Pocket Medicine

CARDIOLOGY

SYNCOPE

Definition

•  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): ↑ sympathetic tone → vigorous contraction of LV → mechanoreceptors in LV trigger ↑ vagal tone (hyperactive Bezold-Jarisch reflex) → ↓ HR (cardioinhibitory) and/or ↓ BP (vasodepressor)
cough, deglutition, defecation, & micturition → ↑ vagal tone and thus can be precipitants
related disorder: carotid sinus hypersensitivity (exagg vagal resp to carotid massage)

•  Orthostatic hypotension (10%)
hypovolemia/diuretics, deconditioning; vasodilat. (esp. if combined w/  chronotropes)

autonomic neuropathy [1° = Parkinson’s, Shy-Drager, Lewy body dementia, POTS (dysautonomia in the young); 2° = DM, EtOH, amyloidosis, CKD] (NEJM 2008;358:615)

•  Cardiovascular

Arrhythmia (15%)

Bradyarrhythmias: SSS, high-grade AV block,  chronotropes, PPM malfunction

Tachyarrhythmias: VT, SVT (syncope rare unless structural heart disease or WPW)

Mechanical (5%)

Endocardial/Valvular: AS, MS, PS, prosthetic valve thrombosis, myxoma

Myocardial: pump dysfxn from MI or outflow obstruction from HCMP (but usually VT)

Pericardial: tamponade

Vascular: PE, PHT, aortic dissection, ruptured AAA, subclavian steal

•  Neurologic (10%): seizure (technically not syncope), TIA/CVA, vertebrobasilar

insufficiency, dissection of cerebral arteries, migraine, narcolepsy

•  Misc. causes of LOC (but not syncope): hypoglycemia, hypoxia, anemia, psychogenic

Workup (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 incident

precipitating factors: exertion (AS, HCMP, PHT), positional Δ (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 sec

associated sx: chest pain, palp., neurologic, postictal, bowel or bladder incontinence (convulsive activity for <10 sec may occur w/ transient cerebral HoTN & mimic seizure)

•  PMH: prior syncope, previous cardiac or neurologic dis.; no CV disease at baseline → 5% cardiac, 25% vasovagal; CV disease → 20% cardiac, 10% vasovagal (NEJM 2002;347:878)

•  Medications that may act as precipitants

vasodilators: a-blockers, nitrates, ACEI/ARB, CCB, hydralazine, phenothiazines, antidep.

diuretics;  chronotropes (eg, bB and CCB)

proarrhythmic or QT prolonging: class IA, IC or III antiarrhythmics (see “ECG”)

psychoactive drugs: antipsychotics, TCA, barbiturates, benzodiazepines, EtOH

•  Family history: CMP, SCD, syncope (vasovagal may have genetic component)

•  Physical exam

VS including orthostatics ( if supine → standing results in >20 mmHg ↓ SBP, >10 mmHg ↓ DBP, or >10–20 bpm ↑ HR), BP in both arms

cardiac: HF (↑ JVP, displ. PMI, S3), murmurs, LVH (S4, LV heave), PHT (RV heave, ↑ P2)

vascular: ✓ for asymmetric pulses, carotid/vertebral/subclavian bruits; carotid sinus massage to assess for carotid hypersensitivity (if no bruits)

neurologic exam: focal findings, evidence of tongue biting; FOBT

•  ECG (abnormal in ~50%, but only definitively identifies cause of syncope in ~10%)

Conduction: SB, sinus pauses/sinus arrhythmia, AVB, BBB/IVCD

Arrhythmia: ectopy, ↓ QT, preexcitation (WPW), Brugada, e wave (ARVC), SVT/VT

Ischemic changes (new or old): atrial or ventricular hypertrophy

Other diagnostic studies (consider based on results of H&P and ECG)

•  Ambulatory ECG monitoring: if suspect arrhythmogenic syncope

Holter monitoring (continuous ECG 24–48 h): useful if frequent events arrhythmia + sx (4%); asx but signif. arrhythmia (13%); sx but no arrhythmia (17%)

Event recorder (activated by Pt to record rhythm strip): limited role as only useful if established prodrome (because must be Pt activated)

Loop recorders (continuously saves rhythm, ∴ can be activated after an event): useful for episodes (including w/o prodrome) likely to occur w/in month.

Implantable loop recorders (inserted SC; can record up to 3 y): useful for infrequent episodes (<1/mo); recommended for recurrent syncope w/o prodrome

•  Echo: consider to r/o structural heart disease (eg, CMP [incl HCMP & ARVC], valvular disease [incl AS, MS, MVP], myxoma, amyloid, PHT, ± anomalous coronaries)

•  ETT: esp. w/ exertional syncope; r/o ischemia- or catecholamine-induced arrhythmias

•  Cardiac catheterization: consider if noninvasive tests suggest ischemia

•  Electrophysiologic studies (EPS): consider in high-risk Pts in whom tachy or brady etiology is strongly suspected, but cannot be confirmed;

50% abnl (inducible VT, conduction abnormalities) if heart disease, but ? significance

3–20% abnl if abnl ECG; <1% abnl if normal heart and normal ECG (Annals 1997;127:76)

•  ? Tilt table testing: utility is debated due to poor Se/Sp/reproducibility; consider only if vasovagal dx suspected but can’t be confirmed by hx

•  Cardiac MRI: helpful to dx ARVC if suggestive ECG, echo (RV dysfxn) or  FHx of SCD

•  Neurologic studies (cerebrovascular studies, CT, MRI, EEG): if H&P suggestive; low yield

Figure 1-6 Approach to syncope

High-risk features (usually admit w/ telemetry & testing; J Emerg Med 2012;42:345)

•  Age >60 y, h/o CAD, HF/CMP, valvular or congenital heart dis., arrhythmias, FHx SCD

•  Syncope c/w cardiac cause (lack of prodrome, exertional, resultant trauma) or recurrent

•  Complaint of chest pain or dyspnea; abnl VS or cardiac exam

•  ECG suggesting tachy or brady-induced syncope; Pt w/ PPM/ICD

Treatment

•  Arrhythmia, cardiac mechanical or neurologic syncope: treat underlying disorder

•  Vasovagal syncope: no proven benefit for midodrine, fludrocortisone, disopyramide, SSRI ? 16 oz of H2O before at-risk situations (Circ 2003;108:2660)

no proven benefit w/ bB (Circ 2006;113:1164)

? benefit w/ PPM if ≥3 episodes/2y & loop recorder w/ asystole >3 sec (Circ 2012;125:2566)

•  Orthostatic syncope: volume replete (eg, 500 mL PO q a.m.); if chronic → rise from supine to standing slowly, compressive stockings, midodrine, fludrocortisone, high Na diet

Prognosis (Ann Emerg Med 1997;29:459; NEJM 2002;347:878)

•  22% overall recurrence rate if idiopathic, else 3% recurrence

•  Cardiac syncope: 2-fold ↑ in mort., 20–40% 1-y SCD rate, median survival ~6 y

•  Unexplained syncope w/ 1.3-fold ↑ in mort., but noncardiac or unexplained syncope w/ nl

ECG, no h/o VT, no HF, age <45 → low recurrence rate and <5% 1-y SCD rate

•  Vasovagal syncope: Pts not at increased risk for death, MI or stroke

•  ✓ state driving laws and MD reporting requirements. Consider appropriateness of Pt involvement in exercise/sport, operating machinery, high-risk occupation (eg, pilot).