Syncope

Marcella O Callaghan
Syncope vs. presyncope
 Syncope: transient loss of consciousness followed by spontaneous
and complete recovery 
 Syncope forms a large component of ED presentations annually –
740,000 ED visits in the US and up to 250,000 admissions 
 Near-syncope less well documented due to variety of descriptors
‘lightheaded, dizzy, hot and cold, spells’
 Near syncope: ‘light-headedness derived from feeling an impending
loss of consciousness’
 Important to remember that the physiology behind both syncope
and presyncope are the same and dependent on underlying patient
comorbidities, medications and concurrent illness 
Types of syncope
 Neurally mediated
 Cardiogenic
 Orthostatic/BP related
Neurally mediated
 AKA ‘reflex’ syncope which is brief LOC secondary to a drop in BP +-
a reduced HR.
 Typically will have prodromal features e.g. sweating, visual
disturbance, light-headed, weak
 3 main categories:
 Vasovagal e.g. secondary to seeing blood, pain, prolonged standing,
emotional stress, phobia of needles
 Situational e.g. urination, straining, after lifting a heavy weight, coughing
 Carotid sinus – massage of carotid sinus results in syncope
 Treatment includes lifestyle changes, avoidance techniques, education
on prodrome, school education
Cardiogenic
 Arrhythmias
 SVT, VT, WPW syndrome, long QT
 Structural
 HOCM, dissection, pericardial tamponade, AS, PE
 Rare cardiac causes:
 Subclavian steal, beta blocker induced, sick sinus syndrome
Supraventricular tachycardia

Ventricular tachycardia

WPW syndrome

WPW syndrome

Long QT

Orthostatic hypotension
 Excessive BP drop by standing up > 20mmHg systolic or diastolic of >
10mmHg after 3 minutes of standing
 Resultant effect is blood pooling, reduced cardiac output and reduced
cranial flow of blood supply = LOC
 Typical causes include medications, dehydration, bleeding, infection
 Medication culprits: beta blockers, diuresis, anticholinergics, anti-
hypertensives
 Degenerative damage to the autonomic nervous system can result in
orthostatic syncope e.g. Parkinsons, amyloidosis, diabetes
Orthostatic hypotension
 Typically symptoms occur upon standing e.g. light-headed, weakness,
tiredness, palpitations, sweatiness

 Diagnosis:
 Confirmed measuring BP after lying flat x 5 minutes by measuring BP at 1
minute, then 3 minutes. HR should also be measured
 A drop of > 20mm Hg systolic or diastolic > 10mmg Hg is confirmatory
 Active stand may also be used to further evaluate which type (initial, classic,
delayed)

 Treatment: increase salf/water, compression stockings, certain medication

if confirmed diagnosis and ongoing syncopal events, medication
reconciliation
Other BP related issues
 Central nervous system ischemia
 TIA/stroke
 Vertebro-basilar arterial disease
 Subarachnoid haemorrhage
History taking – key points
 Preceding symptoms or lack thereof
 Sweating, dizzy, hot flush, visual disturbance, weak, nausea
 Vs. sudden onset; no warning
 Situation e.g. standing, sitting, driving, reaching upwards, positional
 Trauma – fall with headstrike? Injury? Anticoagulation?
 Witnessed vs. unwitnessed (collateral)
 Recovery period
 Vomiting after head injury
 Seizure like activity
 Confusion
 Total recovery or not?
Seizure vs. syncope
 Can resemble each-other
 Common in seizures: tonic-clonic/convulsive movements, post-ictal
state, urinary/bowel incontinence, tongue biting
 None of these are specific to seizures however and certain syncopal
events can look quite convincing for seizure-like activity – history
taking is key/collateral!
 Difference between an explained syncope and ?? seizure is huge for
the patient in terms of driving/career and returning to driving
 Involve the syncope AMAU service
Exam findings – key points
 Vital signs
 Cardiovascular:
 CCF signs
 Murmur
 Arrhythmia
 Prior CABG scan, pacemaker etc.
 Lying and standing BPs
 Respiratory
 Dyspnoea
 Oxygen requirement
 Abdominal:
 AAA/dissection – bilateral BPs, femoral pulses, pulsatile mass
 Neurology! – NB if headstrike and to differentiate from other pathology e.g.
Investigations
 Lying and standing BPs
 Bloods: blood sugar, U&Es, FBC
 ECG
 CXR – pneumonia, pneumothorax, wide mediastinum
 Depending on suspected cause:
 Troponin/BNP/ECHO/Cardiology
 D dimer +- CTPA
 AMAU referral/active stand/R test
 CT brain to outrule haemorrhage
 Seizure/TIA workup
How to risk stratify
 Risk stratification tools:
 San Francisco Syncope rule: (SFSR)
 CHESS mnemonic
 C – history of congestive heart failure
 H – haematocrit < 30%
 E – abnormal ECG
 S – shortness of breath
 S – triage systolic BP < 90mmHg
 Any of the above results in high risk of serious adverse outcomes
including death, MI, arrhythmia, PE, stroke, SAH, significant
haemorrhage
Presyncope vs. syncope
 2018: Comparison of 30-day serious adverse clinical events for
elderly patients presenting to the emergency department with near-
syncope vs. syncope
 3,581 patients > 60 years old included in retrospective cohort study
from ED presentations with both presyncope/syncope
 Key finding: similar rates of 30-day clinical event in older adults
with either syncope or ‘near syncope’ as their presenting complaint
 Study suggested that treating physicians should treat older adults
with near syncope and syncope as the same presenting complaint
Conclusion
 Syncope is a common ED presentation and can have serious
causes that need to be considered
 Good history taking and examination is essential
 Consider the CHESS San Francisco Syncope Rule to assist in a
decision with regard to admission vs. home
 Involve the AMAU Syncope pathway early where possible
 Presyncope and syncope carry the same mortality rate and 30-day
adverse outcomes in patients > 60 years old
Thank you 
 Any questions?