A fast narrow complex rhythm.

A 50-something called 911 for palpitations.

He was tachycardic and diaphoretic.  POCUS cardiac ultrasound was hyperdynamic.

Medics recorded this ECG:

This appears to be atrial flutter with 2:1 conduction, and narrow complex
Medics diagnosed atrial fibrillation with RVR.
It cannot be atrial fibrillation with RVR because it is regular.

The patient arrived in the ED with a heart rate that ranged from 135 to 150 and did NOT look like flutter on the monitor (not available).

A 12-lead was recorded:

There is a regular, narrow complex tachycardia at a rate of 135.
What is it?

It is important to know that the heart rate on the monitor (not recorded), though regular, was varying widely from 115-145.

We never saw P-waves on any of these rhythms.

Another 12-lead was recorded:

Again, there is a regular, narrow complex tachycardia. 
There are no P-waves visible.
Now the rate is 120.

--It is regular, so it cannot be atrial fib.
--There are no flutter waves, and the atrium could only be in flutter if the atrial flutter rate was 250 with 2:1 conduction, resulting in a ventricular rate of 125.  With 1:1 conduction, the ventricular rate would also be 250 (impossible in an adult unless there is an accessory pathway).  So it is unlikely to be atrial flutter.
--Is it PSVT?  At first glance, it could be, but this is far too slow for most PSVT, which is usually at least 140 bpm.  Moreover, PSVT is re-entrant and thus its rate is constant, just as is the rate of other re-entrant rhythms such as atrial flutter and ventricular tachycardia.  This rate is gradually changing between 115 and 145, so it is not PSVT.

Rates that vary gradually up and down are due to automatic rhythms (not re-entrant).  That is to say, there is a pacemaker cell that depolarizes, reaches a threshold, and fires.  Various conditions can cause the "slope" of depolarization to become steeper and therefore reach the threshold sooner and result in a faster rate.   Sinus rhythm is automatic, as are escape rhythms such as junctional escape, ventricular escape, and any accelerated rhythm (junctional, idioventricular).

So this is likely an automatic rhythm.

--How about sinus with hidden P-waves?  How can we figure that out?


Lewis Leads!!

So we moved the monitor leads around into the Lewis Lead position:

1. Placed the Right Arm electrode on the patient’s manubrium.
2. Placed the Left Arm electrode on the 5th intercostal space, right sternal border.
3. Placed the Left Leg electrode on the right lower costal margin.
4. Monitored Lead I.

Here is the result:

A few PVCs, but no P-waves before the QRSs.

It is then that we realized we were probably dealing with junctional tachycardia.  In junctional tachycardia, the junctional autmatic (not re-entrant) rhythm is going faster than the sinus node and thus pre-empts the sinus node.

Later, it was found that this was an overdose of ephedrine, a sympathomimetic, which is likely to cause junctional tachycardia.

Why is the sinus rate not equally affected by the sympathomimetic, such that the sinus rate remains faster than the junction?  I don't know.

With junctional tachycardia, the impulse often also goes towards the atrium, causing a retrograde P-wave that can be before, within, or after the QRS.  I do not see that here.

Junctional Tachycardia

Junctional tachycardia is an uncommon rhythm originating from the AV node or the bundle of His. The mechanism is usually enhanced automaticity producing a regular ventricular rate rarely exceeding 140 bpm. Retrograde P-waves may be seen or may be buried within the QRS complex. The most common etiologies include digoxin toxicity, ischemia, cardiomyopathy, and increased adrenergic stimulation (which is often due to toxins such as sympathomimetics).

Learning Points

1. Most important is to realize that not all non-sinus narrow complex tachycardias are PSVT, flutter, or atrial fibrillation.
2. If you think it is PSVT, but the rate is gradually changing (not constant), it is probably an automatic rhythm (unrecognized sinus is by far the most common)
3. Junctional tachycardia has the same etiologies as sinus tachycardia, with the exception of digoxin toxicity.  This includes toxins, increased adrenergic stimulation, and cardiomyopathy.
4. Therefore, it is not so important to distinguish the two.  It is more important to recognized that a regular rhythm is NOT atrial fibrillation.
5. If there is junctional tachycardia in a young, think about digoxin,

Sinus rhythm with a new wide complex QRS

This is another case written by Pendell Meyers, a G2 at Stony Brook.  As I mentioned before, Pendell will be helping to edit and write the blog.

Case

A middle aged female with type 2 diabetes presented to her endocrinologist for a regularly scheduled follow up appointment for diabetes management. Her history included ischemic cardiomyopathy (CM) with placement of an AICD, CAD s/p CABG, and recent elective LAD stent complicated by ischemic colitis requiring hemicolectomy and colostomy.

During the appointment she complained of several days of off and on dizziness and bilateral leg weakness, and she also told the endocrinologist that she felt as though "life is not worth living anymore" due to multiple concurrent psychosocial stressors as well as her medical issues. Her endocrinologist sent her immediately to the ED for psychiatric evaluation. On the way to the ED she experienced several episodes of left sided chest and abdominal pain described as brief stabbing pains.

On initial exam in the ED she complained of sharp intermittent chest and abdominal pains, increased weakness from baseline, and continued anxiety and tearfulness concerning her overall quality of life given her recent illnesses.

Here is her initial ECG:

What is your interpretation?

There is sinus rhythm at approximately 75 bpm with prolonged PR interval. The QRS complex is wide, approximately 160ms. There are ST deviations which appear appropriate and proportional to the abnormal QRS.

To some long-time readers, the diagnosis will be obvious. I will delay giving away the diagnosis to give learners the best opportunity for reasoning it out.


How to Evaluate a Wide Complex QRS:

When one encounters a wide complex QRS, there should be both an immediate, type 1 thinking, instant-recognition version of evaluation, as well as a more deliberate, logical, double-checking version:

Type 1:
An experienced electrocardiogapher looking at a wide complex may immediately sort it into the most common categories that have earned instant recognition status: LBBB morphology, RBBB morphology (+/- LAFB or LPFB), ventricular paced rhythm (based on pacer spikes and appropriately wide QRS immediately following), or something that doesn't easily fit into any of those categories.

Type 2:
In order to provide a logical approach to the wide QRS that doesn't fit into an obvious category, we must know how a QRS complex becomes wide. A wide QRS complex can only be created by a limited number of ways:

1) Ventricular Origin: The action potential originated in the ventricles, outside of the proximal intrinsic conduction system, or (in the case of WPW) reached the ventricles without using the conduction system:
Examples: Ventricular paced rhythm, ventricular tachycardia, WPW, AIVR, fascicular VTs

2) Supraventricular Origin with Conduction Abnormality: The action potential originated above the ventricles, entered the conduction system correctly, then at least one of the following must have happened:

        2a) Abnormal conduction system: Normal speed of conduction, but structural blockade somewhere within the conduction system
Examples: LBBB, RBBB, nonspecific intraventricular conduction delay, cardiomyopathy

        2b) Abnormal conduction speed: Normal conduction system, but slowed speed of conduction
Examples: Hyperkalemia, Na channel blockade (medication, toxin), severe acidosis

Every wide complex QRS must be a combination of the above causes.

Let's apply this method to our current ECG:

The QRS morphology in some leads (V2-V4) could be mistaken at first glance for LBBB, however the lateral leads in LBBB should show a predominant or mostly monomorphic R wave, which is not the case here, therefore this is not LBBB. There are no pacer spikes. It is something that doesn't fit into a prescribed category.

P-waves before each QRS complex suggest (but do not prove) that the origin of the QRS complex is supraventricular. It does not satisfy the criteria or morphology of RBBB or LBBB, therefore we are left with Non specific intraventricular conduction delay (IVCD) or abnormal conduction speed.

The next obvious step is to look for the patient's prior baseline ECG. Here it is:

Baseline ECG from 1 month prior. How does this ECG affect your reasoning of the presentation ECG?

Here is the presentation EKG again, for easy visual comparison:

The baseline ECG shows SR with normal PR interval and narrow QRS complex. Take a close look at the morphology and QRS components ("up, then down," "small R, then big S") in each lead in the baseline ECG compared to the presentation ECG. What do you notice?

The components are almost exactly the same. The only difference in the QRS complexes between the two ECGs is the width. This suggests that the action potential followed exactly the same pathway down the conduction system, but was SLOWER than before. This patient has a derangement of action potential propagation that is slowing down the speed of conduction and widening the QRS complex.

Of the conditions that cause slowing of action potential speed and wide QRS complexes, there is one condition that is more common, more dangerous, more recognizable, more rapidly life threatening, and more readily treatable than all the others: hyperkalemia.

Now that all readers are on the same page, please notice the corroborating features of hyperkalemia on the presentation ECG: first degree AV block, widened P-waves seen in V4-V6, and peaked T waves in V3-V5.

The possibility of hyperkalemia was not noticed initially by the providers. Initial labs were drawn and sent, and the providers had planned for a broad evaluation including chest pain and abdominal pain workups given her recent colostomy and abdominal pain.

45 minutes after arrival, with no labs back yet, she was suddenly noted to have intermittent periods of obtundation alternating with respiratory distress and worsening pain. Before being rushed to the resuscitation bay, a repeat ECG was performed:

Extremely wide QRS which is difficult to delineate from the ST segment and T wave. This is approaching a sine-wave pattern, and indicates end-stage hyperkalemia which usually precedes an unstable tachy- or bradyarrhythmic cardiac arrest. Even in the absence of electromechanical dissociation which is present in severe hyperkalemia, this disorganized and morbidly wide QRS complex is likely not providing a reasonable cardiac output. 

Hyperkalemia was not suspected immediately after this ECG. Given that the patient had chest pain on arrival, and hyperkalemia had not been suspected on the initial ECG, in a patient with acute worsening, one can understand why acute STEMI +/- intermittent VT/VF may have seemed more likely to explain her acute change. A STEMI alert was called based on perceived ST elevations in the anterior leads V2-V4.

On the way to the resuscitation bay, the patient became unconscious and lost pulses. CPR was initiated. The monitor showed VFib, and she was shocked twice without conversion. On review of the initial ECGs, hyperkalemia was suspected at this point, and the patient received IV calcium and bicarb with ROSC achieved 1-2 minutes later.


Initial labs (~1hour prior to arrest) finally returned showing:
K = 8.1
BUN = 99
Cr = 6.84
Troponin = undetectable


A post-ROSC ECG was obtained just as a change in rhythm occurred:

The first 3-4 QRS complexes are very wide with bizarre morphology of QRS and ST-T-wave. The rhythm then changes to regular and tachycardic, with probable P-waves, (~120 bpm) for the remainder of the ECG.   

The patient's blood pressure on the arterial line dropped acutely:

This shows sustained polymorphic wide complex tachycardia. It is somewhere on the spectrum between polymorphic VT (PMVT) and VFib. The exact point on that spectrum is irrelevant, as the spectrum is more of a vortex ending in VFib arrest. The treatment for either is immediate, unsynchronized defibrillation.

Defibrillation was attempted several times, each with temporary improvement to a more organized wide complex tachycardia, then returning to PMVT/VFib:

Similar to prior

More calcium chloride and bicarb were administered. The exact amount is not available. Within minutes the patient achieved ROSC:

Sinus rhythm with much narrower (but still wide) QRS complex. There is perhaps a short QT and QTc interval here which may be caused by the calcium (a well described finding in hypercalcemia) which appears to have saved this patient's life. 

A dialysis catheter was placed, and the patient underwent immediate CVVHD. No further arrests or deterioration in rhythm occurred. The patient recovered for 1 week in the ICU, then signed out AMA only to return 4 days later with shortness of breath. She had another prolonged admission in which she gradually recovered kidney function, and has not yet required long-term dialysis.



Learning Points:

1) Hyperkalemia is one of the most important causes of a wide QRS complex. Hyperkalemia is immediately life threatening, immediately recognizable on ECG, and immediately treatable.

2) You must become facile with recognizing RBBB, LBBB, and paced rhythms in order to correctly diagnose wide QRS complexes.

3) The initial treatment for life-threatening hyperkalemia is IV calcium. There is no limit to the amount of calcium given if the patient is unstable. Titrate to normalized QRS complex. The serum calcium level is irrelevant.

An irregularly irregular wide complex tachycardia

This was written by Pendell Meyers, a G2 of the Stony Brook residency who has a keen interest in ECGs and who is going to start to help edit this blog.  It was edited by me (Smith).

Below is a common and important ECG that somehow hasn't made it onto this blog yet!

Case

A middle aged man presented with acute shortness of breath. He was hemodynamically stable but in mild respiratory distress, with diffuse B-lines and requiring BIPAP.

Here is his initial ECG:

What is your interpretation? What is the rhythm? Are there signs of acute coronary occlusion?

This shows an irregularly irregular wide complex tachycardia at a rate of about 120. Of course, whenever confronted with a wide complex tachycardia, one must consider ventricular tachycardia. However, unless it is polymorphic VT (which has multiform QRS complexes), VT is never this irregular. An irregularly irregular rhythm must put atrial fibrillation (AF) at the top of the differential.

The QRS complex is classic for LBBB except that V1 and V2 do not show a large, predominant S-wave. It is possible that lead misplacement may account for these two leads, but the rest of the precordial leads and high lateral leads have morphology diagnostic of LBBB. Thus, this is most likely AF with LBBB. Is there coronary occlusion? If there is, it is not evident on this ECG: it does not meet either the original or modified Sgarbossa criteria.  

The differential diagnosis of irregularly irregular wide complex tachycardia is an important one, as it includes dangerous etiologies such as Pre-excited AF (AF with WPW), polymorphic VT, and hyperkalemia-induced arrhythmias, in addition to the more common etiology of Atrial Fib with aberrancy (including LBBB and RBBB).

Unfortunately, the common management for AF with aberrancy (AV nodal blockers to slow the ventricular response) is contraindicated in AF with WPW, as it can precipitate ventricular fibrillation.

How do we know it is NOT AF with WPW?

1) In AF with WPW, the QRS has multiple waveforms. In this ECG, there are slight variations, but they are all basically the same.

2) Most important, in AF with WPW, there can be very short RR intervals because the accessory pathway can have a very short refractory period, allowing it to conduct to the ventricles with RR intervals less than 250 ms. In this case, the shortest RR interval is about 360 ms.

As in all ECG interpretation, finding an old ECG is often very helpful. Identical QRS morphology from a prior known supraventricular rhythm would confirm that the tachycardic rhythm is indeed supraventricular, and would allow a degree of safety in giving AV nodal blocking agents. 

Here is the patient’s prior EKG:

Sinus rhythm with LBBB. All leads have nearly identical morphology as the presentation ECG above, except that V1 and V2 in this prior ECG (in contrast to the presenting ECG) are typical for LBBB. The fact that all other leads match supports the possibility that lead placement is to blame for the first ECG. But it is uncertain.

This ECG was taken as evidence that the first ECG was, as suspected, AF with LBBB. The patient was given 20mg, then 25mg of diltiazem IV, which lowered the rate satisfactorily. 

The patient then spontaneously converted to sinus rhtythm without further therapy (This is not necessarily a result of the diltiazem, which does not generally "convert" AF; it only slow the ventricular response.  Thus, the conversion to sinus is likely coincidental):

Sinus rhythm with LBBB. V1 is slightly more similar to baseline, but the abnormality (from classic LBBB) in V2 remains. There is likely still lead misplacement. 

Learning Points

1) With the exception of polymorphic VT (multiple QRS complexes), VT is fairly regular. 

2) Irregularly irregular wide complex tachycarrhythmias include dangerous etiologies such as Preexcited AFib which must be suspected in order to avoid harms of AV nodal blocking agents.

3) However, AFib with preexisting bundle branch block is the most common overall etiology.

4) A prior ECG with identical morphology is helpful in determining whether a wide complex rhythm is supraventricular.

5) You must memorize the morphology of LBBB and be able to recognize it instantly.

What happens when you give adenosine to a patient with this rhythm?

A 40-something presented with palpitations and had a regular pulse at 170.

Here is his 12-lead ECG:

The computer reads supraventricular tachycardia.
What is it?

It is atrial flutter with 2:1 conduction.  It is not PSVT and not sinus.

There are clear flutter waves in lead II across the bottom.  In V1, there are upright waves that appear to be P-waves but are not: they are atrial waves and it is typical for atrial flutter waves to be upright in V1, whereas sinus P-waves are biphasic in V1.

The flutter rate is relatively fast at 334, such that the ventricular rate is 167 (one half the atrial rate).

As easy as it may seem to make this diagnosis, it is often misdiagnosed as PSVT.  Thus, adenosine is often given.

Such was the case here.

Adenosine was given, during which this rhythm strip was recorded:

The AV node is blocked by adenosine and QRSs disappear.
This "reveals" the flutter waves, which of course continue.
There are some ventricular escape beats.

Adenosine simply blocks the AV node so that there is no QRS to hide the flutter waves, and they become obvious.  So adenosine can help to diagnose atrial flutter, but it will not treat atrial flutter. 

Atrial flutter does not use the AV node for part of its re-entrant loop, as does PSVT [whether AVNRT (a micro-reentrant intranodal loop) or AVRT (a macro re-entrant loop using bypass tract for one leg of the loop)].  Therefore adenosine will not interrupt the loop. 

 The half-life of adenosine is about 10 seconds, and its effect will rapidly wear off (thankfully, otherwise this patient would be dependent on ventricular escape beats for perfusion!)

When the adenosine wears off, the impulse will continue to conduct through the AV node, still at a 2:1.

So atrial flutter must be treated with either:
1) A longer acting AV nodal blocker, such as diltiazem infusion, to slow the ventricular response or 
2) Cardioversion, whether electrical or chemical.  Electrical works better (see article summary at bottom) but has a risk of thromboembolism:

Similarly to atrial fibrillation, patients with atrial flutter do develop atrial thrombi, and thus cardioversion may involve a risk of thromboembolism if the onset of atrial flutter is not within 12-48 hours of ED presentation.  This is primarily because patients with atrial flutter often alternate between fib and flutter, and produce thrombi during episodes of fibrillation.

More cases of misdiagnosed atrial flutter

Here are a couple other cases of atrial flutter which were misdiagnosed.  In these cases, they were misdiagnosed as sinus tachycardia (not PSVT):

Notice there is a "P-wave" just before the QRS in V1
Notice there is a "P-wave" directly superimposed (on top of) the T-wave in V1.
These are atrial flutter waves.

Narrow complex tachycardia at rate of 135.
Notice the "P-waves" are upright in V1
The rhythm strip across the bottom is V1 (it is usually lead II)
Notice there is an extra "P-wave" at the end of each QRS in V1
All these are atrial flutter waves.
True P-waves are not upright in V1; they are biphasic up-down.
The positive deflection of a normal P-wave in V1 is the right atrium
The subsequent negative deflection of the normal P-wave in V1 is the left atrium.
Thus the flutter rate is 270 with 2:1 conduction.

Slow atrial flutter (flutter rate 240, ventricular rate 120)
Misdiagnosed as sinus tach
Here is the case: 

Sepsis with Pulmonary Edema and Elevated Right Sided Pressures

Atrial Flutter rate:

Atrial flutter is usually at a rate of 300, but can be anywhere between 240 and 360.

The ventricular rate depends on AV node conduction and is usually half the atrial rate (2:1 conduction), but may become 1:1 (dangerous) or slow down to less than 2:1 in the presence of AV node blockers

The atrial rate can be much slower in the setting of a sodium channel blocker such as flecainide, quinidine, or procainamide.  Use of these medications without prior AV blockade is dangerous as it will lead to 1:1 conduction!!


Atrial Flutter

--Macro re-entrant loop just above AV Node in right atrium

--Atrial rate 240-360 without medications

--2:1 block, vent rate 150 most common

--Regular, fixed; or regularly irregular: RR interval an integer multiple of the atrial rate

--Narrow if no aberrancy or bundle branch block

--Flutter waves, sawtooth pattern--Nearly always visible in lead II

--Adenosine can help to diagnose, not treat

--Conversion vs. Ventricular slowing

l50 Joules, Ibutilide/Amiodarone

lDiltiazem slows at AV node

Procainamide before Diltiazem is dangerous

---it will slow the atrial rate and allow for 1:1 conduction

---results in a FASTER ventricular rate

See this case:

Wide complex tachycardia at a rate of 270

Relevant literature

Emergency Department Management and 1-Year Outcomes of Patients With Atrial Flutter Scheuermayer FX, et al. Annals of EM 57(6):564-571, June 2011

--122 consecutive patients with a primary ED diagnosis of atrial flutter

--1 year: 3 deaths due to concurrent illnesses and no strokes

--Electrical cardioversion resulted in NSR in 91% (42 of 46)

--8 required > 150 Joules

         --93% discharged home

--Antiarrhythmic treatment resulted in NSR in 27%

--60% discharged home.

         --Same stroke precautions as atrial fib

Sudden weakness with bradycardia and bizarre T-waves

An 60-something man complained of sudden weakness.  There was no chest pain or SOB.  He had normal blood pressure and perfusion and was asymptomatic at rest.  He was well appearing.

An ECG was recorded:

There is a slow, wide rhythm with bizarre T-waves.What is it?  What do you want to do?

You'll note there are P-waves.
Look at lead II across the bottom:
---There is a P-wave immediately after each T-wave (these do NOT conduct).
---There is a P-wave immediately before each QRS.  Even though it appears as if that P-wave does not have enough time to conduct, the PR interval is exactly the same for every one of these, so it is very unlikely to be isorhythmic dissociation.   Therefore, every other P-wave is conducting and it is thus 2nd degree AV block, Mobitz II.

Furthermore, there is a large R-wave in V1, with large S-wave in V5-V6 (RBBB) and also an axis toward aVR, implying a fascicular block as well.

We all know that there is a high incidence of progression from Mobitz II to third degree (complete) AV block, but we don't always get to see it.

Such progression to complete heart block is especially likely when there is high degree block due to disease in the conducting fibers (in contrast to the AV node alone).  And the fact that there is RBBB + fascicular block shows that there is disease in these conducting fibers also.

Here only one fascicle is working, and then it is only working on every other beat!!

Management: Since these patients are at high risk of progressing to complete heart block, especially in the context of acute MI (not applicable here), it is wise to apply the external pacing pads.  Get ready for emergent transvenous pacing and get the patient to an electrophysiologist who can place a permanent pacemaker.

The electrophysiologist was called.  The patient remained stable.

Electrolytes, especially K, were normal. Troponin was negative.


80 minutes later, we have this ECG:

Now what is going on? 

Here the ECG is annotated:

The black lines (lead II across the bottom) indicate the beginning of every P-wave.P-waves are at a rate of about 96.
It appears that every other P-wave conducts [see complexes 1, 4, and 5 -- not including the PVC (red arrow)]
However, you can see that the P-waves encroach closer and closer to the QRS. The PR interval is getting shorter, if it is really a PR interval.
Also, there are clearly P-waves that do NOT conduct.
Thus, the P-waves that appear to conduct are only incidentally going approximately the same rate as the QRS and are not really conducting (isorhythmic dissociation)

Furthermore, the QRS has changed from the first ECG: there is now more of a Left Bundle Branch Block pattern.

This appears to be isorhythmic dissociation with third degree (complete) AV block.
The escape is from the right ventricle, resulting in LBBB morphology, and is regular at a rate of 50 (see green lines of same length).

The QRS has changed because it has gone from a conducted beat to an escape beat.

Alternatively: this could be a junctional escape with alternating bundle branch block: formerly RBBB + fascicular block, now LBBB.  The rate of 50 supports this.

Isorhythmic dissociation:
P-waves are occurring at a rate of 96 and no P-wave is conducting.  The ventricular escape is 50, which is slightly faster than half of the sinus rate (96 divided by 2 = 48).  So every second P-wave occurs at about the same time as the ventricular escape (you have to ignore the PVC).  But since the ventricular rate is slightly FASTER than half the sinus rate, it comes a bit earlier on each beat and therefore the PR interval appears to shorten.  Really they are just coincidentally coming at almost the same time.  

Most isorhythmic dissociation does not also have AV block.  In this case, there is isorhythmic dissociation with complete AV block.

See this post on isorhythmic dissociation without block: What is this rhythm?

Clinical Course

Regardless of whether there was progression to complete heart block or not, the patient would need a pacemaker.

A pacemaker was implanted.  There was no myocardial infarction.  The etiology was not yet found.

How about those T-waves??

These are common in high grade AV block.  You can read more about them here:

Giant Inverted T waves in an Elderly Patient

Bizarre T-wave inversion of Stokes Adams attack (syncope and complete AV block), with alternating RBBB and LBBB

Beware Automated Interpretations of Atrial Fibrillation!

See this ECG:

There is an irregularly irregular rhythm.
The Automated interpretation was "Atrial Fibrillation."
What is it?

Look at the lead II rhythm strip across the bottom.  There are clearly sinus P-waves for the first 6 beats, although they speed up.

This change of rate of the sinus node is called "sinus arrhythmia" and is related to vagal tone from inspiration (which increases vagal tone and slows down the rate, but this takes several seconds and this gets out of phase, which means that by the time it is slowing down, the patient is actually expiring).

Then beats 7 and 8 appear and do not show P-waves in lead II.  Are they junctional?  No!  Look above in V1-V3, and you clearly see an atrial beat but of a different morphology (coming from another focus in the atrium, and thus not a sinus beat).  This is occurring because the vagal tone is slowing the sinus node so much that a different part of the atrium "escapes," taking over the pacemaker function.

Beats 9 and 10 also appear to be preceded by subtle atrial activity, but of yet another morphology and thus from yet another focus in the atrium.

So there appear to be at least 3 atrial pacemakers here (3 foci).

When the rate is tachycardic (greater than 100) and there are at least 3 foci, then it is called multifocal atrial tachycardia (MAT), which is usually associated with COPD.  For more on MAT, see this lecture on Narrow Complex Tachycardias from minutes:seconds 23:44 to 26:50.

Since the rate is normal, this is called a Wandering Atrial Pacemaker.  It is benign.

2 reasons for an irregularly irregular rhythm in a narrow complex*

1. Multifocal atrial tachycardia
2. Atrial fibrillation
* Sinus arrhythmia appears to be irregularly irregular during the 10 seconds of a 12-lead ECG, but it has a regular pattern to it over more time (speeding up, slowing down, speeding up, slowing down).

Automated interpretations in atrial fibrillation

We compared the Veritas automated interpretation [a widely used algorithm on Mortara machines which is a conventional (if, then; instructional) algorithm] and a new deep neural network algorithm (Cardiologs).  We used an expert reference standard, and found that the Veritas had a very large number of false positive reads, more than Cardiologs.(1)

--> A 2004 study of 2298 ECGs from 1085 patients which had a computerized interpretation of AF found that in 442 (19%) of these ECGs, from 382 patients (35%), the interpretation was incorrect, and that, in 92 of these 382 patients, the physician had failed to correct it.  These errors resulted in unnecessary anti-arrhythmic and anticoagulant therapy in 39 patients and unnecessary diagnostic testing in 90 patients, and an incorrect final diagnosis of  paroxysmal AF in 43 patients.(2)

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1.   Smith SW et al. Improved Interpretation of Atrial Dysrhythmias by a New Neural Network Electrocardiogram Interpretation Algorithm.  SAEM.  Abstract 670.  Academic Emergency Medicine 2017; 24(S1):S235. 

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2.   Bogun F, Anh D, Kalahasty G, et al. Misdiagnosis of atrial fibrillation and its clinical consequences. Am J Med 2004;117:636-42.

Learning Point

It is easy to gloss over automated reads without scrutinizing them carefully.  Especially when the read is "Atrial Fibrillation", you must look carefully.  These misreads have adverse consequences!!

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