Fludrocortisone and sleeping in the head-up position limit the postural decrease in cardiac output in autonomic failure

Treatment with head-up tilt sleeping and low-dose fludrocortisone effective ly minimizes orthostatic symptoms and increases orthostatic blood pressure in patients with neurogenic orthostatic hypotension. The aim of the present study was to examine whether the improvement in orthostatic blood pressure during combined treatment with low-dose fludrocortisone and nocturnal head -up tilt in patients with neurogenic orthostatic hypotension can be attribu ted to expansion of plasma volume or to increased total peripheral resistan ce. The effects of a 3-week treatment with fludrocortisone and nocturnal head-u p tilting on the postural changes in arterial pressure, heart rate, and car diac output (pulse contour) were evaluated in eight consecutive patients wi th orthostatic hypotension. The period during which the patients were able to remain in the standing po sition without orthostatic complaints increased minimally from 3 to 10 minu tes. The decrease in arterial pressure after 1 minute of standing-(means wi th standard deviations in parentheses) systolic, 49 (20) mm Hg; diastolic, 18 (11) mm Hg-before treatment was produced by a greater than normal decrea se in cardiac output: 37% (10%) in patients with neurogenic orthostatic hyp otension versus -14% (8%) in control subjects, Treatment increased upright arterial pressure from 83 (19) mm Hg systolic and 55 (13) mm Hg diastolic t o 114 (22) mm Hg systolic and 60 (16) mm Hg diastolic by limiting the decre ase in cardiac output. Body weight increased but hematocrit did not change. Leg pressure-volume relationship decreased in the two patients studied. Th e responses of plasma renin activity and aldosterone to orthostatic stress prior to treatment were subnormal and became even lower after treatment. The improvement in upright blood pressure in orthostatic hypotension during treatment with fludrocortisone and nocturnal head-up sleeping is the resul t of a reduction in the orthostatic decrease in cardiac output. Preliminary data suggest that the expanded body fluid volume is allocated to the periv ascular space rather than to the intravascular space.