ECG Blog #287 — Sinus Tach with ST Depression?

The ECG shown in Figure-1 was obtained from a man in his 50s during hemodialysis. He complained of "chest pain" — but was hemodynamically stable at the time this tracing was recorded.

• Is this Sinus Tachycardia with ischemic ST depression?
• To activate the cath lab?

Figure-1: ECG from a man in his 50s with chest pain.

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My Approach to Today's Case:

Since the patient was hemodynamically stable — there was time for systematic assessment of the rhythm. By the Ps, Qs, 3R Approach (See ECG Blog #185):

• The rhythm is fast and Regular. Since the R-R interval is just over 2 large boxes in duration — I estimate the ventricular Rate to be just under 150/minute.
• The QRS is narrow (ie, clearly not more than half a large box in duration) — which means that the rhythm is supraventricular.
• 
  
• Sinus P waves appear to be absent — because we do not see a clearly defined upright P wave in lead II. It's possible that P waves are hidden within what appears to be terminal positivity of the T wave in lead II — but this is far from certain. In cases like this, until we can demonstrate clear presence of well defined P waves — we have to assume that no sinus P waves are present.
• 
  
• Could there be evidence of some other form of atrial activity? (Maybe — See below).
• In the absence of clearly defined P waves — the 5th Parameter in our systematic Approach (ie, Determining IF P waves are Related to neighboring QRS complexes?) is negative.

MY Impression of the Rhythm: 
By the Ps, Qs, 3R Approach — We have determined that the rhythm in Figure-1 is a regular SVT (SupraVentricular Tachycardia) at just under 150/minute — but without clear sign of sinus P waves.

PEARL #1: Recognition that the rhythm in Figure-1 is a regular SVT without clear sign of sinus P waves (ie, without a definite upright P wave in lead II) — should prompt consideration of the following 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) — these other entities 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: For more on the causes of a regular SVT rhythm (without clear sign of normal atrial activity) — See our Audio Pearl (MP-64) at the bottom of this page in the Addendum.

PEARL #2: How Heart Rate may help in SVT Diagnosis:

• Sinus Tachycardia usually does not exceed 160-170/minute in a "horizontal" adult (ie, in a patient you re 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 rate range is for untreated AFlutter. Patients who are already on antiarrhythmic medication may present with a slower atrial rate (and therefore slower ventricuar 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 will not 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). This is the situation in today's case — since the rate of the regular SVT rhythm in Figure-1 is very close to 150/minute.

PEARL #3: By far, in my experience — the most commonly overlooked arrhythmia (by far!) is AFlutter. The reason for this — is that the atrial activity of AFlutter will often be partially or completely hidden within the QRS complex or the ST-T wave.

• As a result — the BEST way to avoid overlooking the diagnosis of AFlutter is to always Suspect AFlutter with 2:1 AV conduction whenever you encounter a regular SVT rhythm at a rate close to 150/minute, in which sinus P waves are not clearly evident.
• IF you suspect AFlutter in this situation until you prove otherwise — then you will not miss the diagnosis. There are several ways you can then go about proving (or disproving) your suspicion. These include momentarily slowing the ventricular response by a Valsalva maneuver — by "chemical" Valsalva (ie, using Adenosine or other AV nodal slowing drug to see if reducing the ventricular rate brings out underlying flutter activity) — and/or by use of a special lead system, such as a Lewis Lead that may facilitate visualizing atrial activity (See Figure-4 below in the Addendum at the bottom of the page).

PEARL #4: The method that I favor to try first — is to simply LOOK for flutter waves! The diagnosis of AFlutter can be established in a regular SVT at ~150/minute — IF you are able to identify regular atrial activity at ~300/minute. Nothing else results in regular atrial activity at this fast of a rate (Atrial tachycardia will rarely be faster than 250/minute ...).

• The way in which I look for flutter waves is to carefully set my calipers at precisely HALF the R-R interval of the regular SVT (since IF the rhythm is AFlutter — then the atrial rate should be twice the ventricular rate if there is 2:1 AV conduction). The short RED lines in leads II and aVF of Figure-2 confirm that there is indeed 2:1 atrial activity in this tracing — which tells us even before application of a vagal maneuver or administration of Adenosine (or other AV blocker) that the rhythm is virtually certain to be AFlutter.
• 
  
• PEARL #5: My usual "GO TO" leads for identifying atrial activity are i) Lead II — which is typically the BEST lead for identifying atrial activity. In AFlutter — leads III and aVF also usually provide ready evidence of 2:1 atrial activity; ii) Lead V1 — Next to lead II, lead V1 is often the 2nd-best lead in my experience for identifying atrial activity. With AFlutter — one will often see small amplitude positive deflections of AFlutter in this V1 lead; iii) Lead aVR is often surprisingly helpful for identifying atrial activity; and, iv) IF none of the above leads suggest atrial activity — then I’ll survey the remaining 7 leads as I look for atrial activity. That said, AFlutter will almost always provide ready evidence of atrial activity in one or more of my “Go To” leads.
• The reason the diagnosis of AFlutter is so subtle in today's case — is that except for leads II and aVF, flutter waves in other leads are almost perfectly hidden within the QRS complex!

Figure-2: I've labeled atrial activity from Figure-1 (See text).

Case CONCLUSION:

The etiology of the regular SVT at ~150/minute in today's case was AFlutter with 2:1 AV conduction. the reason for "pseudo" ST-T wave inversion was superposition of prominent "sawtooth" flutter activity throughout the cardiac cycle. 

• Looking at the rest of the ECG — there is slight rightward axis (S wave greater than the R wave in lead I) — and probable LVH (very deep anterior S waves in leads V2, V3) — but probably no acute ST-T wave changes once we have accounted for the prominent flutter waves.
• BEST initial treatment of this patient's chest discomfort is to slow the ventricular response (and ideally convert the rhythm). Then repeat the ECG to ensure there are no acute changes once sinus rhythm has been restored.

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Acknowledgment: My appreciation to Mohd Hatif Kamail (from Kota Bharu, Malaysia) for the case and this tracing.

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Relevant LINKS to Today's Case:

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Additional Relevant Material to Today's Case:

• See ECG Blog #185 — for review of the Systematic Ps, Qs, 3R Approach to rhythm interpretation.
• 
  
• See ECG Blog #240 — for Review on the ECG assessment of the patient with a regular SVT rhythm (including distinction between the various types of SVT reentry).
• See ECG Blog #250 — for Review of another case of regular SVT with ST depression.
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• ECG Blog #210 — reviews the Every-Other-Beat Method for rapid estimation of heart rate (See Video Pearl #27 in this post).
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• ECG Blog #220 — reviews my LIST #1: Causes of a Regular WCT and — HOW to assess Hemodynamic Stability (Listen to Audio Pearl #37 in this post).
• 
  
• ECG Blog #229 — reviews distinction between AFlutter vs ATach (and WHY AFlutter is so commonly overlooked). 
• The November 12, 2019 post in Dr. Smith's ECG Blog — in which I review my approach to a Regular SVT rhythm.

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ADDENDUM (2/27/2022):

I've presented this material before — but it bears repeating for reference. These concepts should be automatic for assessment of the patient who presents with a regular SVT rhythm.

—  —

Today's ECG Media PEARL #64 (10:50 minutes Audio) — Reviews my LIST #2: Common Causes of a Regular SVT Rhythm.

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—  —

Today’s ECG Media PEARL #45 (10:00 minutes Audio) — Why is Atrial FIutter so commonly overlooked? Reviews PEARLS regarding the ECG diagnosis of AFlutter — and — What's "New"? in the field, regarding distinction between AFlutter vs Atrial Tachycardia (5/29/2021).

• For those wanting a more advanced review on some newer concepts regarding AFlutter — Check Out this article by García-Cosío F et al (Clinical Approach to ATach and AFlutter, Rev Esp Cardiol 65(4):363-375, 2012).
• Cosio ( Arrhythm & Electrophys Rev 6(2):55-62, 2017).
• For more on distinction between AFlutter vs ATach — Check out Figure-3 below.

 

Figure-3: Distinction between AFlutter vs ATach (excerpted from Grauer K: ACLS-2013-ePub).

Figure-4: Use of a Lewis Lead to facilitate detection of atrial activity during a tachycardia (See text).

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ECG Blog #286 — Challenge: What is the Rhythm?

The long lead II rhythm strip shown in Figure-1 — was obtained from a 60-year old man, who presented with an acute pulmonary problem. He was hemodynamically stable at the time this tracing was obtained. No known prior cardiac history.

• Challenge: How would you interpret this tracing?
• Is there complete AV Block?

Figure-1: Long lead II rhythm strip that was sent to me.

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NOTE: Some readers may prefer at this point to listen to the 7:40 minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to review to My Thoughts on this tracing (that appear below ECG MP-51a).

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—  — 

Today’s ECG Media PEARL #51a (7:40 minutes Audio) — Reviews of "Some Simple Steps to Help Interpret Complex Rhythms" ).

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My APPROACH to the Rhythm in Figure-1:

As always, once I’ve ensured that my patient is hemodynamically stable — I favor use of the Ps, Qs, 3Rs Approach for systematic Rhythm Interpretation (See ECG Blog #185 for review of this system):

• As I often emphasize — it does not matter in what sequence you address the 5 Parameters in the Ps, Qs, 3R Approach — as long as you always look for them all. As a result — I often change the sequence, depending on which of the parameters are easiest to assess.

My initial impression of the rhythm in Figure-1 (which I arrived at within seconds of looking at this tracing) — was the following.

• Although we are only given a single lead to look at — the QRS complex clearly looks narrow (ie, not more than 0.10 second in duration). Therefore, the rhythm is supraventricular.
• The ventricular Rate is not overly fast (ie, about 70-80/minute).
• The rhythm looks almost, but not completely Regular (an observation that I wanted to confirm as soon as I had a moment to use calipers).
• 
  
• Lots of P waves are present! Some of these P waves are easy to see — as they appear before a number of QRS complexes, with PR intervals that could clearly be conducting. But other P waves are either hidden within the ST-T wave (ie, notching the T wave of beat #2) — or — appear before QRS complexes with a PR interval that is clearly too short to conduct (ie, as occurs for the P waves before beats #3, 7, 9, 11 and 13). And, no P wave at all appears before beat #5.
• 
  
• Regarding the 5th Parameter (ie, whether at least some P waves are Related to neighboring QRS complexes) — this was admittedly difficult to determine in my initial (ie, less than 10-second) assessment of the rhythm.

PEARL #1: The most helpful clues for me to determine whether any P waves are conducting (and if so, which ones?) — are the following: i) Look to see if any R-R intervals are clearly much shorter than the other R-R intervals (since the most common reason for there to be much shorter-than-expected R-R intervals — is that the P waves that precede such shorter intervals are being conducted); and, ii) Look to see if there are any PR intervals that repeat — since the finding of PR intervals that repeat (especially if they repeat more than once) — is unlikely to be due to chance.

• These 2 clues almost always provide me with the answer as to whether there are at least some P waves that are being conducted. That said — today’s case was an exception for me, in that: i) The slight variation in R-R interval that we see in Figure-1 has no apparent “pattern” of group beating (and I see no specific R-R intervals that are clearly much shorter than all of the others); and, ii) Although a number of PR intervals look similar — they do not appear to be the same.

BOTTOM LINE: At this point in my interpretation — I did not know for certain what the mechanism of today's rhythm was. All I could say at this point was the following:

• The rhythm was supraventricular — and almost (but not completely) regular.
• The ventricular rate was ~70-80/minute.
• There were lots of P waves — some of which were definitely not conducting — but others which might be conducting.
• I knew that I’d need to use calipers to figure out more.

PEARL #2: When confronted with a rhythm in which some P waves may be conducted, but other P waves are definitely not conducted (as is the case in Figure-1) — I have found the simple step of labeling P waves to be incredibly helpful (Figure-2).

• The reason why labeling P waves is so helpful — is that it instantly facilitates determining which P waves are (or are not) likely to be conducted.
• Recognizing that 1 or more P waves are not conducted raises the possibility of some form of AV block.
• KEY Point: For there to be some form of AV block — the atrial rhythm should be regular (or at least almost regular). Clearly there are exceptions to this general rule (ie, in addition to some form of 2nd-degree AV block — there may also be PACs, PVCs, echo beats, etc.) — but once you establish that there are dropped beats and an underlying regular (or at least fairly regular) atrial rhythm — the possibility of AV block becomes much greater.
• 
  
• On the other hand — recognizing that the atrial rhythm is not regular, especially when P wave morphology is not always uniform — instantly tells you that something other than typical AV block is occurring.

Figure-2: I've labeled the P waves from Figure-1. Using calipers makes this EASY. Since the first few RED arrows are obvious — I simply set my calipers to the P-P interval suggested by these first few RED arrows. This allowed me to "walk out" regular atrial activity throughout the entire rhythm strip (and allowed me to confirm that the "extra peaking" of the T waves of beats #4, 8, 10 and 12 — was clear indication of an "on-time" P wave hidden below).

My THOUGHTS at This Point:

• The labeled P waves in Figure-2 confirm an underlying regular atrial rhythm at a rate slightly greater than 100/minute.
• The rhythm in Figure-2 is supraventricular (narrow QRS). Caliper measurement of R-R intervals confirms slight-but-definite irregularity of the ventricular rhythm. I saw no clear pattern to this slight irregularity in the ventricular rhythm (ie, no "group" beating).
• 
  
• There are many more P waves than QRS complexes (ie, 21 RED arrows, compared to the 14 QRS complexes seen on this tracing). This confirms non-conduction of a number of on-time P waves — which suggests some form of AV block.
• 
  
• I thought complete AV block to be unlikely given irregularity of the ventricular rate (Most of the time — the ventricular rhythm will be regular when there is complete AV block).
• The Mobitz II form of 2nd-degree AV block is uncommon. It seemed highly unlikely here — given the narrow QRS and absence of consecutive P waves with the same PR interval.
• 
  
• By the process of elimination — the rhythm in Figure-1 most likely represents some form of Mobitz I, 2nd-degree AV block ( = AV Wenckebach). But because of the atypical features of today's arrhythmia — I would need to construct a laddergram to prove my suspicion.
• KEY Point: Even though I was unable at this point to come up with a definitive rhythm diagnosis — the above deductions provide sufficient information for appropriate initial clinical management: i) Some form of Mobitz I, 2nd-degree AV block is likely; and, ii) A pacemaker is not needed — since complete AV block is unlikely, and the overall ventricular rate is more than adequate.

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Deriving the LADDERGRAM:

The complex mechanism of today's case is best explained by step-by-step derivation of a Laddergram (See ECG Blog #188 for review on how to read and/or draw Laddergrams).

• NOTE: Today's case provides an example in which I needed to construct a valid laddergram explanation in order to "solve" the arrhythmia.
• Sequential legends over the next 10 Figures illustrate my thought process as I derived this laddergram.

Figure-3: It is usually easiest to begin a laddergram by marking the path of sinus P waves through the Atrial Tier (RED lines drawn directly below the onset of each of the P waves — as shown by the large BLUE arrows). Note that these RED lines in the Atrial Tier are nearly vertical — since conduction of sinus P waves through the atria is rapid. Note also that the P-P interval between successive P waves (vertical RED lines) is equal!

Figure-4: The most challenging part of most laddergrams is construction of the AV Nodal Tier — so I generally save that for last. Therefore, after drawing in all P waves into the Atrial Tier — I prefer to next add indication of all narrow QRS complexes into the Ventricular Tier. The large BLUE arrows show that my landmark for QRS complexes in the laddergram is the onset of the QRS. Note that the RED lines in the Ventricular Tier are also nearly vertical — since conduction of these narrow QRS complexes through the ventricles is rapid.

Figure-5: It's time to begin "solving" what we can in the laddergram. I do this by connecting those P waves in the Atrial Tier that might logically be conducting to narrow QRS complexes in the Ventricular Tier (slanted BLUE lines within the AV Nodal Tier). Although the PR intervals preceding beats #1, 4, 6, 8, 10, 12 and 14 are not all quite equal — Doesn't it appear as if the angle of slant for these BLUE lines in the AV Nodal Tier looks similar? — and — Doesn't there seem to be a "pattern" for these BLUE arrow P waves that do appear to be conducting?

Figure-6: It's time to assess the mechanism we are proposing. IF my initial assumption (ie, that the P waves preceding beats #1,4,6,8,10,12 and 14 are all conducting) — HOW might you most logically connect the unattached atrial lines with the unattached ventricular lines in this Figure-6?
(NOTE: In the 1st grouping [that encompasses beats #1,2,3] — there are 3 unattached atrial lines and 2 unattached ventricular lines. In each of the 5 groupings that follow — there are 2 unattached atrial lines and just 1 unattached ventricular line).

Figure-7: I thought it easiest to address the 1st grouping in this rhythm (that encompasses beats #1,2,3). Doesn't it seem logical to postulate a 4:3 AV Wenckebach cycle for this 1st grouping — in which the PR interval for the RED, PURPLE and GREEN P waves progressively increases — until the YELLOW P wave is blocked. The cycle then begins again with the RED P wave that precedes beat #4, which conducts with a shorter PR interval.

Figure-8: I then addressed the next 5 groupings. The slanted PURPLE lines within the AV Nodal Tier show the only logical option for connecting the unattached atrial lines with the only unattached ventricular line in each grouping.

Figure-9: This means that the single remaining unattached atrial line that we saw for each grouping in Figure-8, must be blocked (slanted YELLOW lines with the butt end that do not make it out of the AV Nodal Tier).

Figure-10: For clarity — I've colored with PURPLE arrows those P waves in the lead II rhythm strip that correspond to the PURPLE lines passing through the Atrial, AV Nodal and Ventricular Tiers in the laddergram. 

Figure-11: For clarity — I've colored with YELLOW arrows those P waves in the lead II rhythm strip that correspond to the YELLOW lines that are blocked, and do not make it out of the AV Nodal Tier.

Figure-12: For my final laddergram illustration — I've colored all laddergram elements in RED. If you step back a little bit from this final illustration — it should be apparent that the mechanism of today's rhythm is 2nd-degree AV block, Mobitz Type I ( = AV Wenckebach) — with 4:3 AV conduction for the 1st grouping (that encompasses beats #1,2,3) — and with 3:2 AV conduction for the remaining 5 groupings.

Final COMMENT on Today's Case:

There are a number of reasons why the rhythm in today's case is so challenging. These include:

• The atrial rate is rapid — with many of the P waves at least partially hidden either within the ST-T wave, or coinciding with the next QRS complex.
• The ventricular rate is faster than is usually seen with AV block. This makes it difficult to tell which P waves are conducting to which QRS complexes.
• The ventricular rhythm is irregular, and without an identifiable pattern of group beating.
• Although a number of PR intervals look to be of similar duration — when measured with calipers, most of these PR intervals manifest slight-but-real differences in PR interval duration. This makes it difficult to tell which of these P waves may be conducting.
• 
  
• PEARL #3: "Not all patients read the textbook" before they develop their arrhythmia. Some cardiac rhythms simply do not follow the rules. It could be that this patient's acute pulmonary problem resulted in hypoxemia that led to the atrial tachycardia and the unexpected variation in PR interval duration. Enhanced autonomic tone (which is common in acutely ill patients) — is another potential reason why the 1st conducted beat in each grouping showed such a variety in PR interval duration.
• 
  
• Final POINT: As emphasized earlier — Even though I was unable to be certain of the etiology of today's rhythm until I drew my laddergram — Application of the Ps, Qs, 3R Approach allowed me within seconds to strongly suspect some form of Mobitz I, 2nd-degree AV block — and — to determine that a pacemaker was unlikely to be needed (since Mobitz II and complete AV block were essentially ruled out — and the overall ventricular rate was more than adequate to maintain perfusion).

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Acknowledgment: My appreciation to Farhan Khan (from Karachi, Pakistan) for the case and this tracing.

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Relevant LINKS to Today's Case:

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Additional Relevant Material to Today's Case:

• See ECG Blog #185 — for review of the Systematic Ps, Qs, 3R Approach to rhythm interpretation.

How to Draw a Laddergram (Step-by-Step Demonstration) 

• See ECG Blog #69 — for a Step-by-Step description on drawing a Laddergram.
• See ECG Blog #188 — for a brief ECG Video review on the basics of what a Laddergram is — with LINKS at the bottom of the page to more than 50 ECG blog posts in which I review illustrative laddergrams.
• See ECG Blog #164 — for a user-friendly rhythm-solving approach to AV Wenckebach, followed by Step-by-Step construction of the Laddergram.
• ECG Blog #236 — Reviews in our 15-minute Video Pearl #52 how to recognize the 2nd-Degree AV Blocks (including "high-grade" AV block). 
• ECG Blog #186 — Reviews when to suspect 2nd-Degree, Mobitz Type I.
• 
  
• CLICK HERE — to DOWNLOAD my Free PowerPoint Laddergram STENCIL for your use as desired.

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ECG Blog #285 — A Wider Irregular Rhythm?

I was sent the ECG and 2-lead rhythm strip shown in Figure-1 — with the following 2 Questions:  

• Is this a NSTEMI ( = Non-ST Elevation Myocardial Infarction)?
• What is the Rhythm?

Figure-1: 12-lead ECG and non-simultaneous 2-lead rhythm strip that was sent to me.

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NOTE: Some readers may prefer at this point to listen to the 8:30-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-60).

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—  — 

Today's ECG Media PEARL #60 (8:30 minutes Audio) — Reviews use of the "Mirror Test" to facilitate recognition of: i) Acute Posterior MI; ii) Acute High-Lateral or Inferior MI (ie, the "magical" reciprocal relationship between leads III and aVL); and, iii) Anterior ST elevation due to LVH (that is not indicative of anterior MI).

• NOTE: I've added LINKS to related ECG blog posts to better illustrate the concepts put forth in today's Audio Pearl (These LINKS are shown below at the end of this blog post).

My Approach to Today's Case:

I was not provided with any history for today's case. I immediately noted that the long 2-lead rhythm strip in ECG #2 of Figure-1 was not recorded simultaneously with the 12-lead ECG ( = ECG #1). Keeping in mind the systematic Ps, Qs, 3R Approach to rhythm interpretation (See ECG Blog #185) — My Thoughts were the following:

• Looking first at the 12-lead tracing ( = ECG #1) — the underlying rhythm is clearly supraventricular (ie, a narrow QRS in all 12 leads).
• In the 12-lead — the rhythm looks to be quite Regular (taking into account that this smart phone photo is somewhat angled — therefore slightly distorted).
• The Rate of the rhythm in the 12-lead ECG is ~85/minute. 
• P waves are present in the 12-lead ECG. Although the P wave in lead II is upright — this P wave in lead II is tiny in size, and the PR interval appears to be shorter than expected (RED arrows in Figure-2). 
• In support that this tiny upright deflection in front of the QRS in lead II is real — is identification of P waves of similar small amplitude, with similar shorter-than-expected PR intervals in other leads (ie, the RED arrow in lead I — as well as unlabeled P waves in leads aVR, aVL and V1).
• All of these P waves are Related to neighboring QRS complexes — as determined by a constant (albeit short) PR interval.
• BOTTOM Line: I suspect that the underlying rhythm in the 12-lead ECG is a low atrial rhythm. To be emphasized — this is not necessarily a pathologic rhythm.

Figure-2: I've labeled KEY features from ECG #1 (See text).

CHALLENGE Question:

The KEY to diagnosis of the tachycardia in ECG #2 lies with appreciation of the appeance of beat #4. WHY do I say this?

ANSWER:

Note that the first 4 P waves in the long lead I rhythm strip are on time! (the 4 consecutive RED arrows in lead I of Figure-2). QRS morphology then changes with beat #4 — which begins a run of an irregular tachycardia with a different (wider) QRS morphology.

• Isn't QRS morphology of beat #4 in both leads I and II of the long lead rhythm strip intermediate between QRS morphology of beat #3 and beat #5. This strongly suggests that beat #4 (that is preceded by an on-time P wave) is a Fusion beat! IF so — this identifies the run of tachycardia that follows as VT (Ventricular Tachycardia), albeit that beats #4-thru-20 are irregular, and the rate slows toward the end of the tracing (See ECG Blog #128 for review of Fusion beats).
• 
  
• I believe the YELLOW arrows in the long lead rhythm strip represent retrograde P waves. This 1:1 VA (retrograde) activity is seen following beats #5-thru-20 — but not after the initial beat in the run (which is the Fusion beat = beat #4).
• I'm uncertain how wide the QRS is for the run of irregular tachycardia — because we only see 2 of the 12 leads. The QRS is wide — but does not look to be overly prolonged. Predominant negativity in both leads I and II could be consistent with origin near the left anterior hemifascicle — though without a 12-lead tracing during the tachycardia, it is impossible to know for certain the origin of tachycardia.
• Although VT (and therefore also Fascicular VT) both tend to be regular (or at least fairly regular) rhythms — on occasion, these rhythms may be surprisingly irregular. I show my Laddergram for the proposed mechanism of the rhythm in the long lead rhythm strip below in Figure-3.
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• To Emphasize: The rate of the wide tachycardia in Figure-3 slows toward the end of the rhythm strip — with a rate of between ~80-100/minute for beats #16-to-20. Thus, the rhythm becomes more consistent with AIVR (Accelerated IdioVentricular Rhythm).
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• In further support that beats #4-thru-20 in Figure-3 represent a ventricular rhythm (becoming most consistent toward the end of the tracing with AIVR) — are the ECG findings in the remainder of the 12-lead tracing (Big HINT in the form of the "mirror-image" picture above the RED insert of inverted leads V2, V3 in Figure-2).
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• Acknowledgment: Although far more irregular than usual for a monomorphic (ie, similar QRS morphology) ventricular rhythm — I am otherwise at a loss to explain the irregular wide tachycardia from beats #4-thru-20, other than to call this rhythm VT that slows and evolves into an irregular AIVR. (AFib would not manifest a fusion beat — nor an on-time P wave before beat #4 — nor retrograde VA conduction during the entire run of tachycardia).

Figure-3: My proposed Laddergram for the rhythm in ECG #2. As noted above — the small size and short PR interval in lead II suggest a non-sinus mechanism for the rhythm (probably a low atrial rhythm). We see 4 consecutively-conducted P waves in lead I (RED arrows in this lead). Then follows a wider and irregular rhythm for beats #4-thru-20. There is 1:1 VA (retrograde) conduction beginning with beat #5 (YELLOW arrows). The fact that beat #4 is preceded by an on-time P wave, and manifests a QRS morphology intermediate between that of beat #3 and beat #5 defines beat #4 as a Fusion beat — which confirms a ventricular etiology for the irregular wide tachycardia.

Returning to the 12-lead ECG in Today's Case:

For clarity — I've isolated the 12-lead ECG in today's case in Figure-4. As always — I favor the use of a Systematic Approach (which I review in ECG Blog #205):

• Rate & Rhythm: We've defined the underlying rhythm in this 12-lead tracing as a low atrial rhythm at ~85/minute.
• Intervals (PR/QRS/QTc): As noted — the PR interval is short, which is not unexpected with a non-sinus rhythm. The the QRS complex is narrow in all 12 leads. The QTc may be slightly prolonged.
• Axis: The frontal plane axis is normal — as determined by predominant positivity in both leads I and aVF (probably about +50 degrees).
• Chamber Enlargement: None. 

Figure-4: The 12-lead ECG in today's case (See text).

Regarding Q-R-S-T Changes:

• Q Waves — There is a small Q waves in lead aVL.
• R Wave Progression — There is a relatively tall R wave in lead V1 — with Transition (where the R wave becomes taller than the S wave is deep) occurring early, between leads V1-to-V2 (Transition normally occurs between leads V2-to-V4).
• ST-T Wave Changes — There is diffuse ST segment flattening and depression in virtually all leads except leads I, aVR and aVL. These latter 2 leads show ST segment elevation.
• Of note — the leads with ST segment flattening and depression all show terminal T wave positivity (with these terminal T waves being peaked and surprisingly tall).

 

Putting It All Together: 

There are a number of important points to consider in the interpretation of the 12-lead ECG shown in Figure-4:

• The ECG finding of diffuse ST segment depression (ie, present in at least 7-8 leads) — in association with ST elevation in lead aVR (and sometimes in lead V1) — suggests the entity of diffuse Subendocardial Ischemia. Although this may be due to non-cardiac disorders (ie, shock, profound anemia, "sick" patient) — the most likely etiology in today's tracing, given the composite of ECG findings is severe coronary disease (due to LMain, proximal LAD, and/or severe 2- or 3-vessel disease).
• 
  
• PEARL #1: When the diffuse ST depression is maximal in leads V2, V3 and/or V4 (as it is in Figure-4) — Posterior Infarction that may be acute is likely.
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• PEARL #2: In support of the likelihood of acute posterior infarction is the positive "Mirror" Test. As discussed in detail in the above Audio Pearl — the Mirror Test is used as a visual aid to facilitate recognition of acute posterior MI. The principle of this test is simple: It is based on the fact that the mirror-image view of anterior leads provides insight to the nature of electrical activity as viewed by the posterior wall of the left ventricle.
• Note that I have vertically flipped anterior leads V2 and V3 in the RED insert of Figure-4 (to show the mirror-image view of these 2 leads). Doesn't the shape of the already tall R waves, the "shelf-like ST depression and terminal T wave positivity seen in leads V2 and V3 of Figure-4, when vertically flipped (as viewed in the Mirror Test) suggest deepening Q waves — worrisome shape and amount of ST elevation — and already deep T wave inversion?
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• PEARL #3: Isolated posterior infarction is possible, but uncommon. Instead — one usually sees inferior lead ST elevation in association with the anterior ST depression of posterior infarction. The fact that the ST depression with terminal T wave positivity is so diffuse — in association with maximal ST depression in leads V2-V4 — suggests a combination of diffuse subendocardial ischemia (from severe coronary disease) + acute posterior infarction may be present.
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• PEARL #4: Although the QRS complex in lead aVL is very small in amplitude — there is a Q wave + ST elevation + T wave inversion in this lead. This suggests acute high-lateral lead involvement. Acute occlusion of the LCx (Left Circumflex) coronary artery may cause the ECG picture of acute Postero-Lateral MI seen in Figure-4. Therefore — today's tracing is not a "NSTEMI" (in the sense of positive troponin but without coronary occlusion) — but rather a patient who likely has severe underlying coronary disease + acute occlusion of the LCx until proven otherwise.
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• PEARL #5: While impossible to date the infarction in today's case without knowing the history — there are a number of features that suggest spontaneous reperfusion has already occurred. These include: i) The surprisingly tall terminal T wave positivity in leads V2, V3, V4 (the mirror image of which [as shown in the RED insert] would show T wave inversion — See ECG Blog #258 and ECG Blog #266); ii) Reperfusion T wave inversion is also seen in lead aVL; and, iii) The rhythm in ECG #2 is an irregular AIVR — and this is an extremely common "reperfusion" rhythm in the context of recent infarction!

Case Follow-Up:

Cardiac cath was performed on the patient in today's case — and revealed multi-vessel coronary disease + recent acute occlusion with the "culprit" artery being the OM (Obtuse Marginal) branch of the LCx (Left Circumflex) coronary artery.

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Acknowledgment: My appreciation to Ahmed Shaaban (from Cairo, Egypt) 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.
• See ECG Blog #185 — for review of the Systematic Ps, Qs, 3R Approach to rhythm 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. (NOTE: Figure-5 in the Addendum of this blog post illustrates the essentials for identifying an isolated posterior MI).
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• ECG Blog #246 — for another example of acute Posterior MI (with positive Mirror Test).
• ECG Blog #80 — reviews prediction of the "culprit" artery (and provides another case illustrating 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.
•  
• The September 21, 2020 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) emphasizes utility of the Mirror Test for diagnosis of acute Posterior MI.
• The February 16, 2019 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) emphasizes utility of the Mirror Test for diagnosis of acute Posterior MI. 
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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 #266 — Reviews distinction between Posterior MI vs deWinter T waves (with anterior terminal T wave positivity reflecting "Reperfusion" T-waves).
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• ECG Blog #258 — How to "Date" an Infarction based on the initial ECG.
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• ECG Blog #108 — Reviews the ECG diagnosis of AIVR (Accelerated IdioVentricular Rhythm) — and clinical implications of this rhythm.
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• ECG Blog #128 — Review the concept of Fusion Beats (and clinical implications of their recognition).
• ECG Blog #133 — Illustrates diagnostic use of Fusion Beats to confirm VT.
• ECG Blog #129 — More on Fusion Beats.

How to Draw a Laddergram (Step-by-Step Demonstration) 

• See ECG Blog #69 — for a Step-by-Step description on drawing a Laddergram.
• See ECG Blog #188 — for a brief ECG Video review on the basics of what a Laddergram is — with LINKS at the bottom of the page to more than 50 ECG blog posts in which I review illustrative laddergrams.
• See ECG Blog #164 — for a user-friendly rhythm solving approach to AV Wenckebach, followed by Step-by-Step construction of the Laddergram.
• CLICK HERE — to DOWNLOAD my PowerPoint Laddergram STENCIL for  your use as desired.

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ADDENDUM (2/18/2022): I've added below in Figure-5 review of a case in which there is an isolated posterior MI (ie, without accompanying inferior lead ST elevation).

 

 

Figure-5: KEY points in the recognition of isolated posterior MI (This figure is taken from ECG Blog #193 — in which I review the "Basics" for predicting the "culprit" artery).