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Not Hyper-Pots, So Why Do Bb's Help Me?


joyagh
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I know many POTSies who do not have hyperadrenergic POTS but are helped by using beta blockers to help control tachycardia. Using a beta blocker to help control the tachycardia POTS has blessed us with can help lessen or eliminate some symptoms.

Here is my understanding... Beta blockers lower your heart rate whether you have excess norepinephrine active in your body or not. When the heart is tachycardic, it is pumping less efficiently and using up more oxygen and energy than it would be if it were pumping at a healthy rate. Since the heart is pumping inefficiently, blood flow around the body is less than optimal. The high oxygen/energy demand of the heart when we are tachycardic also contributes to some symptoms. (If you're interested, look into how your body uses ATP in energy production and how this process if slowed down by age and illness) I would think one of the symptoms it could help a little with is fatigue since the heart requires more energy when it is tachycardic. I know I'm less tired with a beta blocker, but I hear of people being experiencing drowsiness.

Since the main symptom we all share is tachycardia, it makes sense taking a beta blocker helps so many. I am one of those helped by one (Propanolol), but if I were to take it without Midodrine, my blood pressure would be dangerously low. Although my resting/standing heart rates are lower with a beta blocker than without, there is still often a 25-50 beat discrepancy from going from laying to standing

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I was taking Beta Blockers when they drew my blood for the plasma norepi test (supine and standing). Does this affect results?

Plasma norepi levels and the presynaptic uptake of norepi were unchanged in some studies for individuals on beta blockers, while other studies have found that long-term ß-blockade is associated with decreased norepi level.

Alpha-adrenergic agonist, angiotensin II blockers, beta blockers each in their own way are supposed to theoretically lower norepi. levels. For some, it may effect their results and show a reduction in standing norepi levels, while I have heard of other cases (including myself) who were on meds didn't see a difference in results or actually were a bit higher. The way it was explained to me is your body will keep shooting off norepi to constrict blood vessels and may even produce more norepi to overcome what the additional medications are doing.

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I don't have hyper POTS either yet I was prescribed beta blockers and took them for almost 18 months. While they did help with the tachycardia, I couldn't tolerate the side effects (low BP, chest pain, occasional SOB, etc) so I discontinued them.

Also, to the best of my knowledge, beta blockers can decrease the plasma norepi levels but the results of the studies I read are inconclusive.

http://circ.ahajournals.org/content/120/9/725

Propranolol Decreases Tachycardia and Improves Symptoms in the Postural Tachycardia Syndrome

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1401815/

Effect of beta-adrenergic receptor blockade with propranolol on the response of plasma catecholamines and renin activity to upright tilting in normal subjects.

Hope this helps.

Best,

Alex

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These kinds of topics appear a lot. Most treatments are aimed at treating symptoms - if symptoms of excessive sympathetic drive are the major problem which can occur in all forms of POTS - then beta blockers may be helpful. This doesn't depend on whether your serum NE levels are below or above a certain number and increasingly the delineation of POTS that is being adopted is neuropathic v non neuropathic rather than hyper v non hyper because it MIGHT tell people more about the underlying etiology.

The same number of hyper and non hyper POTS patients had QSART abnormalities meaning that some hyper and non hyper POTS patients may have the same underlying mechanism or cause.

Some POTS patients have normal NE but its effects are potently potentiated, others have beta receptor super sensitivity - like some with EDS.

Many patients with NET deficiency did not have overt 'hyperadrenergic' presentations. This was because it appeared that their vesicles ran out of norepinephrine, or alpha 2 receptors blunted NE release, or alpha 2 cerebral stimulatuion reduced sympathetic central outflow. So its murky.

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