This document discusses syncope, which is a brief loss of consciousness caused by transient global cerebral hypoperfusion. It is a common symptom but not a diagnosis. The document summarizes the prevalence, causes, evaluation, and management of syncope. The most common causes are neurally-mediated (50%), cardiac arrhythmias (11%), and orthostatic hypotension (6%). Evaluation involves history, physical exam, ECG, echocardiogram, tilt table testing, carotid sinus massage, and long-term cardiac monitoring depending on the suspected cause. Management depends on the underlying cause but may include lifestyle changes, medications, pacemakers, or treating any identified structural heart issues.

1. SYNCOPE: WHAT HAPPENS
WHEN YOUR LIGHTS GO OUT ?
Syed Raza
MD,MRCP (UK),FCCP, Dip.Card (UK)

2. COMMON SCENARIO !
 Elderly lady
 Lives alone
 Collapse at home
 ? LOC
 No eye witness
 Patient does not remember the event

3. CaseM, 85yo F
Mrs 66yo F
,
Mrs K, 59yo F Mrs L, 64yo F

12. Objectives
 Definition
 Prevalence
 Diagnostic Work Up
 Management
 Implications on driving

13. Syncope:
A Symptom, Not a Diagnosis
 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
Lipsitz 1983
Underlying mechanism:
transient global cerebral hypoperfusion.

14. Impact of Syncope
 40% will experience syncope
at least once in a lifetime1
 1-6% of hospital admissions2
 1% of emergency room visits
per year3,4
 10% of falls by elderly are due
to syncope5
 Major morbidity reported in 6%1
eg, fractures, motor vehicle accidents
 Minor injury in 29%1
eg, lacerations, bruises
1
Kenny RA, Kapoor WN. In: Benditt D, et al. eds. The Evaluation and 3
Brignole M, et al. Europace. 2003;5:293-298.
Treatment of Syncope. Futura;2003:23-27. 4
Blanc J-J, et al. Eur Heart J. 2002;23:815-820.
2
Kapoor W. Medicine. 1990;69:160-175. 5
Campbell A, et al. Age and Ageing. 1981;10:264-270.

15. THE COST
 More than 1 billion pounds per year spent by
NHS for managing falls and syncope.
 Significant portion of the budget is spent on
clinical conditions which have been
misdiagnosed ( i.e. 10% of syncope diagnosed as
epilepsy)

16. Incidence Rates of Syncope According to Age and Sex
Soteriades, E. et al. N Engl J Med 2002;347:878-885

18. Classification
Syncope
rally Mediated 34%
ovagal Others 47%
Cardiac Mediated 18%
otid Sinus Orthostatic Hypotension
Arrythmia
ational Idiopathic
ssopharyngeal Neuralgia
Srtructural Heart Disease
Cardiopulmonary Disease Medications
ebrovascular Psychiatric
onomic Failure

19. Causes of syncope*
Neurally mediated 50%
Cardiac arrhythmia 11%
Orthostatic hypotension 6%
Structural cardiopulmonary 3%
Unknown 9%
* Data pooled from 4 population studies n=1640 patients

20. Neurally Mediated Syncope
 Neuro cardiogenic syncope
 Carotid sinus hypersensitivity
 Visceral syncope (micturition, cough, defecation
etc.)
 Glossopharyngeal neuralgia

21. Neurally Mediated Syncope
(autonomic failure)
 Orthostatic /Postural Hypotension
 Postural Orthostatic Tachycardia Syndrome
(POTS)

22. Neuro-Cardiogenic Syncope
 Commonest cause of syncope
 Most frequently in 30 - 50 age group
 Typical triggers - pain, fear, blood etc
 Prodromal symptoms- warmth, nausea, sweating
 Good history is key to diagnosis
 Usually does not require fancy investigations
 Patient may be discharged the same day

23. Pathophysiology
 Neuro-cardiovascular reflexes severely impaired
or absent.
 Pooling of 500-800 ml blood in distensible
blood vessels of legs on prolonged standing.
 Reduced venous return and cardiac output.
 Reduced brain perfusion.
 Warning signals to brain impaired
 Patient presents with pre syncope or syncope

24. Carotid Sinus Syndrome
 Common in elderly/atherosclerotic ds.
 Sensitive baro receptors at carotid body
 Any pressure i.e. sudden neck turning
or tight collar /shaving
 slowing of heart rate and fall in blood pressure
 Poor brain perfusion → Syncope

25. Carotid Sinus Syncope and Autonomic Dysfunction
Freeman, M. Neurogenic Orthostatic Hypotension. NEJM 2008; 358: 616

27. POSTURAL BP

29. Postural Blood Pressure
 Sadly NOT accurately measured
 Supine position –at least 10 minutes
 Standing/Sitting
 Measure BP immediately, 1 minute , 3 minutes
 Symptoms of pre-syncope or syncope
 Fall in systolic BP by 30 mmHg AND diastolic
BP by 20 mmHg.

30. Orthostatic Hypotension
Common in elderly
most vulnerable
 ↓ Baro receptor sensitivity
 Reduced thirst mechanism
 Poly pharmacy
 Peripheral sympathetic tone impairment
 Diabetic neuropathy, antihypertensive medication

31. POSTURAL ORTHOSTATIC
TACHYCARDIA SYNDROME (POTS)
Patients ( women 15-50)
dizziness or faint on acquiring sudden erect
posture
 Reduced volume of blood reaches the heart
 Stimulation of mechano receptors causes
tachycardia
 Heart rate increases by more than 30 beats/min.
 Heart rate usually above 120 /minute.

32. Initial evaluation: History
Prior to event
Position, activity, situation (urinating etc)
predisposing factors (crowded, warm place etc)
precipitating events (fear, pain, neck movements)
Onset of event
nausea, vomiting, sweating, aura,
About event (eye witness)
Colour, duration, movements, tongue biting
After the event
nausea, vomiting, sweating, confusion, muscle ache, skin colour, wounds

33. Diagnostic tests
 Carotid sinus massage
 Tilt testing
 Others; EP testing, signal averaged (V) ECG,
Echocardiography, ETT, cardiac catheterisation,
neurological/psychiatric evaluation,

34. Carotid Sinus Massage Protocol
 Massage longitudinally, site of maximal impulse, anterior margin
SCM muscle level of cricoid cartilage
 5 –10 seconds, right first, then left after 1-2 minute break
(Newcastle protocol 10secs)
 Continuous ECG and BP monitoring mandatory
 Neurological complication in 0.45% in a series of 1600 patients
(5secs massage)

35. Carotid Sinus Massage
 Stimulation of hypersensitive carotid body can
produce 3 main responses
 Cardio-inhibitory response (70%)
 Vasodepressor response (10%)
 Mixed (20%)

36. Positive CSM Test
 Significant brady /more than 3 s pause on the
ECG
 More than 50 mmHg fall in systolic BP
 Mixed response

37. TILT TABLE TEST

38. Tilt Table Test In Action

39. Indications for Tilt Table Testing
 Unexplained recurrent syncope
 Assessment of recurrent, unexplained fall
 Syncope with suspected autonomic failure
 After a cardiac cause for syncope has been
excluded

40. Upright Tilt Table Test
 Measure HR and BP
while tilting them
upright
 Attempt to elicit
symptoms

41. Tilt Table Testing
 Supine at least 20 minutes prior to tilt
 Tilt angle 70 degrees
 Passive phase min 20 to 45 minutes
 Use either intravenous isoprenaline or sublingual GTN
if passive phase is negative
 Pharmacological phase – 15 to 20 minutes
 End-point: induction syncope

42. Normal test

43. Cardioinhibitory response

44. Vasodepressor response
BP drops from 150/70 to 50/30 but heart rate
stays same

45. Mixed response
BP drops from 150/60 to 50/20 while HR
drops from 65 to 30bpm

47. Orthostatic hypotension
steady drop in BP and rise in HR

48. Heart Monitoring Options
Syncope Occurs Infrequently,
Long-term Monitoring is Likely to be Most Effective
12-Lead 10 Seconds
Holter Monitor 2 Days
Typical Event 7 Days
Recorder
MCOT External 30+ Days
Loop Recorder
ILR 36 Months
ILR = insertable loop recorder
MCOT= mobile cardiac outpatient telemetry

50. Everything is spinning

51. MANAGEMENT
 Patient education and counselling
 Avoid triggers
 Increase in salt and fluid intake
 Sleeping with the head of the bed raised (6-12
inches.
 Elastic stockings
 Preventing LOC or Injury
 Assume supine position upon onset of prodrome
 Avoid driving or other activities that could lead to injury

52. Pharmacological therapy
 Beta blockers
 Dysopyramide
 Fludrocortisone
 SSRIs
 Midodrine

53. Management of Neurally
Mediated Syncope
Grubb BP. NEJM. 2005. 352(10): 1004-1010

54. INDICATION FOR
PACEMAKER
 Syncope with cardio inhibitory or mixed (cardio-
inhibitory plus vasodepressor).
 Severe brady cardia, AV or SA block
 Over drive pacing for some tachy arrhythmia.

55. What are the indications for pacemaker
therapy in neurocardiogenic syncope?
• Non-random, observational
• RCTs comparing vs
• RCTs comparing vs

56. The North American Vasovagal
Pacemaker Study (VPS)
27 dual-chamber pacemakers
Included with rate-drop response
• >6 lifetime episodes
• + tilt-table test
54 pts
27 No pacemaker
– (relative bradycardia)
Primary outcome: first recurrence of syncope
Pacemaker No pacemaker
Excluded
• Vascular, coronary, myocardial or Recurrence of 6/27 (22%) 19/27 (70%)
conduction system disease Syncope
Time to 112 days 54 days
recurrence
J. Am. Coll Cardiol. 1999;33:16-20

57. Overall Survival of Participants with Syncope, According to Cause, and
Participants without Syncope
Soteriades E et al. N Engl J Med 2002;347:878-885

58. Driving Implications
Group 1 Entitlement Group 2 Entitlement
Simple faint –definite No driving restrictions No driving restrictions
provocation with prodromal
symptoms
Unexplained syncope with Can drive 4 weeks after the Can drive 3 months after the
low risk of recurrence event event
Unexplained syncope & Can drive 4 weeks after the Can drive after 3 months if the
high risk of recurrence event if cause identified and cause identified and treated
A abnormal ECG treated If no cause, licence revoked
B structural heart disease If no cause – 6 months off for year
C syncope at the wheel or
results in injury
D more than 1 episode in
last 6 months
Loss of consciousness with Licence revoked for 6 months Licence revoked for 1 year
no clinical pointers
Full neuro/cardiac Ix with
no pointers
Cough syncope Stop driving until symptoms Stop driving
controlled If smokes or respiratory
disease have to be controlled
for 5 years

59. SUMMARY
 Syncope is not an uncommon problem
 The diagnosis of syncope is often missed or it is
misdiagnosed
 Thorough history from eye witness can be very
helpful
 Syncope can be fatal
 Further training to identify the problem and
formulating a plan of management is needed.

61. ANY QUESTION ??