Atrial Fibrillation Pearls from Recent Lectures — Part I
We’ve heard a lot of wisdom in some great lectures about afib managmenet recently, so I wanted to recap some key points and links to resources.
In this month’s M+M, Alan looked at how to manage stable atrial fibrillation with RVR. His first stop was the AFFIRM trial (atrial fibrillation followup investigation of rhythm management, NEJM Volume 347:1825-1833, December 5, 2002), a 4000+ patient, multi-center, randomized trial of rhythm control vs. rate control. This study showed no significant difference in mortality at 5 years, but a trend to benefit in rate control, and increased adverse outcomes in rhythm control group.
Since AFFIRM, we have good reason to typically rate control our afib patients. But the ED approach to some cases (younger patients, known recent onset afib) may warrant a different approach — more on that later.
The general ED approach to stable Afib with rapid ventricular response is 1) Rate Control and 2) Ensure adequate anticoagulation and 3) Usually admit and consideration for cardioversion as inpatient (after adequate anticoagulation and TEE, etc).
Alan focused on which agent(s) are best for rate control. He noted the AFFIRM trial made much use of metoprolol 5mg IVP q3-5 min, though it’s noted to be avoided in LV dysfunction, severe COPD, and hypotension. A short acting agent like esmolol may be helpful in case you want to erase your tracks. And remember to look for other causes — if the patient is thyrotoxic, then the beta-blocker is first line.
CCB are also attractive, however. In a head-to-head prospective randomized trial (Demircan et al, Emerg Med J. 2005) of diltiazem 0.25mg/kg vs. metoprolol 0.15 mg/kg, diltiazem at 20 minutes was 90% successful at brining HR down below 100, compared to 80% success with metoprolol. Diltiazem was quicker, too.
Goldenberg et al 1994 (Am J Cardiology), demonstrated that IV diltiazem (0.25 mg/kg starting dose) was safe in treatment of patients with rapid afib and Class III and Class IV heart failure and evidence of congestion by exam or xray. Several other studies have shown the same. Diltiazem was rare to cause worsening CHF, but there was a 10% incididence of hypotension.
Is there any way to prevent that? Studies have shown that giving calcium prior to verapamil blunts the BP depressing effect of this agent — Kolkebeck et al attempted to study whether same could be for diltiazem. His trial of 78 patients receiving 1/3 amp of 10% CaCl2 showed no sig difference in post-diltiazem BP. But that’s a low dose and the mechanism (and verapamil evidence) is tempting to consider.
How about other agents? Digoxin has fallen out of favor in this country — it takes hours, is tricky to dose, and makes cardioversion undesirable (the release of Ca++ could be fatal).
What about amiodarone? It acts like a beta-blocker. It lowers rate, some (barley any) get conversion, too. Give 150mg IV over 10 min, repeat if needed, then 1g over 24 hours. If they get hypotensive, give fluids. An RCT of Austrian ICU patients (Karth, et al, Crit Care Med 2001 Vol. 29, No. 6) concluded that both amio and diltiazem produced sufficient rate control, but diltiazem had more significant adverse hemodynamic effects.
What about magnesium? Mg controls rate, is likely to convert to NSR as well, it’s very cheap, and comparable to amio in trials even when used alone. Magnesium is best known as an adjunct, however. Give 2-4g in 5 minutes, then 1g an hour. You can repeat bolus. Watch out for ESRD patients, though, they build up a lot of magnesium. We blogged about this from Dinali’s journal club three years ago – much more to read, there.
Alan gave a word of caution, to be expounded upon in Joe’s forthcoming post: If your patient’s ECG shows a wide, irregular QRS (meaning, beat-to-beat morphology variations), never block the AV node with a beta blocker or calcium channel blocker. Treat with procainamide or amiodarone, with the former shown to be more efficacious.
And, of course, if the patient is unstable, don’t be afraid to electrically cardiovert. Most of our data comes from stable patients, but biphasic has shown superiority, with a dose from anywhere between 150J to 360J recommended to maximize first pass success. (Alegret et al, European Society of Cardiology 2007).
Posted
on Sunday, February 22nd, 2009 at 10:47 am by Nick. Filed under
Arrhythmias, Blog.
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Dr G,
Why do most of the Md’s use lower doses of diltiazem than the recommended 0.25mg/kg? And why do they not follow this with a PO dose on the stable patients all of the time?
How long after the initiation of a cardizem drip should we administer Ca?
Is Amio better for new onset Afib than Cardizem?
Comment by Smiles on February 28th, 2009 at 6:28 am
I realize that this has nothing to do with your blog, but Annals placed a study of patients with potential acute coronary syndromes and states that in addition to observation and following cardiac markers, that the patient could receive a coronary CT in the ED… Do we ever do this at Sinai? Should we?
Comment by smiles on March 8th, 2009 at 10:47 pm