Orthostatic hypertension

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] 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.

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
Other namesPostural hypertension

If affecting an individual's ability to remain upright, orthostatic hypertension is viewed as a form of orthostatic intolerance. The body's inability to regulate BP 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.[4] Other mechanisms are proposed for other groups with this disorder.[1]

A prevalence of 1.1% was found in a large population study.[5] The risk of orthostatic hypertension has been found to increase with age, with it being found in 16.3% of older hypertensive patients.[6]

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.[7]

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.[7]

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.[8][9] However, other studies have not found elevated levels of norepinephrine in patients with orthostatic hypertension compared to hypertensive controls.[10] These findings suggest that the causes of orthostatic hypertension may be multifactorial and more research is needed to fully understand the underlying mechanisms.[7]

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.[11][12]

Connections to other disorders

Risks
  • Blood pressure variability is associated with progression of target organ damage and cardiovascular risk.[18]
  • Orthostatic hypertension was positively associated with peripheral arterial disease.[6]
  • Increased occurrence of silent cerebrovascular ischemia[1][4]
  • Systolic orthostatic hypertension increases stroke risk.[19]
  • Orthostatic hypertension was associated with increased all-cause mortality.[20]

Diagnosis

The condition can be assessed by a tilt table test.

Treatments

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,[21] carvedilol,[22] 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.[11]

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 supine to above 90 mmHg in the upright posture.[23]

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.[7]

See also

References
  1. Fessel J, Robertson D (August 2006). "Orthostatic hypertension: when pressor reflexes overcompensate". Nature Clinical Practice. Nephrology. 2 (8): 424–431. doi:10.1038/ncpneph0228. PMID 16932477. S2CID 20184856.
  2. Bell, David S. (May 2000). "Orthostatic Intolerance (OI) Test Results". Lyndonville News. 2 (3).
  3. Streeten, D.H.P. (1987). Orthostatic Disorders of the Circulation. New York: Plenum Medical. p. 116. ISBN 978-1-4684-8962-0.
  4. Kario K, Eguchi K, Hoshide S, Hoshide Y, Umeda Y, Mitsuhashi T, Shimada K (July 2002). "U-curve relationship between orthostatic blood pressure change and silent cerebrovascular disease in elderly hypertensives: orthostatic hypertension as a new cardiovascular risk factor". Journal of the American College of Cardiology. 40 (1): 133–141. doi:10.1016/S0735-1097(02)01923-X. PMID 12103267.
  5. Wu JS, Yang YC, Lu FH, Wu CH, Chang CJ (May 2008). "Population-based study on the prevalence and correlates of orthostatic hypotension/hypertension and orthostatic dizziness". Hypertension Research. 31 (5): 897–904. doi:10.1291/hypres.31.897. PMID 18712045.
  6. Fan 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. PMID 21418863.
  7. Jordan, Jens; Ricci, Fabrizio; Hoffmann, Fabian; Hamrefors, Viktor; Fedorowski, Artur (May 2020). "Orthostatic Hypertension: Critical Appraisal of an Overlooked Condition". Hypertension. 75 (5): 1151–1158. doi:10.1161/HYPERTENSIONAHA.120.14340. ISSN 0194-911X. PMID 32223382.
  8. Streeten, D H; Auchincloss, J H; Anderson, G H; Richardson, R L; Thomas, F D; Miller, J W (March 1985). "Orthostatic hypertension. Pathogenetic studies". Hypertension. 7 (2): 196–203. doi:10.1161/01.HYP.7.2.196. ISSN 0194-911X. PMID 3980066.
  9. Kario, Kazuomi; Eguchi, Kazuo; Hoshide, Satoshi; Hoshide, Yoko; Umeda, Yuji; Mitsuhashi, Takeshi; Shimada, Kazuyuki (2002-07-03). "U-curve relationship between orthostatic blood pressure change and silent cerebrovascular disease in elderly hypertensives: orthostatic hypertension as a new cardiovascular risk factor". Journal of the American College of Cardiology. 40 (1): 133–141. doi:10.1016/s0735-1097(02)01923-x. ISSN 0735-1097. PMID 12103267.
  10. Vriz, O.; Soon, G.; Lu, H.; Weder, A. B.; Canali, C.; Palatini, P. (May 1997). "Does orthostatic testing have any role in the evaluation of the young subject with mild hypertension?: an insight from the HARVEST study". American Journal of Hypertension. 10 (5 Pt 1): 546–551. doi:10.1016/s0895-7061(96)00489-x. ISSN 0895-7061. PMID 9160766.
  11. Streeten DH, Auchincloss JH, Anderson GH, Richardson RL, Thomas FD, Miller JW (1985). "Orthostatic hypertension. Pathogenetic studies". Hypertension. 7 (2): 196–203. doi:10.1161/01.hyp.7.2.196. PMID 3980066.
  12. 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. PMID 3343547.
  13. 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. PMID 8675262.
  14. Jenkins ZM, Eikelis N, Phillipou A, Castle DJ, Wilding HE, Lambert EA (2021). "Autonomic Nervous System Function in Anorexia Nervosa: A Systematic Review". Frontiers in Neuroscience. 15: 682208. doi:10.3389/fnins.2021.682208. PMC 8273292. PMID 34262430.
  15. Tsukamoto Y, Komuro Y, Akutsu F, Fujii K, Marumo F, Kusano S, Kikawada R (December 1988). "Orthostatic hypertension due to coexistence of renal fibromuscular dysplasia and nephroptosis". Japanese Circulation Journal. 52 (12): 1408–1414. doi:10.1253/jcj.52.1408. PMID 2977192.
  16. Takada Y, Shimizu H, Kazatani Y, Azechi H, Hiwada K, Kokubu T (January 1984). "Orthostatic hypertension with nephroptosis and aortitis disease". Archives of Internal Medicine. 144 (1): 152–154. doi:10.1001/archinte.144.1.152. PMID 6362595.
  17. Miranda CL, Henderson MC, Wang JL, Nakaue HS, Buhler DR (October 1986). "Induction of acute renal porphyria in Japanese quail by Aroclor 1254". Biochemical Pharmacology. 35 (20): 3637–3639. doi:10.1016/0006-2952(86)90637-4. PMID 3094542.
  18. Kario K (June 2009). "Orthostatic hypertension: a measure of blood pressure variation for predicting cardiovascular risk". Circulation Journal. 73 (6): 1002–1007. doi:10.1253/circj.cj-09-0286. PMID 19430163.
  19. Yatsuya H, Folsom AR, Alonso A, Gottesman RF, Rose KM (February 2011). "Postural changes in blood pressure and incidence of ischemic stroke subtypes: the ARIC study". Hypertension. 57 (2): 167–173. doi:10.1161/HYPERTENSIONAHA.110.161844. PMC 3214760. PMID 21199999.
  20. 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
  21. Hoshide S, Parati G, Matsui Y, Shibazaki S, Eguchi K, Kario K (January 2012). "Orthostatic hypertension: home blood pressure monitoring for detection and assessment of treatment with doxazosin". Hypertension Research. 35 (1): 100–106. doi:10.1038/hr.2011.156. PMID 21918522.
  22. Moriguchi A, Nakagami H, Kotani N, Higaki J, Ogihara T (March 2000). "Contribution of cardiovascular hypersensitivity to orthostatic hypertension and the extreme dipper phenomenon". Hypertension Research. 23 (2): 119–123. doi:10.1291/hypres.23.119. PMID 10770258.
  23. Schneider, Edward C.; Truesdell, Dorothy (1922-08-01). "A statistical study of the pulse rate and the arterial blood pressures in recumbency, standing, and after a standard exercise". American Journal of Physiology. Legacy Content. 61 (3): 429–474. doi:10.1152/ajplegacy.1922.61.3.429. ISSN 0002-9513.

Further reading
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