Syncope, or fainting, is a relatively common problem that is often misdiagnosed. It is caused by a temporary drop in blood pressure and loss of consciousness. The most common causes are neurally-mediated syncope, cardiac arrhythmias, and orthostatic hypotension. A thorough history, physical exam, and diagnostic tests like carotid sinus massage and tilt table testing can help identify the underlying cause. Treatment depends on the cause but may include lifestyle changes, medications, or pacemaker implantation in severe cases. Proper diagnosis and management of syncope is important as it can occasionally lead to injuries or accidents.

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. Case Mrs L, 64yo F 66yo F , Mrs K, 59yo F Mrs M, 85yo F ? Seizure ? FA L L ? Orthostasis ? Neurocardiogenic

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

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 Neurally Mediated 34% Vasovagal Carotid Sinus Situational Glossopharyngeal Neuralgia Cerebrovascular Autonomic Failure Cardiac Mediated 18% Arrythmia Srtructural Heart Disease Cardiopulmonary Disease Others 47% Orthostatic Hypotension Idiopathic Medications Psychiatric

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 ILR MCOT External Loop Recorder Typical Event Recorder Holter Monitor 12-Lead 2 Days 7 Days 30+ Days 36 Months 10 Seconds 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. Postural hypotension Exclude treatable causes – then: Education Raise bed head Compression stockings Increase salt intake Fludrocortisone – 50 mcg nocte initially Flurbiprofen Desmopressin Midodrine – oral alpha agonist

53. Pharmacological therapy Beta blockers Dysopyramide Fludrocortisone SSRIs Midodrine

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

55. 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.

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

57. 27 dual-chamber pacemakers with rate-drop response 54 pts 27 No pacemaker The North American Vasovagal Pacemaker Study (VPS) Included >6 lifetime episodes + tilt-table test (relative bradycardia) Primary outcome: first recurrence of syncope Excluded Vascular, coronary, myocardial or conduction system disease J. Am. Coll Cardiol . 1999;33:16-20 Pacemaker No pacemaker Recurrence of Syncope 6/27 (22%) 19/27 (70%) Time to recurrence 112 days 54 days

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

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

60. 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.

62. ANY QUESTION ??