Fast Atrial Fibrillation

3 Aug

It is Atrial Fibrillation with a rapid ventricular response. The atrial rate can be more than 300 beats per minute followed by the ventricular rate of up to 170 beats. That is fast. I like to say in my mind Fast AFib. It just sounds cooler.

The intravenous cardizem is infusing giving a better control, or not.What about the or nots? I bet EPS Dr Wes, could give us the facts.

Why does it always have to be intravenous  cardizem?  I have seen Multaq post cardioversion sustain a nice sinus bradycardia. I have a love/hate relationship with Amiodarone.

I am a fan of the digoxin added to a beta-blocker.  I am starting to dig digoxin more and more because it does not drop the blood pressure.


2 Responses to “Fast Atrial Fibrillation”

  1. Dr. Wes August 4, 2010 at 02:03 #

    FAF vs AF w/RVR vs RAF. The there’s ERAF (Early return of AF – usually after cardioversion)… Plenty of pseudonyms for everyone!

    But no matter what it’s called, duration of AF matters. Pharmachologic cardioversion is just as dangerous as electrical cardioversion in terms of potential stroke risk, and AF longer than 48 hours (a convention w/o much data) is risky to convert if the patient is not therapeutically anticoagulated. Using Amiodarone for rate control risks cardioverting the patient in that setting, so beware.

    Often, effective rate control drugs are not administered for fear of hypotension. Yet more often than not, it is the rapid rate that causes the hypotension, not the meds administered. Often, biting the bullet and slowing the rate will paradoxically improve blood pressure since the heart has more time to fill with blood, and therefore can eject blood better. Dig alone is often worthless, but it does potentiate the effects of beta blockers is reasonable to use with beta blockers as you have suggested. Combining beta blockers and calcium channel blockers is occassionally done in refractory cases (thinking lung CA with pulmonary infiltrates, for instance), but risks causing very long conversion pauses with asystole if the atrial fibrillation spontaneously converts back to sinus rhythm.

    Recall that a very important differential exists for AF with RVR when typical doses of meds fail to work: hyperthyroidism, PE (and other causes of hypoxia, including large effusions) and pericardial effusion.

    Okay, enough of my secrets!


    • seejanenurse August 4, 2010 at 12:39 #

      Thank you for sharing your secrets!

      Those long conversion pauses…anticipates….chemical cardioversion.

      We want more secrets. 🙂

      The fear of hypotension and the holding of medications happens a lot, and the cycle just continues. The unfortunate loss of kick, filling time.

      Thank you for the differential…I will think about that, the next time we keep “upping” the cardizem, with no response.

      That reminds me of an experience I had as a very new nurse. I received a transfer from a medical floor, a post-operative patient, being transferred for Sinus Tachycardia. The medical floor was freaking out, calling me to get the patient immediately, so that intravenous lopressor could be administered. The nurse got a STAT cardiology consult for this Sinus Tachycardia. I got the patient to telemetry, gave the lopressor, nothing changed. The telemetry monitor was still, bling, bling, bling. What? I called the cardiologist, who lectured me about Sinus Tachycardia: fever, bleeding, pain etc.

      I sent a STAT CBC, the patient was white as a sheet. Guess what? The hemoglobin was 5.

      I won’t forget. 🙂

      All the lopressor in the world, can not fix that.

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