Phase 4 funny current, phase 0 calcium influx, phase 3 potassium efflux
Mnemonic
“Three phases, not five, and no phase 1 or 2”:
- Phase 4 - spontaneous depolarisation, the pacemaker potential, driven by the funny current (If), a slow inward sodium leak. This is what makes the cell automatic
- Phase 0 - upstroke, driven by calcium through L-type channels, not sodium. This is why it is slow
- Phase 3 - repolarisation, potassium efflux
“Pacemaker cells depolarise with calcium; myocytes depolarise with sodium.” That single difference explains everything else: the slow upstroke gives slow conduction, which is why the atrioventricular node delays the impulse, and why calcium channel blockers and beta blockers slow the rate and the node.
Rate is set by the slope of phase 4: sympathetic stimulation steepens it (raising the rate), vagal stimulation flattens it and makes the maximum diastolic potential more negative.
Ivabradine blocks If specifically, which is why it slows the sinus rate without any negative inotropic or blood pressure effect.
Expansion
- Phase 4 - spontaneous slow depolarisation, the pacemaker potential, driven by the funny current (I-f, a sodium influx) plus calcium influx and falling potassium efflux
- Phase 0 - upstroke driven by L-type calcium channels, not sodium; this makes it slow
- Phase 3 - repolarisation by potassium efflux
There is no phase 1 or 2, and no stable resting potential; the maximum diastolic potential is about -60 mV.
Three consequences:
- The slope of phase 4 sets heart rate. Sympathetic stimulation steepens it, vagal stimulation flattens it and makes the maximum diastolic potential more negative
- The calcium-dependent upstroke explains slow conduction through the sinoatrial and atrioventricular nodes, and why non-dihydropyridine calcium channel blockers slow rate and conduction
- Ivabradine blocks the funny current selectively, slowing rate without any negative inotropic effect