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Review
. 2020 Feb;26(1):154-177.
doi: 10.1212/CON.0000000000000816.

Management of Orthostatic Hypotension

Review

Management of Orthostatic Hypotension

Jose-Alberto Palma et al. Continuum (Minneap Minn). 2020 Feb.

Abstract

Purpose of review: This article reviews the management of orthostatic hypotension with emphasis on neurogenic orthostatic hypotension.

Recent findings: Establishing whether the cause of orthostatic hypotension is a pathologic lesion in sympathetic neurons (ie, neurogenic orthostatic hypotension) or secondary to other medical causes (ie, non-neurogenic orthostatic hypotension) can be achieved by measuring blood pressure and heart rate at the bedside. Whereas fludrocortisone has been extensively used as first-line treatment in the past, it is associated with adverse events including renal and cardiac failure and increased risk of all-cause hospitalization. Distinguishing whether neurogenic orthostatic hypotension is caused by central or peripheral dysfunction has therapeutic implications. Patients with peripheral sympathetic denervation respond better to norepinephrine agonists/precursors such as droxidopa, whereas patients with central autonomic dysfunction respond better to norepinephrine reuptake inhibitors.

Summary: Management of orthostatic hypotension is aimed at improving quality of life and reducing symptoms rather than at normalizing blood pressure. Nonpharmacologic measures are the key to success. Pharmacologic options include volume expansion with fludrocortisone and sympathetic enhancement with midodrine, droxidopa, and norepinephrine reuptake inhibitors. Neurogenic supine hypertension complicates management of orthostatic hypotension and is primarily ameliorated by avoiding the supine position and sleeping with the head of the bed elevated.

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Figures

FIGURE 9-1
FIGURE 9-1
Blood pressure and cerebral blood flow in a patient with neurogenic orthostatic hypotension. The upper tracing shows blood flow velocity as measured by middle cerebral artery (MCA) transcranial Doppler ultrasound, which indicates cerebral blood flow. The lower tracing shows continuous blood pressure acquired with plethysmography. When the patient is in the supine position, both blood pressure (121/84 mm Hg) and mean velocity (Vm) of MCA blood flow (54 cm/s) are normal. When the patient stands up, blood pressure plummets rapidly to 66/54 mm Hg and cerebral blood flow falls by nearly 50% (Vm, 29 cm/s). The patient becomes symptomatic, feels lightheaded and about to faint, and is unable to remain standing. Patient sits down and his blood pressure increases to 93/62 mm Hg. Although this blood pressure is still low, the patient is not symptomatic anymore because the Vm increased to 44 cm/s, indicating almost normal cerebral blood flow. The blood pressure of a patient with symptomatic orthostatic hypotension does not have to return to normal values for the patient to become asymptomatic but only to increase above the lower limit of cerebral autoregulation. Vm = mean velocity.
FIGURE 9-2
FIGURE 9-2
Blood pressure and heart rate of the patient in CASE 9-1 supine and standing. The tracing shows severe orthostatic hypotension with a significant compensatory increase in heart rate, with a change in heart rate (ΔHR)/change in systolic blood pressure (ΔSBP) ratio above 0.5 beats per minute/mm Hg, indicative of non-neurogenic orthostatic hypotension.
FIGURE 9-3
FIGURE 9-3
Flowchart of the management of neurogenic orthostatic hypotension. Removal of aggravating factors and initiation of nonpharmacologic measures must always precede the use of pharmacologic agents. ΔHR = change in heart rate; ΔSBP = change in systolic blood pressure. a Supine.
FIGURE 9-4
FIGURE 9-4
Pressor effect of midodrine and droxidopa versus placebo. Midodrine (A) and droxidopa (B) have a similar short-acting pressor effect profile. Both medications have a fast pressor effect beginning approximately 1 hour after oral administration (green arrows). The pressor effect of midodrine remains for 4 to 5 hours, whereas the pressor effect of droxidopa is slightly longer at 5 to 6 hours. The peak standing systolic blood pressure occurs 1 hour after midodrine administration, whereas the peak standing mean blood pressure occurs 3.5 hours after droxidopa administration. Panel A modified with permission from Wright RA, et al, Neurology. © 1998 American Academy of Neurology. Panel B modified with permission from Kaufmann H, et al, Circulation. © 2003 American Heart Association, Inc.
FIGURE 9-5
FIGURE 9-5
Blood pressure and heart rate of the patient in CASE 9-2 supine and standing. The tracing shows severe orthostatic hypotension with no compensatory increase in heart rate, with a change in heart rate (ΔHR)/change in systolic blood pressure (ΔSBP) ratio below 0.5 beats per minute/mm Hg, indicative of neurogenic orthostatic hypotension.
FIGURE 9-6
FIGURE 9-6
Ambulatory 24-hour blood pressure monitor results of the patient in CASE 9-3. The orange horizontal dashed lines denote arbitrary limits for normal blood pressure (140/90 mm Hg during daytime, 120/70 mm Hg during nighttime). The red tracing denotes systolic and the blue tracing denotes diastolic blood pressure readings throughout one day. A significant drop in blood pressure is seen right after breakfast, lunch, and dinner (arrows), consistent with postprandial hypotension. The tracing also shows nocturnal hypertension while the patient was sleeping, except for an episode of hypotension when standing as the patient got up to urinate (nocturia). OH = orthostatic hypotension.

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