The most effective method for getting a heart that is in atrial fibrillation back to normal rhythm is a called an electrical cardioversion.
I’ve tried to come up with a good alternative or descriptive term for this procedure for my patients, such as “resetting” or “rebooting” the heart, but the term that seems to best resonate with patients is “shocking” the heart.
How Does Electrical Cardioversion Work?
Typically, we all can connect (excuse the pun) to the feeling of a low current electrical shock which occurs when touching an ungrounded electrical source.
Unless the current reaches a certain level, it only results in transient burns and discomfort.
However, at current levels greater than 50 mA, an AC electrical shock traveling through the chest can, if timed properly, cause the heart to go out of normal rhythm into ventricular fibrillation.
We use a “synchronized” electrical cardioversion (termed direct current or DC cardioversion (DCC)) to convert a fibrillating or fluttering atrium back to the normal rhythm by timing the electrical shock so that it doesn’t cause ventricular fibrillation but resets both ventricles and atria safely back to normal.
This may seem like a barbaric and unnecessarily crude and dramatic way to restore normal rhythm, but if patients are properly prepared for this procedure, it is very safe and very effective, resulting in resumption of the normal rhythm 99% of the time.
There are some medications that we can utilize to convert atrial fibrillation (afib) back to normal (antiarrhythmic drugs), but they are far less effective than the electrical cardioversion, and often can bring out more dangerous heart rhythms.
Typically, I do my cardioversions in conjunction with an anesthesiologist, who administers IV propofol (yes, this was Michael Jackson’s sleep aid, his “milk”) to obtain “deep sedation.” At this level of anesthesia, the patient is breathing on his own but will only respond to painful stimulation. The propofol is short-acting and prevents the patient from feeling the intense pain of the cardioversion (often described as like a mule kicking one in the chest), and from recalling any of the events.
The electrical shock is administered through electrodes, consisting of large sticky pads with electrical conducting gel attached to the right anterior chest and the left posterior back (see this brief information from Zoll about optimal placement).
Since I began using “biphasic” energy, the initial cardioversion is successful >95% of the time in my experience, but the heart may revert back to atrial fibrillation anywhere from a few minutes to a few years after the shock. We can reduce the chances of reverting back by the use of anti-arrhythmic drugs.
Multiple Shocks: What Is The Limit?
The DCC may need to be repeated, and we may repeat it after starting one of those anti-arrhythmic drugs I mentioned, in order to increase the time that the heart stays in the normal rhythm.
A common question when I recommend a repeat cardioversion is:
“Doc, how many times can you have your heart shocked?”
One might think it is one and done with the shock but it is not a cure; it is merely a resetting of the chaotic, confused and futile activity of the atria, so that the synchronized and regular electrical pacing provided by the sinus node in the upper right atrium can again resume its rightful role as conductor of the cardiac electrical orchestra that creates the wondrous symphony of normal cardiac contraction.
The factors that brought on the afib in the first place likely are still present: if we don’t address correctable factors we are less likely to maintain the normal sinus rhythm (NSR). Correctable factors include:
- abnormal thyroid function
- abnormal potassium or magnesium
- inflammation of adjacent lung or pericardium
- severe infection
- obesity (see my post on fat sheep and afib)
- certain cardiac valve problems
There is no evidence that the cardioversion per se damages the heart in any way. The major risks of the procedure (again, assuming proper preparation, see below) are related to the anesthesia.
I am more inclined to recommend a repeat cardioversion if there is clear-cut evidence that the patient does poorly when the heart is in afib.
Why Shock The Heart?
In medicine, there are two reasons for giving medications and doing surgery/procedures: to make the patient feel better or to reduce the chances of dying/having a major complication.
The major complication of afib is stroke. Proper anticoagulation is required to prevent this in patients with afib whether or not they are in normal rhythm. Clots can form in the left atrial appendage within hours of the development of afib, and the electrical cardioversion can increase the chance of stroke as any clot present is more likely to be expelled when the quivering, ineffective atrium converts back to a normally pumping, vigorous atrium.
Primarily, then, we utilize cardioversion for the purpose of making patients feel better.
Some patients feel terrible the moment they go into afib: symptoms of palpitations, chest pain, or shortness of breath predominate and are especially prominent if the heart rate is high. Controlling the high heart rate with beta-blockers or diltiazem will reduce many of these symptoms, but I have a large number of patients who still feel terrible when they are “out of rhythm,” even if the heart rate is normal. Such patients who persist in afib are good candidates for one or multiple cardioversions, with or without the addition of anti-arrhythmic drugs.
A second group of patients, I think, benefits the most from maintaining sinus rhythm (rhythm control strategy): patients who develop heart failure when they go into AF.
These patients may not even know they are in AF because they don’t feel the typical symptoms initially. After a few days or weeks or months of being in afib silently, however, they develop shortness of breath, weakness and leg swelling – classic signs of heart failure.
When we look at the heart of such a patient by echocardiography, we often find one of two things causing the heart failure: a weakening of the heart muscle (cardiomyopathy) or significant leakage/backflow from the mitral valve (mitral regurgitation). Following cardioversion and maintenance of SR for weeks to months, the heart muscle strengthens back to normal and/or the mitral regurgitation improves dramatically and the heart failure resolves.
Multiple Shocks: Rationale
Yesterday I did an electrical cardioversion on an elderly patient of mine for atrial fibrillation/flutter; this was her fifth DCC in the last year.
She falls into the second category of afib patients; she had developed severe heart failure due to mitral regurgitation after silently going into afib a year earlier. After long-term loading on the anti-arrhythmic drug amiodarone, followed by her fourth cardioversion, she had stayed in NSR for 10 months, her MR resolved, and she felt great. In patients like her, I think it is particularly important to maintain NSR and thus, multiple shocks are definitely warranted.
On the other hand, if you feel fine in afib without any evidence that it is effecting your heart muscle or valves, then it is hard to justify multiple attempts to shock the heart.
Any patient that has recurrent symptomatic afib or afib associated with heart failure, should be considered a candidate for an atrial fibrillation ablation. The risks and benefits of afib ablation are worthy of another blog post, but the patient-centered afib website stopafib.org has a reasonable discussion here. Suffice it to say, it is a much more complicated and risky procedure than a cardioversion, but it attempts to address the underlying cause(s) of afib, and in some cases creates what could be considered a “cure.”
For additional reading:
Here’s a good article from the European Society of Cardiology on cardioversion (https://www.escardio.org/Guidelines-&-Education/Journals-and-publications/ESC-journals-family/E-journal-of-Cardiology-Practice/Volume-11/Cardioversion-in-Atrial-Fibrillation-Described)
and check out what Dr. John Mandrola, an electrophyiologist (cardiologist who specializes in electrical problems of the heart) has to say about afib ablations at Drjohnm.org (http://www.drjohnm.org/2015/09/a-cautionary-note-on-af-ablation-in-2015/)
Credits-Life Coach of the Skeptical Cardiologist (LCOSC) for review of electrical engineering stuff.
48 thoughts on “Atrial Fibrillation: How Many Times Can You Shock The Heart?”
Fantastic post, I am still processing the enlightened medical management of AF series with my new found clinical experience but this post is more applicable to my question below. On a side note, that had to be pretty cool to press the button and watch NSR happen, its so satisfying watching that discernible p wave return and those RR intervals march.
What kind of risk do you associate PFOs with embolism risk for patients with afib? I have observed several TEEs before sync cardioversions (SCV) and every cardiologist did a bubble test. Apparently a considerable amount of the population walks around with asymptomatic PFOs, if IIRC it was somewhere in the neighborhood of 25%. I was curious if you do/did bubble tests on your patients before SCVs and if a positive bubble test, does it change anything related to the SCV or treatment?
Yes. The cardio version procedure is very rewarding to perform. It is awe-inspiring to watch this mechainical/technical invention applied with its rapid and dramatic force followed by seeing the heart stop beating for a period of time followed by the appearance of normal rhythm. There is always a little tension as we wait to see if it is effective and to make sure the very rare complication of a very slow abnormal response or a more dangerous rhythm doesn’t occur.
I see no risk associated with PFO. I would only perform a bubble study if the atrial septum looked abnormal by 2d and color Doppler and therefore suspicious for an atrial septal defect. Typically, I try to do an abbreviated TEE prior to the cardio version and don’t routinely do bubble tests because I want to shorten the duration (and thus the anesthesia risk to patient) of full sedation.
Yes PFOs are present in 20-30% of autopsies and likely 1/4 people walking around have one and don’t know it.
My brother is currently in the hospital following quadruple bypass surgery. His recovery has been complicated by his transplanted kidney, which stopped working post-surgery, though they are still somewhat hopeful it will resume its job in time. However, it has necessitated dialysis, and each time he undergoes hemodialysis he goes into Afib. The only thing that works is to do the electro-conversion. Since this won’t be practical every single time he goes on dialysis, the doctors are considering ablation and a pacemaker. This may happen in the near future, but in the meantime, the doctors say there is not much they can do during dialysis except continue with the electro-conversion. It had not occurred to me to ask about the procedure – I just assumed my brother was completely out of it, but something made me ask the doctor today if my brother was sedated during the shock. He said that a very light sedation was used and that yes, my brother would feel it and it was most likely a very unpleasant and painful sensation, but my brother would not remember it. Since he is currently on a vent with a tracheostomy, it is not possible to ask him if he recalls these events and if they are painful, but I am naturally very concerned. He has endured so much and I hate to think that he is having to silently endure something that might be causing him long-term stress. He is slowly being weaned off the vent, but still unable to talk.
Newbie at your site. retired ER physician age 84..Wife age 73.( yes- as they used to say” I robbed the cradle”}..she has been healthy except for osteoarthritis requiring bilateral total hip arthroplasties
.About 3 years ago she mentioned “missed beats”. She has always been my patient, so when I took her blood pressure (correctly with 3 repeats -arm at height of heart-relaxed- I had a difficult time determining systole and diastole because of the mix of sinus beats and what has turned out to be frequent PACs. Asymptomatic- but she notes them increasing over past 6 mos ;. Holter of 2019 showed 2477 PACs-normal sinus rhythm; average heart rate 75bpm-minimum heart rate 43 at 5 am; maximum 134 at 9 am, ;238 SV runs;253 SV pairs
Holter in Oct. 2021 now shows 7758 PACs; 7.5%of beats ;sinus rhythm with average heart rate of 71;minimum 41 at 2 AM; maximum 127 at 9AM ;1043 SV pairs; 854 SV runs; ventricular ectopy 42;
Echocardiograms(2) confirm left ventricular diastolic dysfunction. I understand the link between PACs and LVDD .Cardiologist who read the recent Holter recommends Low dose Beta Blockade to reduce frequency of ectopy because of risk of AF;
Jan is on Crestor for carotid artery plaques just raised from 10 mgm to 20 mgm OD by GP as well as low dose asa; serum lipids OK except LDL a ,little sluggish at 2.33 mmol/L and Non HDL Cholesterol at 3.06 mmol/L
;Now here is where the confusion arises. GP wants to start metoprolol ; I am concerned about lowering the heart rate to try to reduce arrhythmias when the rate has hit 41 and 43: if the rate is reduced by 25 % that will leave her at rates in the low 30s..? Inadequate perfusion of vital organs. Also when i read the range of adverse events with Metoprolol, it is mind boggling(scientific phrase?)some of the bloggers are even finding Nebivolol problematic. Will see cardiologist but likely long wait? I’d like to find the safest Beta Blocker with the best antiarrhythmic strength ..Any advice would be appreciated.
This comment likely more appropriate on my post on PACs.
My bottom line answer to your question is
-Beta-blockers don’t act as anti-arrhythmics. There is no evidence that taking one would forestall the development of atrial fibrillation.
It’s great to know that there will be a process done to also bring back the normal rhythm of the heart after the procedure. I just got curious about this since my uncle told me that he might buy one for my aunt. It appears that my aunt is at risk of a heart problem, and he is just being prepared. It might be due to her neglect of her body which made her overweight based on her age and height.
What is your uncle buying?
There are two recent articles that Federico and All might find interesting.
The first suggests a way of regaining sinus rhythm without shock. Simplistically put, the atrial cells are genetically altered to produce a current upon light exposure. A rhythm sensor detects AF, then an LED stimulates an internal atrial current that stops the AF.
So, there’s a long wait for us – should it ever get to us at all.
The second article suggests that simply waiting to do the cardioversion – giving time for the AFing heart to self-correct – is just as good as doing it right away in the ER.
• There is research indicating that repeated shocks can damage myocardial tissue. Is this true of cardioversion as well as of ICDs?
• AF has shown itself to be recurrent and progressive. Would waiting to do the cardioversion not foster remodeling and progression?
• It takes SO long for new ideas, new medications, and new devices to come through the pipeline. Yet, when they do, a hefty percentage is found to be bogus – only after ineffectiveness or harm is shown. (Angina stents, valves by surgery, reducing fats in favor of carbs, etc.)
Also, there’s vernakalant (Brinavess) – IF YOU GO OUTSIDE THE U.S. – which, when added to your IV, will quietly bring you back to sinus.
Why is it taking so long here?
IV vernakalant. I came across a great review of this drug by Dr. Camm about 4 years ago. Converts recent onset AF to SR within 90 minutes in 50%. FDA required additional data that the manufacturer never provided.
What a beautiful article.
I have actually a question, I had my first afib episode 4 years ago, I was 36. All turned out to be perfect, I have a very healthy life style, no pathologies whatsoever, just a bugged heart. Last week I had my second episode, again they had to reboot my pumping muscle.
Now, here is the question. After a proper training, can I learn to reset my heart by myself? For work I’m more often than not in very remote areas, where there is nothing in a few hundreds mile radius. So if it happens out there, I believe I am as good as gone. The bad thing is that my afib gives me quite a few shitty symptoms. Shortage of breath, dizziness and extreme fatigue. I could feel it the second it started.
The good thing is that I am quite cold blooded, I think with the proper tools and knowledge I’d have no problem resetting myself.
Would it be doable?!
Thanks so much!!!!
Firstly I’d like to say how much I enjoyed reading this blog – really useful in setting out issues at (at least for me) the best level of technicality.
Now I’d like to ask you a particular question about ECV to which I’ve not been able to find an answer.
I’m a very fit 66 year old – I fit into the standard definition of an endurance athlete in terms of my lifelong training hours (many times more than the > 1500 hours I see in papers). I have been used to doing 3 x 10k runs a week, as well as other exercise – cycling, and long tough mountain walks (35Km plus, 3000m of ascent).
About a year ago I noticed that i was getting slightly out of breath at the start of my runs, and it slowly got worse. 3 months ago I had an operation under general anaesthetic that prevented meaningful exercise for about 6 weeks. When I went on my first run after that, I was immediately, and throughout the run, having to stop because of breathlessness ever few hundred metres. I went to see my doctor, who diagnosed AF, confirmed by an ECG.
My question relates to WHEN ECV should be done. I’ve had advice that it should be done as soon as possible after the event – apparently the longer it’s left, the harder it is to get a sinus rhythm that is sustained (ie doesn’t revert to AF after a relatively short time). I’ve done a good bit of reading, but haven’t been able to find anything. Can you shed any light on this?
Thanks for your kind words on the blog. Your question is a good one. My answer will be based on my 30 years of experience in the areas as there are no trials to guide us. I think clearly the earlier you do ECV the better your chances of successful subsequent maintenance of SR all things being equal. I usually allow time for spontaneous reversion back to SR which typically occurs within 24 hours. Also, I look for any precipitating or complicating factors which should be corrected prior to the ECV (low potassium/magnesium, infection, recent surgery, hyperthyroidism, mental status changes, etc.)
Many thanks for your very prompt reply. Very much appreciated!
The absolute best article and explanation I’ve read on cardioversion for the treatment of Afib. Thank you for a thoughtful, detailed description of the benefits and risks of cardioversion as well as an easy-to-understand outline of the different patient responses to Afib.
Thanks so much! That makes me feel better because recently a patient told me this post was far too complicated and gave me a one sheet alternative she had written. I was planning to post that alternative and take a reader poll
I’ve had 30 ECV’s over 9 years to maintain NSR, most of them in the first 2-3 years. My question is about the possibility of Brain Damage from the shock traveling up through the Head. I know the Shock goes through the Brain, because, they didn’t get me completely under recently in the ER Room. It felt like a Bomb exploding in my Head, and that was only at 125J. Also wondering if Paddle placement impacts this. My EP said the Anterior/Posterior placement wrong wrong for AFIB, as we only need to shock the Atria, not the whole Heart. At least half of my ECV’s were Ant/Post placement, and I wonder if that Angle sends more Shock up to the Head.
This may be too off-topic but I cannot understand why a cardiologist would not be called to the ER when a presenting, otherwise healthy, 42 year old female appears at the ER with marked, first-time afib, especially given that she had been at the ER two hours earlier with complaints of excruciating left flank pain – or just anyway. Her heart was electro-converted. There was no anesthesia. There were no beta blockers given. There was no order for anticoagulants following the conversion. There was no order for a cardiac workup. But back to why a cardiologist would not be called in to the ER. Thank you.
I’ve pondered the ER cardioversion for atrial fibrillation. I do not advise this unless there is a life-threatening situation which requires immediate cardioversion to stabilize the patient.
It is also my opinion that all patients with atrial fibrillation should be treated by a good cardiologist, preferably one who has a special interest in keeping up with developments in this complex field and one who has no financial or procedural biases.
Yes, great article.
I would add that there is new information about dementia in afib. There’s an increased risk from minor infarcts over time in those who are rate-controlled and still in arrhythmia. Anti-coagulation reduces that risk as well as the risk of a catastrophic infarct. Stroke. But staying on an anti-coagulant is not a perfect solution. Chances of a gastrointestinal bleed or a catastrophic brain bleed increase somewhat depending on the anti-coagulant of choice. On balance, I’m sure it’s best to take your NOAC in such circumstances. We each must trust that the statistics gotten from the masses will apply to the unique individuals we are.
Still, I opted for an ablation myself. There’s nothing like NSR!
The stress of waking every morning with the worry over your mental future bearing down on you can only make your situation worse.
Thanks. I think the dementia link is likely to be causal although this kind of observational study can’t prove it.
Hopefully this will provide more motivation for those afibbers who are balking at anticoagulation to prevent stroke.
I also think that “there is nothing like NSR” for my patients but I know sometimes and especially in incompetent hands the process of maintaining NSR can cause more complications than it prevents.
Also, a successful ablation is not a reason to stop taking anticoagulation.
Hm. If the ablation is successful, that is, NSR for a couple of years, what reasons might there be to stay anticoagulated? Reverse remodeling takes place, yes? The left atrium and its appendage become safe places again, no? Perhaps there’s a worry about rebound coagulation when coming off the med?
I don’t want to burst your bubble but I am unaware of studies proving that ablation lowers stroke risk and I think guidelines recommend anticoagulation post ablation.
My fear is that ablation makes the atrium more mechanically dysfunction and thus more prone to clot formation. In addition, most patient don’t know when they go into afib and ablation failure is common. If patient goes into afib and is unaware, stroke risk returns immediately.
My heart had this procedure done last night and passed away this morning.
Can you clarify what you are saying here?
Ah. I see.
My AF was very symptomatic. I knew the instant it started or stopped. Episodes only got longer, so…
The scarring by ablation of the atrium and its dysfunction though – that I can understand and, um . . . take to heart!
I recall a friend having what I believe to be this procedure 8 years ago without any sedation, and she begged to stop but they said once you started, you couldn’t stop. Is this the same procedure? If so, why was it originally done with no sedation or anesthesia?
In rare circumstances (usually when patient is in shock with extremely low blood pressure) it is necessary to do a cardioversion for atrial fibrillation immediately and without appropriate sedation or anesthesia. The rationale is that the sedating agents can further and potentially dangerously drop the blood pressure.
The other possibility for your friend is that she was in ventricular tachycardia (VT) which is a much more life threatening arrhythmia. VT is usually associated with profound symptoms and low blood pressure, often with the patient being unconscious, thus sedation/anesthesia not required. Sometimes, however patients develop a less malignant form of VT that is sustained and are mentating on arrival to ER.
With this type of patient it is often possible to use medications to convert the rhythm, however, a particularly eager and aggressive ER doctor could conceivably rush in and do an electrical cardioversion right away.
This was very interesting information … as your posts usually are. It’s been a very long time — 10 years since I participated as a nurse in the assistance of treatment of patients undergoing cardioversion for a-fib. It was never a dull moment for me and MY adrenaline (or epinephrine) level was always high. I was always scared for the patient but knew this was a good treatment for them and just loved successful outcomes for them — which seemed to be most of the time!
I’ve always found it interesting when I talk to patients how some know they have a-fib going on and others don’t notice a thing. I think cardioversion is obviously more preferable to being on a medication when possible.
You’ve inspired me to do some more continuing ed in the cardiac arena! <3
Thank you. I too am totally fascinated by the difference in how patient’s feel when in Afib. I think it has to do with how the patient feels discomfort/pain in general-some are naturally stoics, others with extremely low threshold for any body disturbance. More research definitely needed in this area!
Off topic … but kind of on topic (the heart) … I asked an anesthesiologist which was more accurate in determining LVEF (ejection fraction) — an echocardiogram (not TEE) or myocardial perfusion stress test. The anesthesiologist said an echo. I would have thought the myocardial perfusion.
Can you answer why (or better yet) make a post? Just wondering. I know I could Google the heck out of the answer, but there’s some special hearing an answer from a “real life” specialist.
Wow!. The things I could write about ejection fraction, the main measure that we have of the pumping function of the heart.
Good topic for discussion. I can tell you briefly what I teach my residents and previously taught cardiology fellows.
A well-done, well interpreted transthoracic echo EF is far more trustworthy than an ejection fraction obtained from a nuclear or myocardial perfusion stress test. I read them both on a regular basis in multiple areas and have done so at multiple hospitals.
Briefly, the limitations of the nuclear gated imaging-unreliable if heart rhythm irregular, cannot reliably assess if large prior heart attack, unreliably high in people with small hearts. I can’t tell you how many times we’ve gotten a questionably low EF from nuclear and verified normality by echo.
Now, since I review personally the echo on my patients, I can be guaranteed that the EF is correct and is “well done and well interpreted”. If you have read my postings on botched echocardiograms you know that is not always the case 🙂
I’ll have to go back and read many of your posts. I’m happy that the anesthesiologist and his cohorts all agreed with what you’re saying — that the transthoracic echo was more accurate with EF — they said it without hesitation.
While I don’t work directly with cardiologists, I do obtain cardiology records — echos, stress tests, pacer checks, EKGs and office notes.
I read most of them most of the time and yesterday I had an echo that said 60-65% EF and the myocardial perfusion said 81% — I was thinking this was quite a difference since they were performed on the same day. I finally thought to ask the question which was more accurate because I like to document in my nursing history (that is read by the anesthesiologists) the EF … but didn’t know which one to put because of the difference. I wanted to put the higher number, but thought I’d ask. The question had never dawned on me before. I had always thought the two tests would have relatively same results regarding EF … not so yesterday.
That is a typical scenario, abnormally high EF by MPI (likely smallish woman with smallish , normally functioning heart) with echo EF more accurately reflecting the true systolic function.
I would also point out that with echo we are directly looking at the heart muscle on a beat to beat basis.
With MPI it’s a totally indirect image compiled from thousands of beats and the heavily processed and manipulated.
Yes, if my memory does serve me correctly it was a smallish woman — weight no greater than 140 lbs. sent for testing due to abnl EKG, but the stress and echo turned out fine except for some mild MR.
OK, back on topic.
I could not believe it when I first read of some people not actually knowing they were in AF.
Going into AF, to me, means suddenly knowing something is drastically wrong. My ribs are being thrashed from inside by something frightened – wanting to escape. Adrenalin spurts, and then the fright is mine. If I quieten and sit – which I must to catch my breath – I can sense the low buzz of the fibrillation.
I’m thin. Not much covering those ribs.
I wonder – is there a correspondence of cushioning obesity with “silent” AF?
I really think there is. This is based on my anecdotal experience. Some day, I’d like to review all my patients and classify them as silent afibbers or symptomatic afibbers and compare BMI.
That being said, I did see my very thin 94 year old lady yesterday (who self monitors for afib with her iphone/alivecor) who when I first saw her was in afib at 140 BPM and was totally unaware.
I have had 23 Cardioversions,2 Ablations,pacemaker and I am on 200g of Amiodarone. I only seem to stay in sinus rythym or several months. I am 80 years old and as active as I can be. When I go into A fib I go into fiteage,dizziness,shortness of breath. Am I a candidate for a Watchman procedure.
I’m sorry to hear of your ongoing AF problems.
The Watchman will not help you stay in sinus rhythm, it is designed just to reduce your risk of stroke or embolism.
Just became a “follower”, (man does that sound cult-ish), and I am so excited to start reading your posts.
I am the son of an elderly parent who has myriad heart issues – one of which is A-fib. We have done the Caridoversion thing, and it worked very well.
I’ve often found myself having to simplify jargon for my parent, and this was no exception. It helps to calm the nerves by distilling the scary bits down to that which is giggle-some. It also serves to quell fears of distant family who are concerned about such processes.
To that end; I’d like to add/propose my renditions of non threatening names for this procedure – if you will allow.
I have used: “Defribu-Lite”, “Fribu-later Alligator”, and (for the 50 Shades fraternity), “A Firm Yet Gentle Paddling for That Saucy Ticker”.
Please keep the blogs coming.
Brian, London Ontario Canada
Great! I’ll try some of those out on my patients.
As an atrial flutter participant, and a lay person,
Your blog was understandable, informative
Important for family member knowledge.
Very comforting as well. Your picture may need
Some George Lucas help, but yet, good.
Thanks Doc, that’s one of the things I like about you, which is communication.
Continue your fine approach to medicine!
I’m a fan of cardioversion, having had one to eliminate a mixed AF/atrial tachycardia. A nasty combination.
It worked in one. Except for the sticky pads and the normal rhythm, I’d never have known they did it.
My question is about those antiarrhythmia drugs. None is ideal. They range from hardly effective, through dangerous in the context of heart disease, to downright poisonous – as in amioderone.
Could you discuss them?
I would love to discuss the anti-arrhythmic drugs and my personal approach to them. Definitely a complicated area and I don’t want to give it a superficial treatment. I’ll post my summary down the line when time permits.
I will say that I use two drugs for 95% of my patients and that I know these two drugs inside and out and with extreme vigilance and meticulous monitoring coupled with 20 years of experience I find them to be safe and effective.
I’ve had three ablations: AF, flutter, and atrial tachycardia.
I’ve now graduated to dofetilide after a tachycardia of 230 beats/minute, conducted one-to-one, atria to ventricles. Dofetilide and oral diltiazem have been doing the job for three months now. I’ve been told that I might be good for three years on this stuff. That’s all??
What then? Well, then I would be eligible for His bundle pacing after ablating my AV node. Yikes! Sounds drastic.
Your take on this?
Your take on the anti-arrhythmia drugs in general?
Had cardioversion today. Converted, but noted before leaving the hospital diffuse very mild burning across my breasts and upper arms and my middle back. Is it common for the shock to travel under the skin to cause mild burning sensations. Thanks for your input.
Slight irritation/burning would not be unexpected