Syncope Abdul Gofir Blok 18

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.

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

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

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

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?

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

Etiology of Syncope Idiopathic 34% Neurally-mediated Vasovagal 18% Other (situational, carotid sinus) 6% Cardiac Arrhythmia 14% Mechanical 4% Neurologic 10% Orthostatic 8% Medications 3% Psychiatric 2% Linzer, Ann Intern Med, 1997

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

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

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

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 0.8% 0.4% Telemetry “Helpful” 12.6% 16% Mortality 0.9% 0 Linzer, Ann Intern Med, 1997 Estrada, Am J Cardiol, 1995 Glassman, Arch Intern Med, 1997. Estrada, Am J Cardiol, 1995

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%

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.

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

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

Neurocardiogenic Syncope: Pathophysiology

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

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%

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

Tilt table testing Goal: provoke neurocardiogenic syncope Indication: recurrent unexplained syncope without cardiac disease Protocol: passive tilt 45-60 min positive response reproduces symptom Tilt 60-70 degrees. If neg, can add isoproterinol infusion or SL NTG 60-80˚

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

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

“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):878-85. syncope among Framingham Heart Study from 1971 to 1998. 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

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

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

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

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

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 24-48 hrs. If prior hosp didn’t yield Dx, then likelihood of fining cause on subsequent hosp is < 15%

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

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

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.

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?)

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