The EKG is one of the most powerful diagnostic tools in medicine — and it looks terrifying to most students. But the EKG is just a graphical record of the heart's electrical activity. Once you understand what each wave represents physiologically, you can interpret any tracing systematically. This guide walks you through everything: from the cardiac cycle to full EKG interpretation.
AI-generated content. This guide was written by MedAI's AI and is intended as a study aid. Always cross-reference with your official course materials, textbooks, and instructor guidance before your exam.
The heart generates and propagates its own electrical impulses through a specialized conduction system. The sequence of activation determines the waveform pattern on the EKG.
| Structure | Function | Intrinsic Rate | EKG Correlate |
|---|---|---|---|
| SA Node (sinoatrial) | Primary pacemaker of the heart; right atrium near SVC | 60–100 bpm | Sets the heart rate; precedes P wave |
| AV Node (atrioventricular) | Delays signal transmission to ventricles (~100ms); allows atrial filling | 40–60 bpm | PR interval (0.12–0.20 sec) |
| Bundle of His | Conducts signal from AV node to bundle branches | 40–60 bpm | Part of PR interval |
| Bundle Branches (R & L) | Rapidly conduct signal down interventricular septum | ~40 bpm | Part of QRS complex |
| Purkinje Fibers | Final rapid distribution to ventricular myocardium | 20–40 bpm | Completes QRS complex |
| Wave/Interval | Duration (Normal) | Represents | Abnormality |
|---|---|---|---|
| P wave | <120 ms | Atrial depolarization | Absent: atrial fibrillation; Peaked (>2.5mm): right atrial enlargement |
| PR interval | 120–200 ms | Conduction through AV node | >200 ms: 1st-degree AV block; progressively longer then dropped: 2nd-degree Mobitz I (Wenckebach); fixed dropped beats: Mobitz II; no relationship: 3rd-degree |
| QRS complex | <120 ms | Ventricular depolarization | >120 ms: bundle branch block, ventricular tachycardia, hyperkalemia |
| ST segment | Isoelectric (flat) | Plateau phase of ventricular AP (phase 2) | Elevation: STEMI, pericarditis, Brugada. Depression: NSTEMI, ischemia, digitalis effect |
| T wave | Upright in most leads | Ventricular repolarization | Inverted: ischemia, RBBB, LVH. Peaked: hyperkalemia. Flattened: hypokalemia |
| QT interval | <440 ms (corrected) | Total ventricular depolarization + repolarization | Prolonged QTc: risk of Torsades de Pointes (VTach). Drugs: quinidine, haloperidol, macrolides, fluoroquinolones |
| U wave | Small, after T wave | Late repolarization (Purkinje fibers?) | Prominent U wave: hypokalemia |
The 5-Step EKG Interpretation
1) Rate (count large boxes: 300/# boxes between R waves). 2) Rhythm (regular? P before every QRS?). 3) Axis (quadrant method: QRS polarity in leads I and aVF). 4) Intervals (PR, QRS, QTc). 5) Waveform changes (ST elevation/depression, T-wave inversion, Q waves).
The cardiac cycle is the sequence of mechanical events that accompany each heartbeat. Heart sounds, murmurs, and the EKG all map directly onto specific events in the cycle.
| Phase | Valve Status | Pressure Change | EKG | Sound |
|---|---|---|---|---|
| Late diastole (filling) | Mitral + tricuspid OPEN; Aortic + pulmonic CLOSED | LV pressure low, filling from LA | After T wave; P wave begins | S4 if present (atrial kick) |
| Isovolumetric contraction | ALL VALVES CLOSED | LV pressure rises rapidly; volume constant | QRS to start of ejection | S1 (mitral + tricuspid close) — beginning of systole |
| Ejection (systole) | Aortic + pulmonic OPEN; Mitral + tricuspid CLOSED | LV pressure > aortic pressure; SV ejected; volume falls | ST segment | Ejection click (stenotic valve) if present |
| Isovolumetric relaxation | ALL VALVES CLOSED | LV pressure falls rapidly; volume constant | T wave | S2 (aortic + pulmonic close) — beginning of diastole; A2 before P2 |
| Rapid filling (early diastole) | Mitral + tricuspid OPEN | Blood rushes into ventricle from pressure gradient | After T wave | S3 (if present: volume overload, heart failure, mitral regurgitation) |
| Arrhythmia | EKG Findings | Cause | Treatment |
|---|---|---|---|
| Atrial Fibrillation | No P waves; irregularly irregular rhythm; fibrillatory baseline | Hypertension, valvular disease, thyrotoxicosis, alcohol ("holiday heart") | Rate control (β-blockers, CCBs); rhythm control (cardioversion); anticoagulation (stroke prevention) |
| Atrial Flutter | "Sawtooth" flutter waves at 300 bpm; regular ventricular rate (150 bpm with 2:1 block) | Right atrial macro-reentry | Cardioversion; ablation; anticoagulation |
| Ventricular Tachycardia (VT) | Wide QRS (>120ms) ≥3 beats at >100 bpm; AV dissociation; fusion beats | MI scar reentry; cardiomyopathy | Stable: amiodarone. Unstable: synchronized cardioversion |
| Ventricular Fibrillation (VF) | Chaotic, no organized complexes | Ischemia, electrolyte disturbance | Immediate DEFIBRILLATION (unsynchronized). No pulse = VF or pulseless VT |
| Torsades de Pointes | VT with rotating axis ("twisting of points"); prolonged QTc | Prolonged QT (drugs, hypokalemia, hypomagnesemia) | Magnesium sulfate IV; correct electrolytes; remove offending drug |
| 1st-degree AV block | PR > 200ms; every P followed by QRS | Increased vagal tone, digoxin, myocarditis | Usually none required |
| 3rd-degree AV block | Complete AV dissociation; P and QRS independent | Inferior MI (right coronary artery), Lyme disease, structural | Permanent pacemaker |
| Affected Territory | Occluded Artery | EKG Leads with ST Elevation | Reciprocal Changes |
|---|---|---|---|
| Inferior wall | RCA (90%) or LCx | II, III, aVF | I, aVL (lateral) |
| Lateral wall | LCx or diagonal branch of LAD | I, aVL, V5-V6 | II, III, aVF |
| Anterior wall | LAD (diagonal branches) | V1-V4 | II, III, aVF |
| Posterior wall | RCA or LCx | Tall R in V1-V2 + ST depression V1-V3 | ST elevation in V7-V9 (posterior leads) |
| RV infarct | Proximal RCA | ST elevation in V1, V4R | Classic: inferior STEMI + hypotension + JVD + clear lungs |
Hyperkalemia EKG Changes (Know in Order)
As K⁺ rises: (1) Peaked T waves (K 5.5–6.5) → (2) Widened QRS (K 6.5–7.5) → (3) Sine wave pattern (K >7.5) → (4) VF / asystole. TREATMENT: Calcium gluconate (stabilizes membrane), then insulin+glucose (shifts K into cells), then kayexalate/dialysis (removes K).
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