APPROACH TO SYNCOPE

BY ABD RAHIM
 DEFINITION
• Syncope is defined as TLOC due to cerebral
hypoperfusion, characterized by a rapid onset,
short duration, and spontaneous complete
recovery.
• TLOC is defined as a state of real or apparent
LOC with loss of awareness, characterized by
amnesia for the period of unconsciousness,
abnormal motor control, loss of
responsiveness, and a short duration
 CONT..
• presyncope is used to indicate symptoms and
signs that occur before unconsciousness in
syncope
 Epidemiology
• 20-50% of adults experience at least one episode of
syncope during their lifetime.
• 3% of visits to emergency departments
• 6% of all admissions to hospital
• Relatively of tenaged under 18 years.
• 23% in elderly patients in all age groups
• 15% in children aged over 70.
• prevalence and incidence of syncope increase with
advancing age with a 30% recurrence rate
 Classification
TLOC TRAUMATIC

NON TRAUMATIC

SYNCOPE EPILEPTIC SEIZURE PSYCOGENIC RARE CAUSES

Subclavian steal
Reflex syncope, Generalized –tonic, Pseudosyncope, syndrome,
orthostatic hypotension, clonic , tonic-clonic, psycogenic non-epileptic vertebrobasilar TIA,
cardiac Atonic seizure(PNES) SAH, cyanotic breath,
holding spell
 Pathophysiology
• Due to global cerebral hypoperfusion.
• A sudden cessation of cerebral blood flow for as short
as 6–8 s can cause complete LOC. A systolic BP of 50–
60 mmHg at heart level, i.e. 30–45 mmHg at brain
level in the upright position, will cause LOC
• Decreased cerebral perfusion may occur as a result of
decreased cardiac output or decreased systemic
vascular resistance.
• 35% reduction in cerebral blood flow will cause
syncope.
 Cont..
3 PHASES
1. Prodrome
• Sweating, epigastric discomfort, weakness,
nausea,dizziness
• Lasts about 2 minutes
2. LOC- Usually lasts 5-20 seconds
3. Post syncopal pahase:
• Nausea, dizziness, general sense of poor health
• If present, confusion which lasts no more than 30
seconds
 How to approach syncope??
HISTORY (key),
alone identifies the cause up to 85% of the time
• Patient or an Eyewitness
• Before/During and After the event
• The Clinical Background
 Syncope: Important Historical
Features
• Questions about circumstances before the attack
• Position-supine, sitting or standing
• Activity-change in posture, exercise, urination,
defecation, cough, swallowing.
• Predisposing factors-crowds, high temperature,
prolonged standing, postprandial .
• Precipitants-fear, intense pain, neck movements
 Cont..
• Questions about onset of the attack
• Nausea, emesis, aura, abdominal pain,
sweating, blurred vision and dizziness
• Palpitations
• Chest pain
 Cont..
Questions about attack (eye witness)
• Way falling-slumping or kneeling
• Skin color (pallor, cyanotic)
• Duration of loss of consciousness
• Movements ( tonic-clonic, etc.)
• Tongue biting
• Breathing pattern
Questions about the end of the attack
• Nausea, vomiting, sweating, feeling cold, muscle aches,
• confusion, skin color, wounds, chest pain, palpitations, urinary or
fecal incontinence
 Cont..
Questions about background
• Number and duration of syncope spells (Recurrent
• episodes)
• Family history of arrhythmic disease or sudden death
• Presence of cardiac disease
• Neurological disease (Parkinson, epilepsy,narcolepsy)
• Metabolic Disorders (Diabetes)
• Medications (Hypotensive and antidepressant agents)
 Physical Examination
Vital signs • Heart rate
• Orthostatics—most Tachy/brady, dysrhythmia
important • Respiratory rate
• Drop in BP and fixed HR Tachypnea (PE, hypoxia,
->dysautonomia anxiety)
• Drop in BP and increase HR • Bradypnea (CNS,
-> volume depletion/ toxicmetabolic)
vasodilatation • Blood pressure
• Temperature • High (CNS, toxic/metabolic)
Hypo/hyperthermia (sepsis, • Low (hypovolemia,
toxic-metabolic, exposure) cardiogenic shock, sepsis)
 Cont..
• NECK ABDOMEN
Bruits • Pulsatile mass; AAA
JVP (CHF, MI, PE,tamponade) • Tenderness
• HEART
• Occult blood loss
Murmur (valves, dissection)
PELVIS
Rub (pericarditis,tamponade)
• LUNGS • Bleeding, hypovolemia
Sounds may help • Tenderness (PID,
distinguish CHF, infection, ectopic, torsion, sepsis)
pneumothorax
 SKIN NEUROLOGIC
• Signs of trauma, • Mental status; toxic
hypoperfusion metabolic; organic disease;
seizure; hypoxia.
EXTREMITES • focal findings
• Paralysis (CNS) (hemorrhagic/ischemic
• Pulses unequal stroke, trauma, tumor, or
(dissection,embolus) other primary neurologic
disease
• Cranial nerves
• Cerebellar testing
• Blood tests when clinically indicated, e.g.
haematocrit or haemoglobin when haemorrhage
is suspected
• oxygen saturation and blood gas analysis when
hypoxia is suspected
• troponin when cardiac ischaemia-related
syncope is suspected
• D-dimer when pulmonary embolism is
suspected, etc.
 Additional examination
• ECG- suspicious of cardiac syncope
• Carotid sinus massage (CSM) in patients aged
>40 years.
• Head-up tilt testing when there is suspicion of
syncope due to OH or reflex syncope
 CSM
• ventricular pause lasting >3 s and/or a fall in systolic BP
of >50mmHg is known as carotid sinus hypersensitivity.
• Carotid sinus hypersensitivity is a common finding in
older men without syncope;
• abnormal responses are frequently observed (<_40%) in
patients without syncope, especially if they are older
and affected by cardiovascular disease.
• The specificity of the test increases when spontaneous
reproduce syncope during CSM
 Orthostatic challenge
• Changing from the supine to the upright
position produces a displacement of blood
from the thorax to the lower limbs and
abdominal cavity that leads to a decrease in
venous return and cardiac output.
• In the absence of compensatory mechanisms,
a fall in BP may lead to syncope
 Head-Up Tilt Test (HUT)
• Useful as diagnostic test for
patients suspected of having
vasovagal (VVS) syncope.
• Useful in teaching patients to
recognize prodromal symptoms.
• Lying the pt on a table that is
then tilted to angle of 60 for up
to 45min with monitoring of
ECG& BP.
• +ve test if profound bradycardia
(cardio-inhibitory response) & or
hypotension (vasodepressor
response)
 Valsalva manoeuver
• There is strong evidence that the absence
of a BP overshoot and an absence of a HR
increase during the Valsalva is
pathognomonic for neurogenic OH,
• expiration usually correlate with the
degree of autonomic dysfunction
• and related symptoms. In contrast, a
pronounced BP fall beyond what is
normally expected during forced
expiration,
• but a normal chronotropic response
during the manoeuvre, may occur in
• patients with suspected situational
syncope, i.e. syncope occurring during
some forms of singing, and weightlifting,
coughing, playing brass instrument
 General principle of Treatment
• Based on risk stratification and identification
of specific mechanisms when possible.
• Non pharmacological
Education, lifestyle modification, and
reassurance regarding the benign nature of the
condition.
• Physical counter pressure manoevers
 Cont..
• Discontinuation/reduction of vasoactive drugs
(Anti-HPT, nitrates, diuretics, neuroleptic, anti-
depressants, or dopaminergic drugs).
 Pharmacological
• Drug therapy (resistant cases):
• Fludrocortisone (Na & water retention,
expand plasma volume)
• Midodrine (vasoconstrictor alfa-adrenoceptor
agonist)
Thank You