Ilyas K. Colombowala, MD, FACC, FHRS
Cardiac Electrophysiology · Houston, TX · colombowala.com

Condition

Syncope

Transient loss of consciousness from global cerebral hypoperfusion. The clinical job is to separate benign reflex syncope from arrhythmic syncope that needs a device or EP study.

ECG features

  • Sinus bradycardia, pauses, or sinoatrial exit block (sinus node dysfunction)
  • High-grade or complete AV block; alternating bundle branch block; bifascicular block with syncope
  • Pre-excitation (delta wave) — syncope may signal a malignant accessory pathway
  • Prolonged or short QT; Brugada type 1 coved ST elevation
  • Epsilon waves / T-wave inversions V1–V3 (ARVC); deep septal Q waves or LVH (HCM)
  • Ischemic changes; prior infarct (Q waves) raising scar-related VT risk

Differential

  • Reflex (neurally mediated) — vasovagal, situational, carotid sinus hypersensitivity
  • Orthostatic hypotension — volume depletion, drugs, autonomic failure
  • Cardiac arrhythmic — brady (SND, AV block) or tachy (VT, SVT, malignant pre-excitation)
  • Cardiac structural/obstructive — aortic stenosis, HCM, PE, tamponade
  • Non-syncope mimics — seizure, hypoglycemia, psychogenic pseudosyncope

Definition and mechanism

Syncope is transient loss of consciousness due to global cerebral hypoperfusion, with rapid onset, short duration, and spontaneous complete recovery. The unifying final pathway is a drop in cerebral perfusion — whether from vasodilation/bradycardia (reflex), failure to maintain pressure on standing (orthostatic), or a sudden fall in cardiac output (arrhythmic or obstructive).

Classification

  • Reflex (neurally mediated) — the most common and most benign. Vasovagal (emotional or orthostatic stress with a prodrome), situational (cough, micturition, defecation), and carotid sinus syndrome.
  • Orthostatic — hypotension on standing from volume depletion, medications, or autonomic failure.
  • Cardiac — the dangerous group. Arrhythmic (bradyarrhythmia or tachyarrhythmia) or structural/obstructive (severe AS, HCM, PE).

Red flags pointing to a cardiac cause

  • Exertional or supine syncope
  • No prodrome (“I just woke up on the floor”)
  • Palpitations immediately preceding collapse
  • Syncope causing significant injury or occurring while driving
  • Structural heart disease, prior MI, or reduced EF
  • Family history of sudden cardiac death at a young age
  • An abnormal ECG (any of the features above)

ECG clues

The 12-lead is the highest-yield first test. Beyond overt arrhythmia, look for the substrate: conduction disease (AV block, bifascicular block), pre-excitation, channelopathy patterns (long/short QT, Brugada), and markers of structural disease or scar.

Workup

  • History, exam, orthostatic vitals, and 12-lead in everyone — this risk-stratifies most patients
  • Echocardiogram when structural disease is suspected
  • Ambulatory monitoring matched to symptom frequency — Holter (daily), patch (weeks), or an implantable loop recorder for infrequent, unexplained, recurrent events
  • Exercise testing for exertional syncope
  • Tilt-table testing for suspected reflex syncope when the diagnosis is unclear
  • EP study in selected patients with structural disease or conduction disease

Role of the EP study

Targeted, not a screening test. It can demonstrate sinus node dysfunction, infranodal conduction disease (prolonged HV), or inducible VT in the right substrate. A negative study does not rule out an arrhythmic cause, so it is used selectively and interpreted in context.

Management

  • Reflex syncope — education, trigger avoidance, hydration and salt, counter-pressure maneuvers; pacing only for documented reflex asystole in older patients
  • Bradyarrhythmic syncopepacemaker for SND or AV block as the documented cause
  • Tachyarrhythmic syncope — ablation or ICD per the mechanism and substrate
  • Structural/obstructive — treat the lesion (e.g., aortic valve, HCM)

Last reviewed by Dr. Colombowala on May 27, 2026.

Clinical-reference content, not medical advice. This page is written for EP staff and does not create a doctor-patient relationship. It does not replace institutional policy, current device manuals, or attending direction during a case. See the full disclaimer.

© 2026 Ilyas K. Colombowala, MD. All rights reserved. Reproduction, redistribution, or republication of this content in any form without written permission is prohibited.

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