RLR
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Okay, welcome to the forum and I've read your posting. I'll first respond by sharing with you that your predicament is quite common, shared by many persons who experience benign palpitations.
It's important for you to understand that these particular events are extra-cardiac in nature, meaning that they originate from outside the heart and more specifically, by way of the vagus nerve as a consequence of stress, anxiety and in equal instances, GI difficulties. It's purely a matter of physiology in motion and nothing to do with the palpitation events constituting a sign of trouble regarding your heart's performance.
One of the reasons that patients who experience this type of event become so frustrated is that their own perceptions lead them to believe that since the symptom is associated with the heart, then common sense dictates that the underlying cause is associated with the heart as well. Concerns are elevated because most people relate any irregularities associated with their heart to be a potential warning sign that something is wrong and that an impending cardiac event is looming. When you proceed to your primary care physician or specialist, the events more often than not subside and with very good reason; This type of harmless palpitation event is manifested by the parasympathetic nervous system. Apprehension about what the doctor might discover typically causes a rise in sympathetic tone that becomes dominant. Thus, the palpitations events temporarily subside.
From analogous perspective, you can think of the sympathetic nervous system as the accelerator pedal side of things, elevating heart rate and respiration, vasoconstriction and increased BP, decreased GI motility, increased cognitive vigilance and so on. It prepares the body for action. By contrast, the parasympathetic nervous system constitutes the brakes once action is completed, i.e. decreased heart rate and respiration, vasodilation and diminished BO, increased GI motility, decreased cognitive vigilance etc. These two nervous system components components create dynamics between activity and relaxation. So for instance, when your blood pressure rises to significant levels at the doctor's office, a phenomenon we call white-coat hypertension, it is due to elevated sympathetic tone as a consequence of apprehension and discomfort by what the doctor may find. Once everything has been determined to once again be okay, you find that your blood pressure lowers once again to a baseline more normal for you.
When the palpitation events do occur during diagnostic evaluation, they will technically appear as either paroxysmal atrial contractions or paroxysmal ventricular contractions depending upon precisely when they enter the cardiac cycle. The key issue, however, is the origin of the events. Beta-blockers work by reducing the amount of cardiac force necessary by the heart to carry out its functions. We use this drug primarily in instances where patients have experienced a cardiac insult of some type and in the presence of this drug, the heart doesn't have to work as hard. Beta-blockers also help regulate heart rhythm to some extent as well. An added benefit of the drug is that it produces a mild anxiolytic effect and for patients experiencing anxiety, this is a good option. Calcium channel blockers work by tempering the conduction activity of the heart as a means to reduce any irregularities in rhythm.
So we have two instances where drugs either work to reduce mechanical force by the heart or conduction patterns in order to safeguard against problems which might arise. Neither drug is effective in the instance of vagus nerve-induced palpitation events, which are more akin to the factors which produce a muscle twitch elsewhere in the body with the exception that in this particular case the muscle happens to be the heart. The mention of GI problems as one of several precipitating factors which lead to benign palpitation events is due to the fact that the vagus nerve innervates the GI tract as the pneumogastric nerve. Any inflammation, i.e. bloating within the lumen of the intestines, can exert physical pressure against the diaphragm and consequently produce wayward parasympathetic nerve impulses which travel along the vagus nerve to all of the terminal endings, one of which is naturally the heart. All that is taking place during a benign palpitation event is the heart muscle responding to a wayward nerve impulse, nothing more. So the drugs mentioned work quite well with respect to internal mechanical and conductive issues related to the heart, but they are unable to influence a basic external excitation from the vagus nerve. There are drugs such as scopolamine which can dampen vagus nerve activity that could theoretically diminish the potential for palpitations of this type to arise, but the side-effects make it far too contraindicated for use in treating such events.
Benign palpitations are actually quite common and most humans have experienced them in the very isolated context of arising subsequent to being suddenly startled or frightened. I'm sure you've often heard someone speak about the aftermath of a sudden fearful event, exclaiming "Gosh! That made my heart skip a beat!" or "That made my heart leap out of my chest!" What these people are unwittingly describing is a vagus nerve-induced palpitation event. It's temporal proximity to a fearful occurrence establishes reasonable cause and therefore, persons experiencing them do not rush to their doctor with fears that something is wrong with their heart. It is deemed a logical manifestation as a consequence of being suddenly frightened.
In the case of chronicity, however, the patterns are much different. In such instances, persons with frequent palpitations in the absence of a direct known cause results in the establishment of fear and apprehension consistent with the duration of the symptoms.
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