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Sympathethic response to vagal domination

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This is just pure speculation, but has anyone else noticed that just before

and during an AF episode, their blood pressure is abnormally high? I know

some AF patients experience a dangerous fall in blood pressure, but many

have the opposite; I have a theory as to why blood pressure might rise in

those with vagally induced AF (either full or partial vagally induced AF);

Since there is meant to be a delicate balance, and feedback mechanism

between the parasympathetic and sympathetic nervous systems, both of which

are part of the " autonomic " nervous system, an imbalance in one area would

logically cause an imbalance in the order; For example, lets assume that

many of us in here have vagally induced AF, either partial or complete vagal

nerve hypertonicity. A logical response by the cardiac nerve/sympathetic

nervous system, is to " upgrade " itself and become hypertonic itself; This

reaction would in turn cause the vagal nerve to " rebound " and become even

more dominant, and a dangerous neurological feedback pattern could be

established;

In the brain, it has recently been discovered, that certain neural

circuits are formed that can actually change the physical structure of the

brain; This is accomplished because, during any trauma, certain

neurotransmitters are released, which order the brain to physically change

structure, up to a point, to accomodate the trauma; These neurotransmitters

are called " second messengers " , and are a known phenomenon after a stroke,

physical injury, even a profoundly stressful event; Those with both panic

disorders and post traumatic stress disorder are known to many researchers

to have altered brain structures due to these " second messengers " which are

not normally released by the central nervous system, but are held in

specialized cells in the mid brain region.

Hence, taking this research and applying it to AF patients, its entirely

possible if because of vagal nerve dominance the sympathethic nervous system

responds in kind, these second messengers could be released into the brain

and cause neural circuits which will trigger AF, even on a cognitive basis

(by mere thoughts of relaxation paradoxically causing a sympathethic surge,

triggering a hypertonic vagal response, and hence AF).

I postulate that these neural circuits can be bypassed IF a new

medication can be developed which is both " vagolytic " (sedates the vagal

nerve), and adrenergic antagonist (beta blocker effect); Perhaps combining

flecainide (thought to be vagolytic) with a beta blocker might be

considered;

These AF neural circuits would remain, but IF we could control the vagal and

sympathetic nervous systems, over time, we could develop cognitive

mechanisms which would cause the AF neural circuits to be atrophied and

hence of minimal concern;

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> ... I postulate that these neural circuits can be bypassed IF a

new

> medication can be developed which is both " vagolytic " (sedates the

vagal

> nerve), and adrenergic antagonist (beta blocker effect); Perhaps

combining

> flecainide (thought to be vagolytic) with a beta blocker might be

> considered;

> These AF neural circuits would remain, but IF we could control the

vagal and

> sympathetic nervous systems, over time, we could develop cognitive

> mechanisms which would cause the AF neural circuits to be atrophied

and

> hence of minimal concern;

, I only partially follow your message, but I think from what I

have read here that I do not myself have vagal afib - with me so far

as a newbie, stress has always been the trigger, and in fact each

morning when I transition from sleep to being awake I have to

consciously calm down as my heart is racing, etc., just the opposite

of the posting earlier about how relaxation triggers afib for some.

However, I have had anxiety attacks for many years.

I am wondering if taking Ativan (tranq) quite regularly along with my

beta blocker might " reprogram " my brain for less afib and less

anxiety... The only problem with this is that apparently people

adapt to Ativan over time and have to take higher and higher doses.

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If in fact you do not have any of the symptoms of vagally induced AF, then

indeed you probably have adrenergically induced AF (sympathethic nervous

system overstimulation of the heart);

Those with panic attacks, have what is called an " upregulated " sympathethic

nervous system; Attivan which is a benzodiazepine along with a beta blocker

can be generally effective in controlling this type of AF; However, the

body does develop a tolerance to benzodiazepines and hence the potential for

addiction is quite real.

This presents a real dilemma since the only other known treatment,

chemically, that is for an overactive sympathethic nervous system is the use

of anti-depressants; As mentioned a few days ago, these have the potential

of triggering an AF attack, particularly if they block the reuptake of

norepinephrine. The theory behind the use of these antidepressants in the

treatment of panic disorder is that if you actually overstimulate the

sympathethic nervous system chemically, that nervous system will eventually

(within 2 weeks) " downregulate " itself and hence will quit causing both the

panic attacks and the AF as well;

Its a risky strategy, one which might work if you could tolerate the AF

risk for two weeks; I too was diagnosed with a panic disorder back in 94,

and I was never willing to take that risk;

There is another alternative, one which also involves risk, but which is

less of a risk than the antidepressants; That involves moderate exercise, ie

walking around 2 to 4 miles every day; Such walking might also trigger AF,

but at least you would be strengthening the heart muscle which I have found

counteracts the palpitations which can trigger AF;

Re: Sympathethic response to vagal domination

>

> > ... I postulate that these neural circuits can be bypassed IF a

> new

> > medication can be developed which is both " vagolytic " (sedates the

> vagal

> > nerve), and adrenergic antagonist (beta blocker effect); Perhaps

> combining

> > flecainide (thought to be vagolytic) with a beta blocker might be

> > considered;

> > These AF neural circuits would remain, but IF we could control the

> vagal and

> > sympathetic nervous systems, over time, we could develop cognitive

> > mechanisms which would cause the AF neural circuits to be atrophied

> and

> > hence of minimal concern;

>

> , I only partially follow your message, but I think from what I

> have read here that I do not myself have vagal afib - with me so far

> as a newbie, stress has always been the trigger, and in fact each

> morning when I transition from sleep to being awake I have to

> consciously calm down as my heart is racing, etc., just the opposite

> of the posting earlier about how relaxation triggers afib for some.

>

> However, I have had anxiety attacks for many years.

>

> I am wondering if taking Ativan (tranq) quite regularly along with my

> beta blocker might " reprogram " my brain for less afib and less

> anxiety... The only problem with this is that apparently people

> adapt to Ativan over time and have to take higher and higher doses.

>

>

>

>

>

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