Not Sure Where This Is Going?

[havefaitherin]

Hello all. I am a little overwhelmed right now and trying to make sense of things. I was diagnosed with Hyperadrenergic POTS years ago and have dealt with it fairly well by avoiding triggers, etc. This summer I had an ablation done, and things haven't been right since then. A few weeks after the surgery I had a charlie horse in the pool while I was doing laps. It lasted 8 minutes and the only way we stopped it was getting me into the hot shower. Since then, I have been having leg pain (both thigh and calf) frequently. It has been getting much worse as of late, with accompanied tired/weakness. My BP has also been dipping very low along with heart rate, but also high at times. I saw my cardiologist yesterday and he believes for some reason, I have now started developing the symptoms of a "regular" POTS patient, which hasn't happened thus far. He is very confused by this also, and is also contacting my specialist in Toledo. They have to be careful with how to treat me because of the Hyperadrenergic side of things. They can't medicate me the way they would a "regular" POTS patient. This all started after my surgery this summer (which was the first surgery I had after being diagnosed years ago) and has progressively gotten worse. Also, while I was in the hospital this week my IM doc ordered a narcotic for the leg pain which sent things haywire (eyes rolling back in head, tachy heart rate.) My body cannot handle any narcotic drug without really horrible side effects. After my surgery in July they gave me phentanol and I stopped breathing. Just feeling a little desperate and wondering if anyone could shed some light on this for me. Thanks for your time:)

I am 31 years old and have just recently lost 18lbs and started exercising on a recumbent bike 5 weeks ago (appx. 50 miles a week.) I am doing a low glycemic load diet....and felt the best I have felt in years before my symptoms emerged painfully/daily these past couple of weeks.

[Ernie]

Hi,

Your worsening might be caused by the ablation. It depends why and what they ablated.

[persephone]

\i don't want to fresk you but I was told that ablation rarely helps those with POTS, especially if it involves removing the sinus node. For me at least, the tachycardia is what brings my bp back up, so to remove the mechanism that allows my heart to race, my bp would be permanently low. This is how it was explained to me. But I have pots as a secondary to EDS, rather than the type you describe. I'm not sure how much of my own situation applies to you. Hope you feel better soon x

[delphicdragon]

Have you had your potassium and magnesium levels checked?

Sometimes low potassium can cause the pain your describe as well as the heart rate symptoms. Last time I was in a POTS crash my potassium was through the floor and I needed IV potassium to get my heart rate to stop dipping then surging.

Sara

[yogini]

Hi,

I don't know much about ablations, but I don't think hyperandrenergic POTS is treated much differently than other types of POTS...

[havefaitherin]

The ablation was for the uterus....not my heart. Sorry I didn't specify.

Yes, my potassium has been up and down. I am on oral potassium now with compression stockings. I also had an IV with potassium earlier this week, but it didn't really make me feel better. They can't figure out why my potassium keeps dipping down either.

[Dizzysillyak]

Here's some info potassium deficiency. HTH ...

http://www.natural-health-information-cent.../potassium.html

[ramakentesh]

saw my cardiologist yesterday and he believes for some reason, I have now started developing the symptoms of a "regular" POTS patient, which hasn't happened thus far. He is very confused by this also, and is also contacting my specialist in Toledo. They have to be careful with how to treat me because of the Hyperadrenergic side of things. They can't medicate me the way they would a "regular" POTS patient

While your cardiologist might subscribe to the differentiation of POTS based on the researchers at Toledo into 'Normal' POTS as in POTS caused by peripheral neuropathy or patchy denervation and 'hyperadrenergic POTS' based on high NE readings, not all research bodies agree with this differentiation.

Some researchers are still trying to prove that most POTS is based purely on impaired NE reuptake and thus all being hyperadrenergic.

While others dont think that POTS is caused by an overactive or 'hyperadrenergic' autonomic nervous system in ANY POTS patients (Dr.J Stewart).

The problem with these classifications is that there is overlap - most patients who are told they are hyperadrenergic POTS still have blood pooling suggesting impaired baroreflex or venous pooling, whereas most Normal POTS patients will exhibit periods of highly excessive autonomic overactivity.

perhaps this is just a new phase in your existing disease? Have you ever exhibited blood pooling? I suggest your Cardiologist is prescribing to a particular classification of POTS when there isnt concensus on these classifications.

In my experience my pots comes on as adrenal - adrenal surges, very high NE levels in blood during orthostatic stress and then wanes into the dizzy variety where im dizzy all day, less adrenal and my standing BP is around 130 rather than 150 when im adrenal.

Surgery can be a precipitator in many POTS patients.

[havefaitherin]

I find your reply interesting. Yes, my blood does pool 52% in my legs and abdomen per a test that was done in 2005 at the Cleveland Clinic. It was a hemodynamic blood volume test. Although interesting, it wasn't very helpful in treating me. Also, I feel a little puzzled by the idea that the Hyperadrenergic POTS and POTS aren't different. I say this because of the Catecholamines they find in the blood of Hyperadrenergics. I realize many similarities between the two, but markedly different symptoms from others that don't tend to have the Catecholamine problem. I was told by a leading doctor in Autonomic Dysfunction that if they knew back then, what they know now, that Hyperadrenergic POTS wouldn't have been named POTS at all, because they are so markedly different. They would have been their own entity. It is all so complex, I know. I have been dealing with this disease since 2003, so I truly understand the ups and downs and questions we all have with limited research behind us.

Thank you so much for your post. I found it most interesting and am pondering some thoughts you brought up. I love a little mind jogger....especially when the rest of my body isn't working up to par!!

Also, thanks for the Potassium post. I found that website very helpful and am taking oral potassium now.

[flop]

I agree that trying to separate POTS into "hyperadrenergic POTS" and "other POTS" isn't as easy as splitting us into two groups. I had my catecholamines measured last year - sitting and standing were both in the normal range (wasn't done lying down) with the standing (during TTT) result being higher than the sitting one. From the bloods one would conclude that I am not in the hyperadrenergic group.

BUT my BP does some interesting things including regularly putting my diastolic pressure (the lower of the numbers) up to over 100mmHg when I am standing, this is apparently a hyperadrenergic response to orthostatic stress.

The more I read and learn, the more I relaise how complicated POTS is. In fact I don't think that it is one illness at all but a bunch of different problems that cause similar symptoms (at least that explains why we have such different effects from medications).

Flop

[havefaitherin]

I agree Flop. It is so complicated! My BP does the same thing. It is so weird how different, but the same so many of us can be:)

[ramakentesh]

It depends where you are going as to what you are told about POTS.

Most doctors agree with the Toledo breakup of POTS into two primary causes.

That is there is Peripheral or Partial dysautonomia POTS where the autoimmune system creates antibodies that attack the nerves in either the legs or arms or possibily attacks the nerves in the stomach. This means that the nerves no longer constrict veins properly and you get the classic signs of POTS. On standing, dizziness, lethargy, brain fog, blood pooling either in the legs, pelvis, stomach or in all of these.

The problem here is that excessive venous pooling in the extremities would augment sympathetic activition to maintain arterial pressure, which may translate to increased plasma NE levels (to vasoconstrict), excessive sympathetic nerve firing and excessive Adrenaline levels. Therefore a positive NE plasma level for the hyper variety even though the underlying cause is actually partial dysautonomia.

Also if some of the nerves are attacked there is a theory that this patchy distal denervation would possibly cause an overactivity of the other nerves - causing an excessive sympathetic response. (Dr Low and Dr.Jacob et al).

In both these cases the orthostatic intolerance would appear to be sympathetically mediated - that is caused by sympathetic overactivity and the symptoms would be predominantly from high norepinephrine (NE) levels (classic hyper symptoms) despite it being caused by partial dysautonomia.

On the other hand the Hyperadrenegic variety in its case model exhibited swings of postural hypertension and then postural hypotension as NE levels were used up due to faulty reuptake. Induced in mice it showed that the mice responded to stimuli with excessive tachycardia (sound familiar?).

POTS patients who had their vein biospies tested in one study and found to have basically no present NE transporter (a suggested cause of the hyper POTS) did not have elevated NE levels during tilt table, despite there being increased firing of the skeletal sympathetic nerves and lowered reuptake of NE there was no increase found in NE levels (Dr Lambert et al). So these patients were found not to be hyperadrenegic.

When a more accurate estimations were made of sympathetic nervous system activity using total-body NE spillover as used in the study above none of the patients had elevated plasma NE levels. This suggests that the overactivity found in the nerve firing rate could result again from patchy denervation making the remaining nerves more active, or from some sort of alpha or beta hypersensativity (Dr. Jordon et al).

Also there seems to be no explanation as to why a patient with Hyperadrenergic POTS would have blood pooling of any type. These patients are supposed to be suffering from excessive NE levels and thus excessive vasodilation of the carotid and peripheral arteries yet they seem to exhibit blood pooling and reduced thoratic blood volume leading to tachycardia. (Dr.Stewart).

This is where the recent work of Dr.J Stewart seems to provide alternative concepts of POTS. He suggests that POTS is never really caused by sympathetic overactivity or elevated NE levels - and that these hyperadrenergic responses can be seen in all patients.

His theory is that POTS is broken up into three catagories and all are a result of reduced thoratic blood volume (blood moving away from the heart, causing the heart rate increase and the excessive sympathetic response.

The first is High Flow POTS - where patients exhibit high peripheral blood flow and excessive blood pooling in the limbs possibily caused by an auto immune mediated denervation of the legs.

the second is Normal Flow POTS - where patients exhibit normal supine blood flows, excessive peripheral vasoconstriction on standing and blood pooling that seems to be mostly in the stomach region. They also exhibit altered Co levels and excessive sympathetic activity.

The last is Low Flow POTS - where patients demonstrate low peripheral blood flow supine and less so under postural stress, regional blood flow abnormalities that result in some blood pooling and sympathetic overactivity mediated by elevated Angiotenson II levels. These elevated levels also possibily reduce the bioavailability of Nitric Oxide, causing vasoconstriction.

In short the jury is still very much out