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Resuscitation Quick Actions • First 2 Minutes

High-Acuity

San Francisco Rule (CHESS)

High risk if any present: C (Congestive heart failure), H (Hematocrit < 30%), E (abnormal ECG), S (Shortness of breath), S (Systolic BP < 90)

Mandatory 12-Lead ECG

Zero patients can be cleared without an ECG: screen for Brugada, WPW, Long QT, Short QT, HCM dagger Qs, ARVD epsilon waves, and AV blocks

Exertional Syncope Red Flag

Syncope DURING exertion (running, sports) is CARDIAC until proven otherwise (critical aortic stenosis, HCM, aberrant coronary, or VT)

Supine Syncope Red Flag

Syncope occurring while lying flat is virtually never vasovagal or orthostatic; indicates malignant dysrhythmia or neurovascular event

Orthostatic Vitals Criteria

Drop in SBP >= 20 mmHg OR drop in DBP >= 10 mmHg within 3 minutes of standing; confirm orthostasis before attributing cause

Vasovagal Classic Triad

Young healthy patient + Clear precipitant (blood draw, prolonged standing, heat) + Classic prodrome (tunnel vision, pallor, diaphoresis)

Bottom-Line Clinical Pearl

Syncope is defined as a transient loss of consciousness caused by global cerebral hypoperfusion characterized by rapid onset, short duration, and spontaneous complete recovery. The primary emergency goal is NOT diagnosing the exact benign cause, but identifying patients at high risk of sudden cardiac death within 30 days. High-risk red flags include syncope during exertion (aortic stenosis, HCM, channelopathy), syncope while supine, absence of prodrome, and family history of unexplained sudden death under age 40. Every syncope patient requires a 12-lead ECG. The San Francisco Syncope Rule (CHESS) mandates admission if ANY of the following are present: History of Congestive heart failure, Hematocrit < 30%, abnormal ECG, Shortness of breath, or Systolic BP < 90 mmHg.

1. Pathophysiologic Taxonomy of Syncope

Syncope is a symptom characterized by a transient loss of consciousness (TLOC) secondary to abrupt, self-limited global cerebral hypoperfusion, followed by spontaneous, rapid, and complete return to neurological baseline without persistent focal deficits. A cessation of cerebral blood flow for as brief as 6 to 8 seconds, or a drop in mean arterial pressure (MAP) to $< 30\text{ to }40\text{ mmHg}$, is sufficient to cause loss of consciousness.

Syncope CategoryUnderlying MechanismClinical History & Physical Hallmarks
Reflex (Neurally Mediated) SyncopeExcessive vagal tone combined with sympathetic withdrawal, causing profound bradycardia (cardioinhibitory) and/or peripheral vasodilation (vasodepressor)Vasovagal (emotional trigger, blood draw, pain, heat); Situational (micturition, defecation, coughing); Carotid sinus hypersensitivity. Classic prodrome: diaphoresis, nausea, pallor, yawning, tunnel vision, warmth.
Orthostatic HypotensionAutonomic failure or intravascular volume depletion preventing compensatory vasoconstriction upon standingOccurs immediately upon standing from sitting/lying; drop in $SBP \ge 20\text{ mmHg}$ or $DBP \ge 10\text{ mmHg}$. Common in elderly, autonomic neuropathy (diabetes, Parkinson's), volume depletion, and polypharmacy.
Cardiac Syncope (Structural)Fixed mechanical obstruction to left or right ventricular stroke volumeCritical Aortic Stenosis, Hypertrophic Cardiomyopathy (HCM), Cardiac Tamponade, Left Atrial Myxoma, Massive Pulmonary Embolism. Characterized by syncope DURING exertion.
Cardiac Syncope (Dysrhythmic)Sudden paroxysmal bradycardia (high-grade AV block, sick sinus syndrome) or tachycardia (VT, VF, rapid SVT, TdP)Sudden syncope with ZERO warning or prodrome ('drop attack'); syncope while supine; palpitations immediately preceding event; personal or family history of sudden death.

2. High-Risk ECG Screen: The Fatal Channelopathies & Cardiomyopathies

A 12-lead ECG is mandatory in every adult syncope patient. Specifically scrutinize the tracing for the following high-risk electrophysiological entities:

ECG DiagnosisMorphology & Leads InvolvedPathophysiologic Threat
Brugada Pattern (Type 1)Coved ST elevation $\ge 2\text{ mm}$ in V1–V2 followed by a negative T wavePhase 2 re-entry and spontaneous polymorphic ventricular tachycardia/sudden death.
Wolff-Parkinson-White (WPW)Short PR interval ($< 120\text{ ms}$), slurred initial QRS upstroke (delta wave), widened QRSRapid antegrade conduction down accessory pathway during AF, degenerating to VF.
Hypertrophic Cardiomyopathy (HCM)Deep, narrow 'dagger-like' Q waves in lateral (I, aVL, V5–V6) and inferior leads + high LVH voltagesDynamic LV outflow tract obstruction and ventricular fibrillation during exertion.
Arrhythmogenic RV Cardiomyopathy (ARVC)T-wave inversions in V1–V3 + discrete positive deflection at the terminal QRS (epsilon wave)Fibrofatty replacement of RV myocardium predisposing to re-entrant VT.
Congenital/Acquired Long QT$QTc > 470\text{ ms}$ (males) or $> 480\text{ ms}$ (females); risk is extreme if $QTc > 500\text{ ms}$Early afterdepolarizations triggering Torsades de Pointes and syncope/arrest.

3. The San Francisco Syncope Rule (CHESS Mnemonic)

The San Francisco Syncope Rule (SFSR) identifies patients at high risk for serious clinical outcomes within 30 days (death, acute myocardial infarction, serious dysrhythmia, pulmonary embolism, subarachnoid hemorrhage, significant hemorrhage). If ANY of the five CHESS criteria are present, the patient is high-risk and requires hospital admission or prolonged telemetry monitoring:

LetterCHESS CriterionSpecific Diagnostic Definition
CCongestive Heart FailureHistory of CHF, acute pulmonary edema, or EF $< 35\%$
HHematocrit < 30%Anemia secondary to occult GI bleeding, aortic aneurysm rupture, or trauma
EECG AbnormalNon-sinus rhythm, new ischemia, QRS $> 120\text{ ms}$, PR prolongation, or channelopathy pattern
SShortness of BreathAcute dyspnea reflecting PE, acute coronary syndrome, or heart failure
SSystolic Blood Pressure < 90 mmHgHypotension at triage or in the emergency department
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