Syncope

Introduction

  • 1-2% of ED visits 
  • 6% of hospital admissions
  • Near-syncope shares the same pathophysiological processes and may carry the same risks
  • Syncope in the preceding year is the best predictor of recurrence


What features define Syncope?

  • Loss of consciousness, complete loss of motor tone
  • Transient, results in full spontaneous recovery
  • Return to NORMAL conscious state
  • Annual incidence
    • 2% if over 80yo
    • 1.1% if 70-79
    • 0.5% if <70yo
  • No specific age group predominates 
  • Elderly patients with syncope have the greatest morbidity associated with it
  • Prevalence in general population is 19% 
  • 50% of patients that present to ED are admitted, most admitted patients are > 65 years old
  • 15% of children experience at least one episode of syncope
  • Patients with known cardiovascular disease and syncope are greatest risk of mortality

Most cases of syncope are benign, the goal of clinical assessment is to identify any features that might suggest underlying sinister cause

Pathophysiology

  • Common pathway is about 10 seconds of complete disruption of blood flow or nutrient delivery to both cerebral cortices or the reticular activating system, or reduction in cerebral perfusion by 35-50%
  • Even with exhaustive investigation the cause remains unknown in around 40% (60% after ED-only investigations)
  • Risk of death
    • Cardiac syncope 2x
    • Neurologic syncope 1.5x 
    • Syncope of unknown cause 1.3x
  • Vasovagal syncope carries no increased risk of death

Causes

  1. Neurally Mediated (reflex) – 21%
    • Vasovagal Syncope
      • Emotion
      • Pain
      • Instrumentation
      • Valsalva 
    • Situational Syncope
      • Carotid sinus sensitivity (necktie/shaving syncope)
      • Post-exercise
      • GI syncope (swallowing, vomitting, defecating)
      • Post-micturition 
  2. Orthostatic Hypotension Mediated – 9%
    • Volume Depletion
    • Autonomic Failure (diabetes)
    • Drug-Induced
      • Beta-blockers
      • Erectile dysfunction drugs
      • Other anti-hypertensives
      • Anti-arrhythmics 
      • Antiparkinsons drugs
      • Antipsychotics 
  3. Cardiovascularly Mediated – 10% 
    • Dysrhythmia 
      • Tachycardia
        • SVT
        • VT
        • VF
        • WPW
        • Torsades de pointes
        • Arrhythmogenic RV Cardiomyopathy
      • Bradycardia
        • Sick sinus syndrome
        • 2nd/3rd degree AV block
        • Trifascicular Block
      • Prolonged QT
      • Brugada syndrome
      • PPM malfunction
      • ICD malfunction
    • Pulmonary Embolus (obstructive shock)
    • Aortic Stenosis – Critical AS (obstructive shock)
    • Aortic Dissection (Rare) 
    • HOCM
    • Pulmonary HTN
    • Cardiac Tamponade (unlikely to be transient)
    • CVA involving the brainstem (rare)
  4. Other Disorders need to be considered in syncope
    • Vertigo
    • Seizures
    • Hypoglycaemia
    • Psychiatric Disorders (50% in young adults)

Cardiac syncope

  • Most dangerous with 6 month mortality >10%
  • Structural
    • Valvular heart disease (AS/TS/MS)
    • Cardiomyopathy
    • Pulmonary HTN
    • Congenital heart disease
    • Myxoma
    • Pericardial disease
    • Aortic dissection
    • PE
    • Myocardial ischaemia
    • MI
  • Dysrhythmic
    • Brady – Short or long QT, Stokes-Adams, Sinus node disease, second or third-degree HB, pacemaker malfunction
    • Tachy – VT, torsades, SVT, Afib/flutter
  • Always consider AS in the elderly
    • Classic chest pain, dyspnoea on exertion and syncope
  • Dysrhythmic syncope is typically sudden and without prodromal symptoms

Syncope ECG

  • Ischaemia
  • Tachy/Brady/Block
  • WPW
  • Long QT
  • ARVD – Epsilon V1/2/3 + TWI
  • Brugada – V1/2 Saddleback/coved ST elevation with TWI
  • HCM
    • Dagger Q waves laterally and inferiorly
    • High-voltages
    • Tall R wave in V1
    • Mortality 3.5%/year
    • Familial in 55%

Vasovagal syncope

  • Form of reflex-mediated syncope associated with inappropriate vasodilatation, bradycardia or both as a result of inappropriate vagal or sympathetic tone
  • Prodrome of lightheadedness +- nausea, pallor, sweating and feeling of warmth may accompany syncope
  • Slow, progressive onset with associated prodrome is suggestive of vasovagal syncope
  • Situational syncope occurs after coughing, micturition, defecation or swallowing

Carotid sinus hypersensitivity

  • Another type of reflex-mediated syncope
  • Bradycardia and/or hypotension
  • External pressure on abnormally sensitive carotid body results in:
    • Abnormal vagal response (bradycardia and asystole of >3 seconds) AND/OR
    • Vasodepressor response (decrease in BP >50mmHg without bradycardia)
  • Both responses may occur simultaneously
  • More common in men, elderly and in those with ischaemic heart disease, HTN and certain head and neck malignancies
  • Consider in older patients with recurrent syncope and negative cardiac evaluations
  • Can only be definitively diagnosed if clinical hypersensitivity is reproducible and event was associated with an inciting event e.g. shaving/turning head

Orthostatic syncope

  • Postural hypotension with syncope or presyncope
  • Symptom onset is usually within 3 minutes of upright position, but can be delayed in some patients
  • Positive orthostatic changes are seen in 40% of asymptomatic patients >70yo and 25% of those under 60 so orthostasis does not always result in syncope
  • Causes include intravascular volume loss, poor vascular tone or medications
  • Always consider other life-threatening causes, especially in the elderly, as they too may be contributing to orthostatic changes

Psychiatric disorders

  • Found in 40% of those with vasovagal syncope and 62% of those with unexplained syncope
  • Generalised anxiety and major depression most commonly
  • Hyperventilation can lead to syncope through hypocarbia and cerebral vasoconstriction
  • Patients tend to be younger, with repeated episodes of syncope and multiple prodromal symptoms
  • Diagnosis of exclusion

Neurologic syncope

  • Symptoms must be transient with no persistent neurological deficits to meet definition of syncope
  • Brainstem ischaemia, vertebrobasilar atherosclerotic disease and basilar artery migraine may all cause transient decreases in blood flow to the RAS leading to sudden, brief episodes of LOC
  • Typically LOC is preceded by blurred vision, vertigo, focal neurological deficits or nausea
  • Subclavian steal syndrome
    • A rare cause of brainstem ischaemia due to abnormal narrowing of subclavian artery proximal to origin of vertebral artery so that with exercise of the ipsilateral arm, blood is shunted from the vertebrobasilar artery to the subclavian artery to the arm
    • More common on the left and may have reduced pulse volume and BP on affected side
  • Subarachnoid haemorrhage
    • Usually has associated focal neurological deficits, headache or persistent ALOC
    • Can get transient rise in ICP with concomitant reduced CPP and thus get true syncope in rare cases
  • Seizure
    • Most commonly confused diagnosis but a clear history should delineate from other causes of syncope
    • Prodromal aura, post-ictal confusion and muscle ache suggests seizure
    • Prodromal vasovagal symptoms suggest vasovagal
    • Urinary incontinence is not helpful
    • Witnessed head turning, shaking or unusual posturing suggests seizure

Medication syncope

  • Most common means of syncope is orthostasis (especially in elderly)
  • Erectile dysfunction drugs
  • Antihypertensives
  • Beta-blockers and CCB
  • Digoxin
  • Diuretics
  • Proarrhythmic agents may cause dysrhythmias
  • Antipsychotics
  • Antiparkinsonism drugs
  • Antidepressants
  • Phenothiazines
  • Nitrates
  • Alcohol
  • Cocaine

Assessment

Key history

  • Associated events
    • On standing -> Orthostatic
    • Micturition/venepuncture
    • Emotional event
    • Prior episodes
  • Prodromal symptoms
    • Seeing stars, nausea, diaphoresis suggests vagally-mediated
    • Absence suggests cardiac
  • Patient position
    • Lying/sitting concerning for cardiac
    • Upon standing or prolonged standing suggests orthostatic
  • Chest pain – MI, AS, dissection, PE
  • Palpitations – Arrhythmia
  • SOB – PE, CCF, AS
  • Headache – SAH
  • Abdominal or back pain – Ruptured AAA, perforated viscous or ectopic pregnancy
  • No prodrome and events associated with exertion – Cardiac, AS, HOCM
  • Turning head, shaving or neck compression – Carotid sinus hypersensitivity
  • Onset with single limb exercise – Subclavian steal syndrome
  • Previous episodes
    • >5 episodes per year = more likely vasovagal or psychiatric than dysrhythmia
  • Medications and drugs
  • FHx – Brugada, short/long QT, arrythmogenic RV dysplasia, sudden cardiac death, HOCM
  • Special attention to single-car MVA (frequently elderly driving off road) as focus is on trauma when cause may be syncopal
  • Rate of recovery
    • Immediate (<1min) – Vagal or cardiac
    • Slow neurological recovery – Possible post-ictal after seizure

Examination

  • Assess for trauma – If no evidence of protecting themselves, consider sudden LOC i.e. cardiac (but can be seen in both)
  • Bilateral BP – Subclavian steal, dissection
  • Orthostatic BP after 5 min in supine position measured at 1 and 3 minutes after standing
    • Symptomatic drop of >20mmHg is significant as is any drop below 90 independent of symptoms
  • Heart sounds
  • Focal neurological
  • PR testing for GI bleeding

ECG

  • New or old LBBB, LAFB or LPFB or QRS widening are 3.5x more likely to be associated with morbidity
  • Non-sinus rhythms are 2.5x more likely to be associated with morbidity
  • Identifies diagnosis in 5% of syncope
  • Abnormal ECG in patient without obvious cause of syncope has OR of 8 for serious cardiac arrhythmia

Specific diagnoses

  • Ischaemia
  • Arrhythmia
  • Major conduction defect
  • HOCM
  • Ventricular pre-excitation
  • LV strain due to aortic disease
  • Brugada
  • RV dysplasia
  • Prolonged QTc >470ms (>500ms associated with significant outcomes)
  • Short QTc <350ms

Carotid massage

  • Potentially indicated in patients with symptoms suggestive of carotid sinus syndrome
  • Can massage each carotid body for 5-10 sec
  • Positive if symptoms reproduced in presence of asystole >3 seconds or decrease in SBP >50mmHg
  • Do not perform if known carotid stenosis, bruits presents or <3mo hx of stroke or MI or hx of VT or VF
  • Needs informed consent
  • Deficits lasting >24 hours occur in 0.1% of patients
  • Most patients with positive test do NOT have true carotid sinus syndrome so given low risk but potentially catastrophic complications, usually not performed

Hyperventilation manoeuvre

  • Open-mouthed, slow, deep breaths at 20-30/min for 2-3 min with recurrence of prodromal symptoms or syncope significantly correlates with psychiatric causes of syncope

Risk stratification

High risk features for ‘cardiac’ syncope

  • Onset – No prodromal symptoms or while sitting
  • >55yo (OR 5.4)
  • Hx of CCF (OR 3-5) or CAD
  • Ventricular ectopy
  • Abnormal ECG
  • FHx of SCD
  • Significant trauma from syncopal episode

Canadian Arrhythmia syncope risk score

  • Predisposition to vasovagal – -1 points
  • Hx of heart disease – 1
  • SBP <90 or >180 – 1
  • Raised Tn – 2
  • QRS axis <-30 or >100 – 1
  • QRS >130ms – 1
  • QTc >480ms -1
  • ED diagnosis of vasovagal – -2 points
  • ED diagnosis of cardiac syncope – 2 points
  • Score and risk of serious outcome in 30 days (%)
    • -3: 0.4
    • -2: 0.7
    • -1: 1.2
    • 0: 2
    • 1: 3
    • 2: 5
    • 3: 8
    • 4: 13
    • 5: 20
    • 6: 29
    • 7: 40
    • 8: 53
    • 9: 65
    • 10: 76
    • 11: 84

Risk factors for arrhythmias or death at 1 year (Martin et al.)

  • Hx of arrhythmia
  • Hx of CCF
  • Abnormal ECG
  • Age >45

San Francisco Syncope Rule (Quinn et al.)

  • Adverse outcomes at 7 and 30 days with 89% sensitivity and 52% specificity for death at 1 year if 1 of below high risk features:
    • Hx of CCF
    • Abnormal ECG (any new change or non-sinus rhythm – if never seen before, any abnormality at all)
    • Hct <30
    • SOB
    • SBP <90 in the ED
    • Any 1 of above = 12% risk of serious outcome at <7 days (sens 85-95%; speci 50-60%)
  • Note:
    • Isolated PAC, 1st degree AV block likely non-significant across other studies
    • Isolated RBBB, isolated LAFB, frequent PAC’s and the odd PVC are also less worrisome but not entirely okay

OESIL score

  • Age >65
  • Hx of CVD (IHD, CCF, Cerebrovascular or PVD)
  • Abnormal ECG (ischaemia, arrhythmias, prolonged QT, AV block or BBB)
  • Absence of typical prodrome

Other risk factors to consider

  • FHx of sudden cardiac death
  • Syncope while supine
  • Syncope during exercise
  • Syncope without prodromal symptoms
  • Palpitations preceding syncope
  • Age >60 or >65 (no specific age cut-off but <45 is clearly low risk if no other factors present)

Risk stratification (Cameron)

High riskLow risk
Chest pain consistent with IHDAge <45
Hx of CCFOtherwise healthy
Hx of ventricular dsyrhythmiaNormal ECG
Pacemaker, defib dysfunctionNormal CV exam
Age >60Prodrome consistent with vasovagal
Abnormal ECG

Disposition

  • Admission for monitoring is under question as to its utility
  • Echo should be performed in those with known or suspected structural heart disease
    • Usually abnormalities are clinically apparent and will seldom be found in those with normal cardiac exam and ECG
  • Stress testing may be used to identify exercise-induced dysrhythmias or ischaemia or reproduce exertional syncope once HOCM is ruled out
  • EP studies reserved for documented dysrhythmias, preexcitation or underlying cardiac disease
  • Admission criteria
    • Organic cause found
    • Monitored bed if:
      • Suspected cardiac arrhythmia
      • >1 unexplained syncopal episode in last 48 hours
    • Short stay if unsupervised social situation

Outpatient investigation

  • Implantable loop recorders
    • >50% yield for recurrent syncope
  • Tilt table testing
    • Recommended for recurrent, unexplained syncope
    • Identifies reflex-mediated syncope
  • Psychiatric referral
    • For young patients without underlying heart disease who have frequent syncopal events
  • Prolonged QT
    • Referral for genetic testing for LQTS gene
    • If gene negative, patients at very low risk of fatal syncope
  • EEG
    • If suspected seizure

Prognosis

  • No excess of mortality if no underlying heart disease
  • Highest mortality in those with CCF
  • 1/3 of those with syncope and structural heart disease will die within 12 months
  • Mortality rate at 12 months is 25% if cardiac cause vs. 6% if uncertain cause

The elderly

  • There is a gradual continuum of increased risk with increasing age
  • Cardiovascular risk factors are better predictors of poor outcome than age itself
  • Incidence of vasovagal syncope actually decreases with age due to decreased responsiveness of the autonomic nervous systems
  • Less sensitive thirst mechanism and decreased endocrine response to hypovolaemia, exacerbating orthostatic hypotension
  • Postprandial hypotension is more common in the elderly (esp. nursing home residents) due to rapid rate of delivery from stomach into small intestine
  • Baseline hypertension, atherosclerosis and valvular disease also contribute to cerebral hypoperfusion
  • Increased risk of cardiac disease, ischaemia, MI, AS
  • Diabetes leads to autonomic dysfunction and peripheral neuropathy
  • Medication use is far more common with increased risks of orthostasis and decreased autonomic responsiveness to orthostatic stress

Pregnant women

  • Gravid uterus may impair IVC return
  • Incidence of cardiac dysrhythmias (especially PVC’s) increases during normal pregnancy
  • No positive correlation between presyncope or syncope and cardiac dysrhythmia in pregnant women
  • Consider ruptured ectopic and PE in all pregnant women

Syncope vs. seizure

  • Syncope has tongue biting on tip if any
  • Eyes deviate upwards in syncope vs to side in seizure
  • Duration of unconsciousness in syncope <1 min vs. >2 minutes in seizure
  • Post-event confusion <5 min in syncope vs. >5 min in seizure
  • Post-event pulse rate usually slow in syncope (unless tachycardia is cause)

Last Updated on December 20, 2021 by Andrew Crofton