Saturday, May 10, 2025

ECG Blog #481 — New, Old — or in Between?


You are given the ECG shown in Figure-1 — and told that it was obtained from a middle-aged man who presented with epigastric pain and "faints" over the previous 4 days.
  • There was no CP (Chest Pain).
  • No prior tracing — and no additional information is available at the time you are given this tracing.

QUESTIONS:
  • How would you interpret the ECG in Figure-1?
  •    — Should the cath lab be activated?

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


MY Thoughts on Today’s CASE:
There are a lot of ECG findings on the tracing shown in Figure-1. As a result, I favor spending the first ~30 seconds of my assessment of ECG #1 on the basic parameters of Rate & Rhythm, Intervals, Axis and Chamber Enlargement — before focusing on acute Changes (See ECG Blog #205 for review of my Systematic Approach).
  • To Emphasize: Making today's case especially challenging — is the lack of CP and duration of 4 days.
  • The rhythm in ECG #1 is sinus at 80-85/minute.
  • All intervals (PR, QRS, QTc) are normal.
  • The frontal plane axis is markedly leftward — consistent with LAHB (Left Anterior HemiBlock) given the predominantly negative QRS in each of the inferior leads.
  • There is no chamber enlargement.

And now — a look for acute Changes (as I'll be assessing all leads for Q waves, R wave progression — and ST-T wave changes).


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What Caught My "Eye" ...
  • My "eye" was immediately drawn to lead V2 (within the RED rectangle in Figure-2). The amount of J-point ST elevation, and especially the size and "volume" of the ST-T wave in this lead is clearly disproportionate to the modest size of the S wave in this lead.
  • NOTE #1: There is some variation in ST-T wave morphology between the 4 beats that we see in lead V2. The 2nd complex in this lead (to which I’ve added the RED arrow, that highlights the amount of J-point ST elevation) — manifests the most concerning ST segment morphology. This raises the question as to which of these 4 beats in V2 is the most accurate reflection of true ST-T wave morphology in this lead?
  • KEY Point: The way that I instantly knew that my concern about the ST-T wave in lead V2 was real — is by the clear ST segment straightening that we see in leads V4,V5,V6 (RED lines in these leads). These are all hyperacute T waves.
  • There is also ST elevation in these 3 lateral chest leads that should not be there (especially in lead V4).
  • Similar abnormal ST segment straightening is seen in lead II.

  • NOTE #2: At this point, despite the lack of CP — I knew there has been infarction at some point in time, perhaps beginning ~4 days earlier when this patient’s symptoms began. But there is much more going on in this ECG (See below in Figure-3).

Figure-2: My "eye" was immediately drawn to lead V2.

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Reperfusion T Waves?
In Figure-3 — I've added BLUE arrows to highlight subtle-but-real T wave inversion in lead V3 and lead III (and probably also in lead II ).
  • I found lead V3 particularly interesting, in that it is placed in between chest leads with much more remarkable ST-T wave findings (ie, hyperacute ST-T waves in lead V2 — and in leads V4,V5,V6). The terminal T wave inversion that the BLUE arrow highlights in this lead V3 (as well as the cardiac cath findings below) — explain why.

Figure-3: Subtle T wave inversion (BLUE arrows).

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Putting It All Together:
I highlight a series of additional important findings that next caught my "eye" in Figure-4.
  • There has been inferior infarction at some point in time. While difficult to determine if we are seeing QS waves or a tiny initial r wave in leads III and aVF — there clearly does appear to be an initial small q wave in lead II (See magnified insert of this lead in Figure-4).
  • PEARL #1: It is sometimes difficult to distinguish LAHB from inferior MI — as well as from the possibility that there is both LAHB and inferior infarction. The "pseudo-Q" wave that we see here in this lead II magnified insert — indicates that there is more than simple LAHB (which by itself does not produce an inferior Q wave).
  • It is hard to determine the age of the inferior MI in Figure-3 — given the hyperacute T wave in lead II — potential reperfusion T waves in leads II and III (subtle terminal T wave inversion) — but no more than minimal (at most) ST elevation in leads III and aVF.

Q waves and R Wave Progression in the Chest Leads:
With regard to the chest leads — We know there has been anterior infarction at some point in time because:
  • Assuming no electrode lead misplacement — there has been loss of R wave” from lead V2-to-V3 (There may or may not be a tiny initial r wave in lead V3).
  • There is a definite QS complex in lead V4.
  • PEARL #2: It is difficult to “date” this anterior infarction. Perhaps the acute process began ~4 days earlier (ie, at the time the patient developed epigastric pain and began having syncopal spells?). Perhaps the inferior and/or anterior infarction(s) are old — with a superimposed new event? 
  • Although it is possible that this patient has a left ventricular aneurysm from prior infarction — the hyperacute-looking ST-T waves clearly suggest that something more is going on.
  • NOTE: Finding a prior ECG on this patient might be enlightening as to what may be "new" vs "old" vs "new superimposed on old". 
  • BOTTOM Line: Given this patient’s history and the above ECG findings — promp cardiac cath is indicated to clarify the anatomy (since reperfusion with PCI may be needed).

Figure-4: Q waves and R wave progression in today's case.


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Follow-Up in Today's CASE:
  • Troponin came back significantly elevated.
  • Cardiac cath revealed complete occlusion of both the LAD and the LCx artery (which probably explains the relatively modest ST-T wave morphology in transition lead V3 — which is situated in between more marked ST-T wave changes in neighboring leads V2 and V4,5,6). PCI was accomplished.

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Acknowledgment: My appreciation to Tayfun Anil Demir (from Antalya, Turkey) for the case and this tracing.

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ADDENDUM (5/10/2025):
  • For More Material — regarding ECG interpretation of OMIs (that do not satisfy millimeter-based STEMI criteria).


Figure-5: These are links found in the top menu on every page in this ECG Blog. They lead you to numerous posts with more on OMIs.


  • In "My ECG Podcasts" — Check out ECG Podcast #2 (ECG Errors that Lead to Missing Acute Coronary Occlusion).
  • In 'My ECG Videos" — Check out near the top of that page VIDEOS from my MedAll ECG Talks, that review the ECG diagnosis of acute MI — and how to recognize acute OMIs when STEMI criteria are not met (reviewed in ECG Blog #406 — Blog #407 — Blog #408).

  • Please NOTE — For each of the 6 MedAll videos at the top of the My ECG Videos page, IF you click on "More" in the description, you'll get a linked Contents that will allow you to jump to discussion of specific points (ie, at 5:29 in the 22-minute video for Blog #406 — you can jump to "You CAN recognize OMI without STEMI findings!" ).

P.S.: For a sobering, thought-provoking case discussed by cardiologist Dr. Willy Frick — with editorial Commentary by me at the bottom of the page (in the March 17, 2025 post) — Check out this case.
  • As Dr. Frick and I highlight — not only is the current "STEMI paradigm" outdated — but in cases such as the one we describe, because providers waited until STEMI criteria were finally satisfied — cardiac cath and PCI were delayed for over 1 day.
  • BUT — because the cath lab was activated within 1 hour of an ECG that finally fulfilled STEMI criteria — this case will go down in study registers as, "highly successful with rapid activation of the cath lab within 1 hour of the identification of a "STEMI". This erroneous interpretation of events totally ignores the clinical reality that this patient needlessly lost significant myocardium because the initial ECG (done >24 hours earlierwas clearly diagnostic of STEMI(-)/OMI(+) that was not acted on because providers were "stuck" on the STEMI protocol.
  • The unfortunate result is generation of erroneous literature "support" suggesting validity of an outdated and no longer accurate paradigm.
  • The Clinical Reality: Many acute coronary occlusions never develop ST elevation (or only develop ST elevation later in the course) — whereas attention to additional ECG criteria in the above references can enable us to identify acute OMI in many of these STEMI(-) cases.

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Saturday, May 3, 2025

ECG Blog #480 — A Patient with Amyloid ...

 
The ECG in Figure-1 was obtained from a man in his 60s, with a history of cardiac amyloidosis. He reported "some dizziness" recently — but no chest pain.
  • No prior tracing is available at this time. 


QUESTIONS:
  • How would you interpret this ECG?
  •    — Has there been an MI?
  •        — What is the rhythm?
  •            Is the history of cardiac amyloidosis relevant?

Figure-1: The initial ECG in today's case.


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Is the History of Cardiac Amyloidosis Relevant?
In a word — the answer to this question is YES. I review some basics regarding Cardiac Amyloidosis in ADDENDUM #1 below — but for now, keep in mind some of the ECG findings you may encounter in a patient with cardiac amyloidosis. These findings include:
  • Low voltage (especially in the limb leads).
  • Conduction disturbances (ie, LBBB, RBBB, hemiblocks).
  • Various forms of AV Block (1st, 2nd or 3rd-degree).
  • Other arrhythmias (especially AFib).
  • Non-infarction Q waves (ie, pseudo-infarction patterns).
  • OR — Some patients do not manifest ECG abnormalities, especially early in the course of the disorder.
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Back to Today's ECG:
Of note — Today's patient did not have chest pain. Instead, he reported "some dizziness" — but without a well-defined acute onset. As a result — I started with assessment of the long lead II rhythm strip in Figure-1. By the Ps,Qs,3R Approach (as per ECG Blog #185) — I observed the following:
  • The rhythm in the long lead II is not Regular.
  • Given irregularity of the ventrcular rhythm — the Rate of today's rhythm varies, but is not overly fast or overly slow.
  • The QRS looks to be slightly wide (Best appreciated in the chest leads — where the QRS looks to be between 0.11-0.12 second in duration).
  • P waves are clearly present! I've labeled those P waves that we clearly see in the long lead II rhythm strip in Figure-2.

Figure-2: I've labeled with RED arrows the P waves that we clearly can see in today's tracing.

PEARL #1: With the exception of some empty spaces — the overall atrial rhythm looks fairly regular.
  • While impossible to rule out periodic missing P waves — it is far more logical (and much more common) for the underlying atrial rhythm to be regular — with "missing"  P waves to be hidden by near-simultaneous occurrence of QRS complexes.
  • In Figure-3 — I explore the likelihood of there being an underlying regular (or at least almost regular) atrial rhythm — by adding PINK arrows where I suspect additional P waves are likely to be hiding. Using calipers facilitates and expedites figuring out where P waves are likely to be hidden.
  • PEARL #2: Although the colored arrows in Figure-3 are not completely regular — some form of AV block is still likely because: i) There are more P waves than QRS complexes; and, ii) Slight variation in the atrial rate (as we see here) is common with both 2nd- and 3rd-degree AV blocks (known as ventriculophasic sinus arrhythmia — as illustrated in ECG Blog #344).

Figure-3: I've added PINK arrows to the long lead II rhythm strip where I suspect additional P waves are hidden.

PEARL #3 (Beyond-the-Core): We can prove that P waves are hidden where I've added PINK arrows to Figure-3:
  • Note in leads V2 and V3 — that P waves are surprisingly large and peaked. The same is true for the P waves in lead V1.
  • Whereas I initially thought that the changing morphology of QRS complexes in lead V1 was the result of variations in the degree of aberrant conduction — the RED and PINK arrows that I've added in lead V1 are instead the result of superposition of on-time P waves that fall at different points during the QRS. It is this superposition that alters QRS appearance!
  • Therefore — the vertical BLUE lines in lead V1 correspond to the timing of P waves in this lead.
  • Note that the PINK arrow in lead V1 of Figure-3 — corresponds perfectly to the timing of the PINK arrow that I've drawn occurring simultaneous with beat #9 in the long lead II rhythm strip. Thus, this PINK arrow P wave (as well as the other PINK arrow P waves in the long lead II rhythm strip) — are hidden within the QRS complex of beats #2,7 and 11.
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So, What is the Rhythm in Today's CASE?
We've addressed 4 of the 5 parameters of the Ps,Qs,3R Approach:
  • P waves in today's rhythm are fairly regular, albeit with some ventriculophasic sinus arrhythmia (RED arrows in Figure-4).
  • The QRS is slightly wide.
  • The heart Rate varies, but is neither too fast nor too slow.
  • The ventricular rhythm is not Regular. That said, there is a pattern to the ventricular rhythm — in that there appears to be frequent recurrence of shorter intervals of comparable length (ie, The R-R intervals between beats #1-2; 6-7; 8-9; 10-11; and 12-13 look to be the same) — and — longer intervals of comparable length ( = the R-R intervals between beats #3-4; 4-5; 5-6; 7-8; 9-10; 11-12; and 13-14).

PEARL #4: The "pattern" described in the above bullet indicates the presence of group beating!
  • Especially given the almost regular atrial rhythm (RED arrows in Figure-4), in association with the finding of more P waves than QRS complexes — the finding of group beating strongly suggests that some form of Wenckebach block is likely to be present.

Figure-4: Focusing on today's rhythm — RED arrows highlight the underlying fairly regular atrial rhythm.

The 5th Parameter = Related?
As per PEARL #4 — recognition of group beating in today's tracing should immediately suggest the possibility of Wenckebach block.
  • Now look at the P waves in front of each of the QRS complexes that end one of the longer R-R intervals ( = the RED arrow P waves in Figure-5).
  • Then look at the PR intervals between these RED arrow P waves — and the next QRS complex (ie, the PR intervals before beats #1,3,4,5,6,8,10,12 and 14).

PEARL #5: With minimal difference — most of these PR intervals are essentially the same. The finding of PR intervals of equal length that repeat suggests that there is conduction of these equal PR intervals (ie, that at least these P waves with repetititve PR intervals are Related to neighboring QRS complexes!).
  • The exception to the above generality of repetitive PR intervals — is the PR interval before beat #10, which appears to be slightly longer than the other PR intervals.
  • The finding of repetitive PR intervals suggests that in addition to group beating in Figure-3 — there is conduction of the QRS complex that ends each of the brief pauses in this tracing — which virtually ensures that some form of 2nd-degree AV Block, Mobitz Type I (AV Wenckebach) is present!

Figure-5: Focus on the PR intervals between RED arrow P waves — and each of the QRS complexes that end one of the brief pauses.

IF the Rhythm is Mobitz I:
We highlight in Figure-6 — progressive increase in the PR interval until a beat is dropped.
  • I suspect that the RED arrow P waves in Figure-6 — are all conducted (including the slightly longer PR interval before beat #10).
  • Note that these RED arrow P waves that are conducted all manifest a long PR interval (of ~0.32 second) — so an underlying 1st-degree AV Block is present.
  • In 2-beat groups (ie, beats #1,2; 6-7; 8-9; 10-11; 12-13) — the PR interval appears to lengthen. For example, in the first 2-beat group (ie, the group made up of beats #1-2) — the PR interval between the BLUE arrow P wave and beat #2 is longer than the PR interval between the RED arrow P wave and beat #1.
  • YELLOW arrow P waves are non-conducted.

  • Bottom Line: The rhythm in Figure-6 appears to be 2nd-degree AV Block, Mobitz Type I (AV Wenckebach) — with 3:2 and 2:1 AV conduction. In addition — there is an underlying 1st-degree AV Block.

Figure-6: Color coding the P waves in today's rhythm.

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Laddergram Clarification:
The relationship between P waves and neighboring QRS complexes is clarified by use of a laddergram:
  • In 2-beat groups — the PR interval of Blue arrow P waves is increased compared to the PR interval of RED arrow P waves. 
  • BLUE arrow P waves are followed by YELLOW arrow P waves that are non-conducted — after which the next cycle begins with a RED arrow P wave that manifests a PR interval that has shortened.
  • 1-beat groups (that lack a BLUE arrow P wave) — manifest 2:1 AV conduction.

Figure-7: Laddergram of today's rhythm.

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QUESTION:
  • Is the atrial rhythm sinus?or, an ectopic ATach?


ANSWER:
I found it difficult to distinguish between ventriculophasic sinus arrhythmia that is occurring at a rapid rate vs ATach (Atrial Tachycardia) arising from an ectopic atrial focus.
  • The atrial rate is surprisingly fast (about 135/minute). While not ruling out a sinus mechanism — this rapid a rate in a patient this age (ie, over 60) who does not present with an acute onset of symptoms that might predispose to sinus tachycardia — would seem to favor ATach. 
  • As shown by the colored arrows in Figure-7 — the atrial rhythm is clearly not regular. This could be consistent with ATach (although it does not rule out ventriculophasic sinus arrhythmia).
  • Looking ahead to Figure-8, in which I've placed the 12-lead tracing in today's case above the laddergram — P wave morphology in the chest leads looks a bit unusual for a sinus mechanism (ie, pointed P waves that are taller-than-expected for a sinus mechanism in these chest leads).
  • Bottom Line: I therefore suspect ATach for the underlying atrial rhythm. Additional telemetry monitoring, further evaluation of the extent of cardiac involvement from this patient's amyloidosis — and potential use of antiarrhythmic medication will most probably provide the answer.
  • NOTE: Beta-blockers, calcium-channel blockers and digoxin tend to be poorly tolerated in patients with cardiac amyloidosis. Amiodarone may be the antiarrhythmic of choice (Giancaterino et al — JACC: Clin Electrophys 6(4):351-361, 2020).

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Putting It All Together:
Now that we've determined the rhythm — Let's take a closer LOOK in Figure-8 at the 12-lead ECG in today's patient.
  • Overall QRS amplitude in the 12-lead appears reduced — although not quite satisfying voltage criteria for "low" voltage (ie, QRS amplitude is not ≤5 mm in all 6 limb leads — and not ≤10 mm in all chest leads).
  • We noted earlier that the QRS complex in today's tracing is slightly widened. This may be the result of LAHB (Left Anterior HemiBlock) — and/or a nonspecific IVCD (InterVentricular Conduction Defect).
  • Alternatively, slight QRS widening may be the result of the multiple Q waves that are present (QS waves in II,III,aVF — probable Q waves in V1,V2 — and QS waves in V3,V4).
  • Otherwise — there are nonspecific ST-T wave changes that do not appear to be acute.
  • Therefore — ECG findings consistent with cardiac amyloidosis in today's tracings include: i) AV block; ii) Overall reduced voltage; iii) Conduction disturbances (LAHB vs nonspecific IVCD); and, iv) Pseudo-infarction pattern (with multiple Q waves but no apparent history of infarction in this patient).

Figure-8: I've placed the 12-lead tracing above the laddergram.



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Final Overview of Today's CASE:
Assessment of the rhythm in today's case is not simple. The discussion above breaks down my approach to interpretation of the rhythm into "slow motion" — with much more detail than is needed or desired by many emergency providers.
  • To Emphasize: The KEY for emergency providers is to verify that the patient is hemodynamically stable — and then, to determine if any treatment is immediately needed.
  • The "good news" in today's case — is that the history is not acute (ie, some "recent dizziness" — but no chest pain) — so assuming brief exam confirms hemodynamic stability, there should be time for Troponins to rule out an acute event. This non-acute history also means that you probably have a moment of time to contemplate the rhythm.
It Often Helps to Step Back and Look at the Rhythm from Afar ...
  • In Figure-9 — I again show today's initial ECG. Focus on the long lead II rhythm strip. Step back a little bit from this tracing for 2-3 seconds — and ask yourself IF there is a "pattern"?
  • Overall — Aren't there 2 basic R-R intervals (one longer — and one shorter) that repeat? This is unlikely to be due to chance. Instead — it suggests some form of group beating!
  • Aren't many similar-looking P waves are present at what seem to be similar P-P intervals? So, even without calipers — this should quickly suggest that a fairly regular underlying atrial rhythm is probably present.
  • My "eye" then quickly looked in front of each QRS that ends a longer R-R intervals (ie, in front of the QRS of beats #1,3,4,5,6,8,10,12,14) — and it should take only seconds to appreciate that the PR interval in front of each of these beats looks similar ==> therefore P waves that are conducting! (albeit these P waves are conducting with a long PR interval).

  • Putting This Together: Common things are common. The findings of group beating — a seemingly regular underlying atrial rhythm — and P waves that are conducting with a long PR interval at the end of each of the longer PR intervals — suggested to me within seconds that some form of 2nd-degree AV Wenckebach block was almost certain to be present.

Figure-9: Another look at Figure-1.


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Acknowledgment: My appreciation to 林柏 = Po-Chih Lin (from Taiwan) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case: 

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

  • ECG Blog #188 — Reviews how to read and draw Laddergrams (with LINKS to more than 100 laddergram cases — many with step-by-step sequential illustration).

  • ECG Blog #164 — Reviews a case of typical Mobitz I 2nd-Degree AV Block (with detailed discussion of the "Footprints" of Wenckebach).

  • ECG Blog #192 — The Causes of AV Dissociation.
  • ECG Blog #191 — Reviews the difference between AV Dissociation vs Complete AV Block.
  • ECG Blog #389 — ECG Blog #373 — and ECG Blog #344 — for review of some cases that illustrate "AV block problem-solving".
  • ECG Blog #251  Reviews the concepts of Wenckebach periodicity and the "Footprints" of Wenckebach.
  • ECG Blog #344 — thoroughly reviews the Types of 2nd-degree AV block (Mobitz I vs Mobitz II vs 2:1 AV Block).
  • ECG Blog #63 — Mobitz I, 2nd-degree AV block with junctional escape.
  • ECG Blog #262 Low Voltage with acute MI.
  • ECG Blog #272 — Causes of Low Voltage.




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ADDENDUM #1 — about Cardiac Amyloidosis 
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NOTE: I suspect that many (most?) readers of this ECG Blog do not commonly encounter patients with cardiac amyloidosis I didn't in my practice. As a result — I refreshed my familiarity with this entity by brief internet search:
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Is the History of Cardiac Amyloidosis Relevant?
Most clinical providers are familiar with a variety of forms of CardioMyopathy (CM). Most commonly these include dilated CM — hpertrophic CM — and, ischemic CM. Less common CM forms include Takotsubo CM, Arrhythmogenic CM, Post-Partum CM — and a few others.
  • Perhaps the least common CM form (and the least familiar to clinical providers) are the restrictive cardiomyopathies — in which there is infiltration of cardiac tissue by substances that result in stiffening of the ventricles, with impaired ability to relax and contract (leading to impaired ventricular filling and reduced cardiac output).
  • Cardiac Amyloidosis is the most common form of restrictive CM (Cardiac sarcoidosis and cardiac hemochromatosis being less common) — in which the particular substance deposited into myocardial tissue is one of a variety of insoluble protein forms. The relevance of the entity of restrictive CM — is awareness of the particular features of this uncommon CM type that necessitate early diagnosis and specific treatment.

How to Recognize Restrictive Cardiomyopathy?
  • Awareness of the entity of "restrictive" CM — is important for those uncommon occasions in which your patient has one of these forms.
  • Given how uncommon restrictive CM is compared to other cardiomyopathy types (and given the often slow, insidious development of symptoms of a period of years) — a high index of suspicion is usually needed to make the diagnosis.
  • Echo — typically provides the 1st clue. Findings may include: i) Biventricular thickening with normal cavity size; ii) Atrial enlargement; iii) Heart failure from diastolic dysfunction (despite normal systolic function) — often with pericardial effusion; and, iv) A characteristic "sparkling appearance" of the myocardium (See Figure-9).
  • Cardiac MRI — is very useful for confirming the diagnosis.
  • ECG — as listed earlier include: i) Low voltage (especially in the limb leads); ii) Conduction disturbances (ie, LBBB, RBBB, hemiblocks); iii) Various forms of AV Block (1st, 2nd or 3rd-degree); iv) Other arrhythmias (especially AFib) — or — v) Some patients do not manifest ECG abnormalities, especially early in the course of the disorder.

Figure-9: This figure taken from the American Society of Echocardiography page on Echo findings with Cardiac Amyloidosis.




 

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ADDENDUM #2 — about AV Blocks ... 
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  • I've included below an Audio Pearl — a Video Pearl — and links for download of PDFs reviewing the ECG diagnosis of AV Blocks.



ECG Media PEARL #4 (4:30 minutes Audio): — takes a brief look at the AV Blocks — and focuses on WHEN to suspect Mobitz I.



My GOAL in the 15-minute ECG Video below — is to clarify ECG diagnosis of the 2nd-Degree ABlocks, of which there are 3 Types:
  • Mobitz I ( = AV Wenckebach).
  • Mobitz II
  • 2nd-Degree AV Block with 2:1 AV conduction.



This 15-minute ECG Video (Media PEARL #52) — Reviews the 3 Types of 2nd-Degree AV Block — plus — the hard-to-define term of "high-grade" AV block. I supplement this material with the following 2 PDF handouts.
  • Section 2F (6 pages = the "short" Answer) from my ECG-2014 Pocket Brain book provides quick written review of the AV Blocks (This is a free download).
  • Section 20 (54 pages = the "long" Answer) from my ACLS-2013-Arrhythmias Expanded Version provides detailed discussion of WHAT the AV Blocks are — and what they are not! (This is a free download).