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Syncope

Definition
O Syncope is a transient lost of

conciousness due to transient global


cerebral hypoperfusion characterized
by rapid onset, short duration, and
spontaneous complete recovery.
O The adjective pre-syncopal is used to
indicate symptoms and signs that
occur before unconsciousness in
syncope, making it asynonym of
warning and prodromal.
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Causes
O Vascular (62%)
O Reflex (neurally-mediated) syncope
O Vaso-vagal (mediated by emotional and

orthostatic stress)
O Situational (cough, sneeze, GI
stimulation, post-micturition, postexercise, post-prandial)
O Carotic sinus syncope

Causes (cont.)
O Orthostatic hypotension
O Primary autonomic failure
O Secondary autonomic failure

(diabetes, spinal cord injury, uremia)


O Drug-induced orthostatic hypotension
(alcohol, vasodilator, diuretic,
antidepressant)
O Volume depletion (hemorrhage,
diarrhea, vomiting)
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Causes (cont.)
O Cardiac syncope (10%)
O Arrhythmia
O Bradycadia (AV conduction system malfunction,

nodal dysfunction)
O Tachycardia (supraventricular, ventricular)
O Drug induced bradycardia and tachycardia
O Inherited syndrome: Long QT syndrome, Brugada
syndrome
O Structural
O Valvular disease, Acute MI, HOCM, atrial myxoma,

cardiac tamponade, prosthetic valve dysfunction.


O Others: pulmonary embolism, aortic dissection,
pulmonary hypertension.
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Causes (cont.)
O Neurological (5%)
O Migraine or TIA(vertebrobasilar origin)

O Toxic or metabolic (2%)


O Anti-arrhythmic causing pro-arrhythmic

effect
O Anti-hypertensive causing orthostatic
hypotension
O Hypoglycemia
O Psychiatric (1.5%)
O Idiopathic (14%)
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Pathophysiology

Transient insufficiency of global cerebral nutrient flow.


Transient reduction of blood oxygen.
Transient decrease in arterial BP.
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O In healthy young people, cerebral blood flow

represents 12% to 15% of resting cardiac


output.
O A sudden cessation of cerebral blood flow for
only 6 to 10 seconds is sufficient to cause
complete loss of consciousness.
O Syncope occurs due to global cerebral
hypoperfusion. Brain parenchyma depends
on adequate blood flow to provide a
constant supply of glucose, the primary
metabolic substrate. Brain tissue cannot
store energy in the form of high-energy
phosphates found elsewhere in the body.
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O Cerebral perfusion is maintained relatively

constant by an intricate and complex


feedback system involving cardiac output,
systemic vascular resistance, arterial
pressure, intravascular volume status,
cerebrovascular resistance with intrinsic
autoregulation, and metabolic regulation. A
clinically significant defect in any one of
these or subclinical defects in several of
these systems may cause syncope.

Emergencies in
syncope
O Myocardial infarction
O Cardiac arrhytmias
O Aortic dissection
O Cardiac tamponade
O Hypoglycemia
O Addisons disease
O Massive pulmonary embolism

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O 2007 American College of

Emergency Physicians (ACEP) Clinical


Policy on Syncope lists history and
physical examination and 12-lead
ECG as their only current level A
recommendations.

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History
O Precipitating factor (e.g sleep or food

deprivation, warm ambient environment,


alcohol consumption, pain, and strong
emotions such as fear or apprehension.)
O Activity prior to syncope (at rest, change
of posture, on exertion, coughing,
voiding or prolonged standing)
***Syncope happens within 2 minutes of
standing suggest orthostatic hypotension
O Standing? Sitting? Lying?
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Hx (cont.)
O Was lost of consciousness complete?
O Was LOC with rapid onset and short

duration?
O Was recovery spontaneous, complete
and without sequelae?
O Was postural tone lost?

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Hx (cont.)
O Symptoms (pre-syncope)
O Dizziness
O Light-headedness
O Vertigo
O Weakness
O Diaphoresis
O Epigastric discomfort
O Nausea
O Blurred vision
O Pallor
O Paresthesias
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Hx (cont.)
O Syncope vs seizure?
O LOC in syncope about seconds to 1

minutes
O Seizure- post-event confusion, oral
trauma, incontinence, myalgias
O Witnesses
O Convulsive activity, automatismsseizure

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Hx (cont.)
O Medical Hx (drugs that reduce blood

pressure, affect CO, prolong QT


interval, altered sensory system,
alter serum electrolytes)
O Family Hx (MI, arrhytmias, valvular
heart disease, cardiomyopathies,
CHF)
O Other differentials of syncope (Hx of
seizures, diabetes, stroke,
pregnancy)

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Physical examination
O Vital signs
O CVS and Respiratory system examination

(arrhythmias, valvular heart disease,


signs of CCF, carotids stenosis)
O CNS examination
O Signs of Trauma
O Hallpike maneuver (video)
O Tilt Table test (video)
O Carotid sinus massage
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Investigation
O Serum glucose level
O FBC
O Renal Profile
O Cardiac enzyme
O Chest X-ray
O Electrocardiogram
O Echocardiogram
O Holter monitoring
O Stress test
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O Carotid sinus massage has been used with some success

to diagnose carotid sinus syncope.


O Patients are placed on a cardiac monitor and beat-to-beat
BP monitoring device. Atropine is kept at the bedside.
O Longitudinal massage lasting 5 seconds is initiated at the
point of greatest carotid pulse intensity at the level of the
thyroid cartilage on one side at a time.
O The maximal response occurs after approximately 18
seconds, and a positive result is one that produces 3
seconds of asystole or syncope. If the result is negative,
the process is repeated on the other carotid sinus.
O Carotid sinus massage may theoretically precipitate an
embolic stroke in persons with preexisting carotid artery
disease.
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San Francisco Syncope Rule


O The San Francisco syncope rule was developed to

identify patients at risk of a serious outcome within


30 days of presentation and needing admission to
hospital.
O Five criteria (CHESS) used to calculate the San

Francisco syncope rule are:


O Congestive heart failure history
O Haematocrit <30%
O New changes on ECG
O Shortness of breath
O Systolic BP <90 mmHg at triage.
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***Patients with any one risk factor had a 15.2% risk of


serious outcomes.

O Serious outcome was defined as:


O Death
O Myocardial infarction
O Arrhythmia
O PE
O Stroke
O Significant haemorrhage
O Any condition causing a return visit to the

emergency department and admission to


hospital for a related event.
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