I'd love to see a discussion about the different kinds of abnormalities of heart rate and blood pressure during tilt testing that Frans Visser talked about on the NIH ME/CFS Research Roadmap: Circulation Webinar (January 11, 2024): - POTS - Orthostatic hypotension - Syncope - No POTS, normal BP, but OI Here's a quick link to this slide in the recording of the webinar. Visser says "We have patients with POTS with increase in heart rate and patients with orthostatic hypotension with a decrease of the blood pressure, syncope patients. But the most interesting -- intriguing part are those patients with a normal heart rate and normal blood pressure, but with orthostatic intolerance symptoms." Here's a link to the full transcript: https://event.roseliassociates.com/..._Webinar-8_Circulation_Open-Session_final.pdf
I'm one of those patients with normal HR (with chronotropic intolerance+ not high enough HR) normal blood pressure and still OI. Brainfog made me drop out of uni in my final year, but 3 decades later I'm still alive and (a little less) kicking. NASA-lean test and a normal tilt table test would not have conclude that I had OI.
My daughter falls into the “normal BP and HR but experiences OI” during NASA lean test (and in everyday life). Outside the test, she has what seems to be age-related mild hypertension, which arrived 15 years in. It isn’t affected by standing or sitting though. We have been following Dr Peter Novak’s path, as we have approached this from the autonomic angle rather than the ME/CFS angle, just by chance really. But we have also seen Dr Visser’s work. Dr Novak calls patients in this category OCHOS (orthostatic cerebral hypoperfusion syndrome) and he has diagnosed at least three patients who have CFS with OCHOS. https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/26909037/ He feels there are two sub-groups: those with active cerebral vasoconstriction and those with passive increase of peripheral venous compliance. *** On a separate note, South Korean researchers found a similar entity in the same year, although not in CFS patients: https://onlinelibrary.wiley.com/doi/10.1111/ane.12516 They called it OINH, which I fear will not catch on compared to the more catchy OCHOS.
Another normal HR and BP possibility is described by Dr Novak as HYCH (hypocapnic cerebral hypoperfusion): https://journals.plos.org/plosone/doi?id=10.1371/journal.pone.0204419 He has only diagnosed a few people with this, and there’s no mention of co-morbidities, so I don’t know whether any of them had CFS.
In the absence of access to full autonomic testing, a backwards way to try to elucidate whether you lie in the cerebral vasoconstriction group or the venous compliance (poor venous return or low blood volume) group would be to try volume expansion. The ultimate form of volume expansion would be IV saline as it bypasses whatever it is in the body that may be setting the blood volume abnormally low. But this often isn’t considered until all the other forms of volume expansion have been tried, which is a shame. If it could be done early on as a sort of one-off diagnostic then people would know whether they would benefit from volume expansion or not. Ideally, doctors would just measure people’s blood volume, but the equipment and knowledge to do that has gradually disappeared. There is a new, relatively inexpensive device for measuring blood volume, but it hasn’t spread far yet. The technique is called carbon monoxide rebreathing. It has been known for a while, with non-medical versions of the testing equipment being used in space, altitude and sports science, but it was not until last year that a medical version came onto the market in Europe. So it can now be purchased “off the shelf” and run fairly cheaply. It has been validated against the old method (radioactive isotope tracing) and has CE approval in Europe. It can be used in heart and kidney failure, some blood diseases, and plain old blood volume testing, so it would be quite useful in any larger hospital. Some autonomic specialists have tried it out in research settings, but I haven’t heard of it being used in a clinical setting yet. The company’s name is Detalo Health.
If you are in Canada, there is an odd entity that’s been created called “postural symptoms without orthostatic tachycardia (PSWT)”, which is then defined as having POTS symptoms without tachycardia, or without tachycardia sufficient to meet the POTS diagnostic criteria for tachycardia. Given that there are quite a few types of orthostatic intolerance that don’t involve tachycardia, or don’t have it as a diagnostic criterion, this seems like an odd effort to re-categorise everything else with reference to POTS. I don’t think it has caught on, but I just thought I’d mention it in case it came up for anyone in Canada. https://onlinecjc.ca/article/S0828-282X(19)31550-8/fulltext
Another open question that would be important to answer: do the various manifestations of OI reflect stable patient subgroups or can they be the result of adaptations, albeit only partially effective ones, within a single patient over time? My own experience would suggest the latter. Over the decades I've gone through several distinct phases, each lasting for years phase 1: almost immediate outright fainting on standing still with no time for other major OI symptoms to develop before passing out, no problems getting up from sitting or lying down phase 2: standing time before fainting increased but at the cost of significant OI symptoms like jittery cold-sweating with nausea and brain fog phase 3: addition of now also 'greying out' (loosing vision but not quite fainting) on getting up from sitting or lying down, phase 2 symptoms continue phase 4: 'greying out' stopped again, replaced by strong POT, phase 2 symptoms continue phase 5: POT much milder, yet the effect of being upright on cognition feels worse as does the contribution of OI to PEM, phase 2 symptoms continue
@Ravn , I did hear one of the autonomic experts mention the value of retesting patients over time. He mentioned that some patients’ symptoms seem to change or evolve and may need to be re-evaluated to adjust treatment. I think it was Dr Brent Goodman, and he was speaking of autonomic patients, but I am guessing the same idea would apply to any patient with autonomic dysfunction. (He didn’t say anything about the why or how of the changes, unfortunately.)
I felt great for two or so days after general anaesthetic the last two times, always wondered if it was the drip
I've had high blood pressure since I was in my early 20s, now 65. When I look at symptoms, it is clear to me that my ME/CFS started slowly in my late teens. As child my family referred to me as "disgustingly healthy". In university I complained that I couldn't concentrate and could barely stay awke while sitting in lectures. I was drinking many cups of coffee a day. A psychiatrist diagnosed my with "atypical narcolepsy" and I was on ritalin for a few years. When I was teaching I would lie down in my office and fall asleep for an hour. Then I'd go home and lie on the deck and fall asleep for an hour. For years I was frustrated that I would be lying down recomposing an entire email in my head, but if I went immediately and sat at the computer it was gone. I've always said that I felt way better moving then lying down. Even now I go for 40 minute brisk walks because I generally feel good. Now I suspect this is a cerebral perfusion problem. High blood pressure helps push the blood, while sitting, standing and slow walking are... uncomfortable. In my current state, I alternate between an hour or so of "normal regular" activity and two or three hours of lying down to recover and be reenergized. Most doctors seem to believe that orthostatic intolerance must be syncope or tachycardia. I politely disagree.
Canadian Cardiovascular Society Position Statement on POTS syndrome and Related Disorders of Chronic Orthostatic Intolerance This novel classification is on the basis of expert opinion of the Writing Committee on the basis of limitations with the current nomenclature. Suggested diagnostic terms in the spectrum of orthostatic tachycardia and orthostatic intolerance include POTS, POTS plus, postural symptoms without orthostatic tachycardia (PSWT), PSWT plus, and postural tachycardia of other cause (PTOC). The details of these newly defined diagnoses are described in the following sections and summarized enumerated https://onlinecjc.ca/article/S0828-282X(19)31550-8/fulltext
I believe the type of hypovolemia that seems to occur in ME/CFS and POTS does not show up in standard blood tests because there is often nothing wrong with the ratio of components of the blood, there’s just not the right amount of it. To measure blood volume, you need to use a tracer. Funnily enough, getting your blood volume measured used to be easier a few decades ago than it is now. I have read that it was used fairly often to monitor heart and kidney failure. So a reasonable number of large hospitals had the equipment in their nuclear medicine department, like this: https://my.clevelandclinic.org/health/diagnostics/16793-blood-volume-testing Today there are very few hospitals that still have the equipment for various reasons: no longer considered essential for monitoring heart and kidney failure, expensive, loss of knowledege as people retired, consumables (isotope) hard to get. But this could all change soon, as a Danish company has created an off-the-shelf device to measure blood volume using carbon monoxide rebreathing. It got approved as a medical device (CE) in Europe last year (2023). No radiation, no expensive consumables, and it can be operated by a standard medical technician and a phlebotomist (could be one person). (My daughter looked into this a lot when we thought she had low blood volume.)
"novel" Overall not bad, but has significant limitations. They notice a common co-morbidity with ME/CFS, but under special considerations make no mention of PEM/PESE and how it should be a contraindication from their primary recommendation, which is, you guessed it: regular aerobic exercise with a focus on conditioning. Even though POTS has nothing to do with deconditioning and there is no good evidence for this. It's a tiny step that should have been taken decades ago, about the smallest imaginable step. Tiny progress after several generations of stagnation and the single biggest increase of this condition in history, which they make zero mention of. There is zero mention of COVID, or Long Covid, so any MD reading this would be completely unaware of it. Giant facepalm. I'll be speaking with my GP about this soon. I'm unsure if it's worth pointing it to her. I mentioned it a few years ago and she wasn't aware, but this is really only the tiniest possible improvement over not knowing anything.
What I've learnt over the years is to describe the symptoms that you're experiencing, don't even mention POTS or OI, they have no clue what that means and their eyes will glaze over. When I told my GP that I felt pressure in my chest when upright for too long, racing heart at times et, that got me an appointment with a specialist. Most doctors are unfamiliar with POTS, OI or anything in that area of medicine.
@rvallee , I'm not an expert, but in all the lectures and articles by "proper" autonomic experts, specialised exercise is recommended for POTS in order to: address loss of condition due to being unable to undertake normal activity after symptom onset, especially given that the average diagnosis time is something like 5 years increase lower body muscle mass with the hope that that feeds into increased skeletal muscle pump activity, which could pick up the slack for the other mechanisms of venous return that are compromised help get the person back to a reasonable level of functionality once their symptoms are controlled enough to allow them to increase their activity level (i.e. rehabilitation). (Bearing in mind that they are discussing patients with POTS, not patients with POTS and ME/CFS.) I have read cleverer people than me say that the idea of deconditioning was related to early research in space travel, and that knowledge has advanced beyond that. Of course, there will always be people who have read old articles and gotten the wrong end of the stick, so I don't doubt that there are cardiologists out there telling people that POTS is caused by deconditioning, unfortunately. I haven't checked the latest research on exercise in POTS, but I imagine, as with almost anything to do with POTS, there is not enough to conclude anything definitive. Professor Tae Chung would seem to be a reliable source for clinical experience. He has a few lectures on the Dysautonomia International lecture channel. https://vimeo.com/dysautonomia/ Dr Peter Rowe also speaks very passionately and compassionately on this topic in his lectures, as he treats ME/CFS and OI patients.
I'm not aware of any such evidence. It's recommended by clinicians about as often and on the same basis as ME/CFS, usually the Levine or CHOP protocols, but I don't think there are any proper trials of exercise for POTS. The few that are used to justify it all have the same flaws and confounders as the ME/CFS research. All the studies use the exact same framing of cycles of deconditioning and fear of setbacks. For all that POTS is actually objectively measurable, it's been dismissed by medicine just as thoroughly as ME/CFS and funding has been even lower. And really, all I see is MDs suggesting CHOP or Levine, or something like it. Never any references to any research, it's just assumed to work based on their clinical experience. Overall the evidence base is probably even weaker for POTS than for ME. The few trials that exist, all tiny and poorly done, focus on measures of fitness, which improve slightly, but that's just preparing for the test, since POTS isn't a deficit of fitness. But it's always framed as trying to avoid deconditioning, while simply ignoring the actual problem because they don't understand how disabling POTS is, and PEM even less. Here's a good example from a recent Long Covid Reddit thread, a handout from a cardiologist. It just says that exercise is "hugely important" and "extremely effective", recommends the Levine protocol, saying he "has found it to be effective". And this looks like one of the better ones. What a dumpster fire.
If you are full time employed at a desk job and don't go running I suspect that venous pooling capacity is kept stable by the very tiniest of fidgeting movements of the legs from time to time. The idea that you need to strengthen muscles to handle that seems to me pretty implausible, and, as others have said, there is bound to be no evidence. What I am wondering may be important is just the posture itself. We know that the body makes quite major adjustments to plasma protein levels and I suspect blood volume, with prolonged bed rest. We know that most people after prolonged bed rest have to start walking about fairly carefully. What the implications might be for management I don't know, but it may be important to research it.
Three of my last four renin tests have been well above the maximum. Aldosterone has been normal. My blood pressure is being controlled with telmisartan. One of the common causes seems to be stenosis of a kidney blood vessel. The kidney specialist is profoundly uninterested. I'm always amazed that so many doctors are not at all inquisitive about outliers. Now I learned that "idiopathic" really means "it is common but we don't have a clue and we're not really interested in finding out" As far as I can Google there doesn't seem to be a relationship/study between renin and ME/CFS. I'm still wondering what "high blood pressure since early 20's" actually means.
