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For conditions such as POTS (Postural orthostatic tachycardia syndrome) which are unable to regulate appropriate blood pressure / HR on postural changes, they are treated with volume expansion - like an effective chronic hypovolemia - even though technically they are euvolemic.

Various treatments for these conditions include salt tablets and water intake, or regular home IV saline infusions. These have to be done regularly, however, or healthy kidneys will eliminate the excess fluid.

Wouldn't a colloidal volume expander like Gelofusine or Albumin last longer, by maintaining the oncotic pressure?

I recognize that unfortunately, it seems to be hard to get, as wikipedia explains in the article on albumin:

For patients with low blood volume, there is no evidence that albumin reduces mortality when compared with cheaper alternatives such as normal saline, or that albumin reduces mortality in patients with burns and low albumin levels. Therefore, the Cochrane Collaboration recommends that it not be used, except in clinical trials.

However, this research all seems to be about treating acute hypovolemia, such as in cases of blood loss or severe dehydration. In those cases, saline works just as well while being less expensive.

But for EDS patients, the problem isn't low blood volume, but inability to regulate that volume. Saline boosts the quantity of fluid while decreasing oncotic pressure, which is ultimately self-defeating. Maintaining oncotic pressure would, in theory, be ideal. Perhaps we could find a colloid that the kidneys will not eliminate rapidly.

Can blood volume be chronically increased effectively with colloid volume expanders?

  • Welcome to HealthSE Josh! We can't discuss advice for individuals here. But the de-individualized root of your question is an excellent question about the application of concepts to clinical medicine, so I will dramatically alter it to fit site standards. – DoctorWhom Mar 29 '18 at 19:39
  • Kidneys don't excrete protein unless they're sick. – Graham Chiu Mar 29 '18 at 19:58
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Albumin is expensive and potentially dangerous, colloids have never been shown to be better than crystalloids, and there is no good evidence for their effective use in orthostatic hypotension.

Albumin, due to its cost and the traceability requirements inherent to all blood-derived products, is rarely prescribed as first-line treatment 1

Synthetic colloids provide a plasma expansion property of close to 100% (80%–120% depending on the product; Table 2) but with a risk of anaphylaxis, renal failure and clotting disorders. 1

The plasma expansion property of a solution theoretically has direct metabolic effects. A product with a high expansion property corrects blood volume more effectively, limiting the risks of tissue hypoperfusion responsible for lactic acidosis. The expected benefit of a colloid should therefore be logically greater than that of a crystalloid, but this superiority has never been demonstrated. 1

Neurogenic orthostatic hypotension, postprandial hypotension and exercise-induced hypotension are common features of cardiovascular autonomic failure. Despite the serious impact on patient’s quality of life, evidence-based guidelines for non-pharmacological and pharmacological management are lacking at present. Here, we provide a systematic review of the literature on therapeutic options for neurogenic orthostatic hypotension and related symptoms with evidence-based recommendations according to the Grading of Recommendations Assessment, Development and Evaluation (GRADE). Patient’s education and non-pharmacological measures remain essential, with strong recommendation for use of abdominal binders. Based on quality of evidence and safety issues, midodrine and droxidopa reach a strong recommendation level for pharmacological treatment of neurogenic orthostatic hypotension. In selected cases, a range of alternative agents can be considered (fludrocortisone, pyridostigmine, yohimbine, atomoxetine, fluoxetine, ergot alkaloids, ephedrine, phenylpropanolamine, octreotide, indomethacin, ibuprofen, caffeine, methylphenidate and desmopressin), though recommendation strength is weak and quality of evidence is low (atomoxetine, octreotide) or very low (fludrocortisone, pyridostigmine, yohimbine, fluoxetine, ergot alkaloids, ephedrine, phenylpropanolamine, indomethacin, ibuprofen, caffeine, methylphenidate and desmopressin). 2

  1. https://www.medscape.com/viewarticle/730821_2
  2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5686257/
  • Thanks for the response. As for "colloids have never been shown to be better than crystalloids" - I address this point in my question. You are correct that it has been repeatedly demonstrated to be no more effective for treatment of acute hypovolemia, or (as you point out) for preventing lactic acidosis. That research may not apply at all to the issue at hand, though - it certainly has nothing to do with my proposed mechanism of action. – Josh Mar 29 '18 at 21:02
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    Also: EDS-associated POTS may be very different than neurogenic hypotension, despite similar presentation. If the nervous system is "setting" the blood pressure too low, trying to fight it by boosting volume with fluids is likely to fail - the system can compensate by relaxing the arterial walls. But with EDS, the problem is likely caused by the arteries being too elastic to constrict as much as necessary. It is reasonable to expect increased volume to work in the latter case even if it fails in the former. I can confirm that a normal saline infusion did temporarily increase blood pressure. – Josh Mar 29 '18 at 21:10
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    It looks to me like you're assuming: "Since condition X and condition Y have similar symptoms, and treatment A doesn't work for condition X, it probably won't work for condition Y either." That argument can fail when the underlying cause of the observed symptoms is different for conditions X and Y. – Josh Mar 29 '18 at 21:20
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    Anyway, the point is that there is no evidence and theories without data can't be answered. – Graham Chiu Mar 29 '18 at 23:16

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