Electrocardiogram Interpretation
Also known as: ECG, EKG
The electrocardiogram records the electrical activity of the heart from the body surface and remains one of the most valuable and widely available diagnostic tools in clinical medicine. A systematic approach to interpretation ensures abnormalities are not missed, and should be applied consistently regardless of the clinical context prompting the ECG.
Begin by confirming patient details and checking calibration (standard paper speed of 25 mm per second and voltage calibration of 10 mm per millivolt), since deviation from standard settings will distort rate and interval measurements if not accounted for.
Assess rate next, most simply by dividing 300 by the number of large squares between consecutive R waves for a regular rhythm, or by counting complexes over a longer rhythm strip for an irregular rhythm. Normal resting rate is 60 to 100 beats per minute, with bradycardia below this range and tachycardia above it.
Assess rhythm, establishing first whether it is regular or irregular, and whether a P wave precedes every QRS complex with a constant relationship, which together indicate normal sinus rhythm. Irregular rhythms are further characterized as regularly irregular (suggesting a fixed conduction ratio, for example in atrial flutter with variable block, or as a normal variant in sinus arrhythmia related to respiration) or irregularly irregular (classically atrial fibrillation, with no discernible P waves and chaotic baseline activity).
Assess the cardiac axis, most practically by examining leads I and aVF: both positive indicates a normal axis, lead I positive with aVF negative suggests left axis deviation (warranting closer inspection of lead II to confirm), and lead I negative with aVF positive indicates right axis deviation.
Examine each interval and segment in turn. The PR interval (normal range 120 to 200 milliseconds) reflects conduction through the atrioventricular node; prolongation indicates first degree heart block, while a short PR interval raises consideration of pre-excitation syndromes such as Wolff-Parkinson-White. The QRS complex (normal duration under 120 milliseconds) reflects ventricular depolarization; widening suggests bundle branch block, ventricular rhythm origin, or a metabolic disturbance such as severe hyperkalemia. The QT interval, corrected for heart rate (QTc, using Bazett's formula in most routine practice), should generally be under 440 to 460 milliseconds depending on sex; prolongation increases the risk of torsades de pointes and may be congenital or acquired from electrolyte disturbance or QT prolonging medications.
Examine the ST segment and T waves in every lead, looking specifically for ST elevation or depression and T wave inversion, since these findings drive urgent clinical decisions in the context of suspected acute coronary syndrome (see that entry for specific diagnostic thresholds and territorial patterns).
Finally, review for chamber enlargement or hypertrophy criteria (voltage criteria for left ventricular hypertrophy, P wave morphology for atrial enlargement) and any pathological Q waves, which indicate prior myocardial infarction.
ST elevation myocardial infarction and its associated territorial patterns are detailed in the Acute Coronary Syndrome entry. Pericarditis characteristically causes widespread, saddle shaped ST elevation with PR depression, distinguishable from myocardial infarction by its more diffuse distribution not confined to a single coronary territory (see Pericarditis entry).
Hyperkalemia progresses through a recognizable sequence as potassium rises: tall, tented T waves appear first, followed by P wave flattening and PR prolongation, then QRS widening, and finally a sine wave pattern immediately preceding cardiac arrest if untreated, making the ECG a critical bedside tool for assessing the urgency of treatment in suspected hyperkalemia (see Electrolyte and Acid Base Disorders entry).
Atrial fibrillation shows an irregularly irregular rhythm with absent, discrete P waves and a chaotic fibrillatory baseline. Atrial flutter classically shows a sawtooth flutter wave pattern, most visible in the inferior leads, typically with a regular ventricular rate reflecting a fixed conduction ratio, most commonly two flutter waves to one QRS complex.
Bundle branch block patterns are distinguished by QRS morphology in the precordial leads: right bundle branch block shows an RSR pattern in V1 with a broad, slurred S wave in the lateral leads, while left bundle branch block shows a broad, notched R wave in the lateral leads with loss of the normal septal Q wave, and complicates interpretation of ischemic changes given its own baseline repolarization abnormalities.
Wolff-Parkinson-White syndrome shows a short PR interval with a slurred upstroke to the QRS complex, known as a delta wave, reflecting pre-excitation through an accessory pathway, and carries a risk of rapid conduction during atrial fibrillation with potential for degeneration into ventricular fibrillation.
ECG interpretation should always be integrated with the clinical context rather than read in isolation, and a normal ECG does not exclude significant underlying cardiac disease, particularly intermittent arrhythmia or unstable angina between episodes. Serial ECGs, comparison with prior tracings where available, and correlation with symptoms substantially increase diagnostic value beyond a single isolated recording.
Referral: cardiology for any ECG abnormality of uncertain significance, arrhythmia requiring further characterization (for example ambulatory monitoring), or findings suggesting a channelopathy or inherited arrhythmia syndrome warranting family screening.
