Saturday, May 17, 2025

ECG Blog #482 — This Patient got Morphine


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Please NOTE: 

  • After today — No new ECG Blog posts for 3-to-4 weeks ...
  •     — I will also not be prompt in replying to emails ...

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ECG Blog #482 — This Patient got Morphine ...

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The ECG in Figure-1 — was obtained from a man in his 60s, who contacted EMS some time after midnight for new-onset CP (Chest Pain).
  • The patient had risk factors, including hypertension, hyperlipidemia, diabetes — and recent episodes of chest discomfort that sounded like angina.
  • The patient was hemodynamically stable on arrival of the EMS team. He reported CP severity = 7/10 at the time the initial ECG was recorded.

QUESTIONS:
  • How would you interpret the initial ECG in Figure-1?
  •     — Would you activate the cath lab?

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

My Thoughts on the Initial ECG:
In view of the worrisome history in today’s case, with ongoing severe (7/10) CP — ECG #1 is extremely concerning:
  • There is baseline artifact in a number of leads — but the tracing is interpretable.
  • The rhythm is sinus at ~85/minute. All intervals (PR,QRS,QTc) are normal. The frontal plane axis is leftward — but not enough to qualify for LAHB (since the QRS in lead II is still predominantly positive). There is no chamber enlargement.
Regarding Q-R-S-T Wave Changes:
  • Q Waves — It is hard to know if a Q wave is (or is not) present in lead III (The 1st and 3rd complexes in this lead manifest a small initial r wave — but the middle complex does not).
  • R Wave Progression — is normal, with Transition (where the R wave becomes taller than the S wave is deep) occurring normally, here between leads V2-to-V3.

And ST-T Waves?
In this patient with new worrisome CP (still 7/10 at the time ECG #1 was recorded) — there are ST-T wave abns. (abnormalities) in virtually all 12 leads:
  • My “eye” was immediately drawn to the 3 leads within the RED rectangle (leads V1,V2,V3 — as shown in Figure-2). There is no LVH in this tracing (ie, No tall R waves in any lateral lead — and no deep S waves in leads V1,V2). Therefore the ST segment straightening with “fatter”-than-expected T wave peak, as well as ~1 mm. of J-point ST elevation in lead V1 is clearly abnormal.
  • Considering modest R wave amplitude in lead V2 — the nearly 2 mm. of ST elevation with overly large and “bulky” ST-T waves in this lead also represents a hyperacute change until proven otherwise.
  • In the context of leads V1,V2 — the T wave in lead V3 also appears to be “hypervoluminous” ( = hyperacute).
  • Flat (if not scooped) ST depression is seen in 2 of the 3 QRST complexes in lateral chest leads V5,V6 (BLUE arrows in these leads).
  • Lead V4 is distorted by artifact — but appears to manifest ST segment flattening. It is hard to know what this means given the transition position of lead V3 between the 3 anterior leads (that show ST elevation with hyperacute T waves) — and the 2 lateral chest leads (that show “scooped” ST depression in this patient without ECG indication of LVH).
  • In the limb leads — the 2 lateral leads (leads I and aVL) — as well as lead II complement the ST-T wave depression seen in the lateral chest leads (BLUE arrows in these limb leads).
  • ST-T waves in leads III and aVF are nonspecific — but manifest ST-T wave flattening.

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MY Impression of ECG #1:
 In this patient with new and persistent CP — today’s initial ECG strongly suggests acute anteroseptal OMI. This ECG alone (without need for Troponin results) — should prompt the interventionist to take this patient to the cath lab. Unfortunately, this was not done — because the cardiology team felt "STEMI criteria were not met".

  • See the ADDENDUM below for more on the concept acute OMI (acute MI due to acute coronary Occlusion) vs the outdated STEMI paradigm. Regardless of whether the initial Troponin value is elevated (The initial Troponin will be normal in a surprising number of patients with acute coronary occlusion) — and regardless of what additional ECGs might show — ECG #1 is diagnostic of acute LAD OMI in this patient with persistent CP until proven otherwise. Prompt cath with PCI is clearly indicated.

  • More than just acute LAD OMI — the ECG pattern of hyperacute and elevated ST-T waves in leads V1,V2,V3 + the scooped ST depression in leads V5,V6 — strongly suggests there is Precordial "Swirl" (See below Figure-2).

Figure-2: I've labeled today's initial ECG.


What is Precordial "Swirl"?
As I review in ECG Blog #380 — the colorfully descriptive term known as Precordial Swirl — is an intriguing ECG sign that facilitates recognition of a unique ECG pattern strongly suggestive of a very proximal site of acute LAD occlusion (usually proximal to the 1st septal perforator) — with resultant septal ischemia, in addition to anterior wall and apical involvement.

PEARL #1: In the setting of acute LAD OMI (Occlusion-based MI ) — the pattern of Precordial Swirl is recognized by the finding of ST elevation in lead V1 (and often also in lead aVR) — and — reciprocal ST depression in leads V5 and V6.
  • When considering Precordial Swirl — I like to focus on the ST-T wave appearance in leads V1 and V6.
  • Although 1-2 mm of upsloping ST elevation is commonly (and normally) seen in anterior leads V2 and V3 — most of the time we do not see ST elevation in lead V1 (or if we do — it is minimal). Therefore — I become immediately suspicious of "Precordial Swirl" whenever there is suggestion of LAD OMI — and — in addition, lead V1 looks different than expected!

  • NOTE #1: Sometimes recognition that lead V1 looks "different-than-expected" — is only forthcoming after realizing that lead V2 is clearly abnormal.
  • NOTE #2: It's easy to get fooled by LVH! This is because LV "strain" with LVH is sometimes more manifest in anterior rather than lateral chest leads — in which case there may be anterior lead ST elevation (ie, the reciprocal of lateral lead ST-T wave depression). That said — there is no indication of LVH in today's case.

  • Finally, once I've decided that the tracing I am looking at is not an example of LVH that mimics Precordial Swirl — I focus my attention on the shape of the ST-T wave in lead V6 (which tends to be flatter, if not scooped — vs the more typical downsloping ST segment of LV "strain").

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The CASE Continues:
 
The patient was treated en route by the EMS team with ASA and sublingual NTG. 
  • Following NTG — the patient's CP decreased to 5/10 (from the initial rating of 7/10 CP).
  • A repeat ECG was obtained (ECG #2 in Figure-3).

Figure-3: The repeat EMS ECG (done ~14 minutes after ECG #1).


QUESTION:
  • How would YOU interpret the repeat ECG in Figure-3?


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PEARL #2: 
  • Isn't it difficult to assess ECG #2 compared to ECG #1 (that was done ~14 minutes earlier) — without putting both of these ECGs side-by-side?

  • Now LOOK at Figure-4 — in which I have placed both of these tracings side-by-side. Isn't it now much easier to go lead-by-lead — in comparing these 2 tracings?

Figure-4: Side-by-side comparison between the first 2 EMS ECGs.


Comparison of Today's Initial ECG — with the Repeat ECG:
Looking lead-by-lead — I noted the following:
  • Focusing first on the 3 leads that initially caught my attention (Leads V1,V2,V3 — within the RED rectangle in ECG #1) — there clearly has been deflation of the anteroseptal hyperacute ST-T waves in ECG #2.
  • ST depression has clearly decreased in the 5 leads with BLUE arrows in ECG #1.
  • PEARL #3: This improvement in ST-T wave morphology in virtually all leads in ECG #2 (compared to ECG #1) — indicates that these are "dynamic" ST-T wave changes. This finding, that occurs in association with decreased severity of the patient's CP — strongly suggests there has been spontaneous reopening of the "culprit" artery.

  • BOTTOM Line: If there previously was doubt about the indication for prompt cath in today's case — the finding of dynamic ST-T wave changes in association with reduced CP should have put all doubt to rest.

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The CASE Continues:
 
The cardiology team still did not want to perform cardiac cath because "STEMI criteria still were not met".
  • The patient's CP returned (now 10/10! ) — and a 3rd ECG was done (See side-by-side comparison of the 3 ECGs in today's case in Figure-5).
  • Cardiology still did not want to perform cardiac cath.
  • Instead — morphine was given for this patient's CP.

QUESTION:
  • What do you learn from Figure-5?


Figure-5: Side-by-side comparison between ECGs #1,2,3.



What We Learn from the Serial ECGs in Figure-5:
In Figure-4 — We saw improvement in ECG #2 in virtually all leads, that occurred in association with a reduction in CP.
  • Now just 6 minutes later in ECG #3 — the patient's CP has returned to an even more severe degree (10/10 CP! ). The hyperacute ST-T wave changes that we saw in ECG #1 (which had significantly improved at the time ECG #2 was recorded) — have now returned, in association with lateral lead ST depression.
  • Relative to QRS amplitude in leads V1-thru-V4 — it appears that T wave size is even greater in these 4 leads compared to ECG #1.

  • BOTTOM Line: Recurrence of CP, now increasingly severe — in association with return of acute ST-T wave changes in virtually all leads — strongly suggests that the "culprit" LAD has now spontaneously reclosed.
  • Note: This patient's CP has attained a 10/10 intensity despite the administration of morphine. This is not good practice — because often morphine will reduce (relieve) ischemic CP, thereby providing false assurance that the patient is "improving" — when in reality, all the morphine is doing is masking the patient's ischemic symptoms (thereby delaying the need for cardiac cath and definitive treatment).
  • PEARL #4: Morphine should only be given after the decision has been made to perform prompt cardiac catheterization. At that point — generous use of morphine for CP relief is welcomed!
  • PEARL #5: Morphine could have appropriately been given more than 2 hours earlier had the decision to perform prompt cath been correctly made after seeing ECG #1 (or at latest — after seeing the "dynamic" ST-T wave changes on ECG #2).
  • PEARL #6: This final PEARL for today — is essentially a repeat of PEARL #2 — to emphasize how much easier (and how much more time-efficient) it is to compare serial ECGs by putting the tracings you are looking at together, and then going lead-by-lead as you review. There is an "art" to assessment of serial ECGs — as you have to account for potential differences in frontal plane axis, R wave progression (with its effect on QRST morphology), and any change that might result from more or less artifact being present in the lead(s) you are looking at. But can there be any doubt about the "dynamic" ST-T wave changes that we see in Figure-5 that correlate perfectly to the change in relative CP severity?

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

CASE Conclusion:
 
Unfortunately — I was unable to obtain full follow-up. But I did find out the following.
  • The patient continued to have CP despite morphine and IV NTG. As a result — he was finally taken to cath. This raises the question as to whether this patient would have been taken to cath had the morphine relieved his symptoms!
  • The "culprit" artery was confirmed to be the LAD (and given the "Swirl" pattern on ECG — I would bet this was a very proximal LAD lesion).
  • Unfortunately — it took nearly 3 hours after ECG #1 until the decision was finally made to perform cardiac catheterization. Time is muscle — so one can only wonder how much potentially viable myocardium was lost by this delay.

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Acknowledgment: My appreciation to Noah Steege (from Virginia, USA) for the case and this tracing.

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ADDENDUM (5/17/2025):
  • For More Material — regarding ECG interpretation of OMIs (that do not satisfy millimeter-based STEMI criteria).


Figure-6: 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 at a surprisingly early point in the patient's clinical course.

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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.
==================================

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.
==================================

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).