uncontrollable high rate during afib

I've had the problem of uncontrollable high rate (120s-180s steady, 200s for short periods) during afib.
Has anyone else has had this problem and if so, did doctors find a way to bring the rate down (other than converting) ?

Nope, they only know how to inject diltiazem and then look at me reproachfully as though it is my fault it didn't work. They keep injecting diltiazem until they tire of doing it, and eventually go away and leave me attached to assrted monitoring machinery, of which the worst [to me] is the automatic bp cuff, always set at a too-high level of 200, when it only needs to be about 160. This torture device wakes me every 10-15 minutes when it inflates, effectively preventing me from getting any sleep. I complain, and they say that the setting is fixed and they cannot change it. I have found this to be a lie. There is always somebody on each shift who knows how to change the setting, usually a senior nurse. This person will appear like magic once i convince these poor overworked underpaid nurses that if it is not changed i will remove it the next time it hurts me. Sometimes this produces the nurse who knows how, and sometimes i have to actually remove the thing myself in order to get this person to appear. Once the bp cuff is adjusted to a tolerable pressure i can doze off. The doctors reappear the next morning, and sometimes they feel obliged to repeat the same sorry sequence. It does not do anything then either. Eventually they give it up, and usually it converts the second night while i am asleep. If i had stayed home the whole thing would have been over in half the time, but i let somebody convince me to go to the emergency room, and they do not know how to make it stop any better now than they did the last time i did that stupid thing [went to the ER, i mean].

If i stay home the afib will convert spontaneously in about 12 hours, usually after i climb my stairs to my second floor bedroom. This only works toward the end of that 12 hours. I climb the stairs and then sit on the end of my bed to catch my breath, and the afib gives one last big thump and converts back to sweet NSR. I have given up on hospitals for afib. I try to tell them that if they will just let me climb a flight of stairs the afib will convert at the top, but they will not allow me to do that. Once a doctor told me that if i did that i would have a heart attack or a stroke or both. I then left the hospital against his advice, took a cab home, climbed the stairs to my bedroom, sat on the end of my bed, felt the afib convert to sweet NSR, and went to sleep in peace.

I think this diltiazem routine is in whatever textbook they make these young doctors memorize, and they are afraid if they do anything other than what that book says, they will be excommunicated or something. They cling to it even though it does not work. I am only a patient, what could i possibly know?



Edited 1 time(s). Last edit at 05/02/2012 01:55AM by PeggyM.

neginf,

Many of us use a beta blocker to help keep our HR down during an episode. A beta blocker won't necessarily convert you, but can help in many ways. It can make your heart beats easier to tolerate (without you jumping out of your skin). It can help keep your heart from being damaged from the sustained high HR. It can actually help some AADs, such as Flecainide work better in order to facilitate conversion.

lisa
__________________________

So much of medicine is looking solely down the wrong end of the gun barrel, and that is really a pity for all of us---Shannon

Peggy-- Your post gave me a good laugh as I thought back over several hospital experiences I had before I figured out it was better to stay home.



Edited 1 time(s). Last edit at 05/02/2012 01:06PM by Jill.

i think you may find that cardizem and diltiazem are the same drug by 2 different names.

PeggyM

neginf,

Without a beta blocker, my heart rate was 180 while in afib. I was on meds for 6 years for my afib (approx. 2.5 episodes per month) to make it tolerable. I always self converted. Finally a successful ablation 5 years ago.

I was/am in great health and physical condition, so no reason to go to the hospital for anything while in afib.

What you do depends on the frequency of your episodes, your general health and fitness and your Dr. Give us some more information and we can provide more answers.

Neginf,

Have you tried propafenone (rhymol) or flecainide? These are not rate control drugs but they will convert some people back to sinus rhythm. Prior to my surgery I used flecainide pill-in-pocket, 200mg converted me usually within a couple of hours. Some people take a beta-blocker with their flec. Worth a try-

EB

It's well worth trying Acupressure for this. I was surprised to find how effective it can be.

Goggle acupressure point heart 7 and watch the YouTube video. You can treat yourself.

Discharged yesterday from hospital after calling 911 for first time with heart rate of 200 in afib with rvr. Given 2 doses of adenosine which was horrifying and it did not work. The ambulance hit a pot hole and they said I converted. So much for drugs. Everyone in ER saying it was a first pothole conversion. It was funny but not the experience which I apparently been having once a month during sleep over the past 3 months. I dont want ablation, or antiarrhythmics or beta blockers I am healthy exercise and am a health care provider. How do I keep from progressing to persistent a. fib.? Going to see an EPS cardiologist tomorrow. Only happens during sleep. Any advice is helpful for this apparent pothole converter.I also have low low baseline blood pressure.
Mahalo for your input.

I thought my story was funny since Ive been dubbed as the pothole converter but your story is even funnier I hate adenosine and never want it again I tried to sign out AMA yesterday but 2 doctors and a husband made it impossible. Trying to figure out how to prepare for next time Maybe not eat dinner or dont exercise. But I love my treadmill. Do you think I should try dilitiazem? I have ridiculously low blood pressure.

I use diltiazem only when I begin to afib, to help control the heartrate while I wait to self-convert. I take one 240 mg pill.
If you increase your oxygen demand while exercising, it can trigger arrhythmia, as oxygen depletion is a well known reason for foci irritability. What I do is exercise as much as possible without going aerobic. If you can talk easily without breathlessness while you're exercising, you are not likely creating an oxygen demand level that can trigger an episode.

Thanks so much Tom. I can talk and sing at 4 miles per hours but it is a fast walk. I'll slow it down. Do you know why a fib doesn't set in until 5-6 hours after exercising? If I dont do something now what do you think my chances of going into persisten a. fib are? I wonder if I can take diltiazem since my baseline pressure is 88-94/48???

Had afib for 17 years. After about 8 years, 1 to 2 4 hour long episodes per year increased to about 1 per month so I got Flecainide and was ok until a few months ago when I started to have about 1 12+ hour episode about every month. My health is good enough to walk where I want, up hills and stairs fast, lift weights a bit, etc. 53 years old. I take 240mg Dilt each day and 125 mg of Digoxin each day.

I got an ablation and at 3 weeks felt 5 seconds of afib, at 6 weeks PACs started (avg 1 per day), and at 8 weeks went into afib.
After about 20 hours of a 130-199 rate in that episode, I went into a fast 115 rate NSR after 2 100 mg Flecainide and 500?mg Amiodarone drip. They did an echo on me and found mild hypokinesia in my left ventricle (enzyme tests ok) and said I could never take Flecainide again. This was a huge disappointment since it helped convert me even when it was losing its effectiveness on me.
I went back into afib for the next 24 hours or so and my rate kept going up sometimes holding steady at about 170 or 180. I converted and although they said the Diltiazem drip did it, I somehow think they might be wrong.

I had another ablation and at 3 weeks felt 1-2 seconds of afib, at 6 weeks PACs started (avg 1 per day), and at 8 weeks felt 2 seconds of afib.

Very worried about another failed ablation, a high rate episode not converting, and being given an AV node ablation.

elizabeth Perez Wrote:
-------------------------------------------------------
> Thanks so much Tom. I can talk and sing at 4 miles
> per hours but it is a fast walk. I'll slow it
> down. Do you know why a fib doesn't set in until
> 5-6 hours after exercising? If I dont do something
> now what do you think my chances of going into
> persisten a. fib are? I wonder if I can take
> diltiazem since my baseline pressure is
> 88-94/48???


I can't speak to your situation, as we are all different in how we respond to drugs as well as the underlying cause of afib. I can't handle the diltiazem on a regular basis because it slows my heart down too much at night - my natural heart rate can dip into the low 40's then, The diltiazem actually causes apnea in my case - that's why I only take it as a precaution to help manage heart rate during afib.

My afib episodes also follow exercise, but usually a full day or so later - I'm of the opinion that the exercise irritates the vagus nerve which then becomes inflammed - the timing seems to support that perspective. Once inflammed, all it takes is bending over or some movement that causes pressure on the nerve which, in turn, sends a signal to stimulate the heart...hence the trigger. I'm now using valerian root extract to help tone down that sympathetic response. It seems to work. Many here are careful not to bend over when that critical time period occurs, wear loose clothing, etc.

Tom

Exercise is a source of free-radical production ( ROS – reactive oxygen species) – and free radical damage…. which in turn causes inflammation.
When the vagus is exposed continually, it’s going to become irritated unless antioxidants and anti-inflammatory nutrients are plentiful. Eric Braverman, MD, says N- acetyl cysteine – is THE #1 antioxidant. It is a precursor to glutathione which quenches free radicals and everyone needs to be on it. NAC along with the ACEs… vitamin s A, C, E and mineral, selenium …and of course zinc, go a long way toward reducing inflammation and the risk of nerve and other tissue irritation.

Jackie

Hi Elizabeth,
Two clues you gave indicate low cortisol/low adrenal output could well be a major culprit in your case. When you describe 'ridiculously low BP' I'm not sure what BP levels you mean but running consistently low BP below 100/70 of a big red flag for low adrenal reserve and inability to meet short or long term stress demands with adequate cortisol production.

Similarly the delay from excercise to trigger could well coorespond to a the famous cortisol drop soem hours after excerise for those with low to borderline low cortisol production. WHen you excersice ( or eat a big meal) the body will produce more cortisol .. as much as it can anyway. But if you are borderline or truly deficient then at best the excercise might increase cortisol output jsiut enough to make you feel more or less normal or a little better during and for a few hours after the excercise routine. But then as you already marginal adrenal reserve drops below the necessary minimum level you will not be able to marshall any more cortisol for some time and the body will revert to adrenaline as a second class fall back option to meet you immediate cortisol demands.

Adrenaline is our fight or flight hormone and is definitely Not what you want squirting out in place of cortisol .. the longer acting and more calming true stress hormone in appropriate doses ... Adrenaline is great for jumping out the way of a bus or charging tiger , but not so much to replace a drained cortisol reserve during down time after exercise!

It will definitely get you heart going and with the sub-strait and tendency for AFIB already in place adrenaline release like this can become a major trigger for another AFIB episode.

Find a good functional medicine doc (do NOT go to an endocrinologist unless you verify first he or she is among the relatively few enlightened Endo's with respect to managing non-Addison's adrenal insufficiency and is very well versed with Bio-identical hormone therapy as well). That could be worse than staying home for sure.

Have a complete hormone work up with a complete 24 hour urine hormone analysis and selected serum testing as well as a good clinical exam for adrenal and thyroid health and go from there toward helping to support your BP and your adrenals/thyroid as needed.

Maybe all you need to reduce the frequency of those post exercise triggers is a well timed dosing of 5 to 10mg of hydrocortisone (bio-identical cortisol) an hour or two post exercise session?? also make sure you have enough Mag, Potassium AND salt on board ... enough sodium is critical for low cortisol producers but just keep the K to Na intact ratio high around 4 to 1 or so).

Anyway, confirm all this first after comprehensive testing and examination by a skilled functional medicine doc and hopefully that will give you some answers.

Take care
Shannon

Elizabeth,
Sounds a lot like me. A few hours after hard exercise, I get AF, usually when laying down for the night. Heat during exercise exacerbates it. I was having heart rates in the 160-180 range for 2-4 hours. I have now eliminated that (except for a PPI drug-induced series of episodes I posted about and have been discussing the last few days).

What worked for me was to:
Regularly take the Mg glycinate Hans talks about. I did up to 800 mg/day or bowel tolerance, until things were under control. I now do 400 mg/day.
Take potassium gluconate, about a tsp, each day (but sometimes I skip). I make sure to do it the day before and day of heavy exercise especially in heat. And if a really long, tough session (like a 5 hour bike ride at high speed), I'll take more afterwards, maybe another tsp. (these tsp's are dissolved in 12 oz water and drunk, btw). I never do more than 2 tsp of K gluconate (I'm 6'1"/190 lb, btw) because it is dangerous to take too much K. Usually I only take 1 tsp, or maybe 1.5 if a hard day. I have only done 2 tsp a couple times in my life, when I was already experiencing AF.
When exercising, keep my heart rate below a threshhold. For me, that used to be lower, now a bit higher, but I find I can very safely exercise in the 110's, usually in the 120's, and for moderate times (30 minutes or so) in the low 130's. But that is starting to push it. Once I get into the upper 130's/140's for a length of time (20+ minutes) or 150's for even short times (5 minutes), I am very likely to trigger an AF episode a few hours after the exercise.
This can be exacerbated by a big meal. If I go exercise for a long time, then have a big lunch because I'm hungry, I'll likely start AF within 30 minutes or so of completing lunch.
These are typical symptoms of vagal type AF, as I understand it.
I find that taking Potassium (K) gluconate is helpful to ending an AF run at high bpm. It takes 15-20 minutes to start to kick in. Won't work everytime, but helps. But I keep total daily dose within recommended limits, including any dietary sources.

lisa s Wrote:
-------------------------------------------------------
> neginf,
>
> Many of us use a beta blocker to help keep our HR
> down during an episode. A beta blocker won't
> necessarily convert you, but can help in many
> ways. It can make your heart beats easier to
> tolerate (without you jumping out of your skin).
> It can help keep your heart from being damaged
> from the sustained high HR.


Question for the experts:
Is this a true statement? I've heard this, but I don't understand it. Do you really end up with a high ventricular heart rate, or is it just a high atrial rate due to the short circuit, with the second beat creating the 120 bpm or 2 added beats (180 bpm) being relatively weak? Does a fast atrium really do much damage to the heart? (I assume a fast ventricular rate would).
Is the rate of damage less if the heart is conditioned with exercise, even if th conditioning is at lower heart rate?
Any published papers addressing these questions? I have seen the claim made several times, but it isn't clear to me why necessarily.
I know my doctor always wants to run cardiac enzymes after an AF episode. If I did that, I'd be in the hospital getting tested all the time! So far, they say my heart is healthy (except for AF).

The papers I'm familiar with on AF suggest that without other underlying heart disease or stroke, there isn't a higher morbidity for AF patients than controls. That would seem to suggest no real heart damage, wouldn't it? Or am I missing something/remembering wrong?

I first want to thank all of you for your support and posts. It brings tears of joy to know I'm not alone and that there are others who understand and are searching for answers. As you all know I'm a newbie paroxysmal vagal a. fibber and have been dubbed "the pothole converter" that has gone viral on the windward side of Oahu. I need a little humor in this because I'm exhausted. I have a couple of answers to some questions for Robert.
The important information about damage to the heart is told by an echocardiogram and whether there is enlargement due to long standing a. fib with a rapid ventricular response. This answer also depends on age and other health conditions. I had an echo yesterday that showed a normal heart and ejection fraction. If a person has congestive heart failure and say diabetes the risk would be greater for heart damage and the development of atrial or ventricular hypertrophy (an enlarged heart) due to this arrhythmia. A person at an older age even in good health would be at a greater risk for heart damage due to rapid arrhythmias of any kind. We do measure atrial rates however the pulse is the venticular rate and that is the most critical. You can have an atrial rate of 200 but only a pulse ventricular rate of 50. It is the ventricular rate that is important because all of those atrial impulses are not getting through. This is how beta and calcium channel blockers work and this is how dig works. Dig blocks impuses through the AV node.
On another note, my first visit to the EP yesterday, he says for me there might be a serotonin connection because I recall 4 years ago being awakened one night after brain surgery for a benign large meningioma with the same symptoms that hospitalized me this week with a first time diagnosis of a. fib. Apparently there's research about the SSRI (antidepressants) possibly working for those with vagal PAF. I'm going to search for it. Shannon I'm going to follow up on your thoughts because they make alot of sense. I've always had low low blood pressure and recall craving salt since being a kid. Neginf you have been through alot and I hope you dont have to go through more of it. My EP yesterday told me he would not use Dig ever for me. He says many cardiologists dont understand or treat vagal fib appropriately. At this time we are not going with any meds or ablations. But that day may come soon as I fear another episode around the corner. My potassium was mildly low on admission and the sodium mildly high. I will work on this but please be careful with potassium. Too much or too little causes ventricular fibrillation and cardiac asystole.
Thanks so much to all of you.
Aloha the Pothole Converter

RT
The more I read I'm beginning to think that vagal a. fib is a condition not of the heart but of the Autonomic nervous system that controls the heart. What is interesting is that the 2 parts of the ANS which is the sympathetic and the parasympathetic have different effects on different parts of the heart. Usually the sympathetic speeds it up such as described by Shannon and the parasympathetic slows it down. However I undertstand that the atrial tissue under the influence of the vagus nerve actually speeds up under vagal stimulation because the refractory period is reduced and more depolarizations. The opposite is true with the ventricles. The parasympathetic stimulus will the ventricles down. I'm stilll sorting all of this down. Yes the electrolytes you discuss are ultimately responsible for depolarizations and repolarizations. Have you stopped the a. fib with potassium or slowed down the rate or both? I'm going to research the serotonin connection now. I dont want to be on an SSRI but maybe it will work and I imagine if I go on to have frequent episodes I will be depressed and it might be the stone that gets 2 birds at once.

Peggy you have it right on the head... I have been in the ER 13 times... just got of the hospital 7 days ago... Word for word you have it right... except I waited 4 days with a heart rate of 155 .. then converted on the second day there... released the next.. have had two ablations.. take all the meds., supplements... still get Afib 3 to 4 per month or more... end of story. (for now)

Not offering advice, just sharing experience...
When I first had AF and it kept getting more frequent, longer duration, higher intensity (inclg high heart rate like yours), it was scary. The doctors didn't help; the cardiologist I went to scared me even more, and pushed some really potent drugs, which fortunately I didn't take. The best thing he did for me was testing showing no underlying heart disease, heart damage, etc. Normal ejection factor. And, he gave me a "name" for what I had. That was all I needed to launch an internet search, find this site, buy and read Hans' books, talk with Jackie and others on this site, read a ton of published literature, and start to really get a grasp on what I had. That took away most of the fear (which itself is an AF factor via stress). And also the courage to face down the doctors and their fear-mongering, threating me with hospitalization anytime my heart went into mild AF, etc. I put into practice the supplements Hans recommended, took note of triggers, and SLOWLY (a few months) got things under control so that severe AF like yours was extremely rare. Even then, I didn't worry because I always converted on my own within a few hours (usually during the night).

Anyway, the point I was trying to make above in my questions, and I'd be interested for Jackie or Erling or Hans or one of the other better-read people on this site to respond, is that during that period, reading published literature including a big morbidity study of AFibbers, I came to the conclusion that for LAF, morbidity isn't really that different than control groups. That led me to conclude that the risk isn't something to get all worked up about, and that in turn gave me time to implement natural remedies, lose weight, exercise more, reduce stress, etc. That was probably one of the most valuable aspects of all the information--the elimination of fear gave me time to implement slower solutions vs. the fast medical treatments.

Good luck!

Robert - My AF journey lasted 8 years until ablation (’03) and now it’s been almost another 9 years of researching and exploring considerations about what we can do to either alleviate the intensity of events or hopefully, prevent them from happening in the first place.

My opinion is that if one is otherwise healthy, there should be no magnified concern over a fatal event while in AF… but healthy would mean to know the risk factors of adverse clotting which includes blood viscosity status, ferritin levels, fibrinogen levels and HS CRP levels since a degree of inflammation would tend to foster ‘sticky’ blood. The concern comes in because most patients don’t have control over resting the marker testing required to know if their platelets are ‘sticky’ or not.

On the ‘fear factor’…since I’m a healthcare professional, the fear issue was short lived for me once I began my own research. I was fortunate in that my doctors at the time did not voice particular concern over the potential for stroke or dying, but I was healthy and wasn’t on any meds for other conditions, was active and not overweight. It was very annoying for me to have AF and eventually, it led to having to retire from the job that I loved because I was unreliable at maintaining a work schedule by appointments.

I also learned that there are cardiologists and then there are cardiologists… some are conversant and actually know how to manage arrhythmia patients and others only think they know how. My initial cardiologists (2), knew how to prescribe a beta blocker and do a treadmill test but otherwise, offered absolutely nothing useful.

Eventually, I found a cardiologist who specialized in pacing and rhythm disturbances and that was somewhat of an improvement over the former. He acknowledged that eventually, I would most likely need to consult with an Electrophysiologist which did come to pass. But during the time I was under his care prior to ablation, he never did express anything ‘fearful’ about my stroke risk even though I had refused Coumadin as part of my treatment protocol.

With treating arrhythmias, some type of anticoagulants are the Standard of Care. I was fortunate not to have to jump through hoops to avoid using. It was my choice…It’s too bad that the legal liability factor doesn’t alow patients to make up their own mind about using these drugs, assuming they pass the risk marker tests and are in good health, other than AF.

Oh - and I should mention that my events became frequent and of long duration. At times my HR would be high 180 - 220 bpm... very uncomfortable and debilitating. If I knew back then, what I do now... oh my what a difference I would have been able to make.

Jackie

Jackie,
I'm laughing at your experience because that was mine. The cardiologist I was sent to by my local hospital after my first "official" AF episode (the first one in the presence of medical folks and an EKG) was not helpful except for giving me a "name" for it (which as I said, was very helpful). He wanted to put me on aggressive therapy even though I had no other risk factors. Once I read enough to know he was overprescribing I didn't bother filling the prescription and thus never have taken drugs for it. When I asked him about the apparent overtreatment, he told me I should trust him and that it was possible for patients "to read too much." I never went back. Unfortunately, he is the only one making hospital rounds in my smaller town, so I encountered him again a couple weeks ago when I was in for what turned out to be hiatus hernia, not heart. Fortunately, I was able to just smile and say, "I'm not having AF problems anymore." It was almost true; I certainly didn't want him involved again by sharing any details!

Fortunately, I also have access to many EPs in Houston an hour away if I need them. When I switched primary care physicians a couple years ago (mine retired), the new guy was very concerned about my not doing anything for my LAF ("not doing anything", of course, meaning not taking drugs, since I was doing things in the form of Mg/K/taurine). I finally went to a Houston EP just to get his "blessing" on what I was doing so that my PCP would quit bugging me. The EP was fine with what I was doing, disagreed (gingerly and diplomatically) with what the local cardiologist had prescribed but I had refused to take, and said that normally AF progresses and whenever it gets to the point where it is too bothersome, call him. I hope never to have to do that, but if I do, it will be someone like him, not the local cardiologist!

Robert, i am sure that your EP doctor told you this because it is what he has seen in the patients he treats:
"and said that normally AF progresses ..."
and sure enough that is what happens if you just do whatever the doctor says do and take whatever he says take. But for those of us who have figured out [with the help of other posters here] how to make the episodes stop, that progression is not taking place. Session 61 in the archived conference room reports gives 50 examples of people who have done that, and tells exactly what each one did to get this happy result. Go and do likewise.

PeggyM

How do I find session 61?

Elizabeth,
You can find all the conferences off the home page or directly here:
conferences

PeggyM,
You are right. Particularly when you learn that many of the drugs are proarrythmic for ventricular fibrillation, for example! The cardiologist had here had told me ("nicely!") that I'd be a patient for the rest of my life (at the time in my upper 40's) but that there were much worse things that could happen to me. This was as he prescribed Coumadin and the first of what would surely have been a progressive sequence of antiarrythmic medications. Nice business model!

Seriously, that digoxin is not doing you any favors and may wind you up as a permanent afibber. Please take a few minutes and read thru the articles Hans has written about this drug. If my memory is accurate (a rarity, actually, i am reaching the age where my memory is no longer reliable), digoxin reduces the amount of potassium in the heart's cells. The heart needs potassium just as a car needs gasoline. Hopefully somebody will jump in here and give the url for that article. If not, just put the word digoxin into the search function here and you will find plenty support for that view.

PeggyM



Edited 1 time(s). Last edit at 05/09/2012 02:36PM by Hans Larsen.

Once again i am the victim of the underline gremlin.Somebody explained why this happens once a long time ago, but i have forgotten what they said. It might have been George Newman. George, if you are reading this, please make that explanation again?

Peggy M

Hi Peggy,

I edited your posting. The strike-through was caused by a square bracket that you used (articles).

Hans

Thank you, Hans. The square brackets are so much handier to use.

PeggyM