Differentials
Orthostatic syncope (postural or orthostatic intolerance syncope syndromes)
SIGNS / SYMPTOMS
History of fainting with concomitant dehydration, antihypertensive medication or vasodilator use, people who are older, frail, or have underlying conditions associated with autonomic failure.
Symptoms that are reproduced with carotid sinus massage (CSM) are not consistent with orthostatic syncope.
INVESTIGATIONS
Orthostatic BP measurement: a fall in BP (usually >50 mmHg systolic), associated with symptoms of syncope or near syncope. The patient may exhibit the hypotension immediately after standing or it may evolve over the subsequent 3-5 minutes of upright quiet posture. Notably, this observation may not be reliably reproduced, especially in older people. Repeated or 24-hour ambulatory measurements may be necessary to elucidate this diagnosis.
Tilt-table test: hypotension on standing.
Bradycardia
SIGNS / SYMPTOMS
Syncope is possible with long sinoatrial nodal pauses or very slow heart rates.
Occurs owing to bradycardia-induced cerebral hypoperfusion, especially in the setting of left ventricular (LV) dysfunction.
Common in patients with complete heart block and a very slow ventricular escape rhythm with LV dysfunction, and in patients with second-degree atrioventricular (AV) block.
INVESTIGATIONS
ECG: may show sinus bradycardia with or without sinus arrhythmia, AV block with junctional or ventricular escape, His-Purkinje system disease, bradycardia, and AV block in a setting of myocardial infarction; deep T-wave inversions across the precordium indicative of a neurological event may occur in conjunction with sinus bradycardia.
Electrophysiological testing: may be helpful in some cases, but the findings are usually non-specific. It may show quantitative measurement of sinus node, AV node, or His-Purkinje system dysfunction.
Bradycardia: AV conduction disorders
SIGNS / SYMPTOMS
Paroxysmal or persistent atrioventricular (AV) block can cause severe bradycardia and thereby lead to syncope.
INVESTIGATIONS
ECG: patient may have Mobitz type 2 second-degree AV block, third-degree AV block, or alternating left and right bundle branch block; other observations that suggest an AV conduction disorder as the cause of syncope, but are at best considered to be only indirect evidence, include 1) bifascicular block (left bundle branch block, right bundle branch block with left anterior or left posterior fascicular block), 2) Mobitz type 1 second-degree AV block in older people (usually defined as >70 years old).
Mobile cardiac outpatient telemetry: provides long-term ECG monitoring and thereby increases the chance of detecting ECG abnormality (i.e., AV block, possibly transient) if an arrhythmia is the cause of symptoms.
Implantable loop recording: shows evidence of AV block.
Electrophysiological (EP) testing: in the absence of a direct symptom-arrhythmia correlation, a tentative diagnosis can be made in case of ventricular pauses >3 seconds in duration when the patient is awake or if Mobitz type 2 second-degree or third-degree (i.e., complete or high-grade) AV block is discovered. In the setting of nothing more than bifascicular block or non-specific intraventricular conduction delay, invasive EP study may be helpful. On the other hand, these patients often also have underlying structural heart disease, so it is equally important to look for both the conduction abnormalities and susceptibility to tachyarrhythmias.
Supraventricular tachycardias
SIGNS / SYMPTOMS
Very rapid heart rates; infrequently causes a sufficient period of prolonged hypotension to cause syncope. Patients may complain of near syncope.
Associated with reduced circulating volume status (i.e., relative dehydration), upright posture, presence of structural heart disease (especially with diminished ejection fraction or significant valvular or other outflow obstruction), and abnormal reflexes of the peripheral vasculature.
INVESTIGATIONS
ECG: shows heart rate variability and microvolt T-wave alternans.
Holter monitoring, loop recording, or electrophysiological studies: may demonstrate findings of supraventricular tachycardias.
Ventricular tachycardia (VT)
SIGNS / SYMPTOMS
Usually occurs in setting of ischaemic heart disease, valvular heart disease, or certain dilated cardiomyopathies that may result in symptomatic hypotension; VT in obstructive cardiomyopathies and arrhythmogenic right-ventricular dysplasia may cause syncope; torsades de pointes VT is a characteristic feature of the long QT syndromes, arrhythmia may be very fast and is often self-terminating.
INVESTIGATIONS
ECG: shows wide QRS complex (≥120 milliseconds), rate >120 bpm lasting for ≥3 beats, spontaneously resolving in <30 seconds.
Echocardiogram: shows compromised left ventricular function, evidence of structural heart disease, or hypertrophic or idiopathic cardiomyopathy.
Non-sustained VT (NSVT)
SIGNS / SYMPTOMS
NSVT is a common finding during assessment of syncope (whether by Holter or extended-duration ambulatory ECG monitoring) but is diagnostically a much less specific finding than sustained VT.
INVESTIGATIONS
ECG: shows wide QRS complex (≥120 milliseconds), rate >120 bpm lasting for ≥3 beats, spontaneously resolving in <30 seconds.
Echocardiogram: absence of structural cardiac disease.
The isolated presence of NSVT, particularly in the absence of evident structural cardiac disease or ECG evidence of a channelopathy, should not be considered a causative diagnosis. However, if hypotension occurs with NSVT during electrophysiological study, or if monomorphic sustained VT is reproducibly inducible, a basis for syncope seems likely.[5]
Bradycardia or tachycardia: sinus node dysfunction
SIGNS / SYMPTOMS
Lightheadedness, weakness, palpitations, dyspnoea, angina; bradycardia; CSM provokes a sinus pause >3 seconds; heart rate does not change with Valsalva manoeuvre.
INVESTIGATIONS
ECG: shows sinus pauses >3 seconds.
Holter monitoring: indicates sinus pauses >3 seconds, which would indicate bradycardia or tachycardia-bradycardia syndrome. Used for patients with paroxysmal symptoms.
Loop recorder: shows sinus pauses >3 seconds, which would indicate bradycardia or tachycardia-bradycardia syndrome. Used for patients with paroxysmal symptoms.
Electrophysiological study: measures sinus nodal recovery time by overdrive suppression of the sinus node and sinoatrial conduction time.
Acute coronary syndromes (ACS)
SIGNS / SYMPTOMS
Chest pain, palpitations, dyspnoea, weakness, and lightheadedness.
Pale, diaphoretic; may have low BP; heart rate may be brady- or tachycardic; audible S3 or S4; jugular venous distension if right ventricular failure from inferior wall myocardial infarction; signs of congestive heart failure (CHF) such as peripheral oedema and bibasilar rales.
INVESTIGATIONS
ECG: may show ST-segment elevation or depression, dynamic T-wave changes.
Cardiac enzymes: may show elevated troponin and creatine kinase-MB.
CXR: may show increased alveolar markings; cardiomegaly. Pulmonary oedema causes increased alveolar markings and can be caused by ischaemia secondary to ACS. Cardiomegaly suggests concomitant CHF.
Echocardiography: may show wall motion abnormalities, decreased ejection fraction.
Coronary angiography: may show vessel obstruction or coronary anomalies.
Acute aortic dissection
SIGNS / SYMPTOMS
Chest and back pain, tearing in nature; hypotension; unequal pulses or BP in 2 arms; acute pulmonary oedema; focal neurological sign of weakness, dysarthria, or cranial nerve defects if carotid arteries involved.
INVESTIGATIONS
ECG: shows ST- and T-wave ischaemic changes. Cardiac ischaemia occurs if low dissection involving the coronary arteries.
CXR: will indicate widened mediastinum.
Transoesophageal echocardiography: may show false lumen or flap in the ascending or descending aorta, new aortic regurgitation, or pericardial tamponade.
CT chest with contrast: may show false lumen or flap in the ascending or descending aorta.
Severe pulmonary hypertension
SIGNS / SYMPTOMS
Dyspnoea, fatigue, chest pain, palpitations, leg oedema, right-sided third heart sound, right-sided fourth heart sound, pulmonic regurgitation, palpable left parasternal heave, jugular vein distension, peripheral oedema, cyanosis.
INVESTIGATIONS
CXR: shows attenuated peripheral vascular markings (pruning), enlarged pulmonary artery shadows, and opacification of the retrosternal space on the lateral view.
ECG findings of right ventricular hypertrophy: tall R wave and small S wave (R/S ratio >1) in lead V1, qR complex in V1, rSR' in V1, a large S wave and small R wave (R/S ratio <1) in V5 or V6, or a S1S2S3 pattern; right-axis deviation: mean frontal plane QRS axis >100°; right atrial enlargement: P wave ≥2.5 mm in leads II, III, and aVF.
Pulmonary embolism
SIGNS / SYMPTOMS
Dizziness, shortness of breath, pleuritic chest pain, tachycardia, tachypnoea, hypotension, loud P2, jugular venous distension, right ventricular lift.
INVESTIGATIONS
ECG: shows sinus tachycardia; presence of S1, Q3, and T3; usually non-specific.
D-dimer: non-specific if positive; pulmonary embolism excluded if negative. Utility is in its negative predictive value.
CXR: shows decreased perfusion in a segment of pulmonary vasculature (Westermark's sign) and/or presence of pleural effusion.
CT pulmonary angiography: identifies any thrombus in the pulmonary circulation.
Aortic stenosis
SIGNS / SYMPTOMS
Exertional dyspnoea, angina, dizziness, and syncope; in late stages develops into congestive heart failure (CHF) (dyspnoea, paroxysmal nocturnal dyspnoea, peripheral oedema); harsh ejection systolic murmur that radiates to carotids, murmur loudest at the left sternal edge and on squatting, and softer with Valsalva and isometric exercises; slow rising pulse; low carotid volume; S4 with systolic thrill; signs of CHF (pulmonary rales, lower extremity oedema, jugular venous distension, and hepatomegaly).
INVESTIGATIONS
ECG: shows left ventricular (LV) hypertrophy and/or ST depression from LV strain.
CXR: indicates cardiomegaly and/or pulmonary oedema. Aortic stenosis can cause LV hypertrophy and pulmonary oedema.
Echocardiography: assesses the valve area (severity of stenosis), mean atrioventricular gradient, LV hypertrophy, ejection fraction.
Hypertrophic obstructive cardiomyopathy
SIGNS / SYMPTOMS
Systolic ejection murmur (audible at the lower left edge; accentuated by exercise and standing; lessened by lying supine or squatting), dyspnoea, angina.
INVESTIGATIONS
ECG: shows left-axis deviation and prominent Q waves in inferior and lateral leads.
Echocardiography: shows asymmetrical septal hypertrophy; systolic anterior motion of anterior mitral valve leaflet; reversed E:A ratio with diastolic dysfunction; left atrial enlargement.
Electrophysiological studies: show inducible ventricular arrhythmias and/or conduction abnormalities.
Cardiac catheterisation: will show increased left ventricular (LV) outflow tract gradient directly related to severity of obstruction and increased LV filling pressures.
Vertebrobasilar transient ischaemic attack (TIA)
SIGNS / SYMPTOMS
Vertebrobasilar TIA is more likely than carotid-distribution TIAs to present as apparent syncopal episodes but, overall, is extremely rare. Furthermore, vertebrobasilar TIAs are usually marked by other symptoms (e.g., vertigo) indicative of posterior circulation compromise.
INVESTIGATIONS
MRI: shows brainstem infarction.
Carotid Doppler ultrasonography: shows vertebrobasilar stenosis.
CT head: brainstem not well visualised; may have chronic ischaemic changes or evidence of previous infarction. Not a sensitive test for detecting brainstem ischaemia. Commonly used modality because of widespread availability and ease of detecting haemorrhage.
Magnetic resonance angiography (MRA): shows stenosis of vertebrobasilar artery.
Subclavian steal
SIGNS / SYMPTOMS
Subclavian steal is a rare condition and a very rare cause of syncope. Symptoms tend to occur when patients are exercising using the affected arm, and BP differs between the two arms. Because of its rarity, it should be considered only when other causes have been eliminated.
INVESTIGATIONS
Duplex ultrasonography: shows retrograde blood flow in the vertebral artery.
Migraine
SIGNS / SYMPTOMS
Associated with basilar artery migraine; premonitory aura terminates in loss of consciousness, which is slow in onset; occipital headache associated with diplopia, vertigo, tinnitus, visual changes, and syncope; strong association with menstrual cycle; no significant physical finding on examination.
INVESTIGATIONS
MRI and MRA: should be normal and are used to exclude other pathologies.
Non-syncope transient loss of consciousness (T-LOC)
SIGNS / SYMPTOMS
This category mainly comprises three conditions: epilepsy, metabolic, and endocrine disturbances.
Epilepsy is predominated by abnormal movements and complex behaviour patterns; epileptic seizures do not depend on the posture and can occur while the patient is supine; epilepsy is often preceded by an aura or strange sensations, which is not the case with true syncope; after an epileptic seizure, the patient will typically be confused or may have a focal weakness, whereas after a syncopal episode the patient promptly regains their mental and physical faculties (although they may feel fatigued). Temporal lobe seizures are the form of epilepsy most often confused with syncope because they can either mimic or cause reflex bradycardia and hypotension.
Metabolic and endocrine disturbances that can cause non-syncope T-LOC include diabetic coma, hypoglycaemia, and hypercapnia.
In patients with epilepsy, an implantable loop recorder may be able to identify bradycardia or asystole as a cause of syncope. Video recordings on smart phones recorded by friends and relatives may be able to help differentiate between reflex syncope with tonic-clonic movements and true epileptic attacks.[53]
INVESTIGATIONS
Interictal electroencephalogram: may be normal.
Adrenal insufficiency, adrenal crisis
SIGNS / SYMPTOMS
Hyperpigmentation of the skin, abdominal pain, hypotension; related to stressors such as surgery.
INVESTIGATIONS
Cortisol and adrenocorticotropic hormone stimulation test: must be interpreted by an endocrinology specialist.
Diabetic hypoglycaemia
SIGNS / SYMPTOMS
Known diabetes with neuroglycopenic and sympathoadrenal signs and/or symptoms (irritability, shaking, sweating, tremor, palpitations, tachycardia, anxiety, nausea, hunger, pallor).
Seizure and loss of consciousness are signs of severe hypoglycaemia.
INVESTIGATIONS
Serum glucose: low.
Non-diabetic hypoglycaemia
SIGNS / SYMPTOMS
Neuroglycopenic and sympathoadrenal signs and/or symptoms (irritability, shaking, sweating, tremor, palpitations, tachycardia, anxiety, nausea, hunger, pallor).
Seizure and loss of consciousness are signs of severe hypoglycaemia.
No history of diabetes, but may have other known condition associated with hypoglycaemia, or use of non-diabetic, hypoglycaemic medication.
INVESTIGATIONS
Serum glucose: low.
Seizures
SIGNS / SYMPTOMS
Prolonged jerky movements, tongue biting, urinary or faecal incontinence, prolonged post-ictal period.
INVESTIGATIONS
Electroencephalogram: shows epileptiform activity or focal, localising abnormality.
Prolactin level: must be interpreted by a neurology specialist.
Alcohol ingestion
SIGNS / SYMPTOMS
Vomiting, staggering gait, slurred speech.
INVESTIGATIONS
Alcohol level: high or positive.
Stroke
SIGNS / SYMPTOMS
Focal neurological deficit, slurred speech, prolonged reduction in awareness.
INVESTIGATIONS
Head CT: shows hypoattenuation (darkness) of the brain parenchyma; loss of grey/white matter differentiation, and sulcal effacement; hyperattenuation (brightness) in an artery indicates clot within the vessel lumen.
MRI brain: shows acute ischaemic infarct.
Narcolepsy
SIGNS / SYMPTOMS
Excessive daytime sleepiness despite adequate sleep.
INVESTIGATIONS
Overnight polysomnogram: often shows snoring, frequent awakenings, reduced sleep efficiency, periods of rapid eye movement (REM) sleep within the first 20 minutes of sleep, and multiple arousals.
Sleep latency test: shows sleep latency ≤8 minutes plus ≥2 sleep-onset REM periods.
Cataplexy
SIGNS / SYMPTOMS
Loss of muscle tone, often triggered by strong emotions, slurred speech, knee buckling, without loss of awareness.
INVESTIGATIONS
Sleep history.
Sleep actigraphy.
Polysomnogram.
Sleep latency test.
All must be interpreted by specialists in the relevant field.
Pseudosyncope
SIGNS / SYMPTOMS
Generalised anxiety disorder, panic disorder, somatisation disorder, and major depression can present with apparent syncope; usually young; no known cardiac problems; frequent episodes of recurrent syncope (as high as many episodes per day or per week); no specific exam findings.
INVESTIGATIONS
Tilt-table test: negative.
Video electroencephalogram: result must be interpreted by a neurology specialist.[43]
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