Normal versus abnormal: What normative data tells us about the utility of heart rate in postural tachycardia, 2019, Baker and Kimpinski

Another potentially relevant paper from 2010: This descriptive population study of 307 public high school students, ages 15 to 17 years. . . Reference ranges for orthostatic heart rate change in this population at 2 minutes were -2 to +41 beats per minute and at 5 minutes were -1 to +48 beats per minute. . . One-third of participants experienced orthostatic symptoms during testing.
 
Nightsong said:
Another potentially relevant paper from 2010: This descriptive population study of 307 public high school students, ages 15 to 17 years. . . Reference ranges for orthostatic heart rate change in this population at 2 minutes were -2 to +41 beats per minute and at 5 minutes were -1 to +48 beats per minute. . . One-third of participants experienced orthostatic symptoms during testing.
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Yes unfortunately, they do not report how many students had more than 40 bpm HR changes as that would give an indication of the current threshold. They only report the median (20) range (-15 + 61) and 2.5% (-1) and 97.5% (48) quartiles and mention that 23% had a HR increase of more than 30 bpms.

One interesting aspect in this study is that HR changes hardly correlated with orthostatic symptoms (notice the big ranges).
At 5 minutes of standing, those with symptoms had a median heart rate change of 21 beats per minute (range, +6 to +61) and those without symptoms had a median heart rate change of 18 beats per minute (range, -15 to +50).

Receiver operating characteristic curve analysis did identify a significant cutoff in 2- and 5-minute heart rate changes for predicting orthostatic symptoms in adolescents at 18 beats per minute and 20 beats per minute, respectively. However, because of low sensitivity (65% and 61%, respectively) and specificity (53% and 56%, respectively), this cut-off would not be clinically useful for predicting postural orthostatic symptoms
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Nightsong said:
I actually haven't come across a paper that tries to assess pre-test apprehension in head-up tilt, although while searching yesterday I found a Roma et al. paper that briefly considered the potential effects while performing passive-standing tests in POTS patients:
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That's an interesting thought. There are other factors that might influence base line heart rate - for example, the effort of getting to the clinic for those people disabled by their symptoms might result in a much higher baseline heart rate than normal, making it harder to demonstrate an increase upon standing.

I found that periods of worse symptoms did correlate with increased morning resting heart rate, so that would tend to make it harder to demonstrate the necessary heart rate increase. Maybe, as suggested above, more weight should be given to the absolute heart rate when standing after lying down.

ME/CFS Skeptic said:
Same finding here: 9 of the 15 controls (60%) had an HR increase that was higher than 30 bpm after 10 minute passive tilt table testing. With a 10 minute standing test, 5 (33%) met the POT criterium.
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It's a point worth repeating, it definitely doesn't make sense to have the same HR increase in both a tilt table test and a standing test when diagnosing POT.

(and of course, as this thread demonstrates, tilt table testing and HR increases may not be very useful when diagnosing POTS).
 
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@Nightsong Do you know of any studies that measured the prevalence of POTS among OI patients? For example: clinics that report the % of POTS in the patients with OI that get referred to them.

I found this one paper that says that only 19% of their OI patients fulfilled POTS criteria.
Patients with Orthostatic Intolerance: Relationship to Autonomic Function Tests results and Reproducibility of Symptoms on Tilt - PubMed (nih.gov)
The clear message is that symptoms are a poor predictor of autonomic abnormalities. [...] The clinical relevance of our study lies in the finding that even patients who complain orthostatic symptoms do not necessarily have abnormal results in HUT.

Within the OH and POTS groups, BP or HR changes during HUT were not significantly different between symptomatic and asymptomatic groups. In other word, we could not assume the severity of orthostatic symptoms during HUT as indicative of the degree of orthostatic fall in BP or HR rise during HUT
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ME/CFS Skeptic said:
I think the conclusion is more that POT may not be relevant to the symptoms POTS patients experience. Orthostatic tachycardia seems to have little relationship with orthostatic symptoms.
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It may not be, but I think there are a few things to think about before the idea is chucked away. Here are my example measures again. I don't think some of those heart rates on standing are normal, and the days when standing heart rates were high coincided to some extent with worse ME/CFS symptoms.

Screen Shot 2024-06-16 at 11.23.48 pm.png
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So, maybe there's a problem with
  • acknowledging that the increased heart rate phenomenon fluctuates - it's not necessarily a problem every day
  • change measures versus absolute measures - because a raised baseline for whatever reason makes it harder to qualify for a required increase in heart rate.
  • tilt table testing - maybe it has nothing much to do with the impact of standing; maybe it causes problems for healthy people too
  • some people's cardiovascular system may go haywire in different ways, or in different way on different days - e.g. maybe the blood pressure drops, so the heart rate increase is still a problem, but it's not the only one
  • Maybe things are more complicated than just a heart rate change on standing, and other factors need to be taken into account too when working out if a heart rate increase means a system that isn't functioning well. e.g. is the increase sustained? is the increase relative to artery stiffness?
 
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ME/CFS Skeptic said:
@Nightsong Do you know of any studies that measured the prevalence of POTS among OI patients?
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Have you seen this one?
We reviewed the medical records of 246 patients presented with symptoms of OI seen at our centre from January 2010 till March 2019. Out of them, 40 patients included, those qualifying the criteria for POTS on HUTT
...
During the study period, 246 patients underwent the tilt-table test, and 40 of them (16.26%) were diagnosed with POTS
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Hutan said:
acknowledging that the increased heart rate phenomenon fluctuates - it's not necessarily a problem every day
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Yes that is probably an issue and your own measurements show that very clearly: there seems to be a large inter-individual variability: one day you have increases with 45, other times only 11 bpm.

Some argued that orthostatic tachycardia measurements during standing or tilt testing are a bit like measurements of blood pressure: it fluctuates a lot so you have to take multiple measurements before you interpret an increase as an problem.
 
Another interesting one:
Orthostatic Intolerance in Adults Reporting Long COVID Symptoms Was Not Associated With Postural Orthostatic Tachycardia Syndrome - PubMed (nih.gov)
Peak heart rate during the standing test did not predict OI and the majority of Long Covid patients with tachycardia did not have OI during the tilt test.
Of the 53 who had a 10-min tilt, 7 (13%) had an HR increase > 30 bpm without OHtilt (2 to HR > 120 bpm), but six did not report OItilt. POTS was therefore present in n = 1 (1.9%).
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From the above study:
Because a reduction in [lower body negative pressure] tolerance in both [high tolerance to presuncopal symptoms] and [low tolerance] groups after propranolol treatment was most closely associated with reduced tachycardia, the data suggest that a primary autonomically mediated mechanism for maintenance of mean arterial pressure and orthostatic tolerance in healthy subjects is beta adrenergic-induced tachycardia.
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Yes, I don't think we have to see the orthostatic tachycardia itself as pathologic. It may well be a very normal and helpful reaction to some sort of stressor - to blood or oxygen not getting to where it needs to get to, for example.
 
Standing shock index: An alternative to orthostatic vital signs
Blood donation does not affect the supine shock index, but it does result in changes in standing shock index that are similar to changes in more complicated orthostatic vital signs.
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Blood donation resulted in a mean increase in the standing shock index of 0.09 [95% CI, 0.08–0.11] in younger adults and 0.08 [95% CI, 0.05–0.11] in older adults. These changes were similar to those noted for OCSI (young, 95% CI, 0.08–0.10; old, 95% CI, 0.04–0.10). Supine shock index values did not change with donation in younger donors (mean difference 0.0 [95% CI, 0.0–0.01]) or older donors (mean difference 0.0 [95% CI, − 0.01–0.03]).
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This analysis demonstrates that a simple parameter, the standing shock index, is superior to supine vital signs in distinguishing euvolemic patients from those with moderate hypovolemia. The discriminative ability of the standing shock index was similar to that of OCSI, which requires supine vital sign measurement and more involved computation.

In 1980, Knopp demonstrated the superiority of orthostatic vital signs over supine vital signs in detecting blood loss
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Donating 450 ml of blood didn't change supine shock index values in healthy people. It did change standing shock index values by a bit less than 0.1, which is quite significant. And the authors suggest that standing shock index is useful in identifying hypovolemia.

I can't access that paper - I'm interested to know how the shock index changed from supine to standing, before and after the blood donation in these healthy people.
 
Hutan said:
I can't access that paper - I'm interested to know how the shock index changed from supine to standing, before and after the blood donation in these healthy people.
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Hope this works:

1.png
Table 1 shows the effect of a 450-mL blood loss on vital signs as well as the effects of supine versus standing positioning. Supine pulse, sbp, and shock index values showed little effect of blood donation, as evidenced by high CV values and confidence intervals for differences spanning 0 (zero). Standing pulse and sbp values showed clear effects from blood donation, but effects differed in younger and older groups. Of the parameters tested, only standing shock index and OCSI had large effects relative to their variation (low CV) and consistent effects for younger and older groups. The effects of blood donation on OCSI and standing shock index were similar to each other, as measured by mean differences and SD of mean differences.
Table 2 shows test characteristics for a variety of cutpoints for the standing shock index. The vast majority of blood donors had standing shock index values of 0.5 or more after donation (sensitivity 96%), and a cutpoint of 0.6 had a likelihood ratio for a negative test of 0.5. In contrast, a cutpoint ≥1.0 had a specificity of 99%, and a cutpoint ≥0.9 had a likelihood ratio for a positive test of 4.1.
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Thanks very much @Nightsong.

So, similar results to that older study I quoted in my last post.

Standing shock index increased from 0.67 to 0.76 after blood donation

The OCSI (orthostatic change in shock index, the difference between supine and standing shock index) increased from 0.11 to around 0.20 after blood donation.
 
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Also notable in the POTS literature: not a single decent prevalence or epidemiological study. Almost all single-center observational studies which are probably affected by referral and selection bias.

Also no prognosis studies, some say that half of the patients spontaneously recover within 3 years but there seems to be no data about this at all.
 
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