1.12 Syncope: Reflex, Orthostatic & Cardiac Causes

1. The Only Question That Matters

Syncope is transient loss of consciousness from global cerebral hypoperfusion, with spontaneous complete recovery. ABIM lists it as a named subsection under Cardiovascular Disease with three categories: reflex syncope (vasovagal and situational), orthostatic hypotension, and cardiac syncope (structural and electrical).

The exam task is never "what is the diagnosis" in isolation. It is: is this cardiac? Reflex syncope has an excellent prognosis. Cardiac syncope carries meaningful short-term mortality, and the correct answer in those vignettes is admission and monitoring rather than reassurance and discharge.

2. Historical Features That Discriminate

Three features carry disproportionate weight and should be treated as red flags in isolation: syncope during exertion, syncope while supine, and syncope preceded by palpitations.

3. Reflex (Neurally Mediated) Syncope

Reflex syncope results from an inappropriate autonomic response — vasodilation, bradycardia, or both. Subtypes:

• Vasovagal: the classic form, triggered by prolonged standing, heat, pain, emotional distress or the sight of blood, with a well-developed autonomic prodrome.
• Situational: triggered by a specific act — micturition, defecation, coughing, swallowing, or weightlifting.
• Carotid sinus hypersensitivity: in older patients, triggered by head turning, shaving or a tight collar.

Management is largely non-pharmacologic: trigger avoidance, liberal salt and fluid intake if no contraindication exists, and physical counter-pressure maneuvers (leg crossing with tensing, handgrip, arm tensing) at the first symptom. Midodrine or fludrocortisone are reserved for recurrent, disabling episodes. Pacing has a narrow role limited to documented, recurrent asystolic reflex syncope in older patients.

4. Orthostatic Hypotension

The definition is quantitative: a fall of at least 20 mmHg systolic or 10 mmHg diastolic within three minutes of standing. Measure supine after five minutes, then at one and three minutes standing — a seated-to-standing measurement misses cases.

The presence or absence of a compensatory heart-rate rise separates the two mechanisms:

• Compensatory tachycardia present: volume depletion, hemorrhage or medication effect.
• Compensatory tachycardia absent (neurogenic): autonomic failure from diabetic autonomic neuropathy, Parkinson disease, multiple system atrophy or amyloidosis.

Culprit drugs are a favorite: alpha-blockers, diuretics, nitrates, tricyclic antidepressants, antipsychotics and dopaminergic agents. Reviewing and deprescribing the medication list precedes any new prescription.

5. Cardiac Syncope

Structural causes obstruct output or impair filling:

• Severe aortic stenosis — exertional syncope is one of the three cardinal symptoms and mandates evaluation for valve replacement.
• Hypertrophic cardiomyopathy — outflow obstruction worsens with the reduced preload of exertion.
• Pulmonary embolism and cardiac tamponade — acute obstruction to filling or output.
• Aortic dissection and acute myocardial infarction.

Electrical causes are arrhythmic:

• Bradyarrhythmias: sinus node dysfunction, high-grade AV block.
• Ventricular tachycardia, particularly with prior infarct or reduced ejection fraction.
• Inherited channelopathies: long QT syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia.

6. The ECG Is the Highest-Yield Test

Every syncope patient gets a 12-lead ECG. Findings that convert a benign story into an urgent one:

7. Diagnostic Sequencing

1. History, physical examination including orthostatic vital signs, and 12-lead ECG. This trio identifies the cause or the risk category in most patients.
2. Echocardiography when structural disease is suspected by history, murmur or ECG.
3. Rhythm monitoring matched to episode frequency: inpatient telemetry for high-risk patients, ambulatory monitoring for frequent episodes, and an implantable loop recorder for infrequent, unexplained, high-risk syncope.
4. Exercise testing for exertional syncope.
5. Tilt-table testing only when reflex syncope is suspected but the diagnosis remains uncertain after the above.

Two tests that are commonly ordered and rarely helpful: routine head CT and carotid ultrasonography. Syncope is global hypoperfusion; carotid disease causes focal deficits, not transient global loss of consciousness. Neuroimaging is warranted only when head trauma occurred or when focal neurologic findings are present.

8. Seizure Versus Syncope

Brief myoclonic jerking occurs in up to 90% of syncopal episodes and does not indicate a seizure. Features favoring seizure are a preceding aura, prolonged tonic-clonic activity, lateral tongue biting, and postictal confusion lasting minutes. Recovery from syncope is prompt and orientation returns immediately.