[ Home ] [ Up ] [ Exercise Intolerance- the Exercise Pressor Reflex in POTS ] [ Skeletal Muscle Pump ] [ Normal Leg Venous Capacitance ] [ Postural Neurocognitive ] [ Splanchnic Pooling in Normal Flow POTS ] [ Nitric Oxide Dysfunction in Low Flow POTS ] [ Angiotensin-II in POTS ] [ Decreased Upright Cerebral Blood Flow and Cerebral Autoregulation in POTS ] [ Postural Hyperpnea ] [ Nitric Oxide is Decreased in Angiotensin-II dependent Low flow POTS but increased along with Splanchnic pooling Neuropathic POTS ] [ Local Vascular Responses in POTS ] [ Microvascular Filtration in High Flow POTS ] [ POTS as Thoracic Hypovolemia ]
|Chronic orthostatic intolerance is associated
with postural tachycardia syndrome (POTS) in which the diagnosis is made
by abnormal upright tachycardia. Some patients are unable to evoke
baroreflex mediated vasoconstriction and have increased calf blood flow.
Others have low calf blood flow and increased peripheral arterial
resistance. We tested the hypothesis that myogenic, venoarteriolar and
reactive hyperemic responses are abnormal in low flow POTS.
We studied 14 patients aged 13-19 years with POTS and evenly
subdivided among low flow and high flow subgroups compared to 9 healthy
control subjects. POTS was confirmed by findings of a heart rate increase
exceeding 30 beats/min on an initial upright tilt to 70o.
We used venous occlusion strain gauge plethysmography to measure
calf venous pressure and blood flow, while supine and when the calf was
lowered by 40 cm to evoke myogenic and venoarteriolar responses. We
remeasured flow and venous pressure during venous hypertension alone
produced by occlusion cuff pressure to 40 mmHg to evoke only the
venoarteriolar response. We measured reactive hyperemia of the calf using
plethysmography and in the skin using laser Doppler flowmetry. Baseline
blood flow in low flow POTS was reduced compared to high flow and control
subjects (0.8±0.2 vs 4.4±0.5 and 2.7±0.4 ml/min/100ml) but increased
during leg lowering (1.2±0.5). Blood flow decreased in the other groups.
Baseline peripheral arterial resistance was significantly increased in low
flow POTS and decreased in high flow POTS compared to control (39±13 vs
15±3 and 22±5 ml/100ml/min/ mmHg) but decreased to 29±13 in low flow
POTS during venous hypertension. Resistance increased in the other groups.
Maximum calf hyperemic flow and cutaneous flow were similar in all
subjects. The duration of hyperemic blood flow was curtailed in low flow
POTS compared with either control or high flow POTS subjects
(plethysmographic time constant = 20±2 vs 29±4 and 28±4 sec, cutaneous
time constant = = 60±25 vs 149±53 sec in controls). Thus, local
blood flow regulation in low flow POTS patients is impaired.
|The figure shows the design of experiments to examine local
flow regulation in POTS patients. Flow was measured four times by venous
occlusion at supine resting baseline, then the leg was lowered
(hung) off the examining table. We waited at least 4 minutes or until flow
returned to baseline. Subsequently 40 mmHg venous occlusion pressure was
imposed. Finally, after a period of ischemia reactive hyperemic flow was
|The figure shows changes in calf blood flow caused by
lowering the leg. High flow POTS data are shown in the left hand panel,
control data in the middle panel and low flow POTS data are shown in the
right hand panel. The 2 male high flow POTS subjects and 2 male control
subjects are indicated by the darkened lines. Although arterial resistance
is the most appropriate measure of effect it cannot be calculated
accurately during leg dependence because Pv cannot be accurately measured.
Calf blood flow decreases in high flow POTS and control subjects but
increases in low flow POTS patients. This suggests a defect in myogenic
and/or venoarteriolar responses in low flow POTS.
|The figure shows changes in arterial resistance caused by
imposing an increase in venous pressure to 40 mmHg on the leg. High flow
POTS data are shown in the left hand panel, control data in the middle
panel and low flow POTS data are shown in the right hand panel. The 2 male
high flow POTS subjects and 2 male control subjects are indicated by the
darkened lines. Resistance increases in high flow POTS and control
subjects but decreases in low flow POTS patients. This suggests a defect
in venoarteriolar responses in low flow POTS.
|The figure shows the effects of ischemia followed by
reactive hyperemia measured by venous occlusion plethysmography. Although
peak hyperemic blood flows are similar for the different groups there is a
more rapid fall (smaller exponential time constant tau) in subjects
with low flow POTS than either control or high flow POTS subjects.
|Effects of ischemia followed by reactive hyperemia on
laser-Doppler measured cutaneous blood flow are shown. Data are averaged
over all subjects and error lines represent standard errors of the mean.
Peak hyperemic blood flows are similar for control subjects, high flow
POTS patients and low flow POTS patients but there is a more rapid fall
(smaller exponential time constant tau) in low flow POTS patients.