A 50-something called 911 for palpitations.
He was tachycardic and diaphoretic. POCUS cardiac ultrasound was hyperdynamic.
Medics recorded this ECG:
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:
Another 12-lead was recorded:
--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:
Here is the result:
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.
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:
- Placed the Right Arm electrode on the patient’s manubrium.
- Placed the Left Arm electrode on the 5th intercostal space, right sternal border.
- Placed the Left Leg electrode on the right lower costal margin.
- 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,
Nice.... Great pointers for learning. Thanks
ReplyDeleteThanks a lot ..
ReplyDeleteCan we rely on the presence of the PVCs to differentiate junctional tachycardia from PSVT ?
Thanks again
Thanks a lot
ReplyDeleteCan we depend on the presence of the PVCs to differentiate junctional tachycardia from PSVT ?
Thanks again
Either one can have PVCs. It is the variable rate that makes PSVT so unlikely.
DeleteAny follow- up, just wondered..Is it enough just to discontinue digoxin in these cases and wait-watch what happens Dr Smith ?
ReplyDeleteYes. Just withdrawal of the toxin and watchful waiting was all that was necessary. The patient recovered fine.
DeleteI find lewis leads very interesting as a concept, but for the sake of treatement, does it really matter? I mean, should we avoid vagotonic monouvres, adenosine, calcium bloquers or Bbloquers if P waves are present?
ReplyDeleteThankyou for this blog. It is really enlightning!
See these cases and decide for yourself: http://hqmeded-ecg.blogspot.com/search/label/Lewis%20Lead
DeleteSteve...
ReplyDeleteA great teaching case. My thoughts are: The paramedics' ECG is unquestionably a typical, counterclockwise atrial flutter with a very interesting finding - an F wave alternans. I have seen this before but it is quite unusual and well worth saving for teaching purposes. The atrial rate is somewhere between 250 and 300/min. As for the other ECGs, I would certainly agree that they do not look like atrial flutter at all - the rate is much too slow. You speak of a rate that gradually changes but you must not have posted those tracings. Everything I see here is very precise and regular (except for the PVC). As to the origin of the non-flutter tracings, an automatic junctional tachycardia is certainly a possibility, though quite a rarity. You mention an automatic rhythm that is constantly varying which would not be typical of any automatic rhythm other than a sinus rhythm. Enhanced and abnormal automatic rhythms may have a warm-up and a cool-down as they begin and end (respectively), but once the rhythm gets going it's as regular as any re-entrant rhythm. An automatic junctional rhythm would not be subject to the same influence of the autonomic nervous system (though the adrenals could have an effect!). An automatic junctional rhythm would be a rarity in an adult unless the patient were digtoxic or had just had surgery for a congenital heart problem. In addition, while a junctional pacemaker focus may switch to another focus with a different rate, this would not result in a constant, gradual change. If the rate were under 150/min and the rhythm constantly and gradually changing, I would look for more evidence of P waves hidden in the T waves due to a first degree AV block.
I agree that one should never have mistaken ANY of these rhythms for atrial fibrillation. As far as any analogy with sinus tachycardia, sinus tachycardia is almost always physiologic while junctional tachycardia is always pathologic.
Jerry,
DeleteWe did not have tracings at all moments. The rate did vary. Although of course junctional tach is rare and usually associated with cardiac surgery or digoxin, it can also be associated with sympathomimetic toxins, which was the case here. Without intracardiac tracings, I cannot be certain of the diagnosis. It would be the first junctional tach I have ever diagnosed, but I'm still pretty sure that is what it was.
Thanks!
Steve
Steve...
ReplyDeleteSorry. I didn't see the information about the ephedrine ingestion. If the ephedrine level was somewhat variable, that could explain a changing junctional rate but still without autonomic NS involvement. Without that, however, I would not expect an automatic junctional tachycardia to vary except at the onset and offset of the dysrhythmia.