Symptoms that are worse when sitting or standing and improve when lying down, including lightheadedness, vertigo, tinnitus, slurred speech, confusion, coathanger pain in neck and shoulders, grayed or blurred vision, severe fatigue, fainting or near fainting
Complications
Cumulative brain damage, sudden death from falls
Diagnostic method
In-office (lay down for at least 20 minutes, take BP; stand for 3 minutes, take BP), or tilt-table testing by an autonomic specialist
Treatment
Identify and treat causes (medications, dehydration), midodrine, compression garments, bed tilting
Prognosis
Depends on frequency, severity, and underlying cause; neurogenic orthostatic hypotension is a chronic, debilitating, and often progressively fatal condition[1]
Orthostatic hypotension, also known as postural hypotension,[2] is a medical condition wherein a person's blood pressure drops when standing up or sitting down. Primary orthostatic hypotension is also often referred to as neurogenic orthostatic hypotension.[3] The drop in blood pressure may be sudden (vasovagal orthostatic hypotension), within 3 minutes (classic orthostatic hypotension) or gradual (delayed orthostatic hypotension).[4] It is defined as a fall in systolic blood pressure of at least 20 mmHg or diastolic blood pressure of at least 10 mmHg after 3 minutes of standing. It occurs predominantly by delayed (or absent) constriction of the lower body blood vessels, which is normally required to maintain adequate blood pressure when changing the position to standing. As a result, blood pools in the blood vessels of the legs for a longer period, and less is returned to the heart, thereby leading to a reduced cardiac output and inadequate blood flow to the brain.
Very mild occasional orthostatic hypotension is common and can occur briefly in anyone, although it is prevalent in particular among the elderly and those with known low blood pressure. Severe drops in blood pressure can lead to fainting, with a possibility of injury. Moderate drops in blood pressure can cause confusion/inattention, delirium, and episodes of ataxia. Chronic orthostatic hypotension is associated with cerebral hypoperfusion that may accelerate the pathophysiology of dementia.[5] Whether it is a causative factor in dementia is unclear.[6]
The numerous possible causes for orthostatic hypotension include certain medications (e.g. alpha blockers), autonomic neuropathy, decreased blood volume, multiple system atrophy, and age-related blood-vessel stiffness.
Apart from addressing the underlying cause, orthostatic hypotension may be treated with a recommendation to increase salt and water intake (to increase the blood volume), wearing compression stockings, and sometimes medication (fludrocortisone, midodrine, or others). Salt loading (dramatic increases in salt intake) must be supervised by a doctor, as this can cause severe neurological problems if done too aggressively.
^Arnold AC, Raj SR (December 2017). "Orthostatic Hypotension: A Practical Approach to Investigation and Management". The Canadian Journal of Cardiology. 33 (12): 1725–1728. doi:10.1016/j.cjca.2017.05.007. PMC 5693784. PMID 28807522.
^"Orthostatic hypotension" at Dorland's Medical Dictionary
^Ricci F, De Caterina R, Fedorowski A (August 2015). "Orthostatic Hypotension: Epidemiology, Prognosis, and Treatment". Journal of the American College of Cardiology. 66 (7): 848–860. doi:10.1016/j.jacc.2015.06.1084. PMID 26271068.
^"Orthostatic Hypotension Information Page | National Institute of Neurological Disorders and Stroke". www.ninds.nih.gov. Retrieved 2017-03-26.
^Hase Y, Polvikoski TM, Firbank MJ, Craggs LJ, Hawthorne E, Platten C, et al. (January 2020). "Small vessel disease pathological changes in neurodegenerative and vascular dementias concomitant with autonomic dysfunction". Brain Pathology. 30 (1): 191–202. doi:10.1111/bpa.12769. PMC 8018165. PMID 31357238. S2CID 19310855.
^Sambati L, Calandra-Buonaura G, Poda R, Guaraldi P, Cortelli P (June 2014). "Orthostatic hypotension and cognitive impairment: a dangerous association?". Neurological Sciences. 35 (6): 951–957. doi:10.1007/s10072-014-1686-8. PMID 24590841. S2CID 19310855.
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