Syncope iman

1. Approach to Patient with
Syncope
Iman Sulaiman Al-Hatmi

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.

11. Causes

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.

25. Cardiac causes
arrhythmia
Structural
TachycardiaBradycardia
Ventricular tachycardiaSick sinus syndromeAortic stenosis
Ventricular fibrillationAtrioventricular (AV)
block
HOCM
Torsade de pointes VTDrug-inducedPulmonary embolus
Supraventricular
tachycardia
Pulmonary hypertension
Atrial fibrillation/flutterAcute myocardial
infarction
Tamponade
Aortic dissection

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.

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

30. How to approach syncope??

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)

40. PHYSICAL EXAM
 NECK
 Bruits
 JVP (CHF, MI, PE,
tampnade)
 HEART
 Murmur (valves, dissection)
 Rub (pericarditis,
tamponade)
 LUNGS
 Sounds may help
distinguish CHF, infection,
pneumothorax

41. PHYSICAL EXAM
 ABDOMEN
 Pulsatile mass; AAA
 Tenderness
 Occult blood loss
 PELVIS
 Bleeding, hypovolemia
 Tenderness (PID, ectopic,
torsion, sepsis)
 SKIN
 Signs of trauma,
hypoperfusion
 EXTREMITES
 Paralysis (CNS)
 Pulses unequal (dissection,
embolus)

42. PHYSICAL EXAM
 NEUROLOGIC
 Mental status; toxic
metabolic; organic disease;
seizure; hypoxia.
 Focal findings
(hemorrhagic/ischemic
stroke, trauma, tumor, or
other primary neurologic
disease
 Cranial nerves
 Cerebellar testing

43. ECG
WPW
sinus bradycardia ventricular tachycardia
Prolonged QT interval

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