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European Society of Cardiology Task Force Report

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1 European Society of Cardiology Task Force Report
Guidelines on Management (Diagnosis and Treatment) of Syncope Update 2004 Task force members: M. Brignole (Chairman), P. Alboni, D. Benditt, L. Bergfeldt, J.J. Blanc, P.E. Bloch Thomsen, J.G. van Dijk, A. Fitzpatrick, S. Hohnloser, J. Janousek, W. Kapoor, R.A. Kenny, P. Kulakowski, A. Moya, A. Raviele, R. Sutton, G. Theodorakis and W. Wieling Task force member affiliations are available from the ESC, or in the original article published in the European Heart Journal.

2 European Society of Cardiology Task Force Report
Guidelines on Management (Diagnosis and Treatment) of Syncope – Update 2004 Executive summary: Brignole et al. Eur Heart J 2004; 25: 2054 Full text: Brignole et al. Europace 2004; 6: 467 Downloadable for free from Task force members: M. Brignole (Chairman), P. Alboni, D. Benditt, L. Bergfeldt, J.J. Blanc, P.E. Bloch Thomsen, J.G. van Dijk, A. Fitzpatrick, S. Hohnloser, J. Janousek, W. Kapoor, R.A. Kenny, P. Kulakowski, A. Moya, A. Raviele, R. Sutton, G. Theodorakis and W. Wieling Task force member affiliations are available from the ESC, or in the original article published in the European Heart Journal.

3 Guidelines on Management of Syncope
Task Force Report: Guidelines on Management of Syncope Outline: Objectives Background Classification, epidemiology and prognosis Diagnosis Treatment Special issues

4 Part I: Objectives of the Guidelines

5 Objectives To identify: When a diagnosis can be considered likely .
The most appropriate diagnostic work-up. How patients with syncope should be risk stratified. When patients with syncope should be hospitalised. Which treatments are likely to be effective in preventing syncopal recurrences.

6 Part II: Background

7 Background Syncope is a transient symptom and not a disease.
The diagnostic evaluation, and definition of a specific cause of syncope is difficult. There is an international need for: Specific criteria to aid diagnosis Clear-cut guidelines on how to choose tests How to evaluate and use the results of tests to establish a cause of syncope Summary recommendations for treatment

8 Role of the Task Force Develop a comprehensive outline of the issues needing to be addressed. Review applicable literature and develop summaries. Rank the evidence, and develop consensus recommendations. Provide specific recommendations for diagnosis and management of syncope.

9 Part III: Classification, Epidemiology and Prognosis of Syncope

10 The underlying mechanism is a transient global cerebral hypoperfusion
Definition Syncope is a symptom, the defining clinical characteristics of which are: transient self-limited loss of consciousness leads to falling onset is relatively rapid recovery is spontaneous, complete, and usually prompt The underlying mechanism is a transient global cerebral hypoperfusion

11 Classification of Syncope
Syncope must be differentiated from other “non-syncopal” conditions which also lead to transient loss of consciousness. Pathophysiological classification is based on the principal causes of the transient loss of consciousness.

12 ESC Task Force on Management (Diagnosis and Treatment) of Syncope
Real or apparent transient loss of consciousness Non-syncopal attacks With partial or complete loss of consciousness Without any impairment of consciousness Syncope Update 2004

13 Loss of consciousness: I - Syncope
Update 2004 Loss of consciousness: I - Syncope Neurally-mediated Vasovagal faint (common faint): - classical - non-classical Carotid sinus syncope Situational Faint Glossopharyngeal neuralgia Orthostatic hypotension Autonomic failure (primary, secondary, drug and alcohol, post-exercise, post- prandium, volume depletion) Cardiac arrhythmias Bradycardia (sinus & AV diseases) Tachycardia (atrial & ventricular) Inherited (long QT, Brugada s.) Implanted device malfunction Drug-induced pro-arrhythmias Structural cardiac Valvular disease, Acute ischaemia, Obstructive diseases, Tamponade, Pulmonary embolism, Aortic dissection Cerebro-vascular Vascular steal syndromes

14 Loss of consciousness: II - Non-syncopal
Update 2004 Loss of consciousness: II - Non-syncopal Partial or complete loss of consciousness Metabolic Hypoxia,hyperventilation, hypoglycemia Epilepsy Intoxication Vertebro-basilar TIA Any impairment of consciousness Falls Cataplexy Drop attacks Psychogenic ‘pseudo-syncope’ Fictitious disorders, malingering and conversion Carotid TIA

15 Epidemiology of Syncope
The Framingham study reports an incidence of 7.2 per 1000 person-year in a broad population sample. Assuming a constant incidence rate over time, the Framingham study calculates a 10-year cumaulative incidence of 6%. In selected populations, such as the elderly, the annual incidence may be as high as 6%, with a recurrence rate of 30%. The Framingham study included 5209 people over a 26-year period. (Soteriades E et al. Incidence and prognosis of syncope, N Engl J Med 2002; 347: ) The Lipsitz, et al, study reported on an elderly institutionalized population. (Lipsitz LA, et al. Syncope in an elderly instituzionalized population: prevalence, incidence and associated risk. Q J Med 1985; 55: (Note to reviewers: May need to either a) State “Complete references available in the ESC Guidelines”, or b) Add the complete references here.)

16 Syncope: Reported Frequency
Individuals <18 yrs Military Population yrs Individuals yrs* Individuals >70 yrs* 15% 20-25% 16-19% 23% Multiple reports have examined the frequency with which syncope occurs in various populations. This slide provides an overview of such findings. In essence the frequency with which syncope is reported to have occurred in various study groups is approximately 20%. The basis for syncope would be expected to differ substantially among these groups. Younger patients will have a greater proportion of vasovagal syncope, whereas older individuals may reasonably be expected to have a higher likelihood of underlying structural heart disease, and hence a greater predilection to more worrisome etiologies. *during a 10-year period

17 Impact of Syncope Recurrences in ≈ 35% of patients at 3 years.
Cardiac causes result in increased mortality. Syncope can result in other physical injuries to the patient (e.g. broken bones) or to others (e.g. due to motor vehicle accidents). Recurrent syncope has a significant negative impact on quality of life. Recurrences often prompt a hospital admission and expensive testing, resulting in considerable economic implications.

18 Prognostic stratification
Structural heart disease is the most important predictor of total mortality and sudden death in patients with syncope.

19 Prognostic stratification
Poor prognosis: Structural heart disease (independent of the cause of syncope) Excellent prognosis: Young, healthy, normal ECG Neurally-mediated syncope Orthostatic hypotension Unexplained syncope

20 Prognostic stratification
Risk stratification: age >45 history of congestive heart disease history of ventricular arrhythmias abnormal ECG Arrhythmias or death within one year : from 4-7% of patients with 0 factors to % in patients with 3 factors From: Martin TP et al. Risk stratification of patients with syncope Annals Emerg Med. 1997; 29:

21 Part IV: Diagnosis

22 The diagnostic strategy based on the initial evaluation
Management strategy Initial evaluation (history, physical exam, ECG & BP supine/upright) Laboratory investigations guided by the initial evaluation (Reappraisal) Treatment

23 Update 2004 Eur Heart J 2004; 25: 2059

24 Initial evaluation (History, physical exam, ECG & BP supine/upright)
Update 2004 Diagnosis Initial evaluation (History, physical exam, ECG & BP supine/upright)

25 Initial evaluation 3 key questions: Question 1
Syncope or non-syncopal attack ? Question 2 Is heart disease present or absent ? Question 3 Which history of syncope ?

26 Important historical features
Initial evaluation Important historical features 1 - Questions about circumstances just prior to attack Position (supine, sitting or standing) Activity (supine, during or after exercise) Situation (urination, defecation, cough or swallowing) Predisposing factors (e.g., crowded or warm places, prolonged standing, post-prandial period) Precipitating events (e.g., fear, intense pain, neck movements) 2 - Questions about onset of attack Nausea, vomiting, feeling of cold, sweating, aura, pain in neck or shoulders 3 - Questions about attack (eyewitness) Skin colour (pallor, cyanotic) Duration of loss of consciousness Movements (tonic-clonic, etc) Tongue biting

27 Important historical features
Initial evaluation Important historical features 5 - Questions about end of attack Nausea, vomiting, diaphoresis, feeling of cold, confusion, muscle aches, skin colour, wounds 6 - Questions about background Number and duration of syncopes Family history of arrhythmogenic disease Presence of cardiac disease Neurological history (Parkinsonism, epilepsy, narcolepsy) Internal history (diabetes, etc.) Medication (hypotensive and antidepressant agents)

28 The diagnostic strategy based on the initial evaluation
The initial evaluation may lead to: Certain diagnosis Suspected diagnosis No diagnosis (unexplained syncope)

29 Initial evaluation Diagnostic criteria
Vasovagal syncope is diagnosed if precipitating events such as fear, severe pain, emotional distress, instrumentation and prolonged standing are associated with typical prodromal symptoms. Situational syncope is diagnosed if syncope occurs during or immediately after urination, defaecation, cough or swallowing. Orthostatic syncope is diagnosed when there is documentation of orthostatic hypotension associated with syncope or presyncope.

30 ECG diagnostic criteria
Initial evaluation ECG diagnostic criteria Syncope due to cardiac arrhythmia is diagnosed in case of: Symptomatic sinus bradycardia <40 beats/min or repetitive sino-atrial blocks or sinus pauses >3 s. Mobitz II 2nd or 3rd degree atrioventricular block. Alternating left and right bundle branch block. Rapid paroxysmal supraventricular tachycardia or ventricular tachycardia. Pacemaker malfunction with cardiac pauses.

31 ECG diagnostic criteria
Initial evaluation ECG diagnostic criteria Syncope due to cardiac ischemia is diagnosed when symptoms are present with ECG evidence of acute myocardial ischaemia with or without myocardial infarction, independently of its mechanism (*). * The mechanism can be cardiac (low output or arrhythmia) or reflex (Bezold-Jarish reflex), but management is primarily that of ischaemia.

32 Clinical and ECG features that suggest a cardiac syncope
Presence of severe structural heart disease Syncope during exertion or supine Palpitations at the time of syncope Suspected VT (e.g. heart failure or NSVT) BBB Mobitz 1 second degree AVB Sinus bradycardia <50 bpm WPW Long QT ARVD or Brugada Syndrome

33 Clinical and ECG features that suggest a neurally-mediated syncope
Absence of cardiac disease. Long history of syncope. After sudden unexpected unpleasant sight, sound, or smell. Prolonged standing or crowded, warm places. Nausea, vomiting associated with syncope. During or in the absorptive state after a meal. After exertion. With head rotation, pressure on carotid sinus.

34 Laboratory Investigations
Diagnosis Laboratory Investigations

35 Laboratory Investigations
Certain or suspected heart disease yes no Cardiac evaluation -Echocardiogram -ECG monitoring -Exercise test -EP study -ILR NM evaluation -Carotid sinus massage -Tilt testing -ATP test -ILR

36 Laboratory investigations
Useful (when indicated) Carotid sinus massage Tilt testing Echocardiogram Holter/loop monitoring Electrophysiological test Exercise stress testing Implantable loop recorder Almost never useful EEG CT scan & MNR Carotid Doppler sonography Ventricular SAECG Coronary angiography Pulmonary scintigraphy

37 Diagnosis Re-appraisal

38 Re-appraisal Obtaining details of history
Performing NM tests in patients with heart disease Cardiac evaluation in patients without heart disease Neuropsychiatric evaluation

39 Diagnostic Yield Initial evaluation 52% 14% Laboratory tests 34%
Unexplained Data pooled from 7 population-based studies in the 1980’s (N = 1607)

40 Diagnostic Yield Initial evaluation 26% 56% Laboratory tests
Unexplained 18% Data from 3 Syncope Units (total 342 patients)

41 Diagnostic Yield Test APPROPRIATE DIAGNOSTIC NND
Europace 2002; 4: Test APPROPRIATE DIAGNOSTIC NND History/physical exam/ supine-upright BP 308 (100%) 47 (15%) 7 ECG 241 (78%) 25 (10%) 10 Echocardiogram 103 (33%) 3 (3%) 34 ECG monitoring 82 (27%) 13 (16%) 6 Exercise test 22 (7%) 1 (5%) 22 CSM 177 (57%) 44 (24%) 4 Tilt testing 161 (52%) 94 (58%) 2 ATP test 7 (15%) EP study 51 (17%) 14 (27%) In this study diagnostic criteria similar to those recommended in the flow-chart of the ESC Task Force on Syncope were applied to 308 consecutive patients referred to 3 syncope units for syncope. The patients with non-syncopal loss of consciousness at the initial evaluation were excluded. This study shows that when standardized criteria are used, few simple tests are usually needed for diagnosis of syncope. The appropriateness of indications increases the diagnostic yield of the tests. NND= number of tests (patients) needed to diagnosis CSM= carotid sinus massage From: F. Croci, P.Alboni, M. Brignole, et al The Diagnosis of Syncope Using a Standardized Strategy of Evaluation in Patients Referred to 3 Syncope Units. Europace 2002; 4:

42 Number of laboratory test/s necessary (other than Initial Evaluation)
for diagnosis (other than Initial Evaluation) Unexplained 0 test (initial evaluation) 18% 23% >3 test 16% 21% 21% 1 test The same study as above. When standardized criteria are used, few simple tests are usually needed for diagnosis of syncope. The percentage of unexplained syncope at the end of the work-up is low. From: F. Croci, P.Alboni, M. Brignole, et al The Diagnosis of Syncope Using a Standardized Strategy of Evaluation in Patients Referred to 3 Syncope Units. Europace 2002; 4: 2 test Europace 2002; 4:

43 Causes of Loss of Consciousness Data pooled from 4 recent population-based studies (total 1640 patients) Neurally- Mediated Orthostatic hypotension Cardiac Arrhythmia Structural Cardio- Pulmonary Non-syncopal 1 Vasovagal Carotid Sinus Situational Cough Micturition Defaecation Swallow Others 2 Drug Induced ANS Failure Primary Secondary Volume depletion 3 Brady Sick sinus AV block Tachy VT SVT Inherited * 4 AMI Aortic Stenosis HOCM Pulmonary hypertension Others 5 Metabolic Epilepsy Intoxications Drop-attacks Psychogenic TIA Falls This slide provides a simple classification of the principal causes of loss of consciousness. This scheme lists the causes of syncope from the most commonly observed (Left) to the least common (Right). This ranking may be helpful in thinking about the strategy for evaluating syncope in individual patients. Within the boxes,the most common causes of syncope are indicated for each of the major diagnostic groups. The numbers at the bottom of each column provide an approximate value for the average frequency with which that category appears in published report summarizing diagnostic findings (Alboni J Am Coll Cardiol 2001; 37: ). It should be noted that orthostatic causes are not often referred to specialists and consequently tend to be under represented in the literature. Simlarly, non-syncopal attacks (e.g. epilepsy, TIA, somatisation disorders) are generally not referred to syncope clinic as they are easily diagnosed and differentiated from syncope during the initial evaluation. The percentage reported in this slide thus represent those cases misdiagnosed as syncope at the initial evaluation. 50% 6% 11% 3% 9% Unknown Cause = 20%

44 Part V: Treatment

45 Treatment of Syncope: Outline
General principles Neurally-mediated reflex syncopal syndromes Orthostatic hypotension Cardiac arrhythmias as primary cause Structural cardiac or cardiopulmonary disease Vascular steal syndromes Metabolic disturbances

46 Classification of Task Force Recommendations
* Use of Class III is discouraged by the ESC

47 Levels of Evidence

48 Treatment of Syncope: General Principles
Principal goals of treatment: Prevent recurrences Reduce risk of mortality Additional goals: Prevent injuries associated with recurrences Improve quality of life

49 Recommendations Neurally-mediated syndromes: therapy
Initial treatment: Education and reassurance Sufficient for most No treatment Single syncope and no high risk settings Additional treatment High risk or high frequency settings

50 Neurally-mediated syndromes: therapy
Additional treatment (high risk or high frequency) Syncope is very frequent, e.g. alters the quality of life Syncope is recurrent and unpredictable (absence of premonitory symptoms) and exposes patients to “high risk” of trauma Syncope occurs during the prosecution of a ‘high risk’ activity (e.g., driving, machine operation, flying, competitive athletics, etc)

51 Neurally-mediated syndromes: therapy
Class I: Explanation and reassurance Avoidance of trigger events Modification or discontinuation of hypotensive drug treatment Cardiac pacing in CI or M carotid sinus syndrome Class II: Volume expansion (salt supplements, exercise program or head-up tilt sleeping (>10°) in posture-related syncope). Isometric leg and arm counter-pressure manoeuvres in patients with vasovagal syncope. Tilt training in patients with vasovagal syncope. Cardiac pacing in CI vasovagal syncope (>5 attacks per year or severe physical injury or Accident and age >40).

52 Treatment of Orthostatic Hypotension
Treatment Goals: Prevention of symptom recurrence and associated injuries Improvement of quality of life Establishment of the underlying diagnosis The value of these treatments is supported by basic physiological knowledge and small studies, despite the absence of RCT for these treatment strategies.

53 Treatment of Orthostatic Hypotension (cont.)
CAUSE TREATMENT Drug-induced autonomic failure Eliminate the offending agent Primary & secondary autonomic failure Modify physical factors that influence systemic blood pressure* The following should be avoided: Sudden head-up postural changes, prolonged standing, prolonged recumbence during the day, straining during urination or bowel movement, hyperventilation, areas with high environmental temperatures (including saunas, hot showers, etc.), severe exertion, large meals (especially with refined carbohydrates), alcohol and drugs with vasodepressor properties. In addition, the following may be considered for individual patients as needed: Increasing salt and fluid intake, raising the head of the bed during sleep, reduce gravitational-induced pooling by use of abdominal binders and/or waist height support stockings or garments, use portable chairs to avoid prolonged standing, small frequent meals with decreased carbohydrate content, encourage leg crossing and squatting as counter measures, and judicious use of leg and abdominal muscles, especially swimming.

54 Treatment of Orthostatic Hypotension
Class I Recommendations Syncope due to orthostatic hypotension should be treated in ALL patients. In many instances, treatment entails only modification of drug treatment for concomitant conditions.

55 Treatment of Cardiac Arrhythmias as Primary Cause
Treatment Goals: Prevention of symptom recurrence Improvement of quality of life Reduction of mortality risk

56 Treatment of Cardiac Arrhythmias as Primary Cause (cont.)
Class I Recommendations Syncope due to cardiac arrhythmias must receive treatment appropriate to the cause in all patients in whom it is life-threatening and when there is a high risk of injury.

57 Treatment of Cardiac Arrhythmias as Primary Cause (cont.)
Class II Recommendations Treatment may be employed when the culprit arrhythmia has not been demonstrated and a diagnosis of life-threatening arrhythmia is presumed from surrogate data. Treatment may be employed when a culprit arrhythmia has been identified but is not life-threatening or presenting a high risk of injury.

58 Treatment of Cardiac Arrhythmias as Primary Cause (cont.)
Sinus node dysfunction (including bradycardia/tachycardia syndrome) Cardiac pacemaker therapy is indicated and is proven highly effective when bradyarrhythmia is documented as the cause of the syncope (Class I, Level B). Physiological pacing (atrial or dual-chamber) is superior to VVI pacing (Class I, Level A)* Elimination of drugs that may increase susceptibility to bradycardia should be considered (Level C)** Catheter ablation for control of atrial arrhythmias may have a role in selected patients with brady-tachy syndrome (level C)*** *Physiological pacing lowers the risk of developing atrial fibrillation and systemic embolism. It may also improve QOL by reducing symptoms of congestive heart failure, low cardiac output and angina pectoris, and perhaps improve survival. *VVI or VVIR pacing should be avoided in sick sinus syndrome **Cardiac glycosides, beta-adrenergic blockers, calcium channel blockers, and membrane-active antiarrhythmic agents (especially sotalol and amiodarone) are often used to treat concomitant atrial tachyarrhythmias. Elimination of the offending agent is important in preventing syncope recurrence. ***Ablation is not normally used primarily for prevention of syncope.

59 Treatment of Cardiac Arrhythmias as Primary Cause (cont.)
AV conduction system disease Cardiac pacing is first-line therapy for treatment of syncope in symptomatic AV block (Class I, Level B). Pacing improves survival and prevents syncopal recurrences in patients with heart block (Level B). Pacing may be life-saving in patients with BBB and syncope (if suspected mechanism is intermittent AV block) (Level C). Consider VT or VF as a possible cause of syncope in these patients if they also have LV dysfunction.

60 Treatment of Cardiac Arrhythmias as Primary Cause (cont.)
Paroxysmal SVT and VT SVTs are uncommon as a cause of syncope. Syncope due to acquired torsades de pointes (TdP) as a result of drugs is not uncommon. The causal drug should be eliminated immediately. In syncope due to VT, amiodarone may provide benefit in the absence of heart disease. If LV function is depressed, an ICD is warranted. The RV outflow tract and bundle-branch reentry forms of VT may be amenable to catheter ablation. (An ICD is also indicated with LV dysfunction.)

61 Indications for ICD therapy
 Class I Recommendations Documented syncopal VT or VF (Level A) Undocumented syncope, previous MI and inducible SMVT (Level B) Class II Recommendations Unexplained syncope and depressed ventricular function (Level B) Established long QT syndrome, Brugada Syndrome, ARVD or HOCM with a family history of sudden death (Level C) Brugada Syndrome or ARVD and inducible VT/VF (Level C) Abbreviations: VT ventricular tachycardia VF, ventricular fibrillation SMTV, sustained monomorphic ventricular tachycardia ARVD, arrhythmogenic right ventricle tachycardia HOCM, hypertrophic obstructive cardiomyopathy

62 Treatment of Cardiac Arrhythmias as Primary Cause (cont.)
Implanted device (pacemaker, ICD) malfunction Implantable pacing systems are rarely the cause of syncope or near-syncope. If syncope is attributable to the implanted device: Evidence of battery depletion/failure, or lead failure device or lead replacement is indicated. Evidence of pacemaker syndrome, device re-programming or replacement is indicated. In the event an ICD fails to detect and/or treat an arrhythmia, re-programming generally resolves the problem.

63 Treatment of Vascular Steal Syndromes
Syncope associated with upper extremity exercise in the setting of subclavian steal syndrome may warrant surgery or angioplasty. Direct corrective angioplasty or surgery is usually feasible and effective (Class I, Level C). Subclavian steal is rare, but is the most commonly recognized condition in this group. This can occur on a congenital or acquired basis, with low pressure within the subclavian artery causing retrograde flow to occur in the ipsilateral vertebral artery (especially during upper arm exercise). This results in decreased cerebral blood flow.

64 Metabolic Disturbances: Hyperventilation
Hyperventilation resulting in hypocapnia and transient alkalosis may be responsible for confusional states or behavioral disturbances. Clearcut distinction between such symptoms and syncope may be difficult . Frequently associated with anxiety episodes and/or ‘panic’ attacks. Recurrent faints associated with hyperventilation should justify a psychiatric consultation. Metabolic disturbances are relatively infrequent cases of true loss of consciousness. More often these disturbances are responsible for confusional states or irregular behavior. Making a distinction between such symptoms and syncope may not be possible by history alone. Regardless of whether the hyperventilation is the cause of the faint, the frequent clinical association with anxiety episodes and/or ‘panic’ attacks warrants consideration.

65 Part VI: Special Issues in Evaluating Patients with Syncope

66 When to Hospitalise a Patient with Syncope (for Diagnosis)
Suspected or known significant heart disease ECG abnormalities suggesting an arrhythmia Syncope during exercise Syncope occurring in supine position Syncope causing severe injury Family history of sudden death Sudden onset of palpitations in the absence of heart disease Frequent recurrent episodes.

67 When to Hospitalise a Patient with Syncope (for Treatment)
Cardiac arrhythmias as cause of syncope Syncope due to cardiac ischaemia Syncope secondary to structural cardiac or cardiopulmonary diseases Stroke or focal neurologic disorders Cardioinhibitory neurally-mediated syncope when a pacemaker implant is planned. When is it safe not to hospitalize? Patients with isolated or rare syncopal episodes, in whom there is no evidence of structural heart disease and who have a normal baseline ECG (low risk of cardiac syncope – high probability of neurally-mediated syncope). These patients have good survival regardless of results of head-up tilt test.

68 Syncope in the Older Adult: Background
Incidence > 6 % per year Prevalence 10% Two-year recurrence 30% Most common causes of syncope: Orthostatic hypotension (20-30% of patients) Carotid sinus hypersensitivity (up to 20% of patients) Neurally-mediated syncope (up to 15%) Cardiac arrhythmias (up to 20%) Orthostatic hypotension is an attributable cause of syncope in 20-30% of older patients. Up to 25% may have ‘age-related’ orthostatic hypotension, the remainder are predominantly due to medications, primary autonomic failure, secondary autonomic failure (diabetes), Parkinson’s disease and multisystemic atrophy. Carotid sinus hypersensitivity is an age-related diagnosis, rare before age 40, and the prevalence increases with advancing years and with cardiovascular, cerebrovascular and neurodegenerative co-morbidity. Up to 15% of syncope is neurally mediated. In over half, episodes are related to cardiovascular medications. A significant percentage of cardiac arrhythmias are a cause of syncope in the elderly (up to 20%).

69 Syncope in the Older Adult: Diagnostic Evaluation
Pursue witness accounts when possible Include in history taking: Social circumstances, injurious events, impact of events on confidence, ability to perform ADLs independently Determine timing of syncope occurrence: Orthostatic hypotensive events usually occur in the AM Association with meals, medications, nocturnal micturition, etc. Detailed medication history. Co-morbid diagnoses (especially Parkinson’s, diabetes, anaemia, hypertension, ischaemic heart disase, heart failure).

70 Syncope in the Older Adult: Examination
Assessment of neurological and locomotor systems Including observation of gait and standing balance (eyes open & eyes closed). Determine if cognitive impairment is present (mini-mental state examination). Remainder of the clinical examination is the same as for younger adults.

71 Syncope in the Older Adult: Investigations
The diagnostic evaluation should include the same basic components as for younger adult. Exception is routine supine and upright carotid sinus massage. Repeated morning measurements are recommended to determine if orthostatic hypotension exists. 24-hr ambulatory BP may be helpful if meals or medications are suspected. If symptoms continue, or > 1 cause is suspected, further evaluation is indicated. There is no evidence to support the use of head-up tilt studies as part of the initial evaluation although this is common practice in many facilities.

72 Syncope in the Older Adult: Evaluation of the Frail and Elderly
The rigour of assessment should depend on compliance with tests and on prognosis. For patients who have difficulty standing unaided, head-up tilt can be used to assess orthostatic changes. Clinical decisions regarding the value of a syncope evaluation should be made for each patient based on the benefits to the individual.

73 Syncope in the Older Adult: Conclusions
Class I Recommendations: Morning orthostatic blood pressure measurements and supine and upright carotid massage are integral to the initial evaluation unless contraindicated. The evaluation of mobile, independent, cognitively normal older adults is as for younger individuals. In frailer older adults, evaluation should be modified according to prognosis.

74 Syncope in Paediatric Patients: Background
As many as 15% of children may have at least one episode of syncope prior to age 18 Most common causes of syncope: Neurally-mediated syncope (61-71%) Cerebrovascular and psychogenic syncope (11-19%) Cardiac syncope (6%)

75 Syncope in Paediatric Patients: Differential Diagnosis
Careful personal and family history First-degree relative who faints? Any history of: LQTS, Brugada, Kearns-Sayre syndrome, AF, WPW, catecholaminergic polymorphic VT, ARVD, congenital heart disease repair, HOCM, anomalous coronary artery, pulmonary artery hypertension, or myocarditis Cardiac aetilogy should be suspected: In the presence of congenital, structural or functional heart disease Syncope with exertion After history, an appropriate and extensive diagnostic work-up should be started. Abbreviations: LQTS, long QT syndrome AF, atrial fibrillation WPW, Wolff-Parkinson-White VT ventricular tachycardia ARVD, arrhythmogenic right ventricle tachycardia HOCM, hypertrophic obstructive cardiomyopathy

76 Syncope in Paediatric Patients: Diagnostic Work-up
Physical exam and ECG Tilt-testing can probably be deferred until after a second episode if history indicative of neurally-mediated syncope* Tilt test duration should be shorter in teenagers than in adults (< 10 min) 24-hour Holter or loop-recorder should be used for syncope with palpitations Cardiac consult and Echocardiogram for evidence of heart murmur** EEG is indicated for prolonged loss of consciousness, seizure activity, and postictal phase of lethargy/confusion *Tilt protocols used in adults lack specificity in teenage patients. **EPS has minor role in paediatric patients

77 Syncope in Paediatric Patients: Therapy
Neurally-mediated syncope: behaviour modification, salt, increased fluids. Pharmacological therapy reserved for continued symptoms despite behaviour modification. Pacemakers should be avoided whenever possible. Breath-holding spells do not require therapy unless longer asystole is present (potential for cerebral injury). Behaviour modification alone may be as effective as pharmacological therapy and should be tried first in the majority of cases. Drinking salty or sweet liquids without caffeine, ruling out salt avoidance, and performing ‘anti-gravity manoeuvres’ at the earliest recognition of pre-syncope is helpful in many patients.

78 Syncope management facilities
A proposed model of organisation for the evaluation of the syncope patient in a community

79 Organising the Management of Syncope
Eur Heart J 2004; 25:2067

80 Syncope management facilities:
ESC standards Professional skill mix: Core medical and support personnel should be involved full time or most of the time. Experience and training in key components of cardiology, neurology, emergency and geriatric medicine. It is probably not appropriate to be dogmatic

81 Syncope management facilities:
ESC standards Core equipment: Surface ECG recording Phasic blood pressure monitoring Tilt table testing equipment External and internal (Implantable) ECG loop recorder systems 24 hour ambulatory blood pressure monitoring 24 hour ambulatory ECG Autonomic function testing

82 Syncope management facilities:
ESC standards Preferential diagnostic access to: Echocardiography EP studies Stress testing CT and MRI scans Electroencephalography

83 Syncope management facilities:
ESC standards Preferential therapy access to: Pacemaker implantation ICD implantation Catheter ablation of arrhythmias … and to any eventual therapy for syncope

84 Syncope management facilities:
ESC standards Setting The majority of syncope patients should be investigated as out-patients or day cases . A major objective of the syncope facility is to reduce the number of hospitalisations

85 ESC Task Force report on driving and heart disease (1998)*
Driving and Syncope ESC Task Force report on driving and heart disease (1998)* Group 1: Motorcycles, cars and small vehicles with/without trailer Group 2: Vehicles over 3.5 metric tonnes, passenger vehicles > 9 seats Intermediate: – Taxicabs, small ambulances and some other vehicles For Group 1 the Task Force advises minimal restrictions and thus only temporarily should patients with heart disease and syncope in this group be advised not to drive. Driving and heart disease. Task Force Report. Prepared on behalf of the Task Force by MC Petch. Eur Heart J 1998; 19: * Eur Heart J 1998; 19:

86 Disqualifying criteria
Driving and syncope: Disqualifying criteria Cardiac arrhythmias Update 2004 Private drivers Vocational drivers Medical Rx Until successful treatment is established Pacemaker implant Within one week Until appropriate function is established Successful catheter ablation Until long-term success is confirmed (3 mos)

87 Disqualifying criteria
Driving and syncope: Disqualifying criteria Vasovagal/ Carotid sinus Private drivers Vocational drivers Single/mild No restrictions No restriction unless it occurred during driving Severe Until symptoms controlled Permanent restriction unless effective treatment has been established

88 Disqualifying criteria
Driving and syncope: Disqualifying criteria Unexplained syncope Update 2004 Private drivers Vocational drivers Single/mild No restriction unless it occurred during driving Until diagnosis and successful treatment is established Severe

89 Glossary of Uncertain Terms: Panel Advisories
Do not use ‘convulsive’ syncope - it carries the risk of increasing confusion between syncope & epilepsy. Use of ‘drop attacks’ should be restricted to: a fall to ones knees w/out loss of consciousness. The use of ‘dysautonomia’ should be reserved for Riley-Day syndrome. It is unknown whether ‘hyperventilation’ can cause loss of consciousness. Use of ‘pre-syncope’ is an imprecise term for all sensations preceding syncope, regardless of loss of consciousness.

90 Glossary of Uncertain Terms: Panel Advisories (cont.)
‘Neurally-mediated’ syncope is a synonym for ‘reflex’ syncope. ‘Neurocardiogenic’ syncope should be used strictly for reflex syncope in which the reflex trigger originates in the heart. ‘Vasodepressor syncope’ should be used strictly for reflex syncope in which the vasodepressor reflex is documented to occur in the absence of reflex bradycardia. ‘Neurogenic’ syncope is a superfluous alternative for ‘reflex syncope’. ‘Orthostatic intolerance’ should be restricted to summarizing a patient’s complaints.


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