Cardiac Action Potential Flashcards
Major cause of neural action potential
Increase in permeability of the membrane to Na+
Voltage-gated Na+ channels open rapidly
After minimal delay, these channels close automatically
Contributors to repolarization
After peak action potential is reached and membrane potential begins to return to resting
- Na+ channels inactivation gates are closed
- Voltage gated K+ channel are open
- Membrane permiability to Na+ decreases and permeability to K+ continues to rise
Endocardium and Epicardium
Endocardium of ventricles receive action potentials prior to epicardium
Right ventricle epicardium before left ventricle epicardium
Conduction Velocity
Fiber size is important
Large fibers have faster AP transmission; greater velocity
Purkinje (and atrial pathways)> atrial and ventricular muscle >AV node
Delay in AV allows atria to empty into ventricles before ventricles contract
The more rapid the phase 0 occurs-steeper phase 0
Differences in the speed of either voltage gated Na+ or Ca2+ channels
SA Node (Pacemaker)
SA node resting membrane potential gradually depolarizes until it reaches threshold, then it “fires” albeit slower than other regions
This spontaneous depolarization makes the SA node the pacemaker as it has “automaticity”
Opening of funny voltage-gated Na+ channels that open when membrane is repolarized
AV Node similar to SA
Phase 4 has even slower depolatization than the SA Node
Thus, the AV node typically doesn’t reach threshold until it receives a triggering signal from the SA node
Phase 0
Due to opening of slow Ca2+ channels and closing of special K+ channels
This is a balancing act between Ca2+ in and modulating K+ out
Phase 3
Due to closing of Ca2+ gates and opening of special K+ gates
Reversal of phase 0
Action potentials in fast tissues/fibers resting membrane potential
Phases 4-1
Phase 4 is the resting potential and is sustained by high K+ conductance
Phase 0 is rapid upstroke caused by crossing threshold and voltage gated Na+ channels opening
Phase 1 is small repolarization is caused by voltage gated Na+ channels closing and some K+ channels opening
Action potentials in fast tissues/fibers resting membrane potentials
Phase 2-3
Phase 2 or plateau phase is sustained by slow opening of voltage gated Ca 2+ channels and closing of “special”, voltage gated K+ channels. Functionally this prolongs contraction and is fundamentally different than observed in skeletal muscle
Phase 3 or complete repolarization is caused by slow voltage gated Ca2+ channels closing and K+ channels opening
Defective Conduction Velocity
Disruption of these conduction circuits has big impact on heart function
AV node dps–further delays conduction (AV block)
Purkinje fiber dps–disrupts natural conduction and contraction of ventricles (arrhythmias)
Refractory Periods
Refractory periods is when the electrolyte gates have not “reset” sufficiently to allow a second AP to be generated
Refractory period is important to help prevent arrhythmias, and are longer in cardiac cells than neurons
Conduction of action potential is weaker is stimulated during RRP
General Refractory Periods
Absolute refractory period (ARP): No depol
Relative refractory period (RRP): AP can be generated but will have an abnormal conduction
Supranormal period (SNP): Cell is more excitable than normal
Term: Chronotropic
Effect changes rate of depolarization of SA node and therefore heart rate
Positive=faster
Negative=Slower
Dromotropic
Effect is speed of conduction
