Pocket Medicine: The Massachusetts General Hospital Handbook of Internal Medicine by Marc Sabatine Page B

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, S 3 ), murmurs, LVH (S 4 , LV heave), PHT (RV heave, ↑ P 2 )
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