Syncope

An approach to a patient with Syncope

1. AN APPROACH TO A PATIENT WITH SYNCOPE BY: Dr. Tikal Kansara R2 Medicine D Unit

2. What is Syncope? Transient, self-limited loss of consciousness with an inability to maintain postural tone that is followed by spontaneous recovery. with global cerebral hypoperfusion Aka swoon, blackout, collapse, faint

3. Pre-Syncope/ Almost fainting: A state consisting of lightheadedness, muscular weakness, blurred vision, and feeling faint (as opposed to a syncope, which is actually fainting). Faintness Sensation of impending loss of consciousness Giddiness Having a reeling, light headed sensation A feeling of unease and unsteadiness

4. Vertigo A sensation of rotation of one’s self (subjective vertigo) or one’s surroundings (objective vertigo) in any plane. Dizziness Vertigo Syncope Nonsyncope Nonvertigo Patients feel that they cannot keep their balance May become worse on movement

5. Why is it important? Syncope can be an isolated benign, stand alone incident or it can be a trigger of some serious life threatening condition; most likely CARDIAC. Hence, it is important to be vigilante to scrutinize this symptom

6. MECHANISM OF SYNCOPE Syncope is the result of global cerebral hypoperfusion . Brain parenchyma cannot store high energy phosphate bonds like other cells of the body hence depends on the constant supply of glucose for its survival. Typically cessation of blood supply for 3 to 5 seconds results in syncope.

7. Reproduced From: European Heart Journal (2009) 30, 2631–2671

8. BIO DATA Age: Two peaks: With median of 15 years – VVS ( Vasovagal Syncope) is more common With old age patients – Cardiac & OH is more common Sex: More common in females Occupation: Common in painters, formal clothing (tight collar and tie)

9. HISTORY Hx and PE are perhaps the two most important aspects in diagnosis of Syncope. These ( Hx & PE) with 12 lead ECG is the only Level A recommendation for diagnosis of Syncope; according to 2007 American College of Emergency Physicians (ACEP) Clinical P olicy on Syncope.

10. KEY ASPECTS IN HISTORY The three main points on which the etiology of syncope can be determined are: Precipitant Factors Activity the patient was involved in before the incident Patient’s position

11. Precipitant Factors Fatigue Food and water deprivation Warm and ambient enviornment Alcohol Pain Specific Phobias Strong emotional stimuli such as fear and appprehension

12. Activity prior to the episode If occurred at rest Change in posture On exertion / after exertion Specific Situations: Shaving, coughing, voiding or prolonged standing. If occurs within 2 minutes of standing denoted OH (Orthostatic Hypotension – Classical).

13. Position of the patient Whether the patient was standing, sitting, lying down when the syncope occurred. Syncope while sitting or lying down most likely is cardiac

14. Important Hx questions about the attack Was the loss of consciousness complete? Was loss of consciousness with rapid onset and short duration? Was recovery spontaneous, complete, and without sequelae ? Was postural tone lost?

15. Other associated complaints Prior faintness, dizziness, or light-headedness – denotes p/o syncope in 70 % of patients During pre syncopal period – Vertigo, blurred or faded vision, pallor, or paresthesias , diaphoresis – p/o syncope Aura – p/o seizures

16. Some Red Flag Signs These when present should prompt for further evaluation of the patient These includes: Exertional onset Chest Pain Dyspnea Low back Pain Palpitations Severe headache FND (Focal Neurological Deficits) Diplopia , ataxia or dysarthria

17. After episode Ask about the duration of loss of consciousness If in seconds to minutes – p/o Syncope If more than that – p/o Seizures After regaining consciousness, whether the patient was confused, had oral trauma, incontinence or myalgias . Post event confusion rare in syncope, and when it occurs, its always less than 30 seconds.

18. MEDICATION HISTORY Reduce BP - Anti- hypertensives , diuretics, nitrates Affect Cardiac Output – Beta-blockers, digitalis, antiarrythmics Prolong QT-interval – TCAs, phenothiazidines , quinine, amiodarone Alter sensorium – Alcohol, cocaine, analgesics, sedatives Alter serum electrolytes - Diuretics

19. PAST MEDICAL HISTORY Cardiac Etiology MI, Arrythmias , Structural cardiac diseases, Cardiomyopathies , CHF, abdominal aortic aneurysm Neurological Etiologies: H/o Seizure disorder, CVA, DVT Diabetes

20. PHYSICAL EXAMINATION VITALS: Temperature : Fever – UTI or Pneumonia Pulse: Tachycardia – PE, Hypovolemia , tachyarrythmias or ACS Bradycardia – Cardiac Conduction defects, ACS BP – for Orthostatic Hypotension Glucose – Hypoglycemia

21. Higher Functions: Patients with genuine syncope should have a normal baseline mental status If confusion, abnormal behavior, headache, fatigue or somnolence is present – p/o toxic, metabolic or CNS cause should be considered. Signs of Trauma- Head injury, lacerations, extremity fractures Tongue bite – p/o seizures Sos Carotid Sinus massage

22. Causes of Syncope

23. Reproduced From: European Heart Journal (2009) 30, 2631–2671

24. CAUSES OF SYNCOPE Reflex ( Neurally -mediated) syncope NMS Vasovagal Emotional stress, fear, pain, blood phobia, instrumentation Mediated by orthostatic stress Situational Cough, sneeze, Gastrointestinal (swallow, defaecation , visceral pain) Post-exercise Post- prandial Others (laugh, brass instrument playing, weightlifting)

25. Orthostatic Hypotension Fall in systolic BP by 20 mmHg or more and/or fall in diastolic BP by 10 mmHg or more or systolic BP to < 90 mmHg, when a person assumes a standing position from sitting or supine position. Classification Initial OH ( 0 – 30 sec) Classical OH (30 sec – 3 min) Delayed (progressive) OH (3 – 30 min) Delayed (progressive) OH + Reflex syncope (3 – 45 mins )

26. Orthostatic hypotension Primary autonomic failure Pure autonomic failure, Parkinson’s disease with autonomic failure, Lewy body dementia, multiple system atrophy Secondary autonomic failure Diabetes, amyloidosis , uremia, spinal cord injures Drug-induced orthostatic hypotension Alcohol, vasodilators, diuretics, antidepressants Volume depletion Haemorrhage , diarrhoea , vomitting

27. Reproduced From: European Heart Journal (2009) 30, 2631–2671

28. Cardiac Syncope Arrythmias as primary cause: Bradycardia : Sinus node dysfunction AV conduction disease Implanted device failure Tachycardia Supraventricular Ventricular (idiopathic, secondary to structural heart diseases, channopathies ) Drug induced tachycardia and bradycardia

29. Cardiac Syncope Structural disease (Cardiac) Valvular heart disease, Acute MI/ischemia, HOCM, Cardiomyopathy , Cardiac Mass ( Atrial Myxomas , tumors), Pericardial diseasea / tamponade , congenital anomalies of coronary arteries, prosthetic valve dysfunction Structural disease (Extra cardiac) Pulmonary embolus, acute aortic dissection, pulmonary hypertension

30. Reproduced From: European Heart Journal (2009) 30, 2631–2671

31. CONDITIONS MISDIAGNOSED AS SYNCOPE With partial or T-LOC w/o global cerebral hypoperfusion Epilepsy Metabolic disorders including hypoglycemia, hypoxia, hyperventilation with hypocapnia Intoxications Vertebrobasilar TIA W/O impairment of consciousness Cataplexy Drop attacks Falls Functional (psychogenic peudosyncope ) TIA of carotid origin

32. RISK STRATIFICATION SAN FRANCISCO SYNCOPE RULE (SFSR) Abnormal ECG Congestive Cardiac Failure Shortness of breath Haematocrit < 30% SBP < 90 mmHg No risk :: score = 0 Risk of serious events in 7 days :: score >= 1

33. DIAGNOSTIC TESTS

34. ECG

35. ECG is most important investigation which helps suffice the diagnosis in most of the situations If that does not help then, International Study On Syncope Of Unknown Etiology (ISSUE) investigators advise some further tests.

36. Carotid Sinus Massage Indicated in patients > 40 years of age with syncope of unknown etiology after initial evaluation Contraindicated in patients with previous TIA or stroke in prior 3 months and in patients with carotid bruits RESULT: Diagnostic if syncope is reproduced in the presence of asystole longer than 3 seconds and/or fall in SBP > 50 mmHg

37. CAROTID SINUS MASSAGE (CSM)

38. ACTIVE STANDING

39. TILT TABLE TESTING

40. Interpretation Of Tilt Table Test (TTT) VASIS CLASSIFICATION Type 1 – Mixed . Both HR and BP are reduced. BP reduction precedes HR reduction. HR reduction >10% but never < 40 / min Type 2 – Cardioinhibitory . Reduction in both HR and BP. BP decrease precedes HR reduction. Minimum HR is < 40/min or ayatole > 3sec Type 3 – Pure vasodepressor . HR does not decrease to more than 10% Chronotrophic incompetence - no HR increase in spite of the tilt Excessive HR rise – POTS (Positional Orthostatic Tachycardia Syndrome)

41. Reproduced from: Journal of American College Of Cardiology

42. ELECTROCARDIOGRAPHIC MONITORING Conventional Ambulatory Holter Monitoring In-Hospital Monitoring Event Recorders External or implantable loop recorders Remote (at home) telemetry

43. In-Hospital Monitoring Indicated only when the patient is at high risk of a life- threathening arrythmia To be applied immediately after syncope, for a few days, to look for arrhythmic syncope Yield only 16%

44. Holter Monitoring Conventional 24 – 48 hour, or even 7 days, Holter recorders. Yield may be as low as 1 – 2 %

45. External Loop Recorders These devices have a loop memory which records and deletes ECG When activated by the patient typically after the event, they records and saves the pre-activation 5 – 15 minutes of ECG. Very less useful in infrequent syncope and requires high patient compliance

46. Implantable Loop Recorders (ILRs) Life span of 36 months Solid state loop memory that stores retrospective ECGs when activated by bystander or patient, usually after a syncopal episode, or automatically in case of an occurrence of predefined arrythmias .

47. Reproduced From: http://openi.nlm.nih.gov/

48. Reproduced From: Hall-Garcia Cardiology, Texas

49. Remote (at home) Telemetry External and implantable device systems are available that are able to provide continuous ECG recording or 24 hour loop memory, with wireless transmission (real time) to a service center.

50. ELECTROPHYSIOLOGICAL STUDY (EPS)

51. Echocardiography For patients suspected of having a structural heart disease

52. Psychiatric Evaluation Various psychiatric drugs can precipitate syncope through OH and prolonging QT interval However, disruption of anti psychotic medications may have severe psychiatric consequences These patients may present with “Functional Attacks” of T-LOC

53. Functional Attacks Pseudoseizures Pseudosyncopes

54. NEUROLOGICAL INVESTIGATIONS Electroencephalogram CT/MRI Neurovascular Studies Doppler USG

55. TREATMENT Principal goals: Prolong survival Limit physical injuries Prevent recurrences

56. TREATMENT OF REFLEX SYNCOPE Lifestyle modifications Aviodance of possible triggers Early recognition of prodromal symptoms Performing maneuvers to abort the episode Supine position Physical counterpressure maneuvers (PCMs)

57. Pharmacological considerations α – agonists Midodrine Fludrocortisone Some benefits in adults with reflex syncope β – blockers Paroxetine

58. Individual considerations For VVS Tilt table testing To make patients familiarize with prodromal symptoms PCMs (Physical Counterpressure Maneuvers) For Situational Syncope Carotid Sinus Syncope Dual Chamber Cardiac Pacing

59. ORTHOSTATIC HYPOTENSION & OTHROSTATIC INTOLERANCE Principal Goals Expansion of ECF volume In absence of hypertension, patient instructed to take sufficient salt and water intake (target 2 – 3 litres and 10 gm NaCl ) Rapid cool water ingestion Orthostatic intolerance and post prandial hypotension

60. Sleeping with head end of bed elevated (10◦) For gravitational venous pooling Abdominal binders or compressive stocking Pharmacological Midodrine Fludrocortisone

61. Other treatment Modalities Octreotide Post prandial hypotension Erythropoetin Anaemia Pyridostigmine Frequent small meals Judious use of leg and abdominal muscles

62. CARDIAC CAUSE - TREATMENT Treat the underlying cause

63. Syncope in the elderly Most common cause of syncope are OH, reflex syncope (especially CSS) and cardiac arrythmias Syncope in morning favors OH Taking multiple medications, whose withdrawal/overdose leads to syncope

64. OH is not always repeatable in the elderly (particularly medication and age related). Therefore, orthostatic BP appraisal should be repeated, preferably in the morning and/or promptly after syncope CSM is particularly important Tilt testing is well tolerated and safe Twenty-four hour ambulatory BP recordings may be helpful if instability of BP is suspected Due to high frequency of arrythmias , an ILR may be especially useful in elderly with unexplained syncope

65. Driving and Syncope In a large study, 9.8 % had syncope while driving, which was commonly reflex (37 %) or cardiac (12%) The cumulative probability was only 7 % in 8 years Risk of syncope mediated driving accidents was 0.8% per year

66. Refereneces eMedcape Website European Society Of Cardiology (ECS); European Heart Journal www.dizziness-and-balance.com Harrison’s Textbook Of Internal Medicine 17 th Edition Merck Manuals (MSD – online) American Heart Journal PubMed (National Institute Of Health –NIH) Mayo Clinic websites

67. Dr. Tikal Kansara IInd Year Resident SSG Hospital & Medical College, Vadodara