Sunday, February 5, 2023

ECG Blog #361 — Another WCT Rhythm ...


The ECG in Figure-1 is from a middle-aged man — who had just received thrombolytic therapy for presumed acute infarction. No other history available.

QUESTIONS:
  • How would YOU interpret this ECG?
  • How certain are you of your answer?

Figure-1: ECG obtained from a middle-aged man following thrombolytic therapy. (To improve visualization — I've digitized the original ECG using PMcardio).


MY Thoughts on the ECG in Figure-1:
The ECG in Figure-1 — shows a regular WCT ( = Wide-Complex Tachycardia) at ~140/minute, without clear sign of atrial activity.
  • Clinically — The 1st priority in assessing this patient would be to determine hemodynamic status. This is because IF this patient was hemodynamically unstable with this ECG — then regardless of what the rhythm happens to be — synchronized cardioversion would become immediately indicated!
  • On the other hand — IF the patient is completely stable with this rhythm, then by definition — You have at least a “moment of time” to more thoroughly contemplate the etiology of this rhythm.

PEARL #1: As emphasized in many other blog posts (ie, ECG Blog #220 and Blog #196, to name just 2) — the differential diagnosis of a regular WCT rhythm without clear sign of atrial activity should be assumed to be VT (Ventricular Tachycardia) until proven otherwise.
  • Taking all comers in an unselected adult population — statistical likelihood that a regular WCT without atrial activity will be VT is at least 80%.
  • If the patient is at least middle-aged, and especially if there is a history of underlying heart disease — then statistical likelihood that a regular WCT without atrial activity will be VT increases to ~90%. To Emphasize — This is a 90% likelihood of VT even before you look at the ECG!

  • In today's case — Given that the patient was just treated with thrombolytic therapy for a presumed acute MI — the odds that the rhythm in Figure-1 is VT are at least 90% (even before you look at the ECG).

PEARL #2: Use of QRS morphology in the 12-lead tracing during the WCT rhythm can help to refine the statistical likelihood estimate from 80-90% — to an even more precise figure (See ECG Blog #42 for specific criteria I favor for this purpose). This is especially relevant for today’s tracing — because the QRS morphology in Figure-1 is exceedingly atypical for a supraventricular rhythm. Looking at specific ECG findings in today's case:
  • There is extreme axis deviation in the frontal plane during the WCT. This is highly unlikely with a supraventricular rhythm. To Emphasize: By “extreme” axis deviation — the QRS must be entirely negative in either lead I or lead aVF. Even a small positive deflection in either of these leads negates the reliability of this criterion. The 12-lead tracing in Figure-1 satisfies this “extreme” axis deviation criterion — because the QRS is all negative in each of the 3 inferior leads! 

  • The QRS is all positive in right-sided lead aVR. This usually indicates that the origin of the WCT rhythm is from the left ventricular apex — which implies that the rhythm is VT (because supraventricular conduction does not originate from this anatomic location).

  • The QRS is all negative in leads V3-thru-V6. The finding of an all negative QRS in lead V6 — greatly increases the likelihood of VT (for a similar reason as does an all positive QRS deflection in right-sided lead aVR). Seeing an all negative QRS not only in lead V6 — but in each of the last 4 chest leads (ie, in leads V3-thru-V6) overwhelmingly favors VT.

  • Although an all positive QRS in lead V1 can be associated with RBBB-conduction — the lack of additional deflections (ie, there is no triphasic rSR’ complex in lead V1) — is more consistent with VT than with an SVT rhythm.

  • To Emphasize: There are exceptions to the above-cited morphologic criteria. These exceptions are limited to: i) If the rhythm is antidromic AVRT — in which the impulse travels forward over an AP (Accessory Pathway) in a patient with WPW, therefore resulting in a regular WCT rhythm that resembles VT (For more on the various arrhythmias in patients with WPW — See ECG Blog #18); and, ii) If the baseline ECG during sinus rhythm manifests a widened and very abnormal QRS morphology as a result of “scaring” from prior infarction(s). 
  • BOTTOM Line: Other than these 2 exceptions — it’s hard to imagine how the regular WCT rhythm in Figure-1 could be supraventricular (ie, I'd estimate a 98-99% likelihood that the rhythm in Figure-1 was VT).


CASE Conclusion:
Unfortunately — I do not have follow-up on today's patient. That said — it's hard to imagine how today's rhythm could not be VT.
  • ClinicallyImmediate cardioversion would be indicated IF this patient was at all unstable hemodynamically. Even if stable — prompt electrical carioversion would clearly be an appropriate action for a rhythm such as that shown in Figure-1.
  • Alternatively — a trial of antiarrhythmic therapy (ie, with IV Amiodarone or Procainamide) — could be appropriate IF the patient was tolerating the arrhythmia.
  • Although Adenosine is used by many in selected cases for treating a regular WCT rhythm of uncertain etiology — I would not lose time by trying Adenosine in today's case. This is because today's patient by definition has underlying coronary disease (ie, He was just treated with thrombolytic therapy for presumed acute MI). Adenosine may work in the treatment of selected Idiopathic VT rhythms (as per ECG Blog #197) — but Adenosine will not work with ischemic VT.
  • IF at any time during the treatment process the patient's hemodynamic status deteriorates — then immediately cardiovert! 

  • For more on evaluation and management of the regular WCT — See the ADDENDUM below.


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Acknowledgment: My appreciation to Dradam Ahmen (from Nouakchott, Mauritania) for the case and this tracing.

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ADDENDUM (2/5/2023):
  • I've reproduced below from ECG Blog #196 — a number of helpful figures and my Audio Pearl on assessment of the regular WCT rhythm.

 


Figure-2 : My LIST #1 = Causes of a Regular WCT (Wide-Complex Tachycardia) of uncertain Etiology (ie, when there is no clear sign of sinus P waves).



Figure-3: Use of the "3-Simple Rules" for distinction between SVT vs VT.


Figure-4: Use of Lead V1 for assessing QRS morphology during a WCT rhythm.



ECG Media PEARL #13a (12:20 minutes Audio) — reviews “My Take” on assessing the regular WCT (Wide-Complex Tachycardia), when sinus P waves are absent — with tips for distinguishing between VT vs SVT with either preexisting BBB or aberrant conduction.


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Additional Relevant ECG Blog Posts to Today’s Case:

  • ECG Blog #185 — Reviews my System for Rhythm Interpretationusing the Ps, Qs & 3R Approach.

  • ECG Blog #210 — Reviews the Every-Other-Beat (or Every-Third-Beat) Method for estimation of fast heart rates — and discusses another case of a regular WCT rhythm.

  • ECG Blog #220 — Review of the approach to the Regular WCT (Wide-Complex Tachycardia).
  • ECG Blog #196 — Reviews another Case with a Regular WCT Rhythm.
  • ECG Blog #263 and Blog #283More WCT Rhythms ...

  • ECG Blog #197 — Reviews the concept of Idiopathic VT, of which Fascicular VT is one of the 2 most common types. 
  • ECG Blog #346 — Reviews a case of LVOT VT (a less common idiopathic form of VT).

  • ECG Blog #204 — Reviews the ECG diagnosis of the Bundle Branch Blocks (RBBB/LBBB/IVCD). 
  • ECG Blog #203 — Reviews ECG diagnosis of Axis and the Hemiblocks. For review of QRS morphology with the Bifascicular Blocks (RBBB/LAHB; RBBB/LPHB) — See the Video Pearl in this blog post.
  • ECG Blog #211 — WHY does Aberrant Conduction occur?

  • ECG Blog #197 — Review of Fascicular VT.
  • ECG Blog #301 — Reviews a WCT that is SupraVentricular! (with LOTS on Aberrant Conduction).

  • ECG Blog #323 — Review of Fascicular VT.
  • ECG Blog #38 and Blog #85 — Review of Fascicular VT.
  • ECG Blog #278 — Another case of a regular WCT rhythm in a younger adult.
  • ECG Blog #35 — Review of RVOT VT
  • ECG Blog #42 — Review of criteria for distinguishing VT vs Aberration.

  • ECG Blog #133 and ECG Blog #151— for examples in which AV dissociation confirmed the diagnosis of VT.
  • Working through a case of a regular WCT Rhythm in this 80-something woman — See My Comment in the May 5, 2020 post on Dr. Smith’s ECG Blog. 
  • Another case of a regular WCT Rhythm in a 60-something woman — See My Comment at the bottom of the page in the April 15, 2020 post on Dr. Smith’s ECG Blog. 

  • Review of the Idiopathic VTs (ie, Fascicular VT; RVOT and LVOT VT) — See My Comment at the bottom of the page in the September 7, 2020 post on Dr. Smith’s ECG Blog.
  • Review of a different kind of VT (Pleomorphic VT) — See My Comment in the June 1, 2020 post on Dr. Smith’s ECG Blog.





Tuesday, January 31, 2023

ECG Blog #360 — The Patient has Cancer ...


The ECG in Figure-1 was obtained from an older woman. She presented with shortness of breath. The patient was known to have cancer

QUESTIONS:
  • How would YOU interpret this ECG?
  • Why is every-other-beat changing? 

Figure-1: ECG obtained from an older woman with shortness of breath. (To improve visualization — I've digitized the original ECG using PMcardio).


MY Thoughts on the ECG in Figure-1:
The ECG in Figure-1 — shows a regular, supraventricular (ie, narrow-QRS) rhythm at a rate of ~90-95/minute. All intervals (PR,QRS,QTc) and the frontal plane axis are normal. There is no chamber enlargement.  ST-T wave changes do not look acute.

There are 2 “eye-catching” features on the ECG in Figure-1:
  • Diffuse Low Voltage: As discussed in detail in ECG Blog #272 — a series of clinical conditions have been associated with low voltage on ECG. Clinically — the entity of “low voltage” is defined by ECG criteria as the manifestation of a QRS amplitude of ≤5 mm in all 6 limb leads. This low voltage is said to be “diffuse” IF — in addition to satisfying limb lead criteria, QRS amplitude in all 6 chest leads fails to exceed 10 mm. Regarding the ECG shown in Figure-1 virtually all 12 leads show diffuse low voltage.

  • Electrical Alternans: As discussed in detail in ECG Blog #83 — The phenomenon of electrical alternans encompasses a beat-to-beat variation in any one or more parts of the ECG recording. It may occur with every-other-beator with some other recurring ratio (3:1; 4:1; etc.). Amplitude or direction of the P wave, QRS complex, ST segment and/or T wave may all be affected. Alternating interval duration (of PR, QRS or QT intervals) may also be seen. 
  • The ECG in Figure-1 is remarkable — in that further reduction of an already-reduced QRS amplitude is seen in all 12 leads with every-other-beat (The QRS becomes tiny in virtually all 12 leads for every even-numbered beat).


PEARL #1: Regarding Today’s CASE:
Although the list of clinical entities associated with diffuse low voltage and electrical alternans is long (See ECG Blog #272 and ECG Blog #83) — the occurrence of both of these ECG findings in an older patient with known cancer, who presents with shortness of breath — should immediately prompt consideration of a large pericardial effusion as the presumed diagnosis until proven otherwise. 
  • Overall — the sensitivity and specificity of ECG for the diagnosis of pericardial effusion is poor. Clinically — it is rare that the ECG even enters into diagnostic deliberations — because the picture of a large, pear-shaped heart on chest x-ray usually prompts immediate consideration of a large pericardial effusion — that can then be rapidly confirmed by bedside Echo. Seeing low voltage on ECG is most often an “after-thought” to the diagnosis.
  • The above said — the degree of “low voltage” and the prominence of electrical alternans of every-other-beat in Figure-1 is so extreme — that today’s tracing marks one of those truly rare occasions over my many decades of reviewing ECG cases, in which I found myself immediately thinking, “large pericardial effusion” until proven otherwise.

  • A 3rd ECG finding seen in Figure-1 consistent with the diagnosis of a large pericardial effusion — is the rapid heart rate. While not quite satisfying criteria for sinus “tachycardia” (which is a heart rate ≥100/minute) — the overall heart rate of 90-95/minute adds to our suspicion.

  • To Emphasize: Smaller pericardial effusions often do not produce noticeable ECG abnormalities — which highlights the point that the diagnosis will most often not be made from the ECG. That said, what counts clinically — is appreciation whether an enlarging pericardial effusion is evolving toward pericardial tamponade (which would be a medical emergency)

  • PEARL #2: While in most cases, the ECG will not predict impending tamponade — an exception may be seen IF there is development of total electrical alternans (ie, of P wave, QRS complex and T wave) — as this finding suggests there may now be tamponade.

  • PEARL #3: Awareness of the above cited ECG findings may be clinically relevant in the patient with a large pericardial effusion that you are following. While definitive diagnosis of a pericardial effusion will have to be made by Echo — Be alert to the following: i) Progressive reduction in QRS amplitude; ii) Increasing heart rate; and, iii) Evolution of electrical alternans into a pattern involving not only the QRS, but also the P wave and T wave. IF you see this combination of ECG findings — Be ALERT to worsening effusion with potential impending tamponade.


Follow-Up in Today’s CASE:
In today's case — malignant metastasis was suspected in the patient whose ECG is shown in Figure-1. Her large pericardial effusion required drainage — with removal of nearly 1 liter of fluid.


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Acknowledgment: My appreciation to Arron Pearce (from Manchester, UK) for the case and this tracing. 

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Related ECG Blog Posts to Today’s Case:

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.

  • ECG Blog #83 — Reviews the phenomenon of Electrical Alternans.

  • ECG Blog #272 — Review the Causes of Low Voltage on ECG.



    Thursday, January 26, 2023

    ECG Blog #359 — How Many Beats in the 12-Lead?


    The ECG in Figure-1 was obtained from a previously healthy older man — who complained of chest pain and “lightheadedness” while this tracing was recorded. He was not hypotensive. His chest pain had begun the night before.
    • In view of this history — How would YOU interpret the ECG in Figure-1?
    • A total of 12 beats are seen in the long lead II rhythm strip. How many beats are seen in the 12-lead tracing that appears above the rhythm strip?

    Figure-1: 12-lead ECG and long lead II rhythm strip — obtained from an older man with chest pain and “lightheadedness(To improve visualization — I've digitized the original ECG using PMcardio).


    MY Approach to the ECG in Figure-1:
    As always when I encounter a 12-lead tracing with accompanying long lead rhythm strip — I focus first on interpretation of the rhythm (as seen in the long lead rhythm strip that appears below the 12-lead in Figure-1). Keeping in mind the Ps, Qs & 3R Approach to rhythm interpretation (as per ECG Blog #185):
    • The overall rhythm in the long lead II rhythm strip shown in Figure-1 is not regular! That said — there is an underlying sinus rhythm, as determined by upright sinus P waves with fixed PR interval before beats #2,3; 5,6,7; 9,10 and 12The QRS complex of these sinus-conducted beats is narrow. 

    • On the other hand — the QRS complex of beats #1, 4, 8 and 11 is wide. These wide beats manifest a very different QRS morphology compared to that of the sinus-conducted beats — and, these wide beats are not preceded by P waves. Therefore — these 4 beats are PVCs (Premature Ventricular Contractions).

    The "Short" Answer:
     
    • The rhythm in ECG #1 is best described sinus with frequent PVCs.



    QUESTION: 
    • Why is there a short pause after 3 of the PVCs (ie, after beats #1,8,11) — but not after beat #4?

    • Advanced Point: Why is the PR interval before beat #5 slightly longer than all other PR intervals on today's tracing?



    ANSWERS:
    • Like the majority of PVCs that we encounter — beats #1,8,11 are PVCs that manifest a compensatory pause. That is — retrograde (backward) conduction from the PVC lasts long enough (and penetrates backward far enough) — to prevent forward conduction of the next sinus P wave.
    • The reason there is no pause following beat #4 — is that this is an interpolated PVC (ie, this PVC is “sandwiched” between 2 sinus-conducted beats without the compensatory pause that typically follows most PVCs).  

    The above concepts are best explained with the Laddergram that I made of the long lead II rhythm strip in today's tracing (Figure-2):
    • NOTE: I cannot be certain from today's tracing of the extent that PVCs conduct retrograde. I therefore drew this laddergram based on what I think is happening. That said — this laddergram serves well to illustrate what generally occurs with interpolated PVCs.

    Figure-2: My proposed laddergram of the long lead II rhythm strip from ECG #1. Note how the interpolated PVC ( = beat #4) slightly prolongs the PR interval of the next sinus-conducted beat (ie, slight increase in the inclination of the slanted BLUE line in the AV nodal tier).


    PEARL #1: It is good to be aware that the PR interval of the sinus-conducted beat that follows an interpolated PVC may sometimes be prolonged — sometimes to a much greater extent than is seen for beat #5 in this tracing. Such PR interval prolongation is the result of concealed conduction (and not due to 2nd-degree AV block of the Wenckebach type)
    • The reason the PR interval preceding beat #5 in Figure-2 is slightly longer than all other PR intervals on today’s tracing — is that retrograde conduction from the PVC (beat #4) occurs at precisely the point in the cardiac cycle, that it slows but does not completely stop conduction of the next sinus P wave as it passes through the AV node and the ventricles (as shown by slight increase in the inclination of the slanted BLUE line in the AV nodal tier).
    • The technical name for the fact that we can deduce the reason for this slight PR interval prolongation before beat #5 without actually “seeing” this delay in conduction of this next sinus P wave on the surface ECG — is called concealed conduction (ie, the effect of this retrograde conduction from the PVC is “hidden” from our view).

    • Note in Figure-2 — that no PR interval prolongation occurs after the other 3 PVCs. Instead, we see a compensatory pause after PVCs #1, 8 and 11.
    • The slight negative deflection at the very end of the QRS of PVCs #8 and 11 most likely indicates retrograde P waves that have returned all the way to the atria (YELLOW arrows in the laddergram).
    • In contrast — the occurrence of an on-time sinus P wave at the very beginning of the QRS of PVC #1 (first RED arrow in Figure-2) — prevents retrograde conduction from this PVC reaching all the way back to the atria.

    • To EMPHASIZE: The above laddergram provides an "advanced" answer to today's rhythm. The "simple" answer — is that there is sinus rhythm with PVCs, including an interpolated PVC. This simple answer is more than enough for optimal clinical assessment and management of today's patient!

    =================================
    Now that we've interpreted the rhythm in today's tracing — Let's return to the 12-lead ECG. To facilitate assessment — I've reproduced Figure-1 below in Figure-3.
    • As noted in my initial presentation — the patient in today's case is a previously healthy older man who complained of chest pain and "lightheadedness" while the ECG in Figure-3 was being recorded. He was not hypotensive. His chest pain had begun the night before.

    • How would YOU interpret his 12-lead ECG?

    Figure-3: I've reproduced Figure-1. How would you interpret this 12-lead ECG?


    MY Interpretation of the 12-Lead ECG:
    Today’s ECG shows sinus rhythm with frequent uniform (ie, similar morphology) PVCs. Interpretation of ST-T wave changes in this 12-lead tracing initially depends on assessment of sinus-conducted beats in each of the 12-leads. I’ll defer interpretation of ST-T wave changes in the PVCs until later.
    • Regarding Intervals — the PR interval is normal — the QRS of sinus-conducted beats is not wide — and the QTc is normal.
    • Although overall QRS voltage is reduced — criteria for low voltage are not met (ie, the QRS is not ≤5 mm in all 6 limb leads).
    • There is no chamber enlargement.


    Regarding Q-R-S-T Changes in sinus-conducted beats:
    • Q Waves — are present in each of the inferior leads (ie, in leads II,III,aVF). QRS complexes in these leads are extremely small — with especially large and wide Q waves (considering QRS amplitude) in leads III and aVF. A small and narrow q wave is seen in lead II.
    • R Wave Progression — is appropriate for the sinus-conducted beats in the chest leads. Transition (where the height of the R wave becomes taller than the S wave is deep) occurs normally here, between leads V2-to-V3.

    Regarding ST-T wave Changes in sinus-conducted beats:
    • In 2 of the inferior leads ( = leads III and aVF) — there is ST segment coving with slight ST elevation and fairly deep T wave inversion (relative to QRS amplitude in these leads). The ST-T wave in the 3rd inferior lead ( = lead II) is flat (Note that the long lead II rhythm strip gives us a number of additional "looks" at the ST-T wave of lead II — which confirms that it is flat).
    • In high-lateral leads I and aVL — the ST segment is flat and slightly depressed. The ST-T wave in lead aVL presents the mirror-image opposite picture of the ST-T wave in lead III (See ECG Blog #184 for more on this mirror-image opposite relationship).

    • For the sinus-conducted (narrow QRS) beats in the chest leads — there is marked ST elevation in lead V1, that is totally disproportionate to the modest amplitude of the QRS complex in this lead. 
    • A lesser (but still significant) amount of J-point ST elevation is seen in leads V2 and V3.
    • ST-T waves are flat and slightly depressed in lateral chest leads V4,V5,V6.


    Putting It All Together:
    In today's patient, who presented with chest pain (that began the night before) and "lightheadedness" — the ECG in Figure-3 is diagnostic of an acute STEMI (ST Elevation Myocardial Infarction).
    • The frequent PVCs (occurring every third or fourth beat in the long lead II rhythm strip) — is consistent with this diagnosis of a recent acute cardiac event (and this may account for this patient's "lightheadedness").

    • Two Questions that arise are: i) When over the past day this patient's infarct occur? — and, ii) What is the likely "culprit" artery? 

    • I initially thought the ST elevation in anterior leads V1,V2,V3 pointed to acute occlusion of the LAD (Left Anterior Descending) coronary artery as the "culprit" vessel.
    • On further consideration — I suspect the "culprit" artery is the proximal RCA (Right Coronary Artery). The large Q waves in leads III and aVF, in association with a slight (residual) amount of coved ST elevation with moderate T wave inversion — suggest reperfusion T waves from an acute inferior MI that probably began the night before when the chest pain started.
    • The mirror-image opposite ST-T wave picture seen in high-lateral leads I and aVL is a reciprocal change. This is consistent with spontaneous reperfusion of the "culprit" artery — that probably occurred during the hours after RCA occlusion.

    • PEARL #2: Note that the relative amount of ST elevation in the anterior leads is maximal in lead V1 — and progressively decreases as one moves to lead V2 — and then lead V3. We would generally expect the opposite progression if the "culprit" vessel was an occluded LAD. We would also expect that by this time (given onset of symptoms the night before) — that ST elevation from acute LAD occlusion would probably have extended beyond lead V3.
    • In contrast — acute RV infarction is known on occasion to produce marked ST elevation that is maximal in lead V1 on a standard 12-lead tracing. (Obtaining right-sided leads on this patient could have been diagnostic — as acute RV MI with this degree of ST elevation in lead V1 would have certainly produced marked ST elevation in other right-sided leads — See ECG Blog #190 for more on acute RV MI).
    • IF indeed the anterior lead ST elevation in Figure-3 is the result of acute RV MI — this would localize the "culprit" artery to the proximal RCA — because blood supply to the RV is almost always provided from the initial portion of the RCA.

    PEARL #3 (Advanced Point): Most acute OMI (Occlusion-based MI) tracings identified by ECG will be diagnosed on the basis of ST-T wave morphology changes in sinus-conducted beats. Assessment of ST-T wave morphology in PVCs is usually not a reliable indicator of an acute event.
    • That said — On occasion, the shape of ST-T wave elevation or depression in one or more PVCs may be diagnostic of acute infarction.
    • This is the case in Figure-3. QRST morphology of the PVCs in the limb leads and in leads V4,V5,V6 — is consistent with LBBB. Although significant J-point depression is seen in the PVCs in many of these leads — this is not a specific enough finding by itself to diagnose an acute event.
    • In contrast — the amount and shape of the ST elevation for the PVC that we see in simultaneously-recorded leads V1,V2,V3 in Figure-3 — is clearly disproportionate to what one would expect the ST segment of this PVC to look like. This is especially true for the coved ("tombstone"-like) ST elevation of the PVC in lead V1 — that even without the ST elevation we see in sinus-conducted beats, would strongly suggest acute infarction.

    • NOTE: For an example of a case in which assessment of the normal (sinus-conducted) beats was not definitive for acute OMI — such that the diagnosis of acute infarction was only made by recognizing the abnormal ST-T wave morphology of several PVCsSee My Comment at the bottom of the October 8, 2018 post in Dr. Smith's ECG Blog.

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

    Final CHALLENGE in Today's CASE:
    • A total of 12 beats are seen in the long lead II rhythm strip from today's tracing. How many beats are seen in the 12-lead tracing that appears above the long lead rhythm strip?

    • HINT: Why did I repeat the numbers 1 and 2 for each of the 3-lead groupings of simultaneously-recorded beats in Figure-4?

    Figure-4: Why did I repeat the numbers 1 and 2 for each of the 3-lead groupings of simultaneously-recorded beats in today's tracing?


    ANSWER to the Final Challenge:
    It is important to appreciate that the long lead II rhythm strip in today's tracing is not simultaneously-recorded with each of the sets of 3 leads. This is easiest to see — if you look directly above beats #5-thru-12 in the long lead II rhythm strip.
    • There are many different types of recording systems used in the too-numerous-to-count number of different ECG machine systems. The system for recording employed in today's tracing repeats beats #1 and 2 in each of the sets of 3 leads — and — in addition, provides an independent long lead II rhythm strip. (NOTE: We encountered a similar type of recording system for the case presented in ECG Blog #357).

    • Editorial Comment: This is not my favorite system for ECG recording — because I find it confusing. The advantage of this system, is that we do get to see what the first 2 beats in the long lead rhythm strip look like in all 12 leads. The decided disadvantage (in my opinion) — is that we have no idea what the other beats look like in leads other than in the long lead II.
    • Another reason why this system of recording is confusing in today's tracing — is that it looks from the 12-lead ECG in Figure-4, as if the rhythm is ventricular bigeminy. On the contrary — we only see 1 PVC in the entire 12-lead tracing. This is beat #1 in the long lead II rhythm strip — that we see in simultaneously-recorded leads I,II,III. We then once again see beat #1 in simultaneously-recorded leads aVR,aVR,aVF — and again in V1,V2,V3 — and a final time in V4,V5,V6.
    • Imagine how confusing this tracing might have been if instead of the 4 PVCs that we see in the long lead II rhythm strip (ie, beats #1,4,8 and 11) — if beat #1 was the only PVC that occurred. The 12-lead ECG would still look the same as it does in Figure-4 — because with this type of recording system, the first few beats are repeated in each of the 12 leads.


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    • Acknowledgment: My appreciation to Arron Pearce (from Manchester, UK) for the case and this tracing.

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


    Related ECG Blog Posts to Today’s Case:

    • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
    • ECG Blog #185 — Reviews the Ps, Qs, 3R Approach to Arrhythmia Interpretation.

    • ECG Blog #68 — Reviews the concept of interpolated PVCs.

    • ECG Blog #193 — illustrates use of the Mirror Test to facilitate recognition of acute Posterior MI. This blog post reviews the basics for predicting the "Culprit" Artery (as well as reviewing why the term "STEMI" — should replaced by "OMI" = Occlusion-based MI).

    • ECG Blog #184 — and ECG Blog #167 — review the "magical" mirror-image opposite relationship between lead III and lead aVL that helps to confirm acute OMI.

    • ECG Blog #258 — How to "Date" an Infarction based on the initial ECG.

    • ECG Blog #294 — Reviews how to tell IF the "culprit" artery has reperfused.
    • ECG Blog #230 — Reviews how to compare Serial ECGs.
    • ECG Blog #115 — Shows how dramatic ST-T changes can occur in as short as an 8-minute period.
    • ECG Blog #268 — Shows an example of reperfusion T waves.

    • ECG Blog #337 — A "NSTEMI" that was really an ongoing OMI of uncertain duration (presenting with inferior lead reperfusion T waves)

    • ECG Blog #190 — Reviews the concept of acute RV MI.



    Saturday, January 21, 2023

    ECG Blog #358 — A 20-Year Old with Bradycardia


    The ECG in Figure-1 — was obtained from a previously healthy 20-year old man who presented with chest discomfort on inspiration — but no prior history of syncope/presyncope and no sign of heart failure.
    • No prior ECG had been done.
    • Other than a slow pulse — vital signs, oxygen saturation and physical exam were all normal.
    • Screening lab including complete blood count, thyroid function tests and serum electrolytes were unremarkable.


    QUESTIONS:
    • How would YOU interpret the ECG shown in Figure-1?
    • What is your diagnosis?
    • Does this patient need a pacemaker?

    Figure-1: The initial ECG in today's case — obtained from a previously healthy 20-year old man who presented with chest discomfort on inspiration. How would you diagnose this tracing?


    MY Initial Thoughts on Today's Case:
    I found today's case intriguing for 2 reasons: i) The ECG diagnosis; and, ii) Clinical implications of the ECGs in today's case in view of the fact that they were obtained from a previously healthy 20-year old man.


    The Initial ECG in Figure-1:
    As always — I favor starting with the long lead II rhythm strip — and systematically assessing the Ps, Qs & 3Rs (See ECG Blog #185):
    • The ventricular rhythm in the long lead II rhythm strip of Figure-1 — is slow and fairly regular at a rate in the mid-40s.
    • The QRS is wide — with a QRS morphology consistent with LBBB (ie, all upright QRS in lateral leads I and V6 — and predominantly negative QRS in the anterior leads).
    • P waves are present! The PR interval before each of the 7 beats in this tracing is prolonged but constant (ie, at ~0.44 second). The finding of a constant PR interval in front of each beat tells us that there is conduction.
    • Two P waves are seen within each R-R interval. Considering the P-P interval that we see between these 2 P waves — this suggests that a 3rd P wave may be hiding within each of the QRS complexes. If so — this would suggest a fast and regular atrial rate of ~3 X 40-45/minute, or an atrial rate of ~130/minute.

    Looking at the Rest of the 12-Lead:
    As noted above — although the QRS is wide, all beats in Figure-1 appear to be conducted. QRS morphology is perfectly consistent with LBBB conduction.
    • QRS amplitude appears to be significantly increased (ie, with marked overlap of the huge S waves in anterior leads V2,V3). In an older adult — this would suggest LVH in addition to LBBB. However, the specificity of the finding of deep anterior S waves with LBBB is far less in younger adults (ie, today's patient is only 20).
    • T waves are peaked in multiple leads. These T waves are huge (ie, over 20 mm in height in leads V2,V3). Although this appearance would seem to suggest hyerpkalemia — this 20-year old man was previously healthy, and we are told that serum electrolytes were normal!


    The RHYTHM: Putting It All Together
    This initial ECG in today's case is extremely abnormal for a "previously-healthy" 20-year old man!
    • There is 2nd-degree AV Block — most probably with 3:1 AV conduction. The resultant ventricular rate is markedly bradycardic (ie, in the mid-40s).
    • The P waves that conduct do so with a markedly prolonged PR interval.
    • The QRS is wide — with morphology consistent with LBBB conduction.

    • BOTTOM Line: On the basis of this single initial ECG — one has to consider the diagnosis of Mobitz II 2nd-degree AV Block for ECG #1 (See ECG Blog #236for review of the 2nd-degree AV Blocks).


    CASE Follow-Up:
    A detailed work-up was undertaken in search of why this previously-healthy 20-year old man was now for the 1st time presenting for medical attention with the ECG shown in Figure-1:
    • Serum Troponins — negative.
    • Echo — was essentially normal (normal chamber size with ejection fraction ~55-60%).
    • Coronary CT — revealed a zero calcium score, without suggestion of coronary artery abnormalities.
    • Cardiac MRI — negative for fibrosis, scarring or edema.

    • Cardiac Stress Test — revealed chronotropic incompetence!

    • Autoimmune screening — negative.
    • Testing for Lyme Disease — negative.
    • Lamin A/C (LMNA) gene screen for mutations association with familial dilated cardiomyopathy — negative.

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    The Follow-Up ECG:
    The tracing obtained after ECG #1 — is shown below in Figure-2. To facilitate comparison — I have put both of these tracings together.


    QUESTIONS:
    • What is the difference between these 2 tracings?
    • Is a pacemaker still needed?

    Figure-2: To facilitate comparison — I've put the 2 ECGs in today's case together. What is the difference between these 2 tracings?


    Comparison of ECG #1 and ECG #2:
    There are several differences between these 2 tracings: 
    • The QRS complex has narrowed in ECG #2 (ie, LBBB conduction is no longer present!).
    • The ventricular rhythm is no longer regular in ECG #2. The overall ventricular rhythm is still slow (being faster in places than the ventricular rhythm in ECG #1 — but slower than in ECG #1 in other places).
    • The atrial rate has slowed compared to ECG #1.
    • The AV conduction ratio has improved (ie, it looks like there is now 2:1 AV conduction — compared to the 3:1 AV conduction ratio apparent in ECG #1).

    • Advanced POINT: The PR interval in ECG #2 remains constant and prolonged (ie, to ~0.44 second) before the QRS complex of beats #1-thru-5 and before beat #7. That said — careful measurement suggests that the PR interval before beat #6 has become slightly longer (ie, at ~0.48 second) than the other PR intervals in this tracing!


    Looking Closer at Atrial Activity:
    It's easier to appreciate what's happening with atrial activity in today's tracings — IF we add RED arrows over those P waves that we clearly see (Figure-3).
    • Not only has the atrial rate slowed in ECG #2 — but addition of the RED arrows in Figure-3 makes it much easier to appreciate that the P-P interval is now variable in this follow-up tracing. 

    PEARL #1: As is evident for many of the examples of AV block that have appeared in this ECG Blog — it is extremely common for there to be a ventriculophasicsinus arrhythmia in association with 2nd or 3rd degree AV block. 
    • Much of the time (as is the case in Figure-3) — the shorter P-P interval is the one that “sandwiches” a QRS complex (the theory being that perfusion of the heart improves following ventricular contraction — with resultant shortening by a slight amount the P-P interval that contains a QRS).

    Figure-3: I've added RED arrows over those P waves that we can clearly see in today's 2 tracings.


    Atrial Activity in ECG #1:
    For clarity in Figure-4 — I've separated the long lead II rhythm strip in ECG #1, from the rest of the 12-lead that appeared above it in Figure-3.
    • Doing so highlights how much more logical it seems that the underlying atrial rhythm in ECG #1 is Atrial Tachycardia (and that regular on-time P waves continue to occur where I've placed PINK arrows — at a rate of ~130/minute).

    • Advanced POINT: Further support that on-time atrial activity continues (ie, being hidden within each of the QRS complexes in Figure-4) — is suggested by the very subtle-but-real slight deformation of the terminal part of some QRS complexes by these hidden P waves (ie, the slight "extra" hump in the terminal part of the QRS that appears between the slanted BLUE lines for beats #4 and 5 — but which is not seen [GREEN lines] for some beats in which the end of the QRS is smooth).

    Figure-4: I've added a number of PINK arrows to highlight how much more logical it seems that on-time atrial activity continues (hidden within each QRS complex) — throughout the entire long lead II rhythm strip in this tracing.

     
    My Laddergram for ECG #2:
    For clarity in Figure-5 — I've drawn a laddergram for the long lead II rhythm strip from ECG #2 that illustrates the following:
    • Group beating, albeit with slight variation in the atrial rate, as well as slight variation in the R-R intervals.
    • 2:1 AV conduction — in which the PR interval is markedly prolonged and constant (with the exception of slight additional lengthening before beat #6).

    Figure-5: Laddergram for the rhythm in ECG #2.


    KEY Points from Today's Case:
    The unique aspect of today's case — is that this previously healthy 20-year old man only now presents with symptoms from a complex form of AV block that apparently had been present for some period of time. This leaves us with the following QUESTIONS to Answer:
    • Why was the QRS wide in ECG #1 — but not in ECG #2?
    • Why did the conduction ratio improve from 3:1 to 2:1 in the follow-up tracing that was done (as shown in the laddergram in Figure-5)?
    • How best to describe this patient's AV block?
    • Why was this patient without symptoms for so long?
    • Is a pacemaker needed?


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    ANSWERS to these QUESTIONS:
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    PEARL #2: Rather than a fixed intraventricular conduction defect — the transient LBBB conduction that was seen in ECG #1 (but not in ECG #2) — may reflect a rate-related BBB (Bundle Branch Block).
    • As discussed in ECG Blog #242 — Conduction defects may sometimes appear as a result of an increase in heart rate. The interesting feature of this rate-related form of aberrant conduction — is that the rate of "onset" of BBB is not necessarily the same as the rate of "offset"
    • For example — Imagine a rhythm in which there is normal conduction (with a narrow QRS complex) for sinus rhythm at a rate of 70/minute — but, QRS widening occurs when the rate increases to 80/minute. Because the rate of "offset" is not necessarily the same as the rate of "onset" — it may be that the sinus rate needs to drop to as low as 50-60/minute before BBB conduction resolves.

    • This is relevant to today's case — since LBBB conduction appeared in the initial tracing — but not in any of the follow-up ECGs that were done while this patient was hospitalized. The diagnosis of Mobitz II with 3:1 AV Block was made on the basis of the high-grade block with QRS widening that was seen in ECG #1. A finding against the diagnosis of Mobitz II — would be the presence of a narrow QRS complex for conducted beats, as was seen in ECG #2 (and in all subsequent ECGs that were done on this patient).

    • NOTE: The fact that the QRS is narrow and the ventricular rate becomes slower in parts of ECG #2 — suggests that the reason for LBBB conduction in the initial tracing may have been rate-related. But because of the above noted discrepancy between the "rate of onset" and the rate of "offset" of rate-related BBB — it's impossible to prove this relationship with only the 2 tracings that are shown.
    • To Emphasize: Regardless of whether the LBBB conduction in ECG #1 is a reflection of rate-related BBB — development of BBB at a slow rate in the mid-40s is not a "normal" phenomenon in a 20-year old adult. That said, the diagnosis of Mobitz II would seem to be less certain in association with normal QRS duration.
      

    PEARL #3: The reason for the improved AV conduction (from 3:1 in ECG #1 — to 2:1 in ECG #2)may simply be a result of a change in the atrial rate (and not the result of any change in the "severity" of AV conduction). This fundamental concept is all-too-often overlooked!
    • As noted above — the atrial rate in ECG #1 is ~130/minute.
    • The P-P interval becomes longer and irregular in ECG #2 — reflecting the ventriculophasic sinus arrhythmia of this 2nd-degree AV block. The atrial rate in this follow-up tracing varies from ~65-to-85/minute.

    • KEY Point: At the much slower atrial rate seen in ECG #2 — it may be that this patient's diseased AV node may be able to conduct more impulses (compared to the situation when the number of impulses arriving at the AV node is much higher). Therefore — Always take into account the relative atrial rate when assessing whether the "severity" of AV block may be increasing or decreasing.


    PEARL #4: Rather than Mobitz II — I suspect the primary conduction defect in today's patient is a variation of AV Wenckebach (ie, of Mobitz I 2nd-degree AV block).
    • As emphasized in ECG Blog #236Mobitz I ( = AV Wenckebach) is by far the most common form of 2nd-degree AV block. In my experience — as many as 95% of all 2nd-degree AV blocks are Mobitz I. Clinically, the importance of recognizing when the Mobitz II form of 2nd-degree AV block is present — is that pacing is much more likely to be needed for this more severe form of block. 
    • KEY Point: When in doubt as to whether a patient with 2nd-degree AV block has a Mobitz I or Mobitz II defect — Statistics strongly favor Mobitz I.

    • ECG findings in today's case that further support the likelihood of a Mobitz I conduction defect include: i) The likelihood of rate-related BBB as the cause of QRS widening in the initial tracing; ii) The finding of marked 1st-degree AV block for all conducted beats (which is much more commonly seen in patients with Mobitz I than with Mobitz II); and, iii) The subtle-but-real increase in PR interval duration for the P wave before beat #6 in today's 2nd tracing.


    PEARL #5: Some component of vagal tone may be operative in the rhythms seen in today's case. In support of this premise are the following: i) The patient is a previously healthy young adult male (Enhanced vagal tone would become even more likely if it turned out that today's patient performed regular endurance activities); ii) The PR interval is prolonged — and the PR interval is seen to increase for at least 1 of the conducted beats; and, iii) The sinus rate varies substantially in ECG #2.
    • The potential relevance of enhanced vagal tone in today's case — is related to the phenomenon of vagotonic AV Block, in which hard-to-predict variations in rate, PR intervals, and in the degree of AV block may sometimes be the sole result of increased vagal tone (See ECG Blog #61for illustration of this phenomenon)


    PEARL #6: The KEY clinical question to answer in today's case — is whether a permanent pacemaker is indicated for this previously healthy 20-year old man?
    • The "shorter" answer to this question is YES — because: i) The patient is symptomatic; ii) Despite the thorough evaluation described above — no "fixable" cause of this patient's bradycardic 2nd-degree AV block was found; and, iii) There was chronotropic incompetence  on stress testing.

    • The "longer" answer to this question is more complex (See my discussion below regarding AV block in children and younger adults).


    What is Chronotropic "Incompetence"?
    Broadly defined — chronotropic incompetence is the inability to increase heart rate sufficiently to keep up with the increased demand of the patient's activities (Brubaker and Kitzman: Circulation 123:1010-1020, 2011).
    • Although I do not have access to specific stress testing results from today's patient — the report of "chronotropic incompetence" presumably entails the situation reflected above in Figure-4 — in which despite the increase in atrial rate — the reduced (3:1) ratio of AV conduction resulted in a clearly insufficient ventricular rate in the mid-40s.
    • Given the lack of a "fixable" cause of this patient's bradycardia — a permanent pacemaker was deemed necessary.

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    PEARL #7: As discussed in ECG Blog #307 — 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 Potential Causes of AV Block in children and adults (Figure-6)
    • Since some of the causes of AV block in Figure-6 may be treatable and/or resolve with time — a search for the cause is essential.
    • Given the young age of the patient in today's case — the KEY question was whether AV block was congenital, and only presenting for the 1st time at the age of 20.

    Figure-6: Diagnostic considerations for a patient who presents in AV block (adapted from Mangi et al — StatPearls, 2021).


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    PEARL #8: 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).
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    Editorial NOTE: I found review of the literature on AV block in younger patients to be challenging — since there are still many facets of this entity that are uncertain. My summary below is based on review of the following references:

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    What is "Congenital" AV Block?
    The overall incidence of CAVB (Congenital AtrioVentricular Block) is rare — occurring in ~1/20,000 live births. CAVB may occur in isolation — or it may be associated with conduction system abnormality that develops in association with one or more congenital cardiac malformations.
    • The term "congenital" AV block — is reserved for when the conduction defect is diagnosed: i) In utero; ii) At birth; or, iii) During the 1st month of life. 
    • I found it interesting that the way "congenital" AV block is diagnosed in utero — is by fetal echocardiography (ie, by assessing whether the normal sequential relationship exists between atrial and ventricular mechanical events — or is lacking, as it would be with complete AV block). After birth — the diagnosis is made by ECG.
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    • NOTE: The literature I reviewed uses the abbreviation CCHB ( = Congenital Complete Heart Block). I've chosen to alter this to "CAVB" — to allow for cases of significant AV block that do not fit strict definition of "3rd-degree" (complete) AV block. 
    • At least anecdotally — many of the cases of AV block that I've encountered in younger adults do not manifest "complete" (ie, 3rd-degree) AV block. I take this as additional reflection of our suboptimal appreciation for the natural course of AV block that is presumably "congenital" — but which only presents in adulthood.
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    • The entity of CAVB is not uniform — as there may be different etiologies. The 3 main etiologic groups are: i) CAVB with associated congenital cardiac defects; ii) CAVB as the result of maternal autoantibodies; and, iii) Idiopathic CAVB (which is by far the least common etiology).
    • Approximately 90% of patients have CAVB as a result of either associated congenital cardiac defects — or — as the result of maternal autoantibodies. The prognosis of those patients is significantly worse than the ~10% with idiopathic CAVB.
    • Idiopathic CAVB is a diagnosis of exclusion (ie, the patient has CAVB — but no congenital cardiac defects — and negative autoimmune antibodies). Whereas the first 2 categories are almost always diagnosed early (ie, in utero, at birth — or during the 1st month of life)Idiopathic CAVB may pass unnoticed until later in childhood or even adulthood — IF the ventricular escape rate is not overly slow, and the patient is relatively asymptomatic.

    • Physiologically — the reason patients with idiopathic CAVB may pass undetected until adulthood with no more than minimal symptoms — is that overall myocardial function may be adequate with the ability to increase the ventricular escape rate with activity (at least enough for the patient to function to the point that they do not realize their activity level is "less" than it should be).

    • Given a lack of documented cases with detailed follow-up — less is known about the course of patients who presumably have idiopathic CAVB. That said — the report by Li-Na Su et al is fascinating, since it details a specific case with 28 years of follow-up (!) — in which a patient with idiopathic complete AV block did not present until adulthood. Despite symptoms of recurrent syncope — the patient refused pacemaker implantation. Surprisingly, she did amazingly did well for many years (successfully completing an uneventful pregnancy — and participating in normal daily activities, including those with heavy exertion). This patient did well without pacing. She did not have any recurrence of symptoms over her extended follow-up period. 
    • CONCLUSION (based on this report by Li-Na Su): Patients with CAVB (including those with complete AV block) — do not make up a homogeneous group. Some such patients function surprisingly well, participating longterm in normal activities despite their severe conduction defect! Bottom Line: Previous "indications" for permanent pacing — need to be revisited on an ongoing basis, depending on specifics of the case at hand (as we continue to discover information regarding the "natural history" of different patients in the diverse group with CAVB).
    • Pacemaker implantation is not "risk-free" — especially when undertaken in patients at a very young age. Among potential complications that may develop over years of use are wire fracture; need for repeated battery replacement; infection; and pacemaker-induced heart failure, among others.

    • In contrast to patients with idiopathic CAVB — the course of patients with maternal autoantibodies as the etiology of their CAVB tends to be very different and more severe. Complete AV block may be seen in up to 5% of pregnancies in which the mother is positive with anti-Ro/SSA and/or anti-La/SSB antibodies — with a much higher rate of recurrence if the mother goes on to have additional pregnancies. Although these antibodies are most prevalent in mothers with autoimmune diseases (ie, rheumatoid arthritis, lupus, or other collagen vascular diseases) — a significant percentage of women may be asymptomatic carriers without any preexisting diagnosis of an autoimmune disorder. 
    • Presumably, the mechanism for developing CAVB — is immune-mediated injury of the conduction system as a result of transplacental passage of maternal autoantibodies.
    • Because of the very high infant mortality associated with autoimmune-related CAVB (which may attain ~15-30%)early pacing has generally been recommended.

    • In patients with CAVB as a result of congenital cardiac defects — longterm prognosis depends on the nature and severity of associated congenital heart disease, in addition to the severity of the AV block.

    • Overall, among the indications for permanent pacing of patients with CAVB are the following: i) Significant symptoms not due to a reversible cause; ii) Profound bradycardia with CAVB (even when symptoms are modest); iii) Associated left ventricular dysfunction (given high risk of developing dilated cardiomyopathy); iv) QRS widening; and/or, v) A very long QTc. In patients who are not immediately paced — regular follow-up to ensure that these indications do not subsequently develop is essential. 
     

    Final CASE Follow-Up:
    In today's patient — the above described negative work-up resulted in a presumed diagnosis of idiopathic CAVB that had gone undetected for the first 20 years of this patient's life. Because of chronotropic incompetence on stress testing — a permanent pacemaker was placed.


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    Acknowledgment: My appreciation to Mustafa Alalwan (from Abu Dhabi, UAE) for the case and this tracing. 
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    For MORE on Diagnosis of ABlocks/AV Dissociation:
    • ECG Blog #185 — Reviews the Ps, Qs, 3R Approach to Rhythm Intepretation.

    • ECG Blog #188 — for Review on How to Read (and DrawLaddergrams.

    • ECG Blog #307 — Reviews a case of an asymptomatic 40yo man who presented with bradycardia due to previously undetected AV Block.

    • ECG Blog #236 and ECG Blog # 237 — Reviews the 3 Types of 2nd-Degree AV Block (and how to define the term "high-grade" AV block).

    • ECG Blog #63 — Reviews a case of Mobitz I with Junctional Escape.
    • ECG Blog #186 — The AV Blocks (and when to suspect Mobitz I).
    • ECG Blog #191 — How to distinguish between AV Dissociation vs Complete AV Block.
    • ECG Blog #192 — The 3 Causes of AV Dissociation.

    • ECG Blog #242 — Review of Rate-Related BBB.

    • ECG Blog #61 — Review of Vagotonic AV Block.