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SYNCOPE Mechanisms and Management John Telles MD, .

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Slide 1 :

SYNCOPE Mechanisms and Management John Telles MD, FACC August 9, 2006

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Case Study 20 y/o female competitive cyclist Dizzy when stands up quickly Syncope during training ride

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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.

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Maintenance of Postural Normaltension Upright posture results in translocation of 30% of central blood volume to dependent body parts within seconds and transcapillary fluid shifts over 30 minutes further reduce blood volume by 5%. Compensatory responses Muscle pump Nuerovascular compensation Humoral compensation Local vascular

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Bergan J et al. N Engl J Med 2006;355:488-498 Action of the Musculovenous Pump in Lowering Venous Pressure in the Leg

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Maintenance of Postural Normaltension Neurovascular Compensation High pressure mechanoreceptors Low pressure mechanoreceptors

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Syncope is important because…. It is common Costly May be disabling May be only warning sign before sudden death

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Relative Frequency of Syncope 15% of children before the age of 18 16% during 10 year period in men aged 40- 59 19% during 10 year period in women aged 40 –49 23% during 10 year period in elderly > 70 years old Recurrence in 35% in 3 years

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Syncope Mortality Low mortality vs. high mortality Neurally-mediated syncope vs. syncope with a cardiac cause Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. N Engl J Med. 2002;347(12):878-885. [Framingham Study Population]

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Syncope: Key questions to address with initial evaluation Is the loss of consciousness attributable to syncope or not? Is heart disease present or absent? Are there important clinical features in the history that suggest the diagnosis?

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Syncope Mimics Disorders without impairment of consciousness Falls Drop attacks Cataplexy Psychogenic pseudo-syncope Transient ischemic attacks Disorders with loss of consciousness Metabolic disorders Epilepsy Intoxications Vertebrobasilar transient ischemic attacks

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Differential Diagnosis of Syncope: Seizures vs Hypotension

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Causes of True Syncope Orthostatic Cardiac Arrhythmia Structural Cardio- Pulmonary 1 VVS CSS • Situational Cough Post- Micturition 2 Drug-Induced • ANS Failure Primary Secondary 3 Brady SN Dysfunction AV Block • Tachy VT SVT Long QT Syndrome 4 Acute Myocardial Ischemia Aortic Stenosis HCM Pulmonary Hypertension Aortic Dissection Neurally- Mediated Unexplained Causes = Approximately 1/3 DG Benditt, MD. U of M Cardiac Arrhythmia Center

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Causes of Syncope 1Soteriades ES, et al. NEJM. 2002;347:878-885. 2 Linzer M, et al. Ann Intern Med. 1997;126:989-996.

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Causes of Syncope by Age Younger Patient Vasovagal Situational Psychiatric Long QT* Brugada syndrome* WPW syndrome* RV dysplasia* Hypertrophic cardiomyopathy* Catecholaminergic VT Other genetic syndromes Older Patient Cardiac** Mechanical Arrhythmic Orthostatic hypotension Drug-induced Neurally mediated Multifactorial Underlined: benign * Rare, not benign ** Not benign .

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Syncope: Important Historical Features Questions about circumstances just prior to attack Position (supine, sitting , standing) Activity (rest, change in posture, during or immediately after exercise, during or immediately after urination, defecation or swallowing) Predisposing factors (crowded or warm place, prolonged standing post-prandial period) and of precipitating events (fear, intense pain, neck movements) Questions about onset of the attack Nausea, vomiting, feeling cold, sweating, pain in chest, pain in neck, or shoulders,

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Syncope: Important Historical Features Questions about onset of the attack Nausea, vomiting, feeling cold, sweating, pain in chest, pain in neck, or shoulders,

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Syncope: Important Historical Features Questions about attack (eye witness) Skin color (pallor, cyanotic) Duration of loss of consciousness Movements ( tonic-clonic, etc.) Tongue biting Questions about the end of the attack Nausea, vomiting, diaphoresis, feeling cold, muscle aches, confusion, skin color, wounds

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Syncope: Important Historical Feature Questions about background Number and duration of syncope spells Family history of arrhythmic disease or sudden death Presence of cardiac disease Neurological disease (Parkinsons, epilepsy, narcolepsy) Internal history (Diabetes) Medications (Hypotensive, negative chronotropic and antidepressant agents)

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Clinical Features Suggesting Specific Cause of Syncope Neurally-Mediated Syncope Absence of cardiac disease Long history of syncope After sudden unexpected, unpleasant sensation Prolonged standing in crowded, hot places Nausea vomiting associated with syncope During or after a meal With head rotation or pressure on carotid sinus After exertion

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Clinical Features Suggesting Specific Cause of Syncope Syncope due to orthostatic hypotension After standing up Temporal relationship to taking a medication that can cause hypotension Prolonged standing Presence of autonomic neuropathy After exertion

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Clinical Features Suggestion Cause of Syncope Cardiac Syncope Presence of structural heart disease With exertion or supine Preceded by palpitations Family history of sudden death

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Initial Exam: Thorough Physical Vital signs Heart rate Orthostatic blood pressure change Cardiovascular exam: Is heart disease present? ECG: Long QT, pre-excitation, conduction system disease Echo: LV function, valve status, HCM Neurological exam Carotid sinus massage Perform under clinically appropriate conditions preferably during head-up tilt test Monitor both ECG and BP

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Carotid Sinus Massage (CSM) Method1 Massage, 5-10 seconds Don’t occlude Supine and upright posture (on tilt table) Outcome 3 second asystole and/or 50 mmHg fall in systolic BP with reproduction of symptoms = Carotid Sinus Syndrome Absolute contraindications2 Carotid bruit, known significant carotid arterial disease, previous CVA, MI last 3 months Complications Primarily neurological Less than 0.2%3 Usually transient

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Syncope: Diagnostic Testing in Hospital Strongly Recommended Suspected/known ‘significant’ heart disease ECG abnormalities suggesting potential life-threatening arrhythmic cause Syncope during exercise Severe injury or accident Family history of premature sudden death

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Diagnostic Methods and Yields **Structural Heart Disease

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Heart Monitoring Options ILR Event Recorders (non-lead and loop) Holter Monitor 12-Lead 2 Days 7-30 Days Up to 14 Months 10 Seconds OPTION TIME (Months) 0 1 2 3 4 5 6 7 8 9 10 11 12 13 14

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Insertable Loop Recorder (ILR) The ILR is an implantable patient – and automatically – activated monitoring system that records subcutaneous ECG and is indicated for: Patients with clinical syndromes or situations at increased risk of cardiac arrhythmias Patients who experience transient symptoms that may suggest a cardiac arrhythmia

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Symptom-Rhythm Correlation with the ILR CASE: 65 year-old man with syncope accompanied by brief retrograde amnesia. Medtronic data on file. CASE: 56 year-old woman with refractory syncope accompanied with seizures.

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Head-Up Tilt Test (HUT) Protocols vary Useful as diagnostic adjunct in atypical syncope cases Useful in teaching patients to recognize prodromal symptoms Not useful in assessing treatment

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Response to Tilt Table Testing Normal Vasal vagal

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Response to Tilt Table Testing POTS Dysautonomia

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Indication for Tilt Table Testing The evaluation of recurrent syncope, or a single syncopal event accompanied by physical injury, motor vehicle accident, or in high risk setting in which clinical features suggest vasovagal In patients in whom dysautonomias may contribute to symptomatic hypotension Evaluation of recurrent exercise induced syncope in patients without structural heart disease

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Conventional EP Testing in Syncope Greater diagnostic value in older patients or those with SHD Less diagnostic value in healthy patients without SHD Useful diagnostic observations: Inducible monomorphic VT SNRT > 3000 ms or CSNRT > 600 ms Inducible SVT with hypotension HV interval = 100 ms (especially in absence of inducible VT) Pacing induced infra-nodal block

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Diagnostic Limitations of EPS Difficult to correlate spontaneous events and laboratory findings Positive findings1 Without SHD: 6-17% With SHD: 25-71% Less effective in assessing bradyarrhythmias than tachyarrhythmias2 EPS findings must be consistent with clinical history Beware of false positive

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“…cardiac syncope can be a harbinger of sudden death.” Survival with and without syncope 6-month mortality rate of greater than 10% Cardiac syncope doubled the risk of death Includes cardiac arrhythmias and SHD Soteriades ES, et al. N Engl J Med. 2002;347:878.

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Syncope Due to Cardiac Arrhythmias Bradyarrhythmias Sinus arrest, exit block High grade or acute complete AV block Can be accompanied by vasodilatation (VVS, CSS) Tachyarrhythmias Atrial fibrillation/flutter with rapid ventricular rate (eg, pre-excitation syndrome) Paroxysmal SVT or VT Torsade de pointes

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Syncope Due to Structural Cardiovascular Disease: Principle Mechanisms Acute MI/Ischemia 2° neural reflex bradycardia Vasodilatation, arrhythmias, low output (rare) Hypertrophic cardiomyopathy Limited output during exertion (increased obstruction, greater demand), arrhythmias, neural reflex Acute aortic dissection Neural reflex mechanism, pericardial tamponade Pulmonary embolus/ pulmonary hypertension Neural reflex, inadequate flow with exertion Valvular abnormalities Aortic stenosis – Limited output, neural reflex dilation in periphery Mitral stenosis, atrial myxoma – Obstruction to adequate flow

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Neurally-Mediated Reflex Syncope Vasovagal Syncope (VVS) Carotid Sinus Syndrome (CSS) Situational syncope Post-micturition Cough Swallow Defecation Blood drawing, etc. .

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VVS Clinical Pathophysiology Neurally-mediated physiologic reflex mechanism with two components: 1. Cardioinhibitory (? HR) 2. Vasodepressor (? BP) despite heart beats, no significant BP generated Both components are usually present 1 2

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VVS Incidence Most common form of syncope 8% to 37% (mean 18%) of syncope cases Depends on population sampled Young without SHD, ? incidence Older with SHD, ? incidence

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VVS General Treatment Measures Optimal treatment strategies for VVS are a source of debate Treatment goals Acute intervention Physical maneuvers, eg, crossing legs or tugging arms Lowering head Lying down Long-term prevention Tilt training Education Diet, fluids, salt Support hose Drug therapy Pacing

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CSS Carotid Sinus Syndrome Syncope clearly associated with carotid sinus stimulation is rare (=1% of syncope) CSS may be an important cause of unexplained syncope/falls in older individuals Prevalence higher than previously believed Carotid Sinus Hypersensitivity (CSH) No symptoms No treatment

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CSS Etiology Sensory nerve endings in the carotid sinus walls respond to deformation Previous neck surgery may contribute Increased afferent signals to brain stem Reflex increase in efferent vagal activity and diminution of sympathetic tone results in bradycardia and vasodilatation Carotid Sinus

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SAFE PACE Syncope And Falls in the Elderly – Pacing And Carotid Sinus Evaluation Objective Determine whether cardiac pacing reduces falls in older adults with carotid sinus hypersensitivity Randomized controlled trial (N=175) Adults > 50 years, non-accidental fall, positive CSM Pacing (n=87) vs. No Pacing (n=88) Results More than 1/3 of adults over 50 years presented to the Emergency Department because of a falls have CS hypersensitivity With pacing, falls ? 70% Syncopal events ? 53% Injurious events ? 70% Kenny RA. J Am Coll Cardiol. 2001;38:1491-1496.

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Orthostatic Hypotension Etiology Drug-induced (very common) Diuretics Vasodilators Primary autonomic failure Multiple system atrophy Parkinson’s Disease Postural Orthostatic Tachycardia Syndrome (POTS) Secondary autonomic failure Diabetes Alcohol Amyloid

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Treatment Strategies for Orthostatic Intolerance Patient education, injury avoidance Hydration Fluids, salt, diet Minimize caffeine/alcohol Sleeping with head of bed elevated Tilt training, leg crossing, arm pull Support hose Drug therapies Fludrocortisone, midodrine, erythropoietin Tachy-Pacing (probably not useful)

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Syncope and Driving “I want to die peacefully in my sleep like my grandfather did, not like the screaming passengers in his car.” George Burns

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Syncope and Driving: Medical-Legal Concerns State of California requires physicians to report, in good faith, patients who have a physical or mental condition which, in the physician’s judgment, impairs the patient’s ability to exercise reasonable and ordinary control over a motor vehicle. The report may be made without the patient’s informed consent. The physician is obliged to inform the patient of the severity of the condition and that operating a motor vehicle is advised against. This informed advise should be documented in the medical record.

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Syncope and Driving: Medical Legal Concerns Examples of syncopal conditions that would prohibit driving Untreated syncope in patients with heart disease Undiagnosed recurrent syncope which occurs without prodrome and can occur while sitting

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20 y/o female cyclist, dizzy when stands quickly, syncope during training ride

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20 y/o female cyclist, dizzy when stands quickly, snycope during training ride Sitting: HR 65, BP 120/80 , Standing: HR 90, BP 115/80 EKG normal

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20 y/o female cyclist, dizzy with standing quickly, syncope on training ride Sitting: HR 65, BP 120/80 Standing: HR 90, BP 115/80 EKG normal Echo normal

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20 y/o female cyclist, dizzy when stands quickly, syncope during training ride Sitting:HR 65, BP 120/80, Standing HR 90, BP 115/80 EKG normal Echo normal Exercise test normal

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20 y/o female cyclist Dizzy when stands quickly, syncope during training ride Sitting: HR 65, BP 120/80, Standing: HR 90 BP 115/80 EKG normal Echo normal Exercise test normal Tilt test abnormal

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Diagnosis Postural orthostatic tachycardia syndrome POTS Treatment hydration fludrocortisone midodrine welbutrin zoloft procrit atacand @ HS

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Diagnostic Objectives Distinguish true syncope from syncope mimics Determine presence of heart disease and risk for sudden death Establish the cause of syncope with sufficient certainty to: Assess prognosis confidently Initiate effective preventive treatment

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How to Evaluate Syncope *EPS if BBB or LVEF < 40% History: Patient and witnesses Physical: Including carotid massage and ECG Transient or reversible cause? Suspected cardiac or arrhythmic cause? Neurocardiogenic cause? No obvious cause? No heart disease? No work-up or chronic therapy 1st episode? Tilt table Loop recorder Admit, cardiology consult, EPS* - Rx + + + + yes yes yes Rx Rx Rx No Rx yes no - Olshansky B. Syncope: Mechanisms and Management. Futura Pub. Co. 1998. Referral -

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	SlidesOnline 1 Years ago. Category: Cardiology

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... Brugada syndrome, WPW syndrome, hypertrophic cardiomyopathy, arrhythmogenic right ventricula more ... Brugada syndrome, WPW syndrome, hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, and others as possible causes for syncope. ... less

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