Friday, July 31, 2020

OMI-NOMI paradigm established as better than STEMI-NSTEMI with new article


OMI-NOMI paradigm established as better than STEMI-NSTEMI with new article by Emre Aslanger, with some help from Smith

"ACOMI" = Acute Coronary OMI

DIagnostic accuracy oF electrocardiogram for acute coronary OCClUsion resuLTing in myocardial infarction (DIFOCCULT Study)

Free full text:

MY Comment by KEN GRAUER, MD (7/31/2020):
In the April 1, 2018 post in Dr. Smith’s ECG Blog — Drs. Meyers, Weingart and Smith published their OMI Manifesto — in which they extensively document the critically important concept that management of acute MI by separation into a “STEMI” vs “non-STEMI” classification is an irreversibly flawed approach.
  • Their OMI Manifesto details how use of standard STEMI criteria results in an unacceptable level of inaccuracy, in which an estimated 25-30% of acute coronary occlusions are missed! Yet despite this remarkable flaw in the STEMI-paradigm — a substantial number (if not a frank majority) of clinicians continue to apply outdated criteria when interpreting ECGs, by refusing to consider prompt cath for definitive diagnosis and reperfusion therapy just because a millimeter-based definition for acute STEMI is not satisfied.

In the hope of dispelling continued dependence on millimeter-based STEMI criteria — we’ve published numerous cases in recent years in Dr. Smith’s ECG Blog of acute OMI (Occlusion-based Myocardial Infarction), in which patients have benefited from acute reperfusion despite not satisfying “STEMI criteria”.
  • The article by Aslanger, Smith et al that is featured above in today’s post has just been published. It is notable for providing additional evidence in support of making a paradigm shift away from the far less efficient “STEMI” vs “non-STEMI” approach — to acceptance of a newer approach that recognizes other ECG indicators that tell us the patient in front of us who is having new cardiac symptoms is very likely to have ACO (Acute Coronary Occlusion) — and is therefore in need of prompt cath and acute reperfusion despite having an ECG that may lack the millimeter definition of a STEMI.

NOTE: The following ECG findings, when seen in association with new cardiac symptoms are among those that suggest acute OMI despite not satisfying the millimeter-based definition of a STEMI:
  • Hyperacute T waves (that are disproportionately tall and/or fatter-at-their-peak or wider-at-their-base than should be expected given R wave and S wave amplitude in that lead). The more leads in a given lead area that show hyperacute changes — the greater the concern for acute OMI.
  • Terminal QRS distortion (ie, the absence of both a J-wave and an S-wave in either lead V2 or lead V3) — SEE My Comment in the November 14, 2019 post for an illustration and description of T-QRS-D.
  • Suspicious-looking ST elevation not satisfying STEMI-criteria — especially when there is reciprocal ST-T wave depression and/or abnormal ST segment shaping in other leads. The more leads with suspicious findings — the greater the concern for an acute ongoing event.
  • Any ST elevation in inferior leads that occurs in association with mirror-image opposite ST depression in lead aVL.
  • ST depression that is maximal in leads V2-to-V4.
  • The finding of dynamic ST-T wave changes on serial tracings in association with a change in chest pain symptoms (SEE My Comment in the July 21, 2020 post).

  • BOTTOM Line: It takes time (and some practice) — to adjust to the concept that we can get good at accurately and confidently recognizing many cases of acute coronary occlusion, even when millimeter-defined STEMI criteria are not met. The above-cited newly published article by Aslanger, Smith et al provides further support to the growing body of literature of why we should compel ourselves to do so.

Tuesday, July 28, 2020

A Woman with New Dyspnea. Is the extreme left axis deviation, with negative T-wave in lead III, suggestive of RV strain?

MY Comment by KEN GRAUER, MD (7/26/2020):
The ECG in Figure-1 was obtained from a middle-aged woman who presented to the ED with new-onset shortness of breath.
  • QUESTION: Is the inferior lead T wave inversion indicative of RV (Right Ventricular) Strain from acute PE (Pulmonary Embolism)?

Figure-1: ECG obtained from a middle-aged woman who presented to the ED with new dyspnea (See text).

MY THOUGHTS on ECG #1: As always — I favor a systematic approach to ECG interpretation. Without a systematic approach — it might be all-too-easy to overlook that something is “off” here ...
  • Regardless of whichever systematic approach you favor for 12-lead ECG interpretation — the 1st Step should always be to interpret the rhythm. Once you’ve ensured that your patient is hemodynamically stable — the, “Watch Your Ps, Qs and 3Rs” memory aid reminds me of the 5 KEY parameters to assess (CLICK HERE — if interested in more on this Ps, Qs, 3R approach).
  • Although there is no long lead rhythm strip in ECG #1 — the rhythm is regular at a rate of ~80/minute. The QRS complex is narrow.
  • P waves are present — and, these P waves are clearly related to neighboring QRS complexes, because the PR interval is constant. This tells us that P waves are conducting to produce the QRS complex that follows them.
  • Did you recognize that the P wave in lead II is negative?

PEARL #1: If you see P waves that are conducting, but these P waves are negative in lead II — then you do not have a sinus rhythm. The only 2 exceptions to this are: i) If there is dextrocardia; and/orii) If there is some type of lead reversal.
  • PEARL #2: We can easily rule out dextrocardia for ECG #1 — because R wave progression is perfectly normal in the chest leads (there should be reverse R wave progression if the patient had dextrocardia).
  • This leaves us with distinguishing between a low atrial or junctional rhythm (which could be the cause of negative P waves in lead II) — vs some type of lead reversal.

Recognition of Lead Reversal:
Technical errors featuring a variety of lead reversal placements remain a surprisingly common “mishap” of everyday practice. As a result — we like to periodically publish clinical examples of lead misplacement. To review a number of these — GO TO:

PEARL #3 — I’ve summarized in Figure-2 those tips that have helped me most over the years to rapidly recognize tracings in which lead reversal is likely (Taken from My Comment in the February 11, 2020 post in Dr. Smith’s ECG Blog).
  • Applying the tips from Figure-2 to the initial ECG in Figure-1 — not only is the P wave negative in lead II — but lead aVR does not manifest a predominantly negative QRS complex. Instead, the QRS in lead aVR appears to be positive and both the tiny P wave and T wave in this lead also appear to be positive. This shouldn’t normally be ...
  • Increasing my suspicion further that there must be some type of lead reversal in ECG #1 — is the overly similar appearance of the QRST complex in all 3 of the inferior leads.
  • By far — the most common lead reversal is mix-up of the LA (Left Armand RA (Right Arm) electrodes. But this is not the mix-up that occurred in today’s case — because we do not see global negativity (of P wave, QRS and T wave) in lead I (See the February 11, 2020 post).

Figure-2: Tips for recognizing lead reversal. (See text).

PEARL #4 — My favorite on-line “Quick GO-TO” reference for the most common types of lead misplacement comes from LITFL ( = Life-In-The-Fast-Lane). I have used the superb web page they post in their web site on this subject for years. It’s EASY to find — Simply put in, LITFL Lead Reversal in the Search bar — and the link comes up instantly.
  • This LITFL web page describes the 7 most common lead reversals. There are other possibilities (ie, in which there may be misplacement of multiple leads) — but these are less common and more difficult to predict.
  • When I suspect a type of lead reversal that I am less familiar with — I simply review those 7 most common types of lead reversal on the LITFL page — and see if any of the ECG examples they provide seems to apply. In ECG #1 — the key identifying feature that led me to suspect RA-LL reversal was the finding of similar-looking global negativity in each of the 3 inferior leads (See Figure-3).

Figure-3: Features of RA-LL Lead Reversal — adapted from LITFL (See text).

With the essentials from Figure-3 of RA-LL lead reversal in mind — Let’s TAKE ANOTHER LOOK at the initial ECG in this case (TOP tracing in Figure-4):

Figure-4: TOP: The initial ECG in the ED ( ECG #1) — with features of RA-LL lead reversal written below ECG #1. BOTTOM: ECG #2 shows what this initial ECG would look like if corrections were made for RA-LL Lead Reversal (See text).

MY THOUGHTS on ECG #2: Unfortunately (as often occurs) — RA-LL lead reversal went unrecognized in today’s case. As a result, I do not have an actual follow-up ECG. Instead — I constructed ECG #2 in Figure-4 by inverting lead II in ECG #1 — by inverting and switching places for leads I and III — and by switching places for leads aVR and aVF. Isn’t the appearance of P waves, QRS complexes and T waves in the limb leads of ECG #2 now much more logical?
  • The P wave is upright in lead II of ECG #2, as it should be when there is normal sinus rhythm.
  • There is global negativity (of P wave, QRS and T wave) in lead aVR — as most commonly is seen with normal tracings.
  • The appearance of the P waves, QRS complexes and T waves no longer looks so similar in the 3 inferior leads in ECG #2, as it did in ECG #1 when there was RA-LL lead reversal.
  • My Impression of ECG #2: This is a normal ECG. There is normal sinus rhythm — a horizontal (but normal) frontal plane axis of about 0 degrees — and no chamber enlargement. T wave negativity isolated to lead III is not an abnormal finding when the QRS complex is predominantly negative in this lead. There is no longer suggestion of RV strain, since the T wave in leads II and aVF is upright. As stated earlier — R wave progression in the chest leads is normal. T wave inversion isolated in the chest leads to lead V1 is not abnormal. In Summary — This is a normal ECG.

Sunday, July 26, 2020

Prehospital ECG of a 50-something male with Syncope and Chest Pain

This case was sent by an excellent medic:

A 50-something yo male started to chop wood when he experienced a short syncopal episode followed by 8/10 chest pain.  Ground EMS arrived, administered ASA and sublingual nitro to which he passed out again.

Flight crew was called to transport for signs of shock/syncopal episodes, not ACS.

Ground crew had recorded this prehospital ECG:
Sinus rhythm with one PVC (first complex)
And anything else?

These are hyperacute T-waves diagnostic of LAD occlusion.  They begin at V3, and there is no inferior ST depression, so this is probably a mid-LAD occlusion.  The hyperacute T-waves extend to inferior leads, with a reciprocal down-up T-wave in I and aVL. So it is likely that this LAD wraps around to the inferior wall.  But all of that is not important.  What is important is that one recognizes that there is an occlusion somewhere in some kind of coronary artery. There is some ST depression in V5 and V6.

It is Occlusion Myocardial Infarction (OMI).  But it is not a STEMI, as there is very little ST Elevation.  At most about 50% of OMI meet STEMI criteria.  If you do not recognize this immediately, then you need lots of practice.

See this lecture on electrocardiographically subtle LAD occlusion:

Subtle ECG Findings of Left Anterior Descending Artery (LAD) Occlusion -- LAD Occlusion MI (OMI)

The medic continues:

"Everyone stated this was not a STEMI/ did not fall under STEMI guidelines, however I knew (thanks to your blog) this was an occlusion due to hyperacute T waves V3-V4 and Lead III and aVF.  We airlifted the patient with the LUCAS applied/ STAT pads applied and BVM/airway stuff out and ready.  My partner during the flight was wondering why all the precaution.  I pointed out that the patient was experiencing R on T and to be ready.  The cath lab was activated from the air and we were escorted directly to the lab.  The patient’s pain was treated throughout the flight with bumps of Fentanyl since nitro dumped the patient’s pressure twice before.

"The patient was placed on the table and immediately went in to cardiac arrest with ventricular fibrillation for 5 rounds.  They were able to resuscitate and stent the patients LAD (100% occluded).  We got report a couple days later the patient went home with no deficit.

"Many would not have recognized this as hyperacute and went to the ER.  I want to thank you all again for your teachings as they do not go unappreciated."

Here is the outcome:
It was 35 minutes from symptom onset to ECG.  Then another 31 minutes to activation.

As you can see, there is indeed LAD thrombus with poor flow (arrow on left), re-established by stenting (arrow on right).
The ECG was done at the time of the cath, approximately 60 minutes after the first diagnostic ECG. 

Let's put the two ECGs next to each other:

You can see by the ECG done at the time of cath that the hyperacute T-waves have diminished, but some ST Elevation has developed in V3-V6 over the 90 minutes interval.  

Learning Points:

Learn to recognize electrocardiographically subtle LAD occlusion.  There is no better way to do this than to watch this lecture:

Subtle ECG Findings of Left Anterior Descending Artery (LAD) Occlusion -- LAD Occlusion MI (OMI)

Ken Grauer had these comments:

THANKS so much for writing! So glad Dr. Smith’s ECG Blog has been so helpful! YES — this 12-lead ECG does show hyperacute T waves in each of the inferior leads, as well as in V3-thru-V6 (most marked as you state in V3,V4)  — consistent with 100% LAD occlusion (as per your cath). I’d imagine it was mid-LAD + “wraparound” — given lack of ST elevation in aVL, V1, V2 — with ST elevation in inferior as well as anterior leads.

MY Comment by KEN GRAUER, MD (7/26/2020):
Gratifying case for us to see — in which one of our astute medic followers was able to immediately recognize the acuity of this OMI in progress as a result of having learned the pattern from repeated similar cases posted on our blog.
  • Dr. Smith has posted above my immediate impression above (at the end of his discussion) on seeing this tracing and learning that the patient had new-onset chest pain = “this ECG shows hyperacute T waves in each of the inferior leads, as well as in V3-thru-V6 (most marked in V3,V4) — consistent with 100% LAD occlusion. I’d imagine it was mid-LAD + “wraparound” — given lack of ST elevation in aVL, V1, V2 — with ST elevation in inferior as well as anterior leads."

I’d like to add 2 additional points. To do this, I’ve reproduced in Figure-1 the initial ECG in this case.

Figure-1: The initial ECG in this case (See text).

POINT #1: We’ve shown numerous examples of de Winter T waves in Dr. Smith’s ECG Blog. I reviewed features of de Winter T waves in My Comment at the bottom of the page of the May 2, 2019 post — including reproduction of the Figure from the original manuscript by de Winter et al (NEJM 359:2071-73, 2008).
  • I added the following PEARL to that 2019 post — There are many variations on “the theme” of de Winter T waves. In my experience, many of the cases I’ve seen posted that go on to evolve to anterior STEMI do not show J-point ST depression as de Winter et al described (or at most, show minimal J-point depression in only 1-2 leads). The overall pattern is often not “static” — but rather evolves to frank ST elevation in serial tracings. What you see on ECG often depends on when during the process the ECG is obtained ... and, the pattern may evolve!
  • Thus, in ECG #1, the shape of the extremely large, hyperacute T waves (minus the lack of J-point ST depression) resembles the T wave shapes in the Figure I showed in the May 2, 2019 post, which I took from the original manuscript by de Winter et al.

POINT #2: An “R-on-T” phenomenon was said to have been observed in this case. It should be emphasized that this is not what we see for the PVC ( = beat #1) in Figure-1. Unfortunately, we do not see a long lead rhythm strip with onset before the ventricular beat in ECG #1 — but nevertheless, we can still describe what we see in this tracing — and we can still make an accurate determination of the etiology of beat #1.
  • Regular sinus P waves are seen in lead II of ECG #1 (RED arrows).
  • The PR interval preceding beat #1 is clearly shorter than the PR interval preceding sinus-conducted beats #2 and 3.
  • We cannot use lead I in our assessment of the etiology of beat #1 — because artifact distorts the space between the P wave and initial part of the QRS in this lead (BLUE arrow).
  • However, at least in lead II — the very first part of the QRS complex looks identical in beat #1 as in beats #2 and #3 (I’m looking at the initial shape and slope of the very first part of the r wave in lead II). It is the latter part of the QRS complex for beat #1 that becomes very different (at least in leads II and III). These features are characteristic of what happens when there is fusion between a late-cycle ( = end-diastolic) PVC and a sinus-conducted beat.
  • The clinical significance of recognizing late-cycle PVCs in a patient with ongoing acute OMI is comparable to the diagnostic significance of AIVR (Accelerated IdioVentricular Rhythm), when AIVR occurs in the setting of ongoing OMI — which often means there has been spontaneous reperfusion. However, since patients may undergo spontaneous reperfusion — only to be followed a short while later by reocclusion (and then repeat this process over ensuing minutes or hours more than once ...) — it is difficult to correlate events in this patient regarding the repetitive episodes of VFib he experienced, with some resolution of hyperacute T waves, but development of anterior lead ST elevation in the repeat ECG (shown above). This is because we lack more precise awareness of the specific timing of ECG changes correlated to changes in symptom severity. That said — there is a bottom line ...
  • BOTTOM Line: Be aware of the concept of late-cycle PVCs — which can provide insight (in association with symptom and ECG evolution) regarding the likelihood of spontaneous reperfusion (For more on late-cycle PVCs — Please see My Comment at the bottom of the August 13, 2019 post).
  • P.S.: For more on "My Take" regarding late-cycle (end-diastolic) PVCs that result in Fusion Beats (including laddergram illustration) — CLICK HERE

Friday, July 24, 2020

A Complication of the COVID Era

Submitted and written by Gia Coleman MD and Roshan Givergis DO, edits by Meyers and Smith

A woman in her 30s was found crawling in the streets, altered on arrival to the ED. Here is her presenting ECG:

How would you interpret this EKG and what is on your differential?

At first glance, it appears to be a sinus rhythm with PR prolongation at a rate of about 75 bpm. The QRS may appear narrow but is in fact slightly wide (see figure below). The computer measured it to be 136 ms.

Perhaps the most striking finding in this EKG is the almost complete loss/flattening of the T waves. The computer calculated the QTC to be 427. Looking closer, the P waves, particularly in the precordial leads, are not of uniform morphology. Taking the flattened T waves into consideration, this made me question whether the P waves were only P waves, OR were P waves with superimposed U waves, OR only U waves. Most likely these are sinus P waves with superimposed U waves.

Meyers comment: I agree, I cannot tell where the T and/or U wave is or where it ends. I don't think a QT interval can be meaningfully calculated here.

Taking a global look at this EKG, everything just looks long, regardless of the computer calculations. The top two things on my differential when I see EVERYTHING stretched out like this is electrolyte abnormalities or toxins.

The patient then progressed into an irregular wide complex rhythm which unfortunately was not captured on paper. She was treated with an amp of bicarb and an amp of calcium with normalization of her rhythm. She did not lose a pulse.

This is her EKG after calcium and bicarb:

Likely back in sinus rhythm however the U waves are more discernible so it is difficult to see the P waves. The QRS is now narrow and it is regular. Compared to the first ECG, V2 and V3 now show more recognizable T and U wave morphology, showing that there are indeed U waves superimposed on the P waves. The QU interval, if calculated, would be extremely long, in the range of 600 msec.

The patient managed to tell the team through her stupor just prior to intubation that she had taken a bottle of hydroxychloroquine, estimated later to be approximately a 50-gram ingestion. She was given activated charcoal post intubation and started on high dose diazepam, as well as epinephrine for refractory hypotension.

Initial labs returned with a potassium of 3.2; calcium and magnesium were all normal. On repeat labs, potassium dropped to 1.6 with EKG as below.

Ignoring the digital conversion artifact in the inferior leads, there is likely atrial bigeminy. QRS is narrow and QTC by computer is 629 ms (not sure which algorithm) which results from the computer incorporating the U wave into the calculation. To measure the QTc, we must first differentiate the T wave from the U wave, which is easiest to do using V3. See the enlarged view of V3 below. The first beat in V3 is a sinus beat followed by a premature atrial beat resulting in a U wave and a P wave that are superimposed. This becomes more evident when looking at the second beat in V3 where you can clearly see a T wave and a separate U wave.
(Blue arrow = P wave, Red arrow = U wave, Green arrow = T wave)

Below is the most recent EKG, taken four days later.
You can see the P waves are much smaller now, and likely her normal P waves when compared to prior EKGs.
This confirms that what we saw previously were likely U waves superimposed on P waves. The patient was transferred from the Medical ICU down to the floor the following day.

In the COVID era, we should be familiar with signs of potential hydroxychloroquine toxicity if providers are still using and patients are still taking this medication as it has a very narrow therapeutic window and can be lethal.

Hydroxychloroquine/chloroquine are potassium and sodium channel blockers which can lead to QRS widening, ST changes, QTC prolongation and dysrhythmias.

Hypokalemia is a hallmark feature and degree of hypokalemia is associated with mortality risk. Exact mechanism is unclear but is thought to be due to an intracellular shift. While repleting the potassium may be necessary, Goldfrank’s advises caution with aggressive repletion as hyperkalemic complications have been noted later in the course when the potassium then shifts out of cells. Use of bicarb for widened QRS is controversial as it may exacerbate hypokalemia but is reasonable to use if the potassium level is normal taking into consideration the patient’s entire clinical picture.

Management is mainly supportive with early intubation, glucose therapy for refractory hypoglycemia, and epinephrine for hypotension. Several small human and animal studies have shown a benefit in using high dose diazepam (2mg/kg IV over 30 minutes followed by a high dose drip).

If you have a patient with a possible overdose, call your local poison control center at 1-800-222-1222.

For a more in-depth analysis of the QTc interval and U waves in another similar case, check out this article by Dr. Smith, in which cardiac arrest due to Hydroxychloroquine was treated with intravenous fat emulsion

Take home:
1. Know how to measure QTC, the computer is often wrong.

2. Pay close attention to QRS and QTC in potential tox patients.

3. Know the possible EKG findings of hydroxychloroquine as ubiquitous use in the COVID era can cause serious complications.


Barry, James David. "Antimalarials." Goldfrank's Toxicologic Emergencies, 11e Eds. Lewis S. Nelson, et al. McGraw-Hill, 2019,§ionid=21027 3082.

Crouzette, J et al. “Experimental assessment of the protective activity of diazepam on the acute toxicity of chloroquine.” Journal of toxicology. Clinical toxicology vol. 20,3 (1983): 271-9. doi:10.3109/15563658308990070

Riou, B et al. “Treatment of severe chloroquine poisoning.” The New England journal of medicine vol. 318,1 (1988): 1-6. doi:10.1056/NEJM198801073180101

MY Comment by KEN GRAUER, MD (7/24/2020):
GREAT case, with superb explanation and dissection of serial ECGs in this case by Drs. Coleman, Givergis, Meyers & Smith. My comments are brief:
  • I’ll repeat the emphasis that was made on the importance of accurate assessment of QRS duration. As noted above — at 1st glance, the QRS complex appears to be “normal”. However, as was shown by the magnified view (2nd figure above) — vertical BLUE lines clearly document significant QRS prolongation (ie, to >0.13 sec). This is highly relevant — because QRS prolongation >100 msec is a most important predictor of serious sodium channel blocker toxicity (especially as a predictor of potential seizures).
  • PEARL #1: The reason the QRS complex “looks normal” in the 1st ECG shown above (which I’ll call ECG #1) — is that: i) QRS morphology does not resemble any known form of conduction block in ECG #1 (ie, not RBBB nor LBBB); andii) The initial portion of the QRS complex is completely normal (ie, it looks virtually identical to the initial portion of the QRS complex in serial tracings after QRS duration returned to normal). This terminal prolongation effect is commonly seen with sodium channel blockade and with selected other toxicities — in which QRS widening is primarily a result of widening of the latter portion of the QRS complex.
  • PEARL #2: Hydroxychloroquine/chloroquine is a sodium channel blocker. Prominent for its absence in ECG #1 are 2 of the characteristic signs of sodium channel toxicity = i) Right axis deviation; andii) Development of a terminal tall and wide R wave in lead aVR (felt to be due to delay that occurs predominantly in the right bundle branch). It should be appreciated that these 2 ECG signs should be specifically looked for when suspecting sodium channel toxicity — and, it’s insightful to know that despite ingestion of a very large amount of a potent sodium channel blocker (ie, hydroxychloroquine) — that these 2 characteristic ECG signs of sodium channel blockade were absent.

The 3rd 12-lead ECG shown above manifests a bigeminal rhythm. I found this to be the most fascinating tracing in this case.
  • As shown in the magnified view of lead V3 — the KEY that reveals “The Answer” to a problematic tracing will often be found within the pause in the rhythm (even when this pause is brief, as it is here). U waves are really only seen well in lead V3 of this 3rd 12-lead tracing. It is because of the pause that occurs after the early beat — that the P wave in front of the 3rd (and last) beat in this V3 lead becomes isolated, and clearly identified ( = the last BLUE arrow in this magnified view).
  • Knowing that this last BLUE arrow lies over the last P wave in this magnified V3 lead — tells us that the 2nd RED arrow lies over a U wave that is no longer superimposed on the next P wave. Therefore, it is only because of this short pause (that results from this bigeminal rhythm) — that we are finally able to establish with certainty where the U wave ends.
  • Rather than the T wave — I believe the 2nd GREEN arrow in this magnified V3 view lies over a coved (but not elevated) ST segment. I believe the T wave itself has a negative component, that falls in-between the 2nd GREEN and RED arrows, blending imperceptibly with the U wave.
  • Finally — Beyond-the-Core: This 3rd 12-lead ECG shows a bigeminal rhythm. Although difficult to tell because of the electrical interference artifact in the baseline and because each of the early-occurring P waves is superimposed upon a U wave — P wave morphology in all 12 leads for both the 1st and 2nd P waves in each group looks to be virtually the same. IF we could clearly identify a difference in P wave morphology between sinus P waves and the P waves preceding the early-occurring beats — then we could identify this rhythm as atrial bigeminy. But, when there is a bigeminal rhythm with each beat preceded by P waves with the same morphology — we need to include 3:2 SA block of the Wenckebach (Mobitz I) type in our differential diagnosis of the rhythm.

Recommended Resources