Syncope - EDExam
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Transcript Syncope - EDExam
Emergency Department
Management of Syncope
Emilia McGhee
Sept 2010
Syn.co.pe
A transient loss of consciousness and inability to
maintain postural tone due to global cerebral
hypoperfusion.
Characterised by a rapid onset, short duration
and spontaneous complete recovery
Incidence
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1-3 % Emergency Dept visits
6 % of hospital admissions
USA, Japan and Europe
Occurs in up to 50% during lifetime (only 5%
after 40 yrs)
• Recurs in 30%
• Due to cerebral hypoperfusion causing lack of
oxygen and glucose supplly to brain
• Cerebral perfusion maintained by:
– Cardiac output
– Systemic vascular resistance
– Mean arterial pressure
– Intravascular volume
– Cerebrovascular resistance with intrinsic
autoregulation
– Metabolic regulation
What is not syncope
Transient LoC without
global cerebral
hypoperfusion
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Seizure
TIA
Metabolic disorders
Intoxication
Loss of postural tone
without LoC
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Cataplexy
Drop attacks
Falls
TIA of carotid origin
Functional psychogenic
Syncope
vs
• Triggering factor
• Prodrome
• Convulsion after LoC, and
<15 secs
• Short duration
• Quick recovery
• Ongoing lethargy but no
confusion
Seizure
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Pt history
Aura
Automatisms
Convulsions at onset of LoC
Longer duration
Post-ictal phase
Tongue biting, incontinence
Classification
• Reflex – neurally mediated – 30%
• Orthostatic hypotension – 10-15 %
• Cardiac – electrical and mechanical – 10%
Reflex
• Vasovagal
– Emotional stress
– Orthostatic stress
• Situational
– Coughing, micturition
– GI stimulation
– Post exercise, post prandial
• Carotid sinus syncope
– Uncommon, caused by pressure on carotid sinus
– Head turning, tight collars shaving
Orthostatic Hypotension
• Primary autonomic failure
– Pure auntonomic failure, multisystem atrophy,
Parkinson’s Disease, Lewy body dementia
• Secondary autonomic failure
– Diabetes, amyloidosis, uraemia, spinal cord injuries
• Drug induced
– Alcohol, vasodilators, diuretics, phenothiazines,
antidepressants
• Volume depletion
– Vommitting, diarrhoea, dehydration, haemorrhage
“Syncope and sudden
death are the same,
except that in one you
wake up”
Cardiac - Electrical
• Ventricular arrhythmias
– VT, Torsades
– Sudden onset, little prodrome
– Elderly pts with known cardiac disease
• Supraventricular arrhythmias
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SVT, AF with fast ventricular response
Assoc with palpitations, chest pain, dyspnoea
May occur on attempting to stand or walk
Look for evidence of WPW, Brugada, Long QT
• Bradyarrhythmias
– Sick sinus, sinus brady, high grade AV block, adverse medication
reactions, pacemaker malfunction
– Chest pain, dyspnoea, decreased ET, fatigue
Cardiac - Mechanical
• Low CO output states
– Cardiomyopathy, CCF, valvular insufficiency
• Cardiac outflow obstruction
– Sudden onset, no prodrome
– Exertional in nature, murmur present
– Aortic stenosis, HOCM, Mitral stenosis, pulmonary
stenosis, pulmonary embolism, Lt atrial myxoma
HOCM
• Causes of syncope:
– Self terminating ventricular arrhythmias
– SVT
– Severe outflow tract obstruction
– Bradyarrhythmia
– Hypotension in response to exercise
– Reflex syncope
Emergency Department Assessment
• 45% can be diagnosed on history and exam
alone
• A cause will not be found for around 37%
• Management is moving away from firm
diagnosis to risk stratification of patients
Aim in ED
1) Recognise life threatening conditions
2) Recognise low risk conditions for discharge
3) Chose appropriate FU for those who need
further diagnostic testing
4) Recognise those who do not need further
investigation
History – High Yield Questions
• What were they doing
- at rest (arrhythmia)
- exercise / post-exercise (AS, HOCM)
- laughing, micturition etc
• Was there a prodrome?
- vasovagal
• Did they have palpitations?
- an arrhythmia
• Were they SOB?
- PE
- tamponade
• Did they have chest pain?
- PE
- ACS and an arrhythmia
- dissection
• Did they have abdominal pain?
- AAA
- ectopic
• Did they have a headache?
- SAH
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Previous arrythmias
Known CAD
Sudden or unexplained deaths in family
Known CCF
Medications
- QT prolonging medications
- vasodilators
- anti-hypertnesives
Red Flags
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Syncope during exertion
Syncope in lying position
Absence of external factors
Family hx of SCD
Slow recovery from syncope
Examination and bedside tests
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Cardiorespiratory exam
Abdominal exam
Neurological exam
BSL
Orthostatic BP
– A drop of 20mmHg systolic, 10mmHG diastolic or
increase in HR >20
– Systolic BP <90mmHg
– Meaningful if they become symptomatic
Ix that are helpful
• ECG
Consider on case to case basis:
• FBC, EUC
• Troponin, D.dimer, bHCG
• UA
• CXR
• Echo
• CSM
• Tilt table
• EPS
• EST
Ix that are generally low yield
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CTB
MRI
Holter monitor
Carotid dopplers
EEG
Important ECG findings
• Evidence of AV conduction disorder
– Prolonged PR
– Mobitz 1 or 2
– CHB
– RBBB or LBBB
• Evidence of underlying cardiac disease
– Rt or Lt axis deviation
– Significant ST or T wave changes
– Rt or Lt ventricular hypertrophy
ECG findings associated with high risk of
sudden cardiac death
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Hypertrophic cardiomyopathy
Long QT
Ventricular pre-excitation (WPW)
Brugada Syndrome
Short QT
Arrhythmogenic Rt ventricular dysplasia
ECG changes in HOCM
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Normal in up to 15%
Left axis deviation
LVH and strain
flipped T’s
big voltage R waves and deep, narrow Q’s in
lateral leads (I, aVL, V5 and V6)
- infarct Q’s are > 1 small square where as
HOCM Q’s are less than 1 small square
Risk Scores
• Risk scores should be applied once other
identifiable causes have been considered
• Do not replace clinical judgment and using
your brain
• Risk scores may miss rare causes with most
serious outcomes
San Francisco Syncope Rule
C
H
E
S
S
Congestive Cardiac Failure
Haematocrit <30%
ECG abnormal
Shortness of breath
SBP <90 at triage
Any one of these factors predicts high risk and therefore pt
should be admitted and investigated further
SFSR
• Endpoint was ‘serious outcome’ or any condition
causing return to the hospital and admission
• Sensitivity 96% and Specificity 56% for serious
outcome at 7 days
• Revalidated by external study in Canadian ED
finding sensitivity 90%, Specificity 33%
• Other studies found Sensitivity 52-77%
• Blanket application to all syncopes and not just
those with no diagnosis after ED evaluation
ROSE Criteria
• Predictors of serious outcome at 30 days
– Raised BNP
– Positive stool haemoccult
– Anaemia
– Hypoxia
– Prescence of Q waves on ECG
Sensitivity 87%. Negative predictive value 95.5%
ACEP Recommendations
Level A
Level B
Hx and exam suggesting
CCF consistent with high
risk
Elderly, structural heart
disease and coronary
artery disease high risk
Perform ECG
Level C
Echo, CT and other lab
tests should not be
routinely performed in
absence of specific findings
Admit CCF and structural
heart disease.
Other high risk: ECG
abnormalities, haematocrit
<30
What the studies agree on
• Identified risk factors:
– Age >65yrs
– Hx of CCF
– Abnormal ECG
Normal ECG may include sinus tachy, first degree
HB, non-specific ST/T wave changes.
Syncope in the Elderly
Most common causes
• Orthostatic hypotension
– 25% ‘Age related’
– 75% Medication related
• Reflex
– CCS cause in 20%
• Cardiac arrhythmias
– Advanced age, underlying cardiac disease and
comorbidities
Prolonged QT syndrome
Brugada Syndrome
WPW syndrome
HOCM
ECG changes in HOCM
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Normal in up to 15%
Left axis deviation
LVH and strain
flipped T’s
big voltage R waves and deep, narrow Q’s in
lateral leads (I, aVL, V5 and V6)
- infarct Q’s are > 1 small square where as
HOCM Q’s are less than 1 small square
Epsilon waves in arrhythmogenic right ventricular cardiomyopathy
Bifascicular block
Trifascicular block
ECG
CHB
ECG
Tachy-bradycardia syndrome
ECG
Torsades des pointes
Disposition of patients
• Manage indentified cause as appropriate
• Admit high risk for monitoring and investigation
• Consider withdrawing medication likely to be
responsible
• Advise pts on how to avoid further syncope:
– VVS – avoid stimulus
– OH – medication change, good hydration, standing
slowly
– CSS – avoidance of tight collars, pressure on CS
Future plans for Emergency Assessment –
Recommendations from Europe
• Falls and syncope service
– Run by geriatrics, cardiology, neurology
• Direct access to investigation and clinic
– Tilt tables, Echo
• Syncope observation unit
– As part of MAU
– 6 hr telemetry, hourly orthostatic BPs
– Echo
Assessing fitness to drive – National
Transport Commission, Australia
• Unexplained syncope: Private drivers refrain from
driving for 3 months. Commercial for 6 months.
• Recurrent syncope not responsive to treatment:
criteria for conditional license not met
• Cause of syncope identified and assessed as
temporary – NO effect on driving status
In the first 2 instances it is the responsibility of the
patient to inform the RTA
Driving fitness - Research
• ESC: Data suggests that risk of a accident in
pts with syncope is not different to those
without
• Prospective study of 3877 pts with syncope.
Recurrence whilst driving occurred only in 10
pts. Risk of syncope related driving accidents
is 0.8% per year.
Summary
• A syndrome encompassing many physiological
and pathological processes
• Our role is to identify those at risk of sudden
cardiac death
• Benign syncope, while having minimal
mortality, has associated morbidity
• Remember – Cardiac BAD, Non-cardiac Not so
bad
Thank You