Tuesday, January 23, 2024

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:



 


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MY Comment, by KEN GRAUER, MD (1/23/2024):
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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 "ventriculophasicsinus 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; — andiii) 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 intervalIt 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); — andiv) 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 IAll 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); — andiii) 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 — andSink et al — JAHA 12:e028342, 2023] ).

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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).


 



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