Syncope
Introduction
Syncope is a very common presentation to Emergency Department (ED).
Syncope is defined as transient loss of consciousness (TLOC) due to cerebral hypoperfusion, characterized by a rapid onset, short duration, and spontaneous complete recovery. There are several different subtypes of syncope. The final pathway to all types of syncope can either be;
Vasodepressor response where hypotension leads to TLOC. (very common)
Cardio-inhibitory response where bradycardia or transient asystole leads to TLOC. (uncommon)
Types of Syncope
Vasovagal/Reflex Mediated Syncope
Certain triggers result in increased parasympathetic outflow to blood vessels = vasodilation, hypotension and bradycardia resulting in TLOC
Slow progressive onset with prodrome typically of sweating, nausea, blurred vision, light headedness
Triggers
standing for long periods, heat, intense pain, sight of blood, intense emotion
Situational vagal nerve stimulation e.g. with defaecation, micturation, coughing, swallowing.
carotid sinus hypersensitivity
Cardiac Syncope
In cardiogenic syncope arrhythmia is the primary cause of syncope. It can occur due to;
Bradycardia e.g. sinus node dysfunction, AV conduction abnormalities
Tachycardia - SVT or VT
Structural e.g. Aortic stenosis, acute ischemia, cardiomyopathy (e.g. DCM, HOCM), congenital abnormalities, cardiac mass, cardiac tamponade.
Cardiopulmonary e.g. Pulmonary embolism, pulmonary hypertension
Vascular e.g. dissection
Orthostatic Syncope
Defined by a decrease of 20 mmHg systolic and/or 10 mmHg diastolic within three minutes of standing
Syncope usually proceeded by light-headedness
Common in older adults, patients with multiple comorbidities & in polypharmacy where autonomic response to standing up may be blunted.
Common causes
Drug induced e.g. anti-hypertensives, benzodiazepines, antipsychotics, diuretics
Volume depletion e.g dehydration, haemorrhage
Primary autonomic failure e.g. Parkinson’s, multisystem atrophy
Secondary autonomic failure e.g. diabetes
Neurogenic Syncope
Rarely the primary cause of syncope
But must be considered in any patient with syncope and signs or symptoms of CNS pathology
e.g. brain stem stroke, sub arachnoid haemorrhage
Seizures may be confused with syncope as patients may often have very brief tonic clonic movements with their syncope.
Very important to take a thorough history - post ictal confusion/drowsiness, incontinence, tongue biting and epileptic aura make a diagnosis of seizure more likely
Clinical Features
Symptoms
Diaphoresis, nausea, blurred vision, tunnelling of vision, feeling lightheaded.
Cardiac
palpitations, chest pain, SOB
Neurogenic
limb weakness, headache
Signs
Pallor, Bradycardia, Hypotension, loss of responsiveness, abnormal motor response, short duration (seconds to minutes), complete spontaneous recovery.
Postural Hypotension
Lying and standing BP performed 3 minutes apart showing a drop in SBP > 20mmHg = orthostatic hypotension
Lateralizing neurological signs = concerning for neurogenic syncope
Signs of structural heart disease e.g. AS murmur, signs of CCF, HOCM
Red Flags
History of structural heart disease.
History of unexplained collapse
Family history of sudden cardiac death.
Multiple co-morbidities
Poly-pharmacy
Multiple syncopal events in short period
Seated syncopal events (cardiac unless proven otherwise)
Syncope without prodrome (cardiac unless proven otherwise)
Syncope on exertion (cardiac unless proven otherwise)
Differential Diagnosis
Cardiovascular
Heart blocks
Ischaemia
Aortic stenosis
Cardiomyopathy
Arrhythmias
Abdominal
Occult haemorrhage
ruptured ectopic, AAA, GI Bleed
Symptomatic anaemia
CNS & Psychiatry
Seizure
TIA/Stroke
Intracranial haemorrhage
Vertebral artery dissection
Psychogenic pseudosyncope
Conversion disorder
Sepsis
Sepsis/Septic shock form any source
Respiratory
Pulmonary embolism
Tension pneumothorax
Endocrine/Metabolic
Hypoglycaemia
Addison’s disease
Hyponatraemia
Hypokalaemia
Clinical Investigations
Bedside
ECG
ischaemia, arrhythmia, heart block, Brugada, QT prolongation, bradycardia
VBG
Hypoglycaemia, evidence of shock (low pH, high lactate), electrolytes, immediate Hb
BHCG
in all child bearing age females who present with syncope/presyncope
POCUS
severe cardiomyopathy, tamponade, tension pneumo, AAA, intra-peritoneal haemorrhage
Laboratory
FBC
anaemia, elevated WCC, low plts
U&E
assess hydration, renal function, deranged electrolytes
LFTs
liver disease increases risk of bleeding
Troponin
Only if acute ischaemia is suspected. Not a routine test
Radiology
CXR
if concerned about chest sepsis or cardiac cause
CT/MRI Brain
if history/exam suggest neurological cause
CTPA, CT Aortogram
if suspicious for PE or Aortic emergency
Echo
where structural heart disease is suspected
OPD Investigations
GP or OPD specialist may consider referring for OPD holter, 24 hr BP monitor, Tilt table testing, loop recorder etc
Management & Disposition
Vasovagal/Reflex Mediated Syncope
Initial Resusitation
Patients suffering from vaso-vagal / reflex syncope generally get better with lying down in supine position with the feet raised. Occasionally they might require IV access and IV fluids. If symptoms last longer than a few minutes other causes of syncope should be investigated and the patient should be moved to a monitored area.
Specific Treatment
Most of these patients improve considerably with simple lifestyle modifications which include
Keeping hydrated (at least 2000ml of water every day).
Regular meals.
Avoiding alcohol.
Exercise with focus on core muscle strengthening.
Avoiding any specific triggers.
Education regarding intervening by lying down during the prodrome
Disposition
These patients can be safely discharged home with lifestyle advice. If there is recurrence of events, there GP can refer to specialized syncope units for further investigation and treatment.
Orthostatic Syncope
Initial Resusitation
IV access and fluids if hypotension ongoing
Focused examination and investigation to ensure that haemorrhage is excluded as a cause of OH.
Specific Treatment
Treatment must be tailored to the specific cause of OH.
The primary focus in ED is to ensure that life threatening causes of OH are excluded.
Disposition
If life threatening causes e.g. haemorrhage, dehydration are excluded and the patient has fully recovered they can generally be educated regarding how best to avoid recurrence when standing up and discharged home from the ED with outpatient or close GP follow up.
OPD work up if ?autonomic dysfuntion
primary physician to rationalise medications if poly-pharmacy thought to be contributing factor
Cardiac Syncope
Initial Resusciation
All patients with suspected cardiac syncope should be on telemetry/cardiac monitor
If the patient his hypotensive, has a decreased conscious state, has evidence of acute ischaemia, sinister arrhythmia or high grade conduction block they should be moved to the resuscitation room and have cardiac monitor and defibrillation pads attached. Cardiac pacing or defibrillation might be required if this is the case.
Specific Treatment
Seek and treat underlying cause e.g. ischaemia, electrolyte abnormalities, PPM, ICD
Specialist cardiology input will be required
Disposition
All patients with suspicion of cardiac syncope need to be admitted to the hospital.
They need close cardiac monitoring for 24-48 hours at least +/- other cardiac investigations
Neurogenic Syncope
Initial Resuscitation
Patients that collapse secondary to CNS causes generally will have concurrent neuro signs and symptoms.
Low GCS - manage ABCD as clinically indicated
? Stroke - activate urgent in hospital stroke call
? SAH - urgent transfer to CT to confirm diagnosis
Specific Treatment
Seek and treat underlying cause
Disposition
As the underlying pathology for neurogenic syncope is generally sinister with high morbidity and mortality all patients with suspicion of neurogenic syncope need to be admitted to the hospital for work up.
Once the diagnosis is confirmed specialist input will be required e.g. stroke physician, neurology, neurosurgery.
References
Quinn J. Chapter 56 Syncope. Tintinalli’s Emergency Medicine; A Comprehensive Study guide
This blog was written by Dr Mustafa Mehmood and was last updated in January 2021