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Syncope Diagnosis and Management Prabhat Hebbar, MD. Electrophysiologist CHI St. Vincent Heart Clinic Arkansas April 25, 2015.

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Presentation on theme: "Syncope Diagnosis and Management Prabhat Hebbar, MD. Electrophysiologist CHI St. Vincent Heart Clinic Arkansas April 25, 2015."— Presentation transcript:

1 Syncope Diagnosis and Management Prabhat Hebbar, MD. Electrophysiologist CHI St. Vincent Heart Clinic Arkansas April 25, 2015

2 Case 1 72 y/o wm with past medical history sig for HTN, DM, atrial fibrillation, CAD with remote MI was brought to the ER with syncope Pt was going up on a escalator and suddenly passed out. He fell and scraped his back and scalp. He woke up at the top of the escalator and was wondering why so many people had gathered around him. He was awake and alert on regaining consciousness.

3 Case 2 32 y/o female patient with recurrent syncope for the last 7 years. Episodes happen 1-2 times/week EMS was called on one of these episodes and reportedly could not get a blood pressure. Watched in ER for 2 hrs. and then sent home. Drinks plenty of water

4 Objectives I.Etiology II.Diagnosis & Evaluation Options III.Specific Conditions IV.Treatment Options

5 What is syncope? Transient loss of consciousness ( T-LOC) associated with a loss of postural tone rapid onset, short duration, and spontaneous complete recovery. Pathophysiology: sudden decrease or brief cessation of cerebral blood flow.

6 Is it Syncope? The following questions should be answered: Was LOC complete? Was LOC transient with rapid onset and short duration? Did the patient recover spontaneously, completely and without sequelae? Did the patient lose postural tone? Not syncope: Dizziness, presyncope, vertigo Drop attacks Cardiac arrest Seizures.

7 Is this a Seizure or Syncope ? precipitants of the episode the premonitory or prodromal symptoms the symptoms that accompany the episode and the events that follow it.

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9 Syncope: Etiology Orthostatic Cardiac Arrhythmia Structural Cardio- Pulmonary * 1 Vasovagal Carotid Sinus Situational  Cough  Post- micturition 2 Drug Induced ANS Failure  Primary  Secondary 3 Brady  Sick sinus  AV block Tachy  VT  SVT Long QT Syndrome 4 Aortic Stenosis HOCM Pulmonary Hypertension 5 Psychogenic Metabolic e.g. hyper- ventilation Neurological Non- Cardio- vascular Neurally- Mediated Unknown Cause = 34% 24%11%14%4%12% DG Benditt, UM Cardiac Arrhythmia Center

10 Neurally mediated syncope also termed neurocardiogenic or vasovagal syncope largest group of disorders causing syncope result from reflex-mediated changes in vascular tone or heart rate. Triggers - fainting may be triggered in the central nervous system. - activation of receptors in the ventricular wall - or in other organs (the bladder, esophagus, and the carotid sinus)

11 Diagnosis based on history Absence of heart disease Long history of recurrent syncope After sudden, unexpected, unpleasant sight sound smell or pain Prolonged standing or crowded hot places Nausea, vomiting associated with syncope During a meal or post prandial With head rotation or pressure on carotid sinus( shaving, tight collars) After exertion

12 Pathophysiology: a reflex increase in vagal efferent activity and sympathetic withdrawal leading to bradycardia and hypotension. Examples of vasovagal syncope ⁻emotional fainting ⁻situational syncope (e.g., in response to micturition cough, or defecation) ⁻carotid-sinus syncope. ⁻with panic episodes ⁻associated with exercise in athletes without heart disease.

13 Orthostatic Hypotension Syncope usually happens After standing up and standing after exertion. Temporal relation to start or changes in dosage of vasodepressive drugs. Etiology: DAAD Drug-induced (very common) - Diuretics and vasodilators Autonomic failure: primary or secondary - multiple system atrophy and parkinsonism - diabetes, alcohol, amyloid Alcohol Dehydration

14 Syncope Due to Arrhythmia or Structural CV Disease Often life-threatening and/or exposes patient to high risk of injury May be warning of critical CV disease Aortic stenosis, Myocardial ischemia, Pulmonary hypertension Assess culprit arrhythmia / structural abnormality aggressively Initiate treatment promptly

15 Cardiac Arrhythmias Bradyarrhythmias Sinus arrest, exit block High grade or acute complete AV block Tachyarrhythmias Atrial fibrillation / flutter with rapid ventricular rate (e.g. WPW syndrome) Paroxysmal SVT or VT Torsades de pointes

16 Structural Cardiovascular Disease Acute MI / Ischemia Acquired coronary artery disease Congenital coronary artery anomalies HOCM Acute aortic dissection Pericardial disease / tamponade Pulmonary embolus / pulmonary hypertension Valvular abnormalities Aortic stenosis, Atrial myxoma

17 Differential Diagnosis Migraine Acute hypoxemia Hyperventilation Somatization disorder (psychogenic syncope) Acute Intoxication (e.g., alcohol) Seizures Hypoglycemia Sleep disorders

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19 Initial Evaluation Should answer three key questions. -Is it syncope? -Has the etiology been determined? -What is the risk of CV events or death? Detailed history Physical examination Orthostatic blood pressure measurements Electrocardiogram ( ECG)

20 Head-up Tilt Test (HUT) Confirms diagnosis of neurocardiogenic syncope Pooling of blood triggers reflex Tachycardia followed by bradycardia and hypotension. Reproduces symptoms Physician is better able to give prognostic / treatment advice Diagnosis of psychogenic syncope

21 Who is at high risk? Severe structural or coronary artery disease ( CHF, Low EF, prior MI) Clinical features - Syncope with exertion or supine posture - Palpitations at the time of syncope - Family hx of sudden cardiac death EKG features - Frequent PVCs or Non sustained VT - Bifascicular block or QRS > 120 msec - Sinus bradycardia ( < 50bpm) or AV block ( second or third degree) - Pre excited QRS ( WPW syndrome) - Hypertrophic cardiomyopathy - Prolonged QT interval - Brugada pattern - Arrhythmogenic RV cardiomyopathy

22 Evaluation for Underlying Heart Disease A history, a physical examination, and an electrocardiogram are often sufficient ! when the presence or absence of underlying cardiac disease cannot be determined clinically, an echocardiogram, a stress test, or both are needed ECG monitoring: Holter, Event monitor and implantable loop recorder. EP study

23 Testing for Arrhythmias The only certain way is to obtain a rhythm strip during syncope. Ambulatory monitoring: Type of monitoring based on frequency of symptoms. Holter: 24-48 hrs. Event monitor( 1-2 months) Implantable continuous- loop recorder (upto 3 years)

24 Electrophysiologic Study Indications: -Ischemic heart disease and unexplained syncope -Bundle branch block and unexplained syncope -Syncope preceded by palpitations when holter and event have failed to make a diagnosis Findings -Abnormal sinus node function -> Pacemaker -Abnormal AV node function -> Pacemaker -Induction of supraventricular tachycardia -> Ablation -Inducibility for ventricular tachycardia -> ICD +/- ablation

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26 Case 1 Admitted to hospital Telemetry – no arrhythmia Echo – EF 30% Cath: Occluded RCA, mild disease in LAD and LCX Diagnosis: etiology unclear despite initial workup but high risk for sudden cardiac death Underwent single chamber ICD implantation Device Follow up: 2 episodes on NSVT 6 and 8 sec.

27 Case 2 Event monitor: tachycardia and bradycardia Tilt table test: Passive tilt phase neg. After nitroglycerine pt became tachycardic with HR 150 then bradycardic with HR 45 and passed out with reproduction of symptoms. Diagnosis: Neurocardiogenic syncope with predominant cardioinhibitory features Treatment: increase salt and fluid intake, isometric exercises, pay attention of prodrome. Metoprolol trial- no improvement Fludrocortisone 0.1 mg daily – no more syncope

28 Thank you


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