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Eduovisual

Cardiovascular

Syncope: workup, risk stratification, and disposition

Clinical Overview and When to Suspect Syncope

— 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.

Definition: Transient loss of consciousness (TLOC) due to global cerebral hypoperfusion, characterized by rapid onset, short duration (typically <1 min), and spontaneous complete recovery. Distinguish from non-syncopal TLOC (seizure, hypoglycemia, intoxication, concussion) and from "near-syncope" (presyncope), which carries similar short-term risk and warrants identical workup.
Epidemiology and burden:
Three pathophysiologic buckets — drive entire workup:
When to suspect syncope vs mimics:
Step 3 management: First triage question is "Is this cardiac?" — exertional onset, syncope while supine, lack of prodrome, family history of sudden death, or known structural heart disease shifts patient to inpatient telemetry pathway regardless of normal initial ECG.
Solid White Background
Presentation Patterns and Key History

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.

The history is the test — diagnostic yield of focused history + exam + ECG approaches 50–60%, exceeding any single advanced study.
Prodrome characterization:
Circumstance and posture:
Associated symptoms suggesting serious cause:
Medication and substance review — high yield in elderly:
Family history: sudden cardiac death <50, drowning, unexplained MVCs, known channelopathy (long QT, Brugada, CPVT, ARVC), HCM.
Solid White Background
Physical Exam Findings and Hemodynamic Assessment

— 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.

Vital signs — never skip:
Cardiac exam:
Vascular and pulmonary:
Neuro exam (focused, brief):
Other:
Carotid sinus massage (selected ≥40 yo, recurrent unexplained syncope): pause >3 sec or systolic drop >50 mmHg = positive. Contraindicated if carotid bruit, prior TIA/stroke <3 mo, or recent MI.
Solid White Background
Diagnostic Workup — Initial Labs, Imaging, ECG, Biomarkers

— 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.

12-lead ECG — mandatory in every syncope patient. Yield ~5% diagnostic, but identifies high-risk substrate.
Targeted labs (don't shotgun — guideline emphasizes selective testing):
Imaging — only when indicated, not routine:
Telemetry monitoring: All patients admitted or in ED observation should be on continuous monitoring until disposition.
Solid White Background
Diagnostic Workup — Advanced or Confirmatory Studies

— 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.

Echocardiography (TTE):
Ambulatory rhythm monitoring — match device to symptom frequency:
Stress testing:
Electrophysiology study (EPS):
Tilt-table testing:
Autonomic testing: suspected dysautonomia (Parkinson, MSA, diabetic autonomic neuropathy, amyloid).
EEG / brain MRI: only if seizure or focal neuro etiology — not routine syncope workup.
Solid White Background
Risk Stratification and Disposition Logic

— 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.

Goal: identify patients at risk for short-term (≤30 day) serious adverse events — arrhythmia, MI, structural disease, death — who need admission vs those safe for discharge with outpatient follow-up.
High-risk features (mandate admission or ED observation with monitoring):
Low-risk features (support outpatient management):
Validated decision tools (know they exist, but clinical judgment supersedes):
Disposition pathways:
Solid White Background
Pharmacotherapy and Etiology-Directed Treatment

— 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).

Vasovagal/reflex syncope — non-pharm first:
Orthostatic hypotension:
Cardiac syncope — treat the substrate:
Acute interventions in ED:
Solid White Background
Procedures and Device-Based Management

— 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.

Permanent pacemaker indications relevant to syncope:
ICD indications:
Catheter ablation:
Structural interventions:
Driving and activity restrictions post-procedure: vary by state and device; counsel before discharge (see chunk 17).
Solid White Background
Special Populations — Elderly and Renal/Hepatic Impairment

— 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.

Elderly syncope is often multifactorial — combination of orthostasis, medications, mild dehydration, autonomic dysfunction, and subclinical cardiac disease. Single "cause" reasoning often fails.
Higher prevalence of dangerous etiologies:
Polypharmacy review is mandatory:
Renal impairment considerations:
Hepatic impairment:
Frailty and goals of care:
Fall and fracture prevention: Syncope in elderly often results in head trauma, hip fracture, subdural hematoma (especially on anticoagulation — low threshold for CT head).
Solid White Background
Special Populations — Pregnancy, Pediatrics, and Athletes

— 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.

Pregnancy:
Pediatrics:
Athletes:
Solid White Background
Complications and Adverse Outcomes

— 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.

Traumatic injury from syncope:
Sudden cardiac death:
Recurrent syncope:
Procedure-related complications:
Medication adverse effects:
Psychological sequelae:
Missed diagnoses with high morbidity:
Solid White Background
When to Escalate Care — ICU, Consult, and Inpatient Triage

— 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.

ICU admission criteria:
Step-down/telemetry unit:
ED observation unit (≤24 hr):
Consultations:
Transfer considerations:
Discharge from ED criteria:
Solid White Background
Key Differentials — Same-Category (Cardiovascular) Causes

— 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.

Arrhythmic causes — bradyarrhythmias:
Arrhythmic causes — tachyarrhythmias:
Structural cardiac causes:
Ischemic and acute cardiovascular:
Vascular:
Solid White Background
Key Differentials — Other-Category Causes (Syncope Mimics and Non-Cardiac)

— 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.

Reflex (neurally mediated) — most common overall:
Orthostatic hypotension:
Non-syncope TLOC (mimics):
Endocrine/metabolic:
Hematologic:
Solid White Background
Secondary Prevention, Discharge Medications, and Long-Term Plan

— 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.

Etiology-specific long-term plans:
Vasovagal/reflex syncope:
Orthostatic hypotension:
Cardiac syncope:
Channelopathies:
Lifestyle and counseling:
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Follow-Up, Monitoring Parameters, and Counseling

— 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.

Discharge follow-up cadence:
Home monitoring parameters patients should track:
Patient counseling — concrete elements:
Cardiac rehab:
Mental health:
Device patients:
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Ethical, Legal, and Patient Safety Considerations

— 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.

Driving and public safety — high-yield Step 3 territory:
Informed consent edge cases:
Transitions of care — major patient safety vulnerability:
Mandatory reporting:
Capacity assessment:
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High-Yield Associations and Rapid-Fire Clinical Facts

— 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.

Classic ECG–syncope pairings:
Murmur–syncope pairings:
Demographics and patterns:
Drug pearls:
Numbers to know:
Decision tools: Canadian Syncope Risk Score, SFSR ("CHESS"), OESIL.
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Board Question Stem Patterns

— 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.

Stem 1 — Exertional syncope in young athlete:
Stem 2 — Elderly with multifactorial syncope:
Stem 3 — Syncope with abnormal ECG:
Stem 4 — Convulsive syncope vs seizure:
Stem 5 — Long QT after antibiotic:
Stem 6 — PE presenting as syncope:
Stem 7 — Recurrent unexplained syncope:
Stem 8 — Driving counseling:
Stem 9 — Pregnancy + syncope:
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One-Line Recap

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.

The triad that does 60% of the work: focused history (prodrome, trigger, posture, exertion, family history of SCD), targeted exam (orthostatics, bilateral arm BP, cardiac auscultation, neuro screen), and a 12-lead ECG — every syncope patient gets these; CT head, EEG, and carotid Dopplers are usually wrong answers.
High-risk = admit; low-risk = home with follow-up: Red flags are abnormal ECG, exertional or supine syncope, no prodrome, structural/ischemic heart disease, family history of SCD, persistent abnormal vitals, elevated troponin, significant injury, or age >60 with CV risk. The Canadian Syncope Risk Score and clinical gestalt drive the call.
Match treatment to mechanism: Vasovagal → hydration, salt, counterpressure maneuvers (midodrine if refractory); orthostatic → deprescribe + non-pharm + midodrine/fludrocortisone; cardiac → fix the substrate (pacemaker for AV block, ICD for VT/channelopathies, valve replacement for AS, ablation for SVT, anticoagulation/intervention for PE).
Don't forget the Step 3 wrap-up: counsel on driving restrictions per state law and document it, reconcile and deprescribe at discharge, arrange closed-loop follow-up for pending studies (Holter, echo, ILR), and consider implantable loop recorder when initial workup is negative but suspicion for arrhythmia persists — the highest-yield diagnostic for elusive recurrent syncope.
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