Orthostatic hypertension

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Orthostatic hypertension
Other namesPostural 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.

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]

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.[7][8]

Connections to other disorders[]

  • Essential hypertension
  • Other kinds of dysautonomia may coexist, e.g., postural orthostatic tachycardia syndrome (POTS) is common with this condition, orthostatic hypotension with the BP going both high and low at times due to autonomic dysfunction
  • Type 2 diabetes[1]
  • Vascular adrenergic hypersensitivity: Orthostatic hypertension can be secondary to this[9]
  • Anorexia Nervosa: Many people suffering From anorexia experience orthostatic hypertension[citation needed]
  • Hypovolemia can cause orthostatic hypertension
  • Renal arterial stenosis (narrowing of the kidney arteries) with nephroptosis (kidney drops on standing) have been known to cause orthostatic hypertension.[10]
  • 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"[11]
  • Pheochromocytoma[12]

Risks[]

  • Blood pressure variability is associated with progression of target organ damage and cardiovascular risk.[13]
  • Orthostatic hypertension was positively associated with peripheral arterial disease.[6]
  • Increased occurrence of silent cerebrovascular ischemia[1][4]
  • Systolic orthostatic hypertension increases stroke risk.[14]

Diagnosis[]

The condition can be assessed by a tilt table test. If the test is positive, the diagnosis is hyperadrenergic POTS.[citation needed]

Treatments[]

Currently, no treatments are officially recommended for orthostatic hypertension, as it is still little known and can be due to different causes. Hence, treatment for those with this disorder is still a trial-and-error experimental treatment. Some treatments which have been successfully used for this condition are medications doxazosin,[15] carvedilol,[16] 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.[7]

References[]

  1. ^ Jump up to: a b c d Fessel, J.; Robertson, D. (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.
  4. ^ Jump up to: a b Kario, K.; Eguchi, K.; Hoshide, S.; Hoshide, Y.; Umeda, Y.; Mitsuhashi, T.; Shimada, K. (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, J. S.; Yang, Y. C.; Lu, F. H.; Wu, C. H.; Chang, C. J. (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. ^ Jump up to: a b Fan, X. H.; Sun, K.; Zhou, X. L.; Zhang, H. M.; Wu, H. Y.; Hui, R. T. (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. ^ Jump up to: a b Streeten, D. H.; Auchincloss Jr, J. H.; Anderson Jr, G. H.; Richardson, R. L.; Thomas, F. D.; Miller, J. W. (1985). "Orthostatic hypertension. Pathogenetic studies". Hypertension. 7 (2): 196–203. doi:10.1161/01.hyp.7.2.196. PMID 3980066.
  8. ^ Streeten, D. H.; Anderson Jr, G. H.; Richardson, R.; Thomas, F. D. (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.
  9. ^ Benowitz, N. L.; Zevin, S.; Carlsen, S.; Wright, J.; Schambelan, M.; Cheitlin, M. (1996). "Orthostatic hypertension due to vascular adrenergic hypersensitivity". Hypertension. 28 (1): 42–46. doi:10.1161/01.hyp.28.1.42. PMID 8675262.
  10. ^ Tsukamoto, Y.; Komuro, Y.; Akutsu, F.; Fujii, K.; Marumo, F.; Kusano, S.; Kikawada, R. (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.
  11. ^ Takada, Y.; Shimizu, H.; Kazatani, Y.; Azechi, H.; Hiwada, K.; Kokubu, T. (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.
  12. ^ Miranda CL, Henderson MC, Wang JL, Nakaue HS, Buhler DR (1986). "Induction of acute renal porphyria in Japanese quail by Aroclor 1254". Biochem. Pharmacol. 35 (20): 3637–9. doi:10.1016/0006-2952(86)90637-4. PMID 3094542.
  13. ^ Kario, K. (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.
  14. ^ Yatsuya, H.; Folsom, A. R.; Alonso, A.; Gottesman, R. F.; Rose, K. M.; Aric Study, I. (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.
  15. ^ Hoshide, S.; Parati, G.; Matsui, Y.; Shibazaki, S.; Eguchi, K.; Kario, K. (2011). "Orthostatic hypertension: Home blood pressure monitoring for detection and assessment of treatment with doxazosin". Hypertension Research. 35 (1): 100–6. doi:10.1038/hr.2011.156. PMID 21918522.
  16. ^ Moriguchi, A.; Nakagami, H.; Kotani, N.; Higaki, J.; Ogihara, T. (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.
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