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How the Heart's Electrical Signal Works

Your heart is controlled by a biological pacemaker you were born with.

8 min read·February 8, 2025

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A pump with its own spark#

Your heart beats about 100,000 times a day without any conscious effort. Unlike skeletal muscles (which only contract when your brain tells them to), the heart generates its own electrical impulses. It is, in a precise sense, self-driven.

This electrical autonomy comes from specialized cells in a structure called the sinoatrial node — the SA node — tucked in the upper-right chamber of the heart. These cells have an unusual property: they spontaneously depolarize. Their membrane potential drifts toward the threshold for firing, and when it crosses that threshold, an electrical pulse fires, triggering contraction. This happens 60–100 times per minute in a healthy adult at rest.

Depolarization and the action potential#

Cell membranes are electrically polarized — there's a voltage difference across them, with the inside of the cell more negative than the outside. In a resting cardiac cell, this is roughly −90 millivolts.

When stimulated, ion channels in the membrane open. Sodium ions rush in, driven by both electrical attraction and concentration gradient, depolarizing the membrane rapidly to about +30 mV. This is the upstroke of the cardiac action potential. Subsequent potassium outflow and calcium dynamics then repolarize the membrane back to −90 mV, readying the cell for the next cycle.

The Nernst equation describes the equilibrium potential for a given ion — the voltage at which electrical force exactly balances the concentration gradient:

Vm=RTzFln[K+]o[K+]iV_m = \frac{RT}{zF} \ln\frac{[K^+]_o}{[K^+]_i}

where RR is the gas constant, TT is temperature, zz is the ion's charge, FF is Faraday's constant, and the ratio is the concentration of potassium outside versus inside the cell. For potassium in a typical cardiac cell, this gives about −94 mV — close to resting membrane potential, which explains why potassium plays such a central role in setting that baseline.

The conduction system#

Once the SA node fires, the electrical wave doesn't just spread randomly. The heart has a dedicated conduction system that routes the signal with precise timing.

The impulse spreads from the SA node across both atria — the upper chambers — causing them to contract and push blood into the ventricles. This produces the P wave on an ECG.

The signal then reaches the atrioventricular node (AV node), which sits between the atria and ventricles. Here, the signal deliberately slows down — a delay of about 0.1 seconds. This pause is physiologically essential: it gives the atria time to finish contracting and push their blood into the ventricles before the ventricles themselves contract. Rush this step and cardiac output drops.

After the AV delay, the signal travels rapidly down the Bundle of His and through the Purkinje fiber network to the ventricular walls. This produces the QRS complex on the ECG — the sharp spike you recognize as a heartbeat. Finally, the T wave represents ventricular repolarization, the reset before the next beat.

Reading an ECG#

An electrocardiogram is simply a recording of the electrical activity of the heart over time. Each component of the signal corresponds to a stage in the cardiac cycle:

  • P wave: atrial depolarization — the atria contracting
  • QRS complex: ventricular depolarization — the ventricles contracting (the main pumping stroke)
  • T wave: ventricular repolarization — the ventricles recovering

Watch a beat scroll across the monitor and you can read the story of each cycle directly: the small P bump as the atria fire, the sharp QRS spike as the ventricles contract, then the rounded T wave as they reset. Drag the heart rate and the whole pattern simply packs closer together — the shape of a healthy beat stays the same; only the spacing changes.

Doctors read ECGs to diagnose arrhythmias, heart attacks, conduction defects, and electrolyte imbalances. An absent P wave suggests the SA node isn't functioning normally. A wide QRS suggests a problem with ventricular conduction. A specific pattern of ST elevation in the QRS region is the hallmark of a heart attack — muscle cells dying, unable to repolarize normally.

The entire electrical portrait of every beat is legible in that small squiggle of a trace, if you know how to read it.

Key takeaways
  • The heart is self-driven: pacemaker cells in the SA node spontaneously depolarize 60–100 times a minute, no nerve signal required.
  • The conduction path (SA node → atria → AV node → His/Purkinje → ventricles) sequences the squeeze; the ~0.1 s AV delay lets the atria empty before the ventricles fire.
  • Each ECG feature maps to an event: P = atrial depolarization, QRS = ventricular depolarization, T = ventricular repolarization.
  • Potassium's Nernst potential (~−94 mV) sets the resting baseline, which is why electrolyte imbalances show up on the ECG.
  • Deviations are diagnostic — absent P wave (SA node), wide QRS (ventricular conduction), ST elevation (heart attack).
Check your understanding
1. Why is the 0.1-second delay at the atrioventricular (AV) node physiologically critical?
2. According to the Nernst equation, what determines the equilibrium potential for potassium in a cardiac cell?
3. What does an absent P wave on an ECG indicate about the cardiac electrical system?
0 / 3 answered

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