Cardiovascular
Syncope: workup, risk stratification, and disposition
— Lifetime prevalence ~35%; accounts for 1–3% of ED visits and up to 6% of hospital admissions
— Bimodal age distribution: adolescents (vasovagal) and elderly (cardiac, orthostatic, polypharmacy)
— 30-day serious outcome rate in ED syncope ~7–10% (arrhythmia, MI, PE, structural heart disease, hemorrhage)
— Reflex (neurally mediated): vasovagal, situational (cough, micturition, defecation), carotid sinus hypersensitivity — most common, generally benign
— Orthostatic hypotension: volume depletion, autonomic failure (Parkinson, diabetes, amyloid), medications (α-blockers, diuretics, antihypertensives, TCAs)
— Cardiac (highest mortality): arrhythmic (VT, SVT with hemodynamic collapse, sick sinus, AV block) or structural (aortic stenosis, HCM, PE, tamponade, MI, dissection)
— Syncope: pallor, diaphoresis, rapid recovery, brief myoclonic jerks possible (convulsive syncope — does NOT equal seizure)
— Seizure: postictal confusion >5 min, tongue biting (lateral), incontinence less specific, aura
— Pseudosyncope: prolonged "unconsciousness" with closed eyes resisting opening, normal vitals
Board pearl: Syncope during exertion = aortic stenosis, HCM, anomalous coronary, or catecholaminergic VT until proven otherwise; syncope after exertion is usually vasovagal.

— Vasovagal: warmth, nausea, tunnel vision, diaphoresis, lightheadedness over 30–60 sec; triggers include pain, emotion, prolonged standing, blood draw, hot environment
— Orthostatic: lightheadedness within seconds to 3 min of standing or postprandially (autonomic failure)
— Cardiac arrhythmic: no prodrome or brief palpitations; "drop attack" with facial injury suggests sudden arrhythmia (no time to protect face)
— Situational: during/immediately after cough, micturition, defecation, swallowing
— Supine syncope → arrhythmia or seizure
— Exertional syncope → outflow obstruction (AS, HCM), pulmonary HTN, ischemia, exercise-induced VT
— Head-turning or tight collar → carotid sinus hypersensitivity
— Arm exertion with BP differential → subclavian steal
— Chest pain → ACS, dissection, PE
— Dyspnea, pleuritic pain, leg swelling → PE
— Tearing back pain → aortic dissection
— Melena, hematochezia, abdominal pain → GI bleed or ruptured AAA
— Headache, focal deficit → SAH, posterior circulation TIA (rarely causes isolated syncope)
— Antihypertensives, diuretics, α-blockers (tamsulosin), nitrates, PDE5 inhibitors
— QT-prolonging drugs (ondansetron, methadone, fluoroquinolones, antipsychotics)
— Insulin/sulfonylureas (hypoglycemia mimic)
— Alcohol, recreational stimulants
Key distinction: Recurrent syncope with consistent triggers and reliable prodrome over years in a young patient = vasovagal; new-onset syncope in an older patient with cardiac risk factors = cardiac workup until proven otherwise. Witness account of duration, color change, and convulsive activity is often more reliable than the patient's own recollection.

— Bilateral arm BP: >20 mmHg systolic difference suggests aortic dissection or subclavian stenosis
— Orthostatic vitals: drop ≥20 mmHg systolic, ≥10 mmHg diastolic, or HR rise ≥30 bpm within 3 min of standing. Blunted HR response (<10 bpm rise) with BP drop suggests autonomic failure or β-blocker effect
— Persistent tachycardia or hypotension → hemorrhage, PE, sepsis, tamponade
— SpO2 and ETCO2 if obtainable
— Crescendo-decrescendo systolic murmur radiating to carotids, delayed pulse, soft S2 → severe aortic stenosis
— Dynamic murmur louder with Valsalva/standing, softer with squatting → HCM
— Loud P2, RV heave, fixed split S2 → pulmonary HTN/PE
— Muffled heart sounds, JVD, pulsus paradoxus → tamponade (Beck triad)
— Irregularly irregular rhythm → AF with rapid ventricular response
— Asymmetric pulses, abdominal/flank bruit, pulsatile abdominal mass → AAA or dissection
— Unilateral leg swelling, calf tenderness → DVT/PE
— Rales, S3 → decompensated HF
— Focal deficit is not typical of syncope; if present, evaluate stroke/SAH
— Cerebellar findings, vertical nystagmus → posterior circulation event
— Confusion >5 min after event → consider seizure
— Rectal exam if GI bleed suspected (anemia + syncope)
— Inspect for injury (facial, head) — predicts cardiac etiology; absence of protective injury suggests sudden LOC
— Tongue lateral laceration → seizure
CCS pearl: Order "orthostatic vital signs" and "bilateral arm blood pressures" explicitly on the CCS interface within the first 5 simulated minutes — they change the differential immediately and are commonly omitted by test-takers who jump to imaging.

— Ischemic changes (ST elevation/depression, new Q waves, T inversions)
— Arrhythmia: AF/flutter, bradycardia <40, sinus pauses ≥3 sec, 2nd-degree Mobitz II or 3rd-degree AV block
— QTc >500 ms → torsades risk; QTc <340 ms → short QT syndrome
— Brugada pattern: coved ST elevation V1–V2 with T inversion
— WPW: delta wave, short PR
— ARVC: epsilon wave, TWI V1–V3 in adults
— HCM: LVH with deep narrow Q waves inferolateral, giant TWI
— PE: sinus tachycardia (most common), S1Q3T3, RBBB, right axis
— Bifascicular block + syncope → strongly consider EP study/pacemaker
— CBC if bleeding suspected; hemoglobin
— BMP (electrolytes, Cr, glucose) — especially with diuretics, vomiting, DM
— Troponin if chest pain, exertional syncope, ECG changes, or older with CV risk factors
— BNP if HF suspected; elevated BNP predicts adverse outcomes in syncope
— D-dimer only if PE on differential (Wells/PERC-guided); pregnancy test in reproductive-age women
— POC glucose at bedside (hypoglycemia mimic)
— Lactate if sepsis/hemorrhage suspected
— CXR if dyspnea, chest pain, abnormal lung exam, or HF concern
— CT head NOT routine — order only with head trauma on anticoagulation, focal neuro deficit, or seizure suspicion; yield <2% otherwise
— Bedside echo (POCUS) if tamponade, dissection, RV strain, or severe AS suspected
— CT angiography for suspected PE or dissection
Step 3 management: Do not reflexively order CT head, carotid Dopplers, or EEG in uncomplicated syncope — these are low-yield, high-cost choices that are commonly the wrong answer. The correct answer is usually ECG + orthostatics + targeted labs based on history.

— Indicated when structural heart disease suspected: murmur, abnormal ECG, HF signs, exertional syncope, family history of sudden death
— Identifies AS, HCM, severe MR, LV dysfunction, RV strain, pericardial effusion, intracardiac mass (myxoma)
— Routine TTE in all syncope is low yield and not guideline-supported
— Holter (24–48 hr): symptoms daily
— Event monitor / patch (2–4 weeks): symptoms weekly to monthly
— External loop recorder (30 days): less frequent symptoms
— Implantable loop recorder (up to 3 years): recurrent unexplained syncope, suspected arrhythmia, high-risk patients without diagnosis after initial workup — highest diagnostic yield for infrequent events
— Mobile cardiac telemetry: real-time, useful for high-risk outpatients
— Exertional syncope without obstructive findings on echo
— Suspected ischemia or exercise-induced arrhythmia (CPVT, exercise-induced LQTS)
— Structural heart disease + unexplained syncope after noninvasive workup
— Bifascicular block, sinus node dysfunction with inconclusive monitoring
— Suspected SVT/VT not captured
— Low yield in patients with structurally normal hearts and normal ECG
— Recurrent unexplained syncope without structural heart disease when reflex/orthostatic etiology suspected but unclear
— Differentiates vasovagal vs POTS vs orthostatic hypotension vs psychogenic pseudosyncope
— Not first-line and not needed for typical vasovagal history
Board pearl: For recurrent unexplained syncope after a negative initial evaluation, an implantable loop recorder outperforms repeated short-term monitors and tilt testing for arrhythmia detection — a frequent right-answer choice on Step 3.

— Abnormal ECG: ischemia, arrhythmia, BBB, prolonged QT, Brugada, pre-excitation
— Syncope during exertion or supine
— Palpitations preceding syncope
— Family history of sudden cardiac death
— Known structural/ischemic heart disease, HF, prior MI, low LVEF
— Severe anemia, GI bleed, suspected PE/dissection/tamponade
— Persistent abnormal vitals (HR <40 or >100, SBP <90)
— Age >60 with cardiovascular comorbidities
— Significant injury from syncope
— Elevated troponin or BNP
— Young (<40), no cardiac history
— Clear vasovagal or situational trigger with typical prodrome
— Normal ECG, normal exam, normal vitals
— No injury, no recurrence pattern
— Canadian Syncope Risk Score (CSRS): ED-derived, predicts 30-day serious outcomes; incorporates vasovagal predisposition, heart disease history, SBP, troponin, QRS/QTc, ED diagnosis
— San Francisco Syncope Rule ("CHESS"): CHF, Hct <30, ECG abnormal, SOB, SBP <90
— Score thresholds guide observation vs discharge, not used in isolation
— Discharge home: clear reflex syncope, low-risk profile, reliable follow-up, no high-risk features
— ED observation unit (24 hr telemetry): intermediate risk, awaiting echo or stress
— Inpatient telemetry: high-risk features, abnormal biomarkers, arrhythmia concerns
— ICU: hemodynamic instability, ongoing arrhythmia, massive PE, dissection, MI
Step 3 management: A 72-year-old with brief syncope, normal exam, but a new bifascicular block on ECG → admit to telemetry — the correct disposition even with otherwise reassuring presentation. Bifascicular block + syncope = high-grade AV block risk.

— Trigger avoidance, adequate hydration (2–2.5 L/day), liberal salt intake (10 g/day if no HTN/HF)
— Counterpressure maneuvers: leg crossing with tensing, handgrip, arm tensing at prodrome onset — first-line and high yield
— Physical tilt training in selected patients
— Pharm reserved for recurrent disabling cases:
— Midodrine (α1 agonist) — best evidence; avoid in supine HTN, urinary retention
— Fludrocortisone — volume expansion; monitor K+, BP
— β-blockers generally not effective; may help in older patients (≥42 yo) per POST trials
— SSRIs (paroxetine, fluoxetine) — limited evidence
— Review and deprescribe offending agents (diuretics, α-blockers, TCAs, nitrates)
— Slow positional changes, compression stockings (30–40 mmHg waist-high), abdominal binders
— Elevate head of bed 10–20° to reduce supine HTN and nocturnal natriuresis
— Pharm: midodrine, droxidopa (neurogenic OH in Parkinson/MSA), fludrocortisone
— Pyridostigmine for neurogenic OH without supine HTN
— Bradyarrhythmia/AV block → pacemaker
— VT with structural heart disease → ICD ± antiarrhythmic (amiodarone, sotalol), ablation
— SVT → vagal maneuvers, adenosine acutely, β-blocker/CCB chronically, ablation curative
— Long QT → β-blocker (nadolol, propranolol), avoid QT-prolonging drugs, ICD if high-risk or aborted SCD
— Brugada → ICD if symptomatic, avoid fever/sodium channel blockers; quinidine in selected cases
— HCM with outflow obstruction → β-blocker, disopyramide, mavacamten; septal reduction if refractory
— Severe AS → valve replacement (SAVR/TAVR)
— IV fluids for volume depletion
— Blood products for hemorrhagic syncope
— Atropine/transcutaneous pacing for symptomatic bradycardia
— Anticoagulation for PE
Board pearl: Counterpressure maneuvers + hydration + salt are the first-line answer for recurrent vasovagal syncope — choose these before any drug, and before pacemaker (rarely indicated, only for cardioinhibitory subtype with prolonged asystole).

— Symptomatic sinus node dysfunction with documented correlation
— Mobitz II 2nd-degree AV block (with or without symptoms)
— Complete (3rd-degree) AV block
— Alternating BBB
— Syncope + bifascicular block with HV interval >70 ms on EPS or inducible block
— Carotid sinus hypersensitivity with cardioinhibitory response and recurrent syncope
— Selected severe cardioinhibitory vasovagal syncope >40 yo with documented asystolic pauses on ILR (CTOPP, ISSUE-3 data)
— Survivors of cardiac arrest from VT/VF not due to reversible cause
— Sustained VT with structural heart disease
— LVEF ≤35% with NYHA II–III despite optimal medical therapy (primary prevention)
— High-risk HCM, ARVC, LQTS, Brugada with prior syncope from suspected arrhythmia
— Syncope + inducible VT on EPS in structural heart disease
— SVT (AVNRT, AVRT, atrial tachycardia) — curative, first-line in symptomatic patients
— Idiopathic VT (RVOT, fascicular) — high success
— Scar-related VT — adjunct to ICD to reduce shocks
— AF with rapid ventricular response causing syncope
— TAVR or SAVR for severe symptomatic AS with syncope (Class I, urgent)
— Septal myectomy or alcohol septal ablation for obstructive HCM refractory to meds
— Pulmonary endarterectomy or PE thrombectomy for hemodynamically significant PE causing syncope
— Pericardiocentesis for tamponade
— Endovascular or open repair for aortic dissection/AAA
CCS pearl: In a CCS case of syncope with documented complete heart block, the sequence is: continuous monitoring → transcutaneous pacing pads at bedside → atropine if symptomatic bradycardia → cardiology consult → transvenous pacing → permanent pacemaker placement. Don't skip the bridging steps.

— Cardiac syncope rate rises sharply >60 years
— Aortic stenosis, sick sinus syndrome, AV block, AF with pauses, structural disease
— Postprandial hypotension (30–60 min after meals; vasodilator splanchnic shunt)
— Carotid sinus hypersensitivity more common >50 yo
— Antihypertensives, especially α-blockers (tamsulosin, doxazosin)
— Diuretics (volume depletion + electrolyte derangement)
— Psychotropics (TCAs, antipsychotics — orthostasis + QT prolongation)
— Anticholinergics, opioids, benzodiazepines (falls + cognition)
— Insulin and sulfonylureas (hypoglycemia)
— Use Beers Criteria to guide deprescribing
— Adjust dosing of renally cleared antiarrhythmics: dofetilide, sotalol, dabigatran
— Avoid NSAIDs (worsen volume regulation and renal function)
— Contrast for CTA — weigh risk in eGFR <30; pre-hydrate and use iso-osmolar contrast
— Gadolinium contraindicated in eGFR <30 (NSF risk) for unrelated MRI
— Reduce dosing of amiodarone, lidocaine, β-blockers (propranolol, metoprolol)
— Watch for coagulopathy if invasive procedures planned
— Recurrent syncope in advanced frailty may not benefit from aggressive workup or device implantation
— Engage in shared decision-making, especially for ICD/pacemaker in patients with limited life expectancy or significant cognitive impairment
Step 3 management: In an 82-year-old on lisinopril, HCTZ, tamsulosin, and amitriptyline with recurrent syncope, the correct first step is medication reconciliation and deprescribing, not a tilt-table test or ILR — fix the iatrogenic cause first.

— Physiologic causes: aortocaval compression (supine hypotension syndrome, T2/T3) — left lateral decubitus relieves; increased venous pooling, decreased SVR in early pregnancy
— Pathologic concerns: PE (5x risk; D-dimer interpretation tricky — use trimester-adjusted or imaging), peripartum cardiomyopathy (late T3 to 5 months postpartum), arrhythmias (SVT incidence increases), preeclampsia/eclampsia
— Ectopic rupture in early pregnancy with syncope + abdominal pain = surgical emergency
— Imaging: prefer V/Q scan or CTPA when PE suspected — do not withhold; shield as able
— Avoid amiodarone (fetal thyroid), ACEi/ARBs; metoprolol and adenosine are safe; cardioversion safe
— Vast majority (>80%) are vasovagal/reflex or orthostatic; breath-holding spells in toddlers
— Red flags requiring cardiology referral: exertional syncope, syncope while swimming, syncope with chest pain or palpitations, family history of sudden death/drowning/MVC <50, no prodrome, abnormal ECG
— Channelopathies: LQTS (especially LQT1 — exercise/swimming; LQT2 — auditory stimuli; LQT3 — sleep), CPVT (exercise/emotion-triggered polymorphic VT), Brugada
— Structural: HCM (most common cause SCD in young athletes in US), anomalous coronary origin, ARVC, congenital AS
— Mandatory ECG in any exertional syncope
— POTS common in adolescent females; manage with hydration, salt, exercise reconditioning
— Pre-participation screening: history, family history, exam ± ECG (controversial in US; routine in Europe/Italy)
— Exertional syncope = disqualification from competition until full evaluation (echo, stress, sometimes MRI, EPS)
— Commotio cordis: blunt precordial trauma during vulnerable T-wave window → VF; immediate defibrillation
Board pearl: A teenage swimmer with syncope while swimming and a family history of unexplained drowning → Long QT syndrome (LQT1). Order ECG with QTc, refer to cardiology/genetics, start β-blocker (nadolol), and restrict competitive swimming.

— Head trauma — concussion, skull fracture, intracranial hemorrhage (especially on anticoagulation)
— Facial fractures (suggests no prodrome — favors cardiac/arrhythmic etiology)
— Hip and vertebral fractures in elderly — high morbidity/mortality cascade
— MVC if syncope while driving — third-party harm, legal/regulatory implications
— Major concern with cardiac syncope; 1-year mortality up to 30% in untreated cardiac syncope vs <5% in vasovagal
— Missed diagnosis of LQTS, HCM, Brugada, ARVC carries high SCD risk
— Pulmonary embolism with syncope: marker of hemodynamically significant clot, ~2x mortality
— Quality of life impairment, anxiety, social isolation
— Driving restrictions affect employment
— Recurrent falls in elderly → functional decline, nursing home placement
— Pacemaker/ICD: pneumothorax, hematoma, lead dislodgment, infection, endocarditis, inappropriate shocks
— EPS/ablation: vascular access complications, AV block requiring pacemaker, tamponade, stroke (left-sided)
— Tilt-table: prolonged hypotension, rarely asystole
— Midodrine: supine HTN, urinary retention, piloerection
— Fludrocortisone: hypokalemia, HTN, fluid overload, HF exacerbation
— β-blockers: bradycardia, fatigue, bronchospasm
— Antiarrhythmics: proarrhythmia (especially Class IA/IC, sotalol), end-organ toxicity (amiodarone — thyroid, lung, liver, skin, eye)
— Anticipatory anxiety, phobic avoidance
— Pseudosyncope can emerge or coexist with true syncope
— Aortic dissection, ruptured AAA, PE, ACS, subarachnoid hemorrhage, ectopic pregnancy
— Failure to identify QTc prolongation or Brugada on initial ECG
Key distinction: Facial injury or dental injury after a syncopal episode — patient had no time to protect themselves. This pattern strongly suggests a sudden arrhythmic cause without prodrome and should escalate the workup, even if the patient currently appears well.

— Hemodynamic instability (persistent SBP <90, signs of shock)
— Sustained VT/VF requiring drips or post-arrest care
— High-grade AV block requiring transvenous pacing
— Massive or submassive PE on thrombolytics/thrombectomy candidates
— Aortic dissection (post-op or awaiting surgery), tamponade post-drainage
— Acute MI complicating syncope
— Status post-resuscitation with TTM (targeted temperature management) protocols
— High-risk syncope without instability: abnormal ECG, suspected arrhythmia, structural heart disease, troponin elevation
— Intermediate-risk awaiting echo, stress test, or device implantation
— Intermediate-risk patients per CSRS or clinical gestalt
— Requires expedited echo, telemetry, and risk-stratification protocol
— Reduces unnecessary admissions while ensuring safety
— Cardiology/EP: suspected arrhythmia, structural disease, channelopathy, device decisions
— Cardiothoracic surgery: severe AS, dissection, septal myectomy candidate
— Vascular surgery: AAA, peripheral vascular contributors
— Neurology: if seizure mimic confirmed or recurrent diagnostic uncertainty
— Hematology: unexplained anemia, suspected GI bleed coordinating with GI
— Geriatrics/Pharmacy: polypharmacy reviews in elderly
— Facility lacking 24/7 cath lab, EP services, or cardiac surgery → transfer for STEMI, dissection, complex device need
— Stabilize first: airway, IV access, monitoring, reverse anticoagulation if hemorrhage
— Low-risk clinical profile, normal ECG, no high-risk features, reliable follow-up within 1–2 weeks
— Patient understands return precautions, driving restrictions reviewed
— Caregiver support if elderly
CCS pearl: On CCS, when ECG shows complete heart block with syncope, the immediate orders are: continuous cardiac monitoring, IV access, atropine, transcutaneous pacing pads, cardiology consult, admit to CCU/ICU. Sequential orders matter — don't jump to "admit" before stabilizing.

— Sinus node dysfunction (sick sinus, tachy-brady syndrome)
— Mobitz II 2nd-degree AV block
— Complete (3rd-degree) AV block
— Pacemaker malfunction
— Drug-induced bradycardia (β-blockers, CCBs, digoxin, clonidine)
— Sustained VT, polymorphic VT (torsades), VF
— SVT with rapid rates (AVNRT, AVRT, atrial flutter with 1:1 conduction)
— AF with rapid ventricular response, especially with pre-excitation (delta wave + AF = avoid AV nodal blockers; use procainamide)
— Inherited channelopathies: LQTS, SQTS, Brugada, CPVT
— Aortic stenosis — classic exertional syncope triad with angina and dyspnea
— Hypertrophic cardiomyopathy — dynamic LVOT obstruction
— Mitral stenosis — atrial myxoma, severe rheumatic disease
— Atrial myxoma — positional syncope, constitutional symptoms, embolic events
— Prosthetic valve thrombosis or dysfunction
— Severe pulmonary hypertension
— Cardiac tamponade
— Acute MI (especially inferior with bradycardia/AV block, or RV infarct with hypotension)
— Coronary anomaly (anomalous origin) — exertional syncope in young athletes
— Coronary spasm (Prinzmetal)
— Aortic dissection — syncope in ~10%, often with chest/back pain
— Pulmonary embolism (especially saddle/large)
— Ruptured AAA — syncope + abdominal/back pain + hypotension
— Subclavian steal syndrome
— Vertebrobasilar insufficiency (rare isolated syncope cause)
Board pearl: Syncope with wide-complex tachycardia on ECG in a patient with prior MI = VT until proven otherwise. Do not give adenosine or AV nodal blockers; cardiovert if unstable, procainamide or amiodarone if stable, and admit for ICD evaluation.

— Vasovagal (emotional, orthostatic, pain-triggered)
— Situational: cough, micturition, defecation, swallow, post-exercise, sneeze, instrumentation
— Carotid sinus syndrome
— Primary autonomic failure (pure autonomic failure, MSA, Parkinson disease, DLB)
— Secondary: diabetes, amyloidosis, uremia, B12 deficiency, paraneoplastic
— Volume depletion: hemorrhage, vomiting, diarrhea, adrenal insufficiency
— Drug-induced (huge category)
— Seizure — postictal confusion >5 min, tongue laceration (lateral), incontinence, witnessed tonic-clonic, focal aura
— Hypoglycemia — diaphoresis, tremor, prolonged altered mentation until corrected
— Hypoxia — pulmonary disease, CO poisoning
— Intoxication — alcohol, opioids, sedatives
— Concussion / head trauma — preceding mechanism
— Psychogenic pseudosyncope — frequent, prolonged "events," closed eyes resisting opening, normal vitals during event; tilt with monitoring confirms
— Cataplexy (narcolepsy) — preserved consciousness with loss of tone
— Drop attacks (vertebrobasilar, Meniere) — no LOC
— Subclavian steal — arm exertion-induced posterior circulation hypoperfusion
— Adrenal insufficiency (orthostasis + hyperkalemia + hyponatremia)
— Pheochromocytoma (paroxysmal HTN with reflex syncope)
— Carcinoid
— Severe anemia (GI bleed most common occult cause in elderly)
— Mast cell activation/anaphylaxis with distributive hypotension
Key distinction: Convulsive syncope vs seizure — both can have jerking, but convulsive syncope jerks are brief (<15 sec), occur after LOC begins, with rapid recovery and no postictal state. Seizures: longer tonic-clonic activity, postictal confusion >5 min, tongue biting laterally, elevated lactate that clears slowly. EEG is not part of routine syncope workup unless seizure suspected.

— Lifelong trigger avoidance, hydration ≥2 L/day, increased dietary salt if no contraindication
— Daily counterpressure maneuver practice
— Compression stockings for orthostatic component
— Recurrent disabling cases: midodrine 2.5–10 mg TID (last dose by late afternoon to avoid supine HTN)
— Pacemaker only for cardioinhibitory subtype with documented prolonged asystole and refractory recurrent syncope >40 yo
— Deprescribe offending agents; switch to less orthostatic alternatives (e.g., losartan instead of α-blocker)
— Goals of care discussion if BP targets conflict with falls risk — accept slightly higher BP to prevent syncope/falls in frail elderly
— Midodrine, fludrocortisone, droxidopa (neurogenic)
— Head-of-bed elevation, abdominal binders, slow positional changes
— Optimize underlying disease: GDMT for HF (ARNI, β-blocker, MRA, SGLT2i)
— Antiarrhythmics tailored to substrate (sotalol, amiodarone, dofetilide, flecainide where appropriate)
— Anticoagulation for AF per CHA2DS2-VASc
— Statin and aspirin if ASCVD
— Device follow-up (pacemaker/ICD): interrogation every 3–6 months
— LQTS: β-blocker (nadolol or propranolol), avoid QT-prolonging drugs (use credible meds lists), genetic counseling for family
— Brugada: ICD if symptomatic; aggressive fever control with acetaminophen; avoid sodium-channel blockers
— HCM: avoid dehydration and Valsalva-heavy activities; family screening with echo + ECG q1–3 yr
— Driving restrictions (state-dependent; typically 1–6 months symptom-free for cardiac syncope)
— Occupational counseling (commercial drivers, pilots, heavy machinery)
— MedicAlert bracelet for channelopathy or pacemaker/ICD
— Family screening for inherited conditions
Step 3 management: After unexplained syncope with negative initial workup but suspected arrhythmia, implantable loop recorder placement + cardiology follow-up in 2–4 weeks is preferred over repeat ED visits or empirical β-blockers. Document discussion of driving restrictions.

— Low-risk vasovagal/situational: PCP follow-up within 2–4 weeks; reinforce lifestyle measures
— Orthostatic hypotension with medication changes: BP log at home, follow-up in 1–2 weeks
— Post-cardiac syncope hospitalization: cardiology within 1–2 weeks; device check at 2–6 weeks if implanted
— Channelopathy: genetics referral, EP within 2 weeks, family screening initiated
— Symptom diary: date, time, activity, prodrome, duration, recovery
— Home BP and HR (especially orthostatic — supine vs standing at multiple time points)
— Weight (HF patients)
— Glucose logs (diabetics)
— Medication adherence
— Driving restrictions: review state DMV rules; commercial drivers face longer restrictions
— Avoid heights, swimming alone, operating heavy machinery until cleared
— Educate on prodrome recognition and counterpressure maneuvers — practice in office
— Hydration goals, salt intake adjustments
— Avoid prolonged standing, hot showers, alcohol, large carbohydrate meals (postprandial OH)
— Recognize red flags: chest pain, dyspnea, prolonged unconsciousness, focal neuro symptoms, palpitations preceding syncope → call 911
— Indicated post-MI, post-CABG, post-PCI, HF — improves outcomes
— Supervised exercise reconditioning for POTS and deconditioning-related orthostasis
— Screen for anxiety/depression (high prevalence after recurrent syncope)
— Address driving loss and occupational impact
— Psychogenic pseudosyncope: refer to psychiatry/behavioral health; CBT effective
— Pacemaker/ICD interrogation per schedule (in-office or remote monitoring)
— MRI compatibility documentation
— Avoid strong magnetic fields, recognize ICD shock protocol
Board pearl: Patients with cardiac syncope and ICD placement should receive remote monitoring enrollment before discharge — improves arrhythmia detection, reduces inappropriate shocks, and is increasingly a quality measure. Documenting driving counseling is a frequent Step 3 patient safety expectation.

— Physicians must counsel patients with syncope of unclear/cardiac etiology not to drive until cleared
— State laws vary: some are mandatory reporting (e.g., California, Pennsylvania, Oregon, Nevada, New Jersey, Delaware) for conditions causing LOC; others are permissive
— Commercial drivers (CDL): federal FMCSA rules — generally 1-year disqualification after cardiac syncope with no recurrence
— Document counseling clearly in chart — protects patient and physician
— If patient lacks decision-making capacity and continues to drive against advice, escalate to family, social work, and state DMV per local law
— ICD/pacemaker decisions in elderly or those with limited prognosis: discuss alternatives (no device, deactivation policies), goals of care
— ICD deactivation at end of life is ethically and legally permissible at patient/surrogate request — not assisted suicide; analogous to declining CPR. EP can deactivate via programmer
— Genetic testing for channelopathies: implications for family members, insurance (GINA protects health insurance but not life/disability)
— Medication reconciliation at discharge: clearly document started, stopped, and continued meds (especially deprescribed orthostatic offenders)
— Direct verbal handoff to PCP/cardiology when high-risk findings present
— Pending studies (Holter results, outpatient echo) require closed-loop follow-up — assign responsibility before discharge
— Provide written discharge instructions with return precautions, follow-up appointments, and driving restrictions
— Telephone or patient portal follow-up within 48–72 hours for high-risk discharges
— Suspected elder abuse if syncope/injuries from caregiver neglect or polypharmacy mismanagement
— Workplace injuries (occupational health, OSHA)
— Suspected impaired driving leading to MVC (cooperation with law enforcement within HIPAA exceptions)
— Patient refusing admission with high-risk syncope features: assess capacity (understanding, appreciation, reasoning, choice); if intact, document AMA discharge with safety planning; if impaired, involve surrogate
Step 3 management: A 68-year-old with new complete heart block and syncope wants to drive home from the ED. Correct action: assess capacity, explain risks clearly, recommend against driving, arrange alternative transport, document counseling and refusal/agreement, and per state law consider DMV notification. Do not let the patient drive.

— Long QT + syncope with exercise or loud noise → LQTS (LQT1 swimming, LQT2 auditory, LQT3 sleep)
— Coved ST elevation V1–V2 + syncope → Brugada
— Delta wave + syncope → WPW (especially with AF)
— Bifascicular block + syncope → high-grade AV block risk → pacemaker after EPS
— Epsilon wave, TWI V1–V3 → ARVC
— Deep narrow Q waves with LVH + young athlete syncope → HCM
— Crescendo-decrescendo systolic at RUSB radiating to carotids + exertional syncope → AS
— Murmur louder with Valsalva, softer with squat + family history SCD → HCM
— Tumor plop + positional syncope → atrial myxoma
— Young athlete sudden death US: HCM #1; anomalous coronary #2; commotio cordis
— Italy/Europe: ARVC more prominent
— Elderly woman with syncope + slow AF + macular degeneration on digoxin → digoxin toxicity
— Teenager with recurrent syncope on standing, palpitations, fatigue → POTS
— Avoid AV nodal blockers in WPW with AF → use procainamide
— Avoid QT-prolonging drugs in LQTS (check CredibleMeds.org)
— Fever in Brugada → unmask ECG pattern; treat aggressively with acetaminophen
— β-blocker of choice for LQTS = nadolol (or propranolol); not metoprolol
— Midodrine — supine HTN risk; last dose 4 hours before bedtime
— Orthostasis criteria: ≥20 systolic, ≥10 diastolic, or HR ≥30 within 3 min
— QTc >500 ms = torsades risk
— PR >200 ms = 1st degree AV block
— Pause >3 sec or systolic drop >50 mmHg = positive carotid sinus massage
— 30-day serious outcome rate in ED syncope ~7–10%
Board pearl: "Syncope while shaving" or with neck pressure/head turning in an older man → carotid sinus hypersensitivity. Confirm with carotid sinus massage (after excluding bruit and recent stroke); pacemaker for documented cardioinhibitory subtype.

— 17-year-old basketball player, syncope during practice, harsh systolic murmur louder with Valsalva, family history of sudden death → HCM. Order ECG + TTE; restrict from competitive sports; refer to cardiology; family screening.
— 78-year-old on HCTZ, lisinopril, tamsulosin, amitriptyline; recurrent syncope on standing; orthostatic drop 30/15 → medication-induced orthostatic hypotension. Best next step: deprescribe offending agents (NOT tilt-table or ILR).
— 65-year-old with brief syncope, ECG shows RBBB + LAFB (bifascicular block), normal exam → admit to telemetry, cardiology consult, EPS or empirical pacemaker if HV interval prolonged.
— 25-year-old at blood drive, prodrome of nausea/diaphoresis, brief LOC with myoclonic jerks, awake and oriented within seconds → vasovagal syncope, not seizure. No EEG, no MRI needed. Reassure, hydration, counterpressure maneuvers.
— 40-year-old on azithromycin and ondansetron for gastroenteritis, syncope at home, ECG QTc 560 ms → acquired LQTS. Stop offending drugs, correct K+ and Mg2+, monitor on telemetry, consider IV magnesium if torsades.
— Postoperative day 5 patient with sudden syncope, tachycardia, hypoxia, S1Q3T3 → PE. CTPA, anticoagulation, consider thrombolysis if massive/submassive with RV strain.
— Multiple negative workups, infrequent events, structural normal heart → implantable loop recorder is the next step.
— Cardiac syncope patient asks when can resume driving → counsel restriction per state law and condition; document; involve cardiology before clearance.
— Third trimester woman with syncope while supine → aortocaval compression; reposition left lateral decubitus; rule out PE, peripartum cardiomyopathy.
CCS pearl: When a CCS case opens with "syncope," first 5 orders are typically: vital signs (including orthostatics), 12-lead ECG, IV access, continuous cardiac monitoring, point-of-care glucose. Then targeted labs/imaging based on history and exam.

Syncope is global cerebral hypoperfusion whose workup hinges on history + exam + ECG to separate benign reflex/orthostatic causes from life-threatening cardiac etiologies, with risk stratification driving disposition between discharge, observation, telemetry, and ICU.
Board pearl: When in doubt on a Step 3 syncope question, choose the answer that risk-stratifies before it intervenes — ECG before CT, orthostatics before tilt, history before ILR, and deprescribing before adding a new drug.

