EVALUATION OFSYNCOPE IN ADULTS Dr.Venkat Narayana Goutham.V
• Syncope(SING-kə-pee) is a transient, self-limited loss of consciousness with loss of postural tone due to acute global impairment of cerebral blood flow.• The onset is rapid, duration brief, and recovery spontaneous and complete without medical or surgical intervention.
• Other causes of transient loss of consciousness need to be distinguished from syncope.• These include seizures, vertebrobasilar ischemia, hypoxemia, and hypoglycemia
Neurally Mediated(Reflex )Syncope--what happens?• Stress causes an abnormal autonomic reflex• Normal increased sympathetic tone replaced by increased vagal tone• Variable contribution of vasodilation and bradycardia.• Examples include syncope from: – Pain and/or fear – Carotid sinus hypersensitivity – ―situational‖ (cough, micturition, defecation syncope)
Neurally Mediated Syncope
Features of Neurally MediatedSyncope• dizziness, lightheadedness, and fatigue, premonitory features of autonomic activation may be present. These include diaphoresis, pallor, palpitations, nausea, hyperventilation, and yawning.
• During the event proximal and distal myoclonus (typically arrhythmic and multifocal) may occur, raising the possibility of epilepsy.• The eyes typically remain open and usually deviate upward. Urinary but not fecal incontinence may occur.
Treatment: NeurallyMediated Syncope• Reassurance• avoidance of provocative stimuli• plasma volume expansion with fluid and salt are the cornerstones of the management of neurally mediated syncope.
• Isometric counterpressure maneuvers of the limbs (leg crossing or handgrip and arm tensing).• Fludrocortisone, vasoconstricting agents, and beta-adrenoreceptor antagonists are widely used by experts to treat .
Orthostatic Hypotension• Orthostatic hypotension, defined as a reduction in systolic blood pressure of at least 20 mmHg or diastolic blood pressure of at least 10 mmHg within 3 minutes of standing or head-up tilt on a tilt table.
Features• It is a manifestation of sympathetic vasoconstrictor (autonomic) failure .• light-headedness, dizziness, and presyncope (near-faintness)• Visual blurring may occur, likely due to retinal or occipital lobe ischemia.• Patients may report orthostatic dyspnea
• Neck pain—typically in the suboccipital, posterior cervical, and shoulder region (the "coat-hanger headache") most likely due to neck muscle ischemia, may be the only symptom.• Symptoms may be exacerbated by exertion, prolonged standing, increased ambient temperature, or meals
Treatment: OrthostaticHypotension• The first step is to remove reversible causes—usually vasoactive medications .• Nonpharmacologic interventions should be introduced.
Nonpharmacologic interventions• patient education regarding staged moves from supine to upright• warnings about the hypotensive effects of meal ingestion• instructions about the isometric counterpressure maneuvers that increase intravascular pressure (see above).• Intravascular volume should be expanded by increasing dietary fluid and salt.
• If these nonpharmacologic measures fail, pharmacologic intervention with fludrocortisone acetate and vasoconstricting agents such as midodrine and pseudoephedrine should be introduced.
Cardiac Syncope• Cardiac (or cardiovascular) syncope is caused by arrhythmias and structural heart disease.• Both cause the heart to be unable to sufficiently increase cardiac output to meet demand.• Cardiac arrythymias especially in the elderly have high mortality.
Approach to the Patient
Diagnostic Objectives• Distinguish true syncope from syncope mimics• Determine presence of heart disease• Establish the cause of syncope with sufficient certainty to: – Assess prognosis confidently – Initiate effective preventive treatment.
• Generalized and partial seizures may be confused with syncope.
A Diagnostic Plan is Essential•Initial Examination –Detailed patient history –Physical exam –ECG –Supine and upright blood pressure•Monitoring –Holter –Event –Insertable Loop Recorder (ILR)•Cardiac Imaging•Special Investigations.
Diagnostic Flow Diagram Initial Evaluation Syncope Not Syncope Certain Suspected UnexplainedDiagnosis Diagnosis Syncope Cardiac Neurally-Mediated or Frequent or Severe Single/Rare Confirm with Likely Orthostatic Likely Episodes Episodes Specific Test or Specialist Consultation Cardiac Tests for Neurally- Tests for Neurally- No Further Tests Mediated Syncope Mediated Syncope Evaluation + - + - + - Re-Appraisal Re-Appraisal Treatment Treatment Treatment Treatment
HISTORY• HISTORY alone identifies the cause up to 85% of the time• POINTS – Previous episodes – Character of the events, witnesses – Events preceding the syncope – Events during and after the episode
HISTORY• Events preceding the • Events during and syncope after the episode – Prolonged standing – Trauma (implication (vasovagal) important) – Immediately upon – Chest pain (CAD, PE) standing (orthostatic) – Seizure (incontinence, – With exertion (cardiac) confusion, tongue – Sudden without warning laceration, postictal or palpitations (cardiac) behavior) – Aggressive dieting – Cerebrovascular – Heat exposure syndrome (diplopia, dysarthia, hemiparesis) – Emotional stress – Associated with n/v/sweating (vasovagal)
HISTORY• Associated symptoms • Medications – Chest pain, SOB, – Antihypertensives, lightheadedness, diuretics (orthostatic) incontinence – Antiarrthymics (cardiac• Past medical history syncope) – Identifying risk factors – TCA, Amiodarone – Morbidity and mortality (cardiac/prolonged QT) increases with organic causes • Family history • Parkinsons (orthostatic) – Sudden death (cardiac • Epilepsy (seizure) syncope/prolonged QT • DM (cardiac, autonomic or Brugada) dysfunction, glucose) • Cardiac disease
PHYSICAL EXAM• Vital signs – Orthostatics—most – Heart rate important • Tachy/brady, • Drop in BP and fixed dysrhythmia HR ->dysautonomia – Respiratory rate • Drop in BP and • Tachypnea (pe, increase HR -> volume hypoxia, anxiety) depletion/ • Bradypnea (cns, vasodilatation toxicmetabolic) • Insignificant drop in BP – Blood pressure and marked increase in HR -> POTS • High (cns, toxic/metabolic) – Temperature • Low (hypovolemia, • Hypo/hyperthermia cardiogenic shock, (sepsis, toxic- sepsis) metabolic, exposure)
• EKG---Cornerstone of workup – Arrhythmia, long qt, WPW, conduction abn.• Routine Blood work—limited value• Radiology---limited value except if abnormal exam• Other tests—depending of history and exam – Glucose --hemoglobin --troponin --CK (syncope vs seizure)
Starting the ―Workup‖• If young adult and No comorbid conditions or symptomsMost likely VASOMOTOR or ORTHOSTATIC .*Clinicians may forego the ECG in young, healthy patients with an obvious cause of syncope.
The ECGKey Points• Guidelines recommend EKG in the evaluation of all patients with syncope.• Exception: young healthy patients with an obvious cause of syncope• Abnormal ECG in 90% of patient with cardiac syncope• Only 6% of patients with reflex mediated syncope have abnormal ECG.• Syncopal patient with negative cardiac history and normal ECG—unlikely to have a cardiac cause
The ECG patient older, +comorbidsigns/symptoms• If Abnormal ECG – Ischemia/injury – Dysrhythmia • Sinus brady, BBB, AV block, prolonged QT, WPW, HOCM, Brugada• If Normal ECG – Consider holter or event recorder if dysrhythmia suspected
Carotid Sinus Massage(CSM)• Method1 • Absolute – Massage, 5-10 seconds contraindications2 – Don’t occlude – Carotid bruit, known – Supine and upright significant carotid posture arterial (on tilt table) disease, previous CVA, MI last 3 months• Outcome • Complications – 3 second asystole and/or 50 mmHg – Primarily neurological fall in systolic BP with – Less than 0.2% reproduction of – Usually transient symptoms = Carotid Sinus Syndrome
Holter Monitoring• 24-48 hour monitor—limited value because of intermittent nature of arrhythmias• Event recorder—more helpful. Patient must be conscious in order to activate unit.• Establishes diagnosis in only 2-3% of patients with syncope if ECG is normal.• Indicated in patients at highest risk for arrhythmia ie, abnormal ecg, palpitations, cad history, syncope when supine or with exertion.
Loop Event Recorders• Provides longer monitoring—weeks to months• Can activate the monitor after symptoms occur, thereby freezing in its memory the readings from the previous 2-5 minutes and the subsequent 1 minute• In patients with recurrent syncope, arrhythmias were found during symptoms in 8-20%.• Limitations: compliance, use of device, transmission
ECHOCARDIOGRAM• Access structural causes of cardiac syncope – AS, MS, HOCM, atrial myoxoma• Unlikely to be helpful in the absence of known cardiac disease or an abnormal ekg.• INDICATIONS – Abnormal ECG ---history of heart disease – Murmur ---exercise assoc. syncope
Structural Heart Disease• Aortic Stenosis – Most common structural lesion associated with syncope in the elderly• Hypertrophic Obstructive Cardiomyopathy – Vasodilatation (drugs/hot bath) can induce syncope• Obstruction to Right Ventricular Outflow – PE, pulmonary stenosis, pulmonary htn
EXERCISE STRESS TEST• Syncope during exercise is more likely to be related to an arrhythmia• Post-exertional syncope is usually neurally mediated.• Echocardiogram should be done prior to EST to r/o structural abnormality.• INDICATION – Syncope during or shortly after exercise (exertional syncope)
TILT TABLE TEST • Changes in position to reproduce symptoms of the syncopal event. • Positive tilt table test – Induction of bradycardia and hypotension – Considered diagnostic for vasovagal syncope
Indications for Tilt tabletest• Unexplained • Identification of recurrent syncope or neurally mediated syncope associated syncope could alter with injury in absence treatment of structural heart ds. • Evaluation of• Unexplained recurrent syncope or recurrent syncope associated unexplained falls. with injury in setting • Evaluation of near of organic heart syncope or dizziness disease after exclusion of potential cardiac cause of syncope
Tilt Table Test• Unmasks Vasovagal syncope susceptibility• Reproduces symptoms• Positive Tilt Test *Prophylaxis treatment—beta blockers or disopyramide as well as SSRIs *Recurrent symptoms and bradycardia may require pacemaker
Syncope Evaluation FlowChart
Symptoms DiagnosisOccurs after sudden unexpected pain, Vasovagal attacksound, smell, or sightProlonged StandingAthletes post exertionOccurs after micturition, defecation, Situational Syncopecough or swallowingEvent occurs in association with severe Glossopharyngeal or trigeminalthroat or facial pain neuralgiaOccurs with head rotation or pressure Carotid Sinus Syncopeon the carotid sinus-tumors, tight collarsor shavingEpisodes occur immediately on standing Orthostatic hypotensionHeadaches are associated with the event MigrainesMedications taken before Drug induced syncopeEvent is associated with vertigo, TIA/Subclavian Steal Syndromedysarthria or diplopiaEvent is associated with arm exercizePulse/BP differences between arms Aortic dissection/SSSSyncope occurs without prodrome and Arrythmiapatient has underlying structural heart dz.
San Francisco SyncopeRule• Risk Factors – C History of CHF – H Hematocrit less than 30 – E Non-sinus rhythm or new changes in EKG – S Systolic BP less than 90 – S Shortness of breath ------------- is a simple rule for evaluating the risk of adverse outcomes in patient who present with syncope.
SUMMARY• Shotgun approach is Not helpful.• EKG should be considered in all patients.• Tilt table test can diagnosis vasovagal syncope.• Neurologic testing is low yield and often overused.• Holter monitoring, Echo, EST, EP considered in patients at high risk for cardiac syncope.• Patients remain undiagnosed in 34% of cases.