2. Outline
Definition of syncope
Characteristics
Epidemiology
Pathophysiology
Causes & Management
How to approach syncope??
3. Definition
Syncope: transient loss of consciousness
associated with absence of postural tone,
followed by complete and usually rapid
spontaneous recovery.
Pre-syncope: “Lightheadedness where
individual thinks that he or she may black out”.
4. Characteristics
Relatively rapid onset
Variable warning symptoms : light headed, dizzy,
sweating, nausea, blurred vision or feel hot.
Spontaneous, complete, recovery without medical
or surgical intervention
Absence of prolonged confusion
Underlying mechanism is a transient global
cerebral hypoperfusion !!
5. “The only difference between syncope
and sudden death is that in one you
wake up”.
Is It Significant ?
6. 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 often in all age groups
15% in children aged under 18 years.
23% in elderly patients aged over 70.
prevalence and incidence of syncope increase with
advancing age with a 30% recurrence rate
7. Pathophysiology
Normal conscious awareness depends on the
integrated function of the ascending reticular
activating system (ARAS) in the upper brainstem
and the cerebral hemispheres.
Any condition that interrupts
activity in the brain centers (the
brainstem and both hemispheres)
will result in LOC
8. Pathophysiology
Cerebral perfusion is maintained relatively
constant by:
cardiac output
systemic vascular resistance
mean arterial pressure
intravascular volume status
cerebrovascular resistance with intrinsic
autoregulation
metabolic regulation
9. Pathophysiology
Due to global cerebral hypo-
perfusion.
A cessation of cerebral
perfusion lasting only 3-5
seconds can result in 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.
12. Neurally Mediated Reflex Syncope
Vasovagal syncope
Carotid sinus syndrome
Situational syncope
No increased risk for
cardiovascular morbidity
or mortality associated
with reflex mediated
syncope.
13. Vasovagal (neurocardiogenic) syncope
(VVS)
Most common cause of
syncope in young adults
Precipitating event is
often identifiable
Stress, trauma, pain, sight
of blood, prolonged
standing, heat exposure
Patients with VVS younger
than Carotid sinus
syndrome patients
Age range teens to elderly
with mean 43 years
Pallor, nausea, sweating,
palpitations are common
14. Haemodynamic and autonomic changes
characteristic of neurocardiogenic syncope
Arthur W , Kaye G C Postgrad Med J 2000;76:750-753
15. Cont..
3 PHASES
Prodrome
Sweating, epigastric discomfort, weakness, nausea,
dizziness
Lasts about 2 minutes
Loss of consciousness
Usually lasts 5-20 seconds
Postsyncopal phase
Nausea, dizziness, general sense of poor health
If present, confusion which lasts no more than 30
seconds
16. 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 70 for up
to 45min with monitering of
ECG& BP.
+ve test if profound
bradycardia (cardio-inhibitory
response) & or hypotension
17. Treatment
Life style modification:
Salt supplementation
Avoid prolonged standing, dehydration or missing
meals
Drug therapy (resistant cases):
Fludrocortisone (Na & water retention, expand plasma
volume)
B blocker (inhibit initial sympathatic)
Disopyramide (vagolytic agent)
Midodrine (vasoconstrictor alfa-adrenoceptor agonist)
18. Situational Syncope
abnormal or hypersensitive autonomic reflex response to a
specific physical stimulus; may be a component of increased
intracranial or intrathoracic pressure leading to decreased
cerebral perfusion.
urination
defecation
swallowing
Coughing
Mechanoreceptors are present throughout the body (in the
bladder, rectum, esophagus, and lungs), and it is thought that
the sudden activation of a large number of these receptors
also sends afferent signals to the brain, which provokes a
similar response
19. Carotid Sinus Syndrome (CSS)
Carotid sinus hypersensitivity (CSH)
Baroreceptor is senstive to external pressure, so
that pressure over carotid a. causes an
inappropriate & intense vagal discharge.
Syncope related to head turning,
shaving, wearing a tight collar
Pathophysiology
Carotid sinus pressure causes a reflex decrease in
heart rate and blood pressure
CSH predominantly affects older males
20. Carotid sinus massage
Place the patient in the supine position with the neck slightly
extended for a minimum of 5 minutes before carotid sinus massage
is applied.
Massage over the point of maximal carotid impulse, for 5 seconds
on both sides, with a 1-minute interval between massages.
Continuously monitor ECG and blood pressure.
A positive result if any of:
Asystole exceeding 3 seconds (cardioinhibitory response)
Reduction in systolic BP exceeding 50 mm Hg (vasodepressor
response)
Combination of the above (indicates mixed CSH)
Contraindications
Carotid bruit, known but significant carotid arterial disease, previous
21. Treatment of CSH
Most patients can be treated with education,
lifestyle changes & routine follow-up.
Pharmacotherapy. However, no single agent
has been proven to provide long-term
effectiveness in large-scale randomized
controlled trials
Daul-chamber pacing (prevent syncope in pts
with more common cardio-inhibitory response)
22. SAFE PACE
Syncope And Falls in the Elderly – Pacing And Carotid
Sinus Evaluation
Objective
Determine whether cardiac pacing
reduces falls in older adults with
carotid sinus hypersensitivity
Randomized controlled
trial (N=175)
Adults > 50 years, non-accidental
fall, positive CSM
Pacing (n=87) vs. No Pacing
(n=88)
Results
More than 1/3 of adults over 50
years presented to the Emergency
Department because of a falls have
CS hypersensitivity
With pacing, falls 70%
Syncopal events 53%
Injurious events 70%
Kenny RA. J Am Coll Cardiol. 2001;38:1491-1496.
23. Orthostatic Hypotension
Drop in BP: 20 systolic or 10 diastolic within 3 minutes of standing
Present in 40% of patients over 70 years old
May be due to
Drugs (very common) .. Diuretics, vasodilators, antidepressants
Neurologic damage (autonomic failure) ..Parkinson, DM
When vertical,
blood follows
gravity and
pools
Increased
sympathetic
tone
counteracts this
If the response
is inadequate,
syncope occurs
24. Cardiac Syncope
Two basic types
Dysrhythmia
mediated
Structural
cardiopulmonary
lesions
Both cause the
heart to be unable
to sufficiently
increase cardiac
output to meet
demand
Double the risk of
mortality compared with
other syncopal patients.
Up to 50% mortality.
Patients with underlying
cardiac disease are at
greatest risk for cardiac
syncope. Only 3% have
no previous heart
disease.
Cardiac arrythymias
especially in the elderly
have high mortality.
26. Cont..
Key to establish a diagnosis of arrhythmias is to obtain
an ECG recording during symptoms.
Holter monitor, ambulatory ECG device for continuously
monitoring various electrical activity of the CVS for at
least 24 hours (helpful only if Sx. Occur several
times/wk)
Implementable ‘loop recorder’ continuously records
cardiac rhythm and will activate automatically if extreme
brady/tachycardia occurs.
27.
28.
29. Differential Diagnosis of Syncope:
Seizures vs Hypotension
Observation Seizure Inadequate
Perfusion
Onset Sudden More gradual
Duration Minutes Seconds
Jerks Frequent Rare
Headache Frequent (after) Occasional (before)
Confusion after Frequent Rare
Incontinence Frequent Rare
Eye deviation Horizontal Vertical (or none)
Tongue biting Frequent Rare
Prodrome Aura Dizziness
EEG Often abnormal Usually normal
31. Cont..
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
32. 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
33. Cont..
Questions about onset of the attack
Nausea, emesis, aura, abdominal pain, sweating,
blurred vision and dizziness
Palpitations
Chest pain
34. 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
35. 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)
36. Clinical Features Suggesting
Specific Cause of Syncope
Neurally-Mediated Syncope
Absence of cardiac disease
Long history of syncope
After sudden unexpected, unpleasant sensation
Prolonged standing in crowded, hot places
Nausea vomiting associated with syncope
During or after a meal
With head rotation or pressure on carotid sinus
After exertion
37. Clinical Features Suggesting
Specific Cause of Syncope
Syncope due to orthostatic hypotension
After standing up
Temporal relationship to taking a medication that can
cause hypotension
Prolonged standing
Presence of autonomic neuropathy
After exertion
38. Clinical Features Suggesting
Specific Cause of Syncope
Cardiac Syncope
Presence of structural heart disease
With exertion or supine
Preceded by palpitations
Family history of sudden death
39. PHYSICAL EXAM
Vital signs
Orthostatics—most
important
Drop in BP and fixed HR -
>dysautonomia
Drop in BP and increase
HR -> volume depletion/
vasodilatation
Temperature
Hypo/hyperthermia (sepsis,
toxic-metabolic, exposure)
Heart rate
Tachy/brady, dysrhythmia
Respiratory rate
Tachypnea (PE, hypoxia,
anxiety)
Bradypnea (CNS,
toxicmetabolic)
Blood pressure
High (CNS, toxic/metabolic)
Low (hypovolemia,
cardiogenic shock, sepsis)
44. Investigations
ECG---Cornerstone of workup (for all pts)
Arrhythmia, long Qt, WPW, conduction abn.
Routine Blood work—limited value
Radiology---limited value except if abnormal exam
ECHO
Neurologic studies (head CT , MRI , EEG )
Other tests—depending of history and exam
Glucose --hemoglobin --troponin
Ua/culture--CK (syncope vs seizure)
45. Case 1
A 23-year-old nurse presents for evaluation after
having
had five episodes of syncope at work during the
previous three months. All the episodes occurred
while
she was standing and were characterized by a
feeling of
light-headedness lasting one to two seconds and
then
an abrupt loss of consciousness. Two of the
episodes
46. Case 2
A 68-year-old woman with advanced Alzheimer’s
disease and hypertension was admitted to the
hospital after she had a syncopal episode in her
house. The patient was in her usual state of
health until she suddenly collapsed while
standing and lost consciousness for
approximately 2 minutes. She recovered
spontaneously but was too weak to stand and
complained of pleuritic chest pain & dyspnea
47. Case 3
An 18-year-old woman presents to the
emergency department after experiencing a
syncopal event 2 days ago. She does not
recall any chest pain, shortness of breath,
palpitations, or dizziness prior to event. She
denies any past medical problems (except for
a similar syncopal episode with exertion in the
past). She reports that her younger brother
had a similar episode of syncope in the past.
On examination, the patient's vital signs are
normal. ECG done …..
48. References
Davidson ,principles and practice of medicine ,21th edition
Oxford handbook of clinical medicine ,8th edition.
http://pmj.bmj.com/content/76/902/750.full
http://ezproxy.squ.edu.om:2265/contents/reflex-
syncope?source=related_link.
http://apps.mcc.ca/Objectives_Online/objectives.pl?lang=engl
ish&role=expert&id=106#Top
Editor's Notes
(LQTS) is a congenital disorder characterized by a prolongation of the QT interval on electrocardiograms (ECGs) and a propensity to ventricular tachyarrhythmias, which may lead to syncope, cardiac arrest, or sudden death.
Normal QT interval 0.38-0.42 s
