Fast Atrial Fibrillation
AF with RVR – Summary
Seek and treat a cause or exacerbating factor
- (other causes are not immediately treatable in ED but need to be considered later in the workup eg alcohol, valvular disease, COPD, diselectrolyteaemia)
Unstable (eg chest pain, hypotension, CCF)
- Ameliorate eg
- fentanyl for chest pain
- fluids +/- phenylephrine for hypotension
- eg CPAP or BIPAP +/- O2 for CCF +/- nitrate +/- ACEI
Stable or unstable:
- New onset (<48 hours duration): electrically cardiovert (200J, synchronised if patient has a pulse) (see Choice of Anaesthetic below for how to anaesthetise / analgese (for a junior doc unsupervised eg medium dose fentanyl (eg 50µg, as in this case) and low dose midazolam (eg 2mg))
- > 48 hours duration: rate control eg diltiazem 15mg, then 25mg if needed
About once a year I like to present fast-AF case. The last one was Salvage Cardioversion of a Surgical Patient.
AF with RVR a fairly common problem, there are many potential treatments and it can cause a lot of confusion. Every boss has his or her way of managing it.
There is no one right way to treat fast-AF.
A fundamental principle is to find and treat any underlying condition that has caused the AF or made chronic AF faster (eg sepsis, volume depletion, heart failure, hyperthyroidism).
As a general rule new AF (<48 hours) can be cardioverted, > 48 hours -> rate control rather than cardioversion as we don’t want to throw off a clot that has formed in the quivering atria. Also the chances of converting a chronic AF aren’t great.
We had a woman in her late 50s who came in with a productive cough for 2 weeks, dyspnoea, and pleuritic chest pain. She had a distant history palpitations treated with IV medication and “asthma”. Her only medications were asthma inhalers. She stopped smoking 15 years previously. She had no risk factors for PE.
She was tachycardia at 114 at triage, afebrile but BP 70/35, she had no signs of failure and was generally wheezy, RR 30, 99% on RA. Her ECG showed atrial fibrillation with RVR (rapid ventricular response) with widespread, marked ST depression
Not unreasonably the doctors who first saw her in ED had given her nebulisers and some IV fluids. She came to my attention when a monitor announced HR of 180 with BP 70/35. At the bedside the patient was feeling a little better but felt a little faint and tired. Her HR was staying mainly around 180. She was aware of her heart beating rapidly and said this happened only a few times a year and had just started on the day of presentation.
There are many ways to manage this situation, and the approach tends to be different depending on which country you are in. The doctors who were looking after her were keen to give the fluids a chance to work which was not unreasonable, but I wasn’t happy with a HR of 180 and a BP 0f 70 systolic.
So this is what I did, just one way to manage this patient:
Oxygen by mask and nasal prongs (nasal prongs to provide apnoeic oxygenation should we end up needing to intubate her. See No Desat!)
Continue the IV fluid bolus.
Phenylephrine 100µg to attempt to improve the diastolic BP to improve coronary perfusion (see Phenylephrine refresher if you are not familiar with this drug).
Ondansetron 4mg (as etomidate is quite emetogenic)
200J (all shocks synchronised). Still AF.
200J Still AF.
Patient a bit wriggly -> Etomidate 6mg
Sinus rhythm. BP 150/70.
The patient moaned a little during the cardioversion but had no recollection of the shocks and felt great afterwards.
CXR showed a RUL pneumonia and it turned out she had a lung abscess, but no sign of TB. She was treated with a very long course of IV antibiotics.
The choice of anaesthetic
If you need to electrically cardiovert someone in the middle of the night and you don’t have immediate anaesthetic or ED senior support, I would argue a patient like this can’t wait until a senior comes in. If you are not allowed to use an anaesthetic agent I would recommend telling the patient it is going to hurt and giving them medium dose fentanyl (eg 50µg, as in this case) and low dose midazolam (eg 2mg).
If you can use an anaesthetic, your choices are propofol, ketamine or etomidate. I didn’t choose propofol because of its vasodilating and cardiac depressant effects (ie potentially worsening perfusion). I didn’t choose ketamine as it might exacerbate the tachycardia. I chose etomidate and fentanyl because these drugs are usually cardiovascularly stable. Some would say that etomidate is contraindicated in a septic patient due to its adrenal suppressive effects. If you are concerned about this you can give some steroid.
The dose of etomidate for RSI in a haemodynamically normal patient is 0.3mg/kg, for a procedural anaesthesia (maintaining spontaneous respiration) of haemodynamically normal patient is around 0.1mg/kg. It could argued 6mg of etomidate for this 60kg hypotensive patient was a little generous.
What if she had had chronic AF?
The other common situation is the patient with chronic AF who is tachycardic and unstable (eg hypotensive, chest pain or CCF).
As mentioned above we don’t want to cardiovert for fear of throwing of a clot from the quivering atria, and also there is less chance of successfully cardioverting someone who is in chronic AF.
So we aim for rate control rather than rhythm control.
The hypotensive ones we give fluids and pressors (eg phenylephrine) then rate control (eg IV diltiazem) once the BP is respectable.
For chest pain treat the chest pain with fentanyl and rate control with diltiazem.
For fast AF with pulmonary oedema I’ll usually try treating the failure with nitrate and ACE inhibitor +/- diuretic if the BP is OK. If that doesn’t sort the rate out they may need some rate control eg diltiazem. Some people prefer amiodarone. Some like IV magnesium. All these treatments may cause hypotension.
IV calcium before the calcium channel blocker
Some studies suggest that giving some IV calcium gluconate (eg 1-2g) before diltiazem may reduce the hypotensing effects of diltiazem, while still giving rate control. The evidence isn’t great (but there isn’t much evidence about any of these treatments despite this being a fairly common scenario). See http://academiclifeinem.com/calcium-before-diltiazem-may-reduce-hypotension-in-rapid-atrial-dysrhythmias/ by Bryan Hayes
I only heard about giving calcium after this case. I’ll give it a try next time.
ß-Blocker vs CCB
Beta blockers and calcium channel blockers appear to be equally efficacious and safe for fast AF according to this paper from 2013 Safety and efficiency of calcium channel blockers versus beta-blockers for rate control in patients with atrial fibrillation and no acute underlying medical illness
Bryan Hayes in the Academic Life in Emergency Medicine post cited above states that CCBs are superior but says he’ll give the evidence for that in a future post. In our shop we are mainly using diltiazem (eg 15mg over 2 minutes then if needed 25mg over 2 minutes +- 5-15mg/hour)
IV magnesium is another option for rate control. It tends to drop BP but few other side effects. Meta-Analysis of Magnesium Therapy for the Acute Management of Rapid Atrial Fibrillation
However UpToDate says that Mag only lowers the HR by an average of 12 BPM
Why not digoxin?
Some older physicians like digoxin for AF. UpToDate still recommends it for AF with CCF. See Why Billy Mallon doesn’t like digoxin for a critique of digoxin. Basicly it is slow acting and is a poor negative chronotrope and a poor positive inotrope.
Canadians love procainamide to chemically cardiovert AF. Unfortunately procainamide is no longer available in NZ, but I never used in to cardiovert AF as electricity is a lot quicker.
Download audio here (right-click and save or save as) or
Music: Tennis Club by Lorde. https://itunes.apple.com/nz/artist/lorde/id602767352
Lorde is a Kiwi high school student who has just topped the US Alternative Music chart – the first solo female to top the chart in 17 years. What’s that about?