What is orthostatic hypotension?

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What is Orthostatic Hypotension

Orthostatic hypotension is an abnormal drop in blood pressure upon standing—specifically a decrease in systolic blood pressure of ≥20 mmHg or diastolic blood pressure of ≥10 mmHg within 3 minutes of standing from a supine or seated position. 1

Definition and Diagnostic Criteria

  • The European Society of Cardiology defines orthostatic hypotension as a progressive and sustained fall in systolic BP from baseline value ≥20 mmHg or diastolic BP ≥10 mmHg, or a decrease in systolic BP to <90 mmHg, occurring within 3 minutes of active standing or head-up tilt of at least 60 degrees. 1

  • In patients with supine hypertension, a systolic BP drop of ≥30 mmHg should be considered diagnostic. 2

  • The condition may be symptomatic or asymptomatic—patients do not need to experience symptoms for the diagnosis to be clinically significant. 3, 4

Clinical Subtypes Based on Timing

Orthostatic hypotension is classified into distinct subtypes based on when the blood pressure drop occurs:

  • Initial orthostatic hypotension occurs within 15 seconds of standing, with a BP decrease >40 mmHg systolic and/or >20 mmHg diastolic, followed by spontaneous rapid recovery within 40 seconds. 1

  • Classical orthostatic hypotension develops within 30 seconds to 3 minutes of standing and represents sustained hypotension due to impaired vasoconstriction. 1

  • Delayed orthostatic hypotension occurs beyond 3 minutes of standing and is characterized by a slow progressive decrease in BP. 1

Pathophysiology

The fundamental problem in orthostatic hypotension is failure of peripheral vascular resistance to increase appropriately upon standing, not primarily a cardiac pump failure, though cardiac dysfunction can contribute. 5

  • In neurogenic orthostatic hypotension, cardiovascular sympathetic fibers fail to increase total peripheral vascular resistance upon standing, resulting in inadequate vasoconstriction and a blunted heart rate response (usually <10 beats per minute increase). 5, 1

  • In non-neurogenic orthostatic hypotension (such as from hypovolemia), the heart rate response is preserved or enhanced (>10 beats per minute increase). 5, 1

  • Upon standing, approximately 500-800 mL of blood pools in the lower extremities and splanchnic circulation; normally, the autonomic nervous system compensates by constricting veins and arteries while increasing heart rate and cardiac contractility. 6

Common Symptoms

When symptomatic, patients experience manifestations of cerebral and systemic hypoperfusion:

  • Most common symptoms: Dizziness, lightheadedness, pre-syncope, weakness, fatigue, and visual disturbances (blurring, enhanced brightness, tunnel vision). 1, 4

  • Cardiovascular symptoms: Palpitations, chest pain, and dyspnea. 1, 4

  • Characteristic pain pattern: Neck pain in the occipital/paracervical and shoulder region (coat hanger syndrome), low back pain, or precordial pain. 1, 4

  • Other manifestations: Hearing disturbances (impaired hearing, crackles, tinnitus), nausea, sweating, and syncope. 1, 3

Major Causes

Medication-Induced (Most Common)

  • Diuretics cause volume depletion and are among the most common culprits in medication-induced orthostatic hypotension. 5

  • Vasodilators (including nitrates) directly reduce vascular tone. 5

  • Alpha-adrenergic blockers impair vasoconstriction and are particularly problematic in initial orthostatic hypotension. 5

  • Dopamine agonists (such as ropinirole) cause orthostatic hypotension through D2-mediated blunting of the noradrenergic response to standing and subsequent decrease in peripheral vascular resistance. 7

Autonomic Nervous System Dysfunction

  • Primary autonomic failure: Multiple system atrophy, pure autonomic failure, Parkinson's disease, and dementia with Lewy bodies. 5

  • Secondary autonomic failure: Diabetes mellitus with autonomic neuropathy, amyloidosis with autonomic nerve infiltration, spinal cord injuries, and autoimmune/paraneoplastic autonomic neuropathy. 5

Volume Depletion and Other Causes

  • Severe volume depletion from excessive diuresis, dehydration, or blood loss causes non-neurogenic orthostatic hypotension. 5, 6

  • Age-related physiologic changes including stiffer hearts less responsive to preload changes, impaired compensatory vasoconstrictor reflexes, baroreflex dysfunction, and reduced cerebral autoregulation. 5

Clinical Significance and Epidemiology

  • Prevalence ranges from 5% in middle-aged adults to 20% in community-dwelling elderly, and up to 33% in elderly hospital inpatients. 5, 4

  • Orthostatic hypotension accounts for 20-30% of syncope cases in older adults. 5

  • The condition is associated with a 64% increase in age-adjusted mortality, markedly increased cardiovascular morbidity, and up to a 50% increase in relative risk of all-cause mortality. 5, 4

  • Orthostatic hypotension significantly increases the risk of falls, especially backward falls in elderly patients. 5, 4

Diagnostic Testing

  • Measure BP after 5 minutes of lying or sitting, then at 1 minute and 3 minutes after standing. 5, 4

  • If the patient cannot stand safely or clinical suspicion remains high despite normal bedside testing, head-up tilt table testing at 60 degrees or more is recommended. 1, 4

  • Assessment of heart rate response helps distinguish neurogenic (blunted increase) from non-neurogenic (preserved or enhanced increase) causes. 1, 5

References

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Research

Evaluation and management of orthostatic hypotension.

American family physician, 2011

Research

Orthostatic Hypotension: A Practical Approach.

American family physician, 2022

Guideline

Orthostatic Hypotension Causes and Mechanisms

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2026

Research

Orthostatic hypotension.

American family physician, 2003

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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