Atrial fibrillation: irregularly irregular rhythm with absent P waves
Atrial fibrillation is characterized by chaotic atrial electrical activity at rates of 350–600 impulses per minute — far faster than the AV node can conduct. The result is an irregularly irregular ventricular response with no organized P waves visible (replaced by fine fibrillatory baseline). The QRS is narrow (unless aberrant conduction or bundle branch block is present).
The irregularly irregular pattern is the key recognition feature. No two RR intervals are the same — there is no predictable pattern to the ventricular response. Uncontrolled AFib typically presents with ventricular rates of 100–180 bpm; controlled AFib has rates below 100 bpm with rate-control medication.
Clinical priorities in new-onset AFib: assess hemodynamic stability (rate, blood pressure, symptoms); determine duration of onset (onset within 48 hours versus unknown or >48 hours determines anticoagulation approach before cardioversion); assess for acute causes (PE, sepsis, thyrotoxicosis, post-cardiac surgery); initiate rate control (IV metoprolol or diltiazem for most patients; amiodarone if severely depressed EF).
SVT: regular narrow-complex tachycardia, retrograde P waves
Supraventricular tachycardia (SVT) most commonly refers to AVNRT (AV node reentrant tachycardia) in clinical practice. AVNRT uses dual pathways within the AV node to create a rapid reentry circuit, producing a very regular narrow-complex tachycardia at 150–250 bpm.
Key ECG features: The rhythm is regular (fixed RR interval) — this is the critical distinction from AFib. P waves are retrograde and typically buried in or just after the QRS complex. In typical AVNRT, the retrograde P wave appears as a pseudo-S wave in the inferior leads (II, III, aVF) or pseudo-R' wave in V1 — not visible as a separate P wave before the QRS.
Adenosine is diagnostic and therapeutic: IV adenosine 6 mg rapid push terminates AVNRT by blocking AV node conduction, interrupting the reentry circuit. If adenosine terminates the tachycardia abruptly — returning to sinus rhythm — the diagnosis is confirmed as AVNRT (or AVRT). Adenosine will NOT terminate AFib or atrial flutter — it may transiently slow the ventricular rate in flutter and reveal flutter waves, then the rate returns.
AVRT and pre-excitation: when SVT involves an accessory pathway
AVRT (AV reentrant tachycardia) uses the AV node plus an accessory pathway (Kent bundle in Wolff-Parkinson-White syndrome) to create the reentry circuit. Orthodromic AVRT (most common) conducts antegrade through the AV node and retrograde through the accessory pathway — producing a narrow QRS similar to AVNRT. Antidromic AVRT conducts antegrade through the accessory pathway — producing a very wide, bizarre QRS that can mimic VT.
WPW pattern on resting ECG: Short PR interval (<120 ms), delta wave (slurred upstroke of QRS), and wide QRS. The delta wave represents early ventricular pre-excitation via the accessory pathway before normal AV node conduction.
Critical safety note: AFib with WPW is a life-threatening emergency. If the accessory pathway in WPW can conduct rapid rates (short accessory pathway refractory period), AFib may conduct at 250–350 bpm directly to the ventricle via the pathway, bypassing AV node protection. This wide-complex irregular tachycardia can degenerate to VF. AV node blocking agents (adenosine, beta-blockers, calcium channel blockers, digoxin) are CONTRAINDICATED in AFib with WPW — they increase conduction via the accessory pathway. Treat with IV procainamide or electrical cardioversion.