Davis, T. SVT in infants – a crash course, Don't Forget the Bubbles, 2019. Available at:
Carly is a 9 month who is brought in by her parents as she has been unsettled and not feeding well for the last day or so. Her obs at triage show a HR of 277 and she is brought straight round to resus.
Her ECG is as follows:
This post is based on several resources but in particular from Donovan Dwyer’s talk at DFTB17.
What happens in a normal heart?
The sino-atrial (SA) node is the pacemaker of the heart. It is situated in the right atrium and is generates an electrical impulse that conducts through the whole heart and causes it to contract.
The impulses from the SA node, travels to the atrioventricular (AV node). The AV node slows the current (0.1 second pause) and then allows it to pass through the ventricles (via the Bundle of His and the Purkinje fibres). This process allows the atria to contract fully and then allows the ventricles to contract from base to apex.
There are two tracts through the AV node. One is ‘fast‘ and one is ‘slow‘. As you will see from the image below, in a normal heart circuit, the fast pathway will reach the end of the AV node first (and on to stimulate the Bundle of His), and as it starts to travel up the slow pathway they cancel each other out. The end result is that there is a clear path conducting the impulse through the AV node. This produces normal sinus rhythm.
What changes this in SVT?
SVT is usually caused by a re-entrant circuit. In this case a second impulses is triggered before the normal impulse has been fully conducted through the AV node and the tracts reset. This happens where there is increased automaticity in the atrium causing an impulses (from fever, stretch, stimulation etc).
This stimulates the AV node when one part of the tract is refractory. The fast pathway has a longer refractory time, so while the slow pathway may be working again, the fast pathway is in its refractory period.
From Donovan Dwyer’s DFTB17 talk
So the impulse goes down the slow tract and is blocked down the fast tract. By the time is reached the end of the AV node, the refractory period has passed, and it is now able to travel back up the fast pathway.
This causes a retrograde pathway and results in a circuit. SV is an AV node re-entry circuit.
AVRT is similar to AVNRT, but it doesn’t involve the node, it involves an accessory pathway. The idea is the same.
How do we treat this?
The goal of treatment is to stop conduction through the AV node for long enough that the SA node will take over as the primary pacemaker. We can do this in ED physiologically or medically. Importantly – make sure you are recording a rhythm strip while you try to revert the ECG as the cardiologists will need to see this.
The first thing to try is to physiologically revert the SVT. This can be done using valsalva in older children by blowing into a pipe/syringe.
This can be blowing into a pipe attached to a sphygmomanometer to hit 40mmHg for a sustained 15 seconds. Or patients can blow into a 10ml syringe and aim to start moving the plunger. Both are effective.
This works because the extra squeeze on the heart increases the cardiac output and increased carotid and baroreceptor stimulus increasing the BP in the initial stage. After the pressure is sustained, blood volume is forced into the legs and head (causing neck vein distension). The drop in preload means the atrium is stimulated and the heart pumps harder and faster to make up for it, and the blood pressure drops. At the end of the manoeuvre, there is a sudden release, and all the blood flows into the heart causing a huge flow of blood into the carotid and baroreceptors leading to vagal inhibition.
Using a modified valsalva works better – if you lift the patients legs in the air and lie then flat immediately after the release, you will increase the venous return and improve the chances of reversion.
The REVERT study showed that this method reverted SVT in 43% (vs 17%) of (adult) patients.
The diving reflex is another version of this. Young infants cannot do a valsalva manoeuvre (although it can happen when they cry). The diving reflex causes vasoconstriction. It does this because your hands, feet, and face have ten times the heat and cold receptors of the rest of your body. They act to protect you. When you jump into cold water you vasoconstrict to preserve heat at your core. There is a massive shunt of blood to your central circulation that your heart has to manage pumping into your lungs, and that causes you to take a deep breath. When you put a baby into a cold environment, they get profound vasoconstriction in the same way, and blood is shunted to the core. You do, however, need a well-functioning heart for this to work – all the blood that returns needs to be pumped out effectively. This is a potential problem in adults with heart failure. In children with heart failure there is a second pathway – this goes through facial stimulation of cold blood to the hypothalamus. This causes the heart to slow down and decrease metabolism. Because of this, children in heart failure may still respond to the diving reflex (whereas adults will not).
You can use a face mask submerged in ice cold water which is put onto the baby’s face for 30-40 seconds – this is as effective as dunking them in a bucket of ice and a lot more kind.
Adenosine is our first line medical treatment for SVT. It opens the potassium channels briefly and depolarises the AV node – aiming to break the circuit and for the SA node to take over. It only has a half life of 10 seconds. Start with 100mcg/kg as the first dose and then increase to a max of 500mcg/kg (less in neonates). There are five outcomes for what might happen when you give adenosine.
This is what we all hope for where the patient returns to sinus rhythm. Often there is a recovery tachycardia due to a net deoxygenation from being tachycardic for so long. All children with SVT, even if they revert needs cardiology follow up. This is to determine any underlying cause, but also for prophylaxis. Children (particularly infants) cannot tell us when they are in SVT and they may present after several days. Prophylaxis aims to prevent them presenting in collapse or failure.
It’s happened to all of us. When the adenosine doesn’t work, consider the 5 Ds.
- Delivery: remember that it only has a 10 second half life. Give it through a cannula in a large vein, with the arm up in the air, using a three-way tap to ensure a fast bolus and a flush straight after the adenosine.
- Distance: are you giving it through a cannula in the arm, or the foot. If you are using a cannula further away from the heart then a higher dose may well be needed as we need the adenosine to be active by the time it reaches the heart.
- Dose: we are always told to start at 100mcg/kg but actually the evidence shows most children need 170-200mcg/kg to revert. So if you are using IO access, or a cannula in the foot, then consider starting at 200mcg/kg.
- Drugs: theophylline competes at the adenosine receptor, so if you have a child who is on theophylline then you will need a higher dose.
- Diagnosis: patients in fascicular VT will not respond to adenosine and neither does Lown-Ganong-Levine syndrome.
Recurrent or retriggering
Sometimes we see a response to adenosine where the child returns to sinus rhythm but then revert within a minute or two. In this case there is no point in simply continuing with repeated adenosine doses – there is some triggering the SVT and that it what needs to be treated. A second agent is likely needed here and this patient should be discussed with a cardiologist.
After the SVT corrects, it exposes an underlying atrial tachycardia. This looks like SVT to being with but actually when you ablate the AV node it reveals an atrial tachycardia. This cases needs the atrial tachycardia to be treated with a second line agent or another therapy (e.g. cardioversion, pacing). Second line agents can include amiodarone but it is difficulty to get the right dose. If amiodarone is given slowly and at a low dose it’s often ineffective, but given faster and at the higher dose can cause hypertension, asystole, and collapse. Sotalol cardioverts and rate controls so is an alternative second line agent.
Unmask congestive cardiac failure
This is where the child recovers from SVT, but then the BP starts to drop and the child gets more tachycardic. Up to 25% of children with congenital heart disease can present with SVT. But also, children who have had SVT for more than 48 hours are often in heart failure when they present. The prolonged tachycardia causes poor myocardial perfusion, so when they return to their normal rate they have a floppy myocardium that struggles to recover. Myocarditis or myopathies can be unmasked. Rarely they can deteriorate to VT or VF so make sure you are ready for this.