Syncope Simplified: An Evidence-Based Hospitalist’s Guide to Risk Stratification and Management (ACC/AHA/HRS Guidelines)

In this episode of Hospital Medicine Unplugged, we sprint through syncope—recognize the dangerous few, spare the benign many, and let the ECG lead the way.

We open with the do-firsts: define it right—transient LOC from global cerebral hypoperfusion with rapid, spontaneous recovery. Sort into the big three: cardiac, reflex/neurally mediated, and orthostatic. Cardiac etiologies drive morbidity/mortality—find them fast.

Initial evaluation that actually moves the needle: history (context, prodrome, exertion/supine, palpitations, meds), focused exam with orthostatic BPs, and a 12-lead ECG. These three steps often make the diagnosis and set the risk. Add targeted labs only when the story points (bleed, ischemia, electrolyte error).

Risk stratify with bedside red flags—abnormal ECG, known structural heart disease/HF, exertional or supine syncope, no prodrome, age ≥60, palpitations preceding LOC, family hx SCD, persistent hypotension, anemia/bleeding. Use a validated tool (e.g., Canadian Syncope Risk Score) to sharpen 30-day risk and disposition. Low risk? outpatient with education. High risk or unclear? admit/observe with telemetry.

In-hospital diagnostics—be precise, not profligate:
• Telemetry for suspected cardiac syncope, abnormal ECG, or heart disease.
• TTE for murmurs, HF signs, or structural suspicion.
• Neuroimaging/EEG/CTPA/carotids only when the history/exam demands (focal deficits, head trauma, seizure concern, PE clues)—routine use has low yield.

Management—match therapy to mechanism:
• Cardiac syncope: treat the cause—brady/tachy arrhythmias → pacing, ICD, ablation, antiarrhythmics; structural lesions (e.g., AS, HCM) → surgery/intervention; ischemia → ACS pathway. Early cardiology is key.
• Reflex (vasovagal/situational/carotid sinus): education, hydration, salt, physical counterpressure; avoid triggers. For severe/recurrent: midodrine or fludrocortisone; pacing only for select cardioinhibitory phenotypes.
• Orthostatic hypotension: de-prescribe culprits, replete volume, compression/abdominal binders, slow position changes; refractory cases → midodrine, fludrocortisone; treat underlying autonomic failure.

Observation & monitoring plays: structured protocols for intermediate-risk patients reduce unnecessary admissions, speed testing, and keep outcomes steady. Keep telemetry until an arrhythmic cause is excluded or a diagnosis lands.

Pitfalls you don’t want to meet:
• Calling “syncope” with a prolonged post-ictal state—that’s seizure until proven otherwise.
• Blanket ordering head CT, carotids, EEG, or CTPA without clinical signals.
• Missing orthostatics or the med list (diuretics, vasodilators, QT-prolongers).
• Stopping at “vasovagal” in an older adult with no prodrome and abnormal ECG.
• Admitting every syncopal episode—risk tools + bedside clues safely steer many home.

Prognosis reality check: reflex and orthostatic—generally benign (recurrence > mortality). Cardiac syncope—highest short-term risk (arrhythmia, MI, SCD): act swiftly, treat definitively. Unexplained after work-up—risk tracks with age, cardiac history, and ECG.

We close with the system moves—a syncope bundle that (1) auto-captures orthostatic vitals and ECG in triage; (2) runs CSRS to gate observation vs. admission; (3) defaults to telemetry + TTE only when cardiac features present; (4) blocks routine neuro/PE testing without triggers; (5) standardizes reflex/orthostatic counseling + med optimization; (6) fast-tracks pacer/ICD/EP for arrhythmic pathways; (7) embeds clear return precautions and follow-up on discharge.

History + orthostatics + ECG, risk before tests, and mechanism-matched therapy—that’s how you turn a fall into a plan.