Chapter: Pathophysiology & Classifcation of PoTS (2021) pt II: Hypovolemic POTS
This chapter, in the book Postural Tachycardia Syndrome (2021), written by Matthew G. Lloyd & Satish R. Raj, talks about subtypes of Postural Orthostatic Tachycardia Syndrome (POTS). I summarized their Neuropathic POTS section in the last post.
A whole bunch of POTS patients have chronic hypovolemia (Not enough blooood (red blood cells & plasma)), with most presenting with an 11-13% deficit. But some lucky ducks can have blood volumes up to 22% below average. (!!) (I would not be surprised if I was a part of that group sometimes, tbh.)
The way that hypovolemia leads to POTS is because your heart is trying to pump, but it’s just not got enough blood in there to pump properly.
In fact, before I knew this was even a thing, i told my own doctor “it feels like there’s not enough blood to pump! my heart feels too empty when it pumps?? It kinda hurts/does not feel right?” Boy, am i side-eyeing my EP who completely ignored that now and did not say anything in any way related to hypovolemia. -_-
Anyway, when that happens, in response, our body slams that SYMPATHETIC NERVOUS SYSTEM BOOST button to try to compensate (via the baroreflex). That sympathetic activation is what gives us tachycardia and all the rest. (ㅠㅠ)
Blood volume is usually maintained by the Renin-Angiotensin-Aldersterone System (RAAS), which appears to be impaired in hypovolemic POTS, though scientists aren’t sure exactly how.
Studies have been all over the place, with POTSies having been documented having (reduced/normal/increased) circulating renin, (normal/increased) circulating angiotensin II, and (reduced/normal/increased) circulating aldosterone. 🤷
The key to all this conflicting data might be menstrual cycle phases, as RAAS function appears dependent on both cycle phase (and body position,) and the researchers didn’t include menstrual cycle questions in their studies. Hopefully science will, you know, test this properly?? Soon??
As far as I can tell, however, so far studies do seem to agree on a lower aldosterone:renin ratio in POTS patients. Guesses for how/why this is includes low blood vessel capacitance, reduced angiotensin-converting enzyme 2 activity, and because OF COURSE, ~deconditioning.~
(POTS can come from deconditioning. Astronauts get POTSie when they come back to earth! Some (genetically?) predisposed people get POTS when on extended bedrest! But i think the rest of us are quite sick of doctors throwing that word at us constantly, implying we’ve brought this all on ourselves by being lazy, etc.)
(I had an exercise test once at the height of my couch-potato-bc-of-dysautonomia-ness and despite that they said I was not, in fact, deconditioned at all. The amount of vindication and general TOLD YOU SO i felt was intense.)
Anyway, skipping over some reports on deconditioned POTSie astronauts — A recent study found angiotensin II receptor autoantibodies in 12 out of 17 POTS subjects. Another study has already shown that these autoantibodies reduced angiotensin-II-caused vasoconstriction in rabbit (!🐰!) models of POTS.
If that’s also happening in humans, it’s probably what is underlying the reduced pressor response (nerve reflex that constricts small blood vessles called arterioles and increases BP) seen in (some? all? 🤷) human POTSies in response to angiotensin II infusions, despite normal adrenal and kidney responses.
“The importance of hypovolemia to orthostatic intolerance and orthostatic tachycardia in PoTS is illustrated by the observation that expansion of blood volume via intravenous saline or desmopressin (a vasopressin analog) attenuates [reduces] standing heart rate and improves orthostatic symptoms.“
Next up: Hyperadrenergic POTS
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Whose with me on team hypovolemia? (Having multiple subtypes at once is common!) Let us clunk our gatorade bottles together and drink to the scientists who are hopefully investigating these RAAS things further, and will hopefully find better medicine than drinking gallon of salty water a day!
Lloyd MG, Raj SR. Pathophysiology and classification of pots. In: Gall N, Kavi L, Lobo MD, eds. Postural Tachycardia Syndrome. Springer International Publishing; 2021:29-40. doi:10.1007/978-3-030-54165-1_5
Comments are open for discussion, as well as if you have a correction or clarification of anything in this post!