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SYNCOPEDefinition• Symptom of sudden transient loss of consciousness due to global cerebral hypoperfusion• If CPR or cardioversion required, then SCD and not syncope (different prognosis)Etiologies (NEJM 2002;347:878; JACC 2006;47:473; Eur Heart J 2009;30:2631)• Neurocardiogenic (a.k.a. vasovagal, 20%; NEJM 2005;352:1004): c sympathetic tone Svigorous contraction of LV S mechanoreceptors in LV trigger c vagal tone (hyperactiveBezold-Jarisch reflex) STHR (cardioinhibitory) and/or T BP (vasodepressor)cough, deglutition, defecation & micturition Scvagal tone and thus can be precipitantsrelated disorder: carotid sinus hypersensitivity• Orthostatic hypotension (10%)hypovolemia, diuretics, deconditioningvasodilators (espec. if combined w/ chronotropes)autonomic neuropathy (1 Parkinson’s, Shy-Drager, Lewy body dementia, POTS;2 diabetes, EtOH, amyloidosis, renal failure) (NEJM 2008;358:615)• CardiovascularArrhythmia (15%)Bradyarrhythmias: SSS, high-grade AV block, chronotropes, PPM malfunctionTachyarrhythmias:VT, SVT (syncope rare unless structural heart disease or WPW)Mechanical (5%)Endocardial:AS, MS, PS, prosthetic valve thrombosis, myxomaMyocardial: pump dysfxn from MI or outflow obstruction from HCMP (but usually VT)Pericardial: tamponadeVascular: PE, PHT, aortic dissection, ruptured AAA, subclavian steal• Neurologic (10%): seizure (technically not syncope),TIA/CVA, vertebrobasilarinsufficiency, dissection of cerebral arteries, migraine, narcolepsy• No cause identified in 40% of cases• Misc. causes of LOC (but not syncope): hypoglycemia, hypoxia, anemia, psychogenicWorkup (etiology cannot be determined in 40% of cases)• H&P incl. orthostatic VS have highest yield and most cost effective (Archives 2009;169:1299)• History (from Pt and witnesses if available)activity and posture before the incidentprecipitating factors: exertion (AS, HCMP, PHT), positional (orthostatic hypotension),stressors such as sight of blood, pain, emotional distress, fatigue, prolonged standing,warm environment, N/V, cough/micturition/defecation/swallowing (neurocardiogenic),head turning or shaving (carotid sinus hypersens.); arm exercise (subclavian steal)prodrome (eg, diaphoresis, nausea, blurry vision): cardiac 5 sec, vasovagal 5 secassociated sx: chest pain, palp., neurologic, post-ictal, bowel or bladder incontinence(convulsive activity for 10 sec may occur with transient cerebral hypoperfusion)• PMH: prior syncope, previous cardiac or neurologic dis.; no CV disease at baseline S 5%cardiac, 25% vasovagal; CV disease S 20% cardiac, 10% vasovagal (NEJM 2002;347:878)• Medicationsvasodilators: -blockers, nitrates,ACEI/ARB, CCB, hydralazine, phenothiazines, antidep.diuretics; chronotropes (eg, -blockers and CCB)proarrhythmic or QT prolonging: class IA, IC or III antiarrhythmics, et al. (see “ECG”)psychoactive drugs: antipsychotics,TCA, barbiturates, benzodiazepines, EtOH• Family history: CMP, SCD• Physical examVS including orthostatics ( if supine S standing results in 20 mmHg T SBP,10 mmHg T DBP, or 10–20 bpm c HR), BP in both armscardiac: HF (c JVP, displ. PMI, S 3), murmurs, LVH (S 4, LV heave), PHT (RV heave, c P 2)vascular exam: ✓ for asymmetric pulses, carotid bruits, carotid sinus massageneurologic exam: focal findings, evidence of tongue biting; fecal occult blood test• ECG (abnormal in 50%, definitively identifies cause of syncope in 10%)sinus bradycardia, sinus pauses,AVB, BBB, SVT,VTischemic changes (new or old); atrial or ventricular hypertrophymarkers of arrhythmia: ectopy, c QT, preexcitation (WPW), Brugada, wave (ARVC)Other diagnostic studies (consider ordering based on results of H&P and ECG)• Ambulatory ECG monitoring: if suspect arrhythmogenic syncopeHolter monitoring (continuous ECG 24–48 h): useful if frequent eventsarrhythmia sx (4%); asx but signif. arrhythmia (13%); sx but no arrhythmia (17%)Event recorder (activated by Pt to record rhythm strip): useful for infrequent events, butproblematic if no prodrome; yield 20–50% over 30–60 d of monitoringSYNCOPE 1-37