To test whether cerebral autoregulation is impaired in patients with postural tachycardia syndrome
(POTS) we evaluated 17 healthy control subjects and 27 patients with POTS. Blood pressure (BP),
heart rate, and cerebral blood velocity (CBV) (transcranial Doppler) were recorded at rest and during
80o head-up tilt (HUT). Static cerebral autoregulation as assessed from the change in cerebrovascular
resistance during HUT was the same in POTS and in controls. The properties of dynamic cerebral
autoregulation were inferred from transfer gain, coherence and phase of the relationship between BP
and CBV estimated from filtered data segments (0.02-0.8Hz). Dynamic cerebral autoregulation of
patients with POTS did not differ from that of controls. The patients`dynamic cerebral autoregulation
did not change over the course of HUT despite increased tachycardia suggestive of worsening
orthostatic stress. Inflation of MAST pants substantially reduced the tachycardia of patients with
POTS without affecting cerebral autoregulation. Symptoms of orthostatic intolerance were reduced in
half the patients following MAST pants inflation. We conclude that cerebral perfusion and
autoregulation in many patients with POTS does not differ from that of normal control subjects.
Key Words postural tachycardia, cerebrovascular circulation, Fourier analysis, hemodynamics,
The postural orthostatic tachycardia syndrome (POTS) is a form of orthostatic intolerance that is
characterized by symptoms of lightheadedness, fatigue, palpitations, diminished concentration,
blurred vision, tremulousness, shortness of breath, nausea and impaired cognition that mainly occur
during upright posture (5, 24, 31, 33). In order to qualify for the diagnosis of POTS, these symptoms
must occur in conjunction with an increase in heart rate (HR) of over 30 beats per minute (bpm) or a
HR > 120 bpm within the first five minutes of standing (23-25, 31). The HR increase should be
sustained and not associated with orthostatic hypotension (46). Many patients have evidence of
hypovolemia (16, 26) or exaggerated venous pooling with central hypovolemia (32, 48). Inflation of
military anti-shock trousers (MAST pants), which prevent venous pooling in the legs, usually causes
reversal of the tachycardia (49). The pathophysiology of POTS is poorly understood. Various
abnormalities have been described including the presence of an attenuated autonomic neuropathy (25,
43), increased cardiac norepinephrine spillover (19), impaired norepinephrine transporter (45) or
reduced vagal cardiac baroreflex sensitivity (14). Some patients may have evidence of increased
sympathetic activity while supine (17, 18) while others do not (5). Regardless of pathophysiology, all
patients with POTS are significantly disabled by the constellation of symptoms noted above (2).
Lightheadedness and impaired concentration while upright or following other orthostatic stressors are
amongst the most disabling symptoms experienced by patients with POTS. It has generally been
assumed that these symptoms are due to cerebral hypoperfusion despite maintenance of normal blood
pressure (BP) (29). The changes in cerebral perfusion during stand in patients with POTS have been
measured using transcranial Doppler (TCD) sonography of the middle cerebral artery (MCA). Some
investigators did find that MCA cerebral blood velocity (CBV) decreased excessively during
orthostatic stress (23, 34) whereas others found no such change in CBV despite presence of
symptoms suggestive of cerebral hypoperfusion (22, 38). The reduction in CBV during orthostatic
stress has been attributed to excessive hyperventilation (34) or to exaggerated sympathetic activity
directed to cerebral vasculature (28).
Cerebral autoregulation is defined as the intrinsic capacity of cerebral vasculature to maintain
cerebral blood flow constant over a wide range of cerebral perfusion pressures (35, 37). Cerebral
autoregulation has been modelled both as a static and a dynamic process (35, 42, 44), the latter being
somewhat more sensitive index of a threatened cerebral circulation (9). Reduced cerebral perfusion
during orthostatic stress will occur if cerebral autoregulation is overwhelmed or impaired (12).
Normal individuals subjected to high levels of orthostatic stress simulated by lower body negative
pressure (LBNP) have reduced cerebral perfusion and impaired dynamic cerebral autoregulation (4,
54) . Cerebral perfusion is significantly reduced by LBNP in normal individuals made orthostatically
intolerant by prolonged head down bed rest (55). Severe hemorrhagic hypotension in primates also
causes cerebral vasoconstriction (15). We hypothesized that patients with POTS who experience
greater levels of orthostatic stress during stand than do unaffected individuals will have reduced
cerebral perfusion due to impairment of cerebral autoregulation.
We evaluated 27 patients (2 men, 25 women) with POTS as defined above. Although all had
symptomatic orthostatic intolerance, none had recurrent episodes of syncope. In all patients, history,
physical examination, routine clinical chemistry, complete blood count, and other relevant
examinations (Holter monitor, electroencephalogram, electrocardiogram, and echocardiogram) did
not reveal the cause of POTS. Patients participating in this study did not take medication of any kind.
Seventeen healthy subjects (6 men and 11 women) with no history of orthostatic intolerance served as
the control group. Both groups were similar (controls vs. POTS) in age (30.5 + 1.7 vs. 29.2 + 1.6
years), and height (167.7 + 1.6 vs. 165.6 + 1.5 cm). The weights of the control group were greater
(63.5 + 2.0 vs. 55.2 + 1.7 kg, p=0.001).
The hospital internal review board approved the head-up tilt (HUT) test protocols, and informed
consent was obtained from all subjects. All subjects were supine for 30 to 45 minutes before
recordings. The HUT protocol consisted of a 10-minute resting period in the supine position, to a
maximum of 40 minutes of 80° HUT with foot-rest support, and a second 5-minute period with the
subject supine. HUT was discontinued if significant symptoms of orthostatic intolerance were
experienced or if there was a clear precipitous drop in BP or HR. Not all control subjects underwent
the same duration of HUT but in no instance was HUT discontinued because of orthostatic
intolerance. The average duration of HUT in the control subjects was 36.9 + 2.0 min (range 15-40
min) while the average duration of HUT in the POTS patients was 16.9 + 2.1 min (range 3.4- 40
min). Eight of the 27 POTS patients were tilted on a second occasion at which time MAST pants
were inflated to 50 mmHg approximately 5 min after the onset of HUT. The MAST pants remained
inflated for 5-10 min. After deflation of the MAST pants subjects remained tilted for another 5 min.
BP was continuously recorded from the third finger of the left hand with a volume clamp
photoplethysmograph (Finapres model 2300, Ohmeda Monitoring Systems) and was also
intermittently measured from the brachial artery with a sphygmomanometer. The arm was maintained
at the level of the heart. During the recording period, the subject's hand was warmed with a heating
pad to prevent finger vasoconstriction (42). Respiratory movements were measured either with a
nasal thermistor or by using an end tidal CO2 monitor. The right MCA was insonated through the
temporal window at depths ranging between 45 and 55 mm with a 2-MHz Doppler probe (Eden
Medical Equipment TC-64) that was firmly strapped in place with an adjustable headband to ensure a
fixed angle of insonation. The analog ECG, BP, spectral envelope of CBV, and respiratory signals
were analysed by a PC equipped with an eight-channel analog/digital acquisition card and software
(Windaq, Dataq Instruments) and were sampled at 200 Hz.
Beat-to-beat HR, systolic and diastolic BP, and CBV were derived off-line with an automatic peak
and trough detection algorithm. In all cases placement of the cursors was verified by visual inspection
of the waveforms. Stroke volume (SV) and cardiac output (CO) during MAST pants inflation were
derived using the pulse contour method (27). The data were then resampled at 2 Hz with a linear
interpolation algorithm. To obtain a smoothed profile of the hemodynamic response of control and
POTS subjects to HUT, sequential segments of 60 seconds of data were averaged. Cerebrovascular
resistance (CVR) was calculated by dividing mean BP by mean CBV after correcting for the
difference in hydrostatic pressure between the site of BP recording and MCA insonation. Changes in
CVR during HUT served as an index of static autoregulation (35, 41).
The continuous waveforms of BP, CBV and respiration were bandpass filtered between 0.02 and 0.8
Hz. Filtered data segments of 4096 points (204.8 sec) were subsampled at 2.5 Hz. Periodograms were
constructed from Hanning-windowed segments of 256 points overlapped by 50%. The power of the
low frequency BP and CBV bands was integrated using the commonly accepted bandwidth definition
of 0.04 - 0.15 Hz (7, 8, 44). In addition, the power in the frequency band of 0.02 – 0.12 Hz was
integrated for comparison, as this was the frequency band at which the average dynamic gain and
phase were analysed (see below). Transfer functions were constructed from Hanning-windowed
segments of 128 points overlapped by 69%. For each transfer function, squared coherence, phase
delay and transfer gain were calculated. The phase delay is defined as positive when CBV leads BP.
Transfer gain expresses the degree to which oscillations in input (BP) are transmitted to output
(CBV). Dividing transfer gain by mean conductance of the analyzed data segment normalizes the
gain. Normalized gain of less than 1 indicates attenuation of the transmitted BP fluctuations to CBV
i.e. dynamic autoregulation. Minimal dynamic gain was calculated as the average of points between
0.02 and 0.04 Hz, the frequency range at which the best attenuation of transmitted BP fluctuations
was observed. To facilitate comparison of curves of gain and phase between control and POTS
subjects we averaged the points between 0.02 and 0.12 Hz where the normalized gain was less than 1.
3 x 2 ANOVA’s with repeated measures were used for comparisons of baseline, and HUT between
control and POTS subjects for the cardiovascular and cerebrovascular data. Two HUT periods were
sampled, the first beginning approximately one minute after the start of tilt (early HUT) and a second
period beginning approximately 4 minutes before the end of HUT (late HUT). The late HUT period
used for construction of periodograms and transfer functions began approximately three minutes
before the end of the HUT. For comparison of periodograms or of transfer function analyses between
control and POTS groups a 2 x 2 ANOVA with repeated measures was used. If significant
differences were found (p < 0.05) Dunnett’s procedure for multiple comparisons was used to assess
differences between the various groups. For comparisons between groups of patients with greatly
different sample sizes the Mann-Whitney U non-parametric test was used. For other comparisons
between control and POTS groups such as age, height, weight etc. a Student’s t-tests was used. Data
are expressed as mean + SE.
Cardiovascular and cerebrovascular profiles during HUT
Representative beat-to-beat profiles of HR, systolic and diastolic BP, systolic and diastolic CBV and
calculated CVR from a control subject and a POTS patient during HUT are shown in Figure 1. The
complete profiles of the averaged data during early and late HUT from the 17 controls and 27 patients
with POTS are shown in Figure 2 and the averaged raw values from these 3 periods are provided in
Table 1. Supine HR, systolic and diastolic BP and systolic and diastolic CBV were all significantly
increased in POTS patients relative to control subjects. The averaged absolute changes in the
cardiovascular responses from baseline were compared during early and late HUT (all data in this
section expressed as POTS vs. controls). It should be noted that patients with POTS were tilted for a
shorter duration than were control subjects (16.9+2.1 vs. 36.9+2.0 min, p<0.0001). The responses to
late HUT should therefore be considered as being the response to the maximum orthostatic stress
imposed by our experimental protocol. POTS patients had greater increases in HR both during early
(36.5+2.5 vs. 17.5+2.4 bpm, p<0.0001) and late HUT (48.7+1.8 vs. 29.6+2.1 bpm, p<0.0001) and
decreased systolic BP during early (-5.0+2.0 vs. 5.3+4.0 mmHg, p = 0.03) and late (-11.7+2.3 vs.
6.4+4.2 mm Hg, p=0.001) HUT. The increase in diastolic BP during early HUT was similar (9.0+1.8
vs. 7.2+1.4 mm Hg, p=0.5) in both groups but during late HUT was less in POTS (10.0+1.9 vs.
15.9+2.0 mm Hg, p=0.02).
In contrast to the cardiovascular profile, the percent decreases in systolic (early HUT 84.9+2.6 vs.
89.4+2.0% of baseline, p= 0.2; late HUT 78.8+2.1 vs. 77.9+2.5% of baseline, p=0.8) and diastolic
(early HUT 88.0+3.0 vs. 90.7+2.6% of baseline, p=0.5; late HUT 80.0+2.1 vs. 78.2+3.7% of
baseline, p=0.7) CBV were not different. The percent decrease in CVR during early HUT an index of
static cerebral autoregulation, was also similar (85.6 + 3.3% vs. 89.0 + 4.5%, p=0.7) while the
percent decrease in CVR during late HUT was less in POTS than in normal controls(90.3 + 3.6% vs.
108.5 + 6.7%, p=0.02). In 9 POTS subjects ETCO2 was measured. CO2 decreased from 4.57+0.16 %
to 3.86+0.14 % during early HUT (p = 0.0002) and to 3.62+0.15 % by late HUT (no difference
between early and late HUT p=0.3). Respiratory frequency of patients with POTS was similar to that
of normal control subjects (see spectra Fig 4F).
In 8 POTS patients, inflating MAST pants after approximately 5 minutes of HUT reduced the
orthostatic stress of HUT. The profiles of the averaged data from the 8 patients are shown in Figure 3
and averaged raw values are provided in Table 2. MAST pants inflation significantly decreased HR
and increased SV, and systolic CBV. Mean CBV increased from 49.1+4.2 to 53.8 +3.6 cm/s (p=0.01)
which represented an increase from 82.5+3.3 % of the baseline level before MAST pants inflation to
91.1+3.3% of the pre-tilt level during the MAST pants inflation. ETCO2 (measured in only 4
patients) decreased significantly during tilt prior to inflation of MAST pants (4.66+0.29 to 3.91+0.15,
p=0.04) and recovered during MAST pants inflation (4.20+0.17, p=0.01 compared to HUT alone).
Deflation of the MAST pants was associated with an increase in HR, a decrease in SV and a decrease
in CBV (Figure 3). Despite the obvious effect of MAST pants inflation, only 4 patients noted
substantial symptomatic improvement during this maneuver.
Fluctuations in BP and CBV in controls and in POTS subjects during HUT
Both control subjects and POTS patients exhibited similar spontaneous low frequency (<0.1 Hz)
oscillations in BP and CBV although the magnitudes of both the BP and CBV oscillations were
significantly greater in patients with POTS (Fig 4D and 4E; Table 3). The increased magnitude of
these low frequency fluctuations was due to greater response to orthostatic stress. Reduction of
orthostatic stress by MAST pants inflation decreased BP power from 315.8 + 56.4 mmHg /Hz to
134.2 + 22.9 mmHg /Hz (p = 0.005) and CBV power from 209.1 + 22.2 cm/s /Hz to 86.7 + 18.7
cm/s /Hz, (p = 0.0004). The power of the fluctuations during MAST pants inflation did not
significantly differ from that of the normal control BP and CBV oscillations during HUT (p=0.4 for
BP and p=0.7 for CBV).
Dynamic cerebral autoregulation during HUT:
The transfer function signatures of controls and POTS subjects shown in Figs 4A-C were essentially
superimposable. Coherence between BP and CBV remained greater than 0.5 in the frequency range
between 0.06 + 0.01 and 0.36 + 0.03 Hz in control subjects and 0.05 + 0.01 and 0.39 + 0.02 Hz in
patients with POTS (average coherence 0.71 + 0.03 for controls vs. 0.72 + 0.02 for POTS). Phase
was positive in this frequency range revealing that the oscillations in blood flow lead those in
pressure. Gain was <1 at frequencies below 0.12 Hz indicating that flow is stabilized in the presence
of fluctuation in pressure at these frequencies. The values for minimal dynamic gain, average
dynamic gain and average phase, presented in Table 3 show no difference between control and POTS
subjects. Reduction of orthostatic stress by inflation of MAST pants during HUT did not significantly
alter the transfer function curves in the 8 POTS patients tested.
Dynamic cerebral autoregulation in POTS patients remained stable over the duration of the HUT
despite the progressive increase in HR (an index of increased orthostatic stress). Figure 5 presents
data taken from 22 subjects with POTS who had HUTs of sufficient duration to allow for
construction of separate transfer functions from the beginning and from the end of HUT. As shown in
Figure 5 (D-E) the magnitudes of the BP and CBV fluctuations were stable over the duration of the
tilt. Moreover, the transfer function curves from these two times are essentially identical. This visual
impression was confirmed by showing no statistical difference between the paired data of minimal
and average dynamic gain, phase as well as BP and CBV oscillations taken from these 22 subjects.
Dynamic cerebral autoregulation in controls and in subjects with POTS while supine
The dynamic cerebral autoregulation of both groups was also assessed in the absence of orthostatic
stress from data segments obtained during the supine pre-HUT period. As shown in Figure 6 and in
Table 3 there was no difference in the magnitude of the BP or CBV fluctuations at any frequency
range, or in the transfer function signatures of supine controls as compared to those of supine subjects
with POTS. In the absence of orthostatic stress the magnitude of the BP fluctuations was less in both
groups (Table 3). Both the minimal and average dynamic gains were elevated in the supine control
group as compared to HUT. In the POTS patients, the minimal dynamic gain was significantly greater
while supine as compared to HUT, but not the average dynamic gain.
The results of this study provide several new insights concerning cerebral autoregulation in POTS.
First, contrary to our hypothesis, patients with POTS did not have impaired cerebral perfusion as
compared to normal control subjects despite the presence of a cardiovascular profile during HUT
suggestive of increased orthostatic stress. In this regard, our data confirm the observations of others
who did not observe reductions in CBV during orthostatic stress in POTS (22, 38) and are not
consistent with other studies in which CBV was excessively reduced during HUT (23, 34).
Second, reduction of orthostatic stress with MAST pants inflation effectively reversed the HUT-
induced tachycardia but only reduced symptoms of lightheadedness in half of the 8 patients tested.
Third, static autoregulation as assessed from the CVR response to early HUT was similar in POTS
and normal control subjects. Fourth, dynamic cerebral autoregulation of patients with POTS did not
differ from that of controls. Moreover, dynamic cerebral autoregulation did not change over the
course of HUT in patients with POTS even though the cardiovascular response did.
In this study we used TCD to measure cerebral perfusion because this technique is the only one
currently available that permits the non-invasive prolonged monitoring of rapid changes in cerebral
perfusion needed to assess dynamic cerebral autoregulation. We have previously discussed the
limitations of this technique as well as the validity of using linear transfer function analysis to assess
dynamic cerebral autoregulation (42, 44). The MCA was insonated because stable long term
recordings can be easily obtained and because this artery supplies a substantial portion of cerebral
blood flow to the anterior circulation. The dynamic autoregulatory response characteristics of the
MCA largely mirror those of arteries of the posterior circulation (21, 36, 40).
In a study of 9 patients with POTS the alpha-adrenergic blocker, phenotolamine, volume replacement
with isotonic saline or infusion of phenylephrine all acted to reverse the significant CBV reduction
during orthostatic stress (28). These data suggest that in this subgroup of patients with POTS
cerebral hypoperfusion might be due to exaggerated sympathetically-mediated cerebral
vasoconstriction (8, 53). The cerebral vasculature receives a rich sympathetic innervation, but the
effect of this innervation on cerebral blood flow in humans is unclear (20). Whereas numerous
animal experiments have shown that sympathetic denervation does not alter resting cerebral blood
flow (6), in humans, stellate ganglionic blockade increases ipsilateral cerebral blood flow (51).
Similarly, sympathetic denervation does not alter cerebral autoregulation in normotensive animals
(6), but pharmacologic ganglionic blockade with Trimethaphan appears to attenuate dynamic
cerebral autoregulation in humans (53). The effect of generalized sympathoexcitation on cerebral
blood flow in humans is even less well understood. Sympathoexcitation induced by immersing the
hand in ice water, may either increase (39) or decrease (47) CVR while sympathoexcitation induced
by total body surface skin cooling actually improves orthostatic tolerance and increases CBV during
the orthostatic stress of incremental LBNP (11). It is also not clear that exaggerated generalized
sympathoexcitation actually occurs in most patients with POTS. As reviewed in the
INTRODUCTION, not all patients with POTS manifest exaggerated generalized sympathetic
activity. Indeed the same research group that postulated increased sympathetic outflow to cerebral
vasculature in POTS also found that the postganglionic sympathetic response to standing was
blunted in these patients relative to controls (17).
Others have shown that the exaggerated decrease in CBV in patients with POTS is due to
hyperventilation although the cause of this hyperventilation is unknown (34). It has been suggested
that hyperventilation occurred as patients increased depth of respiration to increase venous return and
improve orthostatic tolerance. We have not observed increased respiratory frequency in our patients
nor have we found evidence of hyperventilation in a subgroup of patients in whom CO2 was
measured. Hyperventilation would also be expected to improve dynamic cerebral autoregulation in
these patients (1, 13). However this group of investigators have also documented abnormally
prolonged CBV recovery during phase IV of the Valsalva maneuver, an observation that suggests
that autoregulation is actually impaired in some of their patients with POTS (30).
As noted above, we did not find evidence of impaired cerebral perfusion or impaired static or
dynamic autoregulation in our patients with POTS. It is unlikely that our patients represent a
subpopulation that is distinctly different from that studied by others. Both the symptom and
hemodynamic profiles are indistinguishable from those described by others. Moreover many of the
patients studied by at least one group (34) had evidence of mild POTS only, despite symptoms and
evidence of impaired cerebral perfusion.
Our data clearly show that many with POTS who have symptoms suggestive of cerebral
hypoperfusion during orthostatic stress show normal responsiveness of the anterior circulation during
HUT. What then is the pathophysiology of the symptoms experienced by these patients? One
possibility is that symptoms arise from impaired perfusion of structures (e.g. vestibular nuclei)
receiving blood supply from the posterior circulation. As noted above, there is no evidence that the
dynamic autoregulatory response characteristics of the posterior circulation differs from that of the
anterior circulation (21, 36, 40). Further studies however are required to directly confirm this in
patients with POTS. A second possibility is that cerebral oxygenation is impaired in patients with
POTS. This possibility has been documented in one group of young subjects using near infrared
spectroscopy and recording from probes paced over the forehead (50). It is unlikely that impaired
cerebral oxygenation accounts for these symptoms in our patients. When autoregulation fails, oxygen
extraction fraction increases substantially as a final attempt to maintain cerebral oxygen metabolism
(10, 52). Impaired cerebral oxygenation must therefore be preceded by substantial and measurable
autoregulatory failure. This was not found in our patients. One last possibility is that many of the
symptoms thought to be attributable to cerebral hypoperfusion may occur in patients with POTS in
whom cerebral perfusion is entirely normal. Many patients with POTS seem to have heightened
somatic vigilance and catastrophic cognitions which may predispose them to increased disability (3).
In this regard, it is of interest that in half the patients MAST pants inflation did not substantially have
symptomatic improvement despite significant improvement in cardiovascular and cerebrovascular
In conclusion, this study has shown that the cerebrovascular response as well as static and dynamic
autoregulation during orthostatic stress was comparable between our cohort of patients with POTS
and normal control subjects. Further investigation is required to clarify the underlying
pathophysiology of the symptoms that makes POTS such a disabling condition (2).
Supported by grants to Ronald Schondorf from The CFIDS Association of America and the
Fondation des Maladies du Coeur du Québec
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Figure 1: Representative beat-to-beat profiles of HR, systolic and diastolic BP, systolic and
diastolic CBV and calculated CVR from one control subject and one POTS patient during 800
HUT. Subjects were tilted at 5 minutes and returned to the supine position 5 minutes before end
Figure 2: Averaged profiles from patients and control subjects during rest, early and late HUT.
Figure 3: Averaged profiles from 8 POTS patients while supine, during HUT alone, HUT and
MAST pants inflation and HUT following deflation of MAST pants.
Figure 4: Group-averaged transfer function gain (A), phase (B), coherence (C) and spectral
analysis of the fluctuations in BP (D), CBV (E) and respiration (F) in control subjects and POTS
patients during HUT. AU, arbitrary units.
Figure5: Group-averaged transfer function gain (A), phase (B), coherence (C) and spectral analysis
of the fluctuations in BP (D), CBV (E) and respiration (F) in 22 POTS patients who had HUT of
sufficient duration to allow construction of separate transfer functions at the beginning and end of
Figure 6: Group-averaged transfer function gain (A), phase (B), coherence (C) and spectral analysis
of the fluctuations in BP (D), CBV (E) and respiration (F) in supine control subjects and POTS
Table 1. Averaged cardiovascular and cerebrovascular responses in controls and POTS.
Supine Early HUT Late HUT
Controls POTS Controls POTS Controls POTS
61.2+1.8 75.8+2.5* † † § §
HR (bpm) 79.7+2.3 112.7+2.4* 90.9+ 2.5 123.6+1.8*
108.6+3.0 117.7+2.6* 109.4+3.7 114.0+3.5 115.5+4.6 107.6+3.3*
Systolic BP (mmHg)
56.4+1.9 63.9+1.7* † † §
Diastolic BP 64.5+2.0 73.1+2.7* 72.6+2.3
91.2+4.9 98.0+3.8* † † § §
80.7+4.3 82.0+3.2 70.6+3.5 75.3+2.5
41.0+2.4 45.5+1.7* 37.6+2.7 † 32.2+2.3 §
1.37+0.10 1.34+0.07 † † 1.45+0.12 1.21+0.08*
CVR(mmHg/cm/s) 1.20+0.08 1.15+0.07
*Comparison of POTS with controls during same orthostatic stress;
† Comparison of early HUT vs. supine
§ Comparison of late HUT vs. early HUT
Table 2. Averaged cardiovascular and cerebrovascular responses of patients with POTS to HUT
alone and to inflation of MAST pants during HUT.
Supine HUT MAST Pants
HR (bpm) 81.1+6.6 126.5+3.2* †
SV (ml) 66.8+5.9 39.4+4.9* †
CO (l/min) 5.4+ 0.6 4.9+0.6* 5.1+0.6
Systolic BP (mmHg) 115.3+5.8 110.8+4.8 117.6+6.6
Diastolic BP (mm Hg) 60.6+4.0 71.4+3.6* 72.0+4.8
Systolic CBV (cm/sec) 91.2+6.8 74.4+6.9* †
Diastolic CBV (cm/sec) 43.6+3.1 36.5+3.1* 39.3+2.4
*different from supine, †different from HUT
Table 3. Comparison of Power Spectra and Transfer Function Analysis: Controls vs. POTS
Controls POTS Controls POTS
BP Power (0.02-.012 Hz) 122.8+ 24.7 145.3+25.3 211.0+28.9 322.1+35.6*†
Low Frequency BP Power 68.8+12.8 99.6+17.9 172.9+26.5† 252.5+27.5*†
CBV Power (0.02-0.12 Hz) 123.4+32.2 143.6+23.1 128.3+ 16.3 208.3+25.5*†
Low Frequency CBV Power 58.6+10.7 89.0+13.9 96.4+14.0 162.0+20.8*†
Gain (.02-.04 Hz) 0.82+0.12 0.70+0.07 0.46+0.05† 0.48+0.04†
Gain (.02-.12 Hz) 0.86+0.07 0.79+0.04 0.66+0.03† 0.70+0.04
Phase (.02-.12 Hz) 0.58+0.14 0.76+0.08 0.64+0.08 0.83+0.06
*Comparison of POTS with controls during same orthostatic stress;
† Comparison of HUT vs. supine
Low frequency bandwidth is 0.04-0.15 Hz
0 10 20 30 40 50 0 5 10 15 20 25
Time (min) Time (min)
Mean CBV (% baseline)
% of baseline
0 1 2 1 2 3 -4 -3 -2 -1 0
Baseline Early HUT Late HUT
Mean CBV (% baseline)
% of baseline
0 1 2 1 2 3 0 1 2 3 4 5 1 2 3
Baseline Early HUT Mast Pants Deflation
A POTS HUT D
0.01 0.1 1 0.01 0.1 1
Frequency (Hz) Frequency (Hz)
POTS HUT early
A POTS HUT late
0.01 0.1 1 0.01 0.1 1
Frequency (Hz) Frequency (Hz)
A POTS Supine D
0.01 0.1 1 0.01 0.1 1
Frequency (Hz) Frequency (Hz)