Normal Cardiac Electrical Activity Flashcards
What is the Nernst Equation?
E = (61/z)(log([C]o/[C]i))
Intracellular/Extracellular concentrations of sodium and membrane potential
IC = 10 mM
EC = 145 mM
Eq potential = 71 mV
Intracellular/Extracellular concentrations of potassium and membrane potential
IC = 120 mM
EC = 4.5 mM
Eq potential = -88 mV
Intracellular/Extracellular concentrations of calcium and membrane potential
IC = 10-4 mM
EC = 2 mM
Eq potential = 132 mV
What is the primary transporter that maintains the cell membrane ion gradient?
NA+/K+ ATPase
What are some membrane channel control mechanisms?
Gating
- voltage
- time
- direct agonist
- G protein
- calcium
Modulation
- increases in phosphorylation
- oxidation-reduction
- cytoskeleton
- calcium
- ATP
What is the equation for conductance?
g = 1/R or g = I/E
Phase 4 Depolarization
resting membrane potential
determined mainly by gK which is 100x greater than gNa
the predominant current is the inward rectifier K current
membrane potential is -85 mV to -92 mV
Phase 0 Depolarization
upstroke of the action potential
INa and ICa(L-type)
m gate
the activation gate of sodium channels that open when the threshold potential is reached (about -70 mV)
opening and closing of the gates are both time and voltage dependent
h gate
the inactivation gate that closes after the m gate opens for a brief period of time
prevents excess influx of sodium
L-type calcium channel
controleld by d and f gates, which represent their activation and inactivation probabilities
the f gate closes much more slowly than the h gate
Phase 1 Depolarization
inactivation of INa and more slowly ICa
transient outward potassium current
possible contribution by other species such as Cl-
creates notch in action potential
more prominent in ventricular epicardial than endocardial cells
Phase 2 Depolarization
plateau, mainly due to Ca2+ current because channels remain open much longer than the Na+ channels
residual, very small component of Na+ current
at positive potentials, resistance to K+ is high, so ions can’t contribute as much - called inward rectification
main current during this phase is the delayed rectifier K channel - broken down into IKr and IKs
ultrarapid component IKur in atria - rapid activation, slow inactivation
slow activation gives rise to the plateau
inward rectification
inward rectifier K+ channels cannot conduct ions outward at positive membrane potentials because of an cytoplasmic Mg2+ block (also spermine and spermidine)
K+ can’t contribute to Vm as a result, and only an inward curent can occur