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.
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• 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!

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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!
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• 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.
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• I've reviewed my approach to the ECG diagnosis of LVH often (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.

FINAL QUESTION:

• 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.
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• 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!
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• 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).
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• 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. 

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Acknowledgment: My appreciation to Kim Jiwon (from Seoul, Korea) 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.
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• 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. 
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• 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.
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• ECG Blog #260 and ECG Blog #292 — Reviews when a T wave is hyperacute — and the concept of "dynamic" ST-T wave changes.
• ECG Blog #230 — How to compare serial ECGs. 
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• ECG Blog #254 — What Wellens' Syndrome is and is not ...
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• ECG Blog #337 — an OMI misdiagnosed as an NSTEMI ...
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• 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).
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• 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.
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• ECG Blog #350 — regarding T Wave Imbalance in the Chest Leads.
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• ECG Blog #271 — Reviews determination of the ST segment baseline (with discussion of the entity of diffuse Subendocardial Ischemia).
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• ECG Blog #258 — How to "Date" an Infarction based on the initial ECG.
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• 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.
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• 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).

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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.
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• 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.
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• 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.

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.
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• 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.
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• 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.

QUESTION:

• 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).

QUESTION: 

• 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 #240 — Reentry 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!
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• 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.
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• 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.

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Acknowledgment: My appreciation to Feroz Haroon (from Srinagar, Kashmir) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• ECG Blog #185 — Reviews the Ps, Qs, 3R Approach to Arrhythmia Interpretation.
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• ECG Blog #188 — Reviews the essentials for reading (and/or drawing) Laddergrams, with LINKS to numerous Laddergrams I’ve drawn and discussed in detail in other blog posts. 
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• 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).
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• 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.
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• 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.
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• 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).

ECG Blog #378 — Wenckebach with PVCs?

The ECG in Figure-1 — was obtained from an older woman with chest pain.

• How would YOU interpret this tracing?
• What kind of AV block is present? — OR — Is there no clear evidence of any AV 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:

This tracing is challenging to interpret because of the changing QRS morphology — and because of the uncertainty regarding atrial activity.

• The “good news” — is that although the chief complaint from this older woman was “chest pain” — an initial “quick glance” at the 12-lead does not suggest obvious acute changes. In such cases (assuming the patient is hemodynamically stable) — I favor looking closer at the cardiac rhythm before taking a more detailed look at the 12-lead.

PEARL #1: As noted above — the QRS is changing — and atrial activity is uncertain in parts of this tracing. In such cases — I favor starting with the part(s) of the tracing that I am certain about.

• The underlying rhythm in Figure-1 is sinus — since an upright P wave with constant PR interval is seen before each of the QRS complexes that terminate each of the brief pauses (ie, before beats #3,6,9,12 and 15 — as shown by the RED arrows in Figure-2).
• The PR interval for each of these sinus beats is slightly prolonged (ie, to slightly more than 1 large box in duration = 0.22 second). Therefore — a 1st-degree AV block is present.
• The QRS of sinus beats #3,6,9,12 and 15 looks narrow in this long lead II rhythm strip. Returning for a moment to the 12-lead tracing shown in Figure-1 — confirmation that the QRS of sinus-conducted beats is truly narrow, is forthcoming from the fact that the QRS is clearly narrow in each of the simultaneously-recorded leads for beats #3,6,9,12 and 15 in all 12 leads.
• In contrast — Beats #1, 4, 7, 10 and 13 are wide, different in appearance than the sinus-conducted QRS complexes — and are not preceded by a premature P wave. Therefore — beats #1,4,7,10 and 13 are PVCs (Premature Ventricular Contractions).
• On the other hand — Beats #2,5,8,11 and 14 are clearly supraventricular — because these beats are narrow and virtually identical in QRS morphology to the sinus-conducted beats ( = beats #3,6,9,12 and 15).

The KEY Remaining Question:

• Are there additional P waves in Figure-2?

Figure-2: I've labeled (with RED arrows) the definite sinus P waves in the long lead II rhythm strip from the 12-lead tracing shown in Figure-1.

To EMPHASIZE: Interpretation of today’s rhythm depends on answering the above question regarding whether additional P waves are present in Figure-2?

• Hopefully — You considered the possibility that additional sinus P waves might be “hiding” within the terminal part of the T waves of each of the PVCs (PINK arrows in Figure-3). If this were the case — then the underlying rhythm would be a fairly (but-not-completely) regular rhythm (ie, sinus arrhythmia).
• Ever-so-slight changes in some of the small upright humps in the T waves under each PINK arrow in Figure-3 — supports the possibility that slightly irregular sinus P waves may be hidden here (ie, the hump in the T waves under the PINK arrows of beats #10 and 13 appears slightly narrower than the hump under the PINK arrows in the T waves of beats #1,4,7).
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• PEARL #2: The reason I knew that P waves were indeed hiding in the T waves under each of the PINK arrows in Figure-3 —  is by use of the concept of simultaneously-recorded leads. The RED arrow in lead V1 of Figure-3 shows what the sinus P wave in this lead looks like. Note that the negative deflection just after the PVC in lead V1 — corresponds precisely with the timing of the small positive hump in the T wave under the PINK arrow following beat #10 in the long lead II rhythm strip (as shown by the vertical PINK time-line in Figure-3).

Remaining QUESTIONS:

• What then is the rhythm in today’s tracing?
• WHY is there no “compensatory” pause after each PVC? (ie, after beats #1,4,7,10 and 13)?
• Since each of the arrows in Figure-3 represent sinus P waves, and, since the PR interval is increasing within each “group” of beats — Why is this not Mobitz I 2nd-degree AV block?

Figure-3: I've added PINK arrows to the long lead II rhythm strip in today's tracing — to show where additional sinus P waves are hiding (See text).

ANSWERS to the Above Questions:

It’s easiest to answer the above questions with a Laddergram (See Figure-4 below).

• As I’ve often emphasized, although learning to draw laddergrams takes time and practice — learning to read laddergrams that are already drawn for you is not difficult, and can be quickly learned. (For those interested in practice reading and/or learning to draw laddergrams — there are more than 80 practice examples on my ECG Blog #188).
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• For the laddergram in Figure-4 — it is easiest to appreciate the mechanism of today’s rhythm by ignoring beats #1 and 2, and beginning with beat #3.
• Note that each of the sinus P waves before beats #3,6,9,12 and 15 — are conducted to the ventricles with no more than the very slight delay from the 1st-degree AV block (ie, RED lines passing sequentially through the Atrial, AV Nodal and Ventricular Tiers in the laddergram).
• Beats #1,4,7,10 and 13 are PVCs — which is why I’ve drawn these impulses starting from the ventricles. The PVCs in the Figure-4 laddergram are "interpolated" — because unlike most PVCs, that are associated with a fully “compensatory” post-ectopic pause (ie, a pause equal to twice the normal R-R interval) — “interpolated” PVCs are not followed by this long of a pause (See Figure-5 below for laddergram illustration of a compensatory pause).
• That said — the retrograde conduction that arises from interpolated PVCs (shown in Figure-4 as dotted RED lines extending backward into the AV Nodal Tier) — may delay conduction of the next on-time sinus impulse, causing an increase in the PR interval of the next sinus-conducted beat (ie, the slight increased inclination of the BLUE lines in the laddergram).

PEARL #3: Although the PR interval before beats #2,5,8,11 and 14 is increased (compared to the PR interval before beats #3,6,9,12 and 15) — We can not see why this is happening solely on the basis of the surface ECG that is shown in Figure-3. Instead — We have to postulate that the reason the PR interval lengthens — is that retrograde conduction from the interpolated PVCs must be delaying conduction of the next on-time sinus impulse (as depicted by the dotted RED lines in Figure-4). 

• This phenomenon of trying to explain events that are not evident on the surface ECG — is known as "concealed" conduction. The importance of being aware of this phenomenon — is to recognize that the increase in PR interval for beats #2,5,8,11 and 14 in today's tracing — is the result of concealed conduction (and not due to Mobitz I, 2nd-degree AV block). 

Figure-4: Laddergram illustration of today's tracing.

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Final POINT: As alluded to above — most PVCs are not interpolated. Instead — most PVCs are followed by a "compensatory" pause, as shown for beat #7 in schematic Figure-5.

• The significance of interpolated PVCs is the same as for any other PVC. Clinically — the main reason to be aware of the unusual appearance of interpolated PVCs (sandwiched between 2 sinus beats without a full compensatory pause) — is to recognize this phenomenon when it occurs — and to know that the PR interval of the sinus beat following an interpolated PVC may be prolonged as a result of concealed conduction (and that this is not the result of 2nd degree AV block of the Mobitz I type).

Figure-5: Schematic laddergram illustration of premature beats. Beats #1 and 2 are normal sinus-conducted P waves. Beat #4 is a PAC — beat #7 is a PVC — and beat #10 is a PJC. The PVC is said to be "fully compensatory" — because the R-R interval between beats #6-to-8 equals twice the normal R-R interval. This is because retrograde conduction from the PVC prevents the next on-time P wave from being conducted to the ventricles. 

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P.S.: Now that we've interpreted the rhythm in today's case — it's important to take another LOOK at the rest of the 12-lead ECG (ie, at Figure-3).

• The rhythm is sinus with frequent interpolated PVCs. QRS voltage is overall reduced. Intervals and the axis are normal. There is no chamber enlargement.

Regarding Q-R-S-T Changes: 

• There is a QS in leads V1,V2, with slight delay in transition (ie, the R wave does not become taller than the S wave is deep until between leads V4-to-V5). There are no other Q waves.
• The most remarkable finding — is that T waves in the sinus-conducted beats in chest leads look peaked, and potentially taller-than-they-should-be given R wave amplitude in leads V2-thru-V6.  
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• IMPRESSION: The patient in today's case is an older woman who did present with chest pain. Her ECG does manifest frequent PVCs — and potentially hyperacute T waves. More information and follow-up is needed (ie, serial ECGs, troponins — more history to determine if her symptoms are a result of frequent ectopy or possibly of an acute event). Unfortunately — I have no additional follow-up for this case ...

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Acknowledgment: My appreciation to 유영준 (from Seoul, Korea) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• ECG Blog #185 — Reviews the Ps, Qs, 3R Approach to Arrhythmia Interpretation.
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• ECG Blog #188 — reviews how to read and/or draw Laddergrams (with more than 80 practice examples! ).
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• ECG Blog #68 and ECG Blog #359 — Review of interpolated PVCs.