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,