What kind of AV block is this? And why does she develop Ventricular Tachycardia?

This was written by Magnus Nossen

The patient is a female in her 50s. She presented with a one week hx of «dizziness» and weakness. She was feeling fine prior to the last seven days. There was no chest pain. She did admit to shortness of breath on exertion. She had no known heart condition. Other than being overweight and having an elevated cholesterol she was healthy. She was taking a single perscription drug, a statin.

Below is her presentation ECG. How will you interpret the ECG? 

The ECG above is highly pathological. There are sinus P-waves throughout the tracing. It is immediately apparent that there are more P waves than QRS complexes. Thus some form of AV block must be present. For the majority of the tracing there are two P waves for each QRS. There is a LBBB. 

Whenever there is a fixed 2:1 AV block, it is difficult to determine if the AV block is due AV nodal disease (second degree AV block type I, Wenckebach) or if there is infra-Hisian AV block. Whenever there is a narrow complex 2:1 AV block, you can feel pretty safe that the AV block is second degree type I and therefore the likelihood of progression to complete AV block without stable escape rhythm is quite low.  

However. If there is a 2:1 AV block with a wide QRS complex — it is more likely that the AV block is second degree AV block type II. Why is this an important distinction? 

Mobitz type I AV block is caused by AV nodal disease. The PR interval gradually prolongs until a QRS is dropped and the pattern repeats itself. If there is no BBB the QRS will be narrow.

Mobitz type II AV block usually has a different pathophysiology. In most cases, there is an underlying complete BBB (left or right) and an intermittent block in the other bundle branch. This leads to periods of complete heart block below the His-Purkinje system. If any escape rhythm is present it will be ventricular and very slow.

The ECG above shows LBBB. The P waves that conduct do so with normal PR interval (hinting at normal AV conduction). There is for the most part 2:1 AV block. There is for a short while 3:2 AV conduction. The PR interval seems to be the same, or at least not obviously prolonging. Unfortunately a longer rhythm strip is not available. 

Mobitz type II AV block was suspected. In this case (above ECG) ventricular activation depends on the RBB conducting impulses as there is a permanent LBBB. Intermittent RBBB is causing non-conduction leading to dropped QRS complexes.  If the RBBB worsens and becomes persistent — ventricular escape rhythm is all that is left.

Biochemistry was unremarkable except for a mildy elevated NT-proBNP. Troponins were negative. The patient was admitted with telemetry. During the next 24 hours, she experienced periods of complete AV block with a ventricular escape rhythm in the 20s. She was started on isoprenalin (isoproterenol). 

Shortly after isoprenalin infusion was initiated, there were short runs of ventricular tachycardia. The following ECG was recorded during one of these episodes of VT.

The above ECG initially shows AV block. A run of very fast, irregular polymorphic VT ensues. Isoprenalin was discontinued, and a temporary transveous pacemaker was implanted. The patient stabilized following pacemaker placement.

Discussion: The initial ECG in today's case is pathological for any patient, especially for a 50-year old previously heathy female. Extensive conduction system abnormalities can have various causes (ischemia, genetic, infectious, amyloid, etc). Usually the medical history will provide clues to the cause. 

Even though the primary suspicion was not ischemic heart disease, a CT angiogram was performed, and it revealed normal coronary arteries. This ruled out coronary disease as the cause of conduction system disease. When assessing patients with early onset high grade conduction disorders and ventricular tachydysrhythmia in the absence of coronary disease — cardiac sarcoid should be on the list of differential diagnoses. 

The patient underwent an MRI and cardiac PET scan. Below are videos of the PET scan showing areas of high metabolism/uptake in the myocardium, consistent with cardiac sarcoid.

The patient was transferred to a facility for cardiac biopsy. The biopsy was consistent with cardiac sarcoidosis. Medical treatment with oral steroids and methotrexate was started. She was given CRT-D (Cardiac Resynchronization Therapy-Defibrillator). The ECG below was recorded after her device was implanted. The ECG shows atrial sensing and biventricular paced rhythm. QRS complexes are quite narrow due to both ventricles being paced in a synchronized fasion. 

About sarcoidosis: Sarcoidosis is a multisystem granulomatous disorder. Lung involvement is the typical presentation. Cardiac sarcoidosis (CS) is seen in ~10% of patients with sarcoidosis. The granulomatous inflammation affects the heart, causing an infiltrative cardiomyopathy

The most common manifestations of cardiac sarcoidosis are atrioventricular (AV) block and ventricular tachyarrhythmias (VT). AV block is the first manifestation of CS in more than 30% of patients. VT is the second most common presenting arrhythmia. SCD (sudden cardiac death) from sarcoid heart disease is thought to be caused by either from high-grade AV block or VT.

• Cardiac sarcoidosis is usually associated with lungs sarcoidosis, but can be an isolated finding without other organ involvement. Think of this possibility when you encounter a conduction disorder in a «younger» patient

• 2:1 AV block may pose a diagnostic challenge. In general a wide complex AV block is more dangerous than a narrow complex AV block, which is more likely to have a stable escape rhythm.

• Vaso or inotropic medications are not harmless, and can precipitate life threatening arrhythmias.

Learning points:

 

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

MY Comment, by KEN GRAUER, MD (1/23/2024):

=================================== 

Today's case by Dr. Nossen differs from other cases of AV block we have published over the years in Dr. Smith's ECG Blog — in that the cause of AV block turned out to be CS (Cardiac Sarcoidosis).

• Most of the cases of AV block that we see in practice, are the result of underlying heart disease. That said — it is important to be aware of other potential etiologies that emergency providers will periodically encounter (See Figure-3 in the ADDENDUM below for a LIST of potential etiologies of AV Block).

The 2nd reason I found today's case especially interesting — is the challenge posed by the initial ECG. For clarity in Figure-1 — I have reproduced this initial tracing.

• The KEY decision to make regarding the interpretation of ECG #1 — is to determine the type of 2nd-degree AV block that is present?

Figure-1: The initial ECG in today's case. What type of AV block is present?

MY Thoughts on the ECG in Figure-1:

Today's initial ECG is highly instructive. I'll highlight the following points:

• There is no long lead rhythm strip. Instead, we are only provided with a 5.5 second rhythm strip that only shows 5 beats! It is important to appreciate that we see the same 5 beats in both limb and chest leads (ie, Beats 1,2,3,4,5 in the limb leads are the same as beats 1c,2c,3c,4c,5c in the chest leads).
• 
  
• To Emphasize: It's impossible to determine with certainty the type of AV block from an abbreviated rhythm strip less than 6 seconds in duration, which contains a total of only 5 beats. That said (as per Dr. Nossen) — We can assess the brief rhythm strip that we have, and predict clinical likelihood of what the rhythm etiology is.
• In doing so — I have labeled sinus P waves with RED arrows. As per Dr. Nossen — there are more P waves than QRS complexes, which defines this rhythm as some form of 2nd-degree AV block.
• Even without calipers — it should be obvious that the atrial rhythm is not regular! It is common with 2nd- and 3rd-degree AV block to see a "ventriculophasic" sinus arrhythmia. Usually with ventriculophasic sinus arrhythmia — the P-P intervals that "sandwich" QRS complexes tend to have shorter P-P intervals than those P-P intervals that do not contain a QRS between them. The physiologic reason for this — is thought to be the result of momentarily increased circulation from mechanical contraction arising from the "sandwiched in" QRS complex.
• The QRS complex in ECG #1 is wide. QRS morphology is consistent with LBBB (Left Bundle Branch Block) — in that there are all upright QRS complexes in lateral leads I,aVL,V6 — and predominantly negative QRS complexes in chest leads until lateral lead V6.
• There is some conduction of these LBBB complexes — because the PR interval preceding beats #2,3,4 is constant, as well as normal (ie, not more than 0.20 second in duration).
• ST-T waves in association with LBBB conduction do not suggest acute OMI. That said — there are at the least, some nonspecific ST-T wave abnormalities in the form of ST segment straightening beyond that expected for simple LBBB conduction (ie, in leads II,III,aVF; and in leads V5,V6).
• The ventricular rhythm is fairly (but not completely) regular for the first 4 beats. The reason for this slight irregularity is simply a result of the underlying ventriculophasic sinus arrhythmia.
• Beat #5 occurs earlier-than-expected — and is preceded by a P wave. Determination of the PR interval before beat #5 is KEY for distinguishing between Mobitz I vs Mobitz II forms of AV block — because IF the PR interval before beat #5 is increasing compared to the PR interval before beat #4 — this would suggest Mobitz I ( = AV Wenckebach) as the type of AV block.

CAVEATS and PEARLS: Unfortunately, the P wave before beat #5 in occurs before the end of the preceding T wave. As a result — we do not clearly see the onset of this P wave. This makes it difficult to determine whether or not the PR interval before beat #5 is a little bit longer than the PR interval before beat #4.

• PEARL #1: There are 3 types of 2nd-degree AV block. These are: i) Mobitz I ( = AV Wenckebach) — in which the PR interval progressively increases until a beat is dropped; ii) Mobitz II — in which the PR interval is constant, until one or more beats in a row are non-conducted; — and, iii) 2:1 AV block — with which it is impossible to be certain whether or not the type of 2nd-degree block is Mobitz I or Mobitz II, because we never see 2 QRS complexes in a row that are conducted with the same PR interval. It is for this reason that accurate determination of the PR interval before beat #5 is so important for clinical implications of today's case.
• 
  
• PEARL #2: It is highly unusual for the type of AV block to alternate between Mobitz I and Mobitz II. Therefore, when the predominant rhythm is 2nd-degree AV block with 2:1 AV conduction — IF elsewhere during cardiac monitoring of your patient you see occasional indication of clear Mobitz I (ie, progressive PR interval lengthening before the dropped beat) — then it becomes highly likely that those periods of 2:1 block reflect Mobitz I and not Mobitz II.
• 
  
• PEARL #3: As per Dr. Nossen — the reason distinction between Mobitz I vs Mobitz II is important — is because IF the rhythm is Mobitz II — then pacing is needed (because of a much higher incidence of progression to complete AV block than is seen with Mobitz I — with onset of complete AV block with Mobitz II often being very sudden!). The physiologic reason why pacing is much more likely to be needed with Mobitz II — is that this conduction defect occurs at a lower level in the conduction system (ie, below the AV node) — therefore implying a slower and much less reliable intrinsic rhythm.
• 
  
• PEARL #4: While impossible to know for certain the type of 2nd-degree AV block in today's case from the brief 5-beat tracing we are provided with — certain clinical features can help to predict the clinical likelihood of Mobitz I vs Mobitz II when there is 2:1 AV block. These clinical features include: i) QRS width (As noted — Mobitz II occurs lower in the conduction system — therefore it is usually associated with QRS widening and a ventricular conduction defect); ii) Statistics (In my experience of seeking out every AV block I have been able to locate over the past 40+ years of my career — well over 95% of all 2nd-degree AV blocks I have encountered are Mobitz I, such that my "collection" of Mobitz II tracings remains limited, compared to many hundreds of Mobitz I tracings); iii) PR interval (The finding of a prolonged PR interval for conducted beats is much more commonly seen with Mobitz I AV block); — and, iv) Association with acute or recent MI (Mobitz I is a common accompaniment of inferior MI — whereas Mobitz II is more likely to be seen with anterior MI).
• CAVEAT to PEARL #4: Although the QRS complex is most often narrow with Mobitz I 2nd-degree AV block — it may be wide if there is preexisting BBB. And, although the QRS is most often wide with Mobitz II — it can occasionally be narrow.

LADDERGRAM of Today's Rhythm:

For clarity in Figure-2 — I've drawn a laddergram for the 5-beat rhythm in today's initial ECG.

• As described above — there is 2:1 block for the first 3 beats.
• Beat #4 occurs earlier-than-expected. As best I can tell — the PR interval before beat #5 is not increasing compared to the PR interval before beat #4. That said — IF I was "at the bedside" — I would reserve judgment about the type of 2nd-degree AV block present until I saw a longer period of monitoring (this being the reason for the question mark I placed in the AV Nodal Tier after beat #5).

Figure-2: Laddergram of the rhythm in today's initial ECG.

Putting It All Together:

As noted above — there is a ventriculophasic sinus arrhythmia in today's initial ECG, in which there is some form of 2nd-degree AV block.

• While fully acknowledging that there is need for a longer period of monitoring — I agree with Dr. Nossen that the AV block is most likely Mobitz II because: i) The QRS is wide (ie, there is LBBB); ii) As best I can tell in Figure-2 — the PR interval is not increasing with consecutively conducted beats (albeit the T wave of beat #4 "blocks" our view of the true onset of the P wave before beat #5); — and, iii) The clinical course of today's case is most consistent with Mobitz II AV block — because the patient went on to develop complete AV block, as well as a run of VT (with both of these rhythm disorders being common complications of cardiac sarcoidosis [Hussain and Shetty — StatPearls, 2023 — and — Sink et al — JAHA 12:e028342, 2023] ).

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

ADDENDUM:

There are many potential causes of AV block. Although most commonly seen in adults in association with ischemic heart disease (ie, as the result of recent infarction) — or in older adults as the result of fibrosis or calcification of the atrioventricular conduction system — there are a variety of other Potenial Causes of AV Block in adults, as well as in the pediatric age group (Figure-3).

• KEY Point: As some of the causes of AV block in Figure-3 may be treatable and/or resolve with time — a search for the cause is essential. For example — bradycardia and AV conduction disturbances are not uncommon with Hyperkalemia, with these conduction disturbances most often resolving once serum K+ is corrected.  
• While today's case is the first we have published on cardiac sarcoidosis — we have featured infiltrative cardiomyopathy (ie, with amyloidosis — in the November 15, 2020 post in Dr. Smith's ECG Blog).
• NOTE: The indications for permanent pacing are different in younger patients! Some patients function surprisingly well for long periods of time despite some degree of AV block. As a result — an "optimal balance" is sought between the immediate need for pacing vs the likelihood of pacer malfunction over time (with eventual need for pacer replacement).
• 
  
• P.S.: For those interested in additional examples of AV block (including laddergram illustration) — Please check out My Comment at the bottom of the page in the May 16, 2020 post — the October 25, 2021 post and — the July 30, 2023 post — and, the April 6, 2023 post).

Figure-3: Diagnostic considerations for a patient who presents in AV block (adapted from Mangi et al — StatPearls, 2021).

 

A woman in her 50s with chest pain and lightheadedness and "anterior subendocardial ischemia"

 Written by Pendell Meyers

A woman in her 50s presented with acute chest pain and lightheadedness since the past several hours. Here is her triage ECG during active symptoms:

What do you think?

The ED physician read this as "Normal sinus rhythm. LVH. Marked ST abnormality, possible anterior subendocardial injury."  

Smith: I suspect this was a confirmation of the conventional computer interpretation.  These are often wrong and lead the physician astray.

This is wrong on many levels. 

The rhythm is some form of heart block (see Ken's comments at end of post) with junctional escape. The STD maximal in V1-V4 is diagnostic of acute transmural posterior wall ischemia, most likely due to posterior OMI. Subendocardial ischemia does not localize, and subendocardial ischemia presents with STD maximal in V5-6, II, and STE in aVR.

Here is the Queen of Hearts AI interpretation:

I'm really surprised the confidence isn't higher, I've seen QOH be more confident on more difficult ones that this. Anyway, she does say OMI.

So the patient's OMI was initially missed. It does not meet STEMI criteria. 

Luckily, 45 minutes later, with ongoing pain and a troponin I that resulted at 136 ng/L, the ECG was repeated:

What do you think now?

Easy for anyone.

Obvious STEMI(+) OMI of inferior, posterior, and lateral walls, now with likely 2nd degree heart block type 1 (Wenckebach).

Finally the OMI was realized.

She was taken to cath and found to have total mid RCA occlusion, TIMI 0 flow, stented with excellent result. 

Her heart block resolved quickly. 

Troponin quickly rise to greater than 25,000 ng/L (the lab's reporting limit). 

Echo showed matching wall motion abnormalities.

She survived to discharge.

Learning Points:

We can find OMI on ECG much sooner than STEMI criteria in many cases, and of course many OMIs never meet STEMI criteria at all.

AI can do it too. 

STD maximal in V1-V4, without a QRS abnormality causing it, and in the setting of ACS symptoms, is posterior OMI until proven otherwise.

Subendocardial ischemia does not localize.

The RCA usually supplies the SA and AV nodes, so RCA OMIs can present with heart blocks and bradycardias like in this case.

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

MY Comment, by KEN GRAUER, MD (7/30/2023):

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

There are numerous important points that are brought out by today’s case. For our readers who enjoy the challenge of interpreting cardiac arrhythmias — today’s case offers a “gold mine” of PEARLS regarding the recognition of AV Wenckebach. 

• WARNING: What follows below illustrates my “thought process” in evaluating today’s initial rhythm. Some of the concepts I review are basic, and should be understood, learned and applied by all providers who regularly follow Dr. Smith’s ECG Blog. Other concepts I’ll review go well beyond the basics — and are aimed at advanced interpreters (and those who want get better at interpreting complex rhythms).
• I leave for YOU to decide how deeply you want to “dive” into today’s rhythm. That said, even for less experienced interpreters — KNOW that I clarify KEY basic concepts important for all providers to appreciate. 

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

NOTE: I initially only saw ECG #1 — knowing only what the ED physician wrote in his interpretation. I knew nothing else about the case (For clarity — I've reproduced today's initial tracing in Figure-1).

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

Figure-1: I have reproduced the initial ECG in today’s case.

PEARL #1: Although the rhythm in ECG #1 is complex and extremely challenging — You do not need to figure out what this rhythm is, in order to appropriately manage the patient! 

• So — No worries if you did not recognize AV Wenckebach until later (or even if you never recognized AV Wenckebach at all in today’s case). What counts — is that you appreciate the history ( = ie, A woman in her 50s who presents to the ED with CP and lightheadedness for several hours) — and that you know to immediately elevate your index of suspicion for acute OMI whenever you learn that your patient presents to the ED for new CP! 
• By “elevating” your index of suspicion for acute OMI — I mean appreciating how this history of new CP immediately places your patient in a “higher-prevalence” group for acute OMI — so that you “go on the lookout” for even subtle ECG abnormalities (that in this clinical setting mean acute OMI until proven otherwise).
• In Figure-1 — The ST-T wave abnormality in lead V2 of ECG #1 is obvious. A bit more subtle (but definitely present) — are the ST-T wave abnormalities in neighboring leads (ie, T inversion in lead V1 — ST flattening and depression in leads V3-thru-V5). As per Dr. Meyers — a history of new CP + localized ST-T wave depression that is maximal in leads V2-to-V4 = acute posterior OMI until proven otherwise!
• 
  
• So, to return to Pearl #1 — the reason it does not matter if you even recognize AV Wenckebach at all in this initial ECG — is that assuming this patient is not hypotensive — since the overall heart rate is reasonable and there is ECG evidence that suggests acute posterior OMI until proven otherwise ==> there is indication for prompt cath with PCI as soon as this can be done! The clinical reality — is that any conduction disturbance that might be present, will probably improve (if not resolve) as soon as the “culprit” artery is reperfused!

PEARL #2: Remember that, “Common things are common!” In the setting of acute inferior — or infero-posterior — or isolated posterior OMI — most conduction disturbances that might develop will turn out to be some manifestation of AV Wenckebach (Remembering that “AV Wenckebach” — is a synonym for 2nd-degree AV block, Mobitz Type I ).

• All emergency providers are familiar with the “classic” picture of Mobitz I, 2nd-degree AV block (ie, The PR interval progressively lengthens until a beat is dropped — which produces a slight pause — and then the cycle begins again, as the next beat is conducted with a shorter PR interval).
• That said — there are numerous “variations on this theme” of Mobitz I that when present, can make recognition of Mobitz I quite challenging. Some examples of variation on the "theme" of Mobitz I might include — junctional escape beats, dual AV nodal pathways, simultaneous SA block — or when Wenckebach cycles terminate with PACs or Echo beats, instead of the “classic” non-conducted on-time P wave. NO matter! — because Common things are common. IF your patient has some type of conduction disturbance + an acute inferior or infero-postero or isolated posterior OMI — then even if the “classic” Mobitz I picture is not seen, the chances remain very high that some form of AV Wenckebach is still operative.
• The above statement is especially true IF the QRS complex is narrow (as it is in ECG #1) — since the QRS will almost always be wide when there is Mobitz II.
• Common things are common. In my experience of looking for Wenckebach over the past 40+ years — >95% of 2nd-degree AV blocks are Mobitz I (and not Mobitz II).

PEARL #3: IF you want to try to determine the mechanism of a conduction disturbance — the EASIEST initial step is to label the P waves. You'll note that I also number the beats — since this instantly allows everyone involved to ensure we are all talking about the same part of the tracing (Figure-2).

• For there to be AV block — the atrial rhythm should be regular (or at least almost regular, if there is an underlying sinus arrhythmia). If P wave morphology is changing — or if the P-P interval is clearly irregular — then the chances are that you are dealing with something other than simple AV Wenckebach.
• 
  
• LOOK at Figure-2. Isn’t it much easier now that all P waves are labeled — to appreciate that the underlying atrial rhythm is regular? 
• 
  
• As soon as I labeled all P waves — it became obvious to me that many (most) of these P waves were unrelated to neighboring QRS complexes, which by definition means that there is AV dissociation. 

Figure-2: I've highlighted P waves with RED arrows.

PEARL #4 — AV dissociation is never a “diagnosis”. Instead — it is a condition caused by “something else”. There are 3 Causes of AV Dissociation: i) AV Block itself (of 2nd- or 3rd-degree); ii) "Usurpation" — in which P waves transiently do not conduct because of an accelerated junctional rhythm that takes over (ie, “usurps” control of the rhythm); and, iii) "Default" — in which a junctional escape rhythm takes over by “default” (ie, because of SA node slowing) — as may occur if a medication such as a ß-blocker is being used.

PEARL #5 — Complete AV dissociation is not the same as 3rd-degree AV block! This is one of the most commonly misunderstood concepts in all of arrhythmia interpretation! Complete AV block is just one of 3 possible causes of AV dissociation.

• The KEY to determining if any AV block at all is present — is to determine IF P waves fail to conduct despite having adequate opportunity to do so.

Consider Figure-3. 

• The P waves labeled C, E, G, I, K and M do not realistically have a chance to conduct — because they either occur with a PR interval that is too short (too close to its neighboring QRS) — or the P wave occurs within the QRS — or the P wave occurs too soon after the QRS (within the absolute refractory period — as for M).
• In contrast — the P waves labeled B, D, F, H, J, L, N and P should seemingly conduct — but fail to do so. Therefore, there is at least some form of 2nd-degree AV block in Figure-3.

Figure-3: For clarity — I've denoted P waves by capital letters.

PEARL #6 — The rhythm in Figure-3 is not complete AV block! Most of the time, IF the degree of AV block is complete (3rd-degree) — then the ventricular rhythm should be regular (or at least fairly regular). This is because escape rhythms arising from the AV node, the His or ventricles are usually fairly regular rhythms. Exceptions may occur (ie, during cardiopulmonary resuscitation) — but even then, there will usually be a recognizable pattern of ventricular regularity. 

• Within seconds — I knew that the initial ECG in today's case was not complete AV block.
• 
  
• KEY Point: The BEST clue that there is at least some conduction — is IF in the presence of AV dissociation, you see one or more beats that occur earlier-than-expected.

Take another LOOK at today's initial ECG (which I reproduce in Figure-4). 

• HOW did I immediately know that the rhythm was not complete AV block?

Figure-4: I've reproduced the initial ECG that was shown in Figure-1.

ANSWER:

• I knew the rhythm in Figure-4 was unlikely to represent complete AV block — because beat #7 occurs earlier-than-expected (As shown in Figure-5 — the R-R interval preceding beat #7 = 1040 msec. — whereas the R-R interval preceding all other beats on this tracing = 1160 msec.). As per PEARL #6 — this strongly suggests that beat #7 is conducted.
• Since at least 1 beat is being conducted in Figure-5 — this means that the rhythm is not complete AV block — but instead, some form of 2nd-degree AV block — and by PEARL #2, we know that by far, when there is acute posterior OMI and some form of 2nd-degree AV block with a narrow QRS — that this is almost certain to be some form of AV Wenckebach.
• 
  
• PEARL #7: Not only is the rhythm in this initial ECG not complete AV block — it is also not necessarily a "high-grade" form of 2nd-degree. I define a "high-grade" 2nd-degree block — as when 2-or-more P waves that should conduct, fail to conduct. As discussed above in explanation to Figure-3 — the P waves labeled C, E, G, I, K and M do not realistically have a chance to conduct — because they either occur with a PR interval that is too short (too close to its neighboring QRS) — or the P wave occurs within the QRS — or the P wave occurs too soon after the QRS (within the absolute refractory period — as for M). Therefore — we never see 2 consecutive P waves that should conduct, fail to do so — which means that we have no evidence to suggest this is a high-grade block.

Figure-5: I've measured the R-R intervals in Figure-4.
(8/7/2023 — My THANKS to H.S.Cho for catching my typo ...)

PEARL #8: Realize that IF you want to get good at recognizing complex arrhythmias (especially complex forms of AV dissociation and AV block) — then You HAVE to use calipers. 

• I am not saying that all providers have to use calipers — because as I already emphasized in PEARL #1 — today’s patient has acute posterior OMI until proven otherwise — which means that prompt cath is needed — with the clinical reality that any conduction abnormality that might be present will probably improve as soon as the “culprit” artery is reperfused.
• 
  
• Did YOU realize that beat #7 in Figure-5 occurs slightly early? The chances are that unless you used calipers — that you would not have realized this.
• 
  
• To EMPHASIZE: Using calipers does not slow down your interpretation. On the contrary, using calipers speeds up your interpretation — because you can instantly determine that beat #7 is occurring slightly earlier-than-expected. 
• 
  
• Using calipers also allowed me to quickly determine that the atrial rhythm that I marked out with RED arrows in Figure-2 — is regular! Knowing where to look for those P waves that are partially hidden within QRS complexes or parts of the ST-T wave — is made much easier by setting your calipers to a P-P interval determined by the distance between any 2 consecutive P waves you can clearly identify (such as the distance between B and C — or between C and D in Figure-3). 

PEARL #9: When uncertain if a given beat is or is not being conducted to the ventricles — LOOK for subtle differences in QRS morphology!

• Although both sinus-conducted beats and junctional escape beats are supraventricular impulses that look similar — there sometimes are subtle-but-real differences in QRS morphology between these 2 types of beats! This is because junctional escape beats do not always arise from the center of the AV node — and when they arise either to the right or the left of center, they may manifest subtle differences in morphology (ie, The R wave may be slightly smaller or taller; the S wave may be slightly deeper or wider).
• We see this phenomenon best in lead V5 of Figure-5! BLUE arrows in this lead show that the only beats in the entire rhythm strip with these deeper S waves are beats #7 and #8. This strongly supports my suspicion that beat #7 is sinus-conducted, here with a long 1st-degree AV block (of ~0.42 second).
• 
  
• Acknowlegement I am not sure of the mechanism of beat #8 — because the PR interval that precedes it is slightly shorter than the PR interval of beat #7, which we know is conducted. The BLUE arrow in Figure-5 suggests that beat #8 is also sinus-conducted, perhaps with slight shortening of the PR interval because of the manner in which it ends a 2:1 Wenckebach cycle? Yet beat #8 is preceded by the same R-R interval of 1016 msec. as the other junctional beats. I'm just not certain. 

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

LADDERGRAMS:

I'll conclude my comments with my proposed laddergrams in Figure-6 and Figure-7 — for the 2 tracings shown in today's case.

Figure-6: My proposed laddergram for ECG #1. As suggested by my above discussion — the first 6 beats in ECG #1 appear to be junctional escape, at a rate just over 50/minute. As measured in Figure-5 — the slightly shorter R-R interval preceding beat #7 strongly suggests that this beat is conducted (albeit with a long PR interval). The fact that at least 1 beat is conducted in ECG #1 tells us that this is not complete AV block — but instead, must represent some form of 2nd-degree AV block. Given the clinical setting (ie, apparent acute posterior OMI) and the narrow QRS complex — the conduction disturbance is almost certain to represent some form of AV Wenckebach with junctional escape beats. 

(NOTE: The ? at the end of the laddergram in Figure-6 is to acknowledge that although I suspect beat #8 is also sinus-conducted — I'm uncertain why the PR interval is shorter than the PR before beat #7). 

Figure-7: My proposed laddergram for ECG #2. As per Dr. Meyers — ECG #2 makes the diagnosis of acute infero-postero-lateral OMI obvious — because there is now ST elevation in the inferior leads and in lead V6 — with reciprocal ST depression in lead aVL — and a positive Mirror Test, with marked ST-T wave depression in leads V1-thru-V4 (maximal in leads V2,V3).

As shown in the laddergram — the diagnosis of 2nd-degree AV block, Mobitz Type I (AV Wenckebach) — is now much more evident than it was in ECG #1. Virtually all of the "Footprints of Wenckebach" are now present — including: i) Group Beating (ie, 3:2 AV conduction — with repetitive 2-beat groups); ii) Regular atrial rhythm (RED arrows); iii) Progressive increase in the PR interval within each group until a beat is dropped; and, iv) The pause containing the dropped beat is less than twice the shortest R-R interval.

PEARL #10: The fact that indisputable evidence of AV Wenckebach is seen in ECG #2, that was obtained just 45 minutes after ECG #1 — strongly supports my earlier conclusion that ECG #1 did in fact represent some form of AV Wenckebach, in which the presence of junctional escape beats made this difficult to recognize.

Final Point: The reason every-other QRS complex in Figure-7 looks slightly different from the QRS of the 1st conducted beat in each group — is simply a manifestation of some aberrant conduction. Conditions predisposing to aberrant conduction of beats #3,5,7,9 are set up by the pause preceding beats #2,4,6,8 (Ashman phenomenon).

A Pre-operative ECG on a patient with a hip fracture

An 80-something tripped and sustained a hip fracture.

The patient had no cardiac symptoms, no syncope, no CP or SOB.  He was perfectly fine.

He had a 12-lead ECG in the ED as part of screening:

Interpretation?

You know there is something wrong at least partly because it is on this blog.

But this was looked at in a cursory fashion by a couple very busy emergency physicians and no serious abnormality was noticed.

First note that the QRS complexes are grouped.  Then you can see that there are P-waves which did not conduct (#'s 3 and 8).  There is no PR lengthening prior to the blocked conduction; therefore, it is not Mobitz I (Wenckebach), which would be a benign AV block, but rather Mobitz II.

They did not see that this is 2nd degree AV block Mobitz II.  When I saw it I immediately recognized it, after which it was clear to the providers.

Mobitz II has dropped beats without any prior PR lengthening, and is at risk of progressing to 3rd degree (complete) AV block.  Mobitz II is often below the AV node and therefore often does not respond to atropine.  When the QRS is wide, then it is much more likely to represent blockade below the AV node, and is more likely to be dangerous.

In this case, there is also RBBB with LAFB, which suggests block below the bundle of His.

Clinical Course

Pacer pads were placed on his chest and he was admitted to the ICU with cardiology and EP consultation.

Had he had this rhythm associated with symptoms such as syncope, or associated with acute MI, then he would undergo immediate transvenous pacer placement.

He was kept overnight on telemetry and on the cardiac monitor he was noted to have intermittent bradycardia.  Some of them were during sleep hours, however there was another episode around 10 PM where it is not very clear whether he was asleep or not.  

Of note, the PR interval is normal during the conducted beats.  This is important because it suggests that vagal tone did not have anything to do with the AV block, and suggests a more pernicious etiology.

There was concern that, during hip surgery, he would develop complete AV block.

A temporary pacer was placed.

An EP study to assess need for permanent pacer was undertaken and showed no convincing evidence of Infra-His block.  No permanent pacer was placed.

Learning Point:

Assess the ECG systematically or you will miss something, especially when it is a screening ECG (i. e., the patient does not have cardiac symptoms)!

These are the characteristics of a normal ECG.  

Note that you must assess the rate, rhythm, P-waves, PR interval, and a QRS for every P-wave as part of a systematic approach.

NSR, normal rate

Upright P wave in lead II

Biphasic P wave in V1

PR interval  120 – 200 msec

QRS for every P-wave, same PR interval

QRS less than 110 msec

Normal QRS Axis (-30 to 90 degrees)

Voltage normal

Normal septal Q waves

Normal R-wave progression

Normal ST segments

Normal T-wave size

Normal T wave axis

Normal QT

Normal U-waves

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

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

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

I like nothing better than a good arrhythmia to start of the new decade! So our THANKS to Dr. Smith for doing just that. I’d add the following thoughts to the excellent discussion by Dr. Smith.

• As per Dr. Smith — perhaps the KEY Learning Point is the need to use a Systematic Approach to ECG Interpretation (and especially to rhythm interpretation). Readers of Dr. Smith’s blog know I constantly emphasize this point (See My Comment in the June 28, 2019 post on Dr. Smith’s blog).
• CLICK HERE — For “My Take” on Systematic 12-Lead interpretation.
• CLICK HERE — For “My Take” on Systematic Rhythm interpretation.

Regarding this 12-lead ECG + Rhythm Strip:

• As per Dr. Smith — There is underlying RBBB/LAHB — but there are no acute changes.
• Regarding the rhythm — we look first at the long lead rhythm strip. The underlying rhythm is sinus (ie, upright P wave in lead II) — with slight sinus arrhythmia (slight variation in the R-R interval).
• The QRS complex is wide (as above = RBBB/LAHB).
• The overall R-R interval is fairly regular — but there are 2 pauses on this lead II rhythm strip.
• As per Dr. Smith — the PR interval remains constant for the conducted beats throughout this rhythm strip! PEARL #1 — The KEY to diagnosing Mobitz II, 2nd-Degree AV Block — is that you see consecutively conducted beats, in which the PR interval does not increase. The reason you cannot distinguish with certainty between Mobitz I vs Mobitz II forms of 2nd-Degree AV Block when there is strict 2:1 AV conduction — is that you never get to see 2 conducted beats in a row when there is 2:1 AV block (which means that you can not tell for sure if the PR interval would increase [as in Mobitz I ] IF it had a chance to do so).
• The patient in this case was in his 80s. We have no idea for how long he has lived with bifascicular block + Mobitz II. This AV block could be recent or acute (therefore the rationale for placement of a temporary pacemaker) — but given the subsequent negative EP study — the thought was that permanent pacing was probably not necessary at this point in time (and might never be necessary for this patient in his 80s).
• That said — this potentially serious (life-threatening) form of AV block should not have been overlooked by the initial providers. PEARL #2 — IF emergency providers would begin to routinely carry and use a pair of Calipers — they will doubtlessly surprise themselves by increasing their speed for interpreting complex arrhythmias — and, I bet they will never again miss another case of AV block!
• PEARL #3 — Assuming this 80-something patient maintains his satisfactorily functional lifestyle status — I would recheck a 24-hour Holter monitor on him fairly soon (and perhaps periodically as an outpatient in the future) — to ensure that prolonged bradycardia does not subsequently develop (ie, Despite benign overnight monitoring on telemetry — there still is significant potential risk for subsequent development of prolonged bradycardia).

Additional PEARLS — can be found in my hour-long ECG Video on the Basics of AV Block.

• If you click on SHOW MORE (under the video on the YouTube page) — You’ll find a detailed timed/linked Contents of all in this video.
• CLICK HERE — to go directly to the part (beginning at 30:09) that deals with the 3 types of 2nd-Degree AV Block.

P.S. (1/2/2020): Since there have been some questions regarding atrial activity in this case (P waves are of low amplitude) — I am adding Figure-1, in which I have numbered the beats and labeled P waves.

• Calipers greatly facilitate establishing that P waves are quite regular here (perhaps with slight variation in some P-P interval).
• Calipers also verify that the PR interval is not increasing (ie, this is not Mobitz I ).
• PEARL: The best (easiest) way to tell if the PR interval during a sequence of beats is increasing — is to look at the PR interval just before the pause (ie, the PR interval before beat #2) — and compare this to the PR interval at the end of the pause (ie, the PR interval before beat #3). Do this for each pause in the tracing (ie, Compare the PR interval before beat #6 with the PR interval before beat #7). Note that there is NO difference between any of these PR intervals — thus, the PR interval remains constant throughout, and this is Mobitz II.
• The PR interval is not prolonged. The easiest way to measure the PR interval is to find a P wave on the rhythm strip that begins on a heavy line (BLUE arrow in Figure-1). Note that the QRS complex of beat #2 begins slightly before the next heavy line — which means that the PR interval is definitely not more than 1 large box in duration. This is a normal PR interval (Given the wide range of "normal" PR intervals — my preference is not to call 1st-Degree AV Block until the PR interval is at least 0.22 second in duration).

Figure-1: The ECG in this case (See text).