Rate & rhythm — practical recognition

Rate quick rules

• Regular rhythm: use 300-rule (300 / number of big boxes between R waves).
• Irregular rhythm: count QRS in a 6-second strip and ×10 for bpm estimate.

Common rhythms and what to do

• Sinus rhythm: normal — continue clinical correlation.
• Atrial fibrillation: irregularly irregular; check hemodynamic stability — if unstable: sync cardioversion; if stable: rate control & anticoagulation consideration.
• SVT (AVNRT/AVRT): sudden-onset narrow complex tachycardia — vagal manoeuvres, adenosine (per local protocol) or synchronized DC cardioversion if unstable.
• Ventricular tachycardia (VT): wide complex, often history of structural heart disease; treat as VT until proven otherwise — urgent cardiology/ACLS pathway.
• Paced rhythms & bundle branch blocks: recognize and interpret ischemic changes in the context of wide QRS (see Sgarbossa criteria for LBBB/paced ECGs when suspecting STEMI).

AV blocks — quick guide

• First-degree: PR >200 ms — usually benign, note drugs (beta-blocker, CCB, digoxin).
• Second-degree Mobitz I (Wenckebach): PR progressively lengthens — often at AV node.
• Second-degree Mobitz II: dropped beats without PR lengthening — higher risk, often infra-nodal → consider pacing.
• Third-degree (complete) heart block: AV dissociation — bradycardia, syncope risk → urgent pacing if unstable.

Intervals, axis & hypertrophy — essentials

Intervals

• PR interval: normal 120–200 ms. Prolonged in AV node disease / drugs.
• QRS duration: <120 ms normal. ≥120 ms → BBB or ventricular conduction delay; wide QRS tachycardia differential includes VT.
• QT/QTc: Bazett's formula (QTc = QT / √RR) for quick check — long QT predisposes to torsades (look for drugs, low K/Mg).

Axis

Use leads I & aVF: if I positive & aVF positive → normal axis. Left/right axis deviation clues — large MI, conduction disease, chamber enlargement.

Hypertrophy

Look for large voltages (LVH criteria), P-wave changes for atrial enlargement, and strain patterns (ST depression & T inversion) in LVH.

STEMI recognition — territories & action

The goal is fast identification and activation of reperfusion pathways (PCI/thrombolysis per local protocol).

STEMI territory map (high-yield)

Recognising subtle STEMI & mimics

• Look for new ST elevation ≥1 mm in two contiguous limb leads or ≥2 mm in two contiguous precordial leads (thresholds vary with sex and lead). Follow local STEMI criteria.
• Reciprocal ST depression strengthens the diagnosis (inferior vs anterior patterns).
• Consider posterior leads (V7–V9) when suspicious (horizontal ST depression in V1–V3 may represent posterior STEMI).
• Mimics: early repolarisation, pericarditis (diffuse ST elevation + PR depression), LV aneurysm (chronic Q waves + persistent ST elevation), Brugada pattern — correlate clinically.

Sgarbossa & modified Sgarbossa

When evaluating for STEMI in LBBB or paced rhythm, use Sgarbossa criteria (or modified) to increase diagnostic accuracy — high-specificity rules for acute MI in these settings.

Arrhythmia pearls & electrolyte patterns

• Hyperkalaemia: peaked T waves → wide QRS → sine wave. Treat promptly (calcium, insulin+dextrose, nebulised salbutamol, urgent K removal).
• Hypokalaemia/Hypomagnesaemia: predispose to prolonged QT & torsades — replace electrolytes.
• Torsades de pointes: polymorphic VT with long QT — unsynchronised DC if unstable, magnesium IV if stable, correct electrolytes.
• Pericarditis: diffuse ST elevation and PR depression — pain, positional changes and PR depression help differentiate from STEMI.