Syncope: Assessment of Transient Loss of Consciousness

Introduction

Syncope is transient loss of consciousness due to global cerebral hypoperfusion, defined by rapid onset, short duration and spontaneous complete recovery. All four elements matter: something that is gradual, prolonged, or requires intervention to reverse is not syncope.

It is extremely common - around 40% of people experience at least one episode in their lifetime - and accounts for approximately 1-3% of emergency department attendances. The great majority of cases are benign reflex syncope, requiring reassurance and simple advice.

The clinical task, therefore, is not to explain every faint. It is to identify the small proportion in whom syncope is the warning sign of a condition that can kill: ventricular arrhythmia, complete heart block, severe aortic stenosis, hypertrophic cardiomyopathy, pulmonary embolism or aortic dissection. Everything about the assessment is designed around that separation.

Classification and causes

Reflex syncope

A triggered reflex causes inappropriate vasodilatation, bradycardia, or both, so that blood pressure falls below the threshold for cerebral perfusion.

• Vasovagal syncope - the classic faint. Triggered by prolonged standing, heat, emotional distress, pain, venepuncture or the sight of blood. There is almost always a prodrome.
• Situational syncope - triggered by coughing, micturition (classically a middle-aged man rising at night), defecation, swallowing, or laughter. The common mechanism is a Valsalva-like reduction in venous return combined with vagal activation.
• Carotid sinus hypersensitivity - typically in older men, triggered by head turning, shaving or a tight collar. Diagnosed by carotid sinus massage under monitoring, which reproduces the response.

Orthostatic hypotension

A sustained fall in blood pressure on standing, defined as a drop of 20 mmHg systolic or 10 mmHg diastolic within 3 minutes of standing. Covered in more detail in the article on postural hypotension.

• Drugs - the commonest cause. Antihypertensives, diuretics, alpha-blockers, nitrates, antidepressants, antipsychotics, dopaminergic agents and alcohol.
• Volume depletion - dehydration, haemorrhage, vomiting, diarrhoea, over-diuresis
• Autonomic failure - primary (Parkinson's disease, multiple system atrophy, pure autonomic failure) or secondary (diabetes, amyloidosis, uraemia, B12 deficiency)
• Adrenal insufficiency
• Deconditioning and prolonged bed rest

Cardiac syncope

The group that matters. Cardiac syncope carries a substantially increased risk of death and is the reason syncope is taken seriously.

• Arrhythmia - ventricular tachycardia, complete heart block, sick sinus syndrome with pauses, supraventricular tachycardia with a very rapid rate, long QT syndrome, Brugada syndrome, and pacemaker or ICD malfunction
• Obstructive structural disease - severe aortic stenosis (classically exertional syncope), hypertrophic obstructive cardiomyopathy, mitral stenosis, prosthetic valve thrombosis, and atrial myxoma (positional syncope)
• Ischaemia - acute coronary syndrome may present with syncope, particularly in older patients
• Cardiopulmonary and vascular - massive pulmonary embolism, aortic dissection, cardiac tamponade, and pulmonary hypertension

The history

The history establishes the diagnosis in most cases and is far more valuable than any investigation. Structure it around before, during and after, and always seek a witness account - by telephone if necessary. The patient cannot describe what happened while unconscious, and the witness description of duration, colour and movement is often decisive.

Before

• Position - standing, sitting or lying. Syncope while lying down or sitting is a red flag and points towards a cardiac cause, since reflex and orthostatic mechanisms require an upright posture.
• Activity - during exertion suggests aortic stenosis, HOCM or exercise-induced arrhythmia and is a red flag. After exertion is more often vasovagal.
• Trigger - prolonged standing, heat, a crowded room, pain, emotion, venepuncture, coughing, micturition, head turning, or a sudden loud noise (which suggests long QT type 2)
• Prodrome - nausea, sweating, feeling hot, tunnel or greying vision, tinnitus and light-headedness suggest reflex syncope. Palpitations beforehand suggest an arrhythmia. Chest pain suggests ischaemia, PE or dissection.
• No warning at all - a red flag for arrhythmia, and often the reason the patient has injured themselves

During

• Duration of unconsciousness - syncope is typically seconds; loss of consciousness beyond a few minutes suggests seizure or another cause
• Colour - pallor is characteristic of syncope; cyanosis and a flushed appearance favour seizure
• Movement - brief myoclonic jerking occurs in up to 90% of syncopal episodes and does not indicate epilepsy. The distinction is that syncopal jerking is brief, irregular, arrhythmic and begins after the collapse, whereas a tonic-clonic seizure has sustained rhythmic clonic activity, often lasting a minute or more, that begins with or before the fall.
• Tongue biting - lateral tongue biting is highly specific for seizure. Biting the tip of the tongue is much less discriminating.
• Incontinence - occurs in both and is not useful for distinguishing them, contrary to common teaching
• Eyes - typically open in seizure, and may be closed in psychogenic attacks
• Injury - facial injury or injury without protective reflexes suggests loss of consciousness without warning

After

• Recovery time - rapid and complete recovery within seconds to a minute is characteristic of syncope. Prolonged confusion, drowsiness and disorientation lasting many minutes to hours (a post-ictal state) strongly favours seizure.
• Residual symptoms - fatigue and nausea are common after vasovagal syncope; headache and myalgia after a seizure
• Focal neurological deficit - Todd's paresis after seizure, or a stroke

Background

• Previous episodes - frequency, pattern and whether the current episode felt the same
• Cardiac history - ischaemic heart disease, heart failure, valve disease, cardiomyopathy, previous arrhythmia or a device
• Full drug history - antihypertensives, diuretics, rate-limiting drugs, and any QT-prolonging drug
• Family history of sudden cardiac death under 40, unexplained drowning, or an unexplained single-vehicle road traffic collision - this question is easily forgotten and can be the most important one asked
• Occupation and driving - a professional driver or someone working at height changes the urgency and the advice given

Examination and initial investigations

Examination

• Lying and standing blood pressure - measured lying, then at 1 and 3 minutes standing. Mandatory in every patient.
• Blood pressure in both arms - a differential suggests aortic dissection
• Pulse - rate, rhythm and character. A slow-rising pulse suggests aortic stenosis.
• Cardiac examination - murmurs (particularly an ejection systolic murmur radiating to the carotids in aortic stenosis, or the murmur of HOCM that increases with Valsalva), a third or fourth heart sound, and signs of heart failure
• Neurological examination - focal deficits, and signs of Parkinson's disease or peripheral neuropathy suggesting autonomic failure
• Signs of anaemia, dehydration or gastrointestinal bleeding - including a rectal examination if occult bleeding is suspected
• Evidence of injury, including head injury and fractures
• Carotid sinus massage - in patients over 40 with unexplained syncope, performed with continuous ECG and blood pressure monitoring, and avoided if there is a carotid bruit or previous stroke or TIA

Investigations for every patient

• 12-lead ECG - the single most important test. Look for conduction disease, pre-excitation, a prolonged QT, Brugada pattern, ventricular hypertrophy, Q waves from previous infarction, and evidence of arrhythmia.
• Capillary blood glucose
• FBC - anaemia and gastrointestinal bleeding
• U&Es - electrolytes and volume status

Further investigations, guided by suspicion

• Echocardiogram - where structural heart disease is suspected clinically or from the ECG
• Ambulatory ECG monitoring - matched to symptom frequency: 24-hour Holter for daily symptoms, patch or event recorder for weekly to monthly, and an implantable loop recorder for infrequent syncope with red flags. The loop recorder is the investigation of choice for recurrent unexplained syncope of suspected arrhythmic origin.
• Exercise tolerance test - for exertional syncope
• Tilt table testing - where reflex or orthostatic syncope is suspected but the diagnosis remains uncertain. It is not a first-line test.
• Troponin and D-dimer - only where acute coronary syndrome or pulmonary embolism is clinically suspected, not routinely
• CT head - only if there is a focal neurological deficit, head injury with concerning features, or suspicion of subarachnoid haemorrhage. Routine CT after uncomplicated syncope has a very low yield.
• EEG - only where epilepsy is genuinely suspected on the history, not to exclude it after a typical faint
• Electrophysiological study and genetic testing - in selected patients with suspected arrhythmia or inherited disease

Risk stratification

Differential diagnosis

Other conditions to consider include hypoglycaemia (gradual onset, sweating, no rapid spontaneous recovery without treatment), stroke or TIA (focal deficit, rarely causing isolated loss of consciousness), subarachnoid haemorrhage (thunderclap headache), intoxication, falls without loss of consciousness (particularly in older people, where the distinction is often blurred), and cataplexy (loss of tone with preserved consciousness, triggered by emotion, in narcolepsy).

Management

Reflex syncope

Explanation and reassurance are the main treatment. Patients are frequently frightened, and understanding the mechanism substantially reduces recurrence and anxiety.

• Recognise and avoid triggers - prolonged standing, hot environments, dehydration, missed meals, alcohol
• Recognise the prodrome and act on it - lie down immediately with the legs elevated, or sit and put the head between the knees. Do not try to "walk it off".
• Physical counter-pressure manoeuvres - leg crossing with tensing, handgrip, and arm tensing at the onset of symptoms. These raise blood pressure and can abort an episode, and teaching them is effective.
• Increase salt and fluid intake where not contraindicated
• Review and reduce culprit medication - antihypertensives, diuretics, alpha-blockers and nitrates
• Compression stockings in selected patients
• Midodrine or fludrocortisone - occasionally used in severe recurrent reflex syncope under specialist supervision
• Pacing - reserved for the small number with documented severe cardioinhibitory carotid sinus hypersensitivity or a proven asystolic response with recurrent syncope

Orthostatic hypotension

Review and rationalise medication first, restore volume, encourage slow position changes, raise the head of the bed at night, use compression garments, and consider fludrocortisone or midodrine where non-pharmacological measures fail. Treat the underlying autonomic or endocrine cause.

Cardiac syncope

Treat the underlying cause, and admit for monitoring where an arrhythmia is suspected.

• Bradyarrhythmia - permanent pacemaker
• Ventricular arrhythmia - treat the substrate, consider an implantable cardioverter defibrillator
• Supraventricular tachycardia - drug therapy or catheter ablation
• Severe aortic stenosis - syncope is one of the triad of symptoms mandating valve replacement, and marks a poor prognosis without intervention
• Hypertrophic obstructive cardiomyopathy - risk stratify for sudden death and consider an ICD; avoid vasodilators and dehydration
• Pulmonary embolism, aortic dissection or tamponade - treat as the emergency it is

Red flags

Prognosis

Prognosis is determined by the cause, and the difference between the groups is stark.

Reflex syncope carries no excess mortality. It is benign in prognostic terms, and the main morbidity is from injury during episodes and from the anxiety and restriction that recurrent unexplained collapse causes. Recurrence is common but often reduces once the patient understands the mechanism and learns counter-pressure manoeuvres.

Orthostatic hypotension carries an intermediate prognosis. It is associated with increased mortality, largely reflecting the comorbidity and frailty of the patients in whom it occurs, and it is an important cause of falls and fractures in older people.

Cardiac syncope carries a substantially increased mortality, with historical series reporting one-year mortality of the order of 20-30%, again largely attributable to the underlying cardiac disease. This is the entire justification for the assessment pathway: identifying this group and treating the cause changes outcome, whereas extensive investigation of a classic vasovagal faint does not.

Unexplained syncope in the absence of structural heart disease and with a normal ECG carries a good prognosis. Where red flags are present but no diagnosis has been reached, prolonged monitoring with an implantable loop recorder is worthwhile, since a proportion will have an intermittent arrhythmia that is treatable once documented.