Can we electrically cardiovert stable AF in the ED?

True Story:

A 56 year old anaesthetist presents to your department, he states he started having palpitations while cycling up a large hill.  He took his pulse which felt irregular and so he cycled to the ED.  His HR 107, BP 130/75 RR 18 Sats 98% ORA Apyrexial.  His ECG shows AF, with no ST changes.  He ‘demands’ electrical cardioversion.

For the basics the brilliant RCEM learning website, has a great article on ED management of Atrial Fibrillation.   It doesn’t go into much detail about the nuts and bolts of electrical cardioversion in the ED.

Lets try and go into a bit more detail.

Now what does NICE say?  The relevant verse is here:

1.7.2 In people with atrial fibrillation presenting acutely without life-threatening haemodynamic instability, offer rate or rhythm control if the onset of the arrhythmia is less than 48 hours, and start rate control if it is more than 48 hours or is uncertain. [new 2014]  

1.7.3 Consider either pharmacological or electrical cardioversion depending on clinical circumstances and resources in people with new-onset atrial fibrillation who will be treated with a rhythm control strategy. [new 2014]

 

http://www.nice.org.uk/guidance/cg180/resources/guidance-atrial-fibrillation-the-management-of-atrial-fibrillation-pdf  [page 23]

 

We can consider EC or PC depending on the clinical circumstances and resources.  The implication here is that EC is more resource heavy.  I would argue that it might be in the ED, but that across the organisation as a whole it is less resource intensive to sort in our department than to clog up an acute ward. This is backed up by studies in Ottawa8, Rochester6 and Pennsylvania which show that length of stay (the biggest determinate of health care cost) is less if we just get on and do it9.

So NICE asks us to consider the clinical circumstances of people with new-onset AF.  So what clinical circumstances do we need to consider?

Cause of AF

AF caused by electrolyte abnormalities, ACS, Sepsis, Structural heart disease, or Thyrotoxicosis is unlikely to resolve with a single shock.  After all you will need to treat the underlying cause first.  It is only really appropriate to offer ED EC to patients with idiopathic AF.  It is also important to note that up to 60% of patients with idiopathic AF revert spontaneously with no treatment at all.

Suitability for Procedural sedationbeaker

This depends on the skills present in your department, as well as the patient’s history.  It is unlikely that it is going to be appropriate to perform EC on a patient who has an ASA grade 3 or more.  Similarly you aren’t going to want to sedate someone whose airway looks like Beaker from the muppets.

Choice of sedation technique and agents depends on your skills and preferences.

Risk of thromboembolic complications (before and after EC)

Most guidance, and most studies seem to have a 48 hr cut off mark.  If the AF has been going for less than that time the received wisdom is that you aren’t going to shoot off a thrombus.  There is some opinion out there that EC might stun the right atrial appendage and a thrombus forms AFTER cardioversion.  This remains to be proven.

If the AF has no definitive time of onset, then the safest thing to do is anticoagulation first (depending on centres this can be clexane + warfarin and a clinic, or an admission and IV heparin), and an elective cardioversion later (usually 4 weeks).

What is the incidence of Thromboembolic events (TE) after EC?  I did find a meta-analysis3 from 1998 (Berger et al) which looked at 32 studies, giving 4621 participants.  92 patients had a thromboembolic episode (2%).  The duration of the AF was less than 2 days in the TE group in only 3 patients (0.06%).

Duration of AF Number of patients with TE episode/4621
<2 days 3 (0.06%)
3 days – 1 month 21 (0.45%)
>1 month 42 (0.9%)
Unknown 26 (0.5%)

 

The paper doesn’t tell us how many patients were in each group, so the data has little meaning when broken down as above, so we can only really take from this the overall percentage of 2% for thromboembolic events.

Berger et al was more interested in the timing of thromboembolic event after the cardioversion, this peaks in the first few days following the cardioversion no matter the duration of the AF.  I also found a study looking at NOACs (novel oral anticoagulants eg dabigatran) vs warfarin for anticoagulating patients prior to cardioversion but they got a 30 day thromboembolic rate of 0.8% with warfarin10.

A retrospective study from Denmark of 16 274 DC cardioversions7 without and with anticoagulation was published this year.  Unfortunately they didn’t look at the timing of the AF, but conclude quite reasonably that the risk of TE’s is higher in non-anticoagulated people with AF than people who are.

360/16274 Anticoagulation        n=11 190 No Anticoagulation n=5084 NNT
0-30 days0-360 days 32 [0.28%]144 [1.28%] 54  [1%]216 [4.24%] 12934

Weigner et al looked specifically at incidence of thromboembolic events (TE’s) after cardioverting recent onset AF (<48 hours). They conducted a prospective observational study which was published in 19972.  They identified 375 adults with recent onset AF, 66.7% reverted spontaneously, the rest had some form of active management (electrical or pharmacological or both).  Three patients out of the 375 had a TE event, none of them received electrical cardioversion, all were managed with anticoagulation, and various drug combinations.  All 3 of these patients had essentially benign echoes during that admission, suggesting that the ‘safe’ (drugs and anticoagulation) approach isn’t actually that safe.  All 3 patients were elderly people that had multiple co-morbidities that even the most EC fanatical ED doctor would baulk at doing a cardioversion on.

A 2013 Finnish observational study of acute cardioversion5 (EC within 48 hours of AF onset) pegs the rate of thromboembolic events at less than 1%.  There were 38 thromboembolic events within 30 days in a total of 5116 cardioversions, in 2497 patients, this gives us an incidence rate of 1.5% per patient (or 0.7% per cardioversion).  The study goes on to suggest that using either the CHADS2 score or CHA2DS2-VASC score to risk stratify allows us to reduce that risk further if we only attempt to cardiovert low scoring individuals without anticoagulating them first (it remains to be shown if anticoagulating the high risk group actually reduces thromboembolic events).

afdecThey produce this brilliant decision tree, which I think I might use when discussing the options with patients.  The risk of thromboembolism with delayed elective cardioversion and anticoagulation is also about 1% (confirmed by our study into NOACs10 and the big Danish study7).

I can see myself talking patients through this decision tree to help them make an informed choice about their options.

The question about whether we should be offering this cardioverted group anticoagulation is difficult.  On the one hand the Finnish research suggests that CHADS2VASC scores or similar can help us estimate the risk, but the large study from Denmark seems to suggest blanket prescription (but neglected to sub categorise the time of onset of AF).

This may again come down to giving your patient the choice between nothing, something for 4 weeks and something for longer, depending on their CHADS2VASC score.  So the risk of TE’s following ED EC seems to be about 1%, which is similar to the risk of doing an in-hospital EC with anticoagulation.  So if the risk is the same, is one approach better than another?

Is electrical cardioversion more effective than chemical cardioversion for acute onset AF?

Strangely there is not much to go on here.  Most trials use combination therapy if they study EC at all.  I could only find 3 trials that were in any way useful, and only one compared EC to PC directly.

The first trial I found was a single centre randomised controlled trial that compared electricity alone to pharmacological cardioversion from Italy in 20111.  Patients were excluded if their CHADS2 score was >2, if they were unstable, or if it was felt that the AF was secondary to another process (eg Hyperthyroidism, Sepsis, ACS etc).  All patients had an ED transthoracic ECHO, looking for significant valvular disease.  However the authors neglect to say how many patients they excluded because of their ECHO findings.

Results
N= 247 EC 121 PC 126
Success 108 [89.3%] 93 [73.8%] HR 0.34(CI 0.17-0.68 p= 0.02
Adverse Events 1 6 HR 2(0.22-18.29) p=0.29
Recurrence of AF @2/12 26.3% 

31 lost to follow up

28.3% 

52 lost to follow up

HR 0.9 CI 0.45-1.8 p = 0.86]

 

Patients in the EC arm were more likely to be successfully cardioverted than in the PC arm.  There were more adverse events (flutter, bradycardia and ischeamia) in the PC arm (but this was not significant).  The recurrence rates were broadly similar, but there were a lot more PC patients lost to follow up than EC, so this may have skewed the results in the favour of EC.

The other trial evidence is not as impressive.  Jacoby’s chart review9 compared 30 ED electrical cardioversions with ‘eligible’ controls.  This study also included people with known paroxysmal AF that were managed with a rhythm control strategy (so a few of them got shocked on more than one occasion).  The ED cardioversions were successful 97% of the time.  Follow up was only to 3 weeks, but found no thromboembolic events, however one patient did end up having a mitral valve replacement.  This study was primarily looking at length of stay, and cost per admission.  EC was found to have shorter lengths of stay (23 h vs 56 h), the median cost of admission was also significantly less in the EC group [$1,598 vs $4,274].  This was effectively a small observational study of relatively poor quality, but the conclusions agree with the Italian study.

stiellThis brings me on to my third study – Stiells Ottawa Aggressive protocol for AF6,4.  This was a consecutive cohort study looking at the safety and efficacy of using procainamide and then using electrical cardioversion if cardioversion had not been achieved.

This study included 628 patients with AF. Procainamide successfully cardioverted in 376 (60%) of patients. In the 252 patients where procainamide had failed, EC was attempted in 223 patients of which there was a 92% success rate (203 success, 20 fail). Cardioversion was not attempted in the remainder of the patients (29 patients).

No one was anticoagulated in this study if the onset time was less than 48 hours.  No one in the study had a stroke, no one died, and only 8.6% of patients relapsed, but the follow up was only 7 days.

Conclusion

So in an ED with the right skill set it’s perfectly possible to electrically cardiovert patients with acute onset AF with or without pharmacological cotherapy, in fact electricity might have a better success rate.  The risk of thromboembolic events is also similar to doing a delayed cardioversion with anticoagulation, but recent data suggests it may be worth considering prescribing anticoagulation for a short time afterwards and risk stratifying our patients based on CHADS2VASC score.  If their score is <2 I would offer them EC. If there score is >2 I think I’d try to limit their risk by admitting them for anticoagulation.

Pros and Cons

Pros to ED EC Cons to ED EC
As successful as in-hospital careSame relapse rate

Possibly slightly higher success rate

No side effects from rate control drugs

Risk of thromboembolism 1% same as in hospital care

Can go home faster

Hospital care still an option if ED EC fails

Cheaper for the hospital

Risks of procedural sedationMight not need it (up to 60% revert spontaneously)

Possibly higher risk of thromboembolism after EC if sent home with no anticoagulation

More resource intensive in the ED

 

References

  1. Bellone, Andrea, et al. “Cardioversion of acute atrial fibrillation in the emergency department: a prospective randomised trial.”Emergency Medicine Journal (2011): emj-2010.  [http://emj.bmj.com/content/29/3/188.short]
  2. Weigner MJ, Caulfield TA, Danias PG, Silverman DI, Manning WJ. Risk for Clinical Thromboembolism Associated with Conversion to Sinus Rhythm in Patients with Atrial Fibrillation Lasting Less Than 48 Hours. Ann Intern Med. 1997;126:615-620. doi:10.7326/0003-4819-126-8-199704150-00005 [http://annals.org/article.aspx?articleid=710444]
  3. Berger, Marvin, and Paul Schweitzer. “Timing of thromboembolic events after electical cardioversion of atrial fibrillation or flutter: a retrospective analysis.”The American journal of cardiology12 (1998): 1545-1547.
  4. Safety of Urgent Cardioversion for Patients With Recent-Onset Atrial Fibrillation and Flutter Stiell, Ian G. et al. Canadian Journal of Cardiology , Volume 31 , Issue 3 , 239 – 241 [http://www.onlinecjc.ca/article/S0828-282X(14)01616-X/abstract]
  5. Airaksinen, KE Juhani, et al. “Thromboembolic complications after cardioversion of acute atrial fibrillation: the FinCV (Finnish CardioVersion) study.”Journal of the American College of Cardiology 13 (2013): 1187-1192. [http://www.sciencedirect.com/science/article/pii/S0735109713025266]
  6. Stiell, Ian G., et al. “Association of the Ottawa Aggressive Protocol with rapid discharge of emergency department patients with recent-onset atrial fibrillation or flutter.”Cjem 3 (2010): 181-91.  [http://www.cjem-online.ca/v12/n3/p181]
  7. Hansen, Morten Lock, et al. “Thromboembolic risk in 16 274 atrial fibrillation patients undergoing direct current cardioversion with and without oral anticoagulant therapy.”Europace 1 (2015): 18-23.
  8. Decker, Wyatt W., et al. “A prospective, randomized trial of an emergency department observation unit for acute onset atrial fibrillation.”Annals of emergency medicine 4 (2008): 322-328.
  9. Jacoby, Jeanne L., et al. “Synchronized emergency department cardioversion of atrial dysrhythmias saves time, money and resources.”The Journal of emergency medicine 1 (2005): 27-30.
  10. Nagarakanti, Rangadham, et al. “Dabigatran Versus Warfarin in Patients With Atrial Fibrillation An Analysis of Patients Undergoing Cardioversion.”Circulation2 (2011): 131-136.