Clinical Case 123: How we do SVT Better
This case is inspired by a recent Twitter chat involving Seth Trueger, Chris Hicks, myself and the eternal opposition -Dr le Cong. There were others involved – thanks for joining the conversation to prove Minh wrong 🙂
So here is the case:
Barry is a 27 yo bloke who has never had a sick day in his life.
He was playing beach volleyball as he does every week when he went for a big dive.. He made a great save, hit the sand hard with his chest and jumped up to get the next ball. But he felt his heart racing immediately – it felt like it was jumping out of his chest. He played on until the end of the set. When he sat down for a break he noticed his Fitbit watch showed his pulse at 150/ min. After 5 minutes rest it was still 150 flat. He felt vaguely dyspnoeic, but played on. Now an hour later he is in the ED wondering “what is the problem…”
here is his triage ECG
This is Typical “slow-fast” AVNRT SVT. So easy, we know what to do.
My practice for the previous decade or so has been to try a few budget vagal manoeuvres, then slug in a bolus of adenosine. This almost always works. Patient goes back to sinus rhythm and goes home problem solvered! So what is the problem?
Well we all know that the slug of adenosine comes with a 100% risk of making the patient feel like crap, dying, falling, going mad for half a minute or so. But it is so much fun! For us – not the patient! We get to see a medical miracle on the end of a syringe, impress the Med Students and feel like a God with healing hands… Meanwhile our patient is in a state of abject panic.
Now of course, if it doesn’t work we can just double the dose, maybe even consent the patient to round 2 of la petit mort… Good luck selling that.
Fortunately for Bazza, there is a better way. So how do I do SVT in my ED circa 2015?
I will take you through it step by step.
- Bring Barry into a bay and put him on a monitor, sit him up and explain what is going on. Empathy and reassurance will reduce his endogenous catecholamine load and make all the subsequent steps easier. He will not wonder why you are doing all these odd things to him!
- Grab a sphygmomanometer tube and show him how to blow the meter up to 40+ mmHg as per the REVERT trial. Blow into the tube and hold it up for 15 seconds.
- Now explain the process to him. He will blow into the tube for 15 secs, then we will drop his bed back into mild Trendelenburg and lift his feet up to 45 degrees. The augmented Valsalva, voila! In the REVERT trial this move worked 43% of the time. Nearly half of SVTs were fixed with a 1 minute, no risk, simple, free intervention. There is nothing not to like here!
Here is the video from the Lancet edition in which the REVERT trial was published – 2 minutes….
But 57% of Barrys will still be in SVT after the REVERT-style Valsalva move. So next move?
4. In the past we would usually reach for the adenosine about now – but I think there is a better option. Verapamil. So at this point I will ask the team to make up 20 mg of verapamil in a 20 ml syringe. This usually takes 5 minutes – so in that time I will try the augmented Valsalva a few more times to pass the time. Why not?
There is a metanalysis from 2011 in Europ Journ of EM by Aussie researchers that shows both adenosine & verapamil work in 9 out of 10 cases.
Here is where it gets interesting. Both are equally effective – so which one has the most side effects? Which one would you want if you were in SVT and Valsalva didn’t work?
We know that verapamil has more BP effect – about 4% hypotension vs. 1% for adenosine. But the degree of hypotension seen is not really clinically relevant – about 10 – 15 mmHg in systolic BP.
Adenosine has more side effects (OR of nearly 12:1 ) – and when you consider that SVT is a recurrent problem… adenosine seems particularly torturous. I imagine the side effects counted in these trials are things like BP or other non-patient oriented outcomes. So hard to say how many really didn’t like the death pause of adenosine?!
5. I put in an IV and give 2 mg of the verapamil mix every few minutes until either the patient reverts, or the syringe is empty. I have never had a patient experience anything remotely unpleasant during this titration. In my small experience they have all reverted in the teens – I.e. Between 12 – 16 mg used. A few have had small, asymptomatic BP falls. All went home happy.
6. If they are not reverting then it is not unreasonable to retry the Valsalva trick with the verapamil on board..
7. This is a cognitive STOP point. If we have done all of this and still not winning – then I pause here and reconsider the diagnosis. Send the ECG to my local Cardiologist (2000 km away) to check I am not missing anything. Do a bedside ECHO – just check they don’t have a massive LA or something else that might be an underlying cause.
8. At this point – if all still suggested benign SVT I would consider switching to adenosine. The guidelines all say we should start with 6 mg, then go to 12 and then…. But why? It is a drug that wears off quickly, doses mean little. so why not give a decent whack first time and avoid the potential need to use it 5 minutes later on the now terrified patient ? So my practice is to put in a good proximal IV, put 12 mg in a big syringe and flush it in as fast as I can to get maximal effect.
Chris Hicks suggested sedation for the adenosine pause – and I think this is reasonable if you think the patient is the anxious type. Of course, that sedation will likely drop the BP more than the verapamil would!
That is how I now roll when it comes to treating SVT. Love to hear your thoughts..
Still have access to a manual BP cuff? Mercury or aneroid?