1. Emergency Department Management of Syncope
Emilia McGhee
Sept 2010

2. 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

3. Incidence 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%

4. Cerebral perfusion maintained by:
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

5. What is not syncope
Transient LoC without global cerebral hypoperfusion
Seizure
TIA
Metabolic disorders
Intoxication
Loss of postural tone without LoC
Cataplexy
Drop attacks
Falls
TIA of carotid origin
Functional - psychogenic

6. Syncope vs Seizure Triggering factor Prodrome
Convulsion after LoC, and <15 secs
Short duration
Quick recovery
Ongoing lethargy but no confusion
Pt history
Aura
Automatisms
Convulsions at onset of LoC
Longer duration
Post-ictal phase
Tongue biting, incontinence

7. Classification Reflex – neurally mediated – 30%
Orthostatic hypotension – %
Cardiac – electrical and mechanical – 10%

8. Reflex Vasovagal Situational Carotid sinus syncope 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

10. 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

12. Wyatt W. Decker, M.D.
“Syncope and sudden death are the same, except that in one you wake up”
SYNCOPE: Critical Questions

13. Cardiac - Electrical Ventricular arrhythmias
VT, Torsades
Sudden onset, little prodrome
Elderly pts with known cardiac disease
Supraventricular arrhythmias
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

14. Cardiac - Mechanical Low CO output states Cardiac outflow obstruction
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

15. HOCM Causes of syncope: Self terminating ventricular arrhythmias SVT
Severe outflow tract obstruction
Bradyarrhythmia
Hypotension in response to exercise
Reflex syncope

16. 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

17. Aim in ED Recognise life threatening conditions
Recognise low risk conditions for discharge
Chose appropriate FU for those who need further diagnostic testing
Recognise those who do not need further investigation
Moving away from diagnosis to risk stratification

18. 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

19. Were they SOB?
- PE
- tamponade
Did they have chest pain?
- ACS and an arrhythmia
- dissection
Did they have abdominal pain?
- AAA
- ectopic
Did they have a headache?
- SAH

20. Sudden or unexplained deaths in family Known CCF Medications
Previous arrythmias
Known CAD
Sudden or unexplained deaths in family
Known CCF
Medications
- QT prolonging medications
- vasodilators
- anti-hypertnesives

21. Red Flags Syncope during exertion Syncope in lying position
Absence of external factors
Family hx of SCD
Slow recovery from syncope

22. Examination and bedside tests
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

23. 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

24. Ix that are generally low yield
CTB
MRI
Holter monitor
Carotid dopplers
EEG

26. 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

27. ECG findings associated with high risk of sudden cardiac death
Hypertrophic cardiomyopathy
Long QT
Ventricular pre-excitation (WPW)
Brugada Syndrome
Short QT
Arrhythmogenic Rt ventricular dysplasia

28. ECG changes in HOCM 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

29. 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

30. San Francisco Syncope Rule
C H E 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

31. 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

32. 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%

33. ACEP Recommendations Level A Level B Level C
Hx and exam suggesting CCF consistent with high risk
Elderly, structural heart disease and coronary artery disease high risk
Perform ECG
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

35. 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.

36. 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

37. Prolonged QT
Prolonged QT syndrome

38. Brugada – type 1 – coved type ST elevation with >2mm J point elevation with downsloping AT and negative T. ST elevation in V1-V3 with RBBB appearance but without terminal S waves in lateral leads. PR may be prolonged. Changes over time, with exrecise, fever, medications etc.
Brugada Syndrome

39. WPW. Note Delta wave and short PR. ST and T wave changes.
WPW syndrome

40. HOCM. LVH, large R waves in lateral leads with narrow Qs

41. ECG changes in HOCM 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

42. Epsilon waves in arrhythmogenic right ventricular cardiomyopathy
Epsilon wave, seen in 50% of Arrythmogenic Rt ventricular dysplasia. May also have inverted T waves V1-V3 and RBBB, reflecting slow conduction through myocardium rather than real BBB. 90% will have abnormal ECG but my be subtle.
Epsilon waves in arrhythmogenic right ventricular cardiomyopathy

43. Bifasicular block. RBBB and Lt anterior or posterior hemiblock
Bifascicular block

44. Trifasicular block. Prolonged PR, RBBB, LAD
Trifascicular block

45. ECG
Sinus progressing to CHB. Complete ventricular pause, until ventricular rhythm kicks in
CHB

46. ECG Tachy-bradycardia syndrome
Atrial tachycardia progressing to long sinus pauses
Tachy-bradycardia syndrome

47. ECG
Long QT progressing to Torsades
Torsades des pointes

48. 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

49. 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

50. 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

51. 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.

52. 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

53. Thank You