Synopsis
Measure orthostatic physiology correctly, identify reversible contributors and recognise neurogenic autonomic failure, syncope and autonomic dysreflexia while balancing symptom control against supine hypertension and falls.
- Orthostatic hypotension is a sustained fall of at least 20 mmHg systolic or 10 mmHg diastolic within three minutes of standing or head-up tilt; larger systolic thresholds may be used when supine hypertension is present.
- Measure after adequate supine rest and again after standing, recording symptoms, pulse and exact timing. If the patient cannot stand safely, use the locally accepted lying-to-sitting modification and state the limitation.
- Ask about light-headedness, dim vision, coat-hanger neck pain, weakness, cognitive slowing, falls, syncope, meals, heat, exercise, urination and time of day. Patients with chronic autonomic failure may report fatigue rather than dizziness.
- Review volume loss, anaemia, infection, cardiac disease and medicines before diagnosing neurogenic failure. Diuretics, antihypertensives, nitrates, alpha blockers, dopaminergic medicines, antidepressants, opioids and alcohol can contribute.
- A blunted heart-rate rise during a significant pressure fall can support neurogenic orthostatic hypotension, while marked tachycardia suggests preserved reflexes or a different orthostatic syndrome; beta blockers and pacing confound this distinction.
- Look for the rest of the autonomic phenotype: urinary retention or urgency, constipation, erectile dysfunction, sweating change, heat intolerance, pupillary symptoms, gastroparesis and postprandial hypotension.
- Neurological causes include Parkinson's disease, multiple system atrophy, pure autonomic failure, diabetic and amyloid neuropathy, spinal-cord disease and immune or paraneoplastic autonomic neuropathy.
- First-line treatment combines medication rationalisation, adequate fluid and salt only when safe, slow staged rising, physical counter-pressure manoeuvres, smaller meals, heat avoidance, head-up sleeping and compression selected for the individual.
- Supine hypertension commonly coexists with neurogenic orthostatic hypotension. Check lying as well as standing pressures and avoid taking pressor medicine close to lying down or bedtime.
- Midodrine can improve standing pressure but may cause supine hypertension, piloerection, scalp tingling and urinary retention; it requires specialist or experienced prescriber oversight and timed monitoring.
- Fludrocortisone expands volume but is off-label for postural hypotension in many UK contexts and can cause oedema, hypokalaemia, heart failure and supine hypertension; it is not benign salt replacement.
- Driving, bathing, toileting and night-time falls need explicit advice. Treat functional risk and triggers rather than pursuing a normal clinic blood pressure target that worsens standing symptoms.
Key red flags
Recent vomiting, diarrhoea, bleeding, fever, diuresis or poor intake with thirst, weight loss and tachycardia suggests reduced circulating volume. Oedema does not exclude low effective arterial volume.
Collapse during exertion or while supine, palpitations, chest pain, family sudden death, structural heart disease or an abnormal ECG is not explained safely by an orthostatic reading and needs urgent cardiac assessment.
A person with a lesion usually at or above T6 develops abrupt hypertension, pounding headache, flushing or sweating above the lesion, piloerection and sometimes bradycardia from bladder, bowel or skin stimulation.
Investigation priorities
Demonstrate timing and magnitude of orthostatic change and relate it to symptoms and chronotropic response.
Management branches
Light-headedness, visual dimming, weakness, fall or transient loss of consciousness occurs during standing or soon after rising.
- Check ABCDE and glucose when acute, obtain event and witness history, ECG, injury and red flags, and measure properly timed supine and standing pressure and pulse when safe.
- Treat bleeding, dehydration, infection, arrhythmia or endocrine crisis and review medicines; route exertional, supine, cardiac or focal neurological features to emergency specialist care.
- If orthostatic hypotension persists, implement individual non-drug measures and arrange follow-up or autonomic assessment rather than relying on one asymptomatic clinic reading.
Key medicines
Midodrine for disabling neurogenic orthostatic hypotensionAn experienced prescriber may start 2.5 mg orally three times daily during waking upright hours and titrate weekly to response, commonly up to 10 mg three times daily, keeping the last dose at least four hours before bed.Check supine hypertension, urinary retention, bradycardia, severe heart or renal disease and interacting vasoconstrictors; patients must avoid lying flat after doses and stop or seek review for severe headache or chest symptoms.
Fludrocortisone for selected orthostatic hypotensionWhen specialist or experienced review supports off-label use, start 50–100 micrograms orally each morning and titrate cautiously to symptoms and monitoring rather than a normal standing-pressure target.Monitor supine blood pressure, potassium, renal function, weight and oedema; avoid or use extreme caution in heart failure, significant renal disease and uncontrolled hypertension, and reassess long-term corticosteroid effects.