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Pooling- Can This Msyptom Go Away?


ana_22

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I think it can improve if muscle tone in the legs is poor, or relatively poor, and then improved.

Also there are a number of factors that can cause blood pooling. Liver disease is one ,and so if that condition were improved the pooling would improve also.

"The following are some abnormalities that can result in reduced venous return:

Abnormal veins that stretch excessively can result in pooling blood (Stewart, 2000).

Altered capillary permeability can affect capillary leakiness and cause excessive fluid collection in the lower body (Stewart, 2000). This may be contributing to orthostatic intolerance in a number of POTS patients.

Blood vessels that don't seem to constrict appropriately have been noted in POTS patients. Some physicians believe this subnormal orthostatic venous constriction, resulting from impaired sympathetic innervation, is the cause of blood pooling excessively in the legs of POTS patients (Streeten, 1999). This loss in the ability to vasoconstrict leads to excessive heart rate increases and contractions (Grubb, 2000).

Denervation occurs in some POTS patients. A number of patients do not sweat in various parts of their bodies. Some patients report losing their ability to sweat altogether. This lack of sweating shows that the nerve supply to the area is damaged (Low, 2000). As a result, the vessels that the nerve supplies lose their tone and become slack. Blood volume is normal but vessel capacity is excessive (Low, 2000). This causes decreased venous return of blood flow to the heart, decreased cardiac output and (probably) orthostatic reduction in cerebral blood flow (Streeten, 1999). Peripheral neuropathy may be present in these patients. This neuropathy seems to be selective, with slight responses in some regions being compensated for by overactivity in other regions (Bush, Wight, Brown & Hainsworth, 2000).

Hypovolemia (low blood volume) sometimes occurs in POTS patients. The patients may have a reduced blood volume throughout their body, or the hypovolemia may occur due to blood pooling in the abdomen and legs. Reduced plasma renin activity often accompanies the low blood volume. Reduced levels of renin release consequently result in reduced secretion of aldosterone. This would be expected to impair renal sodium conservation thereby contributing to hypovolemia (Streeten, 1999). Findings suggest that the impaired renin release may possibly result from sympathetic denervation (Jacob & Biaggioni, 1999). Abnormalities in the kidney are also suspected of causing the reduced renin and aldosterone levels (Raj, Biaggioni, Yamhure, Black, Paranjape, Byrne & Robertson, 2005). Physicians believe hypovolemia and inappropriately low levels of plasma renin activity may be important pathophysiological components of orthostatic intolerance (Jacob, Robertson, Mosqueda-Garcia, Ertl, Robertson & Biaggioni, 1997). Decreases in body temperature may result from hypovolemia (Heitz & Horne, 2005, 35).

The findings in hypovolemic POTS patients have been dubbed the "renin-aldosterone paradox" and are explained as follows:

Under normal circumstances, low plasma volume is sensed in the kidney (and in the heart and aorta) and stimulates an increase in plasma renin activity (renin), angiotensin II (A-II), and aldosterone (ALDO). The increase in plasma renin activity and aldosterone promotes salt and water retention, which leads to an increase in extracellular fluid volume and plasma volume. In POTS, there is a failure to sense and appropriately respond to low plasma volume. There is no appropriate increase in plasma renin activity, angiotensin II, and aldosterone given the hypovolemia. Because plasma renin activity and aldosterone are not increased, salt and water retention is not increased, and plasma volume is not increased (Raj, et. al., 2005).

Erythropoietin response impairment may be contributing to a patient's hypovolemia. Erythropoietin is a hormone made by the kidneys. It helps stimulate red blood cell production. Impairment of the normal erythropoietin response to low levels of red blood cell mass could contribute to hypovolemia. Physicians postulate that subnormal erythropoietin response may be resulting from a disorder in the normal sympathetic stimulation of erythropoietin release by the kidney (Streeten, 1999). Read more

Paradoxically, POTS can occur because of hypovolemia or hypovolemia can occur because of POTS. This can happen because hypovolemia may lead to a chronic state of adrenergic activation, which may produce POTS symptoms. Chronic adrenergic activation reduces intravascular volume, which may produce hypovolemia (Stewart & Erickson, 2002). Read more

Impaired venous emptying can cause excessive fluid collection in the lower body. This can lead to blood pooling in the lower limbs and consequently, orthostatic intolerance.

Splanchnic pooling is occurring after meals in some POTS patients. Excessive pooling of blood in the abdomen has been shown to occur while the patient is supine and at rest (Tani, Singer, McPhee, Opfer-Gehrking, Haruma, Kajiyama & Low, 2000). The splanchnic vascular bed contains up to 30% of blood volume. Limited autonomic neuropathy causing peripheral denervation may be the cause of increased resting flow and reduced mesenteric resistance in these patients.

Sympathetic Overactivity is observed in many POTS patients. The sympathetic overactivity can be secondary to a number of factors, some of which may be peripheral denervation, venous pooling, or end-organ dysfunction (Low et al, 1998). Hyperadrenergic states with elevated norepinephrine levels are often found in patients with sympathetic overactivity. One study found that 29% of POTS patients had elevated norepinephrine levels upon standing, and the mean level was 531 pg/mL (Thieben, Sandroni, Sletten, Benrud-Larson, Fealey, Vernino, Lennon, Shen & Low, 2007). Norepinephrine is similar to adrenaline and is a natural vasoconstrictor. Genetic or acquired deficits in norepinephrine activation may result in hyperadrenergic states that lead to orthostatic intolerance (Shannon, Flattem, Jordan, Jacob, Black, Biaggioni, Blakely & Robertson, 2000). These deficits can cause patients to experience symptoms suggestive of not enough norepinephrine simultaneously with high norepinephrine levels. Many of the mechanisms listed here can result in states of chronic adrenergic activation that lead to orthostatic intolerance.

Sympathetic underactivty can also occur in some forms of orthostatic intolerance (Robertson, 2000), such as pure autonomic failure. "

from mechanisims of POTS- www.potsplace.com

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  • 1 month later...

thanks for your answers!

well im still pooling alot, i mentioned it to my dr and the dr said well as long as they're not purple, and i said well actually they are turning purple! then the dr kind of laughed and made a joke about my legs falling off and disregarded the issue. which wasnt very helpful.

i dont thing the dr understands the severity and im kinda getting really worried.

what does everyone elses pooling look like?

my legs go red about after a minute of standing or sitting in a chair and then after about 2-3 minutes they start going a deep purple, sometimes they are more mottled, sometimes there are purple like veiny shaped things, and sometimes there are little white dots in some areas. they only go back to white when i am lying down.

they also pool less when i am walking around the house, but as soon as i stand still they pool again!

can pooling be dangerous?

thanks guys

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Ana,

My legs (and arms) turn a mottled purple color if I am standing or sitting. I wear compression stockings and take midodrine to help with this.

Has your doctor given you anything to help with the pooling? Compression hose help by squeezing the blood back up. Midodrine helps the blood vessels to constrict so that blood doesn't pool in your limbs. Exercise also helps by strengthening your muscles. Good muscle tone improves circulation.

If too much blood pools then you might faint or get a headache, but specialists have told me that the pooling isn't dangerous and doesn't damage veins.

Rachel

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