Atrial fibrillation- acute management

Today we discussed issues related to acute management of atrial fibrillation. A few points:

After establishing that the patient's airway and breathing are stable, the first decision point is whether the patient needs emergent synched cardioversion.
Indications as per ACLS algorithm:
1) Hemodynamic instability, 2) Shock (i.e. hypoperfusion), 3) Pulmonary edema, 4) Ischemia
HOWEVER, remember that clinical judgement is absolutely required; this is not risk-free, and many patients have mild pulmonary edema and borderline hypotension with rapid A-fib and do not all need to be cardioverted.

If emergent cardioversion is indicated, important steps include
1) Consider pre-treatment with antiarrhythmic (e.g. amiodarone); increases the likelihood of success
2) Analgesia and sedation, requiring the capability to deal with the airway; usually requires the help of anesthesia unless in the ICU
3) Application of the pads- "sandwich"- front and back is more successful than sternal and lateral
4) Synchronized cardioversion with 50-100J
5) Anticoagulation for at least 4 weeks post-cardioversion

Watch for
-bradycardia (pts usually have some AV nodal agent "on board" prior that was dosed to their a-fib; if now in sinus, may be bradycardic
-embolic complications

If elective cardioversion (i.e. not emergent), considerations include
1) Embolic risk
If a-fib is present more than 48h (usually difficult to determine) or the patient was not therapeutically anticoagulated for 2 weeks or more prior, there is a significant (but difficult to quantify) risk of systemic embolization with restoration of sinus rhythm. A trans-esophageal echo that shows no evidence of a thrombus makes the risk very low, and is done in situations where emergent cardioversion is not necessary, and the above criteria are not met.
NB- the risk of embolization exists for pharmacologic cardioversion as well, although may be lower than electrical (think about this when using antiarrhythmics like amiodarone)

2) Procedural risk (sedation, analgesia, arrhythmia, etc)

If cardioversion is not indicated, rate control is the next management choice. Options include:
1) Beta-blockers (e.g. metoprolol 2.5-5mg IV over 5-10min)
2) Non-DHP calcium channel blockers (e.g. diltiazem 15-20mg IV over 5-10 min)
3) Digoxin (e.g. 0.25mg IV load)
4) Amiodarone (but note cardioversion risk as outlined above)

There is little evidence to guide us in the acute setting (but lots of evidence in the chronic setting- e.g. AFFIRM)
Reasons to use beta blockers or CCB: Little toxicity, easy to titrate, often the patient has another indication (for B-blocker), rate control is more reliable than digoxin (see below)
Reasons to think twice before using a beta blocker or CCB: LV dysfunction (esp. CCB), pulmonary edema (both), reactive airways (B-blocker), conduction system disease (both)

Reasons to consider digoxin: Is an inotrope, and carries lower risk of hypotension or worsening pulmonary edema. Works particularly well in decompensated aortic stenosis since allows more filling time without affecting contractility
Reasons to think twice before using digoxin: Patient can override it with sympathetic stimulation (that is usually present) since it does not block this, risk of toxicity if levels supratherapeutic, more difficult to use, debatable long-term benefit (definitely no mortality benefit from DIG trial)

Anticoagulation may be initiated in the ED if clearly indicated, but may also wait until the patient is more stable, and risks/benefits (which usually favour anticoagulation) have been discussed.