If we have low blood volume where does it go?

[SOC]

OI - Slow K didnt help, while Florinef helped but caused dangerously high BP that had me visit the ER at doctors orders.

Don't know if this would be any help for you, but just in case -- my doc gave me verapamil to control tachycardia along with Florinef. Without verapamil, my BP increased with Florinef. Withe verapamil, my BP decreased. I think beta blockers would work the same way.

 

[end]

Finally got my brain in gear and thought - surely blood pressure is partly determined by blood volume, so can't be increased as a result of low volume. So I did a search and this page looks useful.

My own bp fluctuates wildly from one minute to the next, which can't be due to changes in volume - must be neurological, I think.

Those in the KDM camp seem to think it is possible - Increased BP in response to Low volume.

MeSci - are you saying they are wrong???

I have that report/opinion some where in my files.

But of course that's there opinion, who really know's with 100% certainty?

 

[end]

Finally got my brain in gear and thought - surely blood pressure is partly determined by blood volume, so can't be increased as a result of low volume. So I did a search and this page looks useful.

My own bp fluctuates wildly from one minute to the next, which can't be due to changes in volume - must be neurological, I think.

Found it! - MeSci message me your email and I can send you a scanned copy.


It also states my strongly positive hydrogen sulfide test indicates increased TH2 activity.

Does anyone think that is wrong too???

 

[MeSci]

Those in the KDM camp seem to think it is possible - Increased BP in response to Low volume.

MeSci - are you saying they are wrong???

I don't know.

 

[Emootje]

"Small changes in total peripheral resistance can significantly influence the vascular capacitance and consequently intravascular BV. For example, a 4% increase in total peripheral resistance reduces the volume of blood flowing through the systemic vasculature by 18%"
http://www.daxor.com/pdfs/contractedpl.pdf

 

[HTester]

"Small changes in total peripheral resistance can significantly influence the vascular capacitance and consequently intravascular BV. For example, a 4% increase in total peripheral resistance reduces the volume of blood flowing through the systemic vasculature by 18%"
http://www.daxor.com/pdfs/contractedpl.pdf

To my mind, this quotation displays a serious misunderstanding of the roles of total peripheral resistance versus vascular capacitance and blood flow versus blood volume in the cardiovascular system. I see this post is almost 6 years old, but if anyone is still thinking about this, I'm happy to write more.

 

[HTester]

Pretty self explanatory question. And then since people recover blood volume must come back. What is the mechanism for this and is there any way to know if you have low volume and the problems it causes?

There are excellent ways to measure blood volume. David Bell used them in the 1980s or early 1990s to demonstrate that most (I forget the percentage, maybe 80%) PWCs have dramatically reduced blood volume (BV). If I recall correctly, BV was so far out of the normal range that Bell suggested it was an excellent biomarker for CFS.

Assuming body weight is pretty constant, the first question is: Is the problem with fluid input or fluid output? Let's start with output. The CDC says glomerular filtration rate (GFR) must be measured in the workup of an ME/CFS patient. GFR is a measure of volume lost per minute from the blood to the kidney proximal tubules. Does anyone know of a study reporting GFR in ME/CFS patients? Between GFR and urine output (UO) there is kidney reabsorption, but UO is the difference. Is UO (liters/day) abnormally increased in ME/CFS?

 

[nandixon]

There are excellent ways to measure blood volume. David Bell used them in the 1980s or early 1990s to demonstrate that most (I forget the percentage, maybe 80%) PWCs have dramatically reduced blood volume (BV). If I recall correctly, BV was so far out of the normal range that Bell suggested it was an excellent biomarker for CFS.

I know that several years ago when David Kaufman was still at the Open Medicine Clinic, he said that the two most common lab findings they were seeing in their ME/CFS patients at the time were low natural killer cell function (which it appears may not occur when the NK cells are isolated from the rest of the blood components?) and low vasopressin (aka AVP and ADH).

I wouldn't be surprised if the low vasopressin finding might correlate pretty well with the reduced blood volume finding, given that one of the functions of vasopressin is to increase blood volume. Perhaps there's not a correlation, though.

(Both decreased NK cell function and decreased vasopressin are rather non-specific findings, unfortunately.)

 

[Inara]

Is the problem with fluid input or fluid output?

I can't answer that for pwME in general, but there seems to be a higher water output (via the kidneys) than input in me (I measured the amount I drank and peed in 24h, which ignores other fluid sources like food and other losses like sweat or diarrhea, but should give an idea). I measured body weight before measurement and after measurement.

An impedance measurement showed a further reduced body water compared to the measurement before. (And it is already reduced...But I think body water can fluctuate.) I found it odd before reading this thread because I drink around 2.5l daily.

 

[Sushi]

Basically, we pee it out. It is possible to measure your blood volume though there are not many medical centers have the equipment.

I just inadvertently discovered another way that blood volume can be measured: I just had a cardiac procedure where part of the monitoring was done through a catheter in an artery. The interventional cardiologist said that he could tell that I had low blood volume through measuring the pressures. This is not a method that would be used unless there was a very good reason to put a catheter in an artery though!

 

[CFS_for_19_years]

Does anyone know of a study reporting GFR in ME/CFS patients?

Tae H Park had two unpublished studies regarding (1) low GFR in ME/CFS and (2) subsequent improvement using IVIG.
Both studies appeared in the 2007 Journal of IIME pages 5-7:
resime.org/Documents/Journals/Journal%20of%20IiME%20Vol%201%20Issue%202.pdf

This is Page 7:

 

[CFS_for_19_years]

David Bell, Nancy Klimas and Peter Rowe have studied blood volume status in ME/CFS patients:

Circulating Blood Volume in Chronic Fatigue Syndrome
1998
David H. P. Streeten, MB, DPhil, FRCP, FACP and David S. Bell, MD, FAAP
http://sci-hub.tw/10.1300/J092v04n01_02 (full text)

In 2015 David Bell gave a talk regarding Blood Volume In ME
www.investinme.org/Documents/Research/David%20Bell%20Blood%20Volume%20in%20ME%20Sep%2015.pdf
He explained the difference between anemia and low blood volume. He treated patients with IV saline. He discussed Streeten's study of MAST (Military Anti-Shock Trousers) trousers on the orthostatic intolerance. This transcript of his talk is much easier to read than any published study.

Chronic fatigue syndrome: Illness severity, sedentary lifestyle, blood volume and evidence of diminished cardiac function
May 2009
Barry E. HURWITZ, Virginia T. CORYELL, Meela PARKER, Pedro MARTIN,
Arthur LAPERRIERE, Nancy G. KLIMAS, George N. SFAKIANAKIS and Martin S. BILSKER
http://sci-hub.tw/10.1042/CS20090055 (full text)

Blood Volume Status in ME/CFS Correlates With the Presence or Absence of Orthostatic Symptoms: Preliminary Results
Nov 2018
C. (Linda) M. C. van Campen, Peter C. Rowe and Frans C. Visser
https://www.frontiersin.org/articles/10.3389/fped.2018.00352/full

All studies and Dr. Bell's talk include methodology for measuring blood volume status.

 

[Float]

Can anyone tell me what the 'good' or 'quality' salt is to use?
I tried to find info in the search box but didn't get anything.

I have always naturally used tons of table salt on my food. And my blood pressure never budged but was always on the low side.

I'm pretty sure I pee it out. Does this mean that I have thick blood?

Sea salt.

 

[HTester]

David Bell, Nancy Klimas and Peter Rowe have studied blood volume status in ME/CFS patients:

More thoughts on blood volume in ME/CFS. As @CFS_for_19_years points out, this question has been studied many times:

David Bell has said in public lectures that blood volume is decreased in a substantial fraction (~80%) of CFS patients. Corroboration of a 20% decrease in plasma volume and a 15% decrease in blood volume in POTS patients was reported by Fu (2010). Fu also found that cardiac output was decreased by 26% and stroke volume by 31%.

Corroborating the Fu results, 30% decrease in cardiac end diastolic volume and 25% decrease in cardiac output was reported by Hollingsworth (2012) in a cohort of CFS patients.

In contrast, Vermeulen (2014) reports no significant difference in cardiac index, Newton (2016) reports a 3.6% decrease in total blood volume in CFS, but no statistical significance, and Farquhar (2002) found no difference in cardiac output (4.1 vs. 4.2 L/min), no significant difference in blood volume, and no significant difference in plasma volume (58.3 vs. 64.2 mL/kg) in 17 (Fukuda) CFS patients compared to 17 age- and gender-matched controls. Moreover, when Bell and colleagues (2000) revisited this subject, they did not find any decrease in plasma volume or total blood volume in 12 women with ME/CFS despite a significant (p<0.01) decrease in red cell volume.

Perhaps, we can conclude that reduced plasma and blood volumes are features of POTS, but not of ME/CFS in general. This appears consistent with the conclusion reached by van Campen (2019) that blood volume is significantly reduced in ME/CFS patients with orthostatic intolerance.

What do you think?


References

Fu, Qi, Tiffany B. VanGundy, M. Melyn Galbreath, Shigeki Shibata, Manish Jain, Jeffrey L. Hastings, Paul S. Bhella, and Benjamin D. Levine. “Cardiac Origins of the Postural Orthostatic Tachycardia Syndrome.” Journal of the American College of Cardiology 55, no. 25 (June 22, 2010): 2858–68. https://doi.org/10.1016/j.jacc.2010.02.043.

Hollingsworth, K G, T Hodgson, G A MacGowan, A M Blamire, and J L Newton. “Impaired Cardiac Function in Chronic Fatigue Syndrome Measured Using Magnetic Resonance Cardiac Tagging.” Journal of Internal Medicine 271, no. 3 (March 2012): 264–70. https://doi.org/10.1111/j.1365-2796.2011.02429.x.

Vermeulen, R. C., and I. W. Vermeulen van Eck. “Decreased Oxygen Extraction during Cardiopulmonary Exercise Test in Patients with Chronic Fatigue Syndrome.” J Transl Med 12 (2014): 20. https://doi.org/10.1186/1479-5876-12-20.

Newton, Julia L., Andreas Finkelmeyer, George Petrides, James Frith, Tim Hodgson, Laura Maclachlan, Guy MacGowan, and Andrew M. Blamire. “Reduced Cardiac Volumes in Chronic Fatigue Syndrome Associate with Plasma Volume but Not Length of Disease: A Cohort Study.” Open Heart 3, no. 1 (June 1, 2016): e000381. https://doi.org/10.1136/openhrt-2015-000381.

Farquhar, William B., Brian E. Hunt, J. Andrew Taylor, Stephen E. Darling, and Roy Freeman. “Blood Volume and Its Relation to Peak O2consumption and Physical Activity in Patients with Chronic Fatigue.” American Journal of Physiology-Heart and Circulatory Physiology 282, no. 1 (January 1, 2002): H66–71. https://doi.org/10.1152/ajpheart.2002.282.1.H66.

Streeten, David H. P., Delsa Thomas, and David S. H. Bell. “The Roles of Orthostatic Hypotension, Orthostatic Tachycardia, and Subnormal Erythrocyte Volume in the Pathogenesis of the Chronic Fatigue Syndrome.” The American Journal of the Medical Sciences 320, no. 1 (2000): 1–8. https://doi.org/10.1016/S0002-9629(15)40790-6.

Campen, C. (Linda) M. C. van, Peter C. Rowe, and Frans C. Visser. “Blood Volume Status in ME/CFS Correlates With the Presence or Absence of Orthostatic Symptoms: Preliminary Results.” Frontiers in Pediatrics 6 (2018). https://doi.org/10.3389/fped.2018.00352.

 

[HTester]

Tae H Park had two unpublished studies regarding (1) low GFR in ME/CFS and (2) subsequent improvement using IVIG.
Both studies appeared in the 2007 Journal of IIME pages 5-7:
resime.org/Documents/Journals/Journal%20of%20IiME%20Vol%201%20Issue%202.pdf

This is Page 7:
View attachment 33424

Normally, decreased GFR would result in hypervolemia rather than the decreased blood volume often (but not always) associated with ME/CFS. So it must be that GFR is reduced secondary to the decrease in blood volume in order to prevent blood volume from falling even further. David Bell said that, when present, low blood volume could be corrected by saline infusion or blood transfusion and this relieved ME symptoms, but only transiently. He even told of a single patient for whom infusion of one liter of saline transiently "cured" the patient's hypertension. That's astonishing and counterintuitive to anyone trained in cardiovascular physiology. Bell's conclusion was that if an ME/CFS patient has low blood volume, low blood volume is secondary to some upstream cause.

 

[Inara]

Perhaps, we can conclude that reduced plasma and blood volumes are features of POTS, but not of ME/CFS in general. This appears consistent with the conclusion reached by van Campen (2019) that blood volume is significantly reduced in ME/CFS patients with orthostatic intolerance.

What do you think?

To make it even more difficult, a recent paper by Baraniuk
https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-019-1935-y
found that some ME patients have orthostatic intolerance symptoms with and without POTS, and a part of those also when lying ("Orthostatic tachycardia did not account for OI symptoms in CFS"). I think the paper has drawbacks (e.g. how OI was defined - lightheadedness and dizzyness; there's more to OI, so maybe people with OI were missed because they had other OI symptoms).

 

[manasi12]

@HTester .. Very glad that you have revived this old thread. Low blood volume and its effects on cardiovascular system is very interesting.
When I first found out about David Bell's theory about five types of orthostatic intolerance, I was really amazed. It made sense why I feel so unwell with orthostatic diastolic hypertension. But volume boosting with either IV fluids or orally doesn't last long. But it definitely helps to bring back my high BP back to almost normal.
Another fascinating area is ayurveda literature which has described a condition known as 'rasa dhatu' depletion. Ras dhatu may be considered analogous to plasma volume. Ayurveda has described in detail the various causes for this like chronic fever, excessive stress, accumulated doshas and other varied causes. I had great relief in my POTS with this approach but I had to stop as I was concerned about possible heavy metal content in few medicines. But it is a very interesting area to look for pathogenesis of chronic low blood volume.

 

[HTester]

But volume boosting with either IV fluids or orally doesn't last long. But it definitely helps to bring back my high BP back to almost normal.

@manasi12 Classically, adding volume should increase pressures in the vascular system. So your experience of decreasing diastolic pressure upon volume loading may point to something unusual in autonomic reflexes, if I have understood your message correctly. Have you explored this either in the literature or in self-experimentation?

 

[manasi12]

@manasi12 Classically, adding volume should increase pressures in the vascular system. So your experience of decreasing diastolic pressure upon volume loading may point to something unusual in autonomic reflexes, if I have understood your message correctly. Have you explored this either in the literature or in self-experimentation?

Sorry , I was not clear about my diastolic hypertension. When I had narrowing of pulse pressure along with slight increase in diastolic pressure, fludrocortisone with lots of salt and water helped my OI. My electrophysiologist insisted on volume boosting and it helped to decrease my diastolic BP along with very low dose atenolol. My diastolic BP went from 96 - 98 to around 75-80.
I have autonomic neuropathy and I get initial orthostatic hypotention and then excessive shooting of BP.

 

[frozenborderline]

@manasi12 Classically, adding volume should increase pressures in the vascular system. So your experience of decreasing diastolic pressure upon volume loading may point to something unusual in autonomic reflexes, if I have understood your message correctly. Have you explored this either in the literature or in self-experimentation?

David Bell documented hypovolemic hypertension in some of his me/cfs patients. I don’t know if he published formal case studies on this, but he mentioned that he had patients with super high blood pressure that went down dramatically with saline infusions. He theorized that there is an adaptive response to low volume where the muscles? Around the blood vessels clamp down to preserve the volume.

I believe hypovolemic hypertension has been documented in the literature.

I have this response to. My bp runs a little high since I’ve been sick and when I get a saline infusion it almost always goes down. I don’t think it’s rare in me/cfs patients , ans in fact I wonder if what people call “hyperadrenergic pots” is an adaptive response to hypovolemia where the body tries to conserve volume and push blood where it needs to go by releasing adrenaline and clamping down on blood vessels to increase pressure.

This is an important area of study bc id you have this issue, many standard treatments for high pressure will harm you. I will find the link to the David bell stuff soon