Syncope Anthony Ho, DO PGY4 Emergency Medicine
Introduction Symptom complex composed of brief loss of consciousness associated with inability to maintain postural tone that spontaneously resolves without medical intervention Epidemiology 2% of ER visits 1 out of 4 persons will have in lifetime Elderly have the highest risk of morbidity Near syncope is the same process Differentiate from vertigo or dizziness
“ Passed Out”
Pathophysiology Lack of blood flow to brainstem reticular activating system for 10-15 seconds Reduction of cerebral perfusion by 35% for 5-10 seconds Most common inciting event is drop in cardiac output Least common is vasospasms or other alterations in flow to CNS
Etiology Causes of syncope Cardiac  Structural cardiopulmonary disease Valvular heart disease, aortic stenosis, tricuspid stenosis, cardiomyopathy, pulmonary HTN, Congenital Heart disease, Myxoma, pericardial disease, aortic dissection, PE, MI, ACS. Dysrhythmias Bradydysrhythmias, Stokes-Adams attack, Sinus node disease, 2 nd -3 rd  degree blocks, pacemaker malfunction, tachydysrhythmias, Vtach, torsades de pointes, SVT, A Fib or Aflutter. Neural/Reflex mediated Vasovagal Situational Cough, micturition, defecation, swallow, neuralgia,  Carotid Sinus Syndrome Orthostatic Psychiatric Neurologic TIA, Subclavian Steal, Migraine Medications
Cardiac Syncope 6 month mortality >10% Underlying Structural Cardiopulmonary disease Think Aortic Stenosis in Elderly Think Hypertrophic Cardiomyopathy in Young PE can lead to Pulmonary outflow obstruction AMI or ischemia can lead to decrease CO Dysrhythmias Both tachy- and bradysrhythmias can lead to transient hypoperfusion Syncope is SUDDEN ONSET without prodromal symptoms
Vasovagal or Neurally/Reflex-Mediated Syncope Syncope associated to inappropriate vasodilation, bradycardia, or both in response to inappropriate vagal or sympathetic tone SLOW PROGRESSIVE ONSET with associated prodrome Carotid Sinus Hypersensitivity, consider in elderly patients with recurrent syncope and negative cardiac evaluations
Orthostatic Syncope Occurs within 3 minutes of standing Orthostatic tests positive if decrease in SBP by >20mmHg or drop in pressure to <90 Non specific test: 40% of asymptomatic patients >70 are positive Many life threatening causes of syncope have orthostatic symptoms, do not attribute as benign just because you have positive orthostatics
Psychiatric Illnesses Diagnosis of exclusion Associated with generalized anxiety and major depressive disorders i.e. Hyperventilation syndrome    hypocarbia   cerebral vasoconstriction
Neurologic Syncope Loss of consciousness with persistent neurologic deficits or AMS are not true syncope Stroke Syndromes with syncope Brainstem ischemia Posterior circulation ischemia (diplopia, vertigo, nausea) Subclavian steal syndrome Seizures often mimic syncope
Medication-Induced Syncope Usually contributes to orthostatic syncope Antihypertensive mediations (BB, CCB), diuretics, and proarrythmics
Elderly Population Cardiovascular risk is the best predictor of mortality with syncope Highest risk group Calcified blood vessels are less compliant LV becomes less compliant, increasing dependence on atrial kick Incidence of vasovagal syncope decreases with age Increased orthostatic syncope
Evaluation ED goal  1. Avoid litigation! 2. Admit patients that will benefit (receive a diagnosis) from admission. 3. Discharge patients that won ’t die (or have complications) before their follow-up. 4. Diagnose in the ED reversible or deadly causes RISK STRATIFICATION Careful history Thorough Physical Exam EKG interpretation
History Symptoms of cardiopulmonary or neurological origin Chest pain, palpitations, shortness of breath, headache, abdomen or back pain, focal deficits. Family history of dysrhythmias, sudden cardiac death, prolonged QT
Physical Exam Focus on cardiovascular and neurological systems Murmurs, rales (think HCM, AS) Focal neurological exam Rectal examination
EKG Cardiopulmonary disease Acute ischemia dysrhythmia (WPW, Brugada) Heart block Prolonged QT
Other test Carotid massage Only small number of patients with hypersensitivity with have true Carotid Sinus Syndrome Hyperventilation maneuver Neurologic Testing CT/MRI not warranted for isolated syncope
Unexplained Syncope Unknown etiology in 40% of patients If diagnosis made, 80% of the time is in the emergency room!
Disposition SF Syncope Rules CHF Hematocrit <30 EKG changes SBP<90 SOB Boston Syncope Criteria 25 criteria
Practice Guideline
Post ED Evaluation Cardiac Syncope Electrocardiographic monitoring Echocardiography Electrophysiology testing Stress testing Neurologic Syncope CT/MRA/Carotid Doppler EEG Reflex-mediated syncope Tilt-table testing Psychogenic Psychiatric testing

Syncope

  • 1.
    Syncope Anthony Ho,DO PGY4 Emergency Medicine
  • 2.
    Introduction Symptom complexcomposed of brief loss of consciousness associated with inability to maintain postural tone that spontaneously resolves without medical intervention Epidemiology 2% of ER visits 1 out of 4 persons will have in lifetime Elderly have the highest risk of morbidity Near syncope is the same process Differentiate from vertigo or dizziness
  • 3.
  • 4.
    Pathophysiology Lack ofblood flow to brainstem reticular activating system for 10-15 seconds Reduction of cerebral perfusion by 35% for 5-10 seconds Most common inciting event is drop in cardiac output Least common is vasospasms or other alterations in flow to CNS
  • 5.
    Etiology Causes ofsyncope Cardiac Structural cardiopulmonary disease Valvular heart disease, aortic stenosis, tricuspid stenosis, cardiomyopathy, pulmonary HTN, Congenital Heart disease, Myxoma, pericardial disease, aortic dissection, PE, MI, ACS. Dysrhythmias Bradydysrhythmias, Stokes-Adams attack, Sinus node disease, 2 nd -3 rd degree blocks, pacemaker malfunction, tachydysrhythmias, Vtach, torsades de pointes, SVT, A Fib or Aflutter. Neural/Reflex mediated Vasovagal Situational Cough, micturition, defecation, swallow, neuralgia, Carotid Sinus Syndrome Orthostatic Psychiatric Neurologic TIA, Subclavian Steal, Migraine Medications
  • 6.
    Cardiac Syncope 6month mortality >10% Underlying Structural Cardiopulmonary disease Think Aortic Stenosis in Elderly Think Hypertrophic Cardiomyopathy in Young PE can lead to Pulmonary outflow obstruction AMI or ischemia can lead to decrease CO Dysrhythmias Both tachy- and bradysrhythmias can lead to transient hypoperfusion Syncope is SUDDEN ONSET without prodromal symptoms
  • 7.
    Vasovagal or Neurally/Reflex-MediatedSyncope Syncope associated to inappropriate vasodilation, bradycardia, or both in response to inappropriate vagal or sympathetic tone SLOW PROGRESSIVE ONSET with associated prodrome Carotid Sinus Hypersensitivity, consider in elderly patients with recurrent syncope and negative cardiac evaluations
  • 8.
    Orthostatic Syncope Occurswithin 3 minutes of standing Orthostatic tests positive if decrease in SBP by >20mmHg or drop in pressure to <90 Non specific test: 40% of asymptomatic patients >70 are positive Many life threatening causes of syncope have orthostatic symptoms, do not attribute as benign just because you have positive orthostatics
  • 9.
    Psychiatric Illnesses Diagnosisof exclusion Associated with generalized anxiety and major depressive disorders i.e. Hyperventilation syndrome  hypocarbia  cerebral vasoconstriction
  • 10.
    Neurologic Syncope Lossof consciousness with persistent neurologic deficits or AMS are not true syncope Stroke Syndromes with syncope Brainstem ischemia Posterior circulation ischemia (diplopia, vertigo, nausea) Subclavian steal syndrome Seizures often mimic syncope
  • 11.
    Medication-Induced Syncope Usuallycontributes to orthostatic syncope Antihypertensive mediations (BB, CCB), diuretics, and proarrythmics
  • 12.
    Elderly Population Cardiovascularrisk is the best predictor of mortality with syncope Highest risk group Calcified blood vessels are less compliant LV becomes less compliant, increasing dependence on atrial kick Incidence of vasovagal syncope decreases with age Increased orthostatic syncope
  • 13.
    Evaluation ED goal 1. Avoid litigation! 2. Admit patients that will benefit (receive a diagnosis) from admission. 3. Discharge patients that won ’t die (or have complications) before their follow-up. 4. Diagnose in the ED reversible or deadly causes RISK STRATIFICATION Careful history Thorough Physical Exam EKG interpretation
  • 14.
    History Symptoms ofcardiopulmonary or neurological origin Chest pain, palpitations, shortness of breath, headache, abdomen or back pain, focal deficits. Family history of dysrhythmias, sudden cardiac death, prolonged QT
  • 15.
    Physical Exam Focuson cardiovascular and neurological systems Murmurs, rales (think HCM, AS) Focal neurological exam Rectal examination
  • 16.
    EKG Cardiopulmonary diseaseAcute ischemia dysrhythmia (WPW, Brugada) Heart block Prolonged QT
  • 17.
    Other test Carotidmassage Only small number of patients with hypersensitivity with have true Carotid Sinus Syndrome Hyperventilation maneuver Neurologic Testing CT/MRI not warranted for isolated syncope
  • 18.
    Unexplained Syncope Unknownetiology in 40% of patients If diagnosis made, 80% of the time is in the emergency room!
  • 19.
    Disposition SF SyncopeRules CHF Hematocrit <30 EKG changes SBP<90 SOB Boston Syncope Criteria 25 criteria
  • 20.
  • 21.
    Post ED EvaluationCardiac Syncope Electrocardiographic monitoring Echocardiography Electrophysiology testing Stress testing Neurologic Syncope CT/MRA/Carotid Doppler EEG Reflex-mediated syncope Tilt-table testing Psychogenic Psychiatric testing