2nd degree AV block: is this Mobitz I or II? And why the varying P-P intervals?

Written by Willy Frick

A middle aged man presented for elective outpatient surgery. The following ECG was obtained in the preoperative area.

What do you think?

The ECG shows sinus rhythm with a rate of about 78 and 2:1 AV conduction along with right bundle branch block and left anterior fascicular block. The PR interval on the conducted beats is prolonged, about 220 ms. Eagle eyed readers might notice PP interval variation.

One differential diagnosis would be blocked PACs, a common cause of pauses on ECGs. However, given that the P waves are all identical in morphology, the more likely explanation is the ventriculophasic response. The exact mechanism is subject to debate, but the characteristic finding is that PP intervals which contain a QRS complex are shorter than PP intervals which lack one. That is exactly what we see here. It can be seen in other forms of heart block as well (such as complete heart block). See Ken Grauer's comment below for more on this.

As this patient is scheduled for imminent elective surgery, it is important to determine whether this is Mobitz I (benign) or Mobitz II (requires pacing).

So...Which is it?

Answer: You cannot be certain from this ECG alone.

The usual way to discriminate between Mobitz I AV block and Mobitz II AV block is by comparing successive PR intervals. If there is PR prolongation from one to the next, this supports Mobitz I physiology which rarely benefits from pacing. Conversely, if the PR interval is constant, this supports Mobitz II physiology, which is an indication for pacing. 2:1 block is a special case, because the tracing lacks successive PR intervals. This pattern can be seen in both Mobitz I and Mobitz II physiology.

History is often helpful. If the patient is otherwise healthy and has a good reason to have high vagal tone (like nausea or somnolence), it is likely Mobitz I. On the other hand, history of syncope does not necessarily prove that it is Mobitz II. This is because high vagal tone can cause reflex syncope, as in this case.

You can also use bedside maneuvers to investigate further. Interventions which increase vagal tone tend to worsen Mobitz I block. Perhaps surprisingly, vagal maneuvers can actually improve conduction in Mobitz II block. This is because the slower sinus rate gives more time for the His-Purkinje system to recover. The opposite is true for maneuvers which reduce vagal tone (i.e., they improve conduction in Mobitz I and worsen it in Mobitz II).

So, for example: atropine and exercise should both improve conduction in Mobitz I block, but make it worse in Mobitz II. Conversely, carotid massage should worsen conduction in Mobitz I block, but make it better in Mobitz II.

In this case, you might suspect Mobitz II block since there is already infra-Hisian disease manifest with the bifascicular block. But this is only a guess. As it turns out, the patient had a repeat ECG obtained prior to evaluation by cardiology.

What do you think?

This is an extremely helpful ECG, because we now have two successive PR intervals to compare to each other (P-waves preceding QRS complexes 4 and 5). I have labeled the P waves below for ease of reference:

P waves 8 and 9 both conduct to the ventricles. You can probably tell just by eyeballing, but caliper measurement confirms that there is PR prolongation, thus confirming Mobitz I block.

So, should the patient go to surgery?

In order to test the hypothesis further, cardiology performed carotid massage while recording 12 leads of rhythm. This is shown below:

A few seconds into the strip you can see the carotid massage artifact (most pronounced in V1-2). Quite surprisingly, carotid massage slows the sinus rate slightly, and as a result instantly improves AV conduction to 1:1, supporting Mobitz II AV block!

The patient went for EP study and had prolonged HV interval which strongly supports placement of a pacemaker. He underwent dual chamber pacemaker implantation and did well.

Learning points:

• Mobitz I and Mobitz II can co-exist in the same patient at the same time

• Bedside maneuvers can help clarify the etiology of 2:1 AV block

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MY Comment, by KEN GRAUER, MD (11/12/2024):

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Questions often arise regarding the various forms of 2nd-degree AV block. Today's case proves insightful, not only by reviewing KEY concepts on this subject — but also by illustrating a case in which bedside maneuvers can help to distinguish between the types of 2nd-degree AV block — and, in which the patient "did not read the textbook".

• I focus my comment on some additional advanced concepts to those discussed in Dr. Frick's excellent review.

To Emphasize: For those in search of "the quick answer" — today's middle-aged man should not be approved for an outpatient elective surgical procedure without further evaluation. As I'll address momentarily — I thought the 2:1 AV block was subtle, and potentially easy to overlook if one was not systematic. But regardless of whether you identified the 2nd-degree block or not — the "quick answer" — is that this patient should not be approved for elective surgery without further evaluation.

• As per Dr. Frick — some history is needed, especially since some patients are at times less than forthcoming with a history of presyncope or syncope unless probing questions are asked.
• Finding a previous ECG from this patient for comparison would be tremendously helpful (Are the conduction defects new or old?).
• To Emphasize: This elective pre-op ECG is not normal. Even if the 2nd-degree AV block is not initially recognized — there are several significant ECG abnormalities (as highlighted by Dr. Frick) which include 1st-degree AV block (PR interval = 0.24 second) — and bifascicular block in the form of RBBB/LAHB. 
• More subtle, but equally important — is the question of when these ECG abnormalities may have occurred? The small-but-definitely-present initial q wave in lead V2 (within the dotted RED circle in Figure-1) is not a normal finding with this RBBB considering that there definitely is a typical triphasic (rsR' ) QRS complex in neighboring lead V1 (ie, So there has been loss of the initial r wave that was seen in lead V1 ).
• Further support that anterior infarction of unknown age may be the cause of the above noted conduction system abnormalities — is forthcoming from the ST segment flattening in multiple leads (BLUE arrows) that is not a typical finding with bifascicular block unless there is underlying heart disease. And although the inferior lead T wave inversion could simply be the result of the predominantly negative QRS complexes of the LAHB — ruling out recent MI seems advisable prior to approval for elective surgery.
• Finally — Regardless of whether the 2:1 AV block is seen — there is marked bradycardia (rate in the 40s), which of itself deserves investigation prior to approval for elective surgery. 
• 
  
• Therefore: The "quick" answer to today's case (obvious within seconds) — is that further evaluation (and potential pacemaker placement) is needed prior to approval for elective surgery.

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What follows is a "deep dive" into some of the intricacies of the 2nd-degree AV block for readers with an interest in advanced arrhythmia interpretation.

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Did YOU See the 2:1 AV Block?

Over the years — I've occasionally encountered tracings for which an unexpected 2:1 AV block makes me STOP for a moment to verify that the rhythm in front of me truly is 2:1 block (and not some masquerading T wave or U wave). This was the case for today's rhythm — for which the marked bradycardia made me suspect 2:1 conduction — but for which the deceptively flat T waves in multiple leads (See the BLUE arrows in leads V4,V5,V6 of Figure-1) made me initially question what was T wave vs U wave vs "extra" P wave vs some superposition of both? And, before cancelling a scheduled elective surgery (with the patient already prepped in the pre-op room) — I would want to be 100% certain that I was truly looking at 2:1 AV block.

• The timing of the potenial "extra deflection" is critical. Using calipers is the fastest and easiest way to check IF what appears to be an extra P wave deflection is real (and not just a look-alike T wave or prominent U wave). 
• As can be seen from the RED arrows in Figure-1 — the timing of these potential P wave deflections is consistent with the presence of an extra P wave.
• One needs to be aware of the phenomenon known as ventriculophasic sinus arrhythmia. It is common with both 2nd- and 3rd-degree AV block to see some variation in the P-P interval beyond that expected with a simple sinus arrhythmia. The proposed rationale for this "ventriculophasic" P-P interval variation — is that the P-P interval that contains a QRS complex "sandwiched" within it, tends to be slightly shorter than the P-P interval located away from the QRS — because coronary perfusion will be a little better immediately following ventricular contraction.
• As per the P-P intervals (in milliseconds) that I have meticulously measured in the lead V5 rhythm strip in Figure-1 — a subtle ventriculophasic sinus arrhythmia is seen in today's case (and it "fits" the typical model of slightly shorter P-P intervals when a QRS is contained within).
• PEARL: The real benefit of being aware of ventriculophasic sinus arrhythmia — is that because the variable P-P interval gently offsets the location of the non-conducted P wave — this allows greater certainty that the potential extra deflection is truly a P wave (ie, This is BEST appreciated in the long lead V1 rhythm strip in Figure-1). Whereas it might be difficult at first glance to distinguish the extra P wave from the T wave in leads II and V5 — Isn't it much easier to recognize the distinct biphasic P wave shape for each P wave in the long lead V1? A T wave would not produce this rounded, terminal negative deflection that so perfectly matches the terminal rounded negative deflection of the sinus P waves before each QRS — such that on seeing this picture in lead V1 — I knew that the rhythm was 2nd-degree AV block with 2 P waves for each QRS complex.

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

The 3 Types of 2nd-Degree AV Block:

Many textbooks still break down the 2nd-degree AV blocks into 2 categories: Mobitz I vs Mobitz II. Instead, I have always favored Marriott's approach for description of the 2nd-degree AV blocks. According to Marriott — there are 3 (not 2) Types of 2nd-degree AV block. These are:

• Mobitz I (which is the same thing as AV Wenckebach) — in which there is progressive PR interval prolongation until a beat is dropped.
• Mobitz II — in which the PR interval is constant, until one or more beats are dropped.
• 2:1 AV Block — in which it is impossible to be certain whether the type of 2nd-degree AV block is Mobitz I vs Mobitz II. As per Dr. Frick — the clinical importance of this distinction — is that Mobitz I is much more likely to be benign (dependent of course on clinical circumstances) — whereas Mobitz II is much more likely to need pacing (because of the disturbing tendency of Mobitz II to suddenly drop conduction of not one, but multiple successive complexes — potentially resulting in ventricular standstill).

How to Tell Mobitz I vs II when there is 2:1 AV Block?

The above said — most of the time we can with high accuracy distinguish between Mobitz I vs Mobitz II — simply by keeping the following clinical features in mind:

• Mobitz I is much more common than Mobitz II. While relative percentages of these 2 conduction disturbances may vary, depending on whether your practice is EP cardiology — outpatient medicine — or treating patients who present for acute care — Statistics strongly favor Mobitz I (ie, Over the 4+ decades that I've studied all AV blocks that have come my way — well over 90% turn out to be Mobitz I ). It's essential not to overlook the Mobitz II cases (because referral for pacing is needed) — but statistically, the overwhelming majority of cases non-EP-cardiologists will see will turn out to be Mobitz I.
• 
  
• The reason Mobitz I has a much better overall prognosis — is that this rhythm disturbance occurs at a higher level within the conduction system (usually within the AV Node). As a result — Mobitz I usually manifests a narrow QRS (unless there is underlying BBB) — Mobitz I is more likely to be influenced by increased vagal tone, and it tends to respond well to Atropine when given during the early hours of acute inferior MI (during which vagal tone is often temporarily increased) — with acute inferior MI probably being the most common clinical situation in which Mobitz I is seen. That said — there are occasions when even Mobitz I 2nd-degree AV block needs permanent pacing (ie, when Mobitz I is associated with marked bradycardia and/or the patient is clearly symptomatic).
• 
  
• In contrast — Mobitz II occurs lower down in the conduction system. As a result — Mobitz II is most often seen with acute anterior MI — there typically is QRS widening (with either BBB and/or hemiblock) — and atropine is unlikely to be effective.
• In general — the PR interval is more likely to be normal with Mobitz II. 
• In contrast — the PR interval is more likely to be prolonged with Mobitz I. This is because with those cases of acute inferior MI that develop AV block — there is often a sequential development of conduction disturbances. That is, there tends to be sequential progression from a normal PR interval — to 1st-degree AV block — to Mobitz I — and on occasion, to 3rd-degree block at the AV nodal level (ie, with a narrow QRS). And, when the AV conduction disturbance with these inferior MI patients resolves — it tends to do so in reverse progression (ie, regressing from 3rd-degree — to Mobitz I 2nd-degree — to 1st degree — until there finally is restoration of sinus rhythm with a normal PR interval).

Unique Features of Today's CASE:

• In general — it is uncommon (rare in my experience) — for a patient to go back-and-forth between Mobitz I and Mobitz II forms of 2nd-degree AV block. Therefore — if you see clear evidence of Mobitz I elsewhere on telemetry monitoring (ie, the 3:2 Mobitz I sequence highlighted by Dr. Frick on today's 2nd tracing) — this usually very strongly suggests that those periods of 2:1 AV block are also a manifestation of Mobitz I.
• KEY Point: Dr. Frick skillfully illustrates in today's case how this usually helpful indicator that the block is Mobitz I fails to hold true in today's case — because both Mobitz I and Mobitz II co-exist in today's patient (who I like to say — "failed to read the textbook" before coming to the hospital).
• Also in today's case — Statistics are wrong — because despite how much more common Mobitz I is than Mobitz II (and despite the prolonged PR interval that is so commonly seen with Mobitz I ) — today's patient also had Mobitz II.
• Then again — the bifascicular block (RBBB/LAHB) and suggestion of anterior MI at some point in time (the abnormal Q wave in V2 in association with multiple conduction disturbances and abnormal ST-T flattening in multiple leads) are factors in favor of Mobitz II.
• Finally — the ingenious use of bedside maneuvers (as described by Dr. Frick) provides a way to suspect in today's case that this patient may turn out to be one of the rare patients in whom Mobitz I and Mobitz II co-exist!

CASE Conclusion: While the need to defer elective surgery and refer today's patient for further evaluation should be obvious within seconds of seeing today's initial ECG — Close scrutiny of the details of today's case makes for a fascinating adventure in advanced arrhythmia interpretation with important lessons for clinical application. Our THANKS to Dr. Frick for sharing this case!

 

See what happens when a left main thrombus evolves from subtotal occlusion to total occlusion.

Written by Magnus Nossen

The patient in today's case is a male in his 70s with hypertension and type II diabetes mellitus. His wife contacted the ambulance service after the patient experienced an episode of loss of consciousness. The syncope lasted about 2-3 minutes according to his wife. He woke up alert and with chest pain which he also had experienced intermittently over the previous few days. The ECG below was recorded about 20 minutes after he regained consciousness. What do you think?

ECG #1

The above ECG shows sinus rhythm at about 60 bpm. There is RBBB and LAHB. The PR interval is normal. The first task when assessing a wide complex QRS for ischemia is to identify the end of the QRS. When you have identified the end of the QRS complex and the beginning of the ST segment you can assess whether there is concordant ST segment elevation, concordant ST depression or whether there are excessively discordant ST segments. Below (Figure A) I have marked the end of the QRS complexes by drawing a vertical line through the J-point of the standard and precordial leads. Blue arrows indicate ST depression and the red arrow ST elevation.

Figure A

It now becomes apparent that there is ST segment depression in almost every lead of the ECG (V1-V6, I, II, aVL and aVF). The ST segment in lead III is close to isoelectric, with perhaps slight ST elevation. There is ST elevation in lead aVR as expected with these widespread ST depressions. The ST segment depression in the precordial leads is excessively discordant. In leads I, II and  aVF there is concordant STD. 

This ECG has widespread ST depression and an almost "Aslanger-like" appearance. The ST segment changes are compatible with severe subendocardial ischemia which can be caused by type I MI from ACS or potentially from type II MI (non-obstructive coronary artery disease with supply/demand mismatch). 

There are multiple possible clinical situations that could account for diffuse subendocardial ischemia that is not due to ACS and plaque rupture. The history in today's case with sudden loss of consciousness followed by chest pain is very suggestive of ACS and type I ischemia as the cause of the ECG changes. In my experience, patients having a type II MI (unless caused by a tachydysrhythmia) usually have a more gradual onset of symptoms reflecting the more gradual onset of most common clinical entities associated with type II MI (e.g sepsis, anemia, hypoxemia, severe hypotension etc., etc.)

The patient was given aspirin and heparin. While preparing for transport the patient became ashen and confused with cool and clammy skin and a very weak pulse. A repeat ECG was recorded about 15 minutes after the initial ECG. What do you think has happened and what is the most likely diagnosis?

Smith: after publication, Pierre Taboulet, who has an amazing French language ECG site, notified that he sees high grade AV block in this ECG:

Arrows point to P-waves

ECG #2

Again there is a wide complex QRS due to RBBB and LAFB. The rhythm now is atrial fibrillation. In the initial ECG (ECG# 1) aVR had ST elevation. Now this lead shows STD depression. Many of the leads that showed ST depression in the initial ECG now show ST elevation! There now is marked ST elevation in leads I, aVL and V2-V6.

In Figure B below I have again marked the J point by vertical lines. The red arrows point to ST segment elevation.

Figure B

At this point, with the ECG changing from diffuse ST depression to widespread ST elevation and the patient presenting in cardiogenic shock, left main coronary artery (LMCA) occlusion is the likely diagnosis. 

There is «shark-fin-like» ST elevation in many leads. This is an ominous sign. The patient was rushed to the nearest emergency department (non-PCI facility) for stabilization. Just prior to arrival he fell out of consciousness with the below ECG on the monitor.

ECG #3

The above ECG  shows a polymorphic VT at a rate of about 180 BPM. The arrhythmia spontaneously converted before defibrillation was achieved. 

On arrival in the emergency department, invasive blood pressure was 35/15mmHg and the patient was in profound cardiogenic shock with severe confusion secondary to brain hypoperfusion. The arterial blood gas showed a lactic acidosis with a lactate level of 17mmol/L. This patient is actively dying from a left main coronary artery OMI and cardiac arrest from VT/VF or PEA is imminent! Unless some LMCA flow is restored he will not survive. You have but one option in this situation as the PCI center is 1 hour away and the patient is too unstable and will not survive transport. 

PUSH THE LYTICS! 

Thrombolytics can be life saving in this situation. The patient was administered thrombolytics and shortly after the lytics were administered, the systolic blood pressure rose to about 80mmHg with ongoing epinephrine infusion. The below ECG (ECG #4) was recorded.

ECG #4

Although the above ECG shows widespread and massive ST depression, these ischemic changes actually represent an improvement over the pre-thrombolytic ECG. (ECG #2). There is now some flow in the LMCA! 

This series of ECGs (ECG #1, #2 and #4) illustrate well that subtotal occlusion of the left main is usually associated with severe subendocardial ischemia (profound and diffuse ST depression), whereas an ECG recorded during total occlusion of the LMCA (ECG #2) will show widespread ST elevations. Complete LMCA occlusion is associated with clinical shock and/or cardiac arrest.

As mentioned above, some flow was restored in the left main coronary artery at the time of recording of ECG #4. Transport to a PCI-capable facility was arranged - and on arrival at the PCI centre, the patient maintained a mean arterial pressure (MAP) of 40-50 mmHg and was alert. His lactate was down to 8. The video below shows the coronary angiography. The image quality is not the best, but you can see the subtotal occlusion of the left main artery. 

Below is a still image with the red arrow indicating the subtotal LMCA stenosis.

Post PCI an intra-aortic balloon pump (IABP) was placed and a combination of norepinephrine and dobutamine was needed to maintain perfusion pressures. Pressors could gradually be tapered within 24 hours. The initial troponin I drawn in the local emergency department prior to transfer to PCI center was 42ng/L (ref < 34ng/L) NT-proBNP was 307ng/L (ref < 300ng/L) 

The below ECG was recorded 12 hours after PCI. There is sinus rhythm with a premature atrial contraction (P wave best seen in leads V1 and V2 superimposed on the T of the second QRS) The PAC conducts to the ventricle with a prolonged PR interval. The profound ST segment and T waves changes are gone. The bifasicular block persists

ECG #5
(12 hours after PCI)

High sensitivity troponin T 16 hours after admission measured 14.877ng/L  (this is a massive infarct!). NT-proBNP was 3753ng/L There was transient liver enzyme elevation as is common with acute shock. The patient spent a couple of days in the cardiac intensive care unit receiving treatment for acute heart failure and aspiration pneumonia. He was later transferred back to his local hospital neurologically intact and without serious sequela. Long term follow up is not available.

How did the Queen of Hearts do on today's ECGs? 

See the the below image with interpretation of ECG #1, #2, #4 and #5

Click here to sign up for Queen of Hearts Access.

See this post for 8 cases of total LM Occlusion:

How does Acute Total Left Main Coronary occlusion present on the ECG?

See this case and this case for more examples of ACS involving the LMCA

Learning points:

• LMCA occlusion carries a poor prognosis, most patients do not make it to the hospital. Those who make it to the ED usually have transient occlusions with reperfusion.
  
  
• Suspect LMCA with sudden shock and widespread ST elevations. 
  
  
• Some patients are too unstable for transfer. Thrombolytics can be life saving, the patient in today's case likely would not have survived had he not been given thrombolytic therapy

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MY Comment, by KEN GRAUER, MD (10/20/2024):

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Today's case marks a tale of gratifying results from astute management of a critically ill patient with cardiogenic shock that resulted from acute LMain occlusion.

• As per Dr. Nossen — it will not be often that emergency providers encounter patients with acute LMain occlusion — simply because survival of most of these patients is so limited. Today's case offers a unique opportunity to track the evolution of a patient during the process of ongoing LMain occlusion.

Before specifically commenting on 2 of the tracings from today's case — it is worth reviewing lessons learned regarding the ECG presentation of patients with acute LMain occlusion. To do this — I have excerpted in Figure-1, my summary of Dr. Smith's major conclusions regarding the ECG appearance of this situation. The KEY Take Home Points are as follows:

• There is no “single” ECG presentation for patients with acute LMain occlusion. Quite literally — You can see almost anything!
• The reason for this highly variable ECG presentation, is that multiple territories may be involved to varying degrees — making it impossible to predict how much ST elevation you will see — and how much opposing (reciprocal) ST depression will attenuate (if not completely cancel out) these initial ST segment vector forces.
• The ST-T wave appearance in lead aVR can be anything when there is acute LMain occlusion.

Figure-1: Reasons for the varied ECG presentation of acute LMain occlusion — excerpted from Dr. Smith’s 8/9/2019 post (This Table from My Comment in the January 16, 2020 post).

Application of Figure-1 to Today's CASE:

What I found so fascinating about today's case — is how dramatically the ECG picture changed within the space of 15 minutes (as shown in Figure-2) — with this being the short amount of time that passed between the recording of the first 2 tracings in today's case.

• As per Dr. Nossen — today's initial ECG (LEFT tracing in Figure-2) shows sinus bradycardia with QRS widening due to bifascicular block (RBBB/LAHB).
• There is marked, diffuse ST segment depression in ECG #1. To facilitate distinguishing between the end of the QRS and the beginning of the ST segment — I highlight the J-point with BLUE arrows. 
• Marked ST elevation is seen in lead aVR (to the right of the RED arrow in this lead).
• As we have noted on many occasions — this ECG picture of diffuse ST depression with ST elevation in lead aVR suggests DSI (Diffuse Subendocardial Ischemia). That said, more than just DSI — ECG #1 also demonstrates the bifascicular block (of RBBB/LAHB) that is so commonly seen in association with acute LAD occlusion.
• Another interesting feature seen in ECG #1 — is that lead III shows a nearly isoelectric baseline. I suspect this is the result of the interplay between electrical forces favoring ST elevation and ST depression.
• 
  
• To Emphasize: DSI does not indicate acute infarction. And although severe underlying coronary disease is often the cause — non-coronary causes may be seen (See My Comment in the March 1, 2023 post for the common causes of DSI ). That said — we have cath confirmation in today's case of subtotal LMain occlusion (which is consistent with the findings in ECG #1).

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And then, 15 minutes later in today's case — this patient was in cardiogenic shock. 

• It is worth taking a moment to compare lead-by-lead what the changes are that occur in the form of ST elevation and ST depression between ECG #1 and ECG #2.
• As per Dr. Nossen — this sudden deterioration in the patient's clinical condition, in association with the ST-T wave changes now seen in ECG #2 — almost certainly indicates evolution to complete LMain occlusion (even though cardiac catheterization done a short time later showed subtotal but not complete occlusion).
• 
  
• PEARL: As noted in the 1st sentence of the Table in Figure-1 — a major reason why the limited data that we have on what the ECG "looks like" with acute LMain occlusion is so varied — is that we never know for certain what the state of the artery was at the time the ECG was recorded (which may be different than the state of the artery when the catheterization was done).
• In particular — Isn't it interesting how the ST-T wave appearance in lead aVR is totally reversed from the marked ST elevation seen with DSI (in ECG #1) — to marked ST depression once LMain narrowing becomes complete (in ECG #2). No wonder the limited data we have shows such variation in the ST-T wave appearance of lead aVR with LMain "occlusion".

Figure-2: Comparison between the first 2 ECGs in today's case. RED arrows are placed at the J-point for judging ST elevation; BLUE arrows at the point for ST depression.

More "Shark-Fin" . . .  

The 1st time I saw "Shark Fin" ST elevation (and "Shark Fin" ST depression) — I had no idea what I was seeing. With practice — this mimic of QRS widening becomes easy to recognize. 

• Today's case adds the extra feature of Shark Fin ST elevation on an already widened QRS complex (because of the RBBB/LAHB). That said — recognition of marked ST elevation or depression remains easy once the J-point is identified (colored arrows in Figure-2).

NOTE: For those wanting more practice recognizing Shark Fin ST-T wave changes — we've shown cases of this entity in the following ECG Blog posts (among others): 

• In the June 11, 2018 post —
• In the October 4, 2019 post —
• In the November 22, 2019 post —
• in the January, 24, 2020 post —
• in the February 16, 2020 post —
• in the April 25, 2020 post —
• in the May 19, 2020 post —
• in the September 27, 2023 post —
• in the May 3, 2024 post —
• 
  
• And — this case of a Shark-Fin-like mimic (My Comment in the August 23, 2024 post).

 

A man in his 60s with syncope. In syncope, what are we looking for on the ECG, and why?

 Submitted and written by Rachel Plate M.D., with some edits by Smith and Meyers

 

A man in his 60s with history of type 2 diabetes, obesity, obstructive sleep apnea requiring nightly CPAP, and hypertension presented for evaluation following a witnessed syncopal episode at home. The patient noted this occurred after standing and he did have prodromal symptoms including lightheadedness. EKG was obtained and shown below.

What do you think?

 

 

The ECG shows sinus rhythm a bifascicular block, both a right bundle branch block and a left anterior fascicular block. The P waves are hard to discern with the artifact present, but I believe there is also likely a prolonged PR interval, also called first-degree AV block (when this is present with bifascicular block, some people use the misnomer "trifascicular block").

There was an old ECG on file from years ago:

Only LAFB here, no RBBB. So the RBBB is new compared to prior.

Unfortunately, the clinicians did not recognize the danger of syncope with new bifascicular block (also probably with first-degree AV block). A urinalysis was ordered and it was reported to show UTI, and the patient was discharged home with antibiotics for UTI.

Two days later he had another syncopal episode at home, woke up on the floor, and again called 911. This time his ventricular rate was notably in the 30s in the ambulance. The following EKG was obtained. 

 

This ECG shows sinus P waves occurring regularly at about 100 bpm, with (most likely) high grade AV block resulting in conduction of only 1 of every 3 P waves, with a resultant ventricular heart rate of about 30-36 bpm. Notice how the QRS occurs at the same distance from the P wave each time - this greatly favors high grade second degree AV block, Mobitz II, over complete heart block with isorhythmic dissociation (in which it just happens to look like the P waves and QRS complexes are associated). Isorhythmic dissociation can be ruled out with a long rhythm strip. 

  

The distinction between high grade second degree AV block and third degree (complete) heart block is not very important, as this patient has already demonstrated high risk to deteriorate into fatal bradyarrhythmia. 

While the team was preparing atropine and transcutaneous pacing, the patient’s ventricular rate spontaneously improved. This EKG was obtained.

 

Now, we again note a bifascicular block with 1st degree AV block.

 

However, an hour later, he subsequently had another syncopal episode associated with asystole lasting 30 seconds after which he spontaneously reverted to complete heart block. No ECG or monitor strip was obtained during asystole.

 

Following, cardiology was able to place a temporary pacing wire and then a permanent pacemaker later the same morning. The patient was discharged after an uncomplicated hospital course on hospital day 2.

 

Here is his ECG after receiving a pacemaker:

The ECG starts in sinus rhythm with first degree AV block, then the sinus rate slows below the atrial pacer rate, and the pacemaker begins pacing the atria. The RBBB and LAFB morphology remains, of course. I am not sure why there appear to be two different atrial pacer spike morphologies. 

 

Learning Points

Syncope + new onset bifascicular block + historical concern for cardiac syncope warrants consideration that the cause of syncope could have been transient further deterioration of the conduction system, including complete heart block and/or asystole. Such a high-risk syncope patient should be recognized and admitted on telemetry for observation of further episodes and consideration of a permanent pacemaker. Deadly bradydysrhythmias due to conduction system failure is an especially preventable cause of death with the availability of the pacemaker.

I teach the "WOBBLER" mnemonic to my learners for syncope ECG evaluation. I believe this mnemonic is attributed to Cliff Reid at Resus.me (https://resus.me/wobbler/). I find this to be an excellent way to keep the important ECG syncope findings in mind, and systematically search each of the many many syncope/lightheadedness/palpitations ECGs I see each shift.

WOBBLER stands for:

WPW

Obstructed AV pathway (meaning AV blocks)

Brugada

Bifascicular block

LVH (including HOCM and other entities with LVH such as aortic stenosis)

Epsilon wave (ARVC)

Repolarization (both short and long QT)

Dr Smith wrote this fantastic post back in 2015 which I highly recommend for a review of the entire approach to ED syncope: 

Emergency Department Syncope Workup: After H and P, ECG is the Only Test Required for Every Patient.....

In this post he describes many high risk features in syncope on the ECG, including:

Long QT (at least 480-500 msec)

Brugada morphology

RV dysplasia (including epsilon wave)

WPW

HOCM

Non-sinus rhythm

SVT or VT (obviously)

AV blocks

Sinus pauses of 2 seconds or more

RBBB with hemiblock (bifascicular block)

LBBB

Any acute ischemia

Pathologic Q waves

LVH or RVH

Click here for 2 more trifascicular block cases:

https://hqmeded-ecg.blogspot.com/search/label/Trifascicular%20block

H/o MI and stents with brief angina has this ED ECG. And what is Fractional Flow Reserve?

A middle-aged man complained of 15 minutes of classic angina that resolved upon arrival to the ED.

Here is his initial ECG:

What do you think?

There is sinus rhythm with RBBB and possible LPFB (see Dr. Grauer's detail below).  There is ST elevation in II, III, and aVF, and reciprocal ST depression in aVL.  And there are Q-waves in both inferior and lateral leads.   So this is indeed diagnostic of myocardial infarction.

Should we activate the cath lab?

No! Not immediately, at least, because this is NOT diagnostic of ACUTE (occlusion) myocardial infarction (Acute OMI).  We need to do some more investigation.

Although diagnostic of MI, it is highly suspicious for "Old inferior MI with persistent ST Elevation" or "inferior aneurysm morphology" because of the well-formed Q-waves and the flat T-waves.

Inferior aneurysm can look a lot like ACUTE inferior MI because it does not usually have QS-waves (as anterior LV aneurysm usually does); instead, inferior aneurysm usually has QR-waves, which in inferior MI are often seen in BOTH acute and old MI.   QS-waves imply no remaining deplorizing forces toward the overlying lead.  To repeat: in contrast, anterior aneurysm is much more easily distinguished from acute MI due to the QS-waves.

I immediately looked for old charts, which were only available from another hospital, and an old echo confirmed inferior "akinesis" (which may also have persistent ST elevation).  A true anatomic aneurysm has "dyskinesis" (systolic outpouching of the ventricular wall) or "diastolic distortion" (diastolic outpouching of the ventricular wall).

See any of these posts for more on anterior LV aneurysm.

Here are other cases of inferior LV aneurysm.

How did I strongly suspect that this was NOT acute?

1.  The patient's chest pain had resolved by the time of the ECG
2.  There are well-formed Q-waves
3.  The T-waves are flat.  Acute T-waves are large, even if not necessarily hyperacute.


Although this ECG does not demand immediate cath lab activation, it is very worrisome.  It could be acute, though probably is not.  But it does prove that the patient has coronary disease and makes the probability that his chest pain is due to ACS very very high.

In fact, his first troponin I returned at 0.128 ng/mL, with a subsequent falling value, diagnostic of MI.

So I made an ED diagnosis of Non-Occlusion Myocardial Infarction (NOMI), and his next day angiogram confirmed NOMI.  He was treated with aspirin and heparin.

Angiogram:

Widely patent RCA and LAD stents.

Culprit Lesion: Angiographically indeterminate 50% stenosis in the proximal OM2 was assessed further with instantaneous wave free ratio (iFR) of 0.96, which is normal (see below for description of iFR*).

"After normalization in the left main, the pressure wire was advanced to the distal OM2, and iFR was 0.96, suggesting no hemodynamic significance, and no significant drift on pull back."

Therefore, no stent was placed.  (No culprit could be identified, and FFR was negative)

Impression and Recommendations:

Widely patient RCA and LAD stents

No evidence for hemodynamic significance of 50% proximal OM2 stenosis

Diffuse mild to moderate CAD without evidence for severe epicardial stenosis
_______________

A bit about fractional flow reserve (FFR) (with my limited understanding of this, and I put a link in to an excellent article on this below): This is an angiographic technique to assess the pressure gradient across coronary lesions.  It is proven better than angiography alone in stable angina, and also has been shown to improve decisions on stenting non-culprit lesions in ACS.  However, if a culprit lesion is identified in ACS, and has low pressure gradient ("negative" FFR assessment), this does NOT mean it should not be stented -- FFR is not a good assessment for culprit lesions.

*Instantaneous wave-free ratio is performed using high fidelity pressure wires that are passed distal to the coronary stenosis. iFR isolates a specific period in diastole, called the wave-free period, and uses the ratio of distal coronary pressure (Pd) to the pressure observed in the aorta (Pa) over this period. During this wave-free period, the competing forces (waves) that affect coronary flow are quiescent meaning pressure and flow are linearly related as compared to the rest of the cardiac cycle.

Very good summary of the data on Fractional Flow Reserve and Instantaneous Wave Free Ratio:  https://www.acc.org/latest-in-cardiology/articles/2017/05/25/08/34/ffr-in-2017-current-status-in-pci-management

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MY Comment by KEN GRAUER, MD (1/31/2020):

===================================

Interesting case to review! We are told that this middle-aged male patient has a history of prior MI with stents. He presents with an episode of brief, new-onset chest pain that had resolved by the time ECG #1 was obtained.

• For clarity — I’ve reproduced and labeled the ECG shown in this case (Figure-1).

Figure-1: The initial ECG that was done in the ED (See text).

I’d add the following thoughts to the comments by Dr. Smith. 

• Although there is resemblance to an rsR’ pattern in lead V1 — this ECG does not represent a “typical" RBBB. YES, there is a RBBB — because there is a predominant positive triphasic complex in lead V1 that occurs in association with wide terminal S waves in lateral leads I and V6. But a closer look at lead V1 reveals marked fragmentation of the QRS complex in both the small S wave downward deflection, as well as in the bifid terminal R’ (Be sure to look at the magnified view of ECG #1, by clicking on the Figure!).
• Fragmentation of the QRS complex is marked, and present in numerous leads in ECG #1 (ie, in each of the inferior leads — and, dramatically so in the upslope of the S wave in lead V2, and to a lesser extent in the S wave of lead V3). The phenomenon of fragmentation has been discussed and illustrated numerous times on Dr. Smith’s ECG Blog (I’ll add reference to THIS CASE of mine). The importance of recognizing fragmentation (especially when it is as marked as it is in ECG #1) — is that it tells us there has been scarring, which may be the result of prior infarction, cardiomyopathy, or some other form of structural heart disease. Such fragmentation does not tell us whether heart disease is acute or has been present long-term — but even IF we had not been told that the patient in this case had prior MI with stents — it would be very clear from the fragmentation we see in ECG #1, that this patient has severe underlying structural heart disease!
• There are 2 clues that scarring in ECG #1 is the result of prior MI: i) There is even fragmentation within 2 of the 3 inferior Q waves (RED arrows); and, ii) Q waves are not only present in the chest leads, but these Q waves begin as early as lead V3 (BLUE arrows) — and extend through to lead V6 (with the Q in V6 being deeper-than-is-likely-to-be-seen with a normal septal q wave). It is uncommon that you will see septal q waves as far over as lead V4. Septal q waves should simply not occur as early as lead V3. And — the presence of RBBB does not account for Q waves in these 4 chest leads. BOTTOM Line: The presence of inferior and antero-lateral Q waves in ECG #1 is diagnostic of inferior and anterolateral MI that must have occurred at some point in time.

Otherwise — I would not diagnose LPHB (Left Posterior HemiBlock) on this tracing ( = my opinion). Instead — I would describe the conduction defection as RBBB alone.

• It is well to keep in mind that among the bifascicular blocks (ie, RBBB/LAHB and RBBB/LPHB) — RBBB/LAHB is far more common (ie, more than 90-95% of the bifascicular blocks in my experience manifest Left Anterior HemiBlock instead of LPHB). The reasons for this are simple: i) The left posterior hemifascicle is much thicker anatomically than the left anterior hemifascicle; and, ii) The posterior hemifascicle has a dual blood supply. As a result of these 2 factors — much more extensive damage is needed to produce true RBBB/LPHB.
• NOTE — It is rare to see a true isolated LPHB. Instead, when LPHB does occur — it is almost always seen in association with RBBB, as a form of bifascicular block. In contrast — isolated LAHB is extremely common, especially in older individuals. And as just mentioned — RBBB/LAHB is by far the most common form of bifascicular block.
• Terminology — While I have seen significant variation among cardiologists regarding the criteria they use for diagnosing LPHB — the criteria I have always used require clear predominant negativity for the QRS complex in lead I. When assessing a tracing for possible LPHB in a patient who also has RBBB — it is the straight downward portion of R wave descent into the S wave in lead I that should be assessed (ie, the portion of the QRS before the terminal delay produced by the RBBB). Predominant negativity of the QRS complex in lead I is not present in ECG #1. Note the positive portion of this straight-line descent (ie, the vertical RED line in lead I) equals the negative portion (ie, the vertical GREEN line in lead I) — so predominant negativity is lacking.

Finally — As per Dr. Smith, the ST-T wave changes we see in ECG #1 do not look acute. Instead, T waves in multiple leads (ie, leads I, aVL, V2-thru-V6) look flat. In addition, ST segments in these leads lack the gentle upsloping that is usually seen in a normal tracing.

• Typically, with simple RBBB — there is slight ST depression with more marked T wave inversion in lead V1 than we see in ECG #1.
• There is ~1 mm of ST elevation in each of the inferior leads. That said — the shape of the ST segment in these inferior leads manifests gentle upsloping (ie, it just doesn’t look acute).
• Although there is some scooping to the ST segment in lead aVL — the J-point in lead aVL is not depressed. Therefore, the “magical” reciprocal relationship seen between leads III and aVL with acute inferior OMI is not seen in ECG #1 (See My Comment in the 1/29/2020 post, among many other references to this phenomenon in Dr. Smith’s blog).
• THE ABOVE SAID — We can not overlook the fact that: i) This middle-aged man has documented severe underlying coronary disease — and, he presents with new (albeit short-lived) chest pain; ii) There is ST elevation in each of the inferior leads in ECG #1; iii) We were not given a prior tracing for comparison (so we do not know for certain which ECG changes are old) — and, iv) It is possible that the ST-T wave flattening we see so diffusely in ECG #1 could be, at least in part, a “net effect” of prior ST-T depression + new ST elevation, in which the "net" result is some cancelling out of opposing forces (ie, "pseudo-normalization"). 
• BOTTOM LINE: I agree entirely with Dr. Smith. The ECG findings we see in ECG #1 do not look acute — BUT — it is impossible to be certain that these findings are not acute from this single ECG, which is why more investigation was indicated for final decision-making.

Our THANKS to Dr. Smith for presenting this case!