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Treating orthostatic hypotension

The concept of head-up tilt sleeping to manage orthostatic hypotension is based on the clinical observations by MacLean and Allen almost 70 years ago [1]. These clinical investigators observed that orthostatic hypotensionin patients with pure autonomic failure appeared to improve symptomatically and objectively during daytime and that this improvement had disappeared in the morning after sleeping in bed at night. The observation of diurnal changes in orthostatic tolerance led MacLean and Allen to the suggestion that patients with orthostatic hypotension should not sleep in a flat bed but should lie in a semi inclined or head-up position [1][2]. Definite symptomatic and objective reversible changes were documented.

The beneficial symptomatic and objective effects of postural treatment at night in patients with debilitating orthostatic hypotension due to autonomic failure were confirmed in several case series [3][4][5]. A consistent finding in these reports is that if a high salt diet or fludrocortisone were added to head-up sleeping the beneficial effects on orthostatic tolerance were enhanced.

An excessive fall in cardiac output underlie the impairment in tolerance to standing after a night’s sleep on a flat bed, systemic vascular resistance does not change [6]. Although nocturnal polyuria is a typical feature of patients with autonomic failure the degree of impairment in orthostatic tolerance after a night's sleep cannot be explained only by the nocturnal polyuria. Marked diurnal variation in orthostatic tolerance can also be found in patients with small diurnal differences in body weight. Transcapillary fluid shifts are thought to play an important role in these patients [6][7][8]. Despite this, treatment with the vasopressin analogue desmopressin has been found effective in reducing both nocturnal polyuria and the postural BP fall in the morning [9]. Adding to complexity, confinement to bed did not substantially alter the diurnal BP changes [10]. Thus various factors may play a role in the diurnal BP changes including orthostatic fluid shifts, transcapillary fluid shifts and neurohumoral rhythms causing changes in sodium and water excretion

Physiological mechanisms

The physiological mechanisms underlying the beneficial effects of head-up sleeping are a decrease in sodium and water excretion during the night resulting in a better maintained and plasma volume; an increase in body weight of 0.5- 1 kg is reported [2][4][5][6][11] (for review see [12]. The observation that head-up sleeping becomes effec¬tive coinci¬dental with appe¬arance of slight edema of the lower legs [1][2][11] suggests that head-up induced volume shifts with an increased content of the extracellular fluid volume in the lower extremities play an important mechanistic role. The lower leg edema is thought to result in diminished pooling of venous blood in the legs and thereby in decreasing the excessive fall in stroke volume and cardiac output during a stand-up in the early morning [1][2][11].

Application

MacLean and Allen accomplished the head-up position by placing the posts of the head of a bed on ordinary kitchen chairs (40-45 cm high) [1][2]. Ten Harkel used a head–up angle of 12 degrees (about 30 cm elevation of the head of the bed) [5]. Sleeping in a sitting position has been applied by Bannister et al. [4] Based on the presumed physiological mechanism discussed above, a steep head-up tilt sleeping position is likely to be the most effective. Gravitational stress is a function of the sine of the angle of tilt and not of the angle itself. Thus a tilt-angle of 5 degrees as used by Fan et al will induce 9% and a tilt-angle of 12 degrees 21% of the full 90 degree orthostatic load. However, a steep tilt-angle is difficult to tolerate by the majority of patients and their partners. We instruct our patients to put the head-end of their bed on 20-30 cm blocks. A hard pillow under the mattress at the level of the thighs has been found useful to prevent sliding down. A footboard is another helpful measure [5]. Head-up tilting also reduces supine hypertension in patients with autonomic failure and also causes an additional gravitationally-induced reduction in cerebral arterial pressure. A 20-25 cm elevation of the head of the bed lowers cerebral arterial pressure by about 15 mmHg [12].

References

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1. 5 MacLean AR, Allen EV. Orthostatic hypotension and orthostatic tachycardia: treatment with the “head-up” bed. JAMA. 1940;115:2162–2167.
2. 6 MacLean AR, Allen EV, Magath TB. Orthostatic tachycardia and orthostatic hypotension: defects in the return of venous blood to the heart. Am Heart J 1944;27: 145-163.
3. 7 Corcoran AC, Browning JS, Page IH. Renal hemodynamics in Orthostatic Hypotension: effects of Angiotonin and Head-up Bed. J Am Med Ass 1942:119:793-794.
4. 8 pmid=4311254
5. 9 pmid=1506810
6. 10 pmid=1961353
7. 11 pmid=11724647
8. 12 pmid=6470562
9. 13 pmid=3089519
10. 14 pmid=6872160
11. 15 pmid=10750642
12. 16 pmid=12357277