Dizziness

Dizziness is a common presentation that accounts for about 5% of primary care visits.
When a patient describes dizziness, it can reflect one of four conditions

Four categories causing a sensation of dizziness
Categories	Pathophysiology	Aetiology
Vertigo = spinning sensation	Vestibular pathology	Vestibular neuritis Labyrinthitis Meniere’s disease
Presyncope = fainting sensation	Reduced cerebral perfusion	Volume depletion Neurocardiogenic syncope
Dysequilibrium = imbalance sensation	Gait disorder	Myelopathy Peripheral neuropathy Parkinson’s disease
Light-headedness = sensation of disconnection from the environment	Psychological disorder	Anxiety Depression

Patients often describe presyncope as a feeling of fainting or dizziness.
Presyncope:
- Described as a feeling of fainting or dizziness.
- Caused by global cerebral hypoperfusion.
- Often accompanied by sympathetic activation (e.g., diaphoresis and tachycardia).
Syncope:
- A transient loss of consciousness with complete and spontaneous recovery.
- Presyncope episodes can lead to syncope.
In general, it can be classified into three broad categories:
1. neurally mediated syncope
  - often affect children and young adults.
2. orthostatic hypotension
  - often in elderly people (>70 years)
  - related to age-related physiological changes, such as :
    - blunting of baroreflex sensitivity
    - reduced intravascular blood volume
    - greater susceptibility to infection
    - reduced myocardial elasticity and increased afterload
3. Cardiac syncope
  - mostly seen in In middle-aged people (40–70 years)
4. Rarer causes include syncope secondary to neurological, metabolic and psychogenic disorder

Etiology of presyncope/syncope
Neurally mediated syncope	Vasovagal syncope	Provoked by pain. fear, emotion, venesection
Neurally mediated syncope	Situational syncope	Provoked by – coughing – Micturition – Defaecation
	Carotid Sinus Syncope	Neck rotation or pressure (e.g. tight collar)
Orthostatic hypotension	Primary autonomic failure	Lewy body diseaseParkinson Multiple system atrophy
	Secondary autonomic failure	Diabetic neuropathy Amyloid neuropathy HIV neuropathy
	Postprandial hypotension
	Postural Tachycardia Syndrome (POTS)	Most common in female young women
	Drug-induced	Anti-hypertensives Diuretics antidepressants
	Volume loss	Haemorrhage Diarrhoea Addison
Cardiac syncope	Arrhythmias	Sinus node dysfunction – bradycardia/tachycardia syndrome Atrioventricular conduction system disease Atrial fibrillation Paroxysmal supraventricular and ventricular tachycardias Inherited syndromes – long/ short QT syndrome – Brugada syndrome – WPW – Arrhythmogenic RV cardiomyopathy Implanted device (pacemaker, ICD) malfunction Drug-induced proarrhythmias
	Structural cardiac disease	Valvular heart disease Aortic stenosis – with exertion Ischaemic heart disease – with exertion Cardiomyopathy – with exertion Pericardial disease
	Vascular disorders	Aortic Dissection Abdominal Aortic Aneurysm rupture Pulmonary Embolism Pulmonary Hypertension Subarachnoid Hemorrhage Subclavian Steal Syndrome (provoked by use of arms)
Neurological	Seizures Migraine Transient ischaemic attacks stroke
Other	Metabolic disorders	Hypoglycaemia (not true syncope as not spontaneously reversible) hypoxia hyperventilation with hypocapnia

By age

1. Children and Young Adults (3–18 years)

Neurally mediated syncope: Vasovagal or situational syncope is common.
Triggers:
- Prolonged standing (30%)
- Movement (13%)
- Change in body position (9%)
- Situational triggers (e.g., micturition, defecating, coughing).
Risk: Generally low-risk in this group.

2. Middle-aged Adults (40–70 years)

Cardiac syncope: Accounts for 10–20% of cases, with potentially high risk.
Common causes:
- Structural heart diseases (e.g., hypertrophic cardiomyopathy, Wolff-Parkinson-White syndrome)
- Arrhythmias and coronary atherosclerosis.
Initial evaluation:
- 12-lead ECG, 24-hour Holter monitoring, 7-day event loop recorder.
- Electrolyte and magnesium levels, echocardiography, cardiac stress tests.
- Family history of sudden death is a key red flag.
Misdiagnosis: Can be fatal—requires thorough investigation.

3. Elderly Adults (>70 years)

Orthostatic hypotension: Common due to:
- Autonomic dysfunction, volume loss, medications.
Contributing factors:
- Blunted baroreflex, decreased cardiac elasticity, increased afterload.
Medication review: Important for drugs affecting:
- Blood pressure (antihypertensives), cardiac output (beta-blockers), QT interval (e.g., amiodarone), and electrolyte balance (e.g., diuretics).

Risk Stratification

Use the San Francisco Syncope Rule (CHESS) (Annals of Emerg Med. 2004; 43;2: 224-232) to identify high-risk cases:
- C: Congestive cardiac failure
- H: Haematocrit <30%
- E: ECG abnormalities
- S: Shortness of breath
- S: Systolic BP <90 mmHg
Validation: 98% sensitivity for predicting serious outcomes.

CHESS was designed to help emergency physicians determine which patients required admission due to the risk of serious outcomes, such as arrhythmias, myocardial infarction, or death.It was highly sensitive in identifying patients at risk of adverse outcomes, meaning it was good at not missing high-risk cases.

A patient with any element of CHESS is considered high-risk for mortality, as these parameters (cardiac issues, low oxygen levels, anaemia, low blood pressure, and ECG changes) suggest severe underlying physiological compromise.

Such patients require closer monitoring and more aggressive management to improve outcomes.

other studies

Risk Score	Criteria	Validation Studies	Sensitivity	Specificity	Limitations
ROSE Score	BNP, Bradycardia Fecal Occult blood Anemia Chest pain Q waves on ECG Oxygen saturations <95%	Did not pass validation (J Am Coll Cardiol 2010;55:713-721)	87%	65%	Low specificity did not pass validation
Boston Syncope Rule	25 predictors including: Signs of ACS Abnormal ECG Cardiac History Family History of sudden death Abnormal vitals Valvular disease	Validated (J Emerg Med. 2007 Oct; 33(3): 233â€“239)	89%	57%	Relatively low specificity includes multiple predictors may lead to over-admission
OESIL Risk Score	Age > 65 Males Hypertension Cardiovascular history Diabetes Previous syncope No prodrome Syncope-related traumatic injuries Abnormal ECG	Validated (Eur Heart J. 2003 May;24(9):811-9)	95%	61%	Limited by retrospective nature specificity moderate
STePS Study	Abnormal ECG No prodrome Male gender Age >65 Structural heart disease Ventricular arrhythmias	Validated (J Am Coll Cardiol. 2008 Jan 22;51(3):276-83)	86%	69%	Limited by short follow-up, specific population studied (elderly and males)

Evaluation of patients with pre-syncope/syncope in GP practice

Cardiac red flags
Symptoms	Chest pain	Coronary artery disease
	Worsening shortness of breath on exertion	Heart failure
	Palpitation or ‘skipped beats’	Arrhythmias
Signs	Fluid overload	Heart failure
	Murmurs	Valvular heart disease
	Carotid bruits	Carotid artery stenosis
Past history	Ventricular arrhythmias, coronary vascular disease
Family history	Sudden death
ECG findings	Ischemic changes	ST and T wave ischaemic changes
	Prolonged QTc	QTc >500 msec
	Atrial fibrillation	New atrial fibrillation
	Persistent sinus bradycardia/tachycardia	HR <40 or >120
	Non-sustained ventricular tachycardia	4 or more VT beat
	Brugada pattern	J-point ST elevation V1–V3 and right bundle branch block
	Wolf-Parkinson-White syndrome or supraventricular tachycardia	Short PR interval and delta wave
	Atrioventricular block	Prolonged PR interval and bundle branch block
	Right ventricular dysplasia	Right bundle branch block with QRS >110 ms in V1, an epsilon wave in V1–V2 and T-wave inversion in right precordial leads

CLINICAL ASSESSMENT

Circumstances just prior to attack
1. Position (supine, sitting or standing)
2. Activity (rest, change in posture, during or after exercise, during or immediately after urination, defaecation, cough or swallowing)
3. Predisposing factors (e.g. crowded or warm places, prolonged standing, post-prandial period)
4. Precipitating events (e.g. fear, intense pain, neck movements)
Onset of attack
1. Nausea, vomiting, abdominal discomfort, feeling of cold, sweating, aura, pain in neck or shoulders, blurred vision
Nature of the attack (eyewitness)
1. Type of collapse (slumping or keeling over)
2. skin colour (pallor, cyanosis)
3. duration of loss of consciousness
4. breathing pattern (snoring)
5. movements (tonic, clonic, tonic-clonic or minimal myoclonus, automatism) and their duration, onset of movement in relation to fall, tongue biting
End of attack
1. Nausea, vomiting, sweating, feeling of cold, confusion, muscle aches, skin colour, injury, chest pain, palpitations
2. urinary or faecal incontinence
Antecedents
1. Family history of sudden death, congenital arrhythmogenic heart disease or fainting
2. Previous cardiac disease: check for scars, pulses, murmurs, pacemakers and other devices?
3. Neurological history (Parkinsonism, epilepsy, narcolepsy)
4. Metabolic disorders (diabetes, etc.)
5. Medication (antihypertensive, antianginal, antidepressant agent, antiarrhythmic, diuretics and QT prolonging agents)

Examination

1. General assessment

Assess conscious state and overall appearance.
Look for pallor, dehydration, diaphoresis and poor peripheral perfusion.
Check for injuries if there has been a collapse or fall.
Record BP, pulse rate/rhythm, respiratory rate, oxygen saturation and temperature.
Check capillary blood glucose in acute dizziness or collapse. aci.health.nsw.gov.au

2. Postural BP and heart rate

Perform only if the patient can stand safely.

Time	Assessment
After lying for 5 minutes	Record baseline BP and HR.
After standing for 1 minute	Record BP, HR and symptoms.
After standing for 3 minutes	Repeat BP, HR and symptoms.

Orthostatic hypotension: sustained reduction of ≥20 mmHg systolic OR ≥10 mmHg diastolic within 3 minutes of standing.
Record dizziness, visual dimming, weakness or presyncope during testing.
Both symptoms and measurements matter: orthostatic hypotension may occur without symptoms.
Stop testing and assist the patient to lie down if significantly symptomatic.
Normal measurements do not exclude intermittent orthostatic hypotension; repeat assessment if clinically indicated. www.racgp.org.au

3. Interpret the heart-rate response

Interpret HR changes in the presence of a postural BP fall.

Finding	Possible interpretation
HR increases >15–20 bpm	Preserved compensatory response; consider hypovolaemia or another non-neurogenic cause. Does not confirm hypovolaemia.
Little or no HR increase	Consider autonomic dysfunction, HR-limiting medication, conduction disease or pacing. Does not confirm autonomic failure.

Review medications, particularly beta blockers, verapamil and diltiazem.
Causes of autonomic dysfunction include diabetic autonomic neuropathy, Parkinson’s disease and multiple system atrophy.
Postural observations alone cannot reliably confirm or exclude dehydration or blood loss. link.springer.com

4. Cardiovascular examination

Pulse rate and rhythm.
Heart sounds and murmurs, particularly an aortic stenosis murmur.
Peripheral perfusion and pulses.
Signs of heart failure: raised JVP, pulmonary crackles and peripheral oedema.
Obtain a 12-lead ECG for syncope/presyncope or suspected cardiac dizziness. www.racgp.org.au

5. Neurological and vestibular examination

Eye movements and nystagmus.
Cranial nerves.
Limb power and sensation.
Cerebellar coordination.
Gait and balance, if safe.
Otoscopy and hearing assessment when vertigo or auditory symptoms are present.
Dix–Hallpike: when brief, position-triggered vertigo suggests BPPV. www.racgp.org.au

6. Additional examination when indicated

Assess for bleeding if suggested by the history or clinical findings.
Abdominal examination when pain or internal bleeding is suspected.
Rectal examination: consider with consent when gastrointestinal bleeding is suspected and findings would influence management; not routine for dizziness.

Urgent findings: persistent hypotension, chest pain, significant arrhythmia, focal neurological signs, marked new gait impairment, significant bleeding or serious injur

note :

POTS = postural orthostatic tachycardia syndrome. Assess with a 10-minute standing test; routine 3-minute postural observations may miss it.

Diagnostic criteria — all required

Sustained HR increase within 10 minutes of standing:
- Age ≥20 years: ≥30 bpm above supine baseline.
- Age 12–19 years: ≥40 bpm above supine baseline.
No sustained orthostatic hypotension: no BP fall of ≥20 mmHg systolic or ≥10 mmHg diastolic.
Frequent orthostatic symptoms that worsen upright and improve on lying down.
Symptoms for at least 3 months.
No alternative condition explaining the tachycardia, such as acute dehydration, anaemia, hyperthyroidism or medication effects. Tachycardia alone does not establish POTS. PMC

Duration criteria vary between references: contemporary consensus uses ≥3 months; the December 2025 RACGP case article uses >6 months

INVESTIGATIONS

Guided by history and examination
Laboratory tests
FBC (anaemia?)
UEC
glucose
blood gas (venous often sufficient)
Consider D-dimers if pulmonary embolism is suspected
Blood alcohol, as clinically indicated.
ECG for causes of sudden collapse:
CT brain:
1. if suspected first seizure
2. if secondary trauma sustained during the syncopal episode (“trauma above the clavicle”)
3. if suspected TIA or stroke
4. if neurological deficit or ongoing altered conscious state / confusion
5. if Age >65
6. if sudden onset headache
7. if patients on warfarin (coumadin)

MANAGEMENT

General Management:
Positioning: Place patient horizontal with legs elevated during an acute episode.
Treat injuries from falls immediately.
Specific Treatments:
Vasovagal Syncope:
- Avoid triggers, increase salt and fluid intake, tilt training.
- Medications: Beta-blockers, SSRIs, fludrocortisone, midodrine if conservative measures fail.
Orthostatic Hypotension:
- Gradual postural changes from sitting or lying down.
- Avoid medications that lower BP (e.g., diuretics, vasodilators).
- Use compression stockings and IV fluids if needed.
- Midodrine for refractory cases.
Lower threshold for hospital presentation and admission if:
1. Syncope unwitnessed
2. Significant risk factors, including:
  - Cardiovascular disease
  - Documented or suspected arrhythmias
  - Known epileptic with greater than one seizure or without home supervision
  - Cardiac pacemaker or other devices
3. Elderly
  - Episodes have been recurrent
  - Significant injuries have occurred
  - Lack of supervision at home
4. Suspected cardiac cause:
  - Age
  - Known electrophysiological abnormalities, or previously documented malignant arrhythmias
  - Diabetes
  - newly abnormal ECG
  - Elevated troponin level
  - Significant depression of ventricular function, documented on echocardiogram
  - Documented IHD including past STEMI, non-STEMI, abnormal cardiac functional study or abnormal angiogram
5. Patients with pacemakers or other cardiac devices:
  - have a high index of suspicion in these patients for arrhythmia and / or cardiac device malfunction
  - All patients with pacemakers with unexplained collapse must be admitted until such time as their pacemaker can be checked
  - Most devices can be interrogated for a record of significant arrhythmia over an extended period of weeks
6. Suspected drug related cause

SEIZURE VERSUS SYNCOPE

Seizure is more likely if:
1. tonic-clonic movements are usually prolonged and their onset coincides with loss of consciousness
2. Hemilateral clonic movement
3. Clear automatisms such as chewing or lip smacking or frothing at the mouth (partial seizure)
4. Tongue biting (especially laterally)
5. Blue face
6. Prior to the event: aura (such as unusual smell)
7. Post-ictal confusion
8. urinary incontinence

Syncope is more likely if:
1. Tonic-clonic movements are always of short duration (<15 sec) and they start after the loss of consciousness
2. Prior to the event: Nausea, vomiting, feeling of cold, sweating (neurally-mediated)
3. short duration