Pathophysiological basis of orthostatic hypotension in autonomic failure

Abstract

In patients with autonomic failure orthostatic hypotension results from an impaired capacity to increase vascular resistance during standing. This fundamental defect leads to increased downward pooling of venous blood and a consequent reduction in stroke volume and cardiac output that exaggerates the orthostatic fall in blood pressure. The location of excessive venous blood pooling has not been established so far, but present data suggest that the abdominal compartment and perhaps leg skin vasculature are the most likely candidates. To improve the orthostatic tolerance in patients with autonomic failure, protective measures that reduce excessive orthostatic blood pooling have been developed and evaluated. These measures include physical counter-manoeuvres and abdominal compression.

Figure 1. The efficacy of sitting, crossing legs, muscle pumping and squatting to improve orthostatic hypotension in patients with autonomic failure

Mean finger arterial blood pressures (Finapres) are expressed as the blood pressure change in the second 30 s of response from the pre-manoeuvre standing blood pressure. For muscle pumping the second 15 s of response from the pre-manoeuvre standing blood pressure. From left to right: sitting on a Derby chair (height 48 cm), a fishing stool (height 38 cm), and a foot stool (height 20 cm), without (^) and with (•) crossed legs; standing in crossed-legs position (CL) without (▴) and with (♦) contraction of lower extremity musculature; standing while muscle pumping (MP), marching on the spot (▿) and toe raising (▾); and squatting (□). The vertical lines represent means and s.d. (Adapted from Smit et al. 1997 with unpublished observations (A. A. J. Smit & W. Wieling) on muscle pumping.)