3. • Syncope(SING-kə-pee) is a transient,
self-limited loss of consciousness
with loss of postural tone due to
acute global impairment of cerebral
blood flow.
• The onset is rapid, duration brief,
and recovery spontaneous and
complete without medical or
surgical intervention.
4. • Other causes of transient loss of
consciousness need to be
distinguished from syncope.
• These include
seizures, vertebrobasilar
ischemia, hypoxemia, and
hypoglycemia
8. Features of Neurally Mediated
Syncope
• dizziness, lightheadedness, and
fatigue, premonitory features of
autonomic activation may be
present. These include diaphoresis,
pallor, palpitations, nausea,
hyperventilation, and yawning.
9. • During the event proximal and
distal myoclonus (typically
arrhythmic and multifocal) may
occur, raising the possibility of
epilepsy.
• The eyes typically remain open and
usually deviate upward. Urinary but
not fecal incontinence may occur.
10. Treatment: Neurally
Mediated Syncope
• Reassurance
• avoidance of provocative stimuli
• plasma volume expansion with fluid
and salt are the cornerstones of the
management of neurally mediated
syncope.
11. • Isometric counterpressure
maneuvers of the limbs (leg
crossing or handgrip and arm
tensing).
• Fludrocortisone, vasoconstricting
agents, and beta-adrenoreceptor
antagonists are widely used by
experts to treat .
12. Orthostatic Hypotension
• Orthostatic hypotension, defined as
a reduction in systolic blood
pressure of at least 20 mmHg or
diastolic blood pressure of at least
10 mmHg within 3 minutes of
standing or head-up tilt on a tilt
table.
13. Features
• It is a manifestation of sympathetic
vasoconstrictor (autonomic) failure .
• light-headedness, dizziness, and
presyncope (near-faintness)
• Visual blurring may occur, likely due
to retinal or occipital lobe ischemia.
• Patients may report orthostatic
dyspnea
14. • Neck pain—typically in the
suboccipital, posterior cervical, and
shoulder region (the "coat-hanger
headache") most likely due to neck
muscle ischemia, may be the only
symptom.
• Symptoms may be exacerbated by
exertion, prolonged standing,
increased ambient temperature, or
meals
15. Treatment: Orthostatic
Hypotension
• The first step is to remove
reversible causes—usually
vasoactive medications .
• Nonpharmacologic interventions
should be introduced.
16. Nonpharmacologic interventions
• patient education regarding staged
moves from supine to upright
• warnings about the hypotensive
effects of meal ingestion
• instructions about the isometric
counterpressure maneuvers that
increase intravascular pressure (see
above).
• Intravascular volume should be
expanded by increasing dietary fluid
and salt.
17. • If these nonpharmacologic
measures fail, pharmacologic
intervention with fludrocortisone
acetate and vasoconstricting agents
such as midodrine and
pseudoephedrine should be
introduced.
18. Cardiac Syncope
• Cardiac (or cardiovascular) syncope
is caused by arrhythmias and
structural heart disease.
• Both cause the heart to be unable to
sufficiently increase cardiac output
to meet demand.
• Cardiac arrythymias especially in the
elderly have high mortality.
20. Diagnostic Objectives
• Distinguish true syncope from
syncope mimics
• Determine presence of heart disease
• Establish the cause of syncope with
sufficient certainty to:
– Assess prognosis confidently
– Initiate effective preventive treatment.
22. A Diagnostic Plan is
Essential
•Initial Examination
–Detailed patient history
–Physical exam
–ECG
–Supine and upright
blood pressure
•Monitoring
–Holter
–Event
–Insertable Loop Recorder (ILR)
•Cardiac Imaging
•Special Investigations
.
23. Diagnostic Flow
Diagram Initial Evaluation
Syncope Not Syncope
Certain Suspected Unexplained
Diagnosis Diagnosis Syncope
Cardiac Neurally-Mediated or Frequent or Severe Single/Rare Confirm with
Likely Orthostatic Likely Episodes Episodes Specific Test or
Specialist
Consultation
Cardiac Tests for Neurally- Tests for Neurally- No Further
Tests Mediated Syncope Mediated Syncope Evaluation
+ - + - + -
Re-Appraisal Re-Appraisal
Treatment Treatment Treatment Treatment
24. HISTORY
• HISTORY alone identifies the cause
up to 85% of the time
• POINTS
– Previous episodes
– Character of the events, witnesses
– Events preceding the syncope
– Events during and after the episode
25. HISTORY
• Events preceding the • Events during and
syncope after the episode
– Prolonged standing – Trauma (implication
(vasovagal) important)
– Immediately upon – Chest pain (CAD, PE)
standing (orthostatic) – Seizure (incontinence,
– With exertion (cardiac) confusion, tongue
– Sudden without warning laceration, postictal
or palpitations (cardiac) behavior)
– Aggressive dieting – Cerebrovascular
– Heat exposure syndrome (diplopia,
dysarthia, hemiparesis)
– Emotional stress
– Associated with
n/v/sweating
(vasovagal)
26. HISTORY
• Associated symptoms • Medications
– Chest pain, SOB, – Antihypertensives,
lightheadedness, diuretics (orthostatic)
incontinence
– Antiarrthymics (cardiac
• Past medical history syncope)
– Identifying risk factors – TCA, Amiodarone
– Morbidity and mortality (cardiac/prolonged QT)
increases with organic
causes • Family history
• Parkinsons (orthostatic) – Sudden death (cardiac
• Epilepsy (seizure) syncope/prolonged QT
• DM (cardiac, autonomic or Brugada)
dysfunction, glucose)
• Cardiac disease
27. PHYSICAL EXAM
• Vital signs
– Orthostatics—most – Heart rate
important • Tachy/brady,
• Drop in BP and fixed dysrhythmia
HR ->dysautonomia – Respiratory rate
• Drop in BP and • Tachypnea (pe,
increase HR -> volume hypoxia, anxiety)
depletion/ • Bradypnea (cns,
vasodilatation toxicmetabolic)
• Insignificant drop in BP – Blood pressure
and marked increase in
HR -> POTS • High (cns,
toxic/metabolic)
– Temperature • Low (hypovolemia,
• Hypo/hyperthermia cardiogenic shock,
(sepsis, toxic- sepsis)
metabolic, exposure)
31. • EKG---Cornerstone of workup
– Arrhythmia, long qt, WPW, conduction abn.
• Routine Blood work—limited value
• Radiology---limited value except if
abnormal exam
• Other tests—depending of history and
exam
– Glucose --hemoglobin --troponin
--CK (syncope vs seizure)
32. Starting the ―Workup‖
• If young adult and No comorbid
conditions or symptoms
Most likely VASOMOTOR or ORTHOSTATIC .
*Clinicians may forego the ECG in young,
healthy patients with an obvious cause of
syncope.
33. Young adult, no
comorbidity, normal
ECG, absent orthostatics
• Vasomotor • Neurologic
– Try carotid massage – CT head (tia, cva, sah)
• (+) carotid sinus – EEG (if suspect Sz)
sensitivity
• (-) reflex or
• Cardiovascular
neurocardiogenic – If Outflow obstruction,
check CT chest, Echo
• Metabolic (PE, valvular, HOCM)
– Check chemistry. – If venous return, check
R/O hypoglycemia, HCG, Echo (pregnancy,
adrenal tamponade)
insufficiency
34. The ECG
Key Points
• Guidelines recommend EKG in the
evaluation of all patients with syncope.
• Exception: young healthy patients with
an obvious cause of syncope
• Abnormal ECG in 90% of patient with
cardiac syncope
• Only 6% of patients with reflex mediated
syncope have abnormal ECG.
• Syncopal patient with negative cardiac
history and normal ECG—unlikely to have
a cardiac cause
35. The ECG
patient older, +comorbid
signs/symptoms
• If Abnormal ECG
– Ischemia/injury
– Dysrhythmia
• Sinus brady, BBB, AV block, prolonged
QT, WPW, HOCM, Brugada
• If Normal ECG
– Consider holter or event recorder if
dysrhythmia suspected
36. Carotid Sinus Massage
(CSM)
• Method1 • Absolute
– Massage, 5-10 seconds contraindications2
– Don’t occlude – Carotid bruit, known
– Supine and upright significant carotid
posture arterial
(on tilt table) disease, previous
CVA, MI last 3 months
• Outcome
• Complications
– 3 second asystole
and/or 50 mmHg – Primarily neurological
fall in systolic BP with – Less than 0.2%
reproduction of – Usually transient
symptoms = Carotid
Sinus Syndrome
37. Holter Monitoring
• 24-48 hour monitor—limited value
because of intermittent nature of
arrhythmias
• Event recorder—more helpful. Patient
must be conscious in order to activate
unit.
• Establishes diagnosis in only 2-3% of
patients with syncope if ECG is normal.
• Indicated in patients at highest risk for
arrhythmia ie, abnormal ecg,
palpitations, cad history, syncope when
supine or with exertion.
38. Loop Event Recorders
• Provides longer monitoring—weeks to
months
• Can activate the monitor after symptoms
occur, thereby freezing in its memory the
readings from the previous 2-5 minutes
and the subsequent 1 minute
• In patients with recurrent
syncope, arrhythmias were found during
symptoms in 8-20%.
• Limitations: compliance, use of
device, transmission
39. ECHOCARDIOGRAM
• Access structural causes of cardiac
syncope
– AS, MS, HOCM, atrial myoxoma
• Unlikely to be helpful in the absence of
known cardiac disease or an abnormal
ekg.
• INDICATIONS
– Abnormal ECG ---history of heart
disease
– Murmur ---exercise assoc.
syncope
40. Structural Heart Disease
• Aortic Stenosis
– Most common structural lesion
associated with syncope in the elderly
• Hypertrophic Obstructive
Cardiomyopathy
– Vasodilatation (drugs/hot bath) can
induce syncope
• Obstruction to Right Ventricular
Outflow
– PE, pulmonary stenosis, pulmonary htn
41. EXERCISE STRESS TEST
• Syncope during exercise is more likely to
be related to an arrhythmia
• Post-exertional syncope is usually
neurally mediated.
• Echocardiogram should be done prior to
EST to r/o structural abnormality.
• INDICATION
– Syncope during or shortly after exercise
(exertional syncope)
42. TILT TABLE TEST
• Changes in position to
reproduce symptoms
of the syncopal event.
• Positive tilt table test
– Induction of bradycardia
and hypotension
– Considered diagnostic
for vasovagal syncope
43. Indications for Tilt table
test
• Unexplained • Identification of
recurrent syncope or neurally mediated
syncope associated syncope could alter
with injury in absence treatment
of structural heart ds.
• Evaluation of
• Unexplained
recurrent syncope or recurrent
syncope associated unexplained falls.
with injury in setting • Evaluation of near
of organic heart syncope or dizziness
disease after
exclusion of potential
cardiac cause of
syncope
44. Tilt Table Test
• Unmasks Vasovagal
syncope susceptibility
• Reproduces
symptoms
• Positive Tilt Test
*Prophylaxis
treatment—beta
blockers or
disopyramide as well
as SSRIs
*Recurrent symptoms
and bradycardia may
require pacemaker
47. Symptoms Diagnosis
Occurs after sudden unexpected pain, Vasovagal attack
sound, smell, or sight
Prolonged Standing
Athletes post exertion
Occurs after micturition, defecation, Situational Syncope
cough or swallowing
Event occurs in association with severe Glossopharyngeal or trigeminal
throat or facial pain neuralgia
Occurs with head rotation or pressure Carotid Sinus Syncope
on the carotid sinus-tumors, tight collars
or shaving
Episodes occur immediately on standing Orthostatic hypotension
Headaches are associated with the event Migraines
Medications taken before Drug induced syncope
Event is associated with vertigo, TIA/Subclavian Steal Syndrome
dysarthria or diplopia
Event is associated with arm exercize
Pulse/BP differences between arms
Aortic dissection/SSS
Syncope occurs without prodrome and Arrythmia
patient has underlying structural heart dz.
48. San Francisco Syncope
Rule
• Risk Factors
– C History of CHF
– H Hematocrit less than 30
– E Non-sinus rhythm or new changes in EKG
– S Systolic BP less than 90
– S Shortness of breath
------------- is a simple rule for evaluating
the risk of adverse outcomes in patient who
present with syncope.
49. SUMMARY
• Shotgun approach is Not helpful.
• EKG should be considered in all patients.
• Tilt table test can diagnosis vasovagal
syncope.
• Neurologic testing is low yield and often
overused.
• Holter monitoring, Echo, EST, EP
considered in patients at high risk for
cardiac syncope.
• Patients remain undiagnosed in 34% of
cases.
