• pacemaker cells: oval; small (3-9m m); reduced # myofibrals, gap junctions; primarily in SA node
• spontaneous electrical activity
• AV and Purkinje have similar cells, but normally do not act as pacemakers
• conducting cells: rod-shaped; large (50 m m diameter); reduced myofibrils; high gap junctions
• found in AV, Purkinje, bundle of His and branches
• conduction slowest through AV node (allows for max ventricular filling and contraction)
• contractile cells: mid-sized (10-15 m m); high myofibrils, gap junctions, T-tubes; main cell type in atria and ventricles
• high gap juntion density leads to fast conduction of impulses

• [Vm = Na (+70), K (-94), Ca (+132)]
• Nernst equation: E_ion= 60 log ([ion]_out/[ion]_in)
• Ohm’s Law: I = G(V_m-E_rev) or (current) = (conductance) x (driving force)
• Parallel batteries model: V _m = G^*_Na E_NA + G^*_Ca E_Ca + G ^*_K E _K
• when membrane becomes more perm to an ion, V_m tends towards E_rev for that ion

Fast response – contractile cells

• 
• phase 4: resting membrane potential
• due to large background K⁺ conductance I_K1 (inwardly rectifying K⁺ channels)
• very large K⁺ conductance stabalizes RMP; little spon depol leading to arrhythmias
• phase 0: upstroke and overshoot
• rapid opening (and inactivation) of voltage gated Na channels
• very similar to channels in nerves; shows positive feedback
• if RMP is slightly depol, some Na⁺ channels cannot reactivate, and upstroke velocity is decreased
• depolarization also causes K⁺ channels (I_K1) to close, so V_m can move away from E_K
• phase 1: initial repolarization
• rapid closing of Na⁺ channels
• transient outward K⁺ channels can make steeper repol; but not found in all cells
• phase 2: plateau
• prolonged AP due to balance of Ca⁺⁺ and K⁺ channels
• Ca⁺⁺ channels: need to be more depol to open; activate and inactivate slower than Na⁺
• delayed rectifier K⁺ channels: open on depol until repol (no inactivation); very slow
• phase 3: final repolarization
• comes when balance of Ca⁺⁺ and K⁺ channels favors K⁺
• Ca⁺⁺ channels slowly inactivate
• slow opening of delayed rectifier channels; also opening of I_K1 once repolarized (RMP)

• 
• phase 4
• no true resting potential (not stable); called maximum diastolic potential (MDP)
• no I_K1 channels, so not as neg as RMP in fast response cells
• two channels responsible for membrane conductance in phase 4
• K⁺ Channels: delayed rectifier (I_K)
• takes time to close so hyperpolarize; analogous to afterhyperpolarization
• Pacemaker channels (funny channels)
• equally permiable to Na⁺⁺ and K⁺ (E_rev ~ -15 mV)
• activated upon hyperpolarization; contribute to depolarization
• phase 0: upstroke
• few Na⁺⁺ channels, so mostly due to Ca⁺⁺ channels which are slower to open and close
• also, phase 4 is more depolarized so Na⁺ channels more likely inactivated
• phase 3: repolarization
• slow decrease in Ca⁺⁺ conductance due to inactivation
• slow increase in K⁺ conductance (I_K)

• purkinje cells: unstable phase 4 because also have funny channels; so can have pacemaker activity
• artrial cells: have I_K(ACh) channels instead of I_K1; less voltage dependent so more open during plateau
• leads to faster repolarization and shorter AP in atria
• activated also by ACh; found in AV and SA nodes

• Na⁺ channel blockers (lidocaine)
• increase threshold for excitation, decrease rate of depolarization in fast response
• results in decrease in rate of conduction of AP
• K⁺ channel blockers (procainamide, quinidine)
• increases AP duration
• few drugs can just block K⁺ channels, usually also Na⁺
• Ca⁺⁺ channel blockers (verapamil, diltiazem)
• decrease rate of depolarization in slow response
• results in slowing of conduction of AP

• depolarizes RMP which causes Na⁺ channel inactivation which results in decrease of upstroke velocity and therefore conduction velocity
• increased K⁺ concentration outside cell acutually increases K⁺ conductance (I_K) during AP which leads to a decreased AP duration

• little effect on RMP
• decreases conductance of K channels (I_K) so increases AP duration