Cardiology
Electrocardiogram (ECG/EKG)
Reading the heart's electrical activity — P, QRS, T waves and their clinical meaning
An electrocardiogram records the electrical activity of the heart from electrodes on the skin. The standard 12-lead ECG provides 12 viewing angles. Each cardiac cycle produces a P wave (atrial depolarization), QRS complex (ventricular depolarization, ~80-100 ms), and T wave (ventricular repolarization). Atrial repolarization is buried in QRS. Standard paper speed is 25 mm/sec; one small box = 0.04 sec, one large = 0.20 sec. Normal PR interval: 120-200 ms. QT interval (corrected): <440 ms men, <460 ms women. Discovered: Willem Einthoven 1903 (Nobel 1924). ECG diagnoses arrhythmias, ischemia, infarction, electrolyte disorders, and structural disease.
- InventorWillem Einthoven (1903; Nobel 1924)
- Standard12-lead ECG (10 electrodes)
- Paper speed25 mm/sec; 1 small box = 40 ms
- Normal QRS80-100 ms (narrow)
- Normal PR120-200 ms (3-5 small boxes)
- STEMI threshold≥1 mm ST elevation in 2 contiguous leads
Interactive visualization
Press play, or step through manually. The visualization is yours to drive — try it before reading on.
Watch the 60-second explainer
A condensed visual walkthrough — narrated, captioned, under a minute.
Why ECG matters
- Chest pain. Triages STEMI vs NSTEMI vs non-cardiac in minutes.
- Palpitations. Identifies arrhythmias (AF, SVT, VT, blocks).
- Syncope. Screens for long QT, Brugada, heart block, WPW.
- Electrolyte emergencies. Hyperkalemia visible before lab results return.
- Drug monitoring. QT prolongation from antipsychotics, antiarrhythmics, antibiotics.
- Preoperative. Baseline rhythm and ischemia screen before surgery.
- Pacemaker/ICD checks. Confirms capture and sensing.
Common misreadings
- Calling a normal ECG "diagnostic." A normal ECG does not rule out unstable angina or NSTEMI — serial ECGs and troponins required.
- Missing posterior MI. ST depression V1-V3 with tall R waves is a posterior STEMI mirror, not subendocardial ischemia.
- Confusing pericarditis with STEMI. Pericarditis has diffuse ST elevation with PR depression and no reciprocal changes.
- Calling AF "irregular sinus." Sinus rhythm requires upright P waves in lead II; AF has none.
- Ignoring lead misplacement. Reversed limb leads invert lead I — repeat before diagnosing dextrocardia.
- Treating hyperkalemia after the labs. Peaked Ts and widened QRS demand calcium immediately.
Frequently asked questions
How is heart rate calculated from ECG?
Two methods. Regular rhythm — divide 300 by number of large boxes between R waves (300/5 = 60 bpm; 300/3 = 100 bpm). Irregular — count QRS complexes in a 6-second strip and multiply by 10. Bradycardia is HR <60 bpm; tachycardia >100. Normal sinus rhythm requires P before every QRS, regular rhythm, and rate 60-100.
What does ST elevation mean?
Acute transmural ischemia — usually a totally occluded coronary artery. STEMI requires ≥1 mm elevation in two contiguous limb leads or ≥2 mm in chest leads V2-V3. Reciprocal ST depression strengthens the diagnosis. Door-to-balloon time goal is <90 minutes for primary PCI. Other causes of ST elevation include pericarditis (diffuse, with PR depression), early repolarization, and LV aneurysm.
How do you localize an MI?
Each lead group views a region. Inferior MI — leads II, III, aVF (right coronary artery in 80%). Anterior — V1-V4 (LAD). Lateral — I, aVL, V5-V6 (circumflex or LAD diagonals). Posterior — tall R and ST depression in V1-V2 (mirror). Right ventricular involvement with inferior MI shows ST elevation in V4R; these patients are preload dependent.
What does atrial fibrillation look like?
No discrete P waves, irregularly irregular R-R intervals, fibrillatory baseline. Most common sustained arrhythmia. Risks stroke (CHA2DS2-VASc score guides anticoagulation). Rate control with beta blockers, diltiazem, or verapamil. Rhythm control with amiodarone, flecainide, or cardioversion. Anticoagulation with apixaban, rivaroxaban, dabigatran, or warfarin.
What is a long QT?
Prolonged ventricular repolarization. QTc >500 ms increases torsades de pointes risk. Causes — congenital (KCNQ1, KCNH2 mutations), drugs (azithromycin, ondansetron, methadone, haloperidol, sotalol), electrolytes (low K, Mg, Ca). Treat torsades with magnesium 2 g IV, correct electrolytes, stop offending drug. Overdrive pacing or isoproterenol for refractory cases.
How do electrolytes show on ECG?
Hyperkalemia — peaked T waves, then PR prolongation, QRS widening, sine wave, asystole. Treat with calcium gluconate (membrane stabilization), insulin/glucose, beta-2 agonists, then dialysis. Hypokalemia — flat T waves, U waves, ST depression. Hypercalcemia — short QT. Hypocalcemia — long QT. These can mimic ischemia.
When do you call a code?
Pulseless rhythms — ventricular fibrillation, pulseless VT (shockable), asystole, and PEA (pulseless electrical activity, non-shockable). Start CPR immediately, defibrillate VF/VT at 200 J biphasic, give epinephrine 1 mg every 3-5 minutes, treat reversible causes (Hs and Ts — hypoxia, hypovolemia, H+, hypo/hyperkalemia, hypothermia, tension pneumothorax, tamponade, toxins, thrombosis).