18 minute read
The paper before the patient
Everything measurable on an ECG rests on two conventions: the paper moves at 25 mm/s and the pen deflects 10 mm per millivolt. That makes one small square 0.04 seconds (40 ms) and one large square 0.20 seconds; five large squares are one second. The calibration pulse at the edge of the tracing is the machine proving both claims: it should be exactly two large squares tall and one wide.
Check the calibration pulse before trusting anything else. Half-standard or double-speed recordings exist, and every 'wide QRS' or 'low voltage' you call inherits their error.
The anatomy of one beat
One cardiac cycle writes five deflections. The P wave is atrial depolarization. The PR interval (P onset to QRS onset, 120 to 200 ms) is mostly the AV node deliberately delaying. The QRS complex (under 120 ms) is both ventricles depolarizing; its first downward deflection is Q, first upward is R, the downward one after R is S. The ST segment is the ventricles fully depolarized, which is why it should sit exactly on the baseline: any current of injury shows up here. The T wave is repolarization, and the QT interval spans the whole ventricular electrical cycle.
The QT must be corrected for rate (QTc), because repolarization naturally shortens as the heart speeds up. A QTc beyond about 440 to 460 ms starts earning attention; beyond 500 ms it is a torsades risk that changes management today.
Twelve views of one event
The twelve leads are twelve cameras filming the same depolarization from different angles. The six limb leads view the frontal plane: lead I looks from the left (0 degrees), aVF from the feet (+90), II from the left hip (+60), and aVR peers from the right shoulder, which is why almost everything looks upside-down in it. The six precordial leads sweep the horizontal plane from the right ventricle (V1) around to the lateral left ventricle (V6).
The angles are why lead groups map to coronary territories: II, III and aVF look at the inferior wall (usually right coronary), V1 to V4 at the septum and anterior wall (left anterior descending), and I, aVL, V5, V6 at the lateral wall (circumflex). A finding confined to one group localizes; a finding everywhere suggests pericarditis, electrolytes, or the machine.
Step 1: rate
For a regular rhythm, find an R wave on a bold line and count large squares to the next one: 300, 150, 100, 75, 60, 50. Two large squares is 150; four is 75. For an irregular rhythm the trick fails, so count complexes across 30 large squares (six seconds) and multiply by ten.
Rate is the first branch point of every arrhythmia algorithm: over 100 sends you down the tachycardia limb, under 60 the bradycardia limb, and the treatment tables differ entirely.
Step 2: rhythm, in five questions
Rhythm yields to five questions asked in order. Is the R-R regular, irregularly irregular, or regularly irregular? Are there P waves at all? Is every P followed by a QRS, and every QRS preceded by a P? Is the P upright in II and inverted in aVR (sinus in origin)? Is the PR interval constant?
The answers sort nearly everything: irregularly irregular with no P waves is atrial fibrillation; sawtooth atrial activity at 300 with a regular ventricular response is flutter; progressive PR lengthening then a dropped beat is Wenckebach; P waves marching independently of the QRS is complete heart block. Name what you see with those five answers before reaching for a diagnosis.
Step 3: axis
The mean QRS axis is where the ventricles' net electrical force points in the frontal plane; normal is roughly -30 to +90 degrees. The two-lead method needs only leads I and aVF: both positive is a normal axis; I positive with aVF negative is left axis deviation; I negative with aVF positive is right axis deviation; both negative is an extreme axis.
Axis rarely diagnoses alone, but it corroborates: right axis fits right ventricular strain (PE, pulmonary hypertension) or a lateral infarct; left axis fits left anterior fascicular block or an inferior infarct; an extreme axis in a wide-complex tachycardia argues for VT.
Step 4: intervals
Three measurements, each with a decision attached. PR over 200 ms is first-degree AV block; a short PR with a slurred QRS upstroke (delta wave) is pre-excitation, which changes which drugs are safe. QRS at 120 ms or more means the ventricles depolarized abnormally: bundle branch block, ventricular origin, pacing, or hyperkalemia; a wide QRS plus a tachycardia is VT until proven otherwise. QTc beyond 500 ms, or clearly lengthening on serial tracings, is an arrhythmia risk you act on: culprit drugs, potassium, magnesium, calcium.
Step 5: the P wave and the atria
The P wave carries the atria's history. A tall peaked P in II (over 2.5 mm) suggests right atrial enlargement, the companion of chronic lung disease. A broad, notched P in II, or a P in V1 with a deep terminal negative portion, suggests left atrial enlargement, the footprint of mitral disease and chronically stiff left ventricles. Absent P waves with an irregular rhythm is fibrillation; inverted P waves after the QRS point to a junctional or retrograde origin.
Step 6: QRS morphology
Wide QRS with an rSR' pattern in V1 and a wide S in V6 is right bundle branch block; wide QRS with a broad notched R in V6 and a deep QS in V1 is left bundle branch block. RBBB can be an incidental finding; a new LBBB never is, and LBBB also rewrites the ST-T rules, so ischemia calls become specialist territory.
Voltage speaks too. Deep S in V1 plus tall R in V5 or V6 (summing over 35 mm) is the classic LVH criterion, often trailed by 'strain' repolarization laterally. Low voltage everywhere suggests effusion, infiltration, obesity or emphysema between the heart and your electrodes. Pathologic Q waves (over 40 ms wide or a third of the R height) are the scar of an old infarct and never 'normal variant' in a regional pattern.
Step 7: ST segments and T waves
The ST segment is compared against the TP baseline in every lead. Elevation in a coronary territory with reciprocal depression in the opposite leads is an occlusion until proven otherwise; the reciprocal change is what separates infarct from the diffuse, saddle-shaped elevation of pericarditis (which also depresses PR segments and spares reciprocity). ST depression that is horizontal or downsloping marks subendocardial ischemia; depression maximal in V1 to V3 should make you ask for posterior leads.
T waves have their own vocabulary: hyperacute broad T waves precede ST elevation in the first minutes of occlusion; deep symmetric anterior T inversions after a pain-free interval (Wellens pattern) mark a critical LAD lesion; tented narrow-based T waves are hyperkalemia. Every ST-T call gains meaning from a comparison tracing: 'new' is the most important adjective in ECG reporting.
Say it in the same order every time
Report the way you read: rate, rhythm, axis, intervals, then morphology by wave (P, QRS, ST-T), then the one-line conclusion in clinical context. 'Sinus tachycardia at 110, normal axis, normal intervals, ST elevation in II, III and aVF with depression in aVL: acute inferior STEMI, activate the lab' is a complete read. The discipline of the fixed order is what stops the dramatic finding in one lead from blinding you to the QT beside it.
Pearls
- Every abnormality is 'compared to what?': hunt down the old ECG before finalizing any read.
- A wide-complex tachycardia is VT until proven otherwise, especially with structural heart disease.
- Tented T waves plus a widening QRS is a potassium emergency; treat the ECG before the lab confirms.
- aVR is not a dead lead: diffuse depression with aVR elevation suggests left main or triple-vessel ischemia.
- The five rhythm questions answered honestly beat a pattern-matched rhythm label every time.
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