Cardiac Action Potentials Flashcards
RMP is set-up by:
NA/K pump (3 Na out, 2 K in) and K leak channels.
When peak action potential is reached and begins to return to RMP, what is going on? (3)
Na channel inactivation gates are closed.
VG K channels are open.
Membrane permeability to Na decreased and permeability to K increases.
Overall conduction pattern:
SA node to AV node to bundle of His (common bundle) to Perkinje fibers (branch to RV and LV).
Timing of transmission of the signal in the ventricles
Endocardium of ventricles receives AP first, then epicardium.
RV epicardium gets AP before LV.
Conduction velocity (slow to fast)
AV node < atrial and ventricular muscle < Purkinje fibers (and atrial pathways).
What is the reasoning for a delay in AV?
It allows atria to empty into ventricles before they contract.
Phase 4 in SA node
RMP gradually depolarizes until threshold, then it “fires”.
It’s opening is due to funny VG Na+ channel.
Has intrinsic, spontaneous depolarization which makes it a “pacemaker” as it has automaticity.
What causes Phase 0 in SA node?
Due to opening of the slow Ca 2+ gates and closing of K+ (b) gates.
Why is there no Phase 1 or 2 in SA APs?
There is too much scarcity of traditional VG Na (m) channels.
What causes Phase 3 in SA APs?
Due to closing of Ca 2+ and opening of K+ (b) gates (reversal of phase 0).
Cardiac AP pacemaker summary
SA node naturally depolarizes to reach threshold w/o electrical stimulation.
AV node is similar to SA node but is much slower.
Bundle of His and Purkinje fibers will remain polarized.
Phase 0 in fast tissues/fibers is caused by:
Rapid upstroke caused by crossing threshold and VG Na channels opening.
Passing threshold and AP is propagated.
Phase 1 in fast tissues/fibers is caused by:
Brief repolarization
Small repolarization via VG Na+ (m) channels closing and K+ (a) channels opening.
Inactivation gates of VG Na+ channels are closed.
Phase 2 in fast tissues/fibers is caused by:
What does it do functionally?
Plateau
Sustained by opening of VG Ca 2+ channels and closing of VG K+ (b) channels.
Prolongs contraction and is fundamentally different than observed in skeletal muscle.
Phase 3 in fast tissues/fibers is caused by:
Slow VG Ca 2+ channels closing and K+ (b) channels opening.
Relationship between phase 0 and velocity
More rapid phase 0 occurs, the steeper phase 3 and faster conduction.
This is also related to differences in the speed of either VG Na or Ca channels.
AV block
AV node damage. Further delays in conduction.
Arrhythmias
Purkinje fiber damage - disrupts natural conduction and contraction of ventricles.
Refractory periods and arrhythmias
RPs are important to prevent arrhythmias and tend to be longer in cardiac cells.
Absolute refractory period
No depolarization
Relative refractory period
AP can be generated but will have abnormal conduction.
Supranormal period
Cell is more excitable than usual.
Conduction of AP is weaker is stimulated during relative refractory period.
Chonotropic effect
Affects changes rate of depolarization of SA node and therefore HR.
Dromotropic effect
Affects speed of conduction.
Inotropic effect
Changes the strength of muscular contraction.
Lusitropic effect
Changes rate of muscular relaxation.
Parasympathetic stimulus in cardiac AP generation
Carried by vagus n.
To SA node and AV node.
NT is ACh and receptor is muscarinic (M2 and M3).
Negative chonotropic effects
Slowed opening of Na+ (f) channels in phase 4.
Hyperpolarization by increasing outward K+ current via K+ ACh channel.
Negative dromotropic effects
Reduced Ca 2+ inward current.
Increased outward K+ current via K+ ACh.
Sympathetic stimulus of cardiac AP generation
To SA node and AV node and to myocytes.
NT is NE and receptor is muscarinic.
Positive chronotropic effects
Increased opening of Na+ (f) channels during phase 4.
Increased Ca 2+ current.
Positive dromatotropic effects
Increased Ca 2+ inward during phase 2.
