A Review Of Postural Orthostatic Tachycardia Syndrome

[Lemons2lemonade]

A review of postural orthostatic

tachycardia syndrome

Sheila Carew, Margaret O. Connor, John Cooke, Richard Conway, Christine Sheehy,

Aine Costelloe, and Declan Lyons*

Blood Pressure Unit, Mid Western Regional Hospital, Limerick, Ireland

Received 4 July 2008; accepted 4 November 2008

Introduction

Postural orthostatic tachycardia syndrome (POTS) is defined as a

sustained heart rate increase of 30 bpm or increase of heart

rate to 120 bpm within the first 10 min of orthostasis associated

with symptoms of orthostatic intolerance1–3 and without significant

orthostatic hypotension (OH).

Patients with POTS are predominately female (4:1) and relatively

young,4,5 but can range in age from 15 to 50 years.6 Differences in

muscle sympathetic nerve discharge characteristics, in the setting

of sympathetic fibre loss associated with POTS, may contribute

to the predisposition to and greater prevalence of POTS in

female individuals.7

There are no accurate epidemiological studies, but it is estimated

that in the USA alone, there are millions of people affected

by POTS.8

Pathophysiology

Normal physiology of standing

When supine, up to 30% of the blood volume is in the thorax.

During orthostasis, 300–800 mL of blood is gravitated downwards

from the thorax into the abdomen and lower extremities. Most of

this pooling into lower limb veins occurs within 10 s. This causes a

decrease in venous return to the right side of the heart with

a subsequent reduction in the stroke volume and cardiac output.

Arterial baroreceptors (carotid sinuses and the aortic arch) and

cardiopulmonary mechanoreceptors (heart and lung) detect a

reduction in pulse pressure and stroke volume. Compensatory

reflexes lead to increased sympathetic nervous system output

(peripheral arteriolar vasoconstriction) and reduced parasympathetic

nervous system output (reduced vagal tone to the heart

with cardio-acceleration). After orthostasis in normal subjects,

there is a 10–15 bpm increase in heart rate, systolic blood

pressure remains stable, and diastolic blood pressure usually

increases (10 mmHg).9

Postural orthostatic tachycardia

syndrome

Postural orthostatic tachycardia syndrome is a clinical manifestation

of multiple underlying mechanisms. It can be divided into a

number of overlapping pathophysiological models as follows.

Neuropathic

This is thought to be associated with partial dysautonomia. The

evidence in support of this is as follows:

† Distal anhidrosis of the legs is commonly found on thermoregulatory

sweat testing and quantitative sudomotor axon reflex

testing (up to 50% of POTS patients).4,10

† Ganglionic acetylcholine receptor antibody is positive in

between 10 and 15% of the cases.4,11

† There is a blunted increase in post-ganglionic sympathetic nerve

discharge (muscle sympathetic nerve activity).12 This peripheral

abnormality might reflect partial dysautonomia. Astronauts

returning from prolonged exposure to microgravity often

display a form of orthostatic intolerance with features similar

to POTS.13 This is felt to be due to abnormal muscle sympathetic

nerve activity.14

† It is shown that leg arteriolar vasoconstriction is impaired.

Therefore, increased arterial inflow can enhance venous filling

and cause venous pooling, despite the fact that venous capacitance

is normal.

[Chaos]

Lemons..would it be possible to perhaps post the link to this? For some reason I can't view it. It's coming thru in programming language.

[Mytwogirlsrox]

Interesting that POTs is defined as a sustained increased HR of 30 bpm or greater that 120 bpm. Seems like isn't always the diagnostic criteria. Some studies just say an increase of 30bpm or greater than 120.... Interesting