Orthostatic hypotension, an acute or progressive decline in mean blood pressure of more than 10 to 15 mm Hg in the erect position, is common in SCI patients, particularly those with cervical injuries when they begin learning to sit and during physiotherapy mobilization (Illman, et al 2000).  Injury at T3 or above may eliminate normal neural cardiovascular responses to mild orthostatic stress (Munakata, et al 2001). The following information on orthostatic hypotension is based largely on an article by J. Blackmer. These articles are cited below.

Pathophysiology and Normalization of Orthostatic Hypotension in SCI

1. The disruption of the effect pathways, from the vasomotor center in the lower brainstem to the sympathetic nerves involved in vasoconstriction, caused by the spinal cord injury, results in the failure of short term blood pressure regulation in SCI

2. The lower resting level of catecholamines, the lack of a significent increase in the release of either epinephrine or norepinephrine when assuming an upright position, and the greater than normal resting skin flow in tetraplegics also contribute to orthostatic hypotension in SCI patients

3. With time and training on a tilt table, the SCI patient being able to adapt to the disruption caused by the injury may be due to:
   • The development of spinal reflex control and/or
   • An increase in vasoconstricting hormones, such as plasma renin and aldosterone which are higher then normal in SCI patients
   • An increased sensitivity to these hormones
   • Normal arginine vasopressin (AVP) release
   • The development of spasticity which causes an increase in central venous volume
     

Treatment

1. Initial strategies to treat orthostatic hypotension in SCI patients include:
   • A progressive increase in the sitting angle with a tilt table, or a tilt-in-space/reclining wheelchair
   • Anti-embolic stockings to increase venous return and abdominal binders
   • Natural recovery per 3. above

2. Pharmacological agents to increase vasoconstriction and peripheral resistance, the effective blood circulating volume, or fluid retention, have been used largely to treat orthostatic hypotension in non-SCI patients, and include:
   • Pseudoephedrine, which has been used in SCI patients:
     • Causes vasoconstriction and an increase in peripheral resistance
     • May cause side effects, such as headaches, dizziness, dry mouth, nausea, and vomiting
     • Should be used in patients with hypertension, diabetes, coronary artery disease, and/or congestive heart failure
     • Have been shown to be somewhat ineffective in some studies

   • Fludrocortisone, which causes blood volume in non-SCI patients and should reduce pressure drop in SCI patients, but which may cuase side effects, such as hypokalemia, fluid retention, and supine hypertension, usually at higher doses only

   • Ergotamine, which:
     • Increase peripheral arteriolar vasoconstriction and does not decrease verebral hemispheric blood flow
     • My control orthostatic hypotension by decreasing venous pooling in an uprightposition, thereby increasing effective peripheral circulatory volume
     • Should be administered at the minimum dose to control orthostatic symptoms, since it may cause severe supine hypertension and aggravate coronary or limb ischemia
     • May be more effective when combined with flurocortisone, as ergotamine or as dihydroergotamine; combination therapy has been used in SCI patients

   • Metoclopramide and Domperidone, dopamine agonists, which may directly antagonize dopamine-induced vasodilation or indirectly block presynaptic inhibition of norepinephrine release, and which may cause extrapyramidal side effects (metaclopramide) and arrythmia and peripheral edema (domperidone)

   • Clonidine, which has an agonist effect that may lead to a paradoxical pressure effect and may cause sedation and dry mouth

   • Midodrine, which has been used in SCI patients:
     • Is a vasoactive agent that can increase standing systolic blood pressure by as much as 22 mm Hg and improve the dizziness, weakness, syncope, low energy level, inablilty to stand, and depression that may accompany orthostatic hypotension in SCI patients
     • May cause scalp pruritus or tingling, supine hypertension, and feelings of urinary urgency

3. Functional electrical stimulation causes a dose-dependent increase in blood pressure independent of stimulation site that may be useful in treating OH (Sampson, et al 2000).
   
   
4. Nitric oxide synthase (NOS) - Blood pressure dysregulation in persons with tetraplegia may reflect increased vascular nitric oxide and suggests a novel treatment of hypotension using NOS inhibition in this population (Wecht, et al 2007).

References

Blackmer J.  Orthostatic hypotension in spinal cord injured patients.  Journal of Spinal Cord Medicine 1997 20(2):212-217 Apr.

Illman A, Stiller K and Williams M. The prevalence of orthostatic hypotension during physiotherapy treatment in patients with an acute spinal cord injury. Spinal Cord 2000 38(12):741-7 Dec.

Munakata M, Kameyama J, Nunokawa T, Ito N and Yoshinaga K. Altered Mayer wave and baroreflex profiles in high spinal cord injury. American Journal of Hypertension 2001 14(2):141-8 Feb.

Sampson EE, Burnham RS and Andrews BJ. Functional electrical stimulation effect on orthostatic hypotension after spinal cord injury. Archives of Physical Medicine & Rehabilitation 2000 81(2):139-43 Feb.

Wecht JM, Weir JP, Krothe AH, Spungen AM and Bauman WA. Normalization of supine blood pressure after nitric oxide synthase inhibition in persons with tetraplegia. [see comment]. Journal of Spinal Cord Medicine 2007 30(1):5-9.