Potassium & the Heartbeat
Your heartbeat is really a wave of electricity, and the single number that tunes it is the potassium in your blood. The normal band is narrow — 3.5 to 5.0 mmol/L — because potassium sets the resting voltage of every heart cell. Drag the Serum K⁺ slider and watch the live ECG morph in real time: push it high and the T waves grow tall and tented, the QRS widens, and the trace slides toward a lethal sine wave; pull it low and the T waves flatten, a stray U wave appears, and the rhythm turns twitchy. This is why a potassium of 6.5 is a genuine emergency.
Try this: start on Normal, then press Hyperkalemia and watch the T waves spike and the QRS balloon — now hit 💉 Calcium and see the complex snap back to normal without the potassium number changing.
Live cardiac readout
What's happening
What is real vs. illustrative: the potassium value (mmol/L), the normal band (3.5–5.0), and the resting-voltage readout — computed live from the real Nernst equation using an intracellular K⁺ of ~140 mmol/L — are genuine physiology. The ECG waveforms are a faithful model of the morphology real potassium disturbances produce (peaked T waves, wide QRS, sine wave, U waves, long QT), and the heart-rate / QRS-width / QT numbers are illustrative of direction and rough magnitude, not a specific patient.
The Science in Plain Language
1. Potassium is the battery your heart runs on
About 98% of your body's potassium lives inside cells, and only a sliver — the 3.5–5.0 mmol/L measured in a blood test — floats in the blood outside them. That steep inside-vs-outside gap is not an accident; it is the charge on the battery. A heart cell at rest sits at about −90 millivolts, meaning the inside is 90 mV more negative than the outside. Where does that number come from? Almost entirely from potassium leaking out down its gradient, which you can calculate with the Nernst equation: EK = −61.5 × log₁₀(K inside / K outside). Plug in 140 inside and 4.0 outside and you get about −94 mV — the readout in the panel. Change the blood number and you change the resting voltage of every cell in the heart.
2. Why the heart is so exquisitely sensitive
Notice that the resting voltage depends on the ratio of inside to outside potassium. Because the outside number is so small, a change that looks tiny on paper — from 4.0 to 6.5 — is actually a huge proportional jump, and it drags the resting voltage a long way. Move the slider and watch the cyan bar climb the ladder toward the orange threshold. When the resting voltage drifts closer to threshold, the fast sodium channels that start each beat begin to inactivate, so the electrical signal spreads through the heart more slowly and clumsily. That is the whole story behind the changing ECG: potassium isn't poisoning the muscle chemically, it's detuning the electrical circuit.
3. Hyperkalemia: tented T waves, then a widening QRS, then a sine wave
Hyperkalemia (high potassium) is one of the true electrical emergencies in medicine, and it announces itself on the ECG in a fairly predictable order. Around 5.5–6.5 mmol/L the T waves grow tall, narrow and “tented” — the repolarization phase speeds up and peaks. As potassium climbs past 6.5–7.5, conduction slows: the QRS widens, the P waves flatten and can vanish. Above roughly 8–9 mmol/L the widened QRS merges with the T wave into a slow, undulating sine wave — a pre-terminal rhythm that slides into ventricular fibrillation or standstill. Press Hyperkalemia and then push the slider higher to watch the trace collapse. This is why an ER treats a potassium of 6.5 as a drop-everything problem, sometimes before the lab result is even confirmed.
4. Hypokalemia: flat T waves, U waves and a stretched QT
Hypokalemia (low potassium, below 3.5 mmol/L) does almost the opposite to the picture but is dangerous in its own way. The T waves flatten, a small extra bump called a U wave appears just after the T, and the electrical recovery drags out, lengthening the QT interval. A long QT is fertile ground for a chaotic, spinning ventricular rhythm called torsades de pointes. Low potassium also makes heart cells irritable and trigger-happy, throwing off extra beats (PVCs). Slide down to 2.8 and watch the T waves melt, the U wave surface and the rhythm start to stutter. People on diuretics (water pills like furosemide or hydrochlorothiazide), or losing fluid through vomiting or diarrhea, are the classic ones to run low.
5. The magnesium connection — why low potassium won't fix
Here is a piece of physiology that trips up even careful clinicians: you often cannot correct a low potassium until you also fix a low magnesium. Magnesium normally acts like a brake on a channel in the kidney called ROMK; when magnesium is low, that brake comes off and the kidney dumps potassium into the urine no matter how much you replace. So the potassium keeps leaking away, and the arrhythmias — especially torsades — keep coming. That's why hospitals give magnesium alongside potassium, and why the “Low Mg²⁺” button in the model makes the low-potassium rhythm even more irritable and hard to settle. Magnesium and potassium travel together; treat them together.
6. What actually moves your potassium up and down
Potassium is pushed into cells (lowering the blood level) by insulin, by adrenaline / beta-agonists like the albuterol inhaler, and by a rising blood pH (alkalosis). It leaks out of cells (raising the blood level) during acidosis, tissue injury, and when certain drugs block the exits. The kidney is the master controller, tuned by the hormone aldosterone. That's why the medicines most likely to raise potassium are the ones that blunt aldosterone: ACE inhibitors and ARBs (blood-pressure pills ending in “-pril” and “-sartan”), and the potassium-sparing diuretic spironolactone — especially in someone with reduced kidney function.
7. The emergency toolkit — and what calcium really does
When potassium is dangerously high, the ER moves in three steps. First, protect the heart: intravenous calcium (gluconate or chloride) raises the firing threshold and stabilizes the membrane within minutes — you can see the QRS narrow. But here is the honest and crucial point the model makes on purpose: calcium does not lower the potassium at all. Press the Calcium button and watch the number stay put while the tracing improves — it buys minutes, not a cure. Second, shift potassium back into cells with insulin plus glucose (and often nebulized albuterol). Third, remove it from the body with diuretics, potassium-binding resins, or, definitively, dialysis. Stabilize, shift, remove — in that order.
8. The myth worth correcting
Two half-truths are worth clearing up. First: “you can't overdose on potassium from food, so supplements are always safe.” For a person with healthy kidneys, that's largely true — the kidney excretes the excess. But add chronic kidney disease, an ACE inhibitor or spironolactone, and a potassium supplement or a heavy hand with salt substitute (which is potassium chloride), and blood potassium can climb into the danger zone quietly, with no symptoms until the ECG changes. Second: “a normal blood potassium means my total-body potassium is fine.” Not necessarily — because 98% is hidden inside cells, the blood level can read normal while total stores are depleted, or shift dangerously fast when pH or insulin changes. The blood number is a snapshot, not the whole account.
9. Reading the ECG at a glance
Here is the rough order in which the ECG changes as potassium climbs and falls. These are teaching landmarks, not rigid cut-offs — individual hearts vary, and the number on the lab report always matters more than any single wave:
- K⁺ 3.5–5.0 (normal): crisp P wave, narrow QRS, a modest rounded T wave.
- K⁺ ~5.5–6.5 (early hyperkalemia): tall, peaked, tented T waves — usually the first sign.
- K⁺ ~6.5–7.5: P waves flatten and lengthen, the QRS widens past 120 ms.
- K⁺ ~8–9+: QRS and T merge into a sine wave, sliding toward fibrillation or asystole.
- K⁺ below 3.5 (hypokalemia): flattening T waves, a rising U wave, and a stretched QT; below ~2.8 the heart turns irritable and torsades-prone.
A quick worked example of the Nernst readout you see in the panel: with intracellular potassium held near 140 mmol/L, a blood potassium of 4.0 gives EK = −61.5 × log₁₀(140/4.0) ≈ −94 mV; raise the blood level to 6.5 and it climbs to about −81 mV (closer to threshold, more sluggish conduction); drop it to 2.8 and it falls to about −104 mV. That's the same equation the model runs every frame.
10. Where potassium comes from — food and “lite salt”
Potassium is abundant in ordinary whole foods, and the amounts are larger than the “banana” stereotype suggests. A medium banana carries roughly 420 mg, but a baked potato with skin has around 900–950 mg, a cup of cooked spinach about 840 mg, half an avocado near 500 mg, and a cup of white beans over 1,000 mg. General adult intake targets sit around 2,600–3,400 mg per day. The one thing to watch is the salt substitute aisle: “lite” or “no-salt” seasonings are usually potassium chloride, and a level quarter-teaspoon can deliver on the order of 600–800 mg of potassium in a single dash. For a healthy person that's harmless; for someone with kidney disease or on an ACE inhibitor, ARB, or spironolactone, it is a hidden way to push blood potassium into the danger zone. Whole foods spread potassium out and come packaged with the kidney doing its job; concentrated potassium chloride does not.
11. What this means for you
For most healthy people, the takeaway is reassuring: eat potassium-rich whole foods — leafy greens, beans, potatoes, avocado, fruit — and your kidneys keep the blood level in that tight 3.5–5.0 window automatically. The people who need to pay real attention are those with kidney disease, those on the blood-pressure and diuretic medicines named above, and anyone with unexplained palpitations, severe muscle weakness, or fainting — all of which can be the body's way of reporting a potassium problem the ECG would confirm in seconds. Potassium is not an exotic supplement to chase; it is the quiet setting that keeps the most important rhythm in your body in tune.