random question about perioperative cardioversion

[stoic]

What's up everyone -

I've got a random question that ya'll are probably most qualified to answer.

If you've got a patient under general, and they go into afib, do you pharmacologically or electrically cardiovert them? would such a patient need to be anticoagulated?

(ps. i'm not talking about a specific patient or experience, i'm just curious)

thanks from a soon to be med student with a new found interest in gas.

luv,
s

---

Members don't see this ad.

 

[apma77]

this is the pearl for A-fib

Atrial Fibrillation:

Irregularly irregular rhythm with variable R-R interval and no p-wave
Seen with MI, hyperthyroidism, mitral valve disease, and dig toxicity
Treatment is based on hemodynamics:

Stable BP : Esmolol or Diltiazem

Unstable BP: Cardioversion (starting with 50 Joules)

therefore, base your treatment in OR depending on the given situation. anticoagulation need not be started in the OR!

 

[stoic]

this is the pearl for A-fib

Atrial Fibrillation:

Irregularly irregular rhythm with variable R-R interval and no p-wave
Seen with MI, hyperthyroidism, mitral valve disease, and dig toxicity
Treatment is based on hemodynamics:

Stable BP : Esmolol or Diltiazem

Unstable BP: Cardioversion (starting with 50 Joules)

therefore, base your treatment in OR depending on the given situation. anticoagulation need not be started in the OR!

thanks for the response.

another quesiton:
i've seen diltiazem used in the ED for patients with afib and mild tachacardia with the intent of slowly their heart rate, but not converting them a normal SA rythym (the cardiologist wanted a TEE before cardioverting them). is the effect of diltiazem heavily dependent on dose? IE would a higher dose cardiovert the patient while a lower dose just slows their heart rate?

thanks again,
s

 

[DrQuinn]

Cardizem is used more for rate control in a. fib, sometimes the patient will convert to NSR but its more important to make sure they are hemodynamically stable and their heart rate is controlled. Old peeps dont' like having their HR 170.

Now in regards to SVTs, the cardizem can and does convert the tachydysrhythmia to NSR by prolonging the refractory period in the AV node and also the accessory pathway (if present), thus allowing NSR to return...

Q

 

[xjohns1]

remember....you will do cardioversion in the OR only when the BP is not stable

 

[MAC10]

thanks for the response.

another quesiton:
i've seen diltiazem used in the ED for patients with afib and mild tachacardia with the intent of slowly their heart rate, but not converting them a normal SA rythym (the cardiologist wanted a TEE before cardioverting them). is the effect of diltiazem heavily dependent on dose? IE would a higher dose cardiovert the patient while a lower dose just slows their heart rate?

thanks again,
s

First of all these are great questions coming out of an MSI.. I didnt start thinking of this stuff untill this year...when I had to mange it

To answer this question
Neither beta blockers nor diltiazem (ca channel blocker) have any direct antiarrhythmic effect that would promote conversion to NSR. Conversion after either drug would be considered spontaneous rather than drug-induced. However, both are effective for first-line acute rate control.

The drugs that chemically cardiovert are antiarrythimic class drugs
amiodarone, ibutilide, procainamide, flecainide, propafenone, sotalol

_______________
VA call at 3AM:

ZZZZZZZZZZZZZZZZZZ
beep beep beep beep....
Ring Ring....
Ha Ha Ha hold on girl....Yes Dr.. I was just calling to tell you that MR blank's feet itch.......Yes his feets itch..he needs something ordered.....
Click
^$&*^#@$*(*(#&$*(#&*()$&(*&(*&&%$#$*&*%

 

[Tenesma]

first of all beta-blockers and certain calcium-channel blockers ARE anti-arrhythmics... In fact they are considered Class II (beta-blockers and that includes sotalol ) and Class IV (diltiazem and verapamil). While they are anti-arrhythmic, they are not well known for spontaneously converting fibrillating rhythms.

There is more than enough literature to show that in a. fib Rate control is more important than Rhythm control (and it is also cheaper and associated with less side-effects).

In the OR, with new onset A. fib w/ RVR (rapid ventricular rate) - I will look for any good reason to electrically cardiovert them. If the rate is too slow (<120) or no evidence of cardiac compromise or no history of valvular problems (IE: patient with severe aortic stenosis i will cardiovert them even before their pressures drop)

If there was any doubt about recurrent A. fib on a patient that hasn't been anticoagulated and the patient is moderately stable, i will throw a TEE down and take a quick look before shocking

 

[stoic]

Are there studies out there that correlate the length of time a patient is in afib with their likelyhood of forming a clot?

ie how long does it take for clots to start forming in patient with afib?

thanks again for humoring my limited knowledge base.

 

[Tenesma]

sure there are studies... but if you really want to be impressed, go to a cardiac OR and look at them doing a TEE while the heart is fibrillating (and full of blood), you can literally see clot starting to form

 

[GasPundit]

Are there studies out there that correlate the length of time a patient is in afib with their likelyhood of forming a clot?

ie how long does it take for clots to start forming in patient with afib?

thanks again for humoring my limited knowledge base.

According to my fuzzy ACLS memories (oh, how the interview season saps your skills away...), I think 48 hours is the "official" length. However, the guidelines are also very keen on TEE. Too bad everywhere doesn't have MGH's easy access to TEE, and that patients do go swinging on through to Community General with no echo backup.

By the by, one of our peds surgeons made a big deal of teaching that 3-5 days post-op, the extra- to intra-vascular fluid shift can often trigger afib. I simply don't think I've had enough experience to see this, but every now and then on the unit I used to wonder if this was contributing to a new onset afib (of course, the varios sympathomimetics probably didn't help either). I'm stepping out on a limb, but stretching out the atria, especially with the new stuff on pulmonary veins/left-atrial junction origins for afib...seems like it could allow this subset of afib patients to be treated with diuretics/vasodilators, anything to improve forward flow.

Anyone with more confidence want to step out onto this flimsy branch of mine?

 

[Tenesma]

there aren't any studies to prove it, but anecdotally it doesn't unreasonable.... usually by day 3 the body is shifting some fluids around, and it could be said that the increased distention of the pulmonary veins/left atria may lead to atrial fibrillation. However, a. fib is a well-known post-operative change in CABG patients (duh...) as well as most thoracic patients.

 

[GasPundit]

there aren't any studies to prove it, but anecdotally it doesn't unreasonable.... usually by day 3 the body is shifting some fluids around, and it could be said that the increased distention of the pulmonary veins/left atria may lead to atrial fibrillation. However, a. fib is a well-known post-operative change in CABG patients (duh...) as well as most thoracic patients.

...I'll bite. Why, exactly, is afib linked to CABG? Is it the torquing on the heart? "Inflammatory mediators"? Oodles of sympathetic stimulation?

 

[Tenesma]

it is "fingers playing with heart" and "irritating it"