2. Syncope is defined as transient loss of
consciousness due to reduced cerebral
blood flow.
Syncope is associated with postural collapse
and spontaneous recovery.
It may preceded by faintness or presyncope
This may include lightheadedness,dizziness
without true vertigo, a feeling of
warmth,diaphoresis, nausea and or visual
blurring
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 (vertigo), hypoxemia, and
hypoglycemia.
The differentiation of syncope from seizure is
an important, sometimes difficult, diagnostic
problem.
5. Syncope may be benign when it occurs as a
result of normal cardiovascular reflex effects
on heart rate and vascular tone or
Serious when due to life threatening
arrythmias.
May be single episode or recurrent
7. Neurocardiogenic / Vasovagal
Most Common
• Pain/Noxious Stimuli
• Situational (micturation, cough,
defecation)
• Carotid Sinus Hypersensitivity (CSH)
• Fear
• Prolonged standing / heat exposure
Cardiovascular
Most Dangerous
• Arrhythmia – Tachy or Brady
• Valve Stenosis (outflow obstruction)
• HOCM (outflow obstruction)
Orthostatic Hypotension
“ D A A D “
• Drugs: BP meds, Diuretics, TCAs
• Autonomic Insufficiency
(Parkinsons, Shy-Dragger, DM,
Adrenal Insufficiency)
• Alcohol
• Dehydration
Neuro / Functional / Psychiatric -
<5%
• Psuedosyncope
• TIA or Vertibro-basilar Insufficiency
8.
9.
10.
11.
12. As blood pools in peripheral vessels and arterial
blood pressure begins to fall, compensatory
mechanisms are activated that attempt to
maintain adequate cerebral blood flow.
These mechanisms include baroreceptors, which
reflexely constrict peripheral blood vessels,
increasing the return of venous blood to the
heart, and the carotid and the aortic arch
reflexes, which increases the heart rate.
These mechanisms work to increase the cardiac
output and the maintenance of a close to normal
blood pressure, all of which are seen during
early presyncopal period
13. If the situation goes unmanaged these
compensatory mechanisms fatigue, which is
manifested through development of reflex
bradycardia. ( cardioinhibitory component and
vasodepressor component )
Slowing of the heart rate to less than 50
beats/min is common & leads to a significant
drop of cardiac output which is precipitous fall
in blood pressure to levels below the critical for
maintenance of consciousness.
In such cases, cerebral ischemia results and the
individual loses consciousness
14. Stress causes an abnormal
autonomic reflex
Normal increased
sympathetic tone replaced
by increased vagal tone
Variable contribution of
vasodilation and
bradycardia.
Examples include syncope
from:
◦ Pain and/or fear
◦ Carotid sinus
hypersensitivity
◦ “situational” (cough,
micturition, defecation
syncope)
15.
16. Dizziness, lightheadedness, and fatigue,
premonitory features of autonomic activation
may be present
These include diaphoresis, pallor,
palpitations, nausea, hyperventilation, and
yawning.
17. 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.
18. Reassurance
Avoidance of provocative stimuli
Plasma volume expansion with fluid and
salt are the cornerstones of the
management of neurally mediated
syncope.
19. 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 .
20. 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.
21. 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
22. 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
23. The first step is to remove reversible causes—
usually vasoactive medications .
Nonpharmacologic interventions should be
introduced.
24. 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.
Intravascular volume should be expanded
by increasing dietary fluid and salt.
25. If these nonpharmacologic measures fail,
pharmacologic intervention with
fludrocortisone acetate and vasoconstricting
agents such as midodrine and
pseudoephedrine should be introduced.
26. 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.
27.
28. 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.
29. Initial Examination
◦ Detailed patient history
◦ Physical exam
◦ ECG
◦ Supine and upright
blood pressure
Monitoring
◦ Holter
◦ Event
◦ Insertable Loop Recorder (ILR)
Cardiac Imaging
Special Investigations
◦ Head-up tilt test
◦ Hemodynamics
◦ Electrophysiology study (EPS)
.
30. Initial Evaluation
Treatment
Syncope Not Syncope
Certain
Diagnosis
Unexplained
Syncope
Cardiac
Likely
Cardiac
Tests
Neurally-Mediated or
Orthostatic Likely
Tests for Neurally-
Mediated Syncope
Frequent or Severe
Episodes
Tests for Neurally-
Mediated Syncope
Single/Rare
Episodes
No Further
Evaluation
Confirm with
Specific Test or
Specialist
Consultation
Suspected
Diagnosis
++
/?
+
- + - + -
Treatment Treatment
Re-AppraisalRe-Appraisal
Treatment
31. 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
32. HISTORY
Events preceding the
syncope
Prolonged standing
(vasovagal)
Immediately upon standing
(orthostatic)
With exertion (cardiac)
Sudden without warning or
palpitations (cardiac)
Aggressive dieting
Heat exposure
Emotional stress
Events during and after
the episode
Trauma (implication
important)
Chest pain (CAD, PE)
Seizure (incontinence,
confusion, tongue
laceration, postictal
behavior)
Cerebrovascular syndrome
(diplopia, dysarthia,
hemiparesis)
Associated with
n/v/sweating (vasovagal)
33. HISTORY
Associated symptoms
Chest pain, SOB,
lightheadedness,
incontinence
Past medical history
Identifying risk factors
Morbidity and mortality
increases with organic
causes
Parkinsons (orthostatic)
Epilepsy (seizure)
DM (cardiac, autonomic
dysfunction, glucose)
Cardiac disease
Medications
Antihypertensives, diuretics
(orthostatic)
Antiarrthymics (cardiac
syncope)
TCA, Amiodarone
(cardiac/prolonged QT)
Family history
Sudden death (cardiac
syncope/prolonged QT or
Brugada)
34. PHYSICAL EXAM
Vital signs
Orthostatics—most
important
Drop in BP and fixed HR -
>dysautonomia
Drop in BP and increase HR
-> volume depletion/
vasodilatation
Insignificant drop in BP and
marked increase in HR ->
POTS
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)
38. 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)
39. 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.
40. Young adult, no comorbidity, normal
ECG, absent orthostatics
Vasomotor
Try carotid massage
(+) carotid sinus
sensitivity
(-) reflex or
neurocardiogenic
Metabolic
Check chemistry. R/O
hypoglycemia, adrenal
insufficiency
Neurologic
CT head (tia, cva, sah)
EEG (if suspect Sz)
Cardiovascular
If Outflow obstruction, check
CT chest, Echo (PE,
valvular, HOCM)
If venous return, check
HCG, Echo (pregnancy,
tamponade)
41. 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
42. 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
43. Carotid Sinus Massage (CSM)
Method1
Massage, 5-10 seconds
Don’t occlude
Supine and upright posture
(on tilt table)
Outcome
3 second asystole and/or
50 mmHg fall in systolic BP
with reproduction of
symptoms = Carotid Sinus
Syndrome
Absolute
contraindications2
Carotid bruit, known
significant carotid arterial
disease, previous CVA, MI
last 3 months
Complications
Primarily neurological
Less than 0.2%
Usually transient
44. 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.
45. 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
46. 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
47. 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
48. 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)
49. Changes in position to
reproduce symptoms
of the syncopal event.
Positive tilt table test
◦ Induction of bradycardia
and hypotension
◦ Considered diagnostic
for vasovagal syncope
50. Indications for Tilt table test
Unexplained recurrent
syncope or syncope
associated with injury in
absence of structural
heart ds.
Unexplained recurrent
syncope or syncope
associated with injury in
setting of organic heart
disease after exclusion
of potential cardiac
cause of syncope
Identification of neurally
mediated syncope could
alter treatment
Evaluation of recurrent
unexplained falls.
Evaluation of near
syncope or dizziness
51. 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
52.
53.
54. Symptoms Diagnosis
Occurs after sudden unexpected pain,
sound, smell, or sight
Prolonged Standing
Athletes post exertion
Vasovagal attack
Occurs after micturition, defecation,
cough or swallowing
Situational Syncope
Event occurs in association with severe
throat or facial pain
Glossopharyngeal or trigeminal
neuralgia
Occurs with head rotation or pressure
on the carotid sinus-tumors, tight collars
or shaving
Carotid Sinus Syncope
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,
dysarthria or diplopia
Event is associated with arm exercize
TIA/Subclavian Steal Syndrome
Pulse/BP differences between arms
Aortic dissection/SSS
Syncope occurs without prodrome and
patient has underlying structural heart dz.
Arrythmia
56. 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.
57. 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.
58. 71y/o M presents after he passed out while walking up
the stairs. He felt slightly lightheaded just prior to the
event. Wife saw him fall but was able to quickly arouse
him. He had no incontinence or tongue biting. Similar
event occurred 2 weeks prior while he was doing yard-
work for which he did not seek medical care. He has a
long history of DM, and hypertension for which he takes
Glipizide, Amlodipine, Lisinopril, and HCTZ. He does not
drink. Vitals, orthostatics, and blood sugar are
unremarkable. ECG shows left axis deviation and LVH.
Exam shows 1+ bilateral edema and 4/6 ejection
murmur radiating to the carotids.
What risk category is this patient and how would
you proceed with workup?
59. H/P, Orthostatics, ECG, Meds
◦ ECG shows evidence of structural heart disease and exam
shows murmur. No orthostasis or suspicious history of
vasovagal syncope. Patient has had multiple episodes.
Based on initial workup, patient is High Risk
o Needs Admission and Cardiac Work-up including
Echocardiogram and Stress Test
Dx: Aortic Stenosis
60. 35y/o healthy M presents with an episode of
syncope while standing. He did not experience any
prodrome symptoms. This has never happened
before. He has no medical history and uses no
medications, drugs, or EtoH. Physical exam and
ECG are normal. No orthostasis. Carotid massage is
negative. Routine labs are unremarkable.
What risk category is this patient and how would
you proceed with workup?
61. H/P, Orthostatics, ECG, Meds - normal with no obvious cause of
syncope
Patient is Low Risk and has had only a Single Episode of syncope
No Further Work-up Indicated
What if the same patient presented with syncope while
working out at the gym and physical exam showed a grade III
systolic murmur that increased with Valsalva?
o Patient is now High Risk given possible structural heart disease
and exertional syncope
Admit to telemetry for cardiac work-up including
Echocardiogram to evaluate for Hypertrophic
Cardiomyopathy.
62. • Key Differential Dx
o Vasovagal/Neurocardiogenic - most common
o Cardiac – HIGH RISK PATIENTS, most dangerous
o Orthostatic – “D A A D”
o Other - Neurologic, Functional, Psych
• Work-up and Risk Stratification
o H/P, Orthostatics, Meds, ECG, +/- Carotid Massage
o Risk Stratify
High Risk - Admit w/ cardiac work-up
Low Risk - Outpatient workup based on frequency of episodes
• Brain Imaging ONLY if focal Neuro Deficits or Head trauma
