Splanchnic Pooling in Normal Flow POTS

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Valsalva Maneuver in Normal Flow POTS ]

Previous investigations have allowed for stratification of POTS patients based on peripheral blood flow. One such subset, comprising “normal flow POTS” patients is characterized by normal peripheral resistance and blood volume while supine but thoracic hypovolemia and splanchnic blood pooling when upright.

We studied 32 consecutive POTS patients aged 14-22 years comprising 13 with low flow POTS, 14 with normal flow POTS, and 5 with high flow POTS compared to 12 comparably aged healthy volunteers. We measured changes in impedance plethysmographic (IPG) indices of blood volume and blood flow within the thoracic, splanchnic, pelvic (upper leg), and lower leg regional circulations while supine and during incremental tilt to 20o, 35o, and 70o. We validated IPG measures of thoracic and splanchnic blood flow against indocyanine green dye dilution measurements. We validated IPG leg blood flow against venous occlusion plethysmography. Control subjects developed progressive vasoconstriction with incremental tilt. In comparison splanchnic blood flow was increased supine in normal flow POTS despite marked peripheral vasoconstriction and did not change during incremental tilt producing progressive splanchnic hypervolemia. Absolute hypovolemia was present in low flow POTS; all supine flows and volumes were reduced; there was absence of vasoconstriction with tilt in all segments, and segmental volumes tended to increase uniformly throughout tilt. Lower body (pelvic and leg) flows were increased in high flow POTS at all angles with consequent lower body hypervolemia during tilt.

Our main finding is selective and maintained orthostatic splanchnic arterial vasodilation in normal flow POTS despite marked peripheral vasoconstriction in these same patients. Local splanchnic vasoregulatory factors may counteract vasoconstriction and venoconstriction in these patients. In addition there was abnormal lower body vasoconstriction in high flow POTS and unchanged vasoconstriction in low flow POTS which was sustained at initially elevated supine levels.

Of interest is that analogous findings were found in normal flow POTS patients during the Valsalva maneuver in which splanchnic pooling was related closely to blunting of the splanchnic vasoconstrictor response.

These findings still hold. However, we currently subscribe to normal flow POTS + high flow POTS as collectively comprising neurogenic POTS in which regional denervation is key. Low flow POTS then corresponds to hyperadrenergic POTS, in which the amounts or effects of norepinephrine, both at the sinus node and in the peripheral circulation (kidney? adrenal?) are amplified.We have rarely found increased supine sympathetic activation.

 

 

The figure depicts changes in mean arterial pressure (top panel) and heart rate (bottom panel) during incremental upright tilt. Mean arterial pressure was increased in low flow POTS at 20o and 35o upright tilt. Heart rate was significantly increased at 35o and 70o upright tilt.

 

 

The figure shows percent changes in thoracic, splanchnic, pelvic, and leg blood volumes during incremental upright tilt averaged over subject groups. Splanchnic changes dominate normal flow POTS. Low flow POTS patients have widespread blood collection. High flow POTS have blood pooling in the lower body.

 

 

The figure shows percent changes in segmental blood flow. From top down changes in thoracic, splanchnic, pelvic and leg (calf) are shown in order. Blood flow decreases for control in all segments. Blood flow does not change in the splanchnic segment for normal flow POTS while leg blood flow is markedly reduced. Blood flow does not change in the peripheral circulation (pelvic and leg) for high flow POTS. There is uniformly blunted blood flow changes in low flow POTS.

 

 

 

 

 


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