Heart rate dropping, need input

I am currently on a 30 day monitor. Right now at about day 18. My heart rate is normally in the 70's or 80's and in past years even been a little tachy.

Anyway, during my first week of monitoring it dropped momentarily to 60 a couple of times. Then this morning to 55 a couple of times. Is this something I should be concerned about? Does this happen to anyone else. I am not one of those super fit types whose normal heart rate is in the 60's or 50's.

Any thoughts?

Lynn,

Are you taking any meds such as a beta blocker?

Marian

No meds. on a daily basis. Could 500 mg. of taurine do this?

Lynn
Re Taurine, it is not my experience and I take 1000 mg four times a day but the only way to see if it is the taurine is to stop taking it at least temporarily. Prior to my ablation I couldn't take taurine as it felt agitating to my heart. We are all slightly different.
Hopefully your cardiologist/EP will be able to advise you after they read the holter results.
Cyndie

Lynn,

I'm guessing it is completely normal. If you've not had monitoring before, you may not have noticed it.

I've had exercise heart rate monitors (HRM) for many years - even before I had afib.

The pre-afib monitors recorded on a 15 second average and the display showed a averaged value (5 second, I think). My heart rate varied, of course, but for any particular exertion level, appeared rock steady.

Once I got a beat to beat recording HRM, I was amazed at the beat to variability. Then, after some investigation, I learned that this variability is considered a sign of health and tends to decrease as we age, and also as our fitness level declines.

These guys use respiratory sinus arrhythmia (i.e. breathing) [en.wikipedia.org] to change heart rate [www.coherence.com]. As you can see, with intention and practice, you can make variability quite large. Their bottom line is a 5 second inhale & 5 second exhale will create the largest variability.

This device [www.resperate.com] similarly uses breath to lower blood pressure (has clinical studies behind it). It is the same technique used by the coherence.com people, they just charge more for the device. A clock with a second hand or a recording with a chime at 5 second intervals would work as well.

In any case, I've lived in the 50's for years (heart rate wise) and my HR can drop into the low 40's during sleep. There are some endurance athletes who've posted about their low 30's HR. At some point, certainly in the 30's, the vagal ANS can be deleterious to an afibber as the vagal ANS will shorten the atrial effective refractory period (AERP) and this can increase the probability that afib will occur. That being said, a few beats in the 50's are not in this category.

George

George:

Thanks that is very interesting. The first time I noticed these low beats I was in a semi-sleep state and it really startled me. I must be extremely sensitive to my heart rhythms. I usually monitor my rate manually or with my BP cuff so I was not aware that such variability existed within 1.5 minutes (100 high, 57 low). Most of my recordings to not reflect such dramatic variability

What concerned me about the low rates is that I am now using a BB for my PIP. The last time I took the BB it seemed to nip an episode in the bud. Whether this will continue remains to be seen, but the low rates made me wonder if the BB will have to go by the wayside or if I was developing sick sinus.

What is ANS?

The effects breathing are remarkable. Maybe you are on to a cure for a-fib. Perhaps if we all trained like Tibetan monks we could overcome this beast.

Lynn,

ANS is autonomic nervous system (i.e. makes you more vagal or adrenergic) see: <[www.afibbers.org];.

As to using a BB for PIP. I don't think this is an issue. Continuous use of a BB would be another story for a vagal afibber. When you use it as PIP, you are already in afib. The issue with continuous use of a BB for a vagal afibber is it will "slow" down an already slow heart.

The issue is AERP <[www.afibbers.org]; I'm referring to this relationship:
Atrial ERP shortening due to (P cells + low potassium + ANS tone) => AF Risk
You can read more about this in PC's explanations I've linked the search to in my link.

The ERP is essentially the "reset" time during which heart cells will not depolarize. The shorter the ERP, the more likely they will depolarize from an errant source (i.e P cell or pacing cell).

This is what is supposed to happen:

"The rhythmic sequence of contractions is coordinated by the sinoatrial (SA) and atrioventricular (AV) nodes. The sinoatrial node, often known as the cardiac pacemaker, is located in the upper wall of the right atrium and is responsible for the wave of electrical stimulation that initiates atrial contraction by creating an action potential. Once the wave reaches the AV node, situated in the lower right atrium, it is delayed there before being conducted through the bundles of His and back up the Purkinje fibers, leading to a contraction of the ventricles. The delay at the AV node allows enough time for all of the blood in the atria to fill their respective ventricles. In the event of severe pathology, the AV node can also act as a pacemaker; this is usually not the case because their rate of spontaneous firing is considerably lower than that of the pacemaker cells in the SA node and hence is overridden."
[en.wikipedia.org]

When a P cell fires before the SA node, this leads to a PAC. However if you have a long atrial ERP, then and the P cell fired before the end of the ERP, nothing happens. So, a longer ERP is better. Reentrant wavelets in the atria end up as afib.

This is a brief, incomplete explanation, but hopefully you get the point.

Whether with meds or a lifestyle/supplement approach, much of what we are trying to do to keep afib at bay is to lengthen the atrial ERP.

An explanation of an approach is here <[www.afibbers.org];

On the med side: in this flecainide study, a conclusion is that it increases atrial ERP [www.ncbi.nlm.nih.gov] "Conclusions: 1) Flecainide suppresses atrial action potential duration accommodation to heart rate changes in vivo, leading to rate-dependent atrial effective refractory period prolongation, which may be important in suppressing atrial fibrillation."

George