Syncope

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Syncope

Definition

Syncope is a symptom defined as an abrupt, transient, complete loss of consciousness (LOC) associated with inability to maintain postural tone, with rapid and spontaneous recovery. The underlying mechanism is transient global cerebral hypoperfusion. Cessation of cerebral blood flow for as little as 10 seconds produces LOC. Recovery of consciousness is usually immediate, though retrograde amnesia can occur (more common in older adults).

Syncope is common, costly, and potentially dangerous - it accounts for 1% of hospital admissions and 3% of ED visits. It can be the only warning sign before sudden cardiac death (SCD).

Braunwald's Heart Disease, p. 1383

Classification and Causes

Syncope is broadly divided into:

1. Neurally Mediated (Reflex) Syncope - MOST COMMON

The cardiovascular reflexes that normally control circulation become inappropriate in response to a trigger, leading to vasodilation ± bradycardia, BP drop, and cerebral hypoperfusion.

Vasovagal (neurocardiogenic) syncope - most frequent cause at any age; triggered by emotional stress, pain, prolonged standing, venipuncture. Mix of vasodepressor (vasodilation) and cardioinhibitory (vagal bradycardia) components. Classic prodrome: nausea, pallor, diaphoresis, lightheadedness.
Carotid sinus hypersensitivity (CSH) - especially in older adults; pressure on the carotid sinus triggers exaggerated reflex.
Situational syncope - cough, sneeze, micturition, defecation, swallowing, post-exercise.
Glossopharyngeal neuralgia - rare, triggered by swallowing.

2. Orthostatic Hypotension

Standing displaces 500-800 mL blood to the abdomen and lower extremities, reducing venous return. Compensatory mechanisms fail, producing hypotension and syncope. Defined as a fall in systolic BP ≥20 mmHg or diastolic BP ≥10 mmHg within 3 minutes of standing.

Causes of orthostatic hypotension:

Category	Examples
Drugs	Diuretics, alpha-blockers (terazosin), ACE inhibitors, antidepressants, MAOIs, phenothiazines, vasodilators (prazosin, hydralazine, CCBs), alcohol
Primary autonomic failure	Pure autonomic failure (Bradbury-Eggleston), multisystem atrophy (Shy-Drager), Parkinson disease with dysautonomia
Secondary neurogenic	Diabetes, Guillain-Barré, amyloid, carcinomatosis, Wernicke encephalopathy, MS
Non-neurogenic	Dehydration, prolonged bedrest, adrenal insufficiency, prolonged fever

3. Cardiac Syncope

Occurs when intrinsic cardiac abnormality interrupts cardiac output. Carries the worst prognosis.

Arrhythmic causes:

Bradyarrhythmias: Sick sinus syndrome, high-degree AV block, pacemaker malfunction
Tachyarrhythmias: SVT, VT, VF
Drug-induced: QT-prolonging drugs

Structural causes:

Aortic stenosis - syncope during exertion; fall in systemic vascular resistance cannot be offset by limited cardiac output; high LV pressure during exercise may also trigger a vasodepressor response
Hypertrophic obstructive cardiomyopathy (HOCM)
Acute MI / ischemia
Cardiac tamponade
Pulmonary embolism
Aortic dissection

Primary electrical disease (rare but dangerous):

Long QT syndrome
Short QT syndrome
Brugada syndrome
Arrhythmogenic right ventricular dysplasia (ARVD)
Catecholaminergic polymorphic VT (CPVT)
Idiopathic VF
Braunwald's Heart Disease, pp. 1383-1390

Conditions Mimicking Syncope (Differential Diagnosis)

Condition	Key Distinguishing Features
Seizure (epilepsy)	LOC simultaneous with motor event, prolonged postictal phase, tongue biting, incontinence
Basilar migraine	Headache, neurologic symptoms, rarely full LOC
Vertigo	Rotation/spinning sensation, no LOC
Hyperventilation	Paresthesias, carpopedal spasm, tachypnea
Hypoglycemia	Confusion progressing slowly to LOC; requires glucose to terminate
Psychogenic (conversion reaction)	No true LOC; indifference to event; common in patients <40 with psychiatric history
TIA/stroke	Usually not complete LOC; focal neurologic deficits persist

Tintinalli's Emergency Medicine, p. 3839

Epidemiology

Accounts for 1-3% of pediatric ED visits; 80% of pediatric fainting is vasovagal.
Up to 50% of young adults report at least one LOC episode in their lifetime.
Prevalence peaks at ages 10-20, then again at ~60 and ~80 years.
Syncope prevalence exceeds 20% in adults ≥75 years; annual incidence approaches 2% in those ≥80.
2-year mortality rate of 25-30% in patients >75 years with syncope (reflects comorbidities and cardiac etiology).

Evaluation

History (Most Important)

Circumstances: posture, activity, emotional triggers, prolonged standing
Prodrome: nausea, sweating, pallor, visual changes (suggests vasovagal)
During event: duration, witnesses, motor activity, incontinence, tongue biting
After event: rapid recovery (syncope) vs. prolonged confusion (seizure)
Past history: cardiac disease, family history of SCD, medications

Physical Examination

Vital signs: heart rate and BP supine, sitting, and standing (orthostatic hypotension)
Cardiovascular exam: murmurs (aortic stenosis), arrhythmias
Neurologic exam
Carotid sinus massage if CSH is suspected (contraindicated if carotid bruit present)

Diagnostic Tests

Test	Indication
ECG	All patients - look for arrhythmia, conduction disease, QT prolongation, Brugada, delta waves
Echocardiogram	Structural heart disease suspected (AS, HOCM, cardiomyopathy)
Ambulatory ECG (Holter/event monitor)	Suspected arrhythmia
Implantable loop recorder (ILR)	Recurrent unexplained syncope - high diagnostic yield
Tilt-table test	Suspected neurally mediated syncope - modest sensitivity/specificity
Electrophysiology (EP) study	Suspected arrhythmic cause, high-risk features
Blood tests	Targeted: glucose (hypoglycemia), CBC, electrolytes
Carotid duplex, head CT, brain MRI, EEG	Very low yield; only in highly selected situations
Stress testing	Only if exertional syncope with suspected ischemia or HOCM

Note: Routine CT head, EEG, and carotid imaging have very low diagnostic yield in syncope and should not be ordered routinely.

Braunwald's Heart Disease, pp. 1390-1394

Risk Stratification

High-risk features (suggest cardiac/serious etiology):

Syncope during exertion
Syncope while supine
No prodrome
Family history of SCD
Structural heart disease
Abnormal ECG (QT prolongation, BBB, ST changes, Brugada pattern)
Age >65 years
Associated chest pain or dyspnea

Low-risk features (suggest vasovagal):

Young age
Clear precipitating trigger (pain, prolonged standing, emotional stress)
Prodromal symptoms (nausea, diaphoresis)
Rapid, complete recovery
No history of cardiac disease
Normal ECG

Management

Management is oriented to the underlying etiology.

Neurally Mediated / Vasovagal Syncope

Education and reassurance - excellent prognosis in young patients
Behavioral measures: avoid triggers, increase fluid/salt intake, avoid prolonged standing
Physical counterpressure maneuvers - leg crossing, hand gripping during prodrome (proven to abort episodes)
Tilt training (for recurrent episodes)
Medications (selected cases): Fludrocortisone (volume expansion), midodrine (alpha-1 agonist), beta-blockers (controversial), SSRIs
Cardioneuroablation - ablation of vagal inputs for selected patients with cardioinhibitory vasovagal syncope (emerging therapy)
Pacemaker - only in cardioinhibitory syncope with documented asystole in older adults (class IIa)

Orthostatic Hypotension

Discontinue/reduce offending drugs
Increase fluid and salt intake
Compression stockings, abdominal binders
Head-of-bed elevation (reduces nocturnal natriuresis)
Midodrine or fludrocortisone
Treat underlying cause (Parkinson disease, diabetes, etc.)

Cardiac Syncope

Arrhythmic: Pacemaker for bradyarrhythmias; ICD or antiarrhythmic drugs for VT/VF; catheter ablation
Structural: Treat underlying condition (valve replacement for severe AS, septal reduction for HOCM, revascularization for ischemia)
Pulmonary embolism: Anticoagulation
Inherited channelopathies (Long QT, Brugada, CPVT): ICD ± medications
Braunwald's Heart Disease, pp. 1394-1397

Special Populations

Older Adults

Syncope is often multifactorial in older patients (age-related CV changes + multimorbidity + polypharmacy).
Neurally mediated syncope remains most common, but cardiac causes (especially bradyarrhythmias, AS) are proportionally higher.
Vasovagal prodrome is often absent in elderly.
Orthostatic hypotension is common due to reduced baroreflex responsiveness.
Syncope may present as an unexplained fall - always consider syncope in falls without witnessed etiology.
Medication review is essential: antihypertensives, diuretics, alpha-blockers are common culprits.

Children / Adolescents

~80% is vasovagal (neurocardiogenic).
~10% neurologic (mostly seizures); ~2-3% cardiac.
Red flags: syncope during exercise, syncope in supine position, family history of SCD, structural or electrical heart disease.
Any child with a pacemaker who develops syncope should be presumed to have pacemaker malfunction until proven otherwise.
Braunwald's Heart Disease, pp. 2886-2912; Tintinalli's Emergency Medicine, p. 3835

Key Takeaways

Syncope = transient global cerebral hypoperfusion → brief LOC → spontaneous full recovery.
Most common cause is vasovagal (neurally mediated) at all ages.
Cardiac syncope is the most dangerous and warrants urgent evaluation.
Always distinguish syncope from seizure, TIA, and metabolic causes.
ECG is mandatory in all patients; further testing is directed by clinical suspicion.
Prognosis is excellent for vasovagal syncope in young patients; cardiac syncope carries significantly higher mortality.

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