PHYS - Cardiac Electrophysiology Flashcards
NERNST EQUATION
- E = 61.5 mV/decade*log([X]o/[X]i)
RESTING MEMBRANE POTENTIAL
- Electrodiffusion - influence of transmembrane ion gradients on RMP
- Influenced by membrane permeability to Na and K
- Approximately equal to Ek because of high Pk
- Some permeability of the membrane to Na+; therefore, RMP =/= Ek by Nernst Equation
- GHK equation, modified to account of Pna/Pk (0.02), value is much closer to actual RMP
- Pna causes a slight (+5 to +10 mV) depolarization of RMP
- At RMP, no Pca or Pcl
- Influenced partially by Na-K pump hyperpolarization (up to -10 mV) to RMP
- Bringing it closer to Ek (net +1 out)
RMP OF DIFFERENT CONDUCTORS
SA
-55 mV to -60 mV
High Na:K permeability, less polarized
Slowest
AV
-60 mV to -65 mV
High Na:K permeability, less polarized
Slow
Atrial/Ventricular fibers
-80 mV
Low Na:K permeability, more polarized
Fast
Purkinje fibers
-90 mV
Low Na:K permeability, more polarized
Fastest
PHASES OF ACTION POTENTIAL:
ATRIAL/VENTRICULAR FIBERS & PURKINJE FIBERS
-
Atrial/Ventricular fibers and Purkinje fibers
- Phase 0: Depolarization
- Pk almost 0, contributes to plateau
- Na+ channels open at -65 mV
- Current: I, Na
- Phase 1: Repolarization
- Na+ channels spontaneously close
- K+ transient outward channels open (at -30 mV)
- Current: I, KO
- Phase 2: Plateau
- Ca2+ channels open (-40 mV)
- K+ delayed rectifier channels open (-20 mV)
- Current: I, Ca and I, K
- Phase 3: Repolarization
- Ca2+ channels close
- K+ inward rectifier channels open (-20 mV)
- These are the “leak channels”
- At depolarized potentials, Mg2+/sporamine/spermine block these inside the membrane
- Repolarized to -20 mV, Mg2+ and polyamines dissociate
- Current: I, K1
- Phase 4: Resting Membrane = Diastole
- Maintained by K+ inward rectifier channels (leak channels)
- Pk highest
- Current: I, K1
- Phase 0: Depolarization
PHASES OF ACTION POTENTIAL:
SA/AV NODES
- Phase 0: Slow depolarization
- Ca2+ channels open at -40 mV
- Deactivate based on time and voltage
- K+ rectifier channels are delayed, open after
- Still depolarize because 2+ vs 1+
- Current: I, Ca2+
- Ca2+ channels open at -40 mV
- Phase 1: Not seen because no Na+ involved
- Phase 2: Not seen because Ca2+ is slow to depolarize, K+ can kind of keep up
- Phase 3: Gradual repolarization
- K+ rectifier already open, starting to inactivate
- Current: I, K at first then I, f
- When MPD reached (Maximum Diastolic Potential -55 to -60 mV), free channels open
- Permeable MAINLY to Na+, but also K+
- I, funny = I, f
- As I, K switches to I, f move into Phase 4
- Phase 4: Resting Membrane = Diastole
- I, f brings current to -40 mV = pacemaker current
- Phase 0 starts again
- No Na+ involvement either because of lack of sodium channels and/or because Na+ channels in a resting membrane are favored to be inactive by sustained depolarization
- SA/AV node RMP = -55 mV to -65 mV, depolarized essentially
ACTION POTENTIAL SPEEDS, MAXIMUM UPSTROKE VELOCITY VS RMP
- At rest/steady-state a depolarized MP will favor the inactivation of Na+ channels
- Ex: if extracellular K+ ([K+]o) is high (ex: ischemia) = depolarized
Low [K+]o
Na+ channels activated
Fast Response
Monophasic
Increase [K+]o
Some Na+ channels inactivated
Depressed Fast Response
Monophasic
Increase [K+]o more
More Na+ channels inactivated
Biphasic upstroke because of greater
Ca2+ channels contribution
Depressed Fast Response
Biphasic
High [K+]o
Na+ channels inactivated
Depolarization by Ca2+ only
Slow Response
Monophasic
- More depolarization of RMP = greater Vmax = faster conduction velocity
- Maximum upstroke velocity depends on number of open Na+ channels
- Hence SA/AV nodes (no Na+ channels) are slower
ACTION POTENTIAL PROPEGATION AND CONDUCTION VELOCITY
- SA/AV = Ca2+
- High automaticity (spontaneous depolarization)
- Purkinje/atrial/ventricular = Na2+
- Threshold level of depolarization must be reached to initiate all-or-none response/propagation of AP
- Action potential is propagated through GJs in a domino effect
- Most cardiac fibers don’t have detrimental conduction, is sustained at full force thru entire muscle
-
Conduction velocity is determined by
- Overshoot (mV above 0)
- Vmax, maximum upstroke velocity
- Diameter of fiber (larger = faster)
REFRACTORY PERIOD
-
Refractory period depends on
- Relationship of sodium conductance (Gna) and membrane potential
- Recovery of Na+ channel inactivation
- Magnitude of K+ efflux during repolarization
-
Absolute/Efferent - impossible to elicit a second AP
- Long!
- Prevents summation of abnormal APs
- Allows ventricles to fill before contraction
-
Relative - a supranormal stimulus can elicit a second AP
- Shorter
Three ways AP is affected by ANS
- Change slope of Phase 4 (change depolarization)
- Change threshold for depolarization
- Change MDP
EFFECTS OF THE ANS ON ACTION POTENTIALS
- Sympathetic (beta-1 adrenergic)
SA node
Increase firing rate by increasing depolarization through increased I, F and I, Ca
AV node
Increase conduction velocity by increasing excitability and propagation
Atria/Ventricles
Increased contractility by increasing I, Ca
- Parasympathetic (M2, Ach)
SA node
Decrease firing rate by lowering MDP and decreasing depolarization
AV node
Decreased excitability (b/c of slower SA firing), reduced propagation to other fibers
Atria
Decreased AP duration by opening Ach ligand-gated K+ channels
Ventricle
No effect
HYPERKALEMIA / HYPOKALEMIA
Hypokalemia
Low [K+]o
Increased automaticity
More negative RMP = increased spontaneous depolarization, proarrhythmia
Increased AP duration
Ventricular arrhythmia
Hyperkalemia
High [K+]o
Decreased automaticity
More positive RMP = decreased depolarization, slowed contractions
Decreased conduction velocity
Slow HR
