Maybe a Dumb Question, But I was Wondering

Chronotropic incompetence

by AgentX86 - 2020-08-02 22:42:24

I'm not sure I understand your question.  The whole idea of rate response is to overcome chronotropic incompetence by mimicing the heart's response to oxygen demand. 

Bradycadia whether caused by sick sinus syndrome or drugs (or SSS caused by drugs) is fixed with the minimum rate setting.  If the heart does't beat on its own in a certain perriod (1s = 60bpm), the PM supplies the impulse to start the heartbeat. 

Chronotropic incompetence is a dynamic heart problem, where Bradycardia is a static problem.  Often the two go together.

Good question

by crustyg - 2020-08-03 06:09:56

Heart output, on a beat-to-beat basis is controlled by rate and how hard each contraction is, and this latter is controlled by calcium channels (calcium ions are necessary to allow the muscle fibres to contract and more calcium ions means harder contraction).

Beta-agonists (adrenaline etc.) and the sympathetic nervous supply to the heart tend to increase the calcium ion supply at the heart cell level =>stronger contraction.  So a beta-blocker should produce *less* powerful heart beats.

Your PM stimulates your heart to contract with a small electrical impulse.  As long as this impulse isn't delivered during the refractory period (while the cells are repolarising/recharging) when no amount of electrical stimulation will have an effect, your PM can drive your HR to any value that it's been set for.  Nothing (except above) will stop this.

So, while the short answer to your Q 'can my PM override the bradycardia of beta-blockers' is YES, it may still leave you feeling weak and breathless if your heart ouput (BPM * strength of contraction) isn't high enough due to your beta-blocker.

The paradox of beta blockers is that observational studies showed that they improved survival in patients with heart failure (odd, because betablockers normally *reduce* the strength of heart contractions as above, and most docs felt that this would make HF worse), and this led to research to understand possible mechanisms.  It seems that beta-blockers can restore the normal control of calcium channels (and hence more normal heartbeat contractions) by modifying the long-term overly active calcium channels which had flooded the muscle fibres with calcium ions.

So, if there's an element of HF in your case then long-term beta-blockers may actually have helped restore more normal heart muscle action, and this, combined with the PM's rate response driving your heart faster, may help increase your heart output when you need it.  We can discuss/argue in another thread what I/we mean by HF...  So it's entirely possible that your perception 'things are getting better as you work hard' may well be correct.

Isn't life strange!

Best wishes.

heart rate

by Gemita - 2020-08-03 07:31:05

Hello Mary,

It is not a dumb question, but a really interesting one.  

No expert here but I feel that medication to slow our heart rate down will continue to cause problems for us as we try to get our heart rates up during exertion.  I do not believe this will improve until and unless we are able to either stop or reduce the medication that we have to take, or perhaps trial other meds/options for effective treatment of our arrhythmias.  

For example when I first got my pacemaker I was taking Digoxin, Flecainide and Bisoprolol.  Even with my pacemaker set at 70 bpm night and day and rate response switched on, I initially struggled during exertion with tachycardia episodes (I also have Flutter as well as AF, SVT and non sustained VT).  It was the tachycardia and my heart rate meds trying to hold me back that were causing the problems.

Then something changed.  I noticed that my anti arrhythmic meds (Digoxin and Flecainide) were making my arrhythmias worse and were found by my pacing clinic from monitoring/data downloads to be causing occasional higher heart rates.  I was told to slowly reduce doses and the tachycardia eased.  I eventually came off both Digoxin and Flecainide without any ill effects and my arrhythmia burden has greatly decreased.  Quite incredible.  I am now on low dose Bisoprolol alone and am able to get my heart rate up without difficulty.  

I would suggest you experiment with your medication.  Metoprolol can be difficult for some of us who report extreme fatigue, weight gain and difficulty exercising.  

So, In answer to your question “is it possible for the rate response feature in a pacemaker to overcome the problems caused by medications such as beta blockers or calcium channel blockers in a patient with sick sinus syndrome” I would say probably not because even with rate response appropriately set, I believe you will certainly still be held back by your medication when trying to exercise.  Additionally during an arrhythmia, exercise is often not possible or at least much more difficult to perform.  I would say try to control your arrhythmia more effectively, reduce your meds to a minimum and you will have far better control and ability to increase your heart rate during exercise in the future - easier said than done I well know !

Not a dumb question !

by IAN MC - 2020-08-03 12:10:29

It seems to me that many different things can cause exercise  intolerance  (  i.e. Chronotropic  Incompetence )

As has been said sinus node dysfunction is a common cause of C.I.  but there are many other causes …  drugs such as beta blockers, digoxin,  amiodarone  can  cause it, as can heart valve problems and of course heart failure.

I have never seen it suggested that rate-adaptive pacemakers be used as a routine treatment for example heart failure ….  So it seems to me that the value of PM –triggered rate response does depend on the cause of the chronotropic incompetence .   So Mary asks a very good question in relation to drug-induced C.I.

“ I don’t know “ is the most honest answer I can give but my simple mind has arrived  at the conclusion that :-

• As I suffer from S.S.S.  together with chronotropic incompetence then I would really avoid any drugs which are known to cause further C.I. if at all possible. I would rather give my Medtronic rate response sensor as easy a life as possible.

Am I missing something ?

Ian

Flecainide

by AgentX86 - 2020-08-03 14:17:27

Flecianide is well known to switch suddenly from an antiarrhythmic to a proarrhythmic overnight. Anyone on it should be aware of this property of the drug.

Metoprolol has no control of the heart rate when exercising and rate response is enabled. That's all the pacemaker, unless of course someone turned on RR for no good reason (and they're going to fight which will likely feel awful). Resting heart rate could be either, depending on the health of the sinus node. If it's above the PM's set minimum,  it's the heart's own pacemaker (the SI node). If it's equal, you don't know and less, there is some sort of arrhythmia going on.

There are several settings for rate response that need to be tuned for different situations and it's rather a balance of all if them to optimally set the PM up for your needs. It's often a tradeoff between activities

I would suggest that you work with an EP to get the drugs and PM balanced.  There are too many variables to guess. A good EP and device technician are very important for an active lifestyle.

Great Responses, lots to think about!

by Marybird - 2020-08-04 00:13:43

Thanks, everybody for the thought-provoking comments. Y'all are great.

Agent X86, I've never been officially diagnosed with CI-  no testing specifically for that, it was the documented symptomatic bradycardia over time, along with the atrial tachycardia, that won the "sick sinus syndrome" diagnosis. Though this was accompanied (before the pacemaker) with the inability to get my heart rate up to decent rates with moderate activity as time went on, and I felt like an old car stuck in first gear. That or it'd go up ok with activity, then fall into the low 40's suddenly, and stay there when I was involved in activity and I'd have to stop, get a grip or pass out. I guess that's what I thought was CI, maybe not?

Before the pacemaker, when I exercised, I often had to stop and get a grip ( with exercise I've been doing for years!), to accomodate the breathlessness, lightheadedness and the chest discomfort that came about at my efforts to work through the lower heart rate. That or I'd sometimes go into tachycardia, and I've found it nearly impossible to exercise though that as it was also symptomatic. I figured the metoprolol was probably partly responsible for the bradycardia/CI, yet if I exercised without taking the previous dose I'd end up with tachycardia. So I took the meds at the regular prescribed intervals, and wished myself luck.

I've had nuclear stress tests with instructions not to take the morning dose of metoprolol before the test. I always had to forego the evening dose too, just to make sure it wouldn't affect my ability to get to my target heart rate, and I was able to do so, though I'd have PVCs and short runs of SVT and EKG changes that muddied up the test interpretation somewhat. The last one in 2019 earned me a cardiac cath, but that showed, according to the cardiologist, that I "had the coronary arteries of a teenager", so no coronary artery disease there.

A couple things you all mentioned about the effects of the beta blocker and calcium channel blocker acting to make the heart rate less "forceful" make sense to me. In that case even with the pacer rate response acting to make the heart beat faster in response to activity, it could be possible, seems to me, that the heart's output in that case might be less than needed by the person for a given activity, even deficient enough to cause SOB, tiredness. In this case the higher the activity level, the more that would be seen. And I guess higher doses of the meds would be more likely to cause these issues in a patient prone to such issues. For some reason, I have the impression that it's the diltiazem, more than the metoprolol, that may slow down my reaching my target heart rate during exercise, if indeed that happens.

Far as I know I don't have heart failure- the testing Ive had in the last year showed a good ejection fraction, and I don't have fluid retention or SOB. CrustyG, I'm sure I could have headed there with some issues in the past that I basically ignored ( such as resistant hypertension-hereditary and that stupid tachycardia) till these came back to bite me you know where. Getting these under control and losing about 50 lbs over the last few years no doubt has improved things heart-wise for me.

I can say the rate response turned on with my pacemaker has made a big difference in my being able to do about anything I want, has given me much more energy and stamina. And apparently if I'm atrial paced at around 91% ( last report), the pacemaker seems to be doing quite a bit of the work. I don't notice any issues during regular activities- the heart rate increases nicely for whatever I'm doing, it's just that trying to get to that target heart rate during exercise can be a challenge sometimes- or perhaps it's just me.

I mentioned this to the pacer tech at my last in-office device check, he said they could increase the rate response to accomodate any exercise or other activity I wanted to do. Well, I thought about it, thought about how that rate response could also increase the heart rate when you really didn't need it to, ie, bending over to pick something up, riding on a bumpy road, rocking in a rocking chair, if it was too sensitive. I hate that feeling when it happens though I know what it is, but where it's set now, it only reacts like that when I ride across one of our old bumpy bridges taking the back way home, when I flip over in bed at night, and when I rock in the rocking chair. I guess with the rate response turned up I might be able to exercise better, but I don't want the tachycardia every time I bend over, so I told the guy I'd like to leave it where it was. Unless, of course, I got into endurance althletics, which in truth will be about when the cows come home. The rates on the pacermaker are lower-55, upper 120. So anything above that is me, but it's hard to get there unless, of course it's tachycardia, LOL. The upper range originally was set at 130, but they set up a "tachycardia alert" at 140, so lowered the upper range so as not to overlap with that.

As for the meds. My two bears which are hard to control at times are the atrial tachycardia, and resistant hypertension. I've had the hypertension since I was in my 30's, my dad was the same, and I have two siblings with the same issues- and they both have afib, one sister also has SSS and a pacemaker. I've taken medication for years for both, have modified my lifestyle to healthy ( most of the time) diet and exercise, and as best I can, avoidance of stress. Still have issues with both at times, but have found the medications including the metoprolol and diltiazem ( along with two other meds for the blood pressure) have done pretty well to control both the tachycardia and the blood pressure. Gemita, I"d love nothing more than to decrease the meds, and have tried over the years, but this resulted in the blood pressure climbing back up, sometimes to dangerous levels, and the tachycardia rearing it's ugly head again. I've been informed by most of the docs I ever saw ( including the PCPs, cardiologists and two EPs over the years) that no matter what, I'd still be taking meds. I even discussed maybe ablation for the atrial tachycardia, and the EP didn't encourage that as he said these are notoriously hard to ablate as they can be hard to induce and sustain in the electrophysiology lab and thus can be hard to locate, or can even aggrevate other spots in the atrium- and I saw this happen with my poor daughter, so I know he wasn't telling tales. He suggested that if it could be controlled with medication, and a pacemaker as needed, that was the way to go. I agreed with him.

The EP had suggested the possibility, in the future, of using antiarrhythmics to control the tachycardia- he mentioned flecainide, propofanol, and even dofetilide ( that's the one they put you in the hospital for 3 days to make sure it doesn't do you in) in the event the meds I was taking stopped working. I informed him, as well as the new EP at that clinic, as well as any doc who'd listen, that I'm leery of antiarrhythmics- having seen family members have severe reactions to them, and really wanted to stick to the rate response drugs I was taking as long as humanly possible. There are always tradeoffs when you take drugs, but I've found these work well for me, are inexpensive and can be used to control both my tachy and blood pressure. At least for now. As you indicate, it's always a work in progress as things change, but for me, I think this is ok for now.

Thanks again for the thoughtful responses. Mary

Good luck

by Gemita - 2020-08-04 08:59:01

Mary, you certainly know yourself well and that is a big help when dealing with tachy arrhythmias and I do appreciate everything you say and would whole heartedly agree with you.  Hypertension is so dangerous and you have to do everything in your power to try to control it, otherwise it would lead to many serious health conditions and trigger worsening arrhythmias like atrial tachycardia.

I agree about anti arrhythmic meds potentially being dangerous (pro arrhythmic in my case) and, in any event, they are just not very effective long term to control our arrhythmias.  An ablation is certainly a better option for a potential cure, but it is not without risk and I declined an ablation a few years ago, choosing to go down the pacemaker and beta blocker route.  It has been a good treatment plan for me.

I agree, a beta blocker or calcium channel blocker is indeed a safer option for heart rate/arrhythmia control as well as blood pressure control.  My cardiologist said the same to me when I started my journey with arrhythmias.  At the time, I didn’t really want to listen to him, assuming he didn’t want to treat me or offer me an ablation.  I was wrong and should have listened to him and not pushed for an anti arrhythmic like Flecainide which certainly caused worsening rhythm disturbances and I believe triggered Atrial Flutter too (since I was not taking an AV nodal blocking agent like a beta blocker for protection at the same time).  

I have very low blood pressure (too low in fact) and this can be equally difficult to manage.  I have tachy/brady syndrome too and hence was given a diagnosis of SSS.  I have lots of different arrhythmias but I can honestly say that with a pacemaker set heart rate of 70 bpm day and night and with minimal medication (beta blocker alone) everything has improved.   My body was crying out for this treatment. I too have a relatively clean heart history (no clogged arteries), although a few insignificant leaky valves.  Am quite a “sensitive” female (71) so perhaps not altogether surprising I have arrhythmias but perhaps this should be another thread ! 

Good luck Mary.  I am sure you will do very well. You sound as though you have got a good team of doctors to work with, with your best interests at heart.

Can a PM take control when medication slows the heart?

by Selwyn - 2020-08-04 16:46:55

Yes, I PM will take over pacing ( that is the heart rate) when the heart rate is too slowed by medication.

My Mother-in-law had a PM fiited especially for that purpose as her heart rate was too slow on her dementia medication ( an anticholinergic side effect).

Having a PM myself, I found that I was not able to exercise with beta-blockers due to breathlessness.. As crustyg says there are other side effects to these drugs affecting contractility of the heart muscle, blood pressure etc.

Selwyn

by Gemita - 2020-08-04 23:59:38

Yes I agree the pacemaker minimum lower rate can be maintained by the pacemaker adequately to provide good support in a resting situation but the question posed I believe is can a higher rate, sufficient to enable a good level of exercise, be maintained by the pacemaker while on rate lowering meds like beta blockers and calcium channel blockers?  I am not sure that the answer is yes.  I see too many folks struggle to meet their full exercise potential on certain medication and throw an arrhythmia into the mix and they struggle even more.  

However I do recall my EP suggesting a pacemaker would allow him to try even higher doses of meds to slow heart rate during my tachy arrhythmias without lowering rate to dangerously low levels because my pacemaker would kick in to prevent rate from dropping below lower limit.  I therefore totally agree that pacemakers in this situation are very very reliable while on rate lowering meds but less so I would suggest when it comes to reaching and maintaining a higher heart rate during exercise. 

It would be helpful to know which rate lowering med (a beta blocker or CCB) might be more likely, in your opinion, to cause more difficulty during exercise ??  I have never tried a CCB but would like to try either Verapamil or Diltiazem.

Rate lowering meds and pacemaker

by AgentX86 - 2020-08-05 15:56:03

Before I got my PM, my EP discussed a PM so he could put me on higher doses of antiarrhythmics for my AFL. My heart rate was already too low and the only antiarrhythmic that we'd tried that worked was ameoderone. That certainly wasn't a long term solution.

I ended up with sotalol but it's a beta blocker as well as an antiarrhythmic. His recommendation was to go the pacemaker route so he could raise the sotalol dose. I tried a couple of ablations after that but the sotalol did in my sinus node so there was no choice but a PM.

Since there was now no choice but a PM I decided that I was tired of screwing around trying to find a solution.  That's when it made sense to go for an AV ablation.

Rate Response and Heart Rate Meds

by Marybird - 2020-08-05 19:10:23

Gemita, you've summarized my original question, and observations about my own experiences so well, in the first sentence of your last post in this thread, in saying " can a higher rate ( response) sufficient to enable a good level of exercise be maintained by the pacemaker while on rate control drugs like beta blockers or calcium channel blockers". It'd seem maybe not as I see it too, though I keep hoping that gradually it'll improve as I push the envelope as I can. 

The ideal would be, of course, not have to take any medications, or as little as possible since the effects of any meds increase as the  dosage goes up ( or so it would seem. Unfortunately those low doses may well not control the tachycardia, ( or blood pressure as applicable), so the tradeoff is control at higher doses for inability to increase the heart rate to accomodate moderate exercise. 

You know this, of course, but the use of a pacemaker to keep heart rates from going too low caused by taking medication "required to control a medical condition, and for which there is no substitute" is considered a Class I ( reasonable and beneficial), by the AAC, AHA and Heart Rhythm Society. This applies to taking rate control drugs for tachycardia, and likely were at least one of the justifications your EP ( and my EP for me-for high blood pressure,too) used as an indication we needed those pacemakers. I'm pretty new to this stuff, and maybe it's my imagination, but it's my impression that the EP's (,and maybe other cardiologists as well) have no problem increasing doses of meds when they don't have to worry about your heart rates going into the toilet anymore. Though the only reason they'd have to do so is if the current dose is not controlling the tachy anymore, or in my case, when the EP doubled my dose of diltiazem to 360 mg/day  at my last visit to get better control of the blood pressure.

It's harder, of course to increase those meds to better control tachycardia when you have low blood pressure issues, since increased doses will drive it even lower. I'd think low blood pressure problems would make tachy control much more difficult than with high blood pressure, I think I could take enough of those meds to bring a horse down and my blood pressure wouldn't go too low!  You mention your tachys seem to be under better control with your lowest pacing rate at 70, that seems to be a good tradeoff. I think my daughter, who has multiple arrhythmia issues and a pacemaker, has low blood pressure issues and they have her lower pacing rate at 80, which I believe has helped her.

You asked about which of the rate control drugs might be more likely to cause exercise issues. It'd probably vary among individuals, but in my own experience, I thought diltiazem caused  more of those issues than metoptolol. I got this impression mainly comparing my exercise at times I was taking metoprolol alone ( a high dose at 150mg/day), with  exercise at180mg/day low dose for diltiazem, no metoprolol ( switched to see if brady stopped, tachy controlled by diltiazem_no on both ). I found I had a much harder time exercising at all on the diltiazem, that heart rate just wouldn't go up at all, unless of course I went into tachycardia, which happened not infrequently. This was before the pacemaker.

Comparing diltiazem and verapamil, they're both calcium channel,blockers andnact similarly. I'm not a doc or pharmacist, but from what I have read verapamil seems to be stronger than diltiazem, it's reported to suppress cardiac activity more than diltiazem. I've never taken verapamil, but it's my impression that a person prone to the heart rate and blood pressure lowering effects of calcium channel blockers might be more affected by these with verapamil, compared with diltiazem. That said, I know of people who take diltiazem as a rate control drug to control their afib ( my sister),  a friend who takes diltizem ( 360 mg/day) to control her SVT and high blood pressure. THey were both told not to take beta blockers-I think that's because it drove their blood pressure too low. They both happy with their diltiazem. 

Might be,worth discussing with your EP, though, everybody's different!

Can a PM increase heart rate whilst on medication that slows the heart rate?

by Selwyn - 2020-08-07 12:08:41

I believe Gemita raises this question.

Ultimately, the heart muscle must respond to the pacing stimulus ( which is why we have PM in the first place!). The rate response, if set correctly, along with the upper rate limit, should not hinder exercise- all things being equal with the stimulus threshold for contraction. 

There are other effects from betablockers, such as the strength of heart muscle contraction ( generally speaking beta blockers have a negative effect). This will limit cardiac output and exercise ability. There is an individual response to this effect. Likewise with some calcium channel blockers such as the nondihydropyridine calcium channel blockers reduce heart  muscle contraction and are contraindicated in heart failure and cardiomyopathies, or at least used in extreme caution. 

Personally, I managed exercise  with verapramil, even with my cardiomyopathy, though could not manage with sotolol, or metoprolol. Everyone is different. '

I expect at the end of the day it all depends on the technology. If you have a good rate response pacemaker, set appropriately,  you should be paced- the heart cannot refuse! It may be that you need to have some adjustments to the threshold stimulus to compensate. An exercise test would achieve this.