Chapter 1 – Electrical Basis of ECG (Foundation Lecture)

To interpret an ECG confidently, you must understand the electrical behavior of cardiac cells. ECG is not a “random graph”—it is the body-surface reflection of millions of cardiac cells undergoing depolarization and repolarization in a coordinated sequence.

Goal: Connect cellular electricity → ECG tracing.

Core chain: RMP → Threshold → Depolarization → Plateau → Repolarization → Conduction.

Exam focus: Na⁺ vs Ca²⁺ depolarization rule (muscle vs nodes).

1) What is an ECG?

An electrocardiogram (ECG) is a time-based graphical recording of the heart’s electrical activity captured by electrodes on the body surface.

What ECG shows

Electrical depolarization and repolarization (timing + sequence)
Rhythm generation and conduction pattern
Indirect clues of ischemia, hypertrophy, and electrolyte effects (because they alter electrical behavior)

What ECG does NOT show

Mechanical contraction strength
Cardiac output / blood pressure
Valve function

Fundamental principle: Electrical activity happens first, mechanical contraction follows.

Clinical importance

Rhythm disorders (e.g., heart block, tachyarrhythmias) are primarily electrical problems. That’s why ECG is a first-line tool for diagnosing arrhythmias—even before mechanical failure becomes obvious.

2) Resting Myocardial Cell & Resting Membrane Potential (RMP)

When a ventricular myocardial cell is not being stimulated, it sits at its resting membrane potential. At rest, the cell is polarized: the inside is negative compared with the outside.

Ventricular myocardial RMP ≈ –90 mV (inside negative)

Why is the resting cell negative?

Ion gradients: K⁺ is high inside, Na⁺ is high outside.
Selective permeability: at rest, the membrane “leaks” K⁺ more than Na⁺.
Na⁺/K⁺ ATPase: pumps 3 Na⁺ out for every 2 K⁺ in → net loss of positive charge from inside.

Exam pearl

The more negative the RMP, the more “stable” the cell. If RMP becomes less negative (e.g., electrolyte disturbance), the cell may become more excitable → arrhythmia risk.

3) Cell Stimulation & Threshold Potential

When a neighboring cell depolarizes, it creates a local current that makes the next cell’s membrane potential less negative. This gradual shift continues until the cell reaches a critical voltage called the threshold potential.

Typical progression: –90 → –80 → –70 mV
Threshold ≈ –70 mV (ventricular muscle)

What happens at threshold?

Voltage-gated sodium channels open abruptly (in ventricular/atrial muscle).
A rapid inward Na⁺ current begins → depolarization accelerates dramatically.

All-or-None law: If threshold is reached → full action potential. If not → no action potential.

4) Depolarization – Phase 0 (Na⁺ Influx in Myocardial Muscle)

Once threshold is reached, fast voltage-gated Na⁺ channels open and Na⁺ rushes into the cell. This causes the membrane potential to rapidly rise and the inside becomes positive.

Approximate change: –70 mV → 0 mV → +10 mV
This rapid upstroke is called Phase 0 in ventricular/atrial muscle.

Clinical correlation (high-yield)

If phase 0 is slowed (e.g., by sodium-channel blocker drugs or severe hyperkalemia), ventricular conduction slows and the QRS can widen.

5) Plateau Phase – Phase 2 (Ca²⁺ vs K⁺ Balance)

Cardiac muscle has a unique feature: after depolarization it enters a plateau phase. Instead of immediately repolarizing, the membrane stays near 0 mV for a short time.

Ionic basis

Ca²⁺ enters through L-type calcium channels.
K⁺ leaves through potassium channels.
These opposing currents partially balance each other → voltage remains relatively stable.

Why plateau matters: It prevents sustained tetanic contraction, allows ventricular filling, and supports effective cardiac output.

6) Repolarization – Phase 3 (K⁺ Efflux)

Repolarization begins when Ca²⁺ channels close and K⁺ efflux dominates. As K⁺ leaves the cell, the inside becomes negative again, returning toward the resting membrane potential.

Membrane potential returns toward –90 mV (resting level) → this is Phase 3.

ECG correlation

Repolarization abnormalities often show up as T-wave changes (peaked, inverted, flattened), and can be triggered by ischemia or electrolyte disturbances (especially potassium changes).

7) Action Potential – The Complete Electrical Event

An action potential is the full electrical cycle of a cardiac cell: depolarization → plateau → repolarization, returning to the resting state.

Key idea: An action potential is not just a local event — it becomes a moving wave across the myocardium.

8) Cell-to-Cell Conduction (Gap Junctions)

Cardiac muscle cells are electrically connected by gap junctions, allowing ions to pass directly from one cell to the next. This enables the heart to behave as a functional syncytium (many cells acting as one electrical unit).

Clinical note: Ischemia can disrupt cell-to-cell coupling and conduction, increasing arrhythmia risk.

9) MOST IMPORTANT EXAM RULE 🔥 (Muscle vs Nodes)

Not all cardiac tissues depolarize using the same dominant ion. This distinction is critical for understanding nodal rhythms and drug effects.

Tissue	Main Depolarizing Ion	What it means (quick logic)
Atrial & Ventricular Muscle	Na⁺	Fast upstroke (Phase 0) via fast Na⁺ channels
SA Node & AV Node	Ca²⁺	Slower upstroke via Ca²⁺ channels → slower conduction

Practical drug connection: Calcium channel blockers mainly affect SA/AV nodal conduction, while sodium channel blockers mainly affect ventricular/atrial conduction.

🔁 Chapter Summary (One-shot Recall)

ECG records electrical activity, not mechanical contraction.
Ventricular cells rest at about –90 mV (polarized).
Stimulus brings the cell to threshold (~–70 mV), triggering an action potential.
Phase 0 in muscle = rapid Na⁺ influx (depolarization).
Phase 2 plateau = Ca²⁺ influx balanced by K⁺ efflux (cardiac uniqueness).
Phase 3 = K⁺ efflux (repolarization).
Signals spread via gap junctions across myocardium.
Exam rule: Muscle depolarization = Na⁺, Nodes depolarization = Ca²⁺.

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