initial tracing in today's case.

  • How would YOU interpret the post-PCI tracing? 
  • Based on the ECGs in Figure-5 — Did PCI succeed in opening the "culprit" artery?

Figure-5: Comparison of the initial ECG in today's case — with a post-PCI tracing. Was PCI successful?

Interpretation of the Post-PCI ECG:
There is significant baseline artifact in the limb leads of ECG #3. Despite this artifact — this tracing is still interpretable.
  • The frontal plane axis in both of the ECGs in Figure-5 is similar — which means that lead-to-lead comparison will be valid. There are no acute changes in Limb Lead ST-T wave appearance.

In contrast — the Chest Leads show that there has been marked evolution of this patient’s anterior MI:
  • There has been significant loss of anterior R wave forces in ECG #3 since the initial ECG. Specifically — the R wave in lead V2 is now smaller — with further loss of R wave from V2-to-V3 — and disappearance of the initial R wave in lead V4 (to form a QS complex in this lead). This loss of anterior forces is consistent with myocardial injury from the large infarction.

  • PEARL #4: Note change (deepening) of the S waves in leads V3,V4 of ECG #3. This is not indicative of LVH — but instead results from the loss of anterior forces, that now leaves posterior forces “unopposed” (with resultant deeper anterior S waves)
  • KEY POINT: It’s good to be aware that QRS amplitudes may undergo hard-to-predict amplitude changes over the course of acute MI evolution.

Chest Leads also show marked changes in ST-T wave appearance:
  • Compared to ECG #1 — there is clearly more ST elevation in leads V2,V3 of ECG #3 — with new ST elevation now present in lead V4
  • That said — an even more striking change in ST-T wave appearance — is the very steep decline of the descending limb of the T wave in leads V2,V3,V4!

  • PEARL #5: It's important to appreciate that although this steep T wave decline appearance looks like the anterior T waves seen in Wellens' Syndrome — this is not Wellens' Syndrome, because infarction has already taken place (whereas Wellens' Syndrome occurs in the absence of CP — and serves as an ECG warning sign that appears before a large infarction with QS waves has taken place — as discussed in ECG Blog #254).

  • Finally — The ST-T wave appearance in leads V5,V6 of the post-PCI tracing ( = ECG #3) — is very different than it was in the initial ECG. Instead of ST segment flattening and depression (that was seen in ECG #1 ) — there is now ST segment coving in lead V5 (a continuation of the ST coving seen in neighboring lead V4, albeit without any ST elevation) — and, there is no longer ST depression in lead V6.

PEARL #6: One of the KEY learning points of today’s case — is the importance of correlating ECG findings with the clinical situation. The more serial tracings recorded (and the better the notation of whether each serial tracing was associated with chest pain — and if so, relative severity of that CP) — the easier it becomes to correlate clinical events.
  • For example — We would not normally expect to see more ST elevation after PCI (as we do in ECG #3) — unless reperfusion of the "culprit" artery with the procedure was not successful — or — unless additional ECGs done prior to PCI showed additional ST elevation occurred before angioplasty opened the occluded vessel. In today's case — presumably this latter possibility is what occurred — in which case (assuming no CP after PCI) — the steep T wave descent with deepening T wave inversion in the anterior chest leads of ECG #3 presumably reflects coronary reperfusion


Acknowledgment: My appreciation to Kim Jiwon (from Seoul, Korea) 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 #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 — as well as the importance of the term, "OMI" ( Occlusion-based MI) as an improvement from the outdated STEMI paradigm.
  • ECG Blog #367 — for another example of acute LCx OMI

  • ECG Blog #294 — How to tell IF the "culprit" artery has reperfused.
  • ECG Blog #194 — AIVR as a sign that the "culprit" artery has reperfused.

  • ECG Blog #260 and ECG Blog #292 — Reviews when a T wave is hyperacute — and the concept of "dynamicST-T wave changes.
  • ECG Blog #230 — How to compare serial ECGs

  • ECG Blog #254 — What Wellens' Syndrome is and is not ...

  • ECG Blog #337 — an OMI misdiagnosed as an NSTEMI ...

  • 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 (with another case to illustrate 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 #350 — regarding T Wave Imbalance in the Chest Leads.

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

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

  • The importance of the new OMI (vs the old STEMI) Paradigm — See My Comment in the July 31, 2020 post in Dr. Smith's ECG Blog.

  • 20 Cases of Precordial Swirl (or "Look-Alikes" ) — Reviewed in the October 15, 2022 post of Dr. Smith's ECG Blog (including My Comment at the bottom of the page).

ADDENDUM (5/24/2023):

Josep Serra Tarragon wrote me asking whether inverted U waves were present in the lateral chest leads of ECG #1. On taking another look — I have to agree with him that they are! (BLUE arrows in leads V4,V5,V6 — in Figure-6).
  • There are 2 QRS complexes in simultaneously-recorded leads V4,V5,V6, in which we see the ST-T wave. I do not see inverted U waves clearly in the first QRS complex — but BLUE arrows that I have drawn into Figure-6 are certainly consistent with inverted U waves for the 2nd QRS complex.
  • Inverted U waves are an uncommon, usually ignored phenomenon. That said — when present in the right clinical situation, they are an indicator of significant ischemia (Correale et al — Clin. Cardiol 27:674-677, 2004).
  • Attention to negative U waves was first pointed out to me by Dr. Barney Marriott in the mid 1980s. Thereafter — I looked for negative U waves over a period of many years, but very rarely found them. Much of the time, there was simply too much "noise" on the tracing to be certain of their presence — or the heart rate was such that it was difficult to distinguish what was "real" inverted U wave vs terminal ST-T wave, baseline movement, or the next P wave. 
  • The mechanism for U wave inversion remains uncertain. Best theory is delayed repolarization of the His-Purkinje system.

  • Bottom Line: The clinical setting in this Blog #380 is certainly consistent with ischemia. I believe Dr. Tarragon is correct that this is highlighted by the BLUE arrows in Figure-6.

  • My THANKS to Dr. Tarragon for pointing this out! 

Figure-6: I've added BLUE arrows to leads V4,V5,V6 of ECG #1 — to indicate inverted U waves.

Friday, May 12, 2023

ECG Blog #379 — Why Tachy on Telemetry?

I was sent the rhythm strip shown in Figure-1 — obtained from telemetry monitoring. I did not know the history.
  • Can YOU explain what happens after beat #4?

Figure-1: Multi-lead rhythm strip obtained from telemetry monitoring.

MY Thoughts on the Rhythm Strip in Figure-1:
The first 4 beats in this 11-beat rhythm strip are sinus — as determined by the presence of regular upright P waves, with a constant PR interval in lead II (RED arrows in Figure-2).
  • The rate of this underlying sinus rhythm is ~57/minute (ie, The R-R interval between these first 4 beats is slightly more than 5 large boxes — therefore a rate slightly less than 300/5 = about 57/minute).
  • The last beat in Figure-2 is another sinus beat ( = RED arrow before this last beat #11).
  • In between the first 4 sinus-conducted beats and the last sinus-conducted beat — is a wide beat ( = beat #5) — which is followed by a run of 5 narrow QRS complexes at a rapid rate (of ~120/minute). A short pause is seen after beat #10.

  • NOTE: Because it is possible for ectopic foci arising from different sites to manifest a similar QRS morphology in one or two leads — but to look very different in other leads — it is worthwhile taking another look at the original 5-lead tracing in Figure-1, to ensure that QRS morphology stays the same for simultaneously-recorded beats #6-thru-10 in each of the 5 leads shown in this multi-lead rhythm strip.

  • The wide beat in Figure-2 (ie, beat #5) — appears to be a PVC (Premature Ventricular Contraction) because in addition to being wide and very different in morphology compared to sinus-conducted beats — beat #5 is not preceded by a premature P wave.

  • Can YOU explain what happens for beats #6-thru-10?

Figure-2: Today's rhythm begins with 4 normal sinus beatas — and ends with a final sinus-conducted beat (RED arrows that precede beats #1-thru-4 — and the RED arrow before beat #11). Beat #5 is a PVC.

What Happens with Beats #6-thru-10?
As noted above — the QRS complex of beats #6-thru-10 is narrow, and similar in morphology to the QRS of sinus-conducted beats in this tracing. These 5 beats represent a short run of an SVT (SupraVentricular Tachycardia) rhythm at a rate of ~120/minute.
  • The KEY to recognizing the mechanism of today’s rhythm — lies with identifying associated atrial activity. Unlike the sinus-conducted beats in this tracing — no upright P wave precedes the 5 beats in this short run of SVT. Instead — YELLOW arrows highlight negative P waves that clearly precede beats #7-thru-10 (ie, theYELLOW arrows in Figure-3).

Important Concepts:
  • Terminology — The terminology used for defining supraventricular rhythms can be confusing. As discussed in detail in ECG Blog #240 — the term, “SVT” — refers to any supraventricular rhythm (ie, with origin at or above the AV node) that manifests a rate of ≥100/minute. By this definition, a variety of rhythms may qualify as “SVTs” — including sinus tachycardia, atrial flutter or fibrillation, MAT, AVRT/AVNRT, among others. Thus, the term “SVT” is a generic (general) one — which is optimally used when we do not yet know the mechanism of a fast, supraventricular rhythm (which is why at this point in the process for today's rhythm — I favored simply calling beats #6-thru-10 a regular SVT at ~120/minute).
  • Why Isn’t this a Run of Atrial Tachycardia?To Emphasize: From this single tracing, we can not rule out the possibility that the negative P waves preceding beats # 7-thru-10 might represent a run of ATach (Atrial Tachycardia). That said — ATach is a far less likely explanation than retrograde conduction because: i) The P-P interval between the YELLOW arrows in Figure-3 is constant (whereas ATach typically begins with a “warm-up” period, in which the the atrial rate gradually accelerates); and, ii) The distance from the preceding QRS to these YELLOW-arrow P waves ( = the RP’ interval) is constant — suggesting that these YELLOW-arrow P waves are related to the preceding QRS (instead of being independent of the previous QRS — as would be likely with ATach).

  • Take another LOOK at Figure-3. Do YOU see any indication of atrial activity after the PVC? If so — Does this provide a clue to the mechanism of today's rhythm?

Figure-3: YELLOW arrows before beats #7-thru-10 highlight atrial activity in the form of negative P waves.

Is There Atrial Activity After the PVC?
  • The WHITE arrow in Figure-4 strongly suggests that there is a P wave after the PVC in today's rhythm. We know this — because the negative deflection under the WHITE arrow appears to manifest a similar RP' interval with respect to the QRS complex that comes before it, as noted for the RP' interval seen between the YELLOW-arrow retrograde P waves.

Figure-4: The WHITE arrow highlights the location of the 1st retrograde P wave in today's rhythm.

LADDERGRAM Illustration:
As discussed in detail in ECG Blog #240Reentry SVT rhythms (both AVNRT and AVRT) are most commonly initiated by a PAC that occurs at "just the right moment" so as to enable retrograde conduction up an alternative AV nodal pathway that allows a reentry circuit to be set up.
  • This is best explained by schematic illustration in the laddergram that I propose in Figure-5. The unusual feature about today's case, is that instead of a PAC initiating the 5-beat reentry SVT rhythm — it is a PVC that does so!

  • The rhythm in Figure-5 begins with 4 normal sinus-conducted beats (which are beats #1-thru-4 in the laddergram). This is followed by beat #5 — which is a PVC (as determined because beat #5 is wide, not preceded by any premature P wave — and very different in morphology from all sinus-conducted beats in this tracing).
  • As suggested by orientation of the BLUE arrow that starts from the ventricles — this PVC conducts retrograde all the way back to the atria to produce the negative deflection under the WHITE arrow (first series of dotted RED lines that depict retrograde conduction back to the atria). Because this retrograde conduction presumably travels over the slower AV nodal pathway — the resulting RP' interval (that produces the retrograde P waves under the YELLOW arrows) is long!
  • Presumably — the timing of retrograde conduction from this PVC was "just right" — such that it found forward conduction back to the ventricles was possible — thereby establishing the reentry circuit that produced the 5 beat run of SVT that extends from beat #6 until beat #10.

  • Note that no retrograde P wave is seen after beat #10! This stops conduction over the reentry circuit — which terminates this short run of reentry SVT. Then, after a suitable short pause — the SA Node recovers sufficiently to produce the next sinus impulse (that results in sinus-conducted beat #11).

Figure-5: Laddergram illlustration of the probable mechanism in today's rhythm.


Acknowledgment: My appreciation to Feroz Haroon (from Srinagar, Kashmir) 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 the Ps, Qs, 3R Approach to Arrhythmia Interpretation.

  • ECG Blog #188 — Reviews the essentials for reading (and/or drawingLaddergrams, with LINKS to numerous Laddergrams I’ve drawn and discussed in detail in other blog posts. 

  • ECG Blog #240 — Reviews the definition of what an "SVT" is — as well as illustrating the different types of reentry SVT rhythms (with assessment of the RP' interval).

  • ECG Blog #229 — Why AFlutter is commonly overlooked? 
  • ECG Blog #137 — AFlutter with an unusual conduction ratio.  
  • ECG Blog #138 — AFlutter vs Atrial Tachycardia
  • ECG Blog #40 — Another regular SVT that turned out to be AFlutter.

  • González-Torrecilla et al: Ann Noninvasive Electrocardiol 16(1):85-95, 2011 — Reviews distinction between AVNRT vs AVRT and other regular SVT rhythms in patients without WPW.

  • Please check out the November 12, 2019 post in Dr. Smith's ECG Blog — in which I reviewed the case of a different kind of regular SVT Rhythm (AFlutter).