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Transcript
Joseph P. Ornato, MD, FACP, FACC, FACEP
Professor & Chairman, Department of Emergency Medicine
 Self-limited loss of consciousness and postural
tone
 Relatively rapid onset
 Variable warning symptoms
 Spontaneous, complete, and usually prompt
recovery without medical or surgical intervention
Underlying mechanism is
transient global cerebral hypoperfusion.
Brignole M, et al. Europace, 2004;6:467-537.
Real or Apparent TLOC
Syncope
Neurally-mediated reflex
syndromes
Orthostatic hypotension
Cardiac arrhythmias
Structural cardiovascular
disease
Brignole M, et al. Europace, 2004;6:467-537.
Disorders Mimicking
Syncope
 With loss of consciousness (i.e.,
seizure disorders, concussion)
 Without loss of consciousness,
i.e., psychogenic “pseudosyncope”
Structural
CardioPulmonary
NeurallyMediated
Orthostatic
1
2
3
4
• Vasovagal
syndrome
• Carotid sinus
syndrome
• Situational
• Drug-induced
• Autonomic
nervous
system failure
• Bradyarrhythmia
• Acute
myocardial
ischemia
• Aortic stenosis
• Hypertrophic
cardiomyopathy
• Pulmonary
hypertension
• Aortic dissection
Cough
PostMicturition
Primary
Secondary
Cardiac
Arrhythmia
Sinus node
dysfunction
AV block
•Tachyarrhythmia
VT
SVT
• Long QT
syndrome
Unexplained Causes = Approximately 1/3
Acute intoxication (e.g., alcohol)
Seizures
Sleep disorders
Somatization disorder (psychogenic
pseudo-syncope)
Trauma/concussion
Hypoglycemia
Hyperventilation
Brignole M, et al. Europace, 2004;6:467-537.

40% will experience syncope
at least once in a lifetime1

1-6% of hospital admissions2

1% of emergency department
visits per year3,4

10% of falls by elderly are due
to syncope5

Major morbidity reported in 6%1
(fractures, motor vehicle crashes)

Minor injury in 29%1
(lacerations, bruises)
1Kenny
RA, Kapoor WN. In: Benditt D, et al. eds. The Evaluation and
Treatment of Syncope. Futura;2003:23-27.
2Kapoor W. Medicine. 1990;69:160-175.
3Brignole
M, et al. Europace. 2003;5:293-298.
Blanc J-J, et al. Eur Heart J. 2002;23:815-820.
5Campbell A, et al. Age and Ageing. 1981;10:264-270.
4
Estimated hospital costs exceeded $10
billion1
Estimated physician office expenses
exceeded $470 million2
Over $7 billion is spent annually in the US
to treat falls in older adults4
1Kenny
RA, Kapoor WN. In: Benditt D, et al. eds. The Evaluation and Treatment of Syncope. Futura;2003:23-27.
v. 6.0. Solucient LLC, Evanston IL.
3Farwell D, et al. J Cardiovasc Electrophysiol. 2002;13(Supp):S9-S13.
4Olshansky B. In: Grubb B and Olshansky B. eds. Syncope: Mechanisms and Management. Futura. 1998:15-71.
2OutPatientView
100
80
73%1
71%2
60%2
60
37%2
40
20
0
1Linzer
2Linzer
Anxiety/
Depression
M. J Clin Epidemiol. 1991;44:1037.
M. J Gen Int Med. 1994;9:181.
Alter Daily
Activities
Restricted
Driving
Change
Employment
 Low mortality vs.
high mortality
 Neurally-mediated
syncope vs.
syncope with a
cardiac cause
Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope.
N Engl J Med. 2002;347(12):878-885. [Framingham Study Population]
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
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 (cardiac cath)
Electrophysiology study
Brignole M, et al. Europace, 2004;6:467-537.
 Circumstances of
recent event
 Eyewitness account of
event
 Symptoms at onset of
event
 Sequelae
 Medications
 Circumstances of
prior events
 Concomitant disease,
especially cardiac
 Pertinent family
history
 Cardiac disease
 Sudden death
 Metabolic disorders
 Past medical history
 Neurological history
 Syncope
Brignole M, et al. Europace, 2004;6:467-537.
 Vital signs
 Heart rate
 Orthostatic blood pressure change
 Cardiovascular exam: Is heart disease present?
 ECG: Long QT, pre-excitation, conduction system disease
 Echo: LV function, valve status, hypertrophic cardiomyopathy
 Neurological exam
 Carotid sinus massage
 Perform under clinically appropriate conditions preferably
during head-up tilt test
 Monitor both ECG and BP
Brignole M, et al. Europace, 2004;6:467-537.
Neurally-mediated
Vasovagal Syncope (VVS)
Carotid Sinus Syndrome (CSS)
Cardiac arrhythmia
Tachy-brady syndrome
Long QT syndrome
Torsade de pointes
Brugada syndrome
Drug-induced
Structural cardio-pulmonary disease
Orthostatic
Vasovagal syncope (VVS)
Carotid sinus syndrome (CSS)
Situational syncope
Post-micturition
Cough
Swallow
Defecation
Blood drawing, etc.
Most common form of syncope
8% to 37% (mean 18%) of syncope cases
Depends on population sampled
Young without structural heart disase, ↑
incidence
Older with structural heart disease, ↓
incidence
 Useful as diagnostic
adjunct to confirm
vasovagal syncope
 Useful in teaching
patients to recognize
prodromal symptoms
Brignole M, et al. Europace. 2004;6:467-537.
60° - 80°
 Etiology
 Drug-induced (very
common)
 Diuretics
 Vasodilators
 Primary autonomic
failure
 Multiple system atrophy
 Parkinson’s Disease
 Postural Orthostatic
Tachycardia Syndrome
(POTS)
 Secondary autonomic
failure
 Diabetes
 Alcohol
 Amyloid
Syncope clearly associated with
carotid sinus stimulation is rare (≤1%
of syncope)
CSS may be an important cause of
unexplained syncope/falls in older
individuals
Kenny RA, et al. J Am Coll Cardiol. 2001;38:1491-1496.
Brignole M, et al. Europace. 2004;6:467-537.
Sutton R. In: Neurally Mediated Syncope: Pathophysiology, Investigation and Treatment. Blanc JJ, et al. eds. Armonk, NY: Futura;1996:138.
 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
1Kenny
RA. Heart. 2000;83:564.
M. Ann Intern Med. 1997;126:989.
3Munro N, et al. J Am Geriatr Soc. 1994;42:1248-1251.
2Linzer
 Absolute
contraindications2
 Carotid bruit, known
significant carotid arterial
disease, previous CVA, MI
last 3 months
 Complications
 Primarily neurological
 Less than 0.2%3
 Usually transient
Ambulatory ECG
Holter monitoring
 Insertable loop recorder (ILR)
Tilt table test
Includes drug provocation (NTG, isoproterenol)
Cardiac catheterization
Electrophysiology study (EPS)
Brignole M, et al. Europace, 2004;6:467-537.
OPTION
12-Lead 10 Seconds
1 day
Holter Monitor
Event Recorders
7-30 days
(non-lead and loop)
Up to 14
Months
ILR
0
1
2
3
4
5
6
7
8
TIME (Months)
Brignole M, et al. Europace, 2004;6:467-537.
9
10
11
12
13
14
Initial Evaluation
History, Physical Exam, ECG, Cardiac Massage
Yield (%)
38-40
Other Tests/Procedures
Head-Up Tilt
External Cardiac Monitoring
Insertable Loop Recorder (ILR)
EP Study
Exercise Test
EEG
27
5-13
43-883-5
<2-5
0.5
0.3-0.5
EEG
Head CT
Brignole M, et al. Europace. 2004;6:467-537.
 Includes cardiac arrhythmias and structural heart
disease
 Often life-threatening
 Suspect if syncope exercise-induced
 May be warning of critical CV disease
 Tachy and brady arrhythmias
 Myocardial ischemia, aortic stenosis, pulmonary
hypertension, aortic dissection
 Assess culprit arrhythmia or structural abnormality
aggressively
 Initiate treatment promptly
Bradyarrhythmias
Sinus arrest, exit block
High grade or acute complete AV block
Can be accompanied by vasodilatation (VVS, CSS)
Tachyarrhythmias
Atrial fibrillation/flutter with rapid ventricular rate
(eg, pre-excitation syndrome)
Paroxysmal SVT or VT
Torsade de pointes
Cardiovascular pathology
Coronary artery disease
Severe left ventricular dysfunction
Cardiomyopathy
Hypertrophic cardiomyopathy
Arrhythmogenic right ventricular cardiomyopathy
Congenital heart disease, especially coronary artery anomalies
Valvular heart disease
Cardiac pacemaker and conducting system disease
Hereditary channelopathies (Sudden Arrhythmic Death Syndrome (SADS))
Brugada syndrome
Early repolarization syndrome (ERS)
Long QT syndrome (LQTS)
Short QT syndrome (SQTS)
Catecholaminergic polymorphic ventricular tachycardia (CPVT)
 Often present as recurrent syncope or brief seizures
in children or young adults before sudden death
occurs
 May have young relatives who have had sudden
death
 ECG findings are often diagnostic
 Effective preventive treatment is available (ICD)
 Astute emergency physician may be the ONLY
healthcare provider who can make the diagnosis and
prevent tragic loss of a young life
 Male predominance
 Autosomal dominant
 Common in Asians
 40-60% prevalence of
life-threatening ventricular
arrhythmias and SCD
 Presents as syncope
 Downsloping ST-segment
elevation in ECG leads V1–3
Type I – 43% ↑ in SCD
 Male predominance
 1-2% of adults
 Normalizes with
exercise
Type II – no ↑ in SCD
Hereditary
Autosomal recessive (Jervell
Lange-Nielsen syndrome) with
hereditary nerve deafness
Autosomal dominant (Romano
Ward syndrome w/out deafness)
Syncope, VF, SCD
Acquired causes
 Hypocalcemia
 Hypokalemia
 Hypomagnesemia
 Ischemia
 Anorexia
 CNS pathology
 QT-prolonging drugs (www.azcert.org)
𝑄𝑇𝑐𝑜𝑟𝑟𝑒𝑐𝑡𝑒𝑑 =
𝑄𝑇𝑚𝑒𝑎𝑠𝑢𝑟𝑒𝑑
𝑅𝑅𝑖𝑛𝑡𝑒𝑟𝑣𝑎𝑙
Bazett Formula
QTc = 0.35-0.44 at HR= 60
Hereditary
Acquired causes
Autosomal dominant
 Hypercalcemia
Atrial fibrillation
 Hyperkalemia
Syncope, VF, SCD
 Acidosis
Early repolarization inferolateral
leads in 65%
 Systemic inflammatory
syndrome
 Myocardial ischemia
 Increased vagal tone
 Anomalous L coronary artery off the pulmonary
artery
 Hypertrophic cardiomyopathy
 Severe aortic stenosis
 Catecholaminergic polymorphic ventricular
tachycardia
 Hereditary defect in myocardial calcium handling
Stress-related syncope, VF, SCD
 ECG – unexplained sinus bradycardia at rest
 50% carry a diagnosis of epilepsy before correct
diagnosis established
Syncope is a common symptom with
many causes
Deserves thorough investigation and
appropriate treatment
Clinical decision (observation) unit at
VCU is an appropriate location to
initiate the evaluation