Cardiac Syncope. spot it, stop it! Syncope is Tranient Loss of Consciousness (T- LOC) due to: transient global cerebral hypoperfusion

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1 Definition Cardiac Syncope spot it, stop it! David Gareth Jones Heart Rhythm Centre Royal Brompton & Harefield NHS Foundation Trust Syncope is Tranient Loss of Consciousness (T- LOC) due to: transient global cerebral hypoperfusion characterized by: Rapid onset Short duration Spontaneous complete recovery Transient Loss of Consciousness Classification of Transient Loss of Consciousness (TLOC) Real or Apparent TLOC Syncope Neurally-mediated reflex syndromes Orthostatic hypotension Cardiac arrhythmias Structural cardiovascular disease Disorders Mimicking Syncope With loss of consciousness, i.e., seizure disorders, concussion Without loss of consciousness, i.e., psychogenic pseudosyncope Syncope A Symptom, Not a Diagnosis Syncope in context Self-limited loss of consciousness and postural tone Relatively rapid onset Variable warning symptoms Spontaneous, complete, and usually prompt recovery without medical or surgical intervention Underlying mechanism is transient global cerebral hypoperfusion.

2 SchematicDrawing Neurally-Mediated Reflex Syncope Pathophysiology Vasovagal Syncope (VVS) Carotid Sinus Syndrome (CSS) Situational syncope Post-micturition Cough Swallow Defecation Blood drawing, etc. Autonomic Nervous System Brignole M, et al. Europace, 2004;6: Benditt D, et al. Neurally mediated syncope: Pathophysiology, investigations and treatment. Blanc JJ, et al. eds. Futura

3 VVS Clinical Pathophysiology Syncope Due to Structural Cardiovascular Disease: Principle Mechanisms 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 2 1 Acute MI/Ischemia 2 neural reflex bradycardia+ vasodilatation, arrhythmias, low output (rare) Previous MI/scar VF/VT! Hypertrophic cardiomyopathy Limited output during exertion (increased obstruction, greater demand), arrhythmias, neural reflex 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 Acute aortic dissection Neural reflex mechanism, pericardial tamponade Wieling W, et al. In: Benditt D, et al. The Evaluation and Treatment of Syncope. Futura. 2003; Syncope Due to Cardiac Arrhythmias Cardiac syncope can be a harbinger of sudden death Bradyarrhythmias Sinus arrest, exit block High grade or acute complete AV block Can be accompanied by vasodilatation (VVS, CSH) Tachyarrhythmias Atrial fibrillation/flutter with rapid ventricular rate (eg, pre-excitation syndrome) Paroxysmal SVT or VT Torsade de pointes 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 Probability of Survival No Syncope Vasovagal and Other Causes Cardiac Cause Follow-Up (yr) Soteriades ES, et al. N Engl J Med. 2002;347:878. Initial Evaluation key questions Is it syncope? 1.Is it a syncopal episode or not? Was LOC complete? 2.Has the aetiological diagnosis been determined? 3.Are there data suggestive of a high risk of cardiovascular events or death? Was LOC transient with rapid onset and short duration? Did the patient recover spontaneously, completely and without sequelae? Did the patient lose postural tone?

4 Aetiology - questions Aetiology - questions Circumstances Position, activites, precipitators Onset Nausea, vomiting, sweating, aura, pain, blurred vision Eyewitness account(s) Nature of fall, colour, duration LOC (often overestimated!) Movements (tonic, clonic, tonic-clonic, myoclonus, automatism) Onset of movements (at start, or delayed), duration Symptoms at end of attack Nausea, vomiting, feeling cold, muscle ache, injury, chest pain, palpitations, confusion, incontinence Background Family history (SCD!), past cardiac Hx, medications Neurological history inc. Parkinsonism, epilepsy Metabolic disorders (DM), alcohol Syncope history Frequency of episodes, individual histories for each when possible Risk stratification Risk stratification in hospital evaluation Abnormal ECG* Cardiac disease (history or exam) Family history of sudden cardiac death Severe injury/accident * SA/AV disease, BBB, acute MI/NSTEMI, Q waves, WPW, LVH/HCM, long QT, short QT, Brugada etc. etc! Heart Monitoring Options Implantable Loop Recorder (ILR) e.g. Reveal OPTION 12-Lead 10 Seconds Holter Monitor 2 Days Event Recorders (non-lead and loop) 7-30 Days ILR TIME (Months) CASE: 83 year-old woman with syncope due to bradycardia: Pacemaker implanted. CASE: 28 year-old man presents to A&E multiple times after falls resulting in trauma. VT: Ablated Brignole M, et al. Europace, 2004;6:

5 Cardiac Rhythms During Unexplained Syncope Composite: N=133 to 7109 Arrhythmia 22% (13-32%) Bradycardia 16% (11-21%) Tachycardia 6% (2-11%) Other 11% No Recurrence 36% (31-48%) Normal Sinus Rhythm 31% (17-44%) Seidl K. Europace. 2000;2(3): Krahn AD. PACE. 2002;25: Medtronic ILR Replacement Data. FY03, 04. On file. Treatment of Syncope Due to Bradyarrhythmia Treatment of Syncope Due to Tachyarrhythmia Class I indication for pacing using dual chamber system wherever possible 08:23:21 0.4nV Atrial tachyarrhythmias AVRT due to accessory pathway ablation of pathway Preexcited AF down accessory pathway ablation!! Ventricular pacing in atrial fibrillation with slow ventricular response :21 8:23:29 :22 :23 :24 :25 :26 :27 :28 : AVNRT ablation of AV nodal slow pathway Atrial fib consider pacing; ablation for paroxysmal AF (also?sss) Atrial flutter ablation if typical (right atrial) flutter Ventricular tachyarrhythmias :29 08:23:37 :30 :31 :32 :33 :34 :35 :36 : Ventricular tachycardia ICD (most, esp. if low EF), ablation in some Torsade de pointes withdraw offending drug or implant ICD (long QT/Brugada/short QT) :37 :38 :39 :40 :41 :42 :43 :44 : Drug therapy may be an alternative in some cases Treatment of neurally mediated syncope Brugada syndrome Lifestyle Avoidance of triggers when possible Maintain hydration and salt intake Physical counter-pressure manoeuvres hand grip, arm tensing, leg crossing Tilt training Difficult need to be motivated! Pharmacological measures Avoid/minimise hypotensive agents when possible Alpha agonists may be helpful (OH vs. VVS) midodrine Beta-blockers not helpful Pacing? controversial - syncope recurrence still >20% (40% unpaced) even if well-selected (cardioinhibitory) Best guided by ILR (evidence of asystole or symptomatic bradycardia)

6 Hypertrophic Cardiomyopathy WPW WPW Preexcited AF Long QT Syndromes Mechanism Abnormalities of sodium and/or potassium channels Susceptibility to polymorphic VT (Torsade de pointes) Prevalence Drug-induced forms Common Genetic forms Relatively rare, but increasingly being recognized Concealed forms: Syncope: Torsade de Pointes From the files of DG Benditt, MD. U of M Cardiac Arrhythmia Center May be common Provide basis for drug-induced torsade Long QT Syndromes: 12-Lead ECG

7 Drug-Induced QT Prolongation (some) Treatment of Long QT Antiarrhythmics Class IA...Quinidine, Procainamide, Disopyramide Class III Sotalol, Amiodarone, Dronedarone Psychoactive Agents Phenothiazines, Amitriptyline, Imipramine, Ziprasidone Antibiotics Erythromycin, Pentamidine, Fluconazole, Ciprofloxacin and other quinolones Nonsedating antihistamines Terfenadine, Astemizole Others Cisapride, Droperidol, Haloperidol Suspicion and recognition are critical Emergency treatment (for recurrent/incessant Torsades de Pointes) Avoid amiodarone Intravenous magnesium Pacing to overcome bradycardia or pauses Isoproterenol to increase heart rate and shorten repolarization If drug induced: Reverse bradycardia Withdraw drug Avoid ALL long-qt provoking agents If genetic: Avoid ALL long-qt provoking agents For more information visit Conclusion Syncope is a common symptom with many causes Thorough history, examination and investigation can facilitate appropriate treatment Cardiac syncope is frequently associated with an adverse prognosis and typically warrants urgent and/or in-patient investigation Seek cardiology opinion if cardiac syncope strongly suspected ESC guidelines (current 2009) offer guidance on best practice Appendix ESC treatment guidelines syncope 2009

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