ECG Blog #456 — Acute MI or Something Else?

Today's case was contributed by Dr. Magnus Nossen (from Fredrikstad, Norway). Dr. Nossen was at his computer — reviewing ECGs from patients recently admitted to his group's hospital service. He came across the ECG shown in Figure-1 — obtained from a woman in her 70s who was admitted to the hospital for new CP (Chest Pain).

QUESTION:

• How would YOU interpret the ECG in Figure-1?

Figure-1: The initial ECG in today's case — obtained from a woman with CP. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on ECG #1:

The rhythm is sinus bradycardia at a rate just under 60/minute. Intervals (PR, QRS, QTc) and the axis are normal. No chamber enlargement.

Regarding Q-R-S-T Changes:

• There may be tiny (normal septal) Q waves in a number of lateral leads.
• R wave progression — shows early transition, with the R wave abruptly becoming predominant already by lead V3. I wonder about precordial electrode lead placement — given the unexpectedly tiny V2 complex that is sandwiched between the deep S wave in V1 and the suddenly tall R wave in lead V3.

The most remarkable finding relates to ST-T Waves:

• Multiple leads in ECG #1 show ST segment straightening with ST depression that appears to be maximal in leads V3 and V4 (BLUE arrows in Figure-2).
• The tiny QRS complex in lead V2 is associated with a disproportionately large and peaked T wave — which is present, but to a lesser extent in neighboring chest leads.
• Prominent U waves are also seen (most marked in leads V2,V3 — but also seen in leads I, II).

My Impression of ECG #1: 

• I shared Dr. Nossen's concern that the ST segment flattening and depression in leads V2-thru-V6 — in association with the disproportionately large upright T wave in lead V2 in this older woman with new CP — strongly suggests posterior OMI (Occlusion-based acute MI), pssibly now with reperfusion T waves in leads V2-thru-V4. Could this be a posterior OMI that was missed by the original providers?
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• Additional Note: Assuming serum electrolytes (K+, Mg++) were normal — the upright U waves in leads II,V2,V3 are clearly larger than expected.

Figure-2: I've labeled the initial ECG. 

The ECG was Repeated:

As shown in Figure-3 — Dr. Nossen's chart review revealed that there was also a 2nd tracing on this patient ( = ECG #2 — which was recorded 21 hours after ECG #1). 

QUESTION:

• Does this repeat ECG (shown below in Figure-3) — change your impression regarding recent posterior OMI, now with reperfusion T waves?

 

Figure-3: The repeat ECG in today's case — recorded 21 hours after ECG #1. (Visualization improved using PMcardio).

MY Thoughts on ECG #2:

There has been dramatic change in the ECG picture since the initial tracing was done (See the comparison between these 2 tracings in Figure-4 below). At this point in time — ECG #2 no longer looked like a recent posterior OMI with reperfusion T waves but instead, like Takotsubo CM (CardioMyopathy). 

• T waves have dramatially filled out in ECG #2 — now with marked prolongation of the QT interval.
• Had I not first seen the prominent U waves in ECG #1 (BLUE arrows) — I would not have known that the extra "shoulder" (projection) seen near the bottom of the T wave descent in multiple leads in ECG #2 (best seen in those leads with the RED arrows) — was the result of a fusion between the upright T waves and U waves that have both significantly enlarged since ECG #1 was recorded. Technically then — rather than marked QT prolongation, we are seeing marked QT-U prolongation in ECG #2.
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• Note #1: Takotsubo on occasion may be associated with large U waves — so, the evolution to prominent T wave positivity with marked QT-U prolongation that we now see in ECG #2 is perfectly consistent with Takotsubo CM.
• Note #2: Retrospectively looking back at ECG #1 — the ECG changes of Takotsubo CM were already evolving 21 hours earlier at the time ECG #1 was recorded (ie, Virtually all leads with upright T waves in ECG #1 already had T waves that were subtly "fatter"-at-their-peak and wider-at-their base than might be expected — and the BLUE arrow U waves in ECG #1 were already larger than is usually seen when serum K+ is normal).
• Note #3: Given the overall better prognosis of Takotsubo CM compared to acute coronary occlusion MI — Dr. Nossen and I took comfort in knowing that acute OMI had not been overlooked (and that cardiac cath was not immediately needed).

Figure-4: Comparison between the initial and repeat ECGs in today's case (done 21 hours apart).

On Further Chart Review of Today's Patient:

Dr. Nossen discovered the following on further chart review:

• Troponin during this patient's hospital admission was modestly increased. This is consistent with Takotsubo CM — which is typically associated with Troponin peaks below that seen with larger MIs (although there is an "overlap range" regarding specific troponin levels — and some OMIs with limited occlusion duration before spontaneous reperfusion occurs, may manifest no more than minimal troponin elevation).
• Serum electrolytes were not abnormal. Neither hypokalemia nor hyperkalemia accounted for the ECG picture seen.
• Today's patient had a history of 3 previous "NSTEMIs". Each time, she underwent cardiac catheterization — and each time, she had patent coronary arteries! In retrospect — this patient never had acute MI (despite the fact that "NSTEMI" was the discharge diagnosis each time).
• For each of this patient's 3 previous hospital admissions that were diagnosed as "NSTEMI" — she had ECGs that showed evolution to the typical ECG picture of Takotsubo CM (See Figure-5 — which shows a representative tracing from one of those prior hospital admissions).

PEARL #1: Both the history and initial ECG from a patient with Takotsubo CM may be very similar to that seen with acute OMI. As a result — it may at first be difficult to distinguish between these 2 entities.

• At times — cardiac catheterization may be needed to rule out acute coronary occlusion.
• On the other hand, if the initial ECG looks similar to the tracing shown in Figure-5 (in which there is diffuse, deep symmetric T wave inversion with a markedly prolonged QT interval) — then, the diagnosis of Takotsubo CM becomes obvious. In such cases — noninvasive imaging (ie, with Echo; CT angiography) may provide sufficient support that the diagnosis truly is Takotsubo CM, such that cardiac catheterization is not needed (especially if the patient is not having ischemic CP).

PEARL #2: The term, "NSTEMI" (ie, a Non ST Elevation Myocardial Infarction) — is greatly overused. In my experience — the term, "NSTEMI" is probably inaccurate most of the time.

• In today's case — on each of this patient's 3 prior hospital admissions, she was diagnosed as having had "NSTEMI" — whereas retrospective review of her chart clearly showed she instead had Takotsubo CM each time.
• I've reviewed on many occasions in this ECG Blog — cases in which acute OMIs were overlooked and misdiagnosed as NSTEMI (See ECG Blog #400 — among many others).
• BOTTOM Line: In 2024 — We should always be suspicious of potential misdiagnosis whenever the label, "NSTEMI" is used. All-too-often this misdiagnosis is applied because providers fail to realize that a history of new CP which spontaneously resolves in association with "an unimpressive ECG" — may potentially reflect "pseudo-normalization" after the phase of ST elevation has begun to evolve into deep reperfusion T waves. And then, all-too-often the "tell-tale" sign of reperfusion T waves is simply overlooked (even when history and significant Troponin elevation say otherwise).

PEARL #3: The correct diagnosis for ECG #2 and ECG #3 is Takotsubo CM. But note how different the ECG pattern is for these 2 tracings!

• ECG #2 (in Figure-4) — is remarkable for large positive T waves with marked QT-U prolongation.
• ECG #3 (in Figure-5) — is remarkable for diffuse, deep and symmetric T wave inversion with a greatly prolonged QT interval.
• 
  
• BOTTOM Line: There is indeed variation in the ECG picture that may be seen with Takotsubo CM. Some of this is a function of when during the course of Takotsubo the ECG is taken. In addition — there are 2 distinct ECG patterns for Takotsubo — and depending on the anatomic region of the heart involved, the ECG picture may differ (See section below for review of Takotsubo ECG findings).

Figure-5: Representative ECG ~2 years earlier, from this patient's prior hospitalization. (Visualization imrpoved using PMcardio).

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ECG Findings with Takotsubo Cardiomyopathy:

By way of review in Figure-6 — I synthesize the findings most commonly seen for the 2 most common ECG patterns in patients with Takotsubo CM (which I've previously discussed in ECG Blog #277).

• As noted below in Figure-6 — the 2 most common ECG Patterns for Takotsubo CM consist of: i) ST elevation on initial ECG; and/or, — ii) Deep, diffuse T wave inversion (especially in the chest leads) with marked QTc prolongation. That said — neither of these patterns is seen in ECG #2 (ie, Rather than either ST elevation or deep, diffuse T wave inversion — there are overly tall, positive T waves present in multiple leads).
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• To Emphasize: I completely agree with Dr. Nossen that the serial ECG evolution that occurs between ECG #1 and ECG #2 in today's case strongly suggests Takotsubo CM (and not acute OMI). That said — the KEY to appreciate is that a variety of ECG patterns are associated with Takotsubo CM.
• Typical Takotsubo CM manifests apical ballooning with hypercontractility of the base. But instead of LV dysfunction localized to the apex — the dysfunction may be of the base = "Reverse" Takotsubo, in which case there will not be apical ballooning. Or, there could be mid-ventricular Takotsubo, in which there is poor function (and ballooning) of the mid-LV, with good function at both the base and the apex (See the June 24, 2014 post — and My Comment in the July 21, 2022 post of Dr. Smith's ECG Blog regarding Takotsubo variant patterns).
• Therefore — I thought the marked increase in QTc with huge, "bulky" upright T waves that we see in ECG #2 (especially given evolution to this ECG picture over the 21 hours since the initial tracing was done) — was perfectly consistent with some form of Takotsubo CM other than the 2 more common patterns described in Figure-6.
• As per Dr. Nossen — Takotsubo on occasion may be associated with large U waves, which accounts for the extra "shoulder" seen deforming the descent of the large T waves in ECG #2 (most prominent in those leads with the RED arrows in Figure-4). Technically then — the terminal part of what was thought to be T wave is actually U wave (ie, producing marked QT-U prolongation).

Figure-6: ECG Findings in Takotsubo Cardiomyopathy — adapted from Namgung in Clin Med Insights Cardiol (See text).

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By way of historical perspective on Takotsubo CM — I've added these 2 pages that I've excerpted from my 2014 ECG-Pocket Brain ePub.

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Figure-7: Brief review of clinical features of Takotsubo Cardiomyopathy (Excerpted from Grauer K — ECG-2014-ePub).

Figure-8: Clinical features of Takotsubo CM — continued (Excerpted from Grauer K — ECG-2014-ePub).

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Acknowledgment: My appreciation to Magnus Nossen (from Fredrikstad, Norway) for the case and these tracings.

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ADDENDUM:  — ECG Evolution in another Patient with Takotsubo:

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As emphasized above — the evolution of ECG changes with Takotsubo Cardiomyopathy is highly variable (and depends on many impossible-to-predict factors). 

• That said — I thought it would be interesting to review the sequential ECG changes as they occurred over time in another patient (different than the patient presented in today’s case) — in he hope that this helps to convey a general idea of the ECG changes to expect.
• My THANKS to Dr. Magnus Nossen for contributing the 8 sequential tracings in this case.

Figure-9: The initial ECG in this 2nd case (contributed by Dr. Nossen). There is sinus tachycardia at ~100/minute — with diffuse ST-T wave depression. The QTc appears to be at least borderline prolonged (being more difficult to assess true QTc duration given tachycardia and terminal T wave positivity vs U wave deflection in many leads).

Figure-10: The 7 sequential tracings that appear in Figures-10-thru-16 are compared with each prior ECG, in order to facilitate recognizing the changes. The rate in ECG #2 is slightly slower than in ECG #1. The differences in ST-T wave morphology in ECG #2 compared to the initial ECG (done 40 minutes earlier) are subtle. There is less J-point ST depression; less ST segment downsloping — and more rounding (coving) of many ST segments in the chest leads.

Figure-11: The rate is slightly faster. ST segment coving continues to increase — and is associated with relative lengthening of the QTc, and deepening of symmetric T wave inversion.

Figure-12: The rate is now significantly slower (~65-70/minute). The presence of this slower heart rate makes it easier to “step back” and better appreciate the overall picture = deep, diffuse symmetric T wave inversion (in all leads except right-sided leads III, aVR, V1 and vertical lead aVF) — with a clearly prolonged QTc. This ECG picture is typical for Takotsubo Cardiomyopathy.

Figure-13: The sinus rhythm rate remains slower than it was for the first 3 tracings. While the amplitude of ST-T wave changes is less in the limb leads of ECG #5 compared to ECG #4 — the symmetric T wave inversion in the chest leads is now clearly deeper.

Figure-14: The amplitude of chest lead T wave inversion has decreased in ECG #6 (ie, the ECG picture of Takotsubo is resolving).

Figure-15: One month has passed — and there is further improvement in ST-T wave appearance, with decidedly more flattening in ST-T waves in the chest leads of ECG #7.

Figure-16: 3 months have now passed — and the ECG has essentially returned to its previous "baseline" appearance. 

ECG Blog #455 — VT Until Proven Otherwise?

I was asked to interpret the ECG in Figure-1 — told only that this 30-ish year old man had a history of having undergone a number of operations for CHD (Congenital Heart Disease) as a child. 

QUESTIONS:

• In Figure-1 — Is the rhythm VT — or — SVT with aberrant conduction — or — potentially neither of these possibilities?
• 
  
• IF told that this patient was hypotensive in association with the rhythm in Figure-1 — Does It Matter what the specific etiology of this rhythm is? If it does matter — Why does it matter?

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-1:

The ECG in Figure-1 shows a regular WCT (Wide-Complex Tachycardia) at ~225/minute, without clear sign of atrial activity.

• QRS morphology — is obviously very abnormal because: i) There is an unusual (indeterminate) frontal plane axis (with predominant negativity in standard leads I,II,III); — ii) There is a monophasic R wave in lead V1 (consistent with RBBB conduction — but lacking the usual triphasic rsR' configuration of RBBB in lead V1); — and, iii) The QRS is essentially all negative in lead V6.
• 
  
• NOTE: In most instances — the finding of a regular WCT rhythm with very abnormal QRS morphology, and without clear sign of atrial activity in an adult has to be assumed VT (Ventricular Tachycardia) until proven otherwise. Statistical odds that such a regular WCT rhythm will turn out to be VT are ≥80%.

The above said — I was not convinced today's rhythm was VT.

• PEARL #1: The KEY feature in today's history is that this patient was diagnosed with CHD as a child, and underwent a number of operations for this. As a result — ALL bets are off as to what his "baseline" ECG might look like! Regardless of how atypical QRS morphology might be in Figure-1 — given this history of multiple surgeries for CHD, there is no predictive value forthcoming regarding QRS morphology in Figure-1 (See ECG Blog #422 for another regular WCT case with abnormal QRS morphology in an adult with CHD).
• PEARL #2: Today's case provides an excellent example for which finding a baseline ECG in this adult with CHD would clearly provide insight. It would probably tell us whether the abnormal QRS morphology that we see in Figure-1 is the result of VT vs SVT (ie, with the abnormal QRS morphology being the result of the patients underlying Congenital Heart Disease). 
• PEARL #3: The survival of children with CHD is much higher than most clinicians realize. At the present time, up to 97% of children with CHD live to reach adulthood — and over 75% of children with CHD who reach 18 years of age, go on to live past middle age (Dellborg et al — Circulation 147(12):930-938, 2023). As a result, it should not be surprising that many children who may have been diagnosed with even severe CHD — are living to later present to the ED with complications (such as tachyarrhythmias) as adults.
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• PEARL #4: Looking closer at today's initial ECG — there is a feature in favor of this rhythm being an SVT (SupraVentricular Tachycardia) instead of VT. Note that the initial deflection of the QRS in several leads is narrow (within the dotted RED ovals in leads I, aVL, V5 in Figure-2). Typically with VT — because the impulse arises from the ventricles (away from the conduction system) — the initial deflection of the QRS tends to be slower (wider) than what we see within the dotted RED ovals in Figure-2.

Figure-2: I've labeled KEY findings in today's WCT rhythm.

• PEARL #5: Figure-2 serves as a reminder of the Every-other-Beat (or in this case, Every-Third-Beat) Method for rapid estimation of heart rate. RED numbers show that in order to record 3 beats — it takes 4 large boxes (BLUE numbers). Thus, 1/3 the heart rate = 300 ÷ 4 = 75/minute X 3 = 225/minute (See ECG Blog #210 for more on the Every-other-Beat Method).
• Fast, accurate estimation of heart rate often provides an important clue to the etiology of certain arrhythmias — though in today's case, a rate of ~225/minute has no value for distinguishing VT from SVT rhythms.
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• PEARL #6: We are told that today's patient was hypotensive in association with the rhythm shown in Figure-1. As a result — it does not matter whether this rhythm is VT or an SVT, because initial treatment is the same! Synchronized cardioversion was applied — and successfully converted the patient to the bottom tracing shown below in Figure-3.
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• PEARL #7: The differential diagnosis that is most commonly cited for the regular WCT rhythm in today's case is between VT vs SVT with aberrancy. More than simply a semantic point — it's important to appreciate that the other common reason for an SVT with QRS widening is a preexisting BBB (Bundle Branch Block). This is different than QRS widening that develops because the very rapid heart rate does not allow sufficient time for recovery of conduction properties in a part of the conduction system (ie, rate-related aberrant conduction — for which a narrow QRS will be seen on the baseline tracing and with return to sinus rhythm after conversion of the fast WCT).

QUESTION:

• Now that we see the post-conversion rhythm ( = ECG #2) — Has this changed your interpretation of the cause of the regular WCT in ECG #1?

Figure-3: Comparison of the initial ECG in today's case — with the repeat ECG done after Cardioversion. (To improve visualization — I've digitized the original ECG using PMcardio).

ANSWER:

The post-cardioversion rhythm in ECG #2 is sinus at a rate of ~110/minute — as we clearly see upright P waves in lead II with a constant PR interval of ~0.20 second.

• Doesn't QRS morphology in the post-cardioversion tracing look very much like QRS morphology during the WCT? Although there are slight differences in QRS morphology between the 2 tracings in Figure-3 — there are many more similarities, including: i) The frontal plane axis is markedly leftward — with very similar-looking predominant negativity in leads II,III,aVF; — ii) The appearance of the monophasic R wave in leads V1,V2,V3 is virtually identical in both tracings; — and, iii) There is predominant negativity for the QRS in leads V4,V5,V6 in both tracings — with a nearly identical almost-all-negative QRS in lead V6.
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• BOTTOM Line: I interpreted the marked similarity in QRS morphology during the WCT and after conversion to sinus rhythm — as indicative of today's tachycardia being the result of an SVT with preexisting RBBB/LAHB in this 30-ish year old man with known CHD, and a history of having undergone a series of operations as a child.
• This impression could be confirmed by obtaining a previous baseline ECG on today's patient. That said, regardless of the likely supraventricular etiology of today's WCT — EP study (with potential ablation treatment) is indicated given hypotension associated with the potential life-threatening arrhythmia that we saw in Figure-1.
• 
  
• P.S.: As a technical point — the PR interval of 0.20 second seen in the post-conversion tracing in Figure-3 is not "long enough" by the standard arrhythmia definition to qualify as 1st-degree AV block. That said, the PR interval generally shortens with tachycardia. As a result — the PR interval in ECG #2 looks longer-than-it-should-be. Considering this patient's history of severe CHD as a child and the presence of bifascicular block (RBBB/LAHB) after conversion to sinus rhythm — I'd interpret this as probable indication of a PR interval conduction disturbance (and another reason for EP consultation).

 

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Acknowledgment: My appreciation for the anonymous submission of this case.

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Additional Relevant ECG Blog Posts to Today’s Case:

• ECG Blog #185 — Reviews my System for Rhythm Interpretation — with use of the Ps, Qs & 3R Approach.
• 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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• ECG Blog #422 and Blog #425 — Cases with Congenital Heart Disease in Adults.
• ECG Blog #220 — Review of the approach to the regular WCT ( = Wide-Complex Tachycardia).
• ECG Blog #196 — Another Case with a regular WCT.
• ECG Blog #263 and Blog #283 — Blog #361 — and Blog #384 — More WCT Rhythms ...
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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.
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• ECG Blog #211 — WHY does Aberrant Conduction occur?
• ECG Blog #301 — Reviews a WCT that is SupraVentricular! (with LOTS on Aberrant Conduction).
• ECG Blog #445 — Another regular WCT rhythm ...
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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 #35 — Review of RVOT VT. 
• ECG Blog #42 — Criteria to distinguish VT vs Aberration.
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• ECG Blog #133 and ECG Blog #151— for examples in which AV dissociation confirmed the diagnosis of VT.

 

 

 

ECG Blog #454 — Look for the "Break" ...

I was sent this ECG recording — and asked for my interpretation of the rhythm in Figure-1. I had little clinical information.

QUESTIONS:

• How was I able to guess the probable correct answer in less than 5 seconds?
• How was I then able to prove that my guess was correct?

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

How did I Know in Less than 5 Seconds?

With experience — it takes only seconds to systematically consider the 5 KEY Parameters for interpretation of any arrhythmia by the Ps, Qs, 3R Approach (See ECG Blog #185):

• While realizing that we only have a single lead to look at in Figure-1 (and that there are times when a single-lead rhythm strip may falsely suggest that the QRS is narrow — whereas in reality, other leads clearly show QRS widening) — the QRS complex in this lead V1 rhythm strip truly appears to be narrow. So — I instantly suspected that today’s rhythm was supraventricular!
• The overall rhythm in Figure-1 looks to be Regular (at a Rate of ~85/minute) — with the exception of a “break” in the rhythm between beats #8-to-#9.
• 
  
• PEARL #1: The BEST Clue to the etiology of a complex arrhythmia tends to be found somewhere within or around any pause that you may find in the rhythm. The RED arrow in Figure-2 shows that whereas P waves were not at all obvious elsewhere in Figure-1 — because of the slight "pause" in the rhythm that we seen between beats #8-to-9 — we are able to clearly identify a P wave in front of beat #9.
• 
  
• PEARL #2: The fact that we clearly see a P wave in front of beat #9 (ie, the RED arrow in Figure-2) — should immediately raise the question as to whether this P wave might be conducting (ie, Related to neighboring beat #9) — albeit this P wave would be conducting with a very long PR interval (ie, of 0.48 second).
• We can "test" this hypothesis — by looking for other "ECG evidence" of "hidden" P waves, keeping in mind that if other P waves were to be found, that they might also be conducting with a very long PR interval.
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• PEARL #3: Looking for "hidden" P waves is tremendously facilitated (and expedited) by using calipers. The reality is that clinicians (including cardiologists) who do not use calipers will typically not be able to interpret complex rhythms such as this one in today's case.
• PEARL #4: The BEST way to find "hidden" P waves — is to determine what a "normal" QRS and ST-T wave look like — and then to carefully look at all QRS complexes and ST-T waves on the tracing. In today's rhythm — I found it easiest to identify hidden P waves by comparing the shape of the "normal" ST-T wave of beat #9 — with the subtle-but-definite deformities present near the beginning of the ST-T waves of beat #10 and beat #11 (ie, the 5th and 6th PINK arrows in Figure-2).
• PEARL #5: Knowing that the 5th and 6th PINK arrows are almost certain to be consecutive "hidden P waves" — allows us to postulate what the P-P interval might be IF there was an underlying regular atrial rhythm (ie, the P-P interval would be the distance between these 5th and 6th PINK arrows).
• PEARL #6: It is common for 2nd-degree and 3rd-degree AV block rhythm to manifest slight irregularity (that is called ventriculophasic sinus arrhythmia) — so this needs to be kept in mind as you set your calipers to the above postulated P-P interval — and attempt to "walk through" P waves through the entire rhythm strip (See ECG Blog #344 for more on ventriculophasic sinus arrhythmia).
• Do YOU see the slight-but-real deformity in the initial part of the QRS for beats #5,6,7,8 (under the first 4 PINK arrows in Figure-2)? This subtle deformity of the initial part of the QRS is notably not present in the QRS of beat #9.
• Do YOU notice that the P-P interval between these first 4 PINK arrows is virtually the same as the P-P interval between the 4th PINK arrow and the RED arrow? 

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

PEARL #7: At this point — I was now able to "walk out" where underlying P waves were "hiding" but present throughout the entire rhythm strip ( = RED arrows in Figure-3). 

• The fact that each of the RED arrows in Figure-3 either occurs over some slight deformity in the QRS or ST-T wave, or at a place in which atrial activity might be entirely hidden by the QRS — supports my suspicion that there is a surprisingly regular underlying sinus rhythm in today's tracing!
• 
  
• To Emphasize: I have described my approach to today's rhythm in "slow motion". In practice — it took me less than 5 seconds to work through these 7 PEARLS.

Figure-3: RED arrows highlight the surprisingly regular underlying sinus rhythm that was are able to "walk out" using calipers set at the P-P interval.

Clinically: What Does this All Mean? 

• PEARL #8: Common things are common. Since we have established that there is an underlying surprisingly regular sinus rhythm — we know that at the least — there is a very markedly prolonged 1st-degree AV Block (PR interval ~0.48 second before beat #9).
• It is very common for 2nd-degree AV Block of the Mobitz I Type (also called AV Wenckebach) — to be associated with a prolonged PR interval for those beats that are conducting.
• Although most cases of Mobitz I 2nd-degree AV Block manifest fairly short groupings of beats with a clearly evident increasing PR interval until a beat is dropped — sometimes there may be very long Wenckebach cycles until the P wave is dropped. Seeing the very long PR interval before beat #9 in today's case immediately prompted me to look for Mobitz I.

PEARL #9: Support for Mobitz I in today's rhythm was immediately forthcoming by quick search for Wenckebach Periodicity (affectionately labeled by Marriott as "The Footprints of Wenckebach). As reviewed in ECG Blog #251 — several of "the Footprints" are present in Figure-3:

• The QRS complex in today's rhythm appears to be narrow (whereas the QRS is much more likely to be wide when the form of 2nd-degree AV block is Mobitz II ).
• There is a regular underlying atrial rhythm (which rules out blocked PACs as the cause for "dropped" beats).
• There is 1st-degree AV block of conducted beats — which is commonly associated with Mobitz I (the prolonged PR interval before beat #9).
• The pause containing the dropped beat is less than twice the shortest R-R interval (as seen here since the R-R interval between beats #8-to-9 is less than twice the R-R interval between beats #7-8).

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Laddergram Confirmation:

As noted — the above discussion outlines my thought process for strongly suspecting a very long cycle of Mobitz I, 2nd-degree AV Block at the etiology of today's rhythm.

• The BEST way to confirm today's rhythm diagnosis — is to prove my suspicion by being able to draw a laddergram that illustrates progressive increase in the PR interval until a beat is dropped. 

Consider the laddergram I have drawn in Figure-4:

• PEARL #10: Because there are so many beats in a long Wenckebach cycle until an on-time P wave is finally non-conducted — there will be minimal increase in the PR interval from one beat-to-the-next. As a result — it may be difficult to appreciate that the PR interval is increasing over the course of the rhythm strip.
• The BEST way to confirm a long cycle of AV Wenckebach is to look at the PR interval just before the pause (which measures 720 msec. in Figure-4) — and to compare this to the PR interval that is seen near the end of the pause (which is 520 msec in Figure-4).
• It can be seen that the PR interval then increases for the next couple of beats (to 600 — and then 640 msec. before beats #10 and 11 in Figure-4). But after these first few beats — the "increment" (ie, increase) in PR interval from one-beat-to-the-next becomes much less in a long Wenckebach cycle.
• In Figure-4 — the on-time YELLOW arrow P wave is not conducted — and this leads to the pause, after which the PR interval "shortens" to 520 msec. as the next long Wenckebach cycle begins.

Figure-4: My proposed laddergram for today's rhythm.

BOTTOM Line: Today's arrhythmia is challenging! That said — my hope is that review of the above 9 PEARLS — and increasing your comfort with the regular use of calipers will increase your confidence in knowing that with a modest amount of practice, you'll be able to dissect complex arrhythmias in a fraction of the time it used to take for interpretation without calipers.

• In "real life" — I do not use calipers to interpret simple arrhythmias, because there is no need to do so.
• There is not time to pull out calipers when the patient in front of you is "crashing" — and you need to administer emergency measures that instant.
• BUT — Today's patient was not hemodynamically unstable with this rhythm — and no matter how much time I might have spent pondering this tracing, I simply could not have definitively solved this rhythm without calipers. Using calipers — it literally took me less than 5 seconds to know with high probability that today's rhythm was a long cycle of AV Wenckebach (which I then proved was the correct interpretation with the above laddergram).

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Acknowledgment: My appreciation to Kianseng Ng (from Malaysia) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #185 — My Ps, Qs, 3R System for Rhythm Interpretation.
• r Rhythm Interpretation.
• ECG Blog #188 — Reviews how to read and draw Laddergrams (with LINKS to more than 100 laddergram cases — many with step-by-step sequential illustration).

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
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• ECG Blog #164 and ECG Blog #251 —Review of Mobitz I 2nd-Degree AV Block, with detailed discussion of the "Footprints" of Wenckebach.
• 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.
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• ECG Blog #404 — Walks you through a step-by-step approach to this AV block case (with links to a VIDEO of this case, and to Blog #344 for more details).
• 
  
• ECG Blog #352 — emphasizes that 1st-degree AV block with a very long PR interval may have hemodynamic consequences.