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Syncope and orthostatic hypotension in older adults

Distinguish syncope from falls, seizure and delirium through witness chronology, identify cardiac and orthostatic danger, measure postural physiology correctly, and restore function with cause-specific, medication-aware and driving-safe management.

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High-risk transient loss of consciousness

Syncope during exertion or supine, abnormal ECG, structural heart disease, new breathlessness, murmur, chest pain, family sudden death, major injury or persistent neurological deficit may indicate malignant arrhythmia, outflow obstruction, embolism or stroke.

Action: Use ABCDE and glucose, obtain a 12-lead ECG promptly, monitor rhythm and physiology, treat bleeding or other acute causes and arrange urgent specialist cardiovascular or neurological assessment according to red flags rather than attributing collapse to age.

Open the sections you need. The overview is shown first.
01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Obtain three histories: the person, witness and records. Establish whether consciousness was lost, posture, trigger, warning, pallor or cyanosis, movements, tongue injury, incontinence, duration and recovery. Brief myoclonic jerks do not prove epilepsy. Ask medication timing, meals, toileting, heat, hydration and previous events. Injuries can be the only evidence when amnesia obscures loss of consciousness.

Examine cardiovascular and neurological systems, hydration and injury. A 12-lead ECG is core and must be reviewed for conduction disease, long or short QT, pre-excitation, Brugada pattern, ventricular hypertrophy or ischaemia. Exertional, supine, abrupt or cardiac-history events require urgent ambulatory monitoring, echocardiography or specialist testing according to suspected mechanism.

Measure orthostatic physiology carefully. Rest supine for at least five minutes, record blood pressure and pulse, then repeat during standing at about one and three minutes and during symptoms. If standing is unsafe, adapt with specialist help. Delayed orthostatic hypotension may require longer measurement. Document symptoms, meals and medicines; one normal test does not exclude intermittent postural disease.

Classical orthostatic hypotension is a sustained systolic drop of at least 20 mmHg or diastolic drop of at least 10 mmHg within three minutes. In people with supine hypertension a larger systolic criterion may be considered by specialists. Pressure below 90 systolic or typical symptoms can be important even when the numerical fall is smaller. Repeat at the time symptoms usually occur.

Review volume, haemoglobin, renal and electrolytes, glucose and infection when indicated. Reconcile diuretics, vasodilators, nitrates, alpha-blockers, antidepressants, antipsychotics, dopaminergic and rate-limiting medicines. Reduce or retime against the original indication and monitor heart failure, angina, urinary symptoms and mental health rather than stopping indiscriminately.

Non-drug treatment includes explaining triggers, adequate fluid when heart and kidney status permit, cautious salt increase, smaller lower-carbohydrate meals for postprandial symptoms, avoiding heat and alcohol excess, slow rising and physical counter-pressure manoeuvres. Abdominal compression is often more effective than stockings but dexterity and carer burden determine feasibility. Elevate the head of bed for neurogenic supine hypertension.

Midodrine, an alpha-1 agonist, is considered for severe neurogenic orthostatic hypotension despite non-drug care. Dose during waking upright hours and avoid within four hours of bed. Check supine and standing pressure and urinary retention. Fludrocortisone is off-label and expands volume but often problematic in heart failure, renal disease, hypokalaemia and supine hypertension.

For recurrent unexplained syncope, select testing from phenotype. Ambulatory ECG duration should match event frequency; implantable monitors may be needed for infrequent high-concern events. Echocardiography follows suspected structural disease. Tilt testing can demonstrate reflex susceptibility. Carotid sinus massage is performed in a monitored specialist setting in selected people over 40, with contraindication review.

Assess function and fear after collapse. Physiotherapy addresses deconditioning and safe transitions; OT reviews bathing, toilet and night routes. Teach what to do during prodrome and how to summon help. Recurrent events may change capacity for independent medication, stairs and bathing, but restrictions should be proportional and reviewed.

Driving advice is part of treatment. The person must stop driving after relevant unexplained blackout and notify DVLA when required. Rules differ by cause, recurrence and Group 1 or 2 licence. Document advice and check current DVLA guidance rather than offering a guessed fixed interval.

Key points

  • Syncope is transient loss of consciousness from global cerebral hypoperfusion with rapid onset, short duration and spontaneous complete recovery.
  • First-line assessment is witness history, examination, capillary glucose when relevant and a 12-lead ECG; classify red flags before ordering broad tests.
  • Ask posture, activity, prodrome, colour, breathing, movements, tongue injury, duration, recovery, injury, medicines and prior or family cardiac history.
  • Measure orthostatic pressure after at least five minutes supine and during standing, including at one and three minutes with symptoms and pulse.
  • Classical orthostatic hypotension is a sustained fall within three minutes of at least 20 mmHg systolic or 10 mmHg diastolic; absolute pressure and symptoms still matter.
  • A blunted heart-rate rise suggests neurogenic failure or rate-limiting medicine; a marked rise may support volume depletion, but neither is diagnostic alone.
  • First-line orthostatic management is cause treatment, medicine review, hydration, safe salt advice, slow transitions, counter-pressure manoeuvres, compression and rehabilitation.
  • Midodrine is a specialist option for severe neurogenic orthostatic hypotension after non-drug care, with supine-pressure and urinary monitoring.
  • Tilt testing and carotid sinus massage are specialist tests for selected recurrent unexplained events, not routine first-line screening.
  • Advise no driving after unexplained loss of consciousness and use current DVLA rules for diagnosis and vehicle group; document the discussion.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
01

Reflex syncope

Vasovagal and situational triggers produce transient vasodilation and bradycardia, often with warmth, nausea, pallor and a recognisable prodrome.

02

Orthostatic hypotension

Volume depletion, autonomic failure and medicines impair vascular compensation after standing, lowering cerebral perfusion and causing dizziness, falls or syncope.

03

Cardiac syncope

Bradyarrhythmia, tachyarrhythmia, aortic stenosis, cardiomyopathy and other structural disease can abruptly reduce cardiac output without warning.

04

Multifactorial older-adult collapse

Frailty, carotid sinus hypersensitivity, postprandial hypotension, impaired thirst and several medicines commonly interact rather than one cause acting alone.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
  1. 1
    Transient cerebral hypoperfusion

    Syncope is brief global loss of consciousness and postural tone from inadequate brain perfusion with spontaneous complete recovery.

  2. 2
    Failed orthostatic vasoconstriction

    Standing pools blood in legs and splanchnic circulation; autonomic or volume impairment prevents sufficient heart-rate and vascular compensation.

  3. 3
    Baroreflex ageing and disease

    Reduced baroreceptor responsiveness, diabetic or neurodegenerative autonomic failure and arterial stiffness increase pressure variability. Symptoms become more likely after meals, heat, exertion or volume loss.

  4. 4
    Medication-amplified preload loss

    Diuretics, vasodilators, alpha blockade and nitrates reduce volume or vascular tone, while rate-limiting drugs restrict cardiac compensation.

  5. 5
    Cerebral autoregulatory vulnerability

    Hypertension, vascular disease and frailty narrow tolerance for rapid pressure falls, producing symptoms at different numerical thresholds.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
Vasovagal prodrome

Warmth, nausea, sweating, pallor and visual dimming after prolonged standing or distress precedes brief loss and rapid recovery.

Orthostatic pattern

Symptoms follow standing, meals, heat or morning medicines and improve on lying, with a reproducible pressure fall.

Arrhythmic patternRed flag

Sudden collapse without warning, during exertion or supine, with palpitations or abnormal ECG is high risk.

Convulsive syncope

Brief irregular jerks can accompany prolonged cerebral hypoperfusion but recovery is usually rapid compared with seizure.

Neurogenic autonomic pattern

Small pulse response, constipation, urinary or sweating dysfunction and Parkinsonian or neuropathic disease accompanies posture hypotension.

Persistent focal signsRed flag

Weakness, aphasia or neglect after the event requires acute neurological care rather than a syncope label.

Red flags requiring action

  • Exertional or supine syncope, no prodrome, palpitations, heart failure, murmur or abnormal ECG requires urgent cardiovascular assessment.
  • Family history of sudden cardiac death under 40 or inherited cardiac disease materially raises arrhythmic concern.
  • Persistent focal neurology is not uncomplicated syncope and requires an acute stroke or neurological pathway.
  • Repeated syncope with head injury, anticoagulation or inability to rise requires injury and immediate safety assessment.
  • Postural symptoms with melaena, anaemia, dehydration, sepsis or adrenal features may reflect acute volume or endocrine disease.
  • New collapse after antihypertensive, diuretic, nitrate, alpha-blocker, insulin or psychoactive change requires prompt medication and physiology review.
05InvestigationsWhat to request, why it matters and how to interpret it.
Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

  1. 01
    Witnessed event historyFirst step
    Why
    Classify loss of consciousness and risk.
    Interpretation and limitations
    Record posture, trigger, prodrome, colour, movement, duration, recovery, injury and cardiac, neurological and family history.
  2. 02
    12-lead ECG
    Why
    Detect arrhythmic and structural clues early.
    Interpretation and limitations
    Conduction block, QT abnormality, pre-excitation, Brugada pattern, ventricular hypertrophy or ischaemia changes urgency and testing.
  3. 03
    Supine and standing pressure
    Why
    Confirm orthostatic physiology during symptoms.
    Interpretation and limitations
    After five minutes supine, measure during standing at one and three minutes with pulse and symptoms; extend when delayed symptoms occur.
  4. 04
    Targeted blood tests
    Why
    Find volume, bleeding and metabolic precipitants.
    Interpretation and limitations
    Use FBC, renal, electrolytes, glucose and other tests from dehydration, anaemia, infection, endocrine or drug suspicion.
  5. 05
    Ambulatory rhythm monitoring
    Why
    Correlate symptoms with intermittent arrhythmia.
    Interpretation and limitations
    Choose Holter, external or implantable duration according to event frequency and pre-test cardiac concern.
  6. 06
    Echocardiography
    Why
    Identify suspected structural cardiac disease.
    Interpretation and limitations
    Use for murmur, abnormal ECG, heart failure or exertional event rather than routine low-risk vasovagal syncope.
  7. 07
    Tilt or carotid sinus testing
    Why
    Diagnose selected reflex or carotid mechanisms.
    Interpretation and limitations
    Specialists use monitored testing after initial assessment when recurrent unexplained events, injury or quality-of-life impact justify it.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
01

Epileptic seizure

Lateral tongue bite, prolonged tonic-clonic movement, post-event confusion and witnessed onset favour seizure, though brief jerks can occur in syncope.

02

Mechanical fall

A clear trip with continuous awareness differs from syncope, but recall may be limited and cardiovascular contributors can coexist.

03

Stroke or TIA

Persistent focal deficit suggests stroke; isolated complete loss of consciousness without focal signs is rarely a TIA.

04

Hypoglycaemia or metabolic event

Glucose, hypoxia, intoxication and metabolic encephalopathy can cause altered consciousness with slower or incomplete recovery. Capillary glucose and directed physiology clarify the diagnosis during the episode.

05

Psychogenic transient unresponsiveness

Long duration, closed eyes, variable movement and recurrent events may suggest psychogenic episodes only after cardiac and neurological danger is assessed.

07ManagementImmediate care, first-line treatment, alternatives and escalation.
01First-line blackout sequenceStabilise, reconstruct and risk-stratifyFirst stepFirst lineA fall may have involved transient loss of consciousness.
  1. 1Perform ABCDE and glucose, assess injury and obtain witness chronology and medicine timing.
  2. 2Examine and obtain 12-lead ECG and correctly measured postural pressure.
  3. 3EscalationEscalate cardiac or neurological red flags and select rhythm, echo or other testing from the suspected mechanism.
02Orthostatic managementTreat causes before pressor escalationEscalationTypical symptoms and a compatible pressure pattern are present.
  1. 1Correct volume or medical triggers and review vasodilating, diuretic, psychoactive and rate-limiting treatment.
  2. 2Teach fluids and salt when safe, staged rising, counter-pressure manoeuvres, meal and heat adaptation and compression.
  3. 3Review symptoms, falls and supine pressure and consider specialist midodrine only for persistent disabling neurogenic disease.
03High-risk cardiac routeProtect against recurrent arrhythmic collapseEvent is exertional, supine, abrupt or accompanied by cardiac history, murmur or ECG abnormality.
  1. 1Arrange urgent cardiology assessment and rhythm monitoring matched to event frequency.
  2. 2Use echocardiography and inherited or structural testing according to findings.
  3. 3Restrict driving and hazardous activity until cause, treatment and current DVLA criteria are addressed.
04Functional recoveryReverse fear and deconditioningPresyncope or syncope has reduced standing, bathing or community mobility.
  1. 1Provide aid and transfer assessment and graded upright and strength rehabilitation with symptoms monitored.
  2. 2Adapt shower, toilet, night route and alarm while avoiding unnecessary permanent restriction.
  3. 3Coordinate medicine timing, carer education and driving or work advice with a named follow-up plan.
Key medicines and prescribing safety2 treatments · regimens, roles and cautions
Specialist treatment for severe orthostatic hypotension due to autonomic dysfunction when cause treatment and non-drug measures are inadequate.

Midodrine

Start 2.5 mg orally three times daily during waking hours and increase weekly according to standing symptoms and pressure, commonly to 10 mg three times daily; take the last dose at least four hours before bed.

Monitor supine hypertension, bradycardia, scalp tingling and urinary retention; avoid severe heart or renal disease and do not dose before lying down.

Volume expansion for selected persistent orthostatic hypotension when alternatives and comorbidity support its use.

Fludrocortisone

An off-label specialist regimen may start 50 micrograms orally each morning and increase to 100 micrograms daily if response and safety permit.

Monitor supine pressure, weight, oedema, potassium and renal function; heart failure, renal impairment and hypokalaemia often make it unsuitable.

08ComplicationsImportant consequences, why they occur and why they matter clinically.
01

Traumatic injury

Sudden loss of tone causes head injury and fracture, particularly without prodrome or with antithrombotic treatment.

02

Falls and activity restriction

Presyncope and fear lead to reduced standing, deconditioning and dependence even when complete syncope is infrequent.

03

Cardiac death

Untreated arrhythmia or structural obstruction can cause recurrent syncope, sudden death and injury to others while driving.

04

Supine hypertension and treatment harm

Pressor treatment for neurogenic hypotension can cause night-time hypertension, fluid overload, urinary retention and stroke risk.

05

Driving and occupational risk

Unexplained or recurrent events require cessation and DVLA-specific restriction, affecting independence and carers. This must be addressed explicitly while diagnosis and treatment continue.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.
  • Record actual syncope, presyncope, falls, injury and activity rather than blood pressure alone.
  • Repeat posture measurements with symptoms, dose changes and time-of-day or meal pattern when initial testing is nondiagnostic.
  • Review supine hypertension, pulse, urinary symptoms, oedema, potassium and renal function during pressor or volume-expanding therapy.
  • Track hydration and salt feasibility in heart failure, CKD and carer-dependent intake.
  • Reassess gait, confidence and home safety after injury or activity restriction.
  • Document driving cessation, DVLA notification and criteria-based return rather than relying on memory of intervals.
10Special situationsVariants, exceptions and circumstances that change the usual approach.

Jerks do not prove seizure

Brief myoclonus can accompany cerebral hypoperfusion; the whole witness sequence and recovery determine interpretation.

One standing test can miss disease

Postprandial, morning and delayed orthostatic hypotension may require measurement in the provoking context.

Symptoms matter with numbers

A clinically important pressure may occur without crossing a single threshold, especially with limited cerebral reserve.

Compression needs to be usable

An effective garment provides no benefit if hand weakness, pain or absent care prevents application.

Pressors shift the problem

Improving standing pressure can worsen supine hypertension and night-time risk, requiring timed dosing and posture review.

Driving is a clinical action

Clear documented advice protects the person and public while diagnostic testing continues.

11Common pitfallsFrequent interpretation and management errors.
  1. 01

    Calling an unwitnessed fall mechanical without exploring loss of consciousness.

  2. 02

    Diagnosing epilepsy from a few brief jerks during a faint.

  3. 03

    Measuring standing pressure without adequate supine rest, symptoms or three-minute readings.

  4. 04

    Using a normal one-off postural test to exclude intermittent or delayed hypotension.

  5. 05

    Stopping several cardiovascular medicines abruptly without indication and response monitoring.

  6. 06

    Starting midodrine without checking supine pressure and urinary retention.

  7. 07

    Giving generic drink more advice to someone with heart failure or care-dependent access.

  8. 08

    Failing to advise driving cessation and current DVLA review after unexplained blackout.

Practice

Two practice questions

Question 1 of 20 correct
Medicine of older adultsOriginal SBA

Measuring orthostatic pressure

An older adult reports dizziness within two minutes of standing. Which bedside measurement best tests classical orthostatic hypotension?

Sources and review status5 sources · checked 27 Aug 2026 · clinical review pending
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.

Authoring stateComplete draftClinical stateAwaiting reviewJurisdictionUnited Kingdom