This article is about the uncommon condition of blood pressure increasing (HYPERtension) when standing up. For the more common condition of blood pressure decreasing (HYPOtension) when standing up, see
Orthostatic hypotension.
Orthostatic hypertension is a medical condition consisting of a sudden and abrupt increase in
blood pressure (BP) when a person stands up.[1] Orthostatic hypertension is diagnosed by a rise in
systolic BP of 20 mmHg or more when standing. Orthostatic diastolic hypertension is a condition in which the
diastolic BP raises to 98 mmHg or over in response to standing,[2][3][4] but this definition currently lacks clear medical consensus, so is subject to change. Orthostatic hypertension involving the systolic BP is known as systolic orthostatic hypertension.
When it affects an individual's to remain upright, orthostatic hypertension is considered as a form of
orthostatic intolerance. The body's inability to regulate blood pressure can be a type of
dysautonomia.
Baroreflex and autonomic pathways normally ensure that blood pressure is maintained despite various stimuli, including postural change. The precise mechanism of orthostatic hypertension remains unclear, but alpha-adrenergic activity may be the predominant pathophysiologic mechanism of orthostatic hypertension in elderly
hypertensive patients.[5] Other mechanisms are proposed for other groups with this disorder.[1]
A prevalence of 1.1% was found in a large population study.[6] The risk of orthostatic hypertension has been found to increase with age, with it being found in 16.3% of older hypertensive patients.[7]
Causes
The causes of this condition are not well understood, but research suggests that it may be caused by a combination of
hemodynamic and
neurohumoral factors.[8]
Some studies have found that orthostatic hypertension may be caused by increased
vascular resistance, possibly due to excess
plasma shifts or increased
blood viscosity. Other studies have suggested that it may be caused by a reduction in
cardiac preload, or an increase in venous pooling.[8]
Research suggests that it may be caused by an overshoot in neurohumoral adjustments to standing. Some studies have found that patients with orthostatic hypertension have normal levels of venous plasma
norepinephrine, but that these levels increase excessively upon standing.[9][10] However, other studies have not found elevated levels of norepinephrine in patients with orthostatic hypertension compared to hypertensive controls.[11] These findings suggest that the causes of orthostatic hypertension may be
multifactorial and more research is needed to fully understand the underlying mechanisms.[8]
Signs and symptoms
Mild or moderate orthostatic hypertension may present without any symptoms other than the orthostatic hypertension BP findings. More severe orthostatic hypertension may present with the typical symptoms of hypertension.
Orthostatic venous pooling is common with orthostatic diastolic hypertension. This occurs in the legs while standing.[12][13]
Renal arterial
stenosis (narrowing of the kidney arteries) with
nephroptosis (kidney drops on standing) have been known to cause orthostatic hypertension.[16]
Aortitis (inflammation of the aorta) with nephroptosis: "This orthostatic hypertension largely may be due to an activation of the renin system caused by nephroptosis and partly due to a reduced baroreflex sensitivity caused by aortitis"[17]
Currently, no treatments are officially recommended for orthostatic hypertension, as it is still little known and has various causes. Hence, treatment for those with this disorder is trial and error.
Some treatments which have been successfully used for this condition are medications
doxazosin,[22]carvedilol,[23]captopril, and
propranolol hydrochloride. Treatment of coexisting conditions, e.g.,
hypovolemia, also is used. Some specialists in severe cases give saline intravenously for hypovolemia, which, if it is the cause, brings the orthostatic hypertension down to a safe level. Pressure garments over the pelvis and the lower extremities may be used as part of treatment, due to the blood pooling issue occurring in many with the disorder.[12]
Epidemiology
The prevalence of this condition has been studied in various populations. In a study conducted in 1922, it was found that 4.2% of 2000 apparently healthy aviators aged 18 to 42 years had an increase in diastolic blood pressure from below 90 mmHg while in the supine position to above 90 mmHg in the upright posture.[24]
Study which defined orthostatic hypertension as a sustained increase in systolic blood pressure of at least 20 mmHg and/or diastolic blood pressure of at least 10 mmHg within 3 minutes of standing, have reported a prevalence rate of orthostatic hypertension ranging from 5% to 30%. This range is generally consistent with the prevalence of orthostatic hypotension.[8]
^
abFan XH, Sun K, Zhou XL, Zhang HM, Wu HY, Hui RT (January 2011). "[Association of orthostatic hypertension and hypotension with target organ damage in middle and old-aged hypertensive patients]". Zhonghua Yi Xue Za Zhi. 91 (4): 220–224.
PMID21418863.
^Streeten DH, Anderson GH, Richardson R, Thomas FD (March 1988). "Abnormal orthostatic changes in blood pressure and heart rate in subjects with intact sympathetic nervous function: evidence for excessive venous pooling". The Journal of Laboratory and Clinical Medicine. 111 (3): 326–335.
PMID3343547.
^Benowitz NL, Zevin S, Carlsen S, Wright J, Schambelan M, Cheitlin M (July 1996). "Orthostatic hypertension due to vascular adrenergic hypersensitivity". Hypertension. 28 (1): 42–46.
doi:
10.1161/01.hyp.28.1.42.
PMID8675262.
^Kostis, W.J., Sargsyan, D., Mekkaoui, C. et al. Association of orthostatic hypertension with mortality in the Systolic Hypertension in the Elderly Program. J Hum Hypertens 33, 735–740 (2019).
doi:
10.1038/s41371-019-0180-4