ECG Characteristics for Diagnosing Cardiac Conditions
Premature Ventricular Beats (PVCs)
Look for wide QRS complexes (>120 ms) occurring earlier than expected, without preceding P waves, followed by a compensatory pause. 1
- Key features: Wide, bizarre QRS morphology that differs from the patient's normal QRS complex 1
- Where to look: Any lead can show PVCs, but they're most easily identified in leads with the tallest QRS complexes 1
- Clinical significance: Multiple PVCs (>2,000 in 24 hours) warrant comprehensive cardiac evaluation including echocardiography and CMR to exclude cardiomyopathy 1
Hypokalemia
Hypokalemia produces prominent U waves, ST depression, and flattened T waves, with the most dramatic changes visible in precordial leads V2-V4. 2
- Characteristic findings: U waves become more prominent than T waves, creating a "double hump" appearance 2
- ST-T changes: Flat or inverted T waves with ST segment depression 2
- Critical pitfall: Severe hypokalemia (≤2.9 mmol/L) can unmask Type 1 Brugada pattern with coved ST elevation in V1-V2, which resolves with potassium correction 2
- Best leads: V2-V4 for U waves; limb leads for QT prolongation 2
Hyperkalemia
Hyperkalemia creates peaked, narrow-based "tented" T waves initially, progressing to widened QRS, flattened P waves, and potentially Brugada-like patterns in severe cases. 3, 4
- Early changes (K+ 5.5-6.5 mEq/L): Tall, peaked T waves with narrow base, best seen in precordial leads V2-V4 3, 4
- Moderate changes (K+ 6.5-8.0 mEq/L): Prolonged PR interval, flattened/absent P waves, widened QRS complex 3, 4
- Severe changes (K+ >8.0 mEq/L): Sine wave pattern, ST elevation mimicking STEMI or Brugada pattern in V1-V3 3, 4
- Critical recognition: ST elevation from hyperkalemia resolves with potassium correction, distinguishing it from true Brugada syndrome 4
- Where to focus: V2-V4 for T wave changes; all leads for QRS widening 3
Atrial Fibrillation
Atrial fibrillation shows irregularly irregular RR intervals with absent P waves, replaced by chaotic fibrillatory waves best seen in leads V1, II, III, and aVF. 1
- Defining feature: Absolutely irregular ventricular response with no discernible P waves 1
- Fibrillatory waves: Small, irregular baseline oscillations best visualized in V1 and inferior leads (II, III, aVF) 1
- QRS morphology: Usually narrow unless pre-existing bundle branch block or aberrant conduction 1
- Rate assessment: Measure ventricular rate over 6 seconds and multiply by 10 for average rate 1
Hypermagnesemia
Hypermagnesemia produces prolonged PR and QT intervals with widened QRS, though ECG changes are less specific than other electrolyte disorders. 1
- Primary findings: PR prolongation, QRS widening, QT prolongation 1
- Severe cases: May progress to complete heart block or cardiac arrest 1
- Best detection: Measure intervals in lead II or V5 for clearest assessment 1
Hypomagnesemia
Hypomagnesemia causes QT prolongation, prominent U waves, and predisposes to torsades de pointes, with changes most evident in precordial leads. 1
- Key findings: Prolonged QT interval, prominent U waves, flattened T waves 1
- Arrhythmia risk: Increases susceptibility to ventricular arrhythmias including torsades de pointes 1
- Where to measure: V2-V4 for U waves; lead II or V5 for QT interval 1
Acute Pericarditis
Acute pericarditis shows diffuse ST elevation with upward concavity (saddle-shaped) in multiple leads, accompanied by PR depression, without reciprocal ST depression. 1
- Hallmark finding: Widespread ST elevation with upward concavity in leads I, II, aVL, aVF, V2-V6 1
- PR segment changes: PR depression in most leads except aVR (which shows PR elevation) 1
- Key differentiator from STEMI: No reciprocal ST depression, ST elevation in multiple non-contiguous territories, preserved R wave amplitude 1
- Evolution: ST segments return to baseline, followed by T wave inversion in the same leads 1
- Best leads: Look at II, aVF, and V5-V6 for characteristic changes 1
Brugada Syndrome
Brugada syndrome Type 1 pattern shows coved ST elevation ≥2 mm in V1-V2 with downsloping ST segment and inverted T wave, often with right bundle branch block. 1
- Type 1 (diagnostic): Coved ST elevation ≥2 mm in V1-V2/V3 with negative T wave and downsloping ST segment 1
- Type 2 (non-diagnostic): Saddleback morphology with ST elevation ≥2 mm but terminal ST segment ≥1 mm above baseline with positive or biphasic T wave 1
- Type 3 (non-diagnostic): Either coved or saddleback with J-point elevation ≥2 mm but terminal ST segment <1 mm 1
- Critical leads: V1-V2 in the 4th intercostal space; consider recording V1-V2 in 2nd intercostal space to unmask pattern 1
- Associated finding: S1S2S3 pattern mimicking left anterior hemiblock due to right ventricular outflow tract conduction delay 1
- Differentiation from early repolarization: Brugada has downsloping ST with ST/ST80 ratio >1, while early repolarization has upsloping ST with ratio <1 1
STEMI (ST-Elevation Myocardial Infarction)
General STEMI Criteria
STEMI requires ST elevation at the J-point in two or more contiguous leads: ≥0.1 mV in all leads except V2-V3, where thresholds are higher and age/sex-dependent. 1, 5
- V2-V3 criteria: ≥0.25 mV in men <40 years, ≥0.2 mV in men ≥40 years, ≥0.15 mV in women 1, 5
- All other leads: ≥0.1 mV ST elevation 1, 5
- Reciprocal changes: ST depression in leads opposite to the infarct territory strongly supports diagnosis 1, 5
- Timing: Obtain ECG within 10 minutes of presentation; repeat every 15-30 minutes if initially non-diagnostic 1, 5
Inferior STEMI
Inferior STEMI shows ST elevation in leads II, III, and aVF, with reciprocal ST depression in aVL and often I. 1, 5
- Primary leads: II, III, aVF show ST elevation ≥0.1 mV 1, 5
- Reciprocal changes: ST depression in aVL (most sensitive), often with depression in lead I 5
- Right ventricular involvement: Record V3R and V4R; ST elevation ≥0.05 mV (≥0.1 mV in men <30 years) indicates RV infarction 1, 5
- Culprit artery clues: Greater ST elevation in III than II suggests right coronary artery; equal or greater elevation in II suggests left circumflex 1
Lateral STEMI
Lateral STEMI demonstrates ST elevation in leads I, aVL, V5, and V6, typically from left circumflex occlusion. 1, 5
- High lateral: I and aVL show ST elevation 5
- Low lateral: V5-V6 show ST elevation 5
- Posterior involvement: Check for ST depression in V1-V3 with tall R waves and upright terminal T waves (posterior STEMI equivalent) 1, 5
- Confirm with posterior leads: V7-V9 at 5th intercostal space; ST elevation ≥0.05 mV (≥0.1 mV in men <40 years) confirms posterior MI 1, 5
Anterior STEMI
Anterior STEMI shows ST elevation in precordial leads V1-V6, with the extent of involvement indicating infarct size. 1, 5
- Septal: V1-V2 ST elevation indicates septal involvement 5
- Anteroseptal: V1-V4 ST elevation 5
- Extensive anterior: V1-V6 plus I and aVL ST elevation indicates large left anterior descending artery occlusion 5
- Poor prognosis markers: ST elevation in ≥8 leads or ST elevation in aVR suggests left main or severe multivessel disease 5
- Loss of R waves: Progressive loss of R wave amplitude in V1-V4 indicates transmural injury 1, 5
STEMI in Bundle Branch Block
In left bundle branch block, concordant ST elevation (same direction as QRS) in leads with positive QRS strongly suggests acute MI. 1
- LBBB criteria: Concordant ST elevation ≥1 mm in leads with positive QRS deflection 1
- RBBB: New ST elevation or Q waves despite common ST-T abnormalities in V1-V3 should raise suspicion for MI 1
- Critical action: New or presumed new LBBB with clinical suspicion warrants immediate reperfusion therapy 5
Hypertrophic Obstructive Cardiomyopathy (HOCM)
HOCM shows deep, narrow Q waves in lateral and inferior leads, giant inverted T waves in precordial leads, and voltage criteria for left ventricular hypertrophy. 1
- Q waves: Deep (>0.3 mV), narrow Q waves in I, aVL, V5-V6 (lateral) and II, III, aVF (inferior) without prior MI 1
- T wave inversion: Giant inverted T waves (≥1 mV) in V2-V6, often symmetric and deep 1
- LVH voltage: Sokolow-Lyon criteria (S in V1 + R in V5 or V6 ≥3.5 mV) or Cornell criteria 1
- ST changes: ST depression in lateral leads (I, aVL, V5-V6) 1
- Where to focus: Lateral leads (I, aVL, V5-V6) for Q waves and ST-T changes; V2-V4 for giant T wave inversion 1
- Differentiation: Unlike MI, Q waves in HOCM are narrow and associated with LVH voltage and giant T waves 1
Bundle Branch Blocks
Right Bundle Branch Block (RBBB)
RBBB shows QRS ≥120 ms with RSR' pattern ("M-shaped") in V1-V2 and wide S waves in lateral leads I, aVL, V5-V6. 1
- V1-V2 morphology: RSR', rSR', or M-shaped pattern with tall R' wave 1
- Lateral leads: Wide, slurred S waves in I, aVL, V5-V6 1
- ST-T changes: ST depression and T wave inversion in V1-V2 are expected (secondary changes) 1
- Incomplete RBBB: Same pattern but QRS 100-119 ms 1
Left Bundle Branch Block (LBBB)
LBBB shows QRS ≥120 ms with broad, notched R waves in lateral leads (I, aVL, V5-V6) and deep S waves in V1-V2, without Q waves in lateral leads. 1
- Lateral leads: Broad, monophasic R waves in I, aVL, V5-V6 with notching or slurring 1
- V1-V2: Deep QS or rS complexes 1
- Absent Q waves: No Q waves in I, V5-V6 (presence suggests additional pathology) 1
- ST-T changes: Discordant ST-T changes (opposite direction to QRS) are expected 1
- Incomplete LBBB: Same pattern but QRS 100-119 ms 1
Left Anterior Fascicular Block (LAFB)
LAFB shows left axis deviation (-45° to -90°), small Q in I and aVL with small R in II, III, aVF, and QRS duration <120 ms. 1, 6
- Axis: Left axis deviation beyond -45° 1, 6
- Lead I: qR pattern (small Q, tall R) 1
- Inferior leads: rS pattern (small R, deep S) in II, III, aVF 1
- QRS duration: <120 ms (if ≥120 ms, consider bifascicular block) 1
Left Posterior Fascicular Block (LPFB)
LPFB shows right axis deviation (+90° to +180°), small R in I and aVL with small Q in II, III, aVF, after excluding other causes of right axis deviation. 1