Patients with autonomic failure may be seriously incapacitated in activities of daily living due to orthostatic hypotension. Their low blood pressure is ascribed to a defective increase in arterial resistance and an excessive venous pooling upon standing. Effective pharmacological treatment is now available, but may aggravate supine hypertension and have other undesirable effects. Additionally, pharmacological treatment is less successful for hypotension with physical exercise or in warm surroundings (Bannister & Mathias, 1992). Non-pharmacological measures are regarded as a cornerstone in the treatment of orthostatic hypotension. These measures consist of chronic expansion of the extracellular volume or reducing the vascular volume in which pooling occurs (Bannister & Mathias, 1992). The latter includes protective measures like physical countermanoeuvres which can be applied by those patients with no major additional neurological and musculo-skeletal disorders, and external support garments which can be recommended to all patients. We reasoned that selection and use of appropriate protective measures would be facilitated by understanding the fundamental physiological mechanisms that prevent excessive orthostatic pooling in healthy subjects, why these mechanisms fail in patients with autonomic failure, and how these protective measures work. Therefore we reviewed the literature and summarized the available data about the amount and location of venous pooling in patients with autonomic failure and the effectiveness of physical countermanoeuvres and external support garments.

The aim of this study was to investigate in patients with neurogenic orthostatic hypotension the mechanism and usefulness of abdominal compression to increase standing blood pressure. In three protocols, 23 patients underwent abdominal compression. Protocol 1 evaluated in a 40-60 degrees head-up-tilt position, the effect of abdominal compression on caval vein and femoral diameter, arterial blood pressure and hemodynamics. Protocol 2 documented the relationship between the level of compression and the arterial pressure response. Protocol 3 investigated the ability to maintain standing blood pressure by an elastic binder. During head-up-tilt, compression (40 mm Hg) resulted in a reduction in diameter of the caval vein (mean -2.6mm, range -1.4 to 0.6), without a change in femoral vein diameter. Stroke volume increased by 14 % (range -1 to 23) and blood pressure (systolic/diastolic) by 30/14 mmHg (range 7/2 to 69/36), both p< 0.05; 40 mmHg compression was associated with a higher pressure response than 20 mmHg (mean 18/8 mmHg, range 6/2 to 43/20 vs. mean 9/4 mmHg, range -1/0 to 18/8, p < 0.05). Elastic abdominal binding increased standing blood pressure with 15/6 mmHg (range -3/3 to 36/14, p < 0.05). We conclude that in patients with neurogenic orthostatic hypotension, abdominal compression increases standing blood pressure to a varying degree by increasing stroke volume.

The occurrence of vasovagal fainting is common in young subjects, but the origin of the precipitating hemodynamic mechanisms involved remain a subject of considerable speculation. Vasovagal fainting is not a sudden onset phenomenon, early failure of vascular resistance responses occurs in faint-prone young subjects. The variability of hemodynamic responses during the actual faint is large, but the main mechanism operative during, is withdrawal of sympathetic outflow to blood vessels in skeletal muscle with impairment of ability to maintain vasomotor tone.

The effect of sitting on a derby chair (height, 48 cm), fishing chair (38 cm), and footstool (20 cm) on the improvement of postural hypotension was studied serially in 8 patients with autonomic failure. The increment in blood pressure during sitting was higher by using a lower portable chair. This was related to an increasing cardiac output at lower sitting heights. The fishing chair was, according to our patients' experience, most useful.