Orthostatic circulatory disorders are frequently the cause of orthostatic i
ntolerance, syncope or dangerous falls. A sufficient therapy should be base
d on a differential diagnosis by means of an active standing test or a tilt
-table test. Three typical pathological reactions of blood pressure and hea
rt rate can be differentiated. The hypoadrenergic orthostatic hypotension i
s characterised by an immediate drop in blood pressure (systolic drop > 20
mmHg below base line within 3 min) with or without compensatory tachycardia
. It is caused by peripheral or central sympathetic dysfunction. Tachycardi
a (> 30 beats per minute above base line within 10 min) without significant
blood pressure drop but with a fall of cerebral blood flow indicates a pos
tural tachycardia syndrome,ln general, there is no further somatic dysfunct
ion. Increased venous pooling is thought to be the assumed pathomechanism.
A reflex mechanism evokes the neurocardiogenic syncope after a certain time
of standing: sympathetic inhibition yields a strong blood pressure drop an
d vagal activation bradycardia. Proved therapies include use of the mineral
ocorticoide fludrocortison (hypoadrenergic orthostatic hypotension), of the
alpha-agonist midodrin (postural tachycardia syndrome) and of beta-blocker
s (neurocardiogenic syncope).