Monday, October 31, 2016

An apparent SVT that does not persistently correct with adenosine

A middle-aged woman presented for abdominal pain.  She was found to have a heart rate of 150.  A 12-lead was recorded:
There is a regular, narrow complex tachycardia.
What is it?

Regular narrow complex tachycardias can be sinus tach, atrial tach, atrial flutter, AV nodal reentrant tachycardia, orthodromic AV reciprocal tachycardia [using a bypass tract (accessory pathway), that is WPW], or junctional tachycardia.

Here is a one hour lecture on Supraventricular Tachycardias; everything you ever need to know.

MAT and atrial fibrillation, other causes of supraventricular tachycardia, are not possible because they are always irregular, and this rhythm is regular.

There are no definite P-waves before the QRS and there are definite retrograde P-waves (see V2 below).
Here the black arrows point out the retrograde P-waves that are clearly present in V2
Once you find this, you go up to V1 and you can see that the retrograde P-wave is all negative.

--Thus, this cannot be sinus tachycardia or atrial tachycardia, which would have upright P-waves in V2.
               Suppose the P-wave was upright in V2 and in the same location in the middle of the QRS?  Then you would have to consider that there is sinus or atrial tach with a very long PR interval.

--When there is a narrow complex tachycardia, especially at a rate of 150, you should also look for flutter waves, which are not present.

--Junctional tachycardia is possible, as it also may have retrograde P-waves.  This is much less common, so let's discard this.

--Thus, we are left with re-entrant tachycardias that use the AV node (AVNRT and orthodromic AVRT).

This can be treated with vagal maneuvers, the best of which is Modified Valsalva, which has a success rate of about 40%.  More reliable is adenosine.

Case continued

A bedside echo showed good LV function.
The patient was given adenosine 6 mg without effect.  Then she was given adenosine 12 mg and had an asystolic pause (without underlying flutter waves), followed by one sinus beat, then one early narrow beat, followed by SVT again.  


Aside: if this were atrial flutter, you would see underlying flutter waves revealed when adenosine blocks the AV node and thus removes the QRS which obscures the flutter waves.  See this image which comes from a great article (the third of the 12 rhythms of Christmas) by Vince DiGiulio on EMS 12-lead and which Vince graciously permitted me to use:
Adenosine blocks AV conduction of flutter to ventricle, resulting in a ventricular escape rhythm and uncovering the flutter waves.

This did NOT happen in our case here.

So what happened?  Did adenosine work?

Yes!  Adenosine's only job is to stop the AV nodal re-entrant circuit.  Its effect is of extremely short duration, so it will be gone immediately and be unable to terminate a subsequently initiated episode of Paroxysmal SVT.  So one may have to prevent initiation of PSVT.

How does PSVT start?  PSVT requires 2 pathways.  In AVRT, one of them is the accessory pathway.   In AVNRT, there are 2 pathways in the AV node, a fast pathway with a long refractory period, and slow pathway with a short refractory period.  PSVT starts with a premature atrial beat (PAB) that reaches the AV node when the fast pathway is still refractory, and the slow one is not.  Then it travels down the slow pathway to the inferior part of the node where it then finds the fast pathway is no longer refractory and ascends that fast limb.  When it gets to the top it goes to BOTH the atrium and back down the slow pathway. Then around and around. For a more detailed explanation with an image, watch this lecture from minute 3:18 to 4:54.

PSVT is stopped by stopping the circuit.  If it recurs, further recurrence can be prevented by either 1) having a continuous AV blockade, as with a longer acting medication such as a calcium channel blocker or 2) preventing PABs.  PABs can be prevented by beta blockers or amiodarone.

Beta blockers may be detrimental in patients with poor LV function because of their negative inotropic effect.  In such cases, I have tried esmolol, as it has a short half-life and can be turned off.  I did not have success.   See this case:

Paroxysmal SVT (PSVT) that repeatedly recurs in spite of successful conversion with adenosine.

In that case in which esmolol did not work, I then gave amiodarone bolus of 150 mg, followed by an infusion, after which intervention the patient stayed in sinus rhythm.

In this case today, the adenosine worked, but within one beat, there was another PAB that initiated the PSVT again.

What to do?  Amiodarone?  Calcium channel blocker?  Something else?  As this patient has good LV function, a calcium channel blocker is an excellent and safe choice.  Before adenosine, verapamil was the standard way to terminate PSVT.

Verapamil IV dosage: the recommend IV dose of verapamil is 5 mg over 2 minutes, followed in 5 to 10 minutes (if no success) by a second 5 to 7.5 mg dose.
Diltiazem IV dosage: The recommended IV dose of diltiazem is 20 mg followed, if necessary, by a second dose of 25 to 35 mg.
An oral dose may be given for ongoing maintenance.

Case continued:

In this case, 2 g of Mg (8 mmoles, 16 mEq) was given by one of my excellent partners, Laura Shrag, and the patient converted!

Here is the post conversion ECG:
What is this? Sinus rhythm?

This was read as sinus rhythm, but it looks more like an ectopic atrial rhythm.  The P-wave in V1 is upright, whereas it should be biphasic.  This means that lead V1 is to the left of the source of the P-wave.  Either the heart is far to the right, or V1 was placed too far left, or there is a left-sided atrial source.  In any case, it is a stable rhythm at a good rate and we shouldn't worry about it any more than that.

--There are no delta waves, so this is less likely to be WPW, though absence of delta waves does not rule out WPW.
See explanation of this at these two posts:

--A large R-wave in lead V1. And why is the PR interval not short?

Also of concern: this patient had tachycardia and was completely unaware of it. She presented only for abdominal pain.  This implies that she is not aware of her PSVT and may live with it for long periods of time.  Long duration tachycardia may lead to cardiomyopathy, so it is particularly important for her to be on long term medications, or have an ablation, so that this does not recur.

Magnesium in PSVT:

Magnesium may be loosely thought of as a nonspecific Calcium channel blocker.  I was unaware of its effect on PSVT until this case.  There is data to show that Magnesium, in a dose of approximately 0.15-0.30 mEq/kg (10.5- 21 mEq per 70 kg, or 1.3-2.6 grams per 70 kg) is often effective for termination of PSVT with a low incidence of mild side effects (transient sensation of warmth, flushing, and diaphoresis).
10 mmoles = 2.5 g = 20 mEq

In the electrophysiologic (EP) literature below, it had variable effects on termination, but consistently prolonged antegrade AV node conduction, which is a necessary component to termination. 
1. In an EP study, after a bolus of 0.3 mEq/kg, followed by a 0.2 mEq (0.025 gm)/ kg/hr maintenance infusion, Mg was shown to increase the tachycardia cycle length by about 10% by slowing the antegrade conduction in the AV node of the re-entrant circuit.  However, it did not appear to convert any of the 4 AVNRT studied or any of the AVRT.  It did not prevent inducibility of SVT or affect the refractory period:

2.  In this EP study, 8 of 10 episodes of SVT that involved the AV node (4 AVRT and 6 AVNRT) were terminated with 2 grams of MgSO4 by rapid bolus, flushed with saline.

3.  In this dose-finding EP study, prolongation of the atrial-His interval was no more pronounced at doses higher than 5 mmols (=1.25 g) than at 5 mmoles:

4.  In this EP study, Mg was effective in termination of 5 of 15 with dual AV node physiology and 0 of 8 cases without dual AV nodal pathways: 

See this post for an explanation of dual AV nodal pathways: 

Wide Complex Tachycardia in a 20 something.

5.  Here is a case report of termination of SVT in the ED, from Annals of EM in the 1990s:


The patient was started on Diltiazem CD 120 mg daily.

Learning Points:

1. SVT that is converted by adenosine to sinus may revert back to SVT.
2. SVT is initiated by PABs.  Prevention of PABs helps to prevent recurrence.
3. Calcium channel blockers are very effective in conversion to, and maintenance of, sinus rhythm.
4. Especially in patients who cannot tolerate calcium channel blockers, it is reasonable to attempt an IV bolus of Mg at 1.25 to 2.5 g.
5. In patients who do not respond to Mg and cannot tolerate calcium channel blockers, amiodarone 150 mg followed by an infusion, may be effective in preventing further episodes of PSVT.  One may have to additionally convert the patient to sinus with adenosine.
6. Chronic tachycardia may lead to cardiomyopathy


  1. Hi Dr. Smith,
    Just some confusion about the paragraph where you describe the pathophys of AVNRT.
    You say that the Premature Atrial beat reaches the AVN while the fast pathway remains refractory, however, then say that this travels down the fast path? Is there a pause at this time to allow for the fast-slow-fast conduction?

    Are there ECG features to differentiate between the fast-slow and slow-fast? Is this really relevant?

    Lastly, what are your thoughts on reverting stable SVT with a CCB as first line? As reviewed by ALiEM here:

    Cheers, Will (House Officer, NZ)

    1. Thanks for pointing out the error. I fixed it! As for CCB, that's fine, but one large study showed significantly higher rates of hypotension with CCB than adenosine, though only 3.6% vs. 0.6%. The vast majority of PSVT which convert with adenosine will stay converted and won't recur for weeks, months, years, or never. So why give a medication that sticks around for hours when you can give one that lasts 10 seconds and is done with?
      Steve Smith

  2. Thanks Dr Smith , nice case , highlights to me the importance of reversion and post reversion strips in further assisting rhythm interpretation. On first look I could appreciate the retrograde P waves in V6 with more clarity.

    Thanks TA

  3. Steve...

    Compare the end of the QRS in V1 in the first tracing with the end of the QRS in V1 in the last (post-conversion) tracing. The first tracing has a pseudo-r' whereas the end of the QRS in the last (post-conversion) tracing doesn't breach the baseline. I don't think there are any negative retrograde P waves in Lead V1 in the first tracing. I think the retrograde P's are upright and attached to the end of the QRS as a pseudo-r'.

    Very interesting post and great teaching case!

  4. Steve...

    Also, regarding the post-conversion tracing, if you measure the P wave duration in Lead II or even Lead V3 and then compare it to the P wave duration in V1, you'll see that the terminal portion of the P wave in V1 is isoelectric. I really don't think there is an ectopic atrial rhythm. The P wave remains upright in both Leads I and II and the P wave is largest in Lead II, so I think this is a sinus rhythm. The P wave axis in the frontal plane is just to the right of +60 degrees (it's closest to the axis of Lead II but it lies slightly in the negative area of Lead aVL). This makes the P wave axis a bit more vertical which could possibly result in a terminal P wave vector in V1 that is nearly perpendicular to the horizontal plane (or at least perpendicular to V1 even within the horizontal plane).

    When I suspect an ectopic atrial rhythm (and there are no retrograde P waves), I look first at the P wave axis. If it falls between +30 and +70 degrees, I feel it is most probably sinus (especially if it is less than +60 degrees).

  5. Thanks for the case.

    Out of interest, did the patient subsequently have an EP study +/- ablation? Would be interesting to know the findings.

    For longer term prevention in this situation of recurrent episodes of SVT in the context of a young patient normal LV function it is also worth considering flecainide. Even in older patients it can be considered in the acute management, but would not be advocated long term. I had a 90yo patient admitted multiple times with SVT. Adenosine sensitive every time, but then she would go home and hardly be able to relax without fear of it happening again! Both bisoprolol and verapamil were ineffective at long term prevention. On one admission she went into SVT 3x overnight, with clear reversion to SR after adenosine each time. I advised one off flecainide that settled things overnight and then took her for an EP study. Classic AVNRT findings and since I ablated her slow pathway she's had no recurrence! :)


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