A young woman presented with palpitations, chest pressure, SOB and weakness.
She had a rapid rate and BP of 140 systolic. She was in no distress.
Her prehospital ECGs showed SVT at 2 different rates: 160 and 240 (approx)
On arrival, this was the first ECG:
She was given 6 mg of IV adenosine, after which she converted to sinus for 2 beats, then had several PACs, then went back into SVT at a rate of 240.
Here is her ECG:
What is going on? What do we do?
To understand SVT, it is necessary to understand how it initiates and propagates:
What do we do about it?
Because this is narrow complex, its antegrade propagation must be traversing the AV node. The temporary blockage by adenosine confirms this.
Management: One suggestion that was offered was to use electrical cardioversion, since adenosine "did not work." However, adenosine did work. But it only lasts for seconds. Then the dysrhythmia was re-initiated (in this case by PACs, which are the basic reason that SVT gets initiated, as above).
Cardioversion will not work! We need to either:
1) prevent re-initiation of the dysrhythmia, by preventing PACs, OR
2) persistently block the AV node transmission with a drug that has a relatively long duration of action (adenosine only does so transiently)
There are 2 primary medication classes for this purpose:
1) Ca channel blockade, with verapamil or diltiazem. Verapamil was the standard treatment in the early 80s, before adenosine. It has a slightly greater chance of hypotension than adenosine (3.5% incidence in one large study)
2) Beta blockade, which will both inhibit PACs and slow AV nodal conduction.
Clinical Course
We decided to use verapamil to block the AV node persistently. Verapamil is a powerful negative inotrope, so it should never be used when there is poor LV function. We did a bedside ultrasound which confirmed excellent contractility.
We gave 5 mg verapamil over 2 minutes.
There was temporary success, but then more PACs, and SVT re-started, this time at a rate of 240.
It would stop and start, randomly at either 160 or 240, always initiated by a PAC.
We gave another 5 mg, without much success.
After this, we turned to beta blockade. It may be hazardous to administer both Verapamil and beta blockade, due to to the possibility of profound negative chronotropy and inotropy. Therefore, we decided on esmolol, which has a short half life and could be turned off if there were adverse effects.
We gave 500 mcg/kg of esmolol and started a 50 mcg/kg/min drip.
This is the result:
Shortly thereafter, a subsequent ECG and all rhythm strips showed sinus rhythm with no PACs. The esmolol worked.
As she tested positive for COVID, no EP study was done. She was discharged on a beta blocker.
Alternative explanation: no accessory pathway.
It is possible also that there is NOT an accessory pathway, but rather only 2 pathways within the AV node. If so, then in one case, the impulse goes down the fast pathway and up the slow pathway (resulting in a very fast rate), and in the other, it goes down the slow pathway and up the fast pathway (resulting in a less fast rate). However, if this is the case, it still needs to traverse both a slow and fast pathway, so this still makes it hard to explain two different rates UNLESS the rate varies depending on the direction.
The rate depends on the time that it takes the impulse to make a complete circuit through the AV node. For the two rates to be different, the rate of conduction would have to be different depending on the direction of the impulse. This is possible.
Procainamide and amiodarone were also suggested by some as management. However, they have very limited success in refractory SVT, especially SVT that involves AV nodal conduction. This article studied their effect in pediatrics:
https://www.ahajournals.org/doi/full/10.1161/CIRCEP.109.901629
She had a rapid rate and BP of 140 systolic. She was in no distress.
Her prehospital ECGs showed SVT at 2 different rates: 160 and 240 (approx)
On arrival, this was the first ECG:
 |
| Narrow complex regular at 160. Not sinus. There is no suggestion of atrial flutter. So this is paroxysmal SVT. |
She was given 6 mg of IV adenosine, after which she converted to sinus for 2 beats, then had several PACs, then went back into SVT at a rate of 240.
Here is her ECG:
 |
| Same as above, but with a rate of 240. |
What is going on? What do we do?
To understand SVT, it is necessary to understand how it initiates and propagates:
Pathophysiology
(From the EmRap compendium chapter written by Pendell Meyers and Steve Smith)
- "Made possible by “dual AV nodal physiology,” in which the AV node is thought to contain 2 pathways that separate briefly and reunite inside the AV node, both conducting from the atria to the bundle of His.
- "The “fast pathway” exhibits faster conduction but a longer refractory period than the “slow pathway.”
- "In sinus rhythm, each AP propagates simultaneously down the dual AV nodal pathways without the opportunity for reentry, since the 2 pathways block each other at the point of re-unification.
- "The normal time between beats ensures that both pathways are available for the next AP.
- "However, a properly timed premature atrial beat may arrive early at the AV node, at a time when the fast pathway is still refractory but the slow pathway is fully repolarized and able to accept the oncoming AP.
- "The AP then proceeds anterogradely down the slow pathway only, during which the fast pathway completes its repolarization.
- "The AP arriving at the reunification point is then able to access the fast pathway, continuing retrogradely up the fast pathway and subsequently anterogradely down the slow pathway, sending APs to both the atria and ventricles.
- "This creates a regular tachycardia with retrograde P-waves that may occur before, during, or after the QRS complex."
- In SVT caused by an accessory pathway, the pathophysiology is similar except that the second conducting limb is the bypass tract, not another limb in the AV node.
Why 2 different rates?
- Suppose there are BOTH 2 pathways in the AV node (which conduct at different speeds) AND an accessory pathway (3 total pathways)?
- Then it could use either AV nodal pathway do descend (at different rates), and the accessory pathway for as the ascending pathway.
Important point: Adenosine or verapamil does not cause the slower rhythm to accelerate into the faster rhythm. A PAC can initiate SVT down either limb of the AV node, it seems this is random. So the rhythm can randomly re-initiate at either rate.
What do we do about it?
Because this is narrow complex, its antegrade propagation must be traversing the AV node. The temporary blockage by adenosine confirms this.
Management: One suggestion that was offered was to use electrical cardioversion, since adenosine "did not work." However, adenosine did work. But it only lasts for seconds. Then the dysrhythmia was re-initiated (in this case by PACs, which are the basic reason that SVT gets initiated, as above).
Cardioversion will not work! We need to either:
1) prevent re-initiation of the dysrhythmia, by preventing PACs, OR
2) persistently block the AV node transmission with a drug that has a relatively long duration of action (adenosine only does so transiently)
There are 2 primary medication classes for this purpose:
1) Ca channel blockade, with verapamil or diltiazem. Verapamil was the standard treatment in the early 80s, before adenosine. It has a slightly greater chance of hypotension than adenosine (3.5% incidence in one large study)
2) Beta blockade, which will both inhibit PACs and slow AV nodal conduction.
Clinical Course
We decided to use verapamil to block the AV node persistently. Verapamil is a powerful negative inotrope, so it should never be used when there is poor LV function. We did a bedside ultrasound which confirmed excellent contractility.
We gave 5 mg verapamil over 2 minutes.
There was temporary success, but then more PACs, and SVT re-started, this time at a rate of 240.
It would stop and start, randomly at either 160 or 240, always initiated by a PAC.
We gave another 5 mg, without much success.
After this, we turned to beta blockade. It may be hazardous to administer both Verapamil and beta blockade, due to to the possibility of profound negative chronotropy and inotropy. Therefore, we decided on esmolol, which has a short half life and could be turned off if there were adverse effects.
We gave 500 mcg/kg of esmolol and started a 50 mcg/kg/min drip.
This is the result:
 |
| Sinus with many PACs So the esmolol is primarily slowing AV nodal conduction and has not stopped the PACs |
Shortly thereafter, a subsequent ECG and all rhythm strips showed sinus rhythm with no PACs. The esmolol worked.
As she tested positive for COVID, no EP study was done. She was discharged on a beta blocker.
More pathophysiology
Here is one likely anatomy for our patient today. For the other, see "Alternative Explanation" below, and Ken's commentary.
However, in our patient today the direction of conduction would be OPPOSITE from this diagram. It goes down one of the AV node pathways, and UP the accessory pathway:
However, in our patient today the direction of conduction would be OPPOSITE from this diagram. It goes down one of the AV node pathways, and UP the accessory pathway:
 |
This schematic comes from this blog post:Wide Complex Tachycardia in a 20 something.
As stated above, the AV node can have 2 pathways and this is the anatomic substrate for AVNRT.
But here there is also an accessory pathway, for a total of 3 pathways. The tachycardia has two different rates because A and B have different conduction speeds. In contrast to the case today, the previous case was wide complex because it went down the bypass tract (causing pre-excitation and a wide complex) and up through the AV node (antidromic). Previous case: the conduction back up through the AV node can go through either limb within the AV node. One is fast and one is slow, and they have differing refractory periods. The rate of the tachycardia depends on which AV node limb it ascends through. Today's case: there is orthodromic conduction. The rate is dependent on which limb of the AV node is conducting. |
It is possible also that there is NOT an accessory pathway, but rather only 2 pathways within the AV node. If so, then in one case, the impulse goes down the fast pathway and up the slow pathway (resulting in a very fast rate), and in the other, it goes down the slow pathway and up the fast pathway (resulting in a less fast rate). However, if this is the case, it still needs to traverse both a slow and fast pathway, so this still makes it hard to explain two different rates UNLESS the rate varies depending on the direction.
The rate depends on the time that it takes the impulse to make a complete circuit through the AV node. For the two rates to be different, the rate of conduction would have to be different depending on the direction of the impulse. This is possible.
Procainamide and amiodarone were also suggested by some as management. However, they have very limited success in refractory SVT, especially SVT that involves AV nodal conduction. This article studied their effect in pediatrics:
https://www.ahajournals.org/doi/full/10.1161/CIRCEP.109.901629
===================================
MY Comment by KEN GRAUER, MD (5/30/2020):
===================================
Fascinating case presented by Dr. Smith (!) — about this young woman who presented with palpitations and sequential reentry SVT rhythms — initially at a ventricular rate of ~160/minute — and then following administration of 6mg IV adenosine, another reentry SVT at a much faster rate of ~240/minute. HOW could this happen?
- For clarity — I have put together the 3 ECGs from today’s case in Figure-1.
- Dr. Smith has reviewed (above) the pathophysiology of dual AV nodal pathways responsible for sustaining reentry SVT rhythms. I focus My Comment on additional insights to be gained from this case.
 |
| Figure-1: The 3 ECGs shown in today’s case (See text). |
ADENOSINE is NOT Always Benign: Adenosine’s reputation as a superb, rapid-acting agent for treatment of reentry SVT rhythms is well established. The drug acts immediately — with a half-life of less than 10 seconds. As a result — any adverse effects that may be produced will almost always be short-lived (typically resolving within 30-to-90 seconds).
- Common adverse effects (that are to be expected) following IV adenosine include: i) chest pain; ii) cough (from transient bronchospasm); iii) cutaneous vasodilatation (transient skin flushing); iv) metallic taste; v) transient nausea, sweating, nervousness, numbness, lightheadedness and a sense of “impending doom”; and, vi) transient bradycardia that may be marked (and which may even cause a brief period of asystole).
- Adenosine may shorten the refractory period of atrial tissue — which could initiate AFib in a predisposed individual. For this reason — Adenosine should be used with caution in patients with known WPW, given theoretic possibility of inducing AFib (which could have significant consequence in a patient with accessory pathways).
- Adenosine may cause a reflex increase in sympathetic tone and circulating catecholamines. This may lead to increase in heart rate; atrial or ventricular ectopy; and/or enhanced conduction over accessory pathways (Mallet ML: Emerg Med J 21:408-410, 2004).
- In addition to AFib — Mallet describes other Proarrhythmic effects of adenosine (in which administration of this drug may cause another arrhythmia). These proarrhythmic effects include: i) PVCs and/or non-sustained VT (including on occasion polymorphic VT and Torsades de Pointes, especially when this arrhythmia is pause-dependent); ii) Induction of other atrial arrhythmias, including ATach and AFlutter; iii) Enhanced AV conduction of established AFlutter (from 2:1 to 1:1 AV conduction); and, iv) Acceleration of the ventricular response to a reentry SVT. This latter effect is the probable explanation for the paradoxical increase in ventricular rate that occurred in this case, with sequential SVT rhythms showing an increase from 160/minute to 240/minute after administration of 6 mg of IV adenosine (Figure-1). As shown by Curtis et al (J Am Coll Cardiol 30[7]1778-84, 1997) — the dual AV nodal pathways referred to by Dr. Smith (above) may manifest different sensitivities to IV adenosine. This property could have facilitated a switching of orthodromic (forward) conduction from the slow to the fast AV nodal pathway at the time the heart rate increased to 240/minute (ECG #2 in Figure-1).
BOTTOM LINE Regarding Use of Adenosine: Adenosine is a great drug — especially in an emergency setting! It works fast. It is highly effective for reentry SVT rhythms (both AVNRT and AVRT!). In addition:
- Adenosine may serve as a “chemical Valsalva” — in which Adenosine is given as a diagnostic/therapeutic trial for a narrow tachycardia (SVT rhythm) of uncertain etiology. Presumably adenosine will convert the rhythm if it is a reentry SVT. If not — it will hopefully slow the rhythm enough (transiently) to allow a definitive diagnosis to be made (just like Valsalva ... ).
- Adenosine can be a valuable agent to be used as a “therapeutic trial” for a regular, monomorphic WCT of uncertain etiology — in which the drug may convert the rhythm if the WCT is either an adenosine-sensitive form of idiopathic VT or a reentry SVT rhythm. And, in the event adenosine does nothing — adverse effects are generally short-lived and well tolerated by most patients.
- BUT — Because adenosine is not benign — the drug should not be used in cases in which it is unlikely to work (ie, when the patient has polymorphic VT or Torsades; or for known VT of ischemic etiology) — and, it should definitely not be used for WPW with rapid AFib.
Some Additional Observations about Figure-1: As per Dr. Smith — the initial ECG in the ED ( = ECG #1) showed a regular SVT rhythm at ~160/minute, without clear sign of atrial activity. After 6 mg of IV adenosine — the rate of the regular SVT increased to 240/minute ( = ECG #2).
PEARL: It can be very helpful to look for sign of retrograde atrial activity during a regular SVT rhythm — as this may provide an important clue to the mechanism of the SVT rhythm. I discuss and illustrate this key concept in detail in My Comment at the bottom of the March 6, 2020 post in Dr. Smith’s ECG Blog. In brief:
- With the usual ( = “slow-fast”) form of AVNRT — the RP’ interval during the SVT is typically very short (ie, with the retrograde P wave either hidden within the QRS complex, or distorting the terminal part of the QRS). This is because with the “slow-fast” form of AVNRT — the reentry circuit is relatively smaller, being completely contained within the AV node (therefore, little distance to travel retrograde — which results in a short RP’ interval).
- In contrast, with AVRT — the RP’ interval during the SVT tends to be longer (with the retrograde P wave most often occurring near the middle of the ST-T wave). This is because the reentry circuit is longer, since it involves an AP (Accessory Pathway) which lies outside of the AV node (therefore, a longer distance for atrial activity to travel retrograde — which results in a longer RP’ interval).
- Unfortunately — there is much baseline artifact in both ECG #1 and ECG #2. As a result — it was exceedingly difficult to look for signs of atrial activity That said — I agree with Dr. Smith that neither sinus P waves nor 2:1 flutter waves seemed to be present in either ECG #1 or ECG #2.
- I do not see any sign of retrograde atrial activity in ECG #1.
- However — I do see a distinct positive notch (pseudo-r’ ) in lead V1 of ECG #2 (RED arrow pointing to this r’ notch within the RED circle in ECG #2). I believe this r’ notch in lead V1 is real — because it was not present in lead V1 in either ECG #1 or ECG #3. Therefore — this r’ notch in lead V1 is almost certain to represent retrograde atrial activity during ECG #2.
My THEORY (Beyond-the-Core): The fact that we see this retrograde P wave in ECG #2 but not ECG #1 suggests that orthodromic conduction has switched from one AV nodal pathway to the other.
- The fact that this r’ notch in lead V1 of ECG #2 manifests a short RP’ interval — suggests to me that retrograde conduction is contained within the AV node (since I’d expect a longer RP’ interval if there was concealed retrograde conduction over an AP).
- I suspect the reason we did not see any retrograde P wave in ECG #1 — was that ECG #1 conducted down the slower AV nodal pathway (therefore the slower rate = 160/minute) — but back up the faster AV nodal pathway (such that the RP’ interval was shorter, and the retrograde P wave in ECG #1 was entirely hidden within the QRS complex!).
- This is the opposite of what I suspect happened with ECG #2 — which conducted down the faster AV nodal pathway (therefore the faster rate = 240/minute) — but then back up the slower AV nodal pathway. This resulted in a slightly longer RP’ interval — that was long enough for the retrograde P wave to emerge from beyond the QRS to porduce a pseudo-r' in lead V1.
- Therefore — I thought it more likely that there was no participation of any AP in the reentry circuit (ie, No AVRT) — but instead, that the SVT rhythms in ECG #1 and ECG #2 were both AVNRT, with the reentry circuit being totally contained within the AV Node. (That said — I fully acknowledge that I could be wrong, and I cannot exclude the possibility of participation by an accessory pathway).
Finally — About ECG #3: We need to remember from Dr. Smith’s presentation that ECG #3 was obtained after two 5 mg doses of verapamil — and after esmolol loading + infusion — and — that the ECG shortly thereafter showed conversion to normal sinus rhythm ( = presumed success in maintaining conversion to sinus rhythm following administration of the ß-blocker).
- Take a look at the long lead II rhythm strip in ECG #3. The rhythm is irregularly irregular — and except for the P wave preceding beat #2, atrial deflections in the long lead II rhythm strip are of extremely small amplitude.
- Wouldn’t it be EASY if you only saw the long lead II rhythm strip of ECG #3, to think this was AFib with a rapid ventricular response? NOTE: Nowhere on this long lead II rhythm strip do we see 2 similar atrial deflections in a row.
- Confession: I was not initially sure what the rhythm in ECG #3 was after looking at this long lead II rhythm strip. It was only after looking at the other 11 leads on this tracing that I was able to confirm that there were definite P waves. P waves are seen best in lead V1, albeit P wave morphology clearly changes from one-beat-to-the-next in this lead (the PURPLE, GREEN and PINK arrows in lead V1). Using the concept of simultaneous-leads — the thin, vertical PURPLE line that begins under the P wave in lead V1 confirms that the tiny upright deflection in front of beat #14 in the long lead II rhythm strip is indeed a P wave.
MORAL of the STORY: Always remember that, “12 Leads are Better than One”. In the case of ECG #3— looking at the simultaneously-recorded leads above the long lead II rhythm strip is instrumental in confirming that this irregularly irregular rhythm is not AFib.
- Technically (since the rhythm in ECG #3 is completely irregular, and P wave morphology does change from one beat to the next) — the rhythm in ECG #3 might best be defined as MAT (Multifocal Atrial Tachycardia).
- That said, practically speaking — I think of the rhythm in ECG #3 rather as a “rhythm in transition” — in this patient who shortly before ECG #3 was in a reentry SVT at 240/minute — for which she received several antiarrhythmic drugs — and then soon after ECG #3, was found to be in normal sinus rhythm without any PACs at all.
Our THANKS to Dr. Smith for presenting this insightful case.
