Thursday, February 20, 2020

What are these wide complexes? If unclear by explanation, the laddergram helps to understand.

An 18 y.o. female who presented for chest pain. Patient reports productive cough and headache x 4 days. She notes persistent sternal chest pain worse at night and waking her from sleep. She also notes intermittent abdominal pain, describing as a "tightness".

"Sinus arrhythmia with variable right bundle origin PVCs"
Is this accurate?












No.

This is sinus bradycardia with a slightly accelerated right ventricular escape, such that sometimes:
1.  the sinus beat is conducted before any ventricular escape (beats 7)
2.  the ventricular beat starts at almost the exact same time as the P-wave, and the P-wave therefore does not conduct (beats 6 and 9)
3. the ventricular beat occurs very shortly after the P-wave such that the P-wave does not conduct (beats 2, 3, 5)
4. The ventricular beat fuses to varying degrees with the conducted beat (beats 1, 3, 4, 8)

This is AV dissociation (not NOT AV block).

Her bedside echo was normal and troponins were negative in the ED.

See Dr. Grauer's extensive discussion below for more detail.

This is not pathologic, and not worrisome.

If you see a patient with such a rhythm, simply walk them around on a monitor to increase the sinus rate.  Then the sinus will usurp the ventricular escape and the ECG will normalize at a faster rate.  If not, there is then a problem.

The patient was referred for Holter and it was normal.



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MY Comment by KEN GRAUER, MD (2/20/2020):
===================================
There are LOTS of excellent Learning Points regarding the ECG in this case. For clarity of explanation — I’ve numbered the beats (Figure-1).
  • A QUOTE to Remember  As Rosenbaum said, “Every self-respecting rhythm has at least 3 possible explanations”. There are some details about this interesting arrhythmia that I am not certain of. That said — I don’t think anyone can be absolutely certain of these details without additional monitoring.

Figure-1: The 12-lead ECG and long lead II rhythm strip in this case (See text).



FIRST — I completely agree with Dr. Smith’s interpretation (given above) — regarding the most important clinical points. I’ll add some additional thoughts.
  • For educational purposes — I think the best way to illustrate the Learning Points from this rhythm, is to address the following clinical questions. Please TAKE ANOTHER LOOK at the rhythm in Figure-1, and answer the following:

BASIC Level QUESTIONS:
  • Is there AV dissociation?
  • Is the P-P interval constant?
  • Is there AV block?
  • The patient is an 18-year old woman. Is AIVR (ie, an Accelerated IdioVentricular Rhythm) common in this age group?
  • WHY do the ventricular beats occur in Figure-1?
  • Are there Fusion beats?
  • HOW would you define the rhythm in Figure-1?

ADVANCED Level QUESTIONS: These questions are Beyond-the-Core. The answers to them do not alter management of this patient — but I think the answers are insightful, and help to hone your ECG interpretation skills beyond the basic level.
  • Are all P waves in the rhythm in Figure-1 the same?
  • Is this really a sinus rhythm?
  • WHICH are the fusion beats in Figure-1Do we really know HOW MANY fusion beats there are?
  • WHY does QRS morphology of the conducted beats (ie, beats #1,4,7,8) change?

HINT: If you do not use calipers — You will not be able to answer many of the above questions ...



Ithere ADissociation? — By definition, there is transient AV dissociation in Figure-1. That’s because, at least for some brief period of time — there are some P waves that are not related to neighboring QRS complexes!
  • I’ve labeled P waves in the long lead II rhythm strip in Figure-2 (BLUE arrows). It looks like beats #1,4,7 and 8 are conducting — because they are all preceded by P waves with a constant and normal PR interval.
  • Since the PR interval preceding beats #2,3,5,6 and 9 is clearly much shorter than the PR interval of conducted beats — this means that beats #2,3,5,6 and 9 are not normally conducted. Therefore — there is AV dissociation for these beats!
  • For more on AV Dissociation — CLICK HERE.

Figure-2: P waves in the long lead II rhythm strip have been labeled with BLUE arrows (See text).



Ithe P-P Interval Constant? — Careful observation of the BLUE arrows in Figure-2 should tell you that the P-P interval is not constant. (IF in doubt — calipers will confirm this for you in 2-3 seconds).
  • At the least — there is sinus arrhythmia ...

Ithere ABlock? — There is no evidence of AV block in Figure-2. That’s because although some of the P waves in this rhythm strip are not conducting — P waves never have a chance to conduct, because the PR interval preceding beats #2,3,5,6 and 9 is clearly too short to allow normal conduction.
  • PEARL #1  Remember that there are potential Causes of ADissociation: i) AV dissociation due to some form of 2nd or 3rd degree AV Blockii) AV dissociation by Usurpation” — in which P waves transiently do not conduct because an accelerated junctional or ventricular rhythm takes over the pacemaking function (because it is faster than the underlying sinus rhythm); and/oriii) AV dissociation by Default” — in which a junctional or ventricular escape rhythm takes over by “default” (ie, because of SA node slowing).

IAIVR Common in an 18yo? — The ventricular beats in Figure-2 are beats #2, 3, 5, 6 and 9. The usual idioventricular escape rate in adults is between 20-40/minute. As per Dr. Smith — since the rate of the ventricular beats in this case is slightly faster than this (ie, ~55-60/minute) — this is a slightly accelerated ventricular rhythm ( = AIVR).
  • For brief review of AIVR — CLICK HERE. The common Clinical Settings in which AIVR may occur include: ias a rhythm during cardiac arrest; ii) in the monitoring phase of acute MI (especially with inferior MI); oriii) as a reperfusion arrhythmia (following thrombolysis, acute angioplasty, or spontaneous reperfusion). AIVR may also occur in patients with underlying coronary disease, cardiomyopathy, and with digoxin toxicity.
  • PEARL #2  On rare occasions, AIVR may occur intermittently in otherwise healthy subjects without underlying heart disease. In such cases — this rhythm is often associated with increased vagal tone. If these individuals are asymptomatic — the rhythm is generally benign, and no treatment is needed. Assuming the Echo is normal for the 18yo woman in this case — and provided that the “chest pain” reported by this patient is not related to the rhythm we see in Figure-2 — no additional evaluation would be needed.

Figure-3: I’ve measured R-R intervals in milliseconds in the long lead II rhythm strip (See text).



WHY do the Ventricular Beats Occur? — To assist in answering this question — I have carefully measured the R-R intervals in the long lead II rhythm strip (Figure-3).
  • PEARL #3  When confronted with a rhythm strip in which there is transient AV dissociation, and you are not certain as to which beat(s) may be conducting — Look for unexpected shortening of the R-R interval. Such shortening usually indicates which beat(s) is being conducted. Conversely — lengthening of the R-R interval often tells you which beat(s) originate from another focus.
  • Beat #4 in Figure-3 is preceded by the shortest R-R interval (865 msec) — and we know this beat is conducting.
  • The next shortest R-R intervals in Figure-3 precede beats #7 and 8 (1045 msec) — which we know are both conducted by the P waves that precede them.
  • The reason all other beats (ie, beats #2,3,5,6 and 9) are at least in part ventricular beats — is that they are all preceded by longer R-R intervals. It is because the appearance of P waves is delayed — that the slightly accelerated ventricular focus “gets tired of waiting”, and puts out a ventricular beat.

Are there Fusion Beats? — To assist in answering this question — I have drawn a Laddergram of the rhythm (Figure-4).
  • PEARL #4  Although becoming comfortable in drawing laddergrams takes time (it literally took me a few decades to get good at this skill!) — learning to read laddergrams is EASY, and takes no more than a few minutes. (IF interested in some user-friendly examples to get you started — CLICK HERE — and HERE — and HERE).
  • P waves precede each of the 9 beats in the long lead II rhythm strip in Figure-4. Isn’t it now much easier to see the irregularity in the P-P interval looking at the Atrial (upper level) tier?
  • Beats #1,4,7 and 8 are conducting.
  • I’ve drawn RED circles at the bottom of the laddergram that represent ventricular origin for beats #2,3,5,6 and 9.
  • My educated guess is that the P waves preceding beats #6 and 9 occur too soon before these ventricular beats to be conducted.
  • On the other hand — the PR interval preceding beats #2,3 and 5 is a little longer than that preceding beats #6 and 9 — such that there may have been time for some conduction from above to have occurred. Although hard to tell — the QRS of beats #2,3 and 5 appears to be a little smaller and narrower than that for beats #6 and 9 — so beats #2,3 and 5 appear to be Fusion beats (schematically represented in the laddergram by simultaneous conduction into the Ventricular tier from above and below).
  • For more on Fusion beats — CLICK HERE.

Figure-4: Laddergram of the long lead II rhythm strip (See text).



WHAT is the Rhythm? — The answer to this question leads us to PEARL #5: The term “AV Dissociation” should never be used as a “diagnosis” per se. Instead — optimal rhythm interpretation indicates there is AV dissociation because of which one or two of the 3 potential causes of AV dissociation discussed in PEARL #1 are operative.
  • The primary problem in the rhythm shown in Figure-4 is bradycardia. It is because of sinus bradycardia and arrhythmia that AV dissociation is seen, with several beats from a slightly accelerated ventricular focus.
  • Thus, the rhythm is not “AV dissociation”. Instead — we see AV dissociation bdefault of the sinus pacemaker that slows enough to allow the slightly accelerated ventricular focus to put out several ventricular beats. NOTE: Semantically — this is not pure AV dissociation by “default” — since rather than simple ventricular “escape” — the ventricular focus is faster than the 20-40/minute rate of a ventricular escape rhythm.


ANSWERS to the ADVANCED Questions: Earlier — I posed the following Beyond-the-Core questions.
  • Are all P waves in the rhythm the same?
  • Is this really a sinus rhythm?
  • WHICH are the fusion beats in the rhythm? Do we really know HOW MANY fusion beats there are?
  • WHY does QRS morphology of the conducted beats (ie, beats #1,4,7,8) change?

Figure-5: I’ve labeled all P waves with letters (See text).



MANSWERS:
  • I believe that P wave morphology is not the same for all of the P waves in Figure-5! Although it is true that there will always be some slight “natural” variation in P wave morphology — DON’T YOU THINK that P waves a,c,d and g are clearly more pointed than P waves e,f and i? (I’m not sure about b, which seems to manifest an in-between morphology).
  • IF in doubt — GO BACK to the 12-lead tracing in Figure-1, and look at P wave morphology in all 12 leads. I believe there are some subtle differences that are real.
  • Note that the rounder P waves (ie, e,f and i) seem to be preceded by a somewhat longer R-R interval. Clinically — I suspect that rather than sinus arrhythmia, this 18yo probably has a wandering atrial pacemaker — with the marked variation in P-P interval (as well as her AIVR) all being manifestations of increased baseline vagal tone. Shift in the site of the atrial pacemaker may be occurring with ongoing variation in vagal tone. That said — to know for certain if the rhythm was a wandering pacer, we'd need a longer period of monitoring — and we'd need to be sure we were seeing at least 3 different P wave morphologies (For more on ECG diagnosis of wandering pacemaker — CLICK HERE).
  • Note that we never see a ventricular beat not preceded by any P wave in Figure-5. As a result — we have NO idea as to what a “pure” ventricular beat looks like. It is therefore possible that even beats #6 and 9 might manifest a slight degree of fusion (ie, we have NO idea as to how many fusion beats we are seeing in this rhythm strip).
  • Finally — Note that the S wave of the earliest conducted beat (ie, beat #4) is slightly wider than the S wave of conducted beats #7 and 8. I do not think beat #4 is a fusion beat — because the PR interval is identical to that of other conducted beats, and it is only the terminal S wave that looks slightly wider. Instead — earlier occurrence of beat #4 is probably the result of some incomplete RBBB aberration.

BOTTOM LINE  Assuming this 18yo has no underlying structural heart disease — her interesting rhythm is almost certainly benign. There are no acute ST-T wave changes on conducted beats in her 12-lead tracing.
  • My hope is that attention to some of the above "picky" details in complex rhythm interpretation are insightful.

Our THANKS to Dr. Smith for presenting this case!


Tuesday, February 18, 2020

32 yo with right sided chest pain. Zero ST Elevation, but that does not matter.



This was sent by a reader.  He does a nice job of examining the whole case, so I leave it (mostly) in his words.

32 yo M Sudden onset localized, ‘sharp’ right sided chest pain for 1 hr. 7/10 at worst, now 4/10 with some radiation to both arms. no associated symptoms.
PMH - MS, Cholesterol, Smoker.
FH - Father MI 45
Obs - BP 133/83, RR 20, Sats 95%, examination unremarkable. Bloods pending.

Reader's interpretation:
ECG 1
Sinus rhythm approx 65bpm
normal axis
non-specific inter-ventricular conduction delay (IVCD) versus incomplete RBBB. QRS 100ms
Subtle 'sagging' ST depression I, aVL, V6. no ST elevation
Very tall anterior T waves V1-5 that are symmetrical and disproportionately large (particularly in V4) but neither very peaked or blunted.
The QTc is normal to short, around 400ms
The R wave progression is slow with potential pathological Q waves V3, I, aVL

Reader's comment:
Although I felt the anterior T waves may be hyperacute suggesting a STEMI equivalent (OMI) I did not feel this was diagnostic at the time. Given the atypical pain and well looking patient the initial plan was serial ECGs, CXR, morphine and review with initial bloods in an hour. Not for lab unless evolving ST elevation. This plan was agreed with the on call cardiology registrar.

This was recorded shortly later, (The reader does not give the exact timing):


Reader's interpretation
Overall very similar to the first trace.
There is a reduction in the T wave amplitude and T wave in version in aVL.
There is reduced R wave amplitude in V3 and a new narrow Q wave in V4.
There is perhaps 0.5-1mm ST elevation in V1 only.
I felt these changes were due to chest lead positioning, V1-2 were placed too high for the initial ECG.

Clinical course
Subsequent ECGs over the next 2 hours were similar. The patient looked well and the pain was now a mild ache 1/10 (Smith comment: because of the morphine?).  The CXR was unremarkable as were bloods except high sensitivity Troponin I at 110 ng/L (99th percentile 34 ng/L).  (Smith comment: this is diagnostic of acute MI, and even with a negative ECG, is reason to activate the cath lab if there is ongoing pain, which of course morphine might eliminate)

I treated him as an NSTEMI with Clopidogrel (already loaded with aspirin), Fondaparinux and commenced atorvastatin and bisoprolol. He was admitted directly to the cardiac ward and placed on telemetry. 

When I returned to check on him later in the night shift the patient was sleeping and there were no further ECGs to review.

The following morning the ECG below was recorded. This shows QS complexes throughout the anterolateral leads that suggests a completed extensive anterior STEMI. Repeat Troponin was greater than 10,000 ng/L (large MI, we do not have the peak)



Angiogram

The patient was taken to the lab and a total occlusion of the mid LAD (after a large diagonal) was treated successfully with PCI and stenting. There was also bystander disease and a staged PCI to the proximal RCA was planned. The patient did well and was discharged without significant LV dysfunction or other complications.

Discussion


In hindsight I feel there are very few alternative causes for an ECG like this other than an acute LAD occlusion. I believe this is one of those 'subtle STEMI' cases where neither the ECG nor the symptoms are very obvious or severe and the usual evolution is not seen.

I think of these cases as 'insidious infarcts' and I have seen this in all infarct territories and I do not think they are particularly rare. Essentially the patient is fairly comfortable and the ECG is not obvious but the patient ended up with Q waves, huge troponins and we missed the opportunity to reperfuse the artery when it counts. These patients tend to be younger and do well but I have no doubt that their future risk of heart failure, arrhythmias and premature death is greatly increased compared to if they had PPCI and standard STEMI treatment. Needless to say cases like this have had a significant impact on me and make me strive to be better at spotting subtle ECG patterns and advocating for patients like this having emergent angios.


What could have been done differently.
Applying Smith's subtle anterior STEMI v early repolarisation (4 variable) equation to the first ECG gives a score of 20.6 suggesting STEMI (> 18.2). Although this is arguably outside it's indications as there is a fairly clear Q wave in V3 (note there are lots of exclusions for using this equation). (Smith comment: if exclusions are there because they are indicative of acute LAD occlusion.  If any one of the 8 are present, it is LAD occlusion until proven otherwise.  Here is a link to use of the formula).

A bedside echo (especially with speckle tracking if available) may have helped if there were regional wall motion abnormalities. 



FOAM resources that promote recognition and early treatment of 'STEMI equivalent' patterns are promoted by Stephen Smith and Pendell Meyers. This is summed up in their proposed OMI/NOMI terminology to replace STEMI/NSTEMI.



Links for the anterior STEMI v early repolarisation equation below.



Smith comment:

1. Morphine should never be given until you are committed to the cath lab.  Pain was 1/10 probably due to morphine.
2. One must learn how to recognize hyperacute T-waves.  These ones are the real thing and cannot be anything else.  The first ECG is absolutely diagnostic of acute LAD occlusion and the cath lab should be activated immediately.
3. Young people do have MI!!


Here are 2 recent cases that are similar:



Case 2. This patient was brought by EMS.  The hyperacute T-waves were immediately recognized by the medics and the patient went expeditiously to the cath lab.   1972765.
Diagnostic hyperacute T-waves in V2-V5Even the small ones are hyperacute, as they are huge in proportion to the QRS and they are "Fat" and symmetric.

This was the patients ED ECG:
Again, diagnostic hyperacute T-waves in V1-V5.




Case 3. Here is a case that was diagnosed and treated immediately, but the myocardium was completely infarcted anyway, without ever developing any ST elevation.

Prehospital ECG:
de Winter's T-waves in V2
Hyperacute in V1-V6, II and aVF
They are symmetric and fat, and also tall.  They tower over the QRS.  The T-wave in V6 is not at all large in any absolute sense, but it is huge in proportion to the QRS.

Here is the ED EDG:
de Winter's T-waves in V3, hyperacute from V1-V6.

And the post-reperfusion ECG:

Notice:
Even though there was never ST Elevation, and the patient underwent rapid reperfusion, there are fully developed QS-waves, indicative of profound anterior wall infarction.


Furthermore, a hyperacute T-wave need not be large, or even proportionally large:  Sometimes a hyperacute T-wave is only symmetric, but not large, as Case 3 below:

Case 3.

Small T-waves that are hyperacute just because they are symmetric.  
The T-waves in II, III, and aVF are hyperacute only because of their symmetry.
I recognized these hyperacute T-waves immediately as part of a study we are doing.  No one else saw them at all.  Another clue is of course the slight STD with T-wave inversion in aVL. 
The next day angiogram, and their disappearance after reperfusion, proved that they were indeed hyperacute Ts due to RCA OMI.

Here is the post reperfusion ECG:


Here is how normal assymetric inferior T-waves look:




Hyperacute T-waves:

Ten (10) Examples of Hyperacute T-waves in Lead V2 (a few in V3), due to acute LAD occlusion








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MY Comment by KEN GRAUER, MD (2/18/2020):
===================================
Our most sincere THANKS to the reader who submitted this case. CREDIT to him/her — for his/her soul-searching account! Hindsight is always much easier in the “retrospectoscope”. I’ll focus my comments on a few additional thoughts to those made by Dr. Smith.
  • For clarity — I’ve reproduced and labeled the first 2 ECGs in this case in Figure-1.

Figure-1: The first 2 ECGs that were shown above in this case (See text).



MTHOUGHTS on this Case  Although the patient in this case is young (32yo) — he is a smoker — his family history is worrisome (father with MI at age 45) — and, his symptoms are new, and these new symptoms led to presentation in the ED.
  • Especially when there are concerning features in the history — The onus has to be on us to rule out (rather than to rule in) the possibility of an acute cardiac event. As a result — IF the initial ECG is not normal, we need to prove that the ECG abnormalities are not acute (rather than the other way around).
  • IF in doubt after evaluating the patient the best you can — Err on the side of caution. Better to cath a patient who doesn’t need it — than not to cath someone who does.

Regarding ECG #1  The reader was systematic in their interpretation, and he/she identified the main abnormal findings. LOOKING CLOSER at ECG #1:
  • In the limb leads — larger and wider-than-expected Q waves are present in leads I and aVL. That said, I wasn’t convinced these limb lead Q waves were significant to the case at hand — and I thought overall ST-T wave changes in the limb leads of ECG #1 were nonspecific.
  • NOT SO in the chest leads. Starting from a definite R wave in lead V1 (3 mm in amplitude) — there is Loss oR wave from V1-to-V2. That this is real-until-proven-otherwise, is supported by the very wide and deep Q wave in lead V3 (BLUE arrow) This suggests anterior MI has occurred at some point in time.
  • The reader correctly identified, “very tall anterior T waves in V1-thru-V5 that are symmetrical and disproportionately large (particularly in lead V4)”. In a patient with new symptoms — especially in association with loss of R wave + the very-large-and-wide Q wave in lead V3 — this description by the reader is how I would define hyperacute anterior T waves.
  • I would add that T waves are fatter-than-they-should-be at their peak (at least in leads V1, V4 and V5) — and, that these T waves are wider-than-they-should-be at their base (at least in leads V1, V3, V4 and V5) — therefore, clearly to be assumed hyperacute in a patient with new symptoms until proven otherwise.

Regarding ECG #2  We are not told how much time passed between the recording of ECGs #1 and #2. The important point, is that although subtle — there has been serial change between these 2 tracings.
  • I thought there was no significant change in the limb leads between ECGs #1 and #2.
  • BUT — there has been further loss of anterior forces — seen as development of a very wide-and-deep Q wave in lead V2 + a Q wave in lead V4 (RED arrows in ECG #2 denoting Q waves).
  • As noted by the reader — T wave amplitude has indeed decreased in multiple leads (ie, the T wave is not as tall in ECG #2 as it was in ECG #1 in leads V1, V2, V3 and V4). Further support that this decrease in T wave amplitude represents a dynamic ST-T wave change — is provided by the unusual short segment of ST straightening that we see in lead V1 (PURPLE arrow) — which replaces the upward-sloping ST segment that we previously saw in lead V1 of ECG #1. This is not artifact. It is real.
  • NOTE: While true that there is now a small negative component to the P wave in leads V1 and V2 of ECG #2 that was not present in ECG #1 — one can not attribute all of the dynamic ST-T changes just described (that occurred in each of the first 4 chest leads) simply to positioning 2 leads (ie, V1,V2) too high on the chest. IF thought that these differences between ECGs #1 and 2 were simply due to lead malposition — then ECG #2 should have been immediately repeated after verifying chest lead placement. This clinical point is important — since IF questions persisted as to whether ECG findings were or were not acutely evolving — demonstration of dynamic ST-T wave change proves that they are.

BOTTOM LINE  Soul-searching cases is TOUGH. But it is an invaluable part of optimizing future treatment. We are indebted to the reader who shared this case with us — so that we can all learn from it.


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