The Lab / Core medicine / Lesson 7
Every heartbeat begins as a tiny voltage swing inside each heart cell. Watch three kinds of charged particle draw that swing, in the cells that set the pace and the cells that squeeze, then see how four classes of heart-rhythm drugs reshape it.
Educational, not for clinical use
Build the signal
Your heart is built from millions of heart muscle cells, joined end to end. Before each beat, a tiny electrical signal sweeps from cell to cell, and each cell squeezes as it passes. This lesson follows that signal inside one cell.
Build the signal
Each cell is wrapped in a thin skin, the cell membrane. The inside carries a different electrical charge from the outside, like a tiny battery. That difference is the cell’s voltage. At rest, the inside is negative.
Build the signal
Salts dissolved in body water split into charged particles called ions. Three matter here: sodium and calcium, crowded mostly outside the cell, and potassium, crowded mostly inside. Each tends to spread toward where it is scarce, carrying its charge.
Build the signal
Ion channels are doors in the membrane, each letting one kind of ion through when open. In a resting heart muscle cell, potassium doors are the main ones open. Potassium seeps out, taking positive charge with it: that leaves the resting potential, negative inside.
Build the signal
Plot the muscle cell’s voltage against time, and each beat draws one shape: a sharp rise, a long flat top, then a fall back to rest. That shape is the action potential. The next three steps build it, piece by piece.
Build the signal
When the signal arrives from a neighbouring cell, fast sodium channels snap open. Sodium floods in, and the voltage leaps from negative to slightly positive in a blink. This upswing is depolarization, and it passes the signal on to the next cell.
Build the signal
The sodium doors shut almost at once, but slower calcium channels open. Calcium trickles in and holds the voltage up in a long, nearly flat stretch: the plateau. That calcium also triggers the squeeze, so the cell contracts during the plateau.
Build the signal
As the calcium doors close, more potassium doors open. Potassium flows out, carrying positive charge away, and the voltage falls back to rest. This return is repolarization. Sodium, calcium, potassium: up, flat, down.
Build the signal
While the voltage is high, the sodium doors stay locked and no new upswing can start: the refractory period. Late in the fall, only a stronger-than-usual signal can start one. This pause keeps the muscle from being driven into one long, unbroken squeeze.
Build the signal
Pacemaker cells, gathered in a small patch called the sinoatrial node, never settle at rest. Sodium leaks in, so their voltage drifts slowly upward. When it reaches a trigger level, the threshold, they fire, and the signal spreads to the muscle.
Build the signal
Pacemaker cells have few working fast sodium channels. Their upswing is carried by calcium channels instead, so it rises gently rather than leaping. Potassium then brings the voltage back down, and the slow drift starts again.
Build the signal
The heart rate is the number of beats each minute. Noradrenaline, from the body’s accelerator nerves, steepens the drift, so beats come sooner. Acetylcholine, from the brake nerves, lowers and flattens it, so they come later. Lesson 6 covers these nerves.
Build the signal
From the sinoatrial node the signal spreads cell to cell, each upswing setting off the next. Fast wiring carries it to the ventricles, the two big pumping chambers, and it sweeps through their muscle. Quicker upswings mean quicker spread.
Build the signal
An electrocardiogram records the heart’s signal through skin pads. Its spike, the QRS complex, is the signal sweeping through the ventricles; slower spread widens it. The Q-T interval runs on to the end of the next bump, when ventricle cells finish their fall.
Build the signal
A pacemaker cell drifts to threshold and fires; the signal spreads, and each muscle cell rises with sodium, holds with calcium and falls with potassium. Two key measures: the heart rate, set by the drift, and the action potential’s length, seen as the Q-T interval.
What changes it
Antiarrhythmic drugs calm abnormal heart rhythms by reshaping the action potential. Class I drugs block fast sodium channels. Class IA slows the upswing, so the QRS complex widens, and also lengthens the plateau and the Q-T interval.
What changes it
Class IB drugs also block sodium channels, but let go quickly between beats, so at a normal heart rate the upswing and the QRS complex barely change. The plateau gets a little shorter, and the Q-T interval shortens.
What changes it
Class IC drugs block sodium channels strongly and let go slowly. The upswing becomes slower and lower, the signal spreads more slowly, and the QRS complex widens. The plateau and fall are untouched, so the Q-T interval stays about the same.
What changes it
Noradrenaline acts on pacemaker cells through beta receptors, docking sites on the cell. Beta-blockers (class II) cover them, so the drift to threshold flattens, each beat comes later, and the heart rate falls. Muscle cells also squeeze less hard.
What changes it
Class III drugs block potassium channels, so potassium leaves the muscle cell more slowly. The plateau lasts longer and the fall comes later, so the refractory period and the Q-T interval both lengthen, giving stray signals less chance to restart a beat.
What changes it
Class IV drugs block the calcium channels that power the pacemaker’s upswing and help its drift. Pacemaker cells reach threshold later and rise more slowly, so the heart rate falls. In muscle cells, the plateau sits lower and the squeeze weakens.
Start with Next, or use the arrow keys. Shapes and timings are illustrative, not measurements.
Loading reference values…
Normal teaching baseline.
The blue line on each bar is an illustrative teaching model, not a patient measurement. A shaded band is the textbook range; a single black tick is a textbook typical value where the book gives no range. Arrows come from the cited source for the selected state.
An illustrative teaching model of one pacemaker cell, one ventricular muscle cell and the electrocardiogram they make. Turn the nerves up or down, block each kind of channel, and watch the shapes change. The faint dashed lines are the normal state.
The shapes are drawn from a few settings, not solved from ion-current equations, and every result is relative to a normal state. The muscle cell’s upswing time grows with the fraction of fast sodium channels blocked, and its peak drops a little. The plateau lengthens with potassium block, shortens a little with late sodium block, and sits lower with calcium block; the fall slows with potassium block. The refractory period ends when the voltage has fallen most of the way back to rest. The QRS width stands for the time the signal takes to spread through the ventricles, which grows as the upswing slows; the Q-T interval stands for the plateau plus the fall. In the pacemaker cell, the voltage between beats rises with the beta signal (sympathetic drive minus beta block) and falls with vagal drive; the drift slope rises with the beta signal and falls with vagal drive and calcium block; calcium block also slows its upswing, and potassium block slows its fall. The heart rate is one over the time from one beat to the next. Squeeze strength rises with calcium entry and the beta signal. Class IB is shown as a very light fast-sodium block (its quick release between beats leaves little block at a normal rate) plus late sodium block. Real drugs often have more than one action, which the model leaves out, along with the atria, the conduction wiring, blood potassium and heart-rate effects on the action potential. In the Clinical values tab, relative results are scaled from the textbook values, as that tab explains.