Electrically induced and voluntary activation of physiologic muscle pump: a comparison between spinal cord-injured and able-bodied individuals

Abstract

FES-induced activation of the physiologic muscle pump during change in position from sitting to standing prevented orthostatic hypotension in spinal cord-injured subjects. During standing it had equal or even greater effect on improving blood circulation when compared with voluntary activation in able-bodied subjects. The use of FES during standing and tilting in spinal cord-injured individuals may prevent orthostatic hypotension and circulatory hypokinesis and improve tolerance to tilting and standing.

Orthostatic hypotension following spinal cord injury: understanding clinical pathophysiology

“…Electrically stimulated leg muscle contractions increased peripheral resistance, heart rate and cardiac output, and blunted the fall in stroke volume that normally occurs during orthostasis. [49][50][51] However, perhaps most importantly, these induced contractions prevented or reduced the orthostatic hypotension normally seen in these SCI patients. Thus, it seems possible that the orthostatic hypotension associated with SCI is due, in part, to the failure to activate skeletal muscle pumps in paralysed dependant limbs during postural challenge.…”

“…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.…”

“…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.…”

“…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. Electrically stimulated leg muscle contractions increased peripheral resistance, heart rate and cardiac output, and blunted the fall in stroke volume that normally occurs during orthostasis.…”

“…25,74 Hyponatremia is also reported in acute SCI. 75 Thus, hyponatremia, probably secondary to supraphysiological ADH activity in SCI, 51 is common among acute and chronic SCI patients. 25,75,76 The combination of increased ADH secretion, low sodium intake, high sodium excretion and the resulting hyponatremia are likely to predispose towards small plasma volumes in SCI patients, and this, in turn, would exacerbate episodes of orthostatic hypotension in these individuals.…”