ECG Blog #425 — Are there P Waves?

I was sent the ECG in Figure-1 — told only that the patient was 70 years old, and had a history of an ASD (Atrial Septal Defect). 

• Serum K+ was normal.
• The patient was hemodynamically stable with ECG #1.

QUESTIONS:

• How would YOU interpret the rhythm in Figure-1?
• Are there P waves?

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

MY Initial Thoughts on Today's CASE:

Knowing that today's patient has a history of an ASD (Atrial Septal Defect) — is relevant to the interpretation of today's interesting tracing!

• There are many variations of ASDs — with severity of this entity and the age at which the patient presents dependent on multiple factors. Surprisingly, patients with an ASD may present for medical attention at any age. 
• Many patients go years without significant symptoms. That said — most patients eventually do become symptomatic (Webb and Gatzoulis: Circulation 114: 1645-1653, 2006).
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• PEARL #1: Given a potentially longterm course for the patient with an ASD — it's important to appreciate that a lack of symptoms does not necessarily exclude the possibility of hemodynamically significant heart disease.
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• PEARL #2: The ECG may provide clues to the underlying severity of the ASD in a given patient — especially in the adult patient who is not overtly symptomatic. Thus, the finding of any of the following may all portend more significant underlying disease: i) Rhythm disturbances (ie, AV block; AFib/AFlutter; other atrial arrhythmias); ii) Signs of RVH and/or pulmonary hypertension (RAA, right axis, tall R and/or qR pattern in lead V1; ST-T wave changes of RV "strain"; incomplete or complete RBBB); and/or iii) LVH.
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• Given complexity of the multiple facets of ASD management during the course of a patient's lifetime — lifelong adult CHD (Congenital Heart Disease) care is recommended, as potential timing of surgical repair in adulthood is a very challenging determination to make (Cotts — Eur Heart J 43:2260-2671, 2022 — and — Lopes and Mesquite — Arq Bras Cardiol 103(6):446-448, 2014).
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• NOTE: For more on ECG recognition of RVH and/or pulmonary hypertension (re the qR pattern in lead V1) — See ECG Blog #234 and Blog #248.

Regarding the Initial ECG in Figure-1:

Realizing some technical faults with ECG #1 (slight folding and angulation of the ECG — therefore some distortion of measurements) — there appears to be a regular WCT (Wide-Complex Tachycardia) at ~135/minute, but without clear sign of sinus P waves.

• I've labeled the initial ECG in Figure-2 — to highlight the areas of uncertainty that I had in assessing this tracing. Specifically — I was not at all certain whether the BLUE arrows and question marks represented P waves with a long PR interval — or — T waves from the preceding QRS with a long QTc — or — the combination of T waves that are "fusing" with underlying atrial activity?
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• KEY Point: Given obvious QRS widening in ECG #1 — distinction between P waves vs T waves vs a combination of both is an essential determination for whether today's rhythm is likely to be supraventricular or VT (Ventricular Tachycardia).
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• PEARL #3: Knowing that today's patient has an ASD led me to suspect some form of SVT (SupraVentricular Tachycardia) instead of VT, because of how common RBBB conduction defects are in the patient with a significant ASD. And although QRS morphology in Figure-2 is somewhat unusual — the findings of QRS widening with a QR pattern in lead V1, with wide terminal S waves in lateral leads I and V6 — especially given marked fragmentation (notching) in multiple leads — could certainly be consistent with adult CHD in which the patient had a longstanding, hemodynamically significant ASD with significant underlying structural abnormality. 

Figure-2: Do the BLUE arrows and question marks represent P waves? — T waves? — and/or a fusion of T waves with underlying atrial activity?

PEARL #4: If the BLUE arrows and question marks in Figure-2 are the result of sinus P waves (that are perhaps fusing with preceding T waves) — then the PR interval would be prolonged.

• That said, as the rate of a sinus rhythm increases — the PR interval tends to shorten, probably the result of reduced basal vagal tone. Because of this, it is uncommon to see sinus tachycardia with a prolonged PR interval.
• While there are some patient who have baseline PR interval prolongation, who continue to manifest a certain amount of PR interval prolongation with sinus tachycardia — most tachycardias that seem to show a "sinus P wave" near the mid-point of the R-R interval turn out to have 2:1 AV conduction (from either ATach or AFlutter).
• As discussed in ECG Blog #227 — this principle is known as the Bix Rule, named after the Viennese cardiologist who first cautioned against "accepting" the diagnosis of "sinus tach with 1st-degree" before meticulous search for an "extra" P wave hidden within the QRS complex.
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• KEY Point: If I was able to identify 2:1 atrial activity — this would virtually confirm my suspicion that today's rhythm was some form of SVT (and not VT) — since coincidental occurrence of 2:1 atrial activity with perfectly timed simultaneous VT is extraordinarily rare.

Searching for Extra P Waves:

I illustrate in Figure-3 — how to assess the possibily of 2:1 atrial activity in today's tracing. 

• IF today's tracing was the result of an SVT with 2:1 AV conduction (from either ATach or AFlutter) — then we would expect to see evidence of an additional atrial deflection (P wave or flutter wave) at that point precisely midway between successive atrial deflections (ie, between successive RED lines in Figure-3).
• Whereas it is impossible to tell if an extra atrial deflection might be lying under the PURPLE lines in leads aVF and V3 (since the PURPLE line occurs in the middle of the QRS in these leads) — I would have expected to see some form of upright deflection under the PURPLE arrow in leads I and V2 if there was 2:1 atrial activity.
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• BOTTOM Line: While important to consider the possibility of an SVT rhythm with 2:1 AV conduction in Figure-3 — I see no evidence to support this theory.

Figure-3: How to assess for possible 2:1 atrial activity.

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Putting It All Together:

At this point in my assessment of today's rhythm — I fully acknowledge that I did not know for certain the etiology of this arrhythmia.

• I had established that today's rhythm was a regular WCT at ~135/minute — but with uncertain (if any) atrial activity. The differential diagnosis is between some form of SVT vs VT (especially since we were told that serum K+ was normal).
• Given the history of an ASD — I thought an SVT would be more likely than VT, because QRS morphology in today's rhythm looked potentially consistent with adult CHD in a patient with longstanding, underlying structural disease (ie, given the widened QR pattern in lead V1 — with wide terminal S waves in lateral leads + marked fragmentation of several QRS complexes).
• I was hoping to find evidence for 2:1 atrial activity — because if present, this would virtually confirm that today's rhythm was supraventricular. Unfortunately — my search for 2:1 atrial activity (as shown in Figure-3) was unsuccessful.
• This could have been an optimal time to try a Lewis Lead — which sometimes reveals atrial activity not evident with standard lead placement (See ECG Blog #223).
• Finding a prior tracing on today's patient could also prove insightful — especially if at a slower heart rate with sinus rhythm, the same QRS morphology is seen as appears in Figure-3. Unfortunately — no prior tracing was available at this time.
• The "good news" — is that today's patient was hemodynamically stable, which meant there was at least a moment of time to try to attain greater certainty as to the etiology of the rhythm.
• Learning more about the patient's history could be insightful.

The CASE Continues:

• The patient's medical record was found. Recent Echo showed a large Ostium Secundum ASD defect — with left-to-right shunting and huge dilatation of right-sided chambers.
• It turns out the patient had been symptomatic — with progressively increasing exertional dyspnea over the past few months.

The initial ECG was repeated — and is shown in Figure-4.

QUESTIONS:

• How would you interpret the repeat ECG shown in Figure-4?
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• Does ECG #2 clarify what the initial rhythm was?

Figure-4: ECG #2 is a repeat ECG, done later that day. 

MY Thoughts on the Repeat ECG in Figure-4:

For clarity with measurements in ECG #2 — I've drawn in 5 large boxes on the ECG grid (seen in between leads I and II in Figure-4). Note when comparing this repeat tracing with the initial ECG in today's case — that because many more beats are captured in ECG #2, that the relative size of a large box on ECG grid paper is different between these 2 tracings.

• Group beating in the form of a bigeminal rhythm (alternating shorter-then-longer R-R intervals) is present in ECG #2. This bigeminal rhythm is most easily appreciated in leads V5, V6. 
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• Sinus rhythm has been restored! (RED arrows in Figure-5 showing clearly defined P waves in this repeat ECG in multiple leads — with return to sinus rhythm defined by the presence of upright P waves with fixed PR interval in lead II).
• Every-other-beat in Figure-5 is a PAC (highlighted by YELLOW arrows that show a slight-but-real different P wave morphology for these PACs, that are clearly narrower than the RED-arrow P waves of sinus beats).

Figure-5: I've labeled the repeat ECG — which shows a bigeminal rhythm in which every-other-beat is a PAC (YELLOW arrows).

CASE Conclusion:

Comparison of the 2 ECGs in today's case allows a definitive diagnosis of the rhythm in the initial ECG to be made retrospectively. Consider Figure-6:

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• Please NOTE in Figure-6: When comparing leads aVF and V6 from ECG #2 — with ECG #1 — that the relative size of a large box on ECG grid paper in my illustration is different between ECG #1 and ECG #2.

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• It is because the overall heart rate has slowed in ECG #2 — that we are able to see sinus P waves emerge from where they were hiding within the preceding T waves. Sinus P waves (RED arrows) are now clearly seen for even-numbered beats in leads aVF and V6 of this repeat tracing.
• We are able to see the pointed P waves of the PACs in lead aVF of ECG #2 (YELLOW arrows).
• However, in lead V6 — we are not able to clearly distinguish the P waves of PACs, because these YELLOW-arrow PACs in lead V6 "fuse" with the preceding T wave.
• Now imagine in your "mind's eye" if the rate of the atrial bigeminy rhythm in lead aVF of ECG #2 was a little bit faster. Wouldn't fusion of the RED-arrow sinus P waves in lead aVF with the T waves preceding them be expected to produce a similar picture of fused P wave and T wave, as is seen in lead aVF of ECG #1?
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• BOTTOM Line: Retrospectively — the return of sinus rhythm with atrial bigeminy in ECG #2 strongly suggests that the rhythm in ECG #1 was sinus tachycardia at ~135/minute, in which tall, pointed inferior lead P waves from this patient's longstanding ASD fused with the T waves that preceded them to produce the unusual QRS appearance in ECG #1.
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• PEARL #5: The KEY to proving that the mechanism of a tachycardia is sinus — is frequent ECG monitoring that once the cause of sinus tachycardia is treated, will result in enough slowing of the tachycardia rate to allow sinus P waves to emerge from where they were hiding in the preceding T waves. This is precisely what we see in Figure-6.

Figure-6: Comparison between today's initial ECG — and leads aVF and V6 in the repeat tracing. Slight slowing of the heart rate with return to a sinus mechanism allows sinus P waves to emerge from where they were hiding in the preceding T waves.

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ADDENDUM (4/14/2024):

Based on some questions that have arisen regarding the PR intervals in ECG #1 and ECG #2 — I've added Figure-7, that I hope will clarify my discussion.

• I fully acknowledge that the difference in size of the ECG grid in the 2 tracings that I show here is potentially confusing. Rather than digitizing both tracings (which risks introducing error inherent with digitization of fine measurements from ECGs that are not completely flat and completely straight) — I thought it better to show the original ECGs.
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• I've added PINK lines in Figure-7 to show that by my measurements — the PR interval in the initial ECG (TOP = lead II rhythm strip) measures just under 1 large box (corresponding to a PR interval = 0.18 second).
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• By my measurements — this is the same PR interval ( = 0.18 second) that I measure for the sinus beats (RED arrow P waves) in lead aVF of ECG #2.
• The PR interval for the PACs (YELLOW arrow P waves) in ECG #2 appear to have a slightly longer PR interval — but PR interval duration of PACs may vary depending on from where in the atria the PACs arise, as well as conduction velocity through the atria, which may be altered by early occurrence of these supraventricular impulses.
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• BOTTOM Line: I wish I had additional tracings. I wish I had tracings that were scanned completely flat and straight. And I wish I had record of ECG monitoring just before — and during — and just after the rhythm changes from the regular tachycardia in ECG #1 — to the bigeminal rhythm in ECG #2. Unfortunately — I lack this information. 
• That said — I thought my discussion in today's case to be a valid explanation based on the 2 tracings that I have (in which I believe that the PR interval is virtually the same for sinus-conducted beats in ECGs #1 and #2). But I fully acknowledge that other explanations may be possible.

As always — Comments from my readers are welcome! — :) 

Figure-7: In the hope of clarifying PR interval duration in ECG #1 and ECG #2 — I've written out the measurements I've made (See text).

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Acknowledgment: My appreciation to Ella Hmayer (from Tunisia) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #185 — Reviews my System for Rhythm Interpretation, using the Ps, Qs & 3R Approach.
• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
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• ECG Blog #210 — Reviews the Every-Other-Beat (or Every-Third-Beat) Method for estimation of fast heart rates — and discusses another case of a regular WCT rhythm. 

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• CLICK HERE — for my 6 new ECG Videos (on Rhythm interpretation — 12-lead interpretation with Case Studies for ECG diagnosis of acute OMI).
• CLICK HERE — for my 2 new ECG Podcasts (on ECG & Rhythm interpretation Errors — and — Errors in assessing for acute OMI).

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• ECG Blog #220 — and ECG Blog #361 — Review of the approach to the regular WCT ( = Wide-Complex Tachycardia).
• ECG Blog #196 — Reviews another Case with a regular WCT rhythm.
• ECG Blog #263 and Blog #283 — More WCT Rhythms ...
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• ECG Blog #227 — Reviews the "Bix Rule" (Looking for 2:1 atrial activity when you see a long PR interval with a tachycardia).
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• For more on ASD in Adults — Webb and Gatzoulis: Circulation 114: 1645-1653, 2006.
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• ECG Blog #197 — Reviews the concept of Idiopathic VT, of which Fascicular VT is one of the 2 most common types. 
• ECG Blog #346 — Reviews a case of LVOT VT (a less common idiopathic form of VT).
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• ECG Blog #204 — Reviews the ECG diagnosis of the Bundle Branch Blocks (RBBB/LBBB/IVCD). 
• ECG Blog #203 — Reviews ECG diagnosis of Axis and the Hemiblocks. For review of QRS morphology with the Bifascicular Blocks (RBBB/LAHB; RBBB/LPHB) — See the Video Pearl in this blog post.
• ECG Blog #211 — WHY does Aberrant Conduction occur?
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• ECG Blog #301 — Reviews a WCT that is SupraVentricular! (with LOTS on Aberrant Conduction).
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• ECG Blog #323 — Review of Fascicular VT. 
• ECG Blog #38 and Blog #85 — Review of Fascicular VT.
• ECG Blog #278 — Another case of a regular WCT rhythm in a younger adult.
• ECG Blog #361 — A regular WCT in a middle-aged man.
• ECG Blog #35 — Review of RVOT VT. 
• ECG Blog #42 — Review of criteria for distinguishing VT vs aberrant conduction.
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• ECG Blog #422 — Reviews another case of adult Congenital Heard Disease.