1. Syncope
Abdul Gofir
Blok 18

2. Syncope (Greek – to interrupt)
Syncope is the sudden transient loss of consciousness and postural tone with spontaneous recovery.
Loss of consciousness occurs within 10 seconds of hypoperfusion of the reticular activating system in the mid brain.

3. Establishing Diagnosis of Syncope
Presyncope & syncope: similar etiologies & workup
Syncope: sudden transient loss of consciousness with loss of postural tone and spontaneous recovery
Mechanism: transient hypoperfusion of brainstem or both cerebral hemispheres
Differential diagnosis:
coma
narcolepsy
seizure
Sudden death- requires elec/mechanical cardioversion
Drop attack -= loss of postural tone w/o loss of consciousness

4. Syncope: scope of the problem
Common
3% Emergency Department visits
1-6% hospital admissions
Costly
Multiple diagnostic tests often performed
Average charge for each diagnostic test ranges from $284 to $4678
Linzer, Ann Intern Med, 1997
Syncope - a symptom, not diagnosis

5. Diagnostic Challenges
History often unclear
Prognosis varies widely
Common etiologies are benign
Potentially high mortality
Need to identify high-risk patient early
Many available tests
40% of patients may elude diagnosis
Hx: was is syncope? Seizure? What were the circumstances? Pt may not remember

6. Syncope: management questions
Diagnostic challenges
What is the best diagnostic test?
How and when to rule out arrhythmia?
How to diagnose neurocardiogenic syncope?
How to decrease the # “idiopathic”?
Management dilemmas
When to admit?
How are the elderly different?
When to resume driving?

7. Case Presentation 50 yo healthy woman, standing at church
Becomes weak, lightheaded, & nauseated
Collapses, awakens after 1 minute
Feels well in ED - “I want to go home”
Normal exam, EKG, labs, CXR
Diagnosis?
Plan - Admit? Further testing?
Glassman, Arch Intern Med, 1997

8. Etiology of Syncope Idiopathic 34% Neurally-mediated Vasovagal 18%
Other (situational, carotid sinus) 6%
Cardiac
Arrhythmia 14%
Mechanical 4%
Neurologic %
Orthostatic 8%
Medications 3%
Psychiatric 2%
Linzer, Ann Intern Med, 1997

9. The Key to Diagnostic Evaluation
History and Exam establish diagnosis in 45%
History: setting, symptoms, medical hx, meds
Exam: HR, BP, cardiovascular, neurologic
EKG adds 5% diagnostic yield
Cheap, non-invasive, readily available
Can indicate important cardiac disease
Prior MI, ventricular hypertrophy, long QT
Bradycardia, conduction block
Abnormalities guide further testing
Setting: trigger for vasovagal
Symptoms: autonomic sx, aura, palpitations/exertional
However, ECG abnormality does not prove causation

10. Diagnostic Algorithm Syncope Noncardiac Idiopathic Cardiac
Syncope definitively dx’d by H & P, ecg: arrhythmia, vasovagal, orthostatic
Arrhythmia
Mechanical
Neurocardiogenic
Orthostatic
Neurologic
Psychiatric

11. Cardiac syncope: inadequate cardiac output, arrhythmia
Cardiac enzymes - only if history or EKG suggestive of MI
1-10% MI’s present with syncope
EKG up to 100% sensitive for MI
Echo - rule out structural heart disease
before stress test if obstruction suspected
yield: 5-10%
Exercise stress test - exertional syncope
identifies exertional arrhythmia
yield: low (1%)
Georgeson, J Gen Intern Med, 1992
Linzer, Ann Intern Med, 1997
Echo: makes Dx for AS, atrial myxoma; can provide evidence of arrhythmia risk if EF low

12. Arrhythmia evaluation - telemetry
Indication: suspected arrhythmia
palpitations, no prodrome
Idiopathic syncope or underlying heart disease
Routine telemetry low yield
2240 non-ICU telemetry patients
10% syncope/dizzy
all syncope
ICU transfer-arrhythmia % %
Telemetry “Helpful” % 16%
Mortality %
Linzer, Ann Intern Med, 1997
Estrada, Am J Cardiol, 1995
Glassman, Arch Intern Med, 1997.
Estrada, Am J Cardiol, 1995

13. Arrhythmia evaluation: 24 hr ambulatory (Holter) monitoring
2612 syncope/dizzy patients
Symptomatic arrhythmia = positive result
Diagnostic arrhythmia in 4%
Symptoms without arrhythmia
Arrhythmia ruled out in 15%
Bottom line
Benefit: monitors during usual activity
Limitation: brief duration limits yield unless daily symptoms
Linzer, Ann Intern Med, 1997
Other studies quote yield for ambulatory monitoring - may establish Dx in 2-3%

14. Arrhythmia evaluation: improving the yield
Loop recorder
Indication: recurrent syncope with normal heart
frequent syncope -> continuous loop recorder (weeks)
infrequent syncope -> implantable loop recorder (years)
Electrophysiologic study
Indication: syncope with organic heart disease
Signal average EKG
Detects late potential in QRS - substrate for VT/VF
indication: normal heart, idiopathic syncope?
Linzer, Ann Intern Med, 1997
Zimetbaum , Ann Intern Med, 1999
Loop recorder: pt needs to regain consciousness and activate to store data
SAECG: most helpful in predicting risk of Vent arrhythmia after MI. Not recommended routinely after syncope; could consider if nl heart, to guide decision about EP study.

15. Neurocardiogenic Syncope
Reflexive
Vasodepressor
Micturition
Orthostatic intolerance
Neurocardiogenic Syncope
Vasovagal
Carotid sinus syncope
Neurally - mediated
Cardioneurogenic

16. Neurocardiogenic Syncope Clinical Presentation
May be predominantly
Cardioinhibitory
(bradycardia)
Vasodepressor
(hypotension) or
Both
Trigger
Patients have autonomic dysfunction, with increase parasympathetic tone causing bradycardia, and decreased sympathetic tone causing hypotension
Syncope

17. Neurocardiogenic Syncope: Pathophysiology

18. Diagnosing neurocardiogenic syncope by history and exam
Precipitant
Vasovagal: pain, emotion, standing
Situational: vagal stimulus
Autonomic symptoms
Rapid recovery of mental status
Bradycardia, pallor may persist
Carotid sinus massage
>3 sec asystole or hypotension=hypersensitivity
Rapid awakening once supine, but Fatigue, depression may follow. Problem: arrhythmia may also be rapid onset\ and short duration.
CSM - for 5-10 seconds
Contraindications to CSM: carotid bruit, stroke, age, MI w/in 6 mo, h/o arrhythmia

19. Neurocardiogenic syncope: treatment
Indicated for frequent syncope
Lifestyle modification
Add salt, avoid triggers
Handgrip, tense arms and legs
Medications
B blocker, SSRI, midodrine, fludrocortisone
Repeat tilt test on therapy?
Pacemaker
Avoid triggers, lie down and elevate feet at onset of Sx, support stockings
Beta blockers - studies w/ mixed results. Pindolol has ISA, may be better choice if baseline bradycardia.
PAXIL -study in JACC - in patients who had failed other therapies, and increased likelihood of subsequent neg tilt, and decreased subsequent syncope from 53% to18%

20. Is Laughter Really the Best Medicine?
“A 63-year-old man was referred with a 20-year history of syncope preceded by intense laughter. We were able to diagnose a gelastic syncope (from the Greek ‘gelos’, laughter). Laughter- related syncope may be induced by the Valsalva manoeuvre.
We advised him not to laugh so hard in the future, and when we saw him again, he had been able to follow this advice, and had suffered no further syncope.”
Braga. Lancet 2005
Rapid awakening once supine, but Fatigue, depression may follow. Problem: arrhythmia may also be rapid onset\ and short duration.
CSM - for 5-10 seconds
Contraindications to CSM: carotid bruit, stroke, age, MI w/in 6 mo, h/o arrhythmia

21. Tilt table testing Goal: provoke neurocardiogenic syncope
Indication: recurrent unexplained syncope without cardiac disease
Protocol: passive tilt min
positive response reproduces symptom
Tilt degrees.
If neg, can add isoproterinol infusion or SL NTG
60-80˚

22. Tilt table testing: why the controversy?
Accuracy difficult to define
Gold standard?
Protocol?
Reproducibility 71-87%
Positive tilt test with idiopathic syncope:
49% with passive tilt
66% with tilt plus isoproterenol
Tradeoff: decreased specificity
Kapoor, Am J Med, 1994
There is no gold standard
Tradeoff b/w sensitivity and specificity

23. Vasovagal syncope: pacemakers ineffective
Randomized double-blind trial
DDD pacer vs. sensing-only pacer %
p = NS
VPSII trial: Three previous small randomized trials found pacemaker is beneficial for patients with severe recurrent vasovagal syncope. - not double blind, OBJECTIVE: To determine if pacing therapy reduces the risk of syncope in patients with vasovagal syncope. randomized double-blind trial of pacemaker therapy in outpatients referred to syncope specialists at 15 centers. In the year prior to randomization, patients had had a median of 4 episodes of syncope. Patients were followed up for up to 6 months. INTERVENTION: After implantation of a dual chamber pacemaker, 100 patients were randomly assigned to receive dual-chamber pacing (DDD) with rate drop response or to have only sensing without pacing (ODO). MAIN OUTCOME MEASURE: Time to first recurrence of syncope. RESULTS: No patients were lost to follow-up. Of the 52 patients randomized to ODO, 22 (42%) had recurrent syncope within 6 months compared with 16 (33%) of 48 patients in the DDD group. The cumulative risk of syncope at 6 months was 40% (95% confidence interval [CI], 25%-52%) for the ODO group and 31% (95% CI, 17%-43%) for the DDD group. The relative risk reduction in time to syncope with DDD pacing was 30% (95% CI, -33% to 63%; 1-sided P =.14). Lead dislodgement or repositioning occurred in 7 patients. One patient had vein thrombosis, another had pericardial tamponade leading to removal of the pacemaker system, and a third had infection involving the pacemaker generator. CONCLUSIONS: did not reduce the risk of recurrent syncope. Because of the weak evidence of efficacy of pacemaker therapy and the risk of complications, pacemaker therapy should not be recommended as first-line.
Connolly, JAMA 2003

24. “Idiopathic” syncope: improving diagnostic yield
Up to 40% patients
Prognosis good
Potential morbidity, lifestyle implications
Consider:
Diagnosis Testing
Neurocardiogenic Tilt table
Anxiety/depression Psychiatric evaluation
Arrhythmia EPS, implanted event monitor
Empiric pacemaker?
Incidence and prognosis of syncope. N Engl J Med 2002 Sep 19;347(12):
syncope among Framingham Heart Study from 1971 to RESULTS: Of 7814 study participants followed for an average of 17 years, 822 reported syncope. most frequently identified causes were vasovagal (21.2 percent), cardiac (9.5 percent), and orthostatic (9.4 percent); for 36.6 percent the cause was unknown. The multivariable-adjusted hazard ratios among participants with syncope from any cause, as compared with those who did not have syncope, were 1.31 (95 percent confidence interval, 1.14 to 1.51) for death from any cause, 1.27 (95 percent confidence interval, 0.99 to 1.64) for myocardial infarction or death from coronary heart disease, and 1.06 (95 percent confidence interval, 0.77 to 1.45) for fatal or nonfatal stroke. The corresponding hazard ratios among participants with cardiac syncope were 2.01 (95 percent confidence interval, 1.48 to 2.73), 2.66 (95 percent confidence interval, 1.69 to 4.19), and 2.01 (95 percent confidence interval, 1.06 to 3.80). Participants with syncope of unknown cause and those with neurologic syncope had increased risks of death from any cause, with multivariable-adjusted hazard ratios of 1.32 (95 percent confidence interval, 1.09 to 1.60) and 1.54 (95 percent confidence interval, 1.12 to 2.12), respectively. There was no increased risk of cardiovascular morbidity or mortality associated with vasovagal (including orthostatic and medication-related) syncope. CONCLUSIONS: Persons with cardiac syncope are at increased risk for death from any cause and cardiovascular events, and persons with syncope of unknown cause are at increased risk for death from any cause. Vasovagal syncope appears to have a benign prognosis.
Pacer, esp if cardioinhibitory or bradycardic suspected

25. Prognosis: Framingham 25 year follow up
Etiology of syncope
Adjusted risk of death
Cardiac
2.01*
Neurologic
1.54*
Idiopathic
1.32*
Vasovagal
1.08
Looked at another way, Framingham data published in 2002 showed increased risk of death about 2X if cardiac syncope, interestingly 1.3 X if idiopathic (signif increase). No increase risk if neurocardiogenic.
*p<0.01
NEJM 2002;347:878

26. Prognosis: ED risk stratification
ED predictors of arrhythmia or mortality
Abnormal EKG
Prior VT/VF
History of CHF
Age > 45
Martin, Ann Emerg Med, 1997

27. Prognosis: Guideline for admission - the San Francisco Syncope Rule
Prediction rule to identify patients at risk of bad outcomes (need admit) over 30 days
Death, MI, arrhythmia, PE, stroke, transfusion
Syncope or related event requiring procedure, ED visit or admit
First assess the patient for cause of syncope
If cause unknown, apply the rule
98% sensitive
56% specific
Quinn, Ann Emerg Med, 2006

28. Prognosis: Guideline for admission - the San Francisco Syncope Rule
CHF - history of
Hematocrit <30%
ECG abnormal
Shortness of breath
Systolic blood pressure <90 mm Hg at triage
Quinn, Ann Emerg Med, 2006
Caveats: single site study, conf intervals wide (up to 11 points) could lower sensitivity to 89%
Remember to evaluate pt first

29. ACP Guidelines for Hospital Admission
Definitely admit
HPI: chest pain
PMH: CAD, CHF, ventricular arrhythmia
Exam: CHF, valve dz, focal neurologic deficit
EKG: ischemia/MI, arrhythmia, bundle branch block
Often admit
HPI: age >70, exertional syncope, frequent syncope
Exam: tachycardia, orthostatic hypotension, injury
Cardiac dz suspected
Linzer, Ann Intern Med, 1997
Hospitalization doesn’t treat syncope. Goal is to prevent death w/in next hrs.
If prior hosp didn’t yield Dx, then likelihood of fining cause on subsequent hosp is < 15%

30. Guidelines for Hospital Admission: implications for practice
Myth: Every syncope patient should be admitted
Recommendation: Establish clear goals for admission, usually diagnostic
Myth: Every syncope patient requires “rule out MI”
Recommendation: Admission not necessary with careful history ruling out symptoms of ischemia and normal EKG
Myth: Telemetry improves outcomes
Recommendation: One-year mortality rarely affected by 24 hours of monitoring

31. Syncope in the elderly: the geriatric challenge
History often obscure
Syncope vs. dizziness vs. fall?
Often multifactorial - elderly at high risk for
Situational syncope
Polypharmacy, adverse drug events
Cardiac, neurovascular disease
Decreased physiologic reserve
Atypical presentation of disease
Abnormalities do not prove causation

32. Recommendations for Driving: following the law
Laws vary by state - available from DMV
California law requires reporting of any loss of consciousness
County health officer receives report
DMV determines fitness to drive
Physician can provide influential prognostic information to DMV
Physicians’ recommendations variable
Awareness of law often poor
California - we report to Dept of Public Health, same form as for reportable diseases. who reports to DMV.

33. American Heart Association Guidelines for Driving
VT/VF (treated with medical or ICD therapy)
Risk greatest 1st 6 mo, up to 10% at 1 year
Resume driving: 6 months arrhythmia free
Bradycardia with syncope
Resume driving: 1 week after pacemaker
Neurocardiogenic syncope -> risk stratify
Mild: presyncope, clear warning & precipitant
Resume driving: immediately
Severe: syncope, no warning or precipitant, frequent
Resume driving: after therapy, waiting period (duration?)

34. Thank for attention
Reference from Lecture Karen E. Hauer, MD University of California, San Francisco