Circulatory hypokinesis and functional electric stimulation during standing in persons with spinal cord injury

Orthostatic hypotension following spinal cord injury: understanding clinical pathophysiology

“…One reason for this may be the fact that although resting supine sympathetic activity (and thus blood pressure) tends to be low after SCI, some studies do report an appropriate increase in peripheral resistance when upright in SCI individuals, despite presumed disruption of the sympathetic control. [49][50][51] It is likely that some other mechanism is responsible for the increased peripheral resistance following orthostasis in SCI individuals. This could be related to production of catecholamines by the adrenal medulla, 50 although recent evidence suggests that this is unlikely (see below), a large and rapid release of vasopressin upon postural change to levels sufficient to exert a pressor effect, 52 spinal reflexes and veno-arteriolar reflexes 6 or peripheral a-adrenoceptor hyper-responsiveness.…”

“…[49][50][51] It is likely that some other mechanism is responsible for the increased peripheral resistance following orthostasis in SCI individuals. This could be related to production of catecholamines by the adrenal medulla, 50 although recent evidence suggests that this is unlikely (see below), a large and rapid release of vasopressin upon postural change to levels sufficient to exert a pressor effect, 52 spinal reflexes and veno-arteriolar reflexes 6 or peripheral a-adrenoceptor hyper-responsiveness. 34 Although circulating supine resting catecholamine levels, particularly noradrenaline, are low in high SCI, there is a coincident hyper-responsiveness of a-adrenoceptors below the lesion site 34 such that if there were to be any increase in noradrenaline levels (eg via activation of the renin-aldosterone-angiotensin system), 6 the peripheral a-adrenoceptors would be likely to respond strongly.…”

“…Sympathetic nervous system dysfunction 6,28 Altered baroreceptor sensitivity 62,64 Lack of skeletal muscle pumps [49][50][51] Cardiovascular deconditioning 69 Altered salt and water balance 74 The level and severity of spinal cord injury, and the extent to which other systems are affected will play a significant role in the development of orthostatic hypotension of cervical SCI individuals in whom catecholamine levels failed to increase following head-upright tilting. 53,54 These data suggest that there is severe impairment of descending tonic cardiovascular control to the spinal autonomic circuits in individuals with cervical SCI, such that there is insufficient sympathetic outflow to release noradrenaline, and consequently impaired vascoconstriction.…”

“…67 SCI patients are lacking this skeletal muscle pumping effect, and this would predispose to circulatory hypokinesis by reducing venous return in the upright position and thus lowering stroke volume, cardiac output and blood pressure. 50 The lack of skeletal muscle contractions during postural challenge has been demonstrated to have a powerful effect upon orthostatic changes in blood pressure in a number of studies. [49][50][51] These investigators performed electrically stimulated leg muscle contractions in paraplegic and tetraplegic volunteers, simulating the skeletal muscle pumping effect normally present in able-bodied persons during standing.…”

Orthostatic hypotension in the first month following acute spinal cord injury

“…Individuals with SCI lack the continuous reciprocal activation of postural skeletal muscles that provides compression on veins and maintains venous return to the heart when in upright position. 25,26 Furthermore, Miller and co-investigators 27 suggested that the skeletal muscle pump is relatively ineffective at competing with the respiratory muscle pump with respect to femoral venous return. Not surprisingly, in our study, the individuals with cervical and high thoracic SCI showed the most severe and prolonged OH.…”