Local Vascular Responses in POTS

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 (0.80.2 vs 4.40.5 and 2.70.4 ml/min/100ml) but increased during leg lowering (1.20.5). 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 (3913 vs 153 and 225 ml/100ml/min/ mmHg) but decreased to 2913 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 = 202 vs 294 and 284 sec, cutaneous time constant = = 6025 vs 14953 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 measured.
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.
 

 


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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