ECG Blog #241 (56) — Fascinating Bigeminy

The 12-lead ECG and long lead II rhythm strip shown in Figure-1 was obtained from a man in his 60s who presented with a complicated course, including high fever and chest pain. The patient was unresponsive without a pulse on arrival in the ED (Emergency Department) — but promptly responded to resuscitation (albeit with hypotension) — at which time ECG #1 was obtained.

• Unfortunately — details of this patient's subsequent course were not available to me. That said — I thought the ECG in Figure-1 was fascinating and instructive enough to present the case without additional clinical follow-up.

 

QUESTIONS:

• What is the rhythm in Figure-1?
• What ELSE is going on in this tracing?
• Are there Osborn waves? IF so — What might this mean?

Figure-1: ECG and long lead II rhythm strip obtained following resuscitation of a patient with fever and chest pain (See text).

 

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NOTE: Some readers may prefer at this point to listen to the 5:35-minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to refer to My Thoughts on this tracing (that appear below ECG MP-56).

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Today's ECG Media PEARL #56 (5:35 minutes Audio) — What are Osborn Waves? (HINT: Osborn waves are not only seen with Hypothermia! ) 

 

 

MY Initial Approach to the ECG in Figure-1:

This is an especially challenging ECG — because QRS morphology is constantly changing in the 12-lead tracing. CONFESSION: I fully acknowledge that I was initially confused as to what was going on.

• PEARL #1: When in doubt about the etiology of a cardiac rhythm — Be systematic! Start with the long lead rhythm strip by addresing the 5 KEY parameters contained in the Ps, Qs & 3Rs Approach (See ECG Blog # 185).
• Because of the confusing, constantly-changing QRS morphology in the 12-lead ECG — I initially ignored the 12-lead — in the hope that understanding the rhythm would help me to sort out what was going on in the 12-lead.

My sequential thought process for assessing the rhythm in Figure-1 is outlined below. As part of my narrative — I include the questions I asked myself.

• There is group beating (ie, repetitive groups of 2 beats in a "long-short" pattern). So, although the ventricular rhythm is not Regular — some type of "organized" pattern to the rhythm is present.
• P waves are present! At least some of these P waves are conducting — as determined by the presence of P waves with a constant (and normal) PR interval preceding each of the QRS complexes that occur at the end of the longer R-R intervals (ie, RED arrows in front of beats #2,4,6,8,10 and 12 in Figure-2). This tells us there is an underlying sinus rhythm.
• The QRS complex is narrow for each of the sinus-conducted beats (ie, beats #2,4,6,8,10 and 12).

Figure-2: I've added RED arrows for those sinus P waves that we know are conducting. (See text).

 

QUESTION: In addition to the P waves highlighted by the RED arrows in Figure-2 — Are there more P waves on this tracing?

• HINT: What does the YELLOW arrow in Figure-2 suggest?

 

 

 

PEARL #2: I find the simple act of labeling P waves to be immensely helpful in facilitating rhythm recognition.

• I was not initially certain whether the hump in the ST segment of beat #3 (YELLOW arrow) represented another sinus P wave. But this hump looked to be about midway between the first 2 RED arrows in this figure — and the shape of this hump looked similar to the shape of other sinus-conducting P waves.
• Use of calipers provided me with the answer in a matter of seconds! (Figure-3).

 

Figure-3: Use of calipers allows us to walk out regular P waves throughout the rhythm strip (RED arrows). The atrial rate is ~80/minute. — NOTE: There is ever-so-slight variation in the P-P interval in Figure-3. This is common — and simply reflects slight sinus arrhythmia. But the presence of an underlying sinus rhythm (with almost regular sinus P waves) should be obvious.

 

QUESTION: Are all of the P waves in Figure-3 conducting? 

• HINT: Are the QRS complexes of beats #3,5,7,9,11 and 13 preceded by a P wave?

 

 

ANSWER: Beats #1,3,5,7,9,11 and 13 are not preceded by a P wave. Instead — an on-time sinus P wave occurs just after the QRS of these beats (PINK arrows in Figure-4).

• The fact that the on-time sinus P waves highlighted by PINK arrows are not followed by a QRS complex tells us that beats #1,3,5,7,9,11 and 13 can not possibly be conducted. Instead — these beats must originate from below the AV node! (ie, beats #1,3,5,7,9,11 and 13 can not possibly be PACs or PJCs — because if they were — they would reset the next sinus P wave!).

 

Figure-4: For clarity — I've colored in PINK the on-time sinus P waves that are not conducting. We know that these PINK P waves can not possibly conduct — because they occur in the refractory period of beats #1,3,5,7,9,11 and 13 — and they are not followed by a QRS complex.

 

PEARL #3: Use of simultaneously-recorded leads saves the day!

• We have just established that beats #1,3,5,7,9,11 and 13 must be originating from below the AV node. This conclusion initially surprised me — because in the long lead II rhythm strip, these beats did not look wide, and they looked similar in morphology to the sinus-conducting beats that occur before them.
• For clarity — I have highlighted within blue-white rectangles in Figure-4 the appearance of beats #3, 9 and 13 in other simultaneously-recorded leads. 12 leads are better than one. It should now be obvious that QRS morphology of beats #1,3,5,7,9,11 and 13 is very different than the QRS morphology of sinus-conducted beats #2,4,6,8,10 and 12.

 

 

QUESTION: If beats #1,3,5,7,9,11 and 13 are not supraventricular — then WHERE are they coming from? 

• HINT: Looking within the blue-white rectangles in Figure-4 — How WIDE are these beats? — and WHAT conduction defect(s) is suggested by their morphology in other simultaneously-recorded leads?

 

 

 

ANSWER: Looking within the simultaneously-recorded leads in Figure-4 — beats #1,3,5,7,9,11 and 13 are slightly (but not greatly) wider than the sinus-conducted beats that precede them. This is best seen for beat #9 in lead V1 — in which the qR complex in this lead measures ~0.11 second in duration.

• QRS morphology for beats #1,3,5,7,9,11 and 13 is consistent with RBBB (widened, qR pattern in lead V1 + wide terminal S waves in lateral leads I and V6) and LPHB (very deep and rapidly descending S wave in lead I + predominant R waves in leads II and III).
• NOTE: For review of how to quickly determine the bundle branch blocks and hemiblocks — See ECG Blog #204 (for BBBs) and ECG Blog #203 (for hemiblocks).

 

 

PEARL #4: We have already established that non-conducting beats #1,3,5,7,9,11 and 13 must be originating from below the AV node. But the fact that these beats are not overly wide — and — that their QRS morphology is consistent with a known type of conduction defect (ie, RBBB/LPHB) — suggests that these bigeminal beats originate from somewhere within the conduction system.

• Simply stated — there are 3 branches to the conduction system. These are: i) the right bundle branch (RBB); ii) the left anterior hemidivision (LAH) of the left bundle branch; and, iii) the left posterior hemidivision (LPH) of the left bundle branch.
• The EASY way to determine the origin of an escape or ectopic beat that manifests a hemiblock pattern — is that the complex arises from the remaining fascicle. Thus, in Figure-4 — since beats #1,3,5,7,9,11 and 13 manifest RBBB/LPHB morphology — these must be fascicular beats arising from the left anterior hemifascicle!
• I schematically illustrate the mechanism of the rhythm in today's case in the laddergram shown in Figure-5.

 

 

Figure-5: Laddergram illustrating the mechanism for the rhythm in today's case. The rhythm is ventricular (or more precisely, fascicular) bigeminy — in which beats #1,3,5,7,9,11 and 13 originate from the left anterior hemifascicle (LAH) in the ventricles.

 

 

What About the REST of the ECG?

Take another look at 12-lead ECG in Figure-5. Keeping in mind that this patient presented to the ED unresponsive, with a history of an acute febrile illness + chest pain — and — knowing that the rhythm in the long lead II rhythm strip is fascicular bigeminy — WHAT are your concerns?

• QUESTION #1: Are there acute ST-T wave changes?
• QUESTION #2: Are there Osborn waves?

 

 

 

PEARL #5: It is often challenging to interpret a 12-lead ECG for acute ST-T wave changes when QRS morphology in each of the leads is constantly changing. To address this challenge — I suggest the following:

• FIRST — Identify sinus-conducted beats in each of the 12 leads! In Figure-5 — the sinus-conducted beats are beats #2,4,6,8,10 and 12.
• Look at leads in a given "lead area" together. For example — beat #2 in both leads II and III shows J-point notching and 1-1.5 mm of ST elevation. The 3rd inferior lead is lead aVF — and sinus-conducted beats #4 and 6 in lead aVF show similar J-point notching and ST elevation as was seen in the other inferior leads.
• The QRS complex is tiny for both of the sinus-conducted beats in high lateral leads I and aVL. It is difficult to draw conclusions regarding ST-T wave appearance in these leads.
• In the chest leads — there is normal R wave progression (with transition between leads V3-to-V4) for sinus-conducted beats #8 and 12. Unfortunately — sinus-conducted beat #10 is obscured by the lead change. Of concern — is ST elevation that begins in lead V2 (for beat #8) — and which then increases (up to 3mm!), and continues through to lead V6 (for beat #12). Small q waves and prominent J-point notching is seen in leads V5 and V6 for beat #12.

 

PEARL #6: It clearly is more difficult to assess ST-T waves for acute changes with premature ventricular beats. That said — there are times when acute ST elevation or abnormal ST depression may only be seen in PVCs. As a result — it is always worthwhile to look at PVCs on the ECG of a patient with new-onset symptoms, because sometimes you will see clear indication of acute ST-T wave changes that may not always be evident in normal sinus-conducted beats!

• Since the PVCs in Figure-5 are of fascicular etiology (ie, originating from within the conduction system) — it is even more likely that we may be able to see acute ST-T wave changes in at least some of these fascicular beats. Note the worrisome shape and marked amount of ST elevation in lateral chest leads V4, V5 and V6 for fascicular beats #11 and 13!

 

 

What about the Osborn Waves?

Note the profound J-point notching in the inferior and lateral chest leads (YELLOW arrows in Figure-6)! This patient was not hypothermic (On the contrary — this patient presented with an acute febrile illness).

• I interpreted the profound J-point notching in Figure-6 as most probably representing Osborn waves. Review of J Wave Syndromes (of which Osborn waves are one of the key entities) — is the subject of today's Audio Pearl (ECG-MP-56).
• An Osborn wave is a deflection with a dome or hump that occurs at the J-point, which is the point where the end of the QRS complex joins with the beginning of the ST segment. While Osborn waves are most commonly associated with hypothermia — it's important to appreciate that this ECG finding has been associated with a number of other conditions, including cardiac arrest and acute myocardial infarction.

 

PEARL #7: More on Osborn waves can be found in my Audio Pearl above (ECG-MP-56). That said — several points merit repetition:

• J Wave Syndromes represent a spectrum of disorders, with certain repolarization variants at one end of the spectrum — and Brugada Syndrome at the other end. Hypothermia-induced Osborn waves represent another part of this spectrum.
• Until recently — awareness was lacking that acute development of exaggerated J waves (ie, Osborn waves) could be a manifestation of acute ischemia (Antzelevitch and Yan and Rituparna et al). This appears to be a transient finding — in which persistence of acute ischemia leads to integration of J-point prominence into the increasingly elevated ST segments. While not commonly reported at the present time — I suspect increased awareness of ischemia-induced Osborn waves will result in more frequent detection of this phenomenon.
• Admittedly — proof is lacking in today's case that J-point prominence in Figure-6 represents ischemia-induced Osborn waves. Support of this assumption could be forthcoming: i) IF a prior baseline ECG on this patient could be found, in which prominent J waves were absent (thus proving that both ST elevation and the J waves were new); and/or, ii) IF serial tracings on this patient showed evolution in the amount of J-point prominence, with resolution after acute reperfusion. That said — given the high (not low) body temperature + the history of chest pain + the ominous shape and amount of diffuse ST elevation in Figure-6 — I felt it likely that J-point prominence highlighted by the YELLOW arrows was ischemia related.
• Clinically — the importance of recognizing ischemia-induced Osborn waves, is that this finding appears to identify patients at high risk for development of malignant ventricular arrhythmias (Rituparna et al). Prompt cath with acute reperfusion seems especially indicated in such patients to reduce risk of VFib. 

Figure-6: I've added YELLOW arrows to the 12-lead ECG from Figure-5 to highlight Osborn waves (See text).

 

In SUMMARY: The rhythm in today's case is fascicular bigeminy. There is diffuse, worrisome ST elevation in multiple lead areas suggestive of an acute evolving STEMI. J-point promience in multiple leads suggests ischemia-related Osborn waves — and adds to concern regarding increased risk for malignant ventricular arrhythmias.

• Unfortunately, additional follow-up in this case is lacking.

 

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Acknowledgment: My appreciation to Ong Hooi Yee (from Malaysia) for allowing me to use this tracing.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #185 — Systematic Approach to Rhythm Interpretation. 
• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation. 
• ECG Blog #188 — Reviews HOW to Read and Draw Laddergrams.
•  
• ECG Blog #204 — Reviews rapid assessment of the Bundle Branch Blocks. 
• ECG Blog #203 — Reviews rapid assessment of the Hemiblocks.
•  
• Antzelevitch C, Yan G-X: J Wave Syndromes. Heart Rhythm 7(4): 549-558, 2010 — is a detailed review by these experts that contains all one could hope to know regarding the etiology and pathophysiology of J Wave Syndromes (including Osborn waves — Brugada Syndrome — and arrhythmogenic Early Repolarization patterns).
• Rituparna S et al: Occurrence of "J Waves" as a Marker of Acute Ischemia (and their Cellular Basis). Pacing Clin Electrophysiol 30(6): 817-819, 2007. 
• ECG Blog #149 — Reviews a case of Osborn Waves from Hypothermia. 
• ECG Blog #172 — Reviews another case of Osborn Waves from Hypothermia. 
• The November 22, 2019 post in Dr. Smith's ECG Blog — Please scroll down to the BOTTOM of the page for My Comment on this case with "Shark Fin" ST elevation and Osborn Waves from acute STEMI. 
• The September 23, 2020 post in Dr. Smith's ECG Blog — Please scroll down to the BOTTOM of the page for My Comment on this additional case of Osborn Waves from acute STEMI.

ECG Blog #240 — What Kind of Regular SVT?

Today's blog is about assessing the regular SVT (SupraVentricular Tachycardia). The patient whose ECG is shown in Figure-1 presented with "palpitations". He was hemodynamically stable.

• How would you interpret the ECG in Figure-1?
• And — Can you tell the mechanism of this rhythm?
• P.S. — How many of the PEARLS listed were new to you?

Figure-1: How would you interpret this ECG? (See text).

  

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NOTE: Some readers may prefer at this point to listen to the 4:20-minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to refer to My Thoughts on this tracing (that appear below ECG MP-55).

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Today's ECG Media PEARL #55 (4:20 minutes Audio) — What does the term, "SVT" mean? This Audio Pearl reviews the semantics and clinical application involved in use of this term. 

 

 

My Initial THOUGHTS on ECG #1:

As usual — I approach rhythm interpretation in systematic fashion by addresing the 5 KEY parameters contained in the Ps, Qs & 3Rs Approach (See ECG Blog # 185).

• NOTE: There is no need to assess the 5 parameters in order (ie, I'll often look at QRS width or regularity of the rhythm before looking for P waves — depending on which of the 5 parameters is easiest to assess for the tracing at hand). 

 

My sequential thought process for the rhythm in Figure-1 was the following:

• The QRS complex is narrow — so the rhythm is supraventricular.
• Sinus P waves are absent (ie, there is no upright P wave in lead II — although, as will be discussed momentarily — it appears that there may be other signs of atrial activity).
• The ventricular rhythm is Regular.
• The R-R interval is just over 2 large boxes in duration — so the Rate of the rhythm is just under 150/minute.

IMPRESSION: The rhythm in Figure-1 is a regular SVT rhythm at ~140/minute — but without clear sign of sinus P waves.

• Looking at the rest of the ECG — there is marked left axis deviation (consistent with LAHB) — no chamber enlargement — early transition (ie, R wave height already equals S wave depth as early as between lead V1-to-V2) — and — some nonspecific ST-T wave abnormalities (that may be rate-related — and which are probably not acute).

 

PEARL #1: Recognition that the rhythm in Figure-1 is a regular SVT — but without clear sign of sinus P waves (ie, without a definite upright P wave in lead II) — should prompt consideration of the followling differential diagnosis LIST:

• i) Sinus Tachycardia (IF there is a possibility that sinus P waves might be hiding within the preceding ST-T wave); 
• ii) A reentry SVT (either AVNRT if the reentry circuit is contained within the AV node — or AVRT if an AP [Accessory Pathway] located outside the AV node is involved); 
• iii) Atrial Tachycardia (ATach);
• iv) Atrial Flutter (AFlutter) with 2:1 AV conduction.

 

KEY Point: Although other entities may also produce a regular SVT (ie, sinoatrial node reentry tachycardia, junctional tachycardia) — they are far less common in practice. Therefore, remembering to think of the 4 entities in the above LIST whenever you encounter a regular SVT rhythm without clear sign of sinus P waves — will greatly facilitate determining the correct diagnosis.

• NOTE: Most SVT rhythms manifest a narrow QRS complex. That said — an SVT rhythm may have a wide QRS if there is either preexisting bundle branch block or aberrant conduction due to the rapid rate.

PEARL #2: How Heart Rate helps in SVT Diagnosis:

• Sinus Tachycardia usually does not exceed 160-170/minute in a "horizontal" adult (ie, in a patient you are examining, who has not just been running). This is not to say that sinus tachycardia will never go faster than 170/minute — but rather to suggest that when the rate of the regular SVT rhythm you are assessing is well over this rate range — then the rhythm will probably not be sinus tachycardia. NOTE: All bets are off in children — in whom sinus tachycardia over 200/minute is not that uncommon.
• With AFlutter — the most common ventricular response in the patient who is not being treated with an antiarrhythmic medication is ~150/minute (usual range ~140-160/minute). This is because the atrial rate in untreated AFlutter is most often ~300/minute (usual range ~250-350/minute) — and since untreated AFlutter most often presents with 2:1 AV conduction — 300/2 ~150/minute. As a result — IF the ventricular rate of the regular SVT rhythm you are assessing is over ~170-180/minute — then AFlutter is less likely, because this rate would be faster-than-expected for 2:1 AV conduction, and too slow for 1:1 AV conduction. 
• NOTE: This ~140-160/minute range is for untreated AFlutter. Patients who are already on antiarrhythmic medication may present with a slower atrial rate (and therefore slower ventricular response) for flutter.
• It is well to remember that ATach is less common as a cause for a strictly regular SVT, especially in an otherwise healthy young-to-middle-aged adult. ATach is more likely to be seen in patients referred for EP (ElectroPhysiologic testing) — and in older adults with SSS (Sick Sinus Syndrome). I include ATach in the above differential diagnosis LIST for completeness — but take into account that it won't be seen as often as AFlutter and the reentry SVTs.
• Therefore — IF the rate of a regular SVT without clear sign of sinus P waves is substantially faster than 160-170/minute — then a reentry SVT rhythm (ie, AVNRT or AVRT) becomes the most likely diagnosis. However, IF the rate of the regular SVT is close to 150/minute (ie, 140-160/minute) — then any of the 4 diagnostic entities in the above LIST could be present ( = sinus tach — AVNRT-AVRT — ATach — AFlutter).

PEARL #3: Other Helpful Diagnostic Features:

In addition to the ventricular rate of a regular SVT rhythm — there are a number of other ECG findings that may help with differential diagnosis. These include:

• Detection of Atrial Activity! — I have reviewed on many occasions how using calipers can facilitate detection of 2:1 AV conduction diagnostic of AFlutter (ie, See my discussion in the November 12, 2019 post of Dr. Smith's ECG Blog). As I'll discuss momentarily — detection of retrograde atrial activity can be diagnostic of a reentry SVT rhythm.
• Look for a “Break” (or subtle change) in the Rhythm! — Even a slight pause in the SVT rhythm, may be all that is needed to reveal underlying atrial activity that had been hidden by the regular tachycardia. 
• Look for the “Onset” (and/or Termination) of the Rhythm! — The KEY clue to the etiology of an SVT often lies with capturing either the beginning and/or the end of the SVT. ATach often begins gradually, with progressive acceleration of the ectopic focus (ie, “warm-up” phenomenon). Then, there may be gradual slowing (ie, “cool-down”) of the rhythm as it ends. In contrast — SVT reentry rhythms often start with 1 or more PACs that block conduction down one of the AV nodal pathways, which serves to promptly set up the reentry circuit as the impulse starts down the other pathway. The onset of a reentry SVT is often abrupt (ie, accounting for the previous term used to designate this rhythm = PSVT = Paroxysmal SVT). The termination of reentry SVT rhythms is also usually quick (though this may occur over several beats).

 

PEARL #4: While our goal is to arrive at as precise of a rhythm diagnosis as possible — the "good news" is that for practical purposes — initial diagnostic and/or treatment measures in the field or in the ED for an undifferentiated regular SVT rhythm are similar (ie, consideration of a vagal maneuver — and/or use of an AV nodal blocking agent such as Verapamil/Diltiazem; a ß-Blocker, and possibly Adenosine).

 

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The CASE Continues:

Take another look at the rhythm in Figure-1.

• QUESTION: Do you see any sign of atrial activity?

 

 

 

 

ANSWER:

We have emphasized how sinus P waves are not seen in Figure-1 — as there is no upright P wave that precedes the QRS complex in lead II.

• That said — RED arrows in Figure-2 indicate that there are retrograde P waves! 

 

PEARL #5: Retrograde atrial activity is most easily recognized by the finding of negative P waves in one or more of the inferior leads. This negative P wave deflection may be seen as a notch in the terminal portion of the QRS complex — as a notch in the ST-T wave — or sometimes beyond the end of the T wave. 

• In Figure-2 — retrograde atrial activity is best seen in leads III and aVF (as a negative notch) — and in lead V1 (as a small positive notch that appears just after the r' of the QRS complex). I suspect the negative deflection of the QRS in lead II reflects a combination of S wave + retrograde P wave, though it is more difficult to distinguish a distinct retrograde P wave in this lead.
• KEY Point: The distance from the onset of the R wave until the beginning of the retrograde P wave — is known as the RP' interval.
• IF retrograde P waves are seen in a regular SVT rhythm — and the RP' interval is short (ie, ≤70 msec.) — then AVNRT ( = AtrioVentricular Nodal Reentrant Tachycardia) is likely! (González-Torrecilla et al: Ann Noninvasive Electrocardiol 16(1):85-95, 2011).
• Because precise measurement of the RP' interval is often difficult — I consider the RP' interval to be "short" (ie, predictive of AVNRT) — if retrograde P waves either notch the end of the QRS, or occur very soon after the QRS (as they do in Figure-2, as shown by the RED arrows).

 

Figure-2: I've added RED arrows to Figure-1 to indicate retrograde atrial activity. The RP' interval is short (ie, retrograde P waves immediately follow the end of the QRS complex) — therefore suggesting AVNRT as the mechanism for this SVT rhythm (See text).

Looking Closer at the Retrograde P Waves:

Consider the 3 tracings shown in Figure-3. They each show a regular SVT rhythm, in which sinus P waves (ie, upright P waves in lead II) are not clearly seen.

• ECG #2 — shows a regular SVT at just under 150/minute. The upright deflection near the midpoint in the R-R interval in lead II is almost certainly just a T wave. Against there being a sinus P wave hidden within this T wave — is the fact that this would make the PR interval long (ie, ~0.26 second) — and if anything, the PR interval shortens when there is tachycardia. Although a rate of ~150/minute should always make you think about the possibility of AFlutter — other than possibly lead V6, none of the other 11 leads even remotely suggest 2:1 AV conduction. Instead — the RED arrows in ECG #2 suggest retrograde atrial conduction with a very short RP' interval that notches the terminal portion of the QRS complex (with a positive deflection in lead V1 — and — with suggestion of a negative notch in each of the inferior leads). This rhythm is unlikely to be ATach — because if that upright deflection in lead V1 was a forward-conducting P wave — it would make for an exceedingly long PR interval. This leaves us with a reentry SVT rhythm as the probable diagnosis for ECG #2 (ie, AVNRT or AVRT).
• ECG #3 — shows a regular SVT at ~210/minute. For practical purposes, this rate is too fast to be Sinus Tachycardia. It is also too fast to be AFlutter with 2:1 AV conduction — since this would result in an atrial rate = 210 X 2 = 420/minute, which is much faster than the maximum atrial rate for flutter. AFlutter with 1:1 AV conduction is extremely uncommon, and a flutter rate of 210/minute would be uncharacteristically slow (unless the patient is on antiarrhythmic therapy). ATach is possible, but in the absence of clear sign of ectopic P waves — ATach is far less likely than a reentry SVT, which is a much more common rhythm (as per Pearl #2). While difficult to prove from this single tracing — I suspect that the RED arrows in ECG #3 (that highlight probable negative deflections in the inferior leads, with sharp angulation in lead V3) — represent retrograde atrial conduction with a moderately long RP' interval that occurs well after the QRS complex (within the latter part of the ST segment).
• ECG #4 — shows a regular SVT at ~160/minute. There is a slow, gradual upslope to and beyond the ST segment, that leads up to a very deep, negative P wave (highlighted by RED arrows) in front of each of the inferior leads. This deflection before the QRS is positive in lead aVR. P wave negativity in the inferior leads rules out Sinus Tachycardia. Lack of 2:1 atrial activity rules out AFlutter. This essentially leaves us having to decide between ATach (in which case we'd have to postulate huge negative P waves) vs AVNRT, in which there is retrograde atrial conduction with a very long RP' interval.

Figure-3: For illustrative purposes — Consider the 3 regular SVT rhythms in this Figure. RED arrows represent retrograde atrial activity. (See text).

  

What the RP' Interval Tells Us in Figure-3:

The KEY to the probable etiology for each of the regular SVT rhythms shown in Figure-3 lies with he relative length of the RP' interval. 

• ECG #2 in Figure-3 shows a very short RP’ interval, in which the retrograde P wave distorts the terminal portion of the QRS complex. This is virtually diagnostic of the "slow-fast" form of AVNRT — in which the impulse travels first down the "slow" AV nodal pathway — and back up the "fast" AV nodal pathway. It is because the impulse travels back up (ie, retrograde) over the “fast” AV nodal pathway that the RP’ interval is so short. This “slow-fast” form of AVNRT is by far the most common AVNRT form, so much so that we generally assume “slow-fast” conduction when we simply say “AVNRT”.
• ECG #3 in Figure-3 shows a moderately long RP' interval. This suggests that there may be an AP (Accessory Pathway) participating in the reentry pathway — and that the type of reentry SVT is AVRT. Because the AP lies outside of the AV node with AVRT — the time to circulate around the reentry pathway and conduct back to the atria (retrograde) is longer than when the entire reentry circuit is contained within the AV node. As a result, the retrograde P wave will often be seen to occur within the ST segment, instead of notching the terminal portion of the QRS complex. A follow-up ECG was done on this patient, and did indeed show WPW (See My Comment in the October 16, 2019 post of Dr. Smith's ECG Blog).
• ECG #4 in Figure-1 either shows a very long RP’ interval or an Atrial Tachycardia. Although definitive distinction between an ectopic ATach vs a reentrant SVT rhythm would require EP study — I favor the diagnosis of a reentrant SVT because: i) the shape of the ST segments in ECG #4, leading up to the large negative deflection highlighted by RED arrows looks more like retrograde activity; and, ii) If the rhythm was ectopic ATach, we'd have to postulate huge negative P waves! Therefore — IF we are indeed seeing a very long RP' interval in ECG #4 — then this would represent the far less common "fast-slow" form of AVNRT — in which the impulse travels first down the “fast” AV nodal pathway — and back up the “slow” AV nodal pathway. Retrograde conduction back up the “slow” AV nodal pathway would account for the very long RP’ interval.

 

PEARL #6: Note the PVC toward the end of the long lead II rhythm strip in ECG #4. This illustrates a concept mentioned in Pearl #3 — namely, that clues to etiology will often be found when there is a "break" in the underlying SVT rhythm.

• Note that retrograde atrial activity from "fast-slow" AV nodal reentry continues unaffected by the PVC (vertical GREEN lines in Figure-3).
• The finding of one or more PVCs during a reentrant SVT rhythm that do not convert the rhythm, favors AVNRT over orthodromic AVRT. This is because a premature impulse arising from the ventricles is much more likely to interrupt a reentrant SVT (such as AVRT) in which a part of the cycle passes through the ventricles (via an accessory pathway) on its way back to the AV node. 
• In contrast — the reentrant cycle with AVNRT is entirely contained within the AV node, and therefore far less likely to be "penetrated" and interrupted by a PVC.
• Bottom Line: While EP study would be needed for definitive diagnosis — I strongly suspect the "fast-slow" form of AVNRT for the etiology of the SVT rhythm in ECG #4 instead of AVRT or ectopic ATach.

Help from the Post-Conversion Tracing:

It's important to always repeat the ECG after conversion to sinus rhythm (Figure-4). This is because definitive determination of SVT etiology may only be possible after comparison of the ECG during and after the tachycadia.

• PEARL #7: The BEST way to prove that suspicious deflections during the SVT rhythm were indeed reflective of retrograde atrial conduction — is to obtain a post-Conversion tracing. Note that retrograde atrial activity during the SVT (RED arrows in Figure-4) — is no longer present after conversion to sinus rhythm (BLUE arrows now showing smooth transition from the end of the QRS to the beginning of the ST segment). The only possible explanation is that the RED arrows represented retrograde P waves from a reentrant cycle with a very short RP' interval — such that the rhythm in ECG #2 was AVNRT.

Figure-4: Comparison of the SVT rhythm in ECG #2 with the post-Conversion tracing proves that the SVT rhythm was AVNRT (See text).

  

The Mechanism of the "Fast-Slow" form of AVNRT:

Finally — Consider the rhythm shown in Figure-5.

• QUESTION: Can you explain what is happening in Figure-5?

 

Figure-5: A final example of a regular SVT rhythm. How does this SVT begin? (See text).

 

 

ANSWER:

The laddergram in Figure-6 reveals the mechanism operative for the SVT rhythm in ECG #5. This illustrates another concept mentioned in Pearl #3 — namely, that the onset and/or termination of the SVT rhythm may provide an invaluable clue to etiology.

• Note that we see the onset of the tachycardia in Figure-6. After a sinus beat (ie, beat #3 in Figure-6) — a PAC (ie, beat #4) initiates the process.
• This PAC presumably finds the slow AV nodal pathway amenable to retrograde conduction at the moment it is traveling toward the ventricles (ie, dotted, slanted lines in the AV Nodal Tier of Figure-6). IF the timing is “just right” (as shown in this laddergram) — then a reentry circuit utilizing the slow AV nodal pathway (which produces the very long RP’ interval) can be set up.
• I’m uncertain why this “fast-slow” AVNRT terminates after beat #13 (perhaps because the R-R interval of beats #12-13 is a little bit shorter than preceding R-R intervals during the tachycardia?).
• Following 1 sinus beat ( = beat #14) — it looks like the “fast-slow” AVNRT is about to begin again.

 

PEARL #8: ATach typically begins with gradual acceleration of an ectopic atrial focus (ie, "warm-up" phenomenon). It often terminates with gradual deceleration (ie, "cool-down" phenomenon). This is not what we see in Figure-6!

• Reentrant SVT rhythms typically begin with one or more PACs, that serendipitously find one of the AV nodal pathways amenable to retrograde conduction. This serves to initiate the reentrant cycle.
• There is no "warm-up" in Figure-6. After one retrograde beat — a constant reentrant R-R interval is set up for the 8 beats in the run of SVT that follows (ie, beats #6-thru-13).
• There is no "cool-down". Instead — we see abrupt conversion to sinus rhythm with beat #14 (albeit the very next beat seems about to initiate another run).
• A similarly abrupt termination (ie, without "cool-down") is observed at the beginning of ECG #5 (prompt cessation of SVT after beat #2).
• Bottom Line: The sequence for "onset" and "offset" of the SVT rhythm in Figure-6 is typical for the uncommon "fast-slow" reentrant form of AVNRT.

Figure-6: Laddergram illustration of the mechanism for the SVT rhythm in Figure-5.

 

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #185 — Reviews the Ps, Qs & 3Rs Approach to systematic rhythm interpretation.
• 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. 
• ECG Blog #229 — Why is AFlutter so 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.

 

Other sites where I've discussed some of the cases shown in today's blog:

• The March 6, 2020 post in Dr. Smith's ECG Blog.
• The October 31, 2016 post in Dr. Smith's ECG Blog.
• The October 16, 2019 post in Dr. Smith's ECG Blog. 
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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).