Findings in POTS

Home ] Up ][Circulatory Findings in POTS]


  • Circulatory Variants in POTS (this page)

  • Systematic Investigations

  1. Skeletal Muscle Pump

  2. Leg Venous Capacitance

  3. Local Factors in POTS

  4. Evidence for POTS as Thoracic Hypovolemia

  5. Peripheral Vasodilation and Microvascular Filtration in High Flow POTS

  6. Splanchnic Pooling in Normal Flow POTS

  7. Postural Hyperpnea in Normal Flow POTS

  8. Diminished Upright Cerebral Autoregulation and Cerebral Blood Flow

  9. A Relation to Angiotensin-II in Low Flow POTS

a. Blockade of AT1R by losartan reverses reduced bioavailability of nitric oxide in low flow

b. ACE-II is Deficient causing Ang-II Excess and reduced vasodilator Ang-(1-7) in Low Flow POTS

  1. Microcirculatory Dysfunction of Nitric Oxide (NO) in Low Flow POTS

  2. But, Neuronal Nitric Oxide is Specifically Decreased in Low Flow POTS

  3. Origins of Exercise Intolerance in POTS

  4. Postural neurocognitive and neuronal activated cerebral blood flow deficits in young chronic fatigue syndrome patients with postural tachycardia syndrome

  5. Return to Home Page






Circulatory Variants in POTS - Original Classification Scheme by Lower Extremity Blood Flow 

The pathophysiology of chronic orthostatic intolerance comprises abnormalities in compensatory mechanisms that excessively restrict venous return to the heart during upright stance. As a result, reflex tachycardia is invariably present during upright posture and chronic orthostatic intolerance is often denoted postural tachycardia syndrome (POTS). POTS is usually defined by symptoms of orthostatic intolerance (e.g. lightheadedness, headache) associated with an excessive increase in heart rate early during orthostatic stress; typically in adults this is defined by an increase of >30 beats per minute. The presence of POTS does not indicate a specific cause for such orthostatic intolerance but rather signifies a common final pathway producing thoracic hypovolemia.

We therefore expect and observe pathophysiologic heterogeneity in POTS.  Our initial studies of POTS focused on peripheral venous pressure (Pv) and found that there were [at least] two separate populations of patients present, which at that time we distinguished on the basis of supine leg venous pressure: a group of POTS patients with high Pv (exceeding control limits of 20mmHg) and a group with normal Pv.

 However, later when we examined supine peripheral blood flow in POTS patients prospectively grouped by calf Pv, as shown in figure 1 (a synthesis of data from previous papers), we found that the high Pv data were unimodal with decreased calf peripheral blood flow and increased peripheral resistance, but the normal Pv data were bimodal with increased supine calf blood flow and decreased supine arterial resistance in some patients, and normal supine calf blood flow and normal supine arterial resistance in others. This suggests that there are [at least] two subgroups within the normal Pv group: a group of patients with increased blood flow and a group of patients with unchanged blood flow compared to control. 
We currently think that peripheral blood flow and arterial resistance furnish useful and physiologically important markers to classify POTS. We therefore subscribe to 3 groups of POTS patients distinguished by peripheral blood flow and peripheral arterial resistance.

They are:

  1. A high blood flow, low arterial resistance group with normal to decreased Pv, now denoted “high flow POTS”. 
  2. A low blood flow, high arterial resistance, high Pv group now denoted “low flow POTS”. 
  3. A normal blood flow, normal arterial resistance group with normal Pv, currently denoted “normal flow POTS”. 


More specifically linked pages show that:

1)      High Flow CFS/POTS is characterized by normovolemia, peripheral vasodilation, and increased peripheral blood flow, cardiac output and microvascular filtration. Evidence indicates a mechanism of defective adrenergic-mediated vasoconstriction associated with post-viral peripheral neuropathy. Therefore, investigations of high flow POTS will not be pursued further in the current proposal.

2)      Normal Flow CFS/POTS is characterized by normovolemia and normal supine heart rate, peripheral resistance and blood flow. Upright, splanchnic vascular regulation is abnormal producing venous pooling, intense peripheral vasoconstriction and acrocyanosis. Patients are often hyperflexible and may fulfill criteria for the Ehlers-Danlos Syndrome.

3)      Low Flow CFS/POTS is characterized by mild hypovolemia and general decreased regional blood flows related to defects in local blood flow regulation, most notable in the dependent parts of the body and the cutaneous circulation. Peripheral vasoconstriction decreases when upright. The phenotype is distinguished by generalized pallor, cool skin, and often marked resting tachycardia.