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10 common ecg findings

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Here are 10 common ECG findings with their key features, clinical significance, and underlying mechanisms - sourced from Harrison's Principles of Internal Medicine 22E, Tintinalli's Emergency Medicine, Roberts and Hedges' Clinical Procedures, and Braunwald's Heart Disease.

1. ST-Segment Elevation

What you see: ST segment raised ≥1 mm above baseline in two or more contiguous leads.
Mechanism: Transmural (full-thickness) ischemia shifts the injury current vector toward the epicardium. This produces ST elevations over the ischemic zone and reciprocal ST depressions in opposite leads.
Localization:
  • Anterior (V1-V6 + I, aVL) - LAD territory
  • Inferior (II, III, aVF) - RCA territory
  • Lateral (I, aVL, V5-V6) - LCx territory
  • Posterior - reciprocal ST depression in V1-V3
Also caused by: Pericarditis (diffuse, concave-up "saddle-shape" elevation with PR depression), Takotsubo syndrome, early repolarization, LBBB.
  • Harrison's Principles of Internal Medicine 22E, p. 1915

2. Atrial Fibrillation (AF)

What you see:
  • Absence of distinct P waves; flat or chaotic isoelectric baseline (fibrillatory f-waves)
  • Irregularly irregular narrow QRS complexes (unless bundle branch block or pre-excitation is present)
  • Ventricular rate typically 100-180 bpm if uncontrolled
Mechanism: Multiple chaotic reentrant wavelets in the atria depolarize at 350-600 impulses/min; the AV node filters these, producing an irregularly irregular ventricular response.
Clinical significance: Loss of atrial kick reduces cardiac output by ~20% in compensated hearts (more in stiff ventricles). Major risk of thromboembolism - CHA2DS2-VASc score guides anticoagulation.
  • Tintinalli's Emergency Medicine, p. 149

3. Left Ventricular Hypertrophy (LVH)

What you see (voltage criteria):
  • SV1 + RV5 or RV6 ≥ 35 mm (Sokolow-Lyon)
  • R in aVL ≥ 11 mm (Cornell)
  • Often accompanied by ST depression + T-wave inversion in lateral leads (the "strain" pattern)
  • Left atrial abnormality (broad, notched P in II; deep negative terminal P in V1) increases specificity
Caveat: Prominent precordial voltages are a common normal variant in young, athletic individuals. Sensitivity of voltage criteria is low in middle-aged/older adults, obese patients, and those with COPD.
  • Harrison's Principles of Internal Medicine 22E, p. 1914

4. Bundle Branch Blocks

RBBB vs LBBB comparison in V1 and V6
Comparison of normal, RBBB, and LBBB patterns in V1 and V6 - Harrison's, Figure 247-10
QRS duration ≥120 ms is required for complete block.
Right Bundle Branch Block (RBBB):
  • rSR' ("M-shaped" or "rabbit ears") in V1
  • Wide, slurred S wave in V6 and lead I
  • Secondary T-wave inversion in V1-V3
  • RBBB alone is often benign; also seen with pulmonary embolism, ASD, RV strain
Left Bundle Branch Block (LBBB):
  • Wide, predominantly negative (QS) in V1
  • Broad, tall, entirely positive (R) in V6
  • Septal activation reversal - no septal Q wave in V6
  • LBBB is almost always pathological - associated with coronary artery disease, hypertension, dilated cardiomyopathy, valvular disease; a new LBBB in ACS is treated like STEMI (Sgarbossa criteria apply)
  • Harrison's Principles of Internal Medicine 22E, p. 1914-1915

5. Atrioventricular (AV) Block

1st Degree AV Block:
  • PR interval >200 ms (>5 small squares); every P conducts
  • Often benign; can be from increased vagal tone, inferior MI, digoxin
2nd Degree - Mobitz I (Wenckebach):
  • Progressive PR lengthening until a P wave fails to conduct (dropped QRS)
  • Usually at the AV node level; often benign
2nd Degree - Mobitz II:
  • Fixed PR interval with sudden, unpredictable dropped QRS beats
  • At or below the bundle of His; high risk of progressing to complete heart block
3rd Degree (Complete Heart Block):
  • No relationship between P waves and QRS complexes (AV dissociation)
  • Escape rhythm: junctional (narrow, ~40-60 bpm) or ventricular (wide, <40 bpm)
  • Requires urgent pacing
  • Harrison's Principles of Internal Medicine 22E; Robbins & Kumar Basic Pathology

6. Prolonged QT Interval

What you see: Corrected QT (QTc) ≥440 ms in men, ≥460 ms in women (Bazett's formula: QTc = QT / √RR).
Mechanism: Delayed ventricular repolarization due to reduced outward K+ currents or increased inward Na+/Ca2+ currents. Creates dispersion of repolarization, predisposing to early afterdepolarizations and Torsades de Pointes (polymorphic VT).
Causes:
  • Congenital: LQTS1 (KCNQ1), LQTS2 (KCNH2), LQTS3 (SCN5A)
  • Drugs: antiarrhythmics (sotalol, amiodarone), antipsychotics, macrolides, fluoroquinolones
  • Electrolytes: hypokalemia, hypomagnesemia, hypocalcemia
  • Hypothyroidism, hypothermia, myocarditis
  • Fuster and Hurst's The Heart 15E; Harrison's 22E

7. Hyperkalemia

ECG changes in hyperkalemia across severity levels
Sequential ECG changes in hyperkalemia - Harrison's, Figure 247-14
Progressive ECG changes with rising K+:
K+ levelECG change
5.5-6.5 mEq/LTall, peaked ("tented") T waves - earliest sign
6.5-7.5 mEq/LWidening QRS, PR prolongation, P-wave flattening
>7.5 mEq/LP waves disappear, sine-wave pattern
>8-9 mEq/LVentricular fibrillation or asystole
Emergency: Calcium gluconate stabilizes the myocardium. Sodium bicarbonate, insulin+glucose, and albuterol shift K+ intracellularly.
  • Harrison's Principles of Internal Medicine 22E, p. 1918

8. Pericarditis / Pericardial Effusion

Pericarditis - 4 evolutionary stages:
  1. Diffuse, concave-up ST elevation with PR segment depression (most leads except aVR/V1)
  2. ST and PR normalization
  3. Diffuse T-wave inversions
  4. T-wave normalization
Pericardial effusion ECG signs:
  • Sinus tachycardia
  • PR depression
  • Low voltage QRS (amplitude ≤5 mm in all limb leads or ≤10 mm in precordial leads)
  • Electrical alternans - beat-to-beat alternation in QRS amplitude/axis; total (P+QRS+T) alternans with sinus tachycardia is relatively specific for cardiac tamponade
ECG sensitivity for pericardial effusion is only 1-17%, so echo is mandatory for confirmation.
  • Roberts and Hedges' Clinical Procedures in Emergency Medicine, p. 393

9. Sinus Bradycardia and Sinus Tachycardia

Sinus Bradycardia: Rate <60 bpm; normal P morphology (upright in II, inverted in aVR), regular rhythm.
  • Causes: high vagal tone (athletes, vasovagal), hypothyroidism, hypothermia, sick sinus syndrome, inferior MI, beta-blockers/calcium channel blockers, raised ICP
Sinus Tachycardia: Rate >100 bpm; same P morphology; typically gradual onset/offset.
  • Causes: pain, fever, hypovolemia, anemia, heart failure, PE, hyperthyroidism, sepsis, sympathomimetics
  • A reflex sinus tachycardia with a clearly identifiable cause should prompt treatment of the underlying condition, not the rate itself.

10. Pathological Q Waves

What you see: Q wave width ≥40 ms (≥1 small square) or depth ≥25% of the R wave amplitude in the same lead.
Mechanism: Electrically silent infarcted myocardium creates a "window" toward the cavity; leads overlying the infarct record negative (away) vectors as Q waves.
Localization mirrors the ST elevation distribution:
  • Anterior Q waves (V1-V4): LAD infarction
  • Inferior Q waves (II, III, aVF): RCA infarction
  • Lateral Q waves (I, aVL, V5-V6): circumflex infarction
Note: Small septal Q waves (<40 ms, <2 mm) in I, V5, V6 are normal. Q waves in aVR are always normal. Q waves in III alone (without II and aVF) are often positional and non-pathological.
  • Harrison's Principles of Internal Medicine 22E, p. 1916

Quick Reference Summary

FindingKey ECG FeaturePrimary Concern
ST elevation≥1 mm elevation in ≥2 contiguous leadsSTEMI / pericarditis
Atrial fibrillationIrregularly irregular, no P wavesStroke risk, rate control
LVHTall R waves (SV1+RV5 ≥35 mm)Hypertension, HCM
RBBB/LBBBWide QRS, specific morphologyLBBB: often pathological
AV blockPR prolongation / dropped beats3rd degree: urgent pacing
Long QTQTc ≥440-460 msTorsades de Pointes
HyperkalemiaPeaked T waves → sine waveLife-threatening arrhythmia
PericarditisDiffuse saddle ST + PR depressionTamponade if effusion
Sinus bradycardia/tachyRate <60 or >100, normal P axisTreat underlying cause
Pathological QWide/deep Q in ≥2 contiguous leadsOld/evolving infarction

Give me images with marked changes compared to normal

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Here are textbook ECG images for each finding, with the key changes explained:

1. ST Elevation - Mechanism

Subendocardial vs transmural ischemia ST changes
A (left): Subendocardial ischemia - ST vector points inward → ST depression in overlying leads. B (right): Transmural/epicardial ischemia - ST vector points outward → ST elevation in overlying leads (the STEMI pattern).
  • Harrison's 22E, Fig. 247-11

2. Anterior STEMI - Evolving ECG Sequence

Anterior STEMI acute and evolving ECG across all 12 leads
Top row (Acute): ST elevation in I, aVL, V2-V6. Tall, peaked "hyperacute" T waves. Reciprocal ST depression in II, III, aVF. Bottom row (Evolving): Deep Q waves developing in V2-V4. ST elevation resolving. T-wave inversions appearing.
  • Harrison's 22E, Fig. 247-13A

3. Inferior STEMI - Evolving ECG Sequence

Inferior STEMI acute and evolving ECG across all 12 leads
Top row (Acute): ST elevation in II, III, aVF (RCA territory). Reciprocal ST depression in I, aVL, V1-V4. Bottom row (Evolving): Deep Q waves in II, III, aVF. ST settling. T inversions in inferior leads.
  • Harrison's 22E, Fig. 247-13B

4. Anterior STEMI - Real 12-Lead Tracing

Real 12-lead ECG showing acute inferior MI with ST elevation in inferior leads
What to see: Marked ST elevation in II, III, aVF with deep reciprocal ST depression in I, aVL, V1-V2. This is a real-patient inferior STEMI tracing.
  • Textbook of Family Medicine 9E, Fig. 27-12 - "Acute inferior MI with ST elevation in inferior leads"

5. Wellens T-Wave Pattern (Anterior Ischemia / LAD Stenosis)

Deep T-wave inversions V1-V6 Wellens sign precordial leads
Key change: Deep, symmetric T-wave inversions across V1-V6. No ST elevation. No Q waves. Significance: The "Wellens T-wave sign" - almost always indicates critical high-grade LAD stenosis. High risk for impending anterior STEMI. Do NOT stress-test these patients.
  • Harrison's 22E, Fig. 247-12

6. Bundle Branch Blocks (RBBB vs LBBB)

RBBB vs LBBB morphology in V1 and V6 compared to normal
V1V6
NormalSmall r, deep SNarrow qR, upright T
RBBBrSR' ("rabbit ears"), inverted TqRS with wide slurred S
LBBBWide, entirely negative (QS)Broad, monophasic tall R, inverted T
  • Harrison's 22E, Fig. 247-10

7. Atrial Fibrillation

ECG tracing of atrial fibrillation - no P waves, irregularly irregular QRS
Key changes vs normal:
  • No P waves - chaotic fibrillatory baseline
  • Irregularly irregular QRS complexes (note the varying R-R intervals)
  • Narrow QRS unless BBB is present
  • Pye's Surgical-Handicraft, Fig. 17.35

8. Complete Heart Block (3rd Degree AV Block)

ECG of complete heart block showing dissociated P waves and slow escape rhythm
Key changes vs normal:
  • Small P waves (atrial rate ~70-80 bpm) firing independently
  • Wide, slow QRS complexes (ventricular escape rhythm, ~30-40 bpm)
  • No relationship between P waves and QRS complexes (AV dissociation)
  • The long flat stretches after each QRS represent the slow ventricular rate with no conducted beats
  • Pye's Surgical-Handicraft, Fig. 17.34

9. Hyperkalemia - Progressive Changes

ECG changes in hyperkalemia from mild to very severe - peaked T waves, wide QRS, sine wave
Left (Mild-Moderate ~5.5-6.5 mEq/L): Narrow, tall, peaked ("tented") T waves in V1-V2. Normal QRS. Middle (Moderate-Severe ~6.5-7.5 mEq/L): QRS widens markedly. P waves flattening. T waves remain tall and peaked. Right (Very Severe >7.5 mEq/L): Sine-wave pattern - P waves gone, QRS and T wave merge into a continuous oscillation. Precedes VF/asystole.
  • Harrison's 22E, Fig. 247-14

10. Hypokalemia - Prominent U Wave

ECG of hypokalemia showing flat T wave and prominent U wave in lead II and V3
Key changes vs normal:
  • Flat or inverted T waves
  • Prominent U wave (the rounded deflection after the T wave, labeled "U" in V3) - represents delayed Purkinje fiber repolarization
  • Apparent QT prolongation (actually QU prolongation)
  • Risk of Torsades de Pointes
  • Harrison's 22E - Hypokalemia panel

Summary of What to Look for

FindingAbnormal FeatureNormal comparator
STEMIST elevation ≥1 mm, hyperacute TFlat ST, smooth upright T
Wellens signDeep symmetric T inversions V1-V6Upright T precordially
Inferior STEMIST ↑ in II, III, aVF + reciprocal ↓ in I, aVLIsoelectric ST everywhere
RBBBrSR' in V1 / wide S in V6Small r, deep S in V1
LBBBQS in V1 / monophasic R in V6rS in V1, qR in V6
AFNo P waves, irregular QRSRegular rhythm, clear P waves
Complete heart blockP-QRS dissociation, slow escape1:1 PR relationship
HyperkalemiaPeaked T → sine waveNormal T amplitude
HypokalemiaFlat T + prominent U waveNo U wave visible

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ECG Quick Reference Guide

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What's inside the guide:
SectionContent
Cover pageStyled title page listing all 10 findings
Findings 1–10Each on its own section with colour-coded cards
Textbook ECG imagesAnterior STEMI, Inferior STEMI, Wellens sign, RBBB/LBBB comparison, AF, Complete heart block, Hyperkalemia progression, Hypokalemia U waves, ST deviation mechanism diagram
Mechanism boxesBrief pathophysiology for each finding
Urgency badgesEmergency / Urgent / Monitor / Benign colour coding
Quick-reference summary tableAll 12 findings in one table with key ECG features, normal comparators, and urgency
ECG interpretation checklist9-step systematic approach (Rate → Rhythm → Axis → P → PR → QRS → ST → T → QT)
Sources cited throughout: Harrison's 22E, Tintinalli's Emergency Medicine, Braunwald's Heart Disease, Roberts & Hedges, Textbook of Family Medicine 9E.
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