Narrow Complex Tachycardia at a Rate of 220

40-something yo who is on flecainide and diltiazem had sudden onset chest pain, palpitations, shortness of breath and diaphoresis:

Rate is 220.  What do you think?

It is fast, narrow, and regular, without P-waves.  So it is not atrial fib and not VT.   It is a regular narrow complex tachycardia.   There is a lot of ST depression -- this is ischemia caused by the very fast rate and is an indication for emergent electrical cardioversion.

What is the DDx?  

----PSVT (which includes AVNRT and orthodromic AV reciprocating tachycardia) [AVRT uses an accessory pathway, a "bypass tract" and thus is seen in WPW; about 30% of PSVT is orthodromic AVRT] 

----Atrial Flutter with 1:1 conduction.

Which is it?

The fact that the patient is on Flecainide and Diltiazem is good evidence that this is atrial flutter with 1:1 conduction.  These medications are primarily given to patients with atrial fib or flutter (the flecainide keeps the patient in sinus rhythm, and the diltiazem prevents 1:1 AV conduction when the patient is in flutter).

If you look closely at lead II across the bottom, it appears there are flutter waves.

This is atrial flutter with 1:1 conduction.  The patient is not on anticoagulants, but the very fact that he is on flecainide is evidence that he probably spends most time in sinus rhythm.

The providers thought this was AVNRT.

He was given adenosine 6mg, then 12mg, with no change.  If AVNRT, then one would expect conversion.  If flutter, one would expect AV blockade and uncovering of obvious flutter waves.  But the dose of adenosine clearly was not high enough to sufficiently block the AV node.  One could escalate to 18 mg.  This was not done.

Instead, they appropriately decided on electrical cardioversion.  The decided to sedate with etomidate. After giving the etomidate, but before cardioversion, they noticed that the patient had "converted":

Here is the 12-lead:

What happened?  Rate is now 120.

Ischemia is gone.

The providers thought that the patient had spontaneously converted.  

However, look closely (this explanation is fascinating -- pay attention!!): there are still flutter waves.  The flutter rate is 240 and there is 2:1 conduction with a ventricular rate of 120.  Go back to the first ECG, and the ventricular rate was 220, which means that the atrial flutter rate has INCREASED from 220 to 240!!

The reason that the ventricular rate has slowed is that the flutter rate has increased!!

The AV node cannot conduct as a rate of 240, but it can conduct at a rate of 220.  When the atrial flutter rate increased, the AV node could not keep up and the patient got much better because of a decreased ventricular rate.

Why did the flutter rate increase?  Not certain, but just a change in sympathetic tone would do it.

A short time Later the patient actually converted to sinus:

What would have a happened with a higher dose of adenosine?  The AV node would have blocked the conduction for a brief time and the flutter waves would have become obvious. Then the adenosine would be quickly metabolized, and the AV node would resume 1:1 conduction.  So adenosine does not treat this, but sometimes makes the diagnosis obvious.

Learning Points:

1. Patients who get atrial flutter and are kept in sinus rhythm with a type I antidysrhythmic, usually flecainide, must be on an AV nodal blocker to prevent 1:1 conduction.  In this case, it is uncertain if he had not taken his diltiazem, or if he needed a higher dose.

2. Regular Narrow complex tachycardia, if not sinus tach, is AVNRT, AVRT, or atrial flutter with 1:1 or 2:1 conduction.

3.  Never try to convert atrial flutter with a drug such as procainamide without first giving an AV nodal blocker.  You will cause a slowing of the atrial flutter rate with potential to INCREASE the ventricular rate.