General MedicineTier 1Disease (DEADMAN)

Autonomic dysfunction - postural hypotension

Description

Sustained fall in BP within 3 minutes of standing: >=20 mmHg systolic, or >=10 mmHg diastolic
- Or >=30 systolic if supine hypertension is present
Variants
- Initial orthostatic hypotension - transient fall >40 systolic within 15 s, resolves by 30 s; needs beat-to-beat monitoring, not a manual cuff
- Delayed orthostatic hypotension - beyond 3 min; often an early marker of degenerative autonomic failure
- Postprandial hypotension - within 2 h of a meal; common and under-recognised in the elderly
- Neurogenic OH - no compensatory rise in heart rate (HR rise <15 bpm, or a ratio of HR change to systolic BP change <0.5)
Discriminator: does the pulse rise?
- Rises appropriately -> volume depletion, blood loss, drugs
- Does not rise -> neurogenic (autonomic failure), or beta-blockade, or a paced/denervated heart

~5-10% of community-dwelling elderly; 20-30% over 75; up to 50% of nursing home residents
Rare under 50 unless neurogenic or drug-induced
Present in ~30-60% of Parkinson disease, and near-universal in multiple system atrophy and pure autonomic failure
Independently predicts falls, fracture, cognitive decline, cardiovascular events and mortality

Normal response to standing

500-1000 mL pools in the legs and splanchnic bed
-> dec venous return -> dec cardiac output -> dec carotid/aortic baroreceptor firing
-> baroreflex: inc sympathetic outflow, dec vagal tone
-> inc HR (10-20 bpm) + peripheral vasoconstriction -> BP maintained

Why the elderly fail

The primary mechanism in older people is impaired baroreceptor reflex sensitivity, reducing the compensatory heart rate and vasoconstrictor response to the fall in blood pressure on standing
Compounded by
- Arterial stiffening -> less buffering
- Diastolic dysfunction -> steeply preload-dependent stroke volume
- Reduced thirst and renal sodium conservation -> chronic subclinical hypovolaemia
- Polypharmacy

Causes

A. Neurogenic - central

Multiple system atrophy (severe early OH with relatively preserved cognition and poor levodopa response)
Parkinson disease, dementia with Lewy bodies, pure autonomic failure
Spinal cord lesion, brainstem stroke

B. Neurogenic - peripheral

Diabetic autonomic neuropathy - the commonest peripheral cause
Amyloidosis (AL and hereditary ATTR), Sjogren, paraneoplastic, HIV, B12 deficiency, chemotherapy (vincristine, platinum), Guillain-Barre, autoimmune autonomic ganglionopathy

C. Non-neurogenic

Hypovolaemia - haemorrhage, dehydration, diuretics, adrenal insufficiency, diabetes insipidus
Cardiac - aortic stenosis, HFpEF, arrhythmia, constrictive pericarditis
Drugs - always the first thing to review
- Antihypertensives (esp. alpha-blockers, diuretics), nitrates, levodopa and dopamine agonists, TCAs, antipsychotics, SSRIs, opioids, PDE5 inhibitors, alcohol
Deconditioning, prolonged bed rest, large varicose veins

The measurement itself

Supine for 5 minutes, then BP and HR at 1 and 3 minutes standing (standing, not sitting - sitting misses up to half of cases)
Repeat in the morning and after a meal if the history is suggestive but the test is negative
Calculate the HR response - it is the key discriminator and is almost always omitted

History

Symptoms: light-headedness, "coat-hanger" neck and shoulder ache (highly specific for OH - suboccipital muscle ischaemia), visual greying, fatigue, cognitive slowing, syncope, falls
Timing: morning, post-prandial, post-exertional, hot weather, after alcohol
Full medication review including timing of doses
Autonomic review of systems: constipation, urinary symptoms, erectile dysfunction, sweating change - their presence points to a generalised autonomic disorder

Examination

Investigations

FBE, UEC, glucose/HbA1c, B12, TSH, morning cortisol/short synacthen if indicated
SPEP/free light chains - amyloid
ECG; echo if a cardiac cause is suspected
Tilt table testing if the diagnosis is uncertain or syncope is unexplained
Formal autonomic testing (Valsalva ratio, heart rate variability, sweat testing) in specialist centres
Supine and standing plasma noradrenaline: fails to rise on standing in neurogenic OH; low supine level suggests peripheral, normal suggests central

Target symptoms and falls, not the number. Aim for standing systolic >90 mmHg.

A. Deprescribe first - the highest-yield step

Review and withdraw or reduce antihypertensives, alpha-blockers, nitrates, TCAs, antipsychotics, diuretics
If antihypertensives are still needed, dose at night and prefer agents with less orthostatic effect

B. Non-pharmacological - always before drugs

Rise slowly and in stages; sit on the bed before standing
Increase salt (up to 6-10 g/day) and fluid (2-2.5 L/day) unless heart failure or renal disease
Rapid bolus of 500 mL cold water raises BP within 5-15 min for ~1 h - useful before rising or before a meal
Physical counter-manoeuvres: leg crossing, squatting, toe-raises, tensing buttocks and abdomen
Compression: abdominal binder is more effective than stockings (the splanchnic bed holds more blood than the legs); waist-high stockings if used
Head-up tilt of the bed by 10-20 degrees at night - reduces nocturnal natriuresis and morning OH
Small, low-carbohydrate, frequent meals; avoid alcohol and large hot meals
Avoid straining, hot baths, prolonged standing
Exercise: recumbent - swimming, rowing, cycling

C. Pharmacological - if symptoms persist

Drug	Dose	Note
Fludrocortisone	0.1-0.2 mg daily	Volume expansion. Monitor K+, weight, oedema; worsens supine hypertension
Midodrine	2.5-10 mg tds	Alpha-1 agonist. Last dose >=4 h before bed - supine hypertension. Scalp tingling, urinary retention
Droxidopa		Not available in Australia
Pyridostigmine	30-60 mg tds	Modest; does not worsen supine hypertension - useful when it coexists
Desmopressin	low dose	Nocturnal polyuria; monitor sodium
Octreotide		Postprandial hypotension

D. Supine hypertension - the therapeutic dilemma

Present in ~50% of neurogenic OH; treating OH worsens it
Never lie flat during the day; sleep head-up
Short-acting agent at bedtime if severe (nitrate patch removed on waking, losartan, or captopril)
Accept moderate supine hypertension in exchange for symptom control and fall prevention - falls kill sooner than nocturnal BP

Falls, fractures, syncope
Parkinson disease, multiple system atrophy, dementia with Lewy bodies, pure autonomic failure
Diabetic and amyloid autonomic neuropathy
Supine hypertension (~50% of neurogenic cases)
Cognitive impairment and dementia - repeated cerebral hypoperfusion
Adrenal insufficiency, anaemia, dehydration
Polypharmacy and frailty

Independently associated with increased all-cause mortality, cardiovascular events, stroke, falls and incident dementia - it is not a benign nuisance
Neurogenic OH is progressive and reflects the underlying degenerative process
Drug- and volume-related OH is often fully reversible
In multiple system atrophy, severe early OH is a defining feature and a poor prognostic marker

Monitor

6 more sections, plus exam facts

Premium unlocks every note across every specialty, and the full exam fact library behind it.