What to do at onset

The history of my experience with AF has undergone a rather significant change lately. Prior to 2007 I had had episodes separated by years, but starting last November I began having weekly episodes. Most episodes start early in the morning. I’m not certain, but I don’t believe I awoke in AF. My most recent episode started late in the afternoon while I was lying on the couch watching the Rose Bowl. Typically my episodes end in between 4 to 8 hours. Only during my last episode did I go to the ER. There I was infused with a calcium channel blocker to slow my heart (140 bpm) and later after the tests were back I was given a liquid potassium supplement.

My question concerns how I should respond to future episodes. It’s a sixty mile drive to my VA hospital. If I could slow my heart rate down below 100bpm on my own I’d like to handle the problem at home. I would very much appreciate hearing how other members of the forum approach this situation.

Josiah

Hello Josiah,

I have most episodes shortly after going to bed of woke up after 1 hour of sleep in AF.

My heart calms down or goes back to NSR (normal heart beat) after walking around in the house for 30 minutes. Staying in bed made the episode just worse. This seems to be typical for a vagal afibber.

I don't know whether your episodes are of a vagal or adrenergic nature, but I am sure more people will help you clarify this.

By the way, did your episodes return after you were given a liquid potassium supplement? Most members of this forum benefit from magnesium and porassium supplements.


Ritze

P.S. I should add that I haven't had an episode for 4 months, but this is because I take constant medication (flecainide). So I was talking about my situation as it was some months ago. Nevertheless, moderate exercise definately helped me.

Josiah,

See Jackie's post here:

<[www.afibbers.org];

She says, "At the onset, I take 25 mg. Toprol XL. Wait 30 minutes and take 100 mg. Flecanide. If not converted within an hour, take another 100 mg. Flecanide. I've only had to take the second flecanide dose once. These were my instructions from Dr. Natale."

The Toprol XL should help keep heart rate down, they the flec should help with quick conversion.

You might have a conversation about this on-demand approach with your doctor.

George

I have not had another episode since taking the potassium supplement. Because potassium passes through the body very rapidly, I'm sure the dose I was given on New Years day is long gone, but I've significantly increased my daily potassium intake. I'm hoping it makes a difference.

Josiah

Take 25 to 50 mg of Metoprolol extended release. If you do not convert by yourself, you also have to get a prescription for an antiarrhythmic drug.

I use Sotalol together with Metoprolol with 100% success rate. Others here also use Flecainide and a beta blocker. Both drugs prolong the action potential. Flecainide and Sotalol achieve that, each in a different way. Sotalol by blocking the potassium channel, which prolongs the refractory period. Flecainide by blocking the sodium channel to prolong the contraction and the reduce the strength of the contraction.

Sotalol also works as a beta blocker, which is good, as at a lower heart rate the effect of the potassium blocking is more efficient. This is phenomena is called "reverse use dependency". For me, the beta blocking from Sotalol is not enough, as I also need a "pure" beta blocker like Metoprolol-XL to convert.

A beta blocker is also used with Flecainide, as there is a risk that with higher heart rates Flecainide can convert the AF to flutter with 1:1 conduction. 1:1 conduction means that every contraction of the atria results in a contraction of the ventricle. As Flecainide works on the "upstroke" of the action potential, it becomes more efficient at higher heart rates, "use dependency" which can be a dilemma for the physician, when he has to decide the dosage for a symptomatic afibber. Further more, the sodium blocking acts as an anesthetic for the heart muscle, so it should not be used by patients that already have a reduction of the output of the heart, low ejection fraction, which is common for a patient with a prior heart attack, resulting a partially deceased heart muscle (The CAST trial).

In both cases the lowering of the heart rate by beta blocking will reduce the load on the heart and make it work more efficient, less oxygen consumption/volume pump out from the heart. Loss of atrial kick, when in AF.

Both Sotalol and Flecainide can cause ventricular arrhythmias due to the "reverse use respective use dependency" if the dosage is too large. The work load on the ventricles, which are affected as much as the atria becomes too much and the ventricles start to fibrillate. The effect of the dosage can be seen as a prolonged QT or a widened QRS interval.

There is a good summery in the Wikipedia.

It is also believed that beta blocking will reduce the contraction and contraction rate from ectopic foci and thereby stopping the fibrillation. How beta blockers affect the heart is not completely understood.

The use of a beta blocker may seem as a paradox for a vagal afibber. A reason for the transformation of PACs to AF, is believed to be the faulty dispersion of the refractory period at lower heart rates. Areas in the atria, that have a too short refractory period in regards to the heart rate, do not give the protection of letting the contractions induced by ectopic foci to form wavelets of contractions in the atria. At lower heart rates impulses from the SA-node will not overrun impulses from ectopic foce, overdrive suppression. For many, PACs and even AF can stop, if the heart rate is increased, e.g. getting up from bed, jogging, etc. Unfortunately the same conditions, that favour AF, will occur again, when you go back to rest, if it is not just a temporary condition caused by increased vagal tone after a big meal or after exercise. A temporal increase in heart rate can give an antiarrhythmic drug the time to start working, even if the heart rate gets low from the beta blocker, as a normal refractory period/prolonged action potential is instated and the conditions for wavelets no longer exist.

Hi, Josiah, George & Jackie,

I, myself, would be 100% in agreement with what Jackie evidently said, ie, Toprol, Flecainide.

When I was diagnosed, April 1999, I was a silent afibber with 160 pulse, ie I did not even know I was fibrillating. I was put on rate control with warfarin, digoxin, Toprol and lisinopril. Toprol and digoxin slowed my heart to a resting pulse below 90. I fibrillated continuously til electroconverted in June 1999, but felt great and walked 16 miles a week.

In a few days, I fibrillated again and was converted with amiodarone, which gave me continuous NSR from June til Dec. 1999. Amiodarone instead of flecainide was used because echo & stress testing in June 1999 showed my heart was weak (from prolonged fibrillation). In Oct. 1999, an echo test showed my heart was back up to normal strength, so I was allowed to discontinue warfarin, digoxin and toprol. I continued with amiodarone (antifibrillation) and lisinopril (to reduce my slightly high blood pressure). I was told I should resume Toprol if my pulse became too high, but it was never necessary.

March 2000, an echo test confirmed that my heart strength was still normal. In Sept. 2000, I requested to be put on flecainide instead of amiodarone to avoid the possibility of irreversible lung damage or death risks of amiodarone. I'm very happy with flecainide. I've fibrillated on an average of every 132 days for the last few years with 2090 mg/day flecainide, average length of fibrillation 4 hours. Even when fibrillating, my resting pulse is seldom over 130. 70-75 is my normal rsting pulse when in NSR.

Oct. 2007, an echo and a stress test showed my heart strength is still normal. Afib and "mild plaque" in arteries are the only known heart problems that I have.

If I had your afib history instead of mine, I would ask my cardiologist to prescribe the use of Toprol and flecainide just as Jackie recommended.

A; 1/6 Sun. 2 PM CST

GeorgeN wrote:

> Josiah,
>
> See Jackie's post here:
>
> <[www.afibbers.org];
>
> She says, "At the onset, I take 25 mg. Toprol XL. Wait 30
> minutes and take 100 mg. Flecanide. If not converted within an
> hour, take another 100 mg. Flecanide. I've only had to take the
> second flecanide dose once. These were my instructions from Dr.
> Natale."
>
> The Toprol XL should help keep heart rate down, they the flec
> should help with quick conversion.
>
> You might have a conversation about this on-demand approach
> with your doctor.
>
> George

Thanks Gunnar. Nice post. Josiah what meds do you take

Mark

Let me say that I appreciate all the responses I've received to this post.

In response to your question, Mark, I currently take 25mg of Metoprolol three times a day, 25mg of Chlorthalidone in the morning and 5mg of coumadin.

Josiah

Josiah - were you lying down after a meal? If so, it's known to be one of the triggers. Don't lie down or sit slouched or with the abdomen scrunched.

Better to sit upright for at least an hour or more or remain on your feet.

Jackie

Jackie, i was on flec back about 3 years ago and woke up one night in afib. I rushed to the er and was at a very high rate. I was scared. They hit me with the paddles without putting me under. Now i am supposedly allergic to flec. However some friends of mine ask me why i was not taking toprol along with the flec. Maybe if i took it the rate would not have gone so haywire. What are your thoughts. Steve

Group, I went out early sunday morning also and i am on Sotolol but I never seem to be able to get back in nsr naturally. I am cardioverted. I had been however afib free for 6 months. Its so strange this thing. Steve

Josiah,

You state above that "Prior to 2007 I had had episodes separated by years, but starting last November I began having weekly episodes". How many years PRIOR to 2007 did you fist have AF?

Al,

I assume you mean 200mg of Flec/day and not 2090mg/day!!

Best to all,

Mike F.

Josiah,

Many thanks for the reply. One more thing please - have you for at least the last twenty years experienced quite frequent ectopy? Either several tens or more single PACs/PVCs/day and/or one or several short (few seconds) 'runs' of such beats/day?

TIA

Mike F.

Mike F.

Until I started following this forum about 2 weeks ago I had never heard of PACs/PVCs. My pulse seemed to be rock solid when I was in NSR and totally haywire when I was in AF. Six months ago I experienced one exception to that, I was taking my pulse and I percieved that though my pulse was quite regular, I was missing every third beat. It may be the case that I do have PAC's/PVCs that I just wasn't aware of.

Josiah

Josiah,
Many thx for the further info.
Best,
Mike F.