ramakentesh
Senior Member
- Messages
- 534
Ofcourse I am working with a doctor. I would struggle to prescribe myself midodrine 
. You realise that there isnt a clear understanding of the etiology of POTS in any cases therefore the treatment options work sporadically, are rarely supported with little more a conjectural basis and are 'more guesswork than science'? (this statement coming from a leading researcher in orthostatic circulatory control.
You realise that 'experts on treating OI' base most of their experience on clinical results rather than research? And that in pots two similar patient presentations can have paradoxical results from treatments?
The aim of the exercise is to find a medicine or combination that works before for me which i am doing. My observations were purely about midodrine.
POTS and NMH have very different mechanisms. In NMH there is a reduction in vasoconstrictive responses to standing, a reduction in sympathetic outflow or perhaps an excessive parasympathetic response to standing. In POTS there is either increased peripheral blood flow exaccerbated by postural challenge and redistributive thoratic hypovolumia, increased splanchnic (stomach/pelvis) blood pooling and again redistributive thoratic hypovolumia or there are low flow states characterised by increased peripheral resistance, reduced vasomotor or NO mediated flow dilation, sympathoexcitation and chronic reductions in absolute blood volume.
If you have orthostatic hypotension and tachycardia you do not have POTS you have NMH or NCS. POTS is characterised by an increase in orthostatic heart rate without a measurable reduction in blood pressure. There is however redistributed changes, flow abnormalities, sympathetic excess and changes in cerebral autoregulation that occur mimicing the effects of postural hypotension.
. You realise that there isnt a clear understanding of the etiology of POTS in any cases therefore the treatment options work sporadically, are rarely supported with little more a conjectural basis and are 'more guesswork than science'? (this statement coming from a leading researcher in orthostatic circulatory control.You realise that 'experts on treating OI' base most of their experience on clinical results rather than research? And that in pots two similar patient presentations can have paradoxical results from treatments?
The aim of the exercise is to find a medicine or combination that works before for me which i am doing.
My observations were purely about midodrine. POTS and NMH have very different mechanisms. In NMH there is a reduction in vasoconstrictive responses to standing, a reduction in sympathetic outflow or perhaps an excessive parasympathetic response to standing. In POTS there is either increased peripheral blood flow exaccerbated by postural challenge and redistributive thoratic hypovolumia, increased splanchnic (stomach/pelvis) blood pooling and again redistributive thoratic hypovolumia or there are low flow states characterised by increased peripheral resistance, reduced vasomotor or NO mediated flow dilation, sympathoexcitation and chronic reductions in absolute blood volume.
If you have orthostatic hypotension and tachycardia you do not have POTS you have NMH or NCS. POTS is characterised by an increase in orthostatic heart rate without a measurable reduction in blood pressure. There is however redistributed changes, flow abnormalities, sympathetic excess and changes in cerebral autoregulation that occur mimicing the effects of postural hypotension.
