Transcript SYNCOPE EVALUATION AND MANAGEMENT

SYNCOPE
EVALUATION AND
MANAGEMENT
Jayne Barr, MD
Clinical Assistant Professor
The Ohio State University
Case #1
• 42 year old female
• Chief complaint: passing out at work
• Works in a pharmaceutical lab. Was
sitting at her desk, felt nauseated and
knew she was going to pass out.
• Per witnesses, was slump over chair and
was unconscious for a few seconds.
Case continues
• No chest pain, palpitations, shortness of
breath
• Similar episodes 10 years ago.
• No family history of sudden cardiac death
• No medications.
• No smoking. No alcohol. No drugs.
Case #2
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82 year old male.
Found unresponsive by his son
Past medical history—HTN
Medications—HCTZ
Exam—BP 160/98. P 70. Now alert and
oriented. Facial contusions. Otherwise normal
exam.
Q: How would you manage these 2 patients?
Syncope: Definition
• Abrupt and self-limited loss of consciousness
associated with absence of postural tone
• Relatively rapid onset. Variable warning
symptoms.
• Followed by rapid and complete recovery. Last
only a few minutes.
• Absence of prolonged confusion
• Presyncope---prodromal symptom of fainting
and typically has the same work up as syncope.
Significance of Syncope
• “The only difference between syncope
and sudden death is that in one you wake
up”. [1]
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--anonomymous
Syncope: Epidemiology
• 20-50% of adults experience at least one
episode of syncope during their lifetime.
• Explained 53-62%
• Infrequent, unexplained 38-47%
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500,000 new syncope patients each year.
3-5% of ER visits.
6% of hospital visits.
More common in the elderly.
• Up to 23% in age >70 years.
Syncope: Economic Burden
• Per recent data, the
overall cost per hospital
admission was estimated
to be about $10,600.
• One study found to be
$17,000 of
“unnecessary” testing to
diagnosis vasovagal
syncope
• Overall cost in US
estimated to be in
excess of $1 billion.
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Costs of Test
Troponin
EKG
Telemetry
Head CT
MRI brain
Carotid US
EST
Echocardiogram
EEG
$78
$221
$255/d
$1545
$2216
$1294
$2492
$809
$1115
Causes of Syncope
Morbidity and Mortality
• Most cases benign.
• Syncope of cardiac origin
has the highest morbidity
and mortality.
• 1 year mortality of 1833%
• Recurrence in the elderly
population is 30%
• Syncope of unknown
origin.
• 1 year mortality of 6-12%.
Syncope in Children
• Generally a benign
event.
• Most common causes
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Vasovagal (40%)
Simple faint (29%)
Breathholding (4%)
Unknown (15%)
• Rare but serious
causes of syncope in
children
– Hypertrophic
cardiomyopathy
– Anomalous origin of left
coronary artery
– Myocarditis
– Long QT syndrome
– Cystic medial necrosis
– WPW
Syncope: Pathophysiology
• Decreased cerebral
perfusion is common to
all causes of syncope
• Cessation of cerebral
perfusion for as little as
3-5 seconds can result in
syncope
• Decreased cerebral
perfusion may occur as a
result of decreased
cardiac output or
decreased systemic
vascular resistance.
More Pathophysiology
• Bilateral hemisphere
dysfunction or reticular
activating system (RAS)
midbrain knockout.
• Generally acute
hypoperfusion is
responsible.
– Regional
(vasoconstriction)
– Systemic (global
hypotension)
• Loss of consciousness
causes loss of postural
tone leading to collapse
• 35% reduction in
cerebral blood flow will
cause syncope.
• Modifying factors
– Cardiac output
– Systemic and local
vascular
resistance/occlusion
– Blood volume
– Ability to compensate
Syncope: Etiology
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Mnemonic: PASSOUT
P-ressue (hypotensive causes)
A-rrthymias
S-eizures
S-ugar (hypo/hyper glycemia)
O-utput (cardiac)/ O2 (hypoxia)
U-nusual causes
T-ransient (TIAs, strokes, CNS diseases)
More specifics
• OUTPUT
– Cardiac
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AS, PA, MS,IHSS
Cardiomyopathies
Atrial myoxomas
Cardiac tamponade
Aortic dissection
MI, CHF
– Pulmonary
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PE, acute hypoxemia
Pulmonary HTN
COPD exacerbation
CO poisoning
• UNUSUAL CAUSES
• Anxiety, Panic disorder
• Major depressive disorder
• Somatization disorder
(psychogenic syncope)
• Hyperventilation
syndrome
• Migraine, sleep disorder
• TRANSIENT
• TIA (vertebrobasilar),
CVA, subdural hematoma
• Subarachnoid
hemorrhage
• CNS mass effect (tumor)
• Basilar artery migraine.
Syncope
• CAUSES (Head---Heart---Vessels)
– Reflex mediated
• Vasovagal, carotid sinus, situational
– Cardiac
• Mechanical , arrhythmias
– Orthostatic
• Drugs, autonomic failure
– Cerebrovascular
– Unknown
– Nonsyncopal causes
Neurally mediated reflex syncope
(36-62%); average (24%)
• Vasovagal, carotid sinus, situational
• No increased risk for cardiovascular
morbidity or mortality associated with
reflex mediated syncope.
Neurally Mediated Reflex Syncope
--what happens?
• 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)
Vasovagal syncope
• Most common cause
of syncope in young
adults
• Precipitating event is
often identifiable
– Stress, trauma, pain,
sight of blood,
prolonged standing,
heat exposure
Vasovagal Syncope
• 3 PHASES
• --Prodrome
• Diaphoresis, 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
Prevalence of VasoVagal
Syncope
• Prevalence poorly known (8-37% with mean of
18%)
• Important points
– Patients with VVS younger than Carotid sinus
syndrome patients
– Age range teens to elderly with mean 43 years
– Pallor, nausea, sweating, palpitations are common
– Amnesia for warning symptoms in older patients
Vasovagal Syncope Management
Management for Vasovagal
syncope
• Optimal management is source of debate
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Patient education, reassurance, instruction
Fluids (sports drinks), salt, diet
Tilt training
Support hose (waist high)
• Drug therapies
• Pacing (DDD pacing)
– Class II indication if positive tilt test and
cardioinhibitory or mixed reflex
Drug therapies for Vasovagal
syncope
• Salt/volume
– Salt, sports drinks,
fludrocortisone
• Beta-adrenergic blockers
– 1 positive control study
using atenolol
– Use if hx of htn
• Disopyramide
• SSRIs
– 1 controlled study
– Use if hx of depression
• Vasoconstrictors (eg,
midodrine)
– 1 negative controlled study
(etilephrine)
– ? Efficacy of
neosynephrine
– Use midodrine if
significant hypotension
Postural Orthostatic
Tachycardia Syndrome
• Upright symptoms without hypotension.
• Upright tachycardia—excessive HR response
to maintain a low normal BP.
• 500,000 Americans, usually young women
• Partial dysautonomia
• Antecedent infection, surgery, pregnancy
• Treatment—low dose propanolol 10mg tid
Carotid Sinus Syncope
• Syncope related to
head turning,
shaving, wearing a
tight collar
• Pathophysiology
– Carotid sinus
pressure causes a
reflex decrease in
heart rate and blood
pressure
Carotid sinus massage
• Site
– Carotid arterial pulse just
below thyroid cartilage
• Method
– Massage, not occlusion.
– Right followed by left,
pause between
– Duration:5-10 seconds
– Posture: supine and erect
• Risks
– 1/5000 massages
complicated by TIA
• Outcome
– 3 sec asystole and/or
50mmHg fall in systolic
blood pressure with
reproduction of symptoms
==CAROTID SINUS
SYNDROME
• Contraindications
– Carotid bruit, known but
significant carotid arterial
disease, previous CVA, MI
last 3 months.
Situational Syncope
• Related to micturition,
defecation, swallowing or
coughing
• Induced by baroreceptor
and mechanoreceptors
causing vagal stimulation
• Circumstances of the
event are typically
diagnostic
Orthostatic syncope
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When vertical, blood follows gravity and pools.
Increased sympathetic tone counteracts this.
If the response is inadequate, syncope occurs.
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
– Volume loss
– Neurologic damage
More on Orthostatic
Hypotension
• Volume loss
– Assoc. with tachycardia
• Medications
– Seen in elderly 45% of
time
• Situational
– Micturition, cough,
postprandial, carotid sinus
sensitivity, defecation,
laughing
• Adrenal insufficiency
• Primary autonomic
disease
– Idiopathic, parkinsons
disease, multisystem
atrophy (Shy-Dragger)
• Secondary autonomic
disease
– Neuropathic (dm, amyloid,
alcoholism, autoimmune,
vitamin deficiency, etc)
– CNS (cva, MS, tumors,
spinal cord)
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.
Neurologic Syncope
• Rarely the primary cause of syncope
• Ischemia to the RAS in the brainstem may
cause “drop attacks”
• Results from Vertebrobasilar insufficiency due to
TIA (sometimes basilar migraine)
• Usually accompanied by vertigo, ataxia,
dysarthia, diplopia
• Other examples
• Subclavian steal—occurs with arm activity. Systolic BP in
arms (difference of 10mmHg)
• Subarachnoid hemorrhage
Psychiatric causes
• Most commonly associated with
• Anxiety
• Panic
• Major depressive disorders
• Variety of mechanisms may be involved
• Hyperventilation
• Increased vagal tone
Syncope-like States
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Migraine
Acute hypoxia
Hyperventilation
Somatization disorder (psychogenic syncope)
Acute intoxication (ie alcohol)
Seizures
Hypoglycemia
Sleep disorders
An Approach to Syncope
History
Physical Exam
EKG
Neurological
Evaluation
ENT
Evaluation
Head CT scan/ Skull films
Carotid Doppler
MRI brain
EEG
Psychological
Evaluation
Cardiovascular
Evaluation
Other
Cardiovascular
testing
Holter/ELR/ILR
Tilt Table
Echocardiogram
EPS
Angiogram
Exercise test
Endocrine
Evaluation
HISTORY
• RAPID ASSESSMENT
– Identify Life-Threatening causes
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Dysrhythmias
cardiac ischemia
Critical aortic stenosis
Aortic dissection
Pulmonary embolus
CVA
SAH
Toxic-metabolic derangement
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
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)
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)
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)
PHYSICAL EXAM
• HEENT
– Tenderness/deformity
(trauma)
– Papilledema (increased
icp, head injury)
– Breath (alcohol, dka)
• NECK
– Bruits
– JVD (chf, mi, pe,
tampnade)
• HEART
– Murmur (valves,
dissection)
– Rub (pericarditis,
tamponade)
• LUNGS
– Sounds may help
distinguish chf,
infection,
pneumothorax
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,
steal)
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
Seizure or Not?
• SEIZURE
– Frothing at mouth
– Tongue biting
– Disorientation/
postictal
– Age < 45 year
– LOC over 5 minutes
*tongue biting found only in seizure
(99% specificity); absence did not
exclude the possibility of a
seizure (24% sensitivity)
• NOT A SEIZURE
– Sweating prior to
episode
– Nausea prior to
episode
– Oriented after event
– Age > 45 years
Ancillary Studies
• 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
– Ua/culture
--hemoglobin
--troponin
--CK (syncope vs seizure)
Starting the “Workup”
• If young adult and No comorbid conditions or
symptoms
Most likely VASOMOTOR or ORTHOSTATIC .
*Clinicians may forego the EKG in young, healthy
patients with an obvious cause of syncope.
Normal EKG
• If Normal EKG:
– Check orthostatics
– Check hemoglobin
• If low---Anemia
• If normal or high--Volume loss, dehydration, drug
induced
Young adult, no comorbidity,
normal EKG, 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)
The EKG
Key Points
• Guidelines recommend EKG in the evaluation
of all patients with syncope.
• Exception: young healthy patients with an
obvious cause of syncope
• Abnormal EKG in 90% of patient with cardiac
syncope
• Only 6% of patients with reflex mediated
syncope have abnormal EKG.
• Syncopal patient with negative cardiac history
and normal EKG—unlikely to have a cardiac
cause
The EKG
patient older, +comorbid signs/symptoms
• If Abnormal EKG
– Ischemia/injury
– Dysrhythmia
• Sinus brady, BBB, AV block, prolonged QT, WPW,
HOCM, Brugada
• If Normal EKG
– Consider holter or event recorder if
dysrhythmia suspected
sinus bradycardia
ventricular tachycardia
3 or more beats
WPW
Prolonged QT interval
Other: sinus pause> 2 sec, SVT, afib, 2nd or 3rd AV block, PM malfunction
Summary of the Cardiovascular
Diagnostic Pathway
SYNCOPE
History
Physical Exam
EKG
Known Structural
Heart Disease
Echocardiogram
EPS
Positive
Negative
Treat
Tilt table
ELR/ILR
No Structural
Heart Disease
>30 days
> 2 events
< 30 days
Tilt table
ILR
tilt table
Holter/ELR
ILR
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 EKG is normal.
• Indicated in patients at highest risk for
arrhythmia ie, abnormal ekg, palpitations, cad
history, syncope when supine or with exertion,
+FH
Holter results--summary
• PACs and PVCs
– Usually not significant
– Exception: ie 3 consecutive 3 PVCs at 100 bpm
• Bigeminy—may be significant
• AV block---is important
• Bradycardia---if signs and symptoms correlate
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
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 EKG
– Murmur
---history of heart disease
---exercise assoc. syncope
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
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)
EPS—Intracardiac EPS
• Rarely indicated in
patients with structurally
normal hearts and
normal ekg.
• Diagnostic yield greatest
in patients with known
heart disease but nondiagnostic ekg
monitoring.
• Heart disease-------5080%
• No heart disease---1850%
• Difficult to correlate
spontaneous events and
laboratory findings
• Ineffective for assessing
bradyarrhythmias
• Often must settle for an
attributable cause
• Abnormal finding on EPS
does not guarantee that
this was what caused the
patient’s syncope.
• EPS is abnormal in 1868% of patients with
syncope of unknown
cause.
EP testing—Useful Diagnostic
findings
• Inducible monomorphic VT
• Sinus node response time > 3000 ms or
carotid sinus response time >600 ms
• Inducible SVT with hypotension
• HV interval > 100ms (especially in
absence of inducible VT)
• Pacing induced infra-nodal block
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
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
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
NEUROLOGIC TESTING
• Tend to be overused
• Includes EEG, CT head, MRI head, Carotid
dopplers
• In contrast, Cardiovascular tests are
underused.
• INDICATION
– Only if history and physical exam suggests a
neurologic cause or testing for other causes is
complete.
EEG
• Not a first line of testing
• To differentiate syncope from seizure
• Abnormal EEG in the interval between
two attacks -> Epilepsy
• Normal EEG -> does not tell us anything
Tests and Diagnostic Yield
Test/procedure
yield (%)
history and physical
49-85
EKG
2-11
EPS without SHD
11
EPS with SHD
49
Tilt table test without SHD
11-87 (syncope pt
+TTT 24-75%)
Ambulatory EKG
holter
2
loop recorder 2-3wks
20
implantable LR upto 14mo
65-88
Neurological (ct, carotid)
0-4
Syncope Evaluation Flow Chart
Syncope Evaluation Flow Chart
When to Admit
• Consider admitting if age greater than 40 years
• Discharge if benign etiology
– Vasovagal, micturition, psychogenic syncope
• Admit if
– Suspected or known significant heart disease ie
cardiac ischemia, CHF, structural heart ds or +family
hx of SCD
– EKG suggestive of arrhythmia or syncope during
exercise
– Stroke
– Syncope causing severe injury
– Severe orthostatic hypotension
ACEP guidelines
Clinical Risk Score for Predicting 1
year Mortality in Patients with Syncope
• Risk Factors
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Abnormal ekg
Age >45 years
History of CHF
History of ventricular
arrhythmia
Number
of risk
factors
1 year
mortality
(%)
0
1
1
9
2
16
3/4
27/80
Congestive Heart Failure
• CHF = poor outcome
– N=491; 12% with syncope
– Cardiac syncope; 49% dead 1 year
– Noncardiac syncope; 39% dead 1 year
– No syncope; 12% dead 1 year
*CHF is a risk factor for poor outcome in
multiple studies
San Francisco Syncope Rule
• Risk Factors
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C
H
E
S
S
History of CHF
Hematocrit less than 30
Non-sinus rhythm or new changes in EKG
Systolic BP less than 90
Shortness of breath
• Predicting Serious Outcome (at 7 days)
– Low risk (no risk factor)---0.3% serious outcome
– High risk (1+risk factor)---15.2% serious outcome
Predictor of 30 day serious events
in older patients with syncope
• Predictors of increased risk
– Age >90y, male gender, arrhythmias, SBP> 160,
abnormal EKG, Abnormal troponins
• Predictor of decreased risk
– Near syncope
• Stratified in low (0), intermediate (1-2) and High
(>2) risk groups.
• CHF was not associated with increased risk
• Even low risk group—2.5% risk
• Needs validation
Annals Emerg Med 2009.
Driving and Return to Work
• Vasovagal syncope---can return to work
• VT---no driving for 3-6 months
• In Ohio, can not be a Commercial Driver
if diagnosed with syncope
Case #1 Continues
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Physical exam: Normal
Orthostatics: Normal
EKG: Normal
Labs: no anemia. Glucose normal.
ECHO: Normal
Tilt Table Test: after 7 minutes of 70 degrees
upright, HR 36, BP 51/41, LOC. Regained
consciousness with supine position.
Case #1 Conclusion
• DIAGNOSIS----Vasovagal Syncope
• TREATMENT---Florinef, Ted hose, Fluids
• OUTCOME---No reoccurence of
symptoms when followed up at 3 months,
6 months, and 1 year later.
Case #2 Continues
• Emergency Room workup—negative.
Electrolytes, CBC normal. EKG showed NSR
with occasional PVCs.
• Decision made to ADMIT.
• 2 hours later---Nonsustained Vtach.
• EP study—Inducible Vtach. Automated internal
defibrillator placed.
• Cardiac cath---diffuse coronary artery disease.
SUMMARY
• Syncope is a transient loss of consciousness
due to decreased cerebral blood flow.
• Most common causes: vasovagal, cardiac
(cardiac arrhythmia), and orthostatic
hypotension. Seizures are rare.
• Patients with cardiac syncope are at increased
risk of death.
• History and Physical exam are the MOST
important to identify the cause
• Orthostatic BPs should be done on all pts.
SUMMARY
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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.
Clues to the Etiology of Syncope
• Cough, micturition, defecation, swallowing--situational syncope
• Syncope with arm exercise---subclavian steal
• Syncope with shaving---carotid sinus syncope
• Syncope with change of position---orthostatic
• Prodromal symptoms (nausea, diaphoresis)--neurally mediated reflex (vasovagal)
Clues to the Etiology of Syncope
• Syncope with exertion---AS, IHSS, arrhythmias
• Abrupt onset---cardiac syncope
• Blood pressure/pulse differential---Aortic
dissection, subclavian steal syndrome
• Post-syncopal disorientation; incontinence--seizure
REFERENCES
• Engel. Ann Internal Med. 1978. 89; 403412
• Kapor, W. Medicine. 1990. 69; 160-175.
• Krahn. Cardiology Clinic. 1997
• ACEP Clinical Policy on Syncope.
• Ann Emerg Med. 2009.
• Mayo Clinic Proceedings. Nov 2008.