Wednesday, August 23, 2017

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


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

Sunday, August 13, 2017

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





Friday, August 11, 2017

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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