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Every measurement made on a living patient is, ultimately, an attempt to read out the electrical or mechanical activity of tissue without disturbing it. The electrocardiogram (ECG) is the oldest, most-used and most-taught biopotential measurement in medicine, and it sits at the intersection of cell biophysics, electromagnetism and instrumentation engineering. Understanding it properly requires three things: the cellular physics of action potentials, the macroscopic projection of cardiac electrical activity onto the body's surface, and the design choices forced on the front-end amplifier by signals of millivolt amplitude in the presence of much larger interference. This lesson covers all three. The same instrumentation principles transfer directly to the electroencephalogram (EEG) and to electromyography (EMG) — the ECG is just the most accessible example.
Spec mapping: This lesson sits under AQA 7408 section 3.10.3 (Biological measurement). It covers the basic structure of nerve and muscle cells; the resting potential and the action potential as ion-driven membrane events; the cardiac action potential as a special case with a distinctive plateau phase; the conduction system of the heart (SA node → AV node → bundle of His → Purkinje fibres) and its mapping onto the cardiac cycle; the ECG as a body-surface recording of cardiac electrical activity; the standard 12-lead configuration and the meaning of the P, QRS and T waves; clinical interpretation including rate and basic arrhythmia recognition; and the instrumentation requirements of high input impedance and common-mode rejection. (Refer to the official AQA specification document for exact wording.)
Synoptic links:
- Section 3.7.3 (electric fields and potential): the ECG is literally the time-varying electric potential at body-surface electrodes produced by cardiac current sources inside the thorax. The potential at a point is set by V = kq/r summed over all current sources, and the dipolar approximation used in ECG vector cardiography is a direct application of this.
- Section 3.7.4 (capacitance): cell membranes have a measurable capacitance per unit area (≈ 1 μF cm⁻²), and the time constants of action-potential rising and falling phases are RC times set by membrane capacitance and ion-channel conductance. The capacitor work from earlier in the course gives the physical basis.
- Section 3.10.4 (ultrasound) and 3.10.5 (X-rays/CT): the ECG complements anatomical imaging — ultrasound shows mechanical motion, X-ray CT shows anatomy, and ECG shows electrical timing. A complete cardiac diagnosis usually triangulates all three.
Every excitable cell — neuron, skeletal muscle fibre, cardiac myocyte — maintains a resting potential of typically -70 mV (inside negative with respect to outside). This potential difference exists because the cell membrane is selectively permeable to certain ions and because active ion pumps maintain concentration gradients.
The membrane houses two relevant species of channel at rest:
The equilibrium between diffusive efflux and electrical attraction yields the Nernst equation for the equilibrium potential of an ion species:
V_K = (RT/zF) ln([K⁺]_out / [K⁺]_in) ≈ -90 mV at 37 °C
The resting potential of -70 mV sits between the Nernst potential of K⁺ (-90 mV) and that of Na⁺ (+60 mV), much closer to the K⁺ value because the membrane is mostly permeable to K⁺. The Na⁺/K⁺-ATPase pump maintains the concentration gradients against passive leakage, exporting 3 Na⁺ and importing 2 K⁺ per ATP hydrolysed.
When the membrane is depolarised past a threshold of about -55 mV, voltage-gated sodium channels open en masse, the membrane permeability flips from K-dominated to Na-dominated, and the membrane potential swings rapidly toward the Na⁺ Nernst potential of ~+60 mV. This is the depolarisation phase. The Na⁺ channels then inactivate; voltage-gated K⁺ channels open with a delay; K⁺ efflux repolarises the membrane back toward -70 mV. The whole event lasts a few milliseconds in a nerve cell.
The cardiac myocyte adds a critical wrinkle: a plateau phase lasting around 200-250 ms, mediated by L-type calcium channels that admit Ca²⁺ slowly while K⁺ efflux is suppressed. The plateau gives the cardiac muscle cell its long absolute refractory period and prevents tetanus — the heart cannot be tetanically stimulated like skeletal muscle, which is essential to its function as a pump.
| Phase | Cardiac myocyte | Mechanism |
|---|---|---|
| 0 — depolarisation | -90 → +30 mV in ~1 ms | Fast Na⁺ channels open |
| 1 — initial repolarisation | +30 → 0 mV | Na⁺ channels inactivate; K⁺ transient outward |
| 2 — plateau | 0 mV held for ~200 ms | L-type Ca²⁺ inward balances K⁺ outward |
| 3 — repolarisation | 0 → -90 mV | Delayed-rectifier K⁺ channels |
| 4 — resting | -90 mV | K⁺ leak dominates |
The heart is an electrically organised muscle. A specialised conduction pathway times the contraction of the four chambers:
SA node (sinoatrial node) — in the right atrial wall. The pacemaker. Spontaneously depolarises at about 60-100 beats per minute (bpm) in adults.
Atrial spread — depolarisation spreads across both atria, triggering atrial systole (~80 ms).
AV node (atrioventricular node) — at the boundary between atria and ventricles. Imposes a built-in conduction delay (~100 ms) that allows atrial systole to complete before ventricular systole begins.
Bundle of His → bundle branches → Purkinje fibres — high-velocity conduction system that delivers the depolarising wavefront from the AV node to the apex of the ventricles and then back upward through the ventricular myocardium. Conduction velocity in Purkinje fibres is ≈ 2-4 m s⁻¹, an order of magnitude faster than in working myocardium.
The whole sequence — atrial depolarisation, AV delay, ventricular depolarisation, ventricular repolarisation — repeats roughly once per second. Each event produces a characteristic deflection in the ECG.
A single ECG cycle consists of:
P wave — depolarisation of both atria. Small, rounded, upward deflection in most leads. Duration ≈ 80-100 ms.
PR interval — onset of P to onset of QRS. Includes the AV node delay. Normal range ≈ 120-200 ms.
QRS complex — depolarisation of both ventricles. The largest deflection of the ECG (∼1 mV in lead II). Duration ≈ 60-100 ms. The mass of ventricular myocardium dwarfs the atria, so the ventricular deflection dominates.
ST segment — corresponds to the plateau phase of ventricular myocardium. Normally isoelectric (flat at baseline). Elevation or depression of the ST segment is the cardinal sign of acute myocardial ischaemia or infarction.
T wave — repolarisation of the ventricles. Small, rounded, upward in most leads.
| Feature | Typical duration / amplitude | Clinical significance |
|---|---|---|
| P wave | 80-100 ms; ≈ 0.1-0.2 mV | Atrial enlargement (peaked or notched) |
| PR interval | 120-200 ms | Lengthened in AV block |
| QRS | 60-100 ms; ≈ 1 mV in lead II | Widened in bundle branch block or ventricular origin |
| ST segment | Isoelectric | Elevated in STEMI; depressed in ischaemia |
| T wave | ≈ 0.1-0.3 mV | Inverted T-waves indicate ischaemia or previous infarct |
| QT interval | < 440 ms (men), < 460 ms (women) | Prolonged QT — torsades de pointes risk |
An ECG is recorded at the standard paper speed of 25 mm s⁻¹. The distance between consecutive R waves is measured to be 22 mm. Calculate the heart rate in bpm.
The time between R waves is t = 22/25 = 0.88 s. The heart rate is f = 60/t = 60/0.88 = 68 bpm. This falls comfortably within the normal sinus range of 60-100 bpm.
A modern diagnostic ECG records twelve simultaneous leads, each looking at the heart's electrical activity from a different vantage point. The set comprises:
Conceptually, each lead provides a "view direction" — a particular projection axis along which cardiac dipole activity is sampled. Lead II (right arm to left leg) typically gives the largest QRS because its axis closely matches the mean electrical axis of the heart (about +60° in most adults). The clinical reasoning is geometric: ischaemia of the inferior wall manifests in leads II, III and aVF; of the lateral wall in I, aVL, V5, V6; of the anterior wall in V1-V4.
The full taxonomy of arrhythmias is the substance of cardiology specialty training; A-Level expects recognition of a small number of canonical patterns.
Sinus tachycardia — sinus rhythm at > 100 bpm. Normal response to exercise, fever, anxiety, hypovolaemia.
Sinus bradycardia — sinus rhythm at < 60 bpm. Common in athletes; may be drug-induced (beta-blockers) or pathological (sick sinus syndrome).
Atrial fibrillation (AF) — disorganised atrial depolarisation, no discrete P waves, irregularly irregular ventricular response. Common in older patients; increases stroke risk.
Ventricular tachycardia / fibrillation — wide-QRS tachycardia or chaotic ventricular activity. Cardiac arrest if sustained; defibrillator response.
An ECG shows no discernible P waves, a baseline that fluctuates irregularly, QRS complexes of normal width but with grossly irregular R-R intervals. Heart rate calculated over a 10-s strip averages 130 bpm. Interpret.
The absence of P waves, the irregular baseline (fibrillatory waves) and the irregularly irregular QRS spacing are the textbook triad of atrial fibrillation. The QRS width remains normal because conduction below the AV node is unaffected — only the AV node's filtering of chaotic atrial impulses produces the irregular ventricular response. The rate of 130 bpm puts this in AF with rapid ventricular response, which clinically calls for rate control (e.g. beta-blockers, calcium-channel blockers) and consideration of anticoagulation to reduce stroke risk.
graph LR
A["Cardiac dipole<br/>~1 mV at surface"] --> B["Electrodes<br/>Ag/AgCl + gel"]
B --> C["Differential amplifier<br/>high Z_in, high CMRR"]
C --> D["Filter<br/>0.5 - 40 Hz typ."]
D --> E["ADC + display<br/>25 mm/s, 10 mm/mV"]
E --> F["Interpretation"]
style C fill:#3498db,color:#fff
style D fill:#3498db,color:#fff
The cardiac signal at the body surface is about 1 mV. The mains-frequency electromagnetic environment in a typical hospital room induces a common-mode interference signal of tens of millivolts on every electrode lead — well over an order of magnitude larger than the cardiac signal itself. Three instrumentation choices defeat this:
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