The Heart’s Electrical System & the ECG
Your heart makes its own electricity — it needs no nerve to beat, which is why a transplanted heart still beats. Every heartbeat starts as a tiny spark in the SA node, spreads across the atria (the P wave), pauses for a crucial tenth of a second at the AV node, then races down the His–Purkinje wiring so both ventricles squeeze together (the big QRS) before resetting (the T wave). Press play and watch the spark travel, drawn beat-for-beat alongside a live ECG.
Try this: start on Normal and watch the spark pause at the AV node. Then switch to Heart block to see the pause become a wall — and to Atrial fibrillation, where you can hit Defibrillate and watch an orderly rhythm snap back.
Live ECG readout
What's happening
Real clinical values: the SA node’s 60–100 bpm intrinsic rate, the ~0.1 s AV-node delay, the 120–200 ms PR interval, and a normal QRS under 120 ms. The ECG’s shape (P–QRS–T) and the spark’s sequence are real; the exact voltages and timing here are a smooth illustrative model, not a recording from one person.
The Science in Plain Language
Your heart runs on its own electricity
Here is the fact that surprises almost everyone: the heart does not wait for a signal from the brain to beat. It generates its own electrical pulse, over and over, for a lifetime — roughly 2.5 billion beats without a single day off. That is why a transplanted heart still beats even though every nerve connecting it to the donor’s brain was cut. The nerves only adjust the tempo; the beat itself is homegrown. Cut all the nerves and a healthy heart simply settles into its own steady rhythm.
The SA node: a battery that leaks on purpose
The spark starts in the sinoatrial (SA) node, a patch of specialised cells in the wall of the right atrium about the size of a grain of rice. Ordinary heart cells sit still at rest, but SA-node cells cannot: they slowly leak positive ions inward through a channel nicknamed the “funny current” (carried by HCN channels). That slow leak drifts the cell’s voltage upward until it hits threshold and fires itself — about 60–100 times a minute at rest. This self-firing (automaticity) is what sets your resting heart rate.
Why nerves speed you up and slow you down
The SA node is wired to two opposing controls. The vagus nerve (the “rest and digest” brake) releases acetylcholine onto M2 receptors, which slows the leak and drops the rate — a fit person’s heart can dip into the 40s during deep sleep. The opposite drive, adrenaline/noradrenaline acting on beta-1 receptors, steepens the leak and speeds you up when you climb stairs or feel afraid. Try the Vagal brake button in the animation to watch the rate fall, or Exercise to watch it climb — the sequence is identical, just faster or slower. Beta-blocker drugs (metoprolol, bisoprolol) work by blunting that adrenaline drive.
The P wave: the atria squeeze
Once the SA node fires, the wave sweeps across both atria and they contract, giving the ventricles a final top-up of blood — the so-called atrial kick, worth roughly 20–30% of a beat’s filling. On the ECG this atrial activity is the small first bump: the P wave. When you lose organised atrial contraction (as in atrial fibrillation, below), you lose that kick, which is one reason people feel breathless and tired in AFib.
The AV node: the pause that makes it all work
The atria and ventricles are separated by a ring of insulating fibrous tissue — electrically, the top and bottom of the heart are two separate rooms with one door between them: the atrioventricular (AV) node. The AV node deliberately delays the signal by about a tenth of a second. It manages this because it conducts unusually slowly — roughly 0.05 metres per second, against about 0.5 m/s in atrial muscle — so the wave crawls through it. That tiny pause is not a flaw; it is essential. It lets the atria finish emptying before the ventricles fire, so the pumps don’t clash. On the ECG this shows up as the flat gap between the P wave and the QRS — the PR interval, normally 120–200 ms. The AV node has a second job, too: it acts as a gatekeeper, refusing to pass impulses faster than the ventricles can safely handle — which is exactly what protects you in atrial fibrillation. Watch the spark visibly stop and wait at the AV node in the animation; that stillness is the whole point.
His–Purkinje and the QRS: both ventricles, together, bottom-up
Past the AV node, the signal drops into the heart’s express wiring: the bundle of His, its left and right bundle branches, and the fine Purkinje fibres that thread through the ventricle walls. This system is fast — the Purkinje network conducts at roughly 2–4 metres per second, dozens of times quicker than ordinary muscle — so the whole ventricular mass depolarises almost at once and contracts from the apex upward, wringing blood toward the great arteries. That coordinated squeeze is the tall QRS complex, the biggest deflection on the ECG, and it is what you feel as your pulse. A normal QRS is narrow — under 120 ms. When a bundle branch is damaged, the QRS widens (a bundle branch block) because the signal has to abandon the express lanes and crawl through muscle instead.
The T wave, and how to read the tracing
After contracting, the ventricles have to reset (repolarise) before they can fire again; that recovery is the T wave. Because each part of the ECG maps to one step of the electrical journey, the tracing is a live window on the wiring: P = atria, PR gap = AV delay, QRS = ventricles firing, T = ventricles resetting. This is why an ECG is so powerful in a chest-pain emergency — a blocked coronary artery starving the muscle of oxygen shifts the ST segment (the stretch between QRS and T), and that shift is often how a heart attack is diagnosed in the first ten minutes.
When it fails: heart block, AFib, and cardiac arrest
If the SA node runs too slowly, or the pathway breaks, things go wrong in recognisable ways. In heart block the AV node stops passing the signal; in complete (third-degree) block the atria and ventricles beat on separate clocks, and a slow backup pacemaker lower in the heart escapes to keep you alive: a junction near the AV node fires at about 40–60 bpm, while a pacemaker down in the ventricles manages only ~20–40 bpm — enough to survive, rarely enough to feel well. The fix is usually an implanted pacemaker device, a matchbox-sized generator that watches for missed beats and delivers a tiny timed pulse through a wire in the heart. If the atria fire chaotically instead of in step, that is atrial fibrillation: an irregularly irregular pulse, a lost atrial kick, and pooled blood that raises stroke risk (which is why AFib is often treated with blood thinners such as apixaban or warfarin, guided by a risk score). And if the ventricles fibrillate, there is no pumping at all — that is cardiac arrest, and it is fatal within minutes without help.
What a defibrillator actually does (a common myth)
Films show a defibrillator “jump-starting” a flat, silent heart — that is backwards. A defibrillator is useless against a truly flatline heart (asystole is not a shockable rhythm). What the shock actually does is the opposite of a jump-start: it stops everything at once, depolarising every cell in a single instant so the disorganised, quivering electrical storm has nowhere to go. With the chaos wiped clean, the SA node — the fastest natural pacemaker — gets the first word again and can restart an orderly rhythm. That is exactly what the Defibrillate button models here: in atrial fibrillation it resets the atria back to sinus rhythm (a planned version of this is called cardioversion). The real lifesaver in a cardiac arrest is fast CPR plus an AED — survival falls by roughly 7–10% for every minute that a shockable arrest goes untreated, which is why public defibrillators and bystander CPR matter so much.