Rapid Afib

I totally agree with you. We did have them on our floor until about four months ago. It was decided that to be in accordance with patient safety standards that all meds must come up from the pharmacy after a doctor's order has been faxed to them.( We do not even have stock tylenol now). Thus the wait for the meds.

Sad but true and one day it will cost someone their life.

This would infuriate me. I can think of numerous times I've gone to our pyxis that HAS meds and had to override to obtain meds based on verbal stat orders. For example- I had to get dopamine the other night. I've had to get lasix for flash pulmonary edema, haldol to calm a pt who required 6 people to hold her down, iv lopressor... I couldn't imagine having to wait for a fax to pharmacy, then have the med sent/delivered before giving it. I'd like to think I didn't waste my time getting a BSN only to be treated like a child with excessive safety measures. As an educated adult, I'd like to be treated as one.

If I remember correctly, you posted this patient has a history of AFib w/RVR, and he was asymptomatic. What antiarrhythmic meds has he taken in the past regards to his AFib HX? Calcium Channel Blockers, such as Diltiazem, usually are an excellent measure to slow the ventricular rate in AFib. However, looks like your patient's cells were not very receptive to Diltiazem. I'm curious as to why Amiodarone was not considered D/T its ability to decrease automaticity rate of ventricular ectopic foci, therefore useful for its anti-fibrillatory actions. However, Amiodarone may be proarrhythmic R/T its ability to prolong the QT interval. Plus, liver enzymes must be watched with Ami's long half-life. Another consideration would be Rythmol, a Class IC medication. However, this, too, can have proarrhythmic potential.

So, is it safe to assume the dig f/by lopressor decreased his rate? Usually digoxin alone does not suppress ectopy such as AFib.

BTW, what did the 12 lead ECG indicate & what about labs such as lytes and cardiac enzymes like Troponin I?

BTW2, even though this patient is asymptomatic I wonder if a visit to the EP lab has been considered?

This so reminds me of a patient I had last week : /

Lady came in through the ER with AFib c RVR rate 180s- totally asymptomatic. Recieved 2 cardizem boluses, IV Dig and Lopressor and some po Toprol. She comes up to our tele floor still taching away, she gets more Dig and we start the Cardizem gtt, titrate up to 20. Nothing is touching this lady. To top it all of, she doesn't speak any English expect for a few basic phrases, and keeps gesturing to me and saying 'toilet, now, toilet'. So I am offering her the bedpan, and she is saying 'No, toilet, now' and I am trying to explain to this woman that I am not letting her get up and walk to the bathroom with her heart beating so fast. Finally she agrees to use the bedpan, I help her turn over onto it, and she's gone- like she fainted, a mask came over her face that was ashen......seven second pause on the monitor (longest I have ever seen)....then she's back in sinus brady at 40 and totally symptomatic with a low BP, respirs of near 40, needing multiple boluses. Total craziness, thank the Lord my other patients didn't need a whole lot then : )

But this is why I love my cardiac floor : P I am an adrenaline girl.

What did he weight? 10 mgs to start is a low dose...20 is more a standard dose...

You mentioned wide complexes. I would want a cardiologist to look at that, because it's suggestive of a conduction problem. When folks start throwing everything in the formulary at afib c RVR, and this typically includes lopressor and cardizem, you're just asking for trouble. Those two together can cause blocks in patients who don't already have 'em, let alone those whose strips suggest they do (some sources say we should NEVER combine a cardizem drip with a beta blocker). I've had 3 pts on a cardizem drip in the past 2 weeks with recent administration of beta blockers where the HR/BP took a rapid dive, another reason to keep everyone on a cardizem drip on a telemon. Protocol says I ought to check their vitals Q2H. Q15min feels much better to me.

Can someone explain what does RVR mean?

Also, when some of you mentioned that you need to see the labs including lytes, are you specifically looking at K, Na, Mg and Ca? Does increased in BUN and Creatinine has anything to do with the A Fib?

RVR means Rapid Ventricular Response. Here's what you have: you have a patient whose atria are fibrillating and so blood is not being pumped through the heart adequately. A lot of patients have that problem and as long as they're getting meds for rate control and anticoagulation (since A-fib tends to produce micro-clots that put the patient at great risk for stroke and heart attack), they can live with it. But if this same patient (let's say it's an elderly woman) becomes anemic from a GI bleed, that affects the volume of her RBC's and therefore, the amount of oxygen her heart will get.

When the atria are fibrillating and the heart is not getting enough oxygen, the ventricles try to pump harder and faster to get that oxygen. If the ventricles are pumping at a rate of over 100 bpm and sustain somewhere around that area, the patient might have A-fib w/ RVR. This needs to be confirmed with a 12-lead EKG. Sometimes the patient does not have any symptoms, sometimes they'll feel faint or c/o fluttering in their chest. But as the cardiac output decreases, you will begin to see symptoms such as a dropping blood pressure. That's why A-fib with RVR needs to be addressed stat. If the patient's BP is OK now, just wait because it won't be in awhile. So treat it while you have a good BP.

Put O2 on the patient, get a 12-lead EKG, monitor vital signs and get the doc immediately. Treat it immediately and you will usually avoid big problems later. If a patient is already on Coumadin and a rate controller medication like Lopressor, that's a clue that the patient may have a history of this.

As to the Lytes: anything that can cause the heart to have less oxygenation could be the root cause of a patient going into A-fib RVR, so you have to treat those to get the patient stable again.

Thanks Angie for that clear explanation.

We had a pt from who recently transferred from oncology unit to our tele unit because of A fib as well. Her HR was around 150's when we received her from previous shift. MD put her on Cardizem drip of 5 mg/hr (10 max). Three hours later, her HR still remained in the 150's at 10 mg/hr. I told my preceptor that the Cardizem was not working, and should we contact the MD. She just ignored my comment. Later, when the MD came in to see the pt. He was furiuos no one took action on that poor lady. He stoppped the Cardizem and started her on Lopressor 5 mg IVP Q4hr. Her HR instantly dropped to 100's after we gave her the push. I thought that was pretty amazing. The pt was not on coumadin, but she was on Lovenox.

RVR=Rapid Ventricular Response.

In people with AF with a controlled ventricular rate (typically 50s to low 100s), the decrease in cardiac output is negligible and primarily due to loss of atrial kick, so the biggest concern is with prevention of thrombosis, hence anticoagulation with warfarin.

When the ventricles are being driven at an excessive rate (usually 120s to 180s), ventricular filling time is shortened, resulting in a decrease in cardiac output. Since decreased cardiac output means decreased perfusion of vital organs, rapid AF can be dangerous. Since calcium channel blockers such as diltiazem also have prodysrhythmic effects, particularly the potential for Torsades, the benefit of using the drug should outweigh the potential hazards. The primary effect of diltiazem in the treatment of rapid AF is slowed conduction through the AV node.