How to Interpret an ECG: A Systematic Approach
Use a standardized, step-by-step method to analyze every ECG, beginning with rate and rhythm assessment, followed by interval measurements, axis determination, and morphologic analysis of waveforms—this systematic approach minimizes diagnostic errors and ensures no critical findings are missed. 1, 2
Step 1: Calculate Heart Rate and Assess Rhythm
Calculate heart rate by counting QRS complexes in a 6-second strip and multiplying by 10, or use the 300-divided-by-large-boxes method (count large boxes between consecutive R waves and divide 300 by that number). 1, 2
Determine rhythm regularity by examining R-R interval consistency:
- Normal sinus rhythm requires a P wave before each QRS with consistent PR interval and rate 60-100 bpm 1, 2
- Sinus bradycardia (<60 bpm) may be normal in athletes 2, 3
- Note any irregularities suggesting premature beats, pauses, or atrial fibrillation 2
Step 2: Measure Critical Intervals
PR interval (normal 120-200 ms or 3-5 small squares): Assess AV conduction; prolongation suggests AV block 1, 2
QRS duration (normal <120 ms or <3 small squares): Widening indicates ventricular conduction delay or bundle branch block 1, 2
QT interval: Measure manually in lead II or V5 using the tangent method, then correct for heart rate (QTc) using Bazett's formula:
- Normal QTc: <450 ms for men, <460 ms for women 1, 2, 3
- Prolonged QTc increases risk of torsade de pointes 4
Step 3: Determine Electrical Axis
Quick axis determination using leads I and aVF:
- Normal axis (-30° to +90°): Both leads I and aVF positive 1, 2
- Left axis deviation (-30° to -90°): Lead I positive, aVF negative 1, 2
- Right axis deviation (+90° to +180°): Lead I negative, aVF positive 1, 2
- Extreme axis deviation (+180° to -90°): Both leads I and aVF negative 2
Axis deviation reflects chamber enlargement, myocardial hypertrophy, or conduction abnormalities and directly impacts morbidity and mortality assessment. 1
Step 4: Analyze P Wave Morphology
Normal P wave characteristics:
- Duration <120 ms and amplitude <2.5 mm 1
- Upright in leads I, II, aVF; biphasic in V1 1
- Consistent morphology before each QRS in sinus rhythm 1, 2
Abnormal P waves suggest atrial enlargement or non-sinus rhythms. 1
Step 5: Examine QRS Complex Morphology
Look for pathologic Q waves (>1 mm wide and >1/3 the height of R wave or >0.04 seconds duration), which suggest prior myocardial infarction. 1, 2
Assess R wave progression across precordial leads V1-V6:
- R wave amplitude should increase from V1 to V4, then decrease toward V6 1
- Poor R wave progression may indicate anterior infarction
Apply voltage criteria for left ventricular hypertrophy:
- Sokolow-Lyon criterion: S in V1 + R in V5 or V6 >3.5 mV (35 mm) 5, 2
- Cornell voltage: S in V3 + R in aVL (specify which criterion used, as different criteria have different sensitivities) 5
Critical caveat: QRS voltage criteria decline with age and vary by population; specify which criteria you use, as only 11.2% of hypertensive patients meet both Sokolow-Lyon and Cornell criteria simultaneously. 5
Step 6: Evaluate ST Segments
Measure ST deviation at the J point (junction of QRS and ST segment):
- ST elevation >0.1 mV in limb leads or >0.15-0.2 mV in precordial leads suggests acute injury requiring emergent reperfusion therapy 2, 6
- ST depression in leads other than V1-V3 indicates subendocardial ischemia 6
- ST elevation in V1-V3 with upward convexity may indicate Brugada syndrome (J-wave syndrome) 4
Always correlate ST changes with clinical symptoms: ST elevation with active chest pain indicates acute coronary occlusion; the same finding in an asymptomatic patient may represent early repolarization, pericarditis, or ventricular aneurysm. 6
Step 7: Analyze T Wave Morphology
Normal T waves: Upright in leads I, II, V3-V6; inverted in aVR; variable in III, aVL, aVF, V1, V2 1
T wave abnormalities:
- Inversion, hyperacute appearance, or flattening suggests ischemia 2
- T waves represent transmural dispersion of repolarization; excessive prolongation with enhanced dispersion predisposes to torsade de pointes 4
- In children >1 month, T wave inversion in V1-V3 is normal 2
Step 8: Identify Additional Features
Look for U waves (small deflections after T waves), which may indicate hypokalemia, bradycardia, or pathologic repolarization abnormalities. 1, 4
Assess for conduction abnormalities: Bundle branch blocks, AV blocks, or pre-excitation patterns. 2
Critical Pitfalls to Avoid
Never rely solely on computer interpretation—physician verification is mandatory, as computer errors remain common and the same ECG pattern may occur in different pathophysiologic states. 1, 2, 3
Avoid electrode misplacement, particularly precordial leads, which significantly alters interpretation and causes false diagnoses. 2
Always compare with previous ECGs when available to identify new changes. 2, 3
Consider technical factors: Inadequate high-frequency response (minimum 150 Hz for adults) causes systematic underestimation of signal amplitude and smoothing of Q waves. 2
Interpret ECG in clinical context—the same finding has different implications depending on symptoms; ST elevation with active chest pain requires emergent catheterization, while the same finding in an asymptomatic athlete may be benign early repolarization. 2, 6
Account for age and gender differences: QT intervals are longer in women; QRS voltages decline with age; sinus bradycardia to 30 bpm may be normal in athletes. 5, 1, 2
Monitor medications affecting ECG: Antiarrhythmics, psychotropics, anti-infectives, and antihypertensives can alter conduction and repolarization. 1, 3