Syncope- Study Notes

Definition:

• Syncope = transient global cerebral hypoperfusion → transient loss of consciousness (LOC) with spontaneous, rapid recovery to baseline.

• Key point: always due to reduced cerebral perfusion.

Major Categories of Syncope

1. Reflex (neurally mediated) syncope

   • Vasovagal

   • Situational

   • Carotid sinus hypersensitivity

2. Orthostatic syncope

3. Cardiogenic syncope

   • Arrhythmogenic

   • Mechanical

1. Reflex Syncope (Neurocardiogenic)

Mechanism

• Trigger → ↑ vagal outflow (cranial nerve X).

• Vagal effects:

  • Cardioinhibitory: ↓ HR → ↓ CO → ↓ SBP.

  • Vasodepressor: vasodilation → ↓ SVR → ↓ DBP.

• Net result: ↓ BP + ↓ cerebral perfusion → transient LOC.

Subtypes

• Vasovagal syncope

  • Trigger: pain, phobia, prolonged standing.

  • History: prodrome (nausea, diaphoresis, blurry vision).

• Situational syncope

  • Triggered by straining events (coughing, micturition, defecation).

• Carotid sinus hypersensitivity

  • Trigger: carotid compression.

  • Causes: carotid sinus massage, tight collar, shaving, head turning.

2. Orthostatic Syncope

Mechanism

• Standing → ↓ venous return → ↓ preload → ↓ stroke volume → ↓ CO → ↓ BP → ↓ cerebral perfusion → LOC.

Causes

1. Volume depletion

   • Vomiting, diarrhea, diuretics, bleeding, burns, excessive sweating.

2. Vasodilation

   • Medications: calcium channel blockers (amlodipine, nifedipine), α1-blockers (tamsulosin, prazosin, doxazosin).

3. Autonomic neuropathy

   • Failure of sympathetic vasoconstriction (e.g., diabetic neuropathy).

3. Cardiogenic Syncope

Mechanism

• Primary cardiac problem → ↓ cardiac output → ↓ BP → ↓ cerebral perfusion → LOC.

Causes

1. Arrhythmias

   • Tachyarrhythmias (e.g., VT >150 bpm → ↓ diastolic filling).

   • Bradyarrhythmias (e.g., AV block, sinus node dysfunction → ↓ HR).

2. Mechanical

   • ↓ Contractility: MI, severe HF.

   • ↓ Filling: cardiac tamponade, tension pneumothorax.

   • ↑ Afterload/obstruction:

     • Hypertrophic cardiomyopathy (HCM).

     • Aortic stenosis.

     • Pulmonary embolism.

Clinical Features

• Sudden onset, often no prodrome.

• May occur with exertion (classic for HCM, aortic stenosis).

Clinical Differentiation:

• Reflex syncope: prodrome (nausea, diaphoresis, blurry vision).

• Orthostatic syncope: positional change (supine/seated → standing).

• Cardiogenic syncope: sudden, exertional, or without warning.

Diagnostic Approach

1. Initial tests

   • Orthostatic vitals:

     • ↓ SBP ≥20 mmHg or ↓ DBP ≥10 mmHg = orthostatic syncope.

   • 12-lead ECG:

     • Arrhythmias (e.g., AV block, VT).

2. Further evaluation

   • Holter monitor / EP study → occult arrhythmia.

   • Echocardiography → structural/mechanical causes (HCM, aortic stenosis, EF, tamponade).

   • Carotid sinus massage → diagnostic if SBP ↓ >50 mmHg or asystole >3 sec.

   • Tilt table test → vasovagal/situational.

3. Rule out seizure

   • Seizure features: tonic-clonic activity, aura, tongue biting, incontinence, postictal confusion.

   • Syncope: prodrome, transient LOC, rapid recovery, no postictal state.

Management

• Reflex syncope: avoid triggers.

• Orthostatic syncope:

  • Rehydrate, treat hypovolemia.

  • Stop vasodilator drugs.

  • Pharmacologic: midodrine (vasoconstrictor), fludrocortisone (↑ Na+/water retention).

• Cardiogenic syncope:

  • Arrhythmias: ICD (VT/VF), pacemaker (bradyarrhythmias).

  • Mechanical: treat underlying cause (valve replacement, HF management, PE treatment, pericardiocentesis for tamponade).

The Takeaways

• Syncope = transient global cerebral hypoperfusion.

• Categorize: reflex, orthostatic, or cardiogenic.

• Prodrome → reflex, positional → orthostatic, sudden/exertional → cardiogenic.

• Always distinguish from seizure.

• Management is cause-specific.