Week 9: Cardiovascular
1. Describe ion transport during each phase of cardiac conduction
Action Potentials:
● Cardiac myocyte - much longer than nerve cell action potential
○ Can’t fire as strong as nerve bc life
● Five phases of non-pacemaker action potential (Myocyte = contractile cell)
○ Phase 0: depolarization
■ Depolarizing currents from adjacent cells - reach threshold (-70mV)
→ threshold opens voltage gated Na channels → K channels from
phase 4 close = rapid depolarization of this cell (fast channels) open for
almost no time (maybe millisecond or two)
■ Na channels open (at threshold = -70mV)
○ Phase 1: Partial Repolarization
■ Transient K+ channels open and K+ efflux (out of cell)
■ Na channels close; K channels open
○ Phase 2: Plateau
■ L = Long (L type channels open longer)
■ L type Ca channels open simultaneously with K channels → you get a
plateau (Ca into cell is + so it offset the K+ leaving the cell)
■ At end of phase 2: Ca channels close K stays open
● Ca channels open (flow in)
● K channels still open (flow out)
○ Phase 3: Repolarization
■ Ca channels close but K+ remains open → repolarizing back to RMP
● Moves closer to RMP
○ Phase 4: Resting Membrane Potential of -80 bw action potentials
■ -90mV (repolarized at below threshold) Na channels close (Na channels
responsible for repolarizing currents) K channels open (keep RPM at
-90 → K is leaving taking + charge and keeping cell at repolarization)
● K channels open, moving in both directions (mostly out)
● Na channels also open
● Refractory Period: in atria and myocytes (contractile cells)
○ During phases 0,1,2 and part of 3 the cell is refractory to the initiation of new
action potentials → cannot accept new PAs
○ Why do we have refractory pd?
■ Many antiarrhythmic drugs increase increase the Refractory Period
which reduces myocyte excitability (essentially elongate action
potentials)
● Limits the frequency of cardiac contractions
● Allows for adequate filling time
● Prevents sustained contractions
Pacemakers - SA node
● Cells within the sinoatrial (SA) node comprise the primary pacemaker site
● No true resting potential
○ Generate regular, spontaneous action potentials
● Depolarizing current is carried primarily by relatively slow, inward CA++ currents
○ No Na channels channels in SA nodes
● Three phases of pacemaker Action potential:
, ○ Phase 0: Rapid depolarization (no resting membrane potential)
■ Voltage gated Ca channels open, calcium moves in and we get
depolarization
■ Open voltage-gated L-type Ca channels
● Close at end of phase 0
● Stimulus that causes an opening of voltage gated calcium
channels
○ Phase 3: Repolarization
■ Open of K channels → in response to voltage that is achieved when
depolarize the cell → K efflux from the cell → membrane potential
down
● Open K channels
○ Phase 4: Slow depolarization
■ K channels close → at this voltage opening of unique voltage gated
Na channels (funny channels) open at mV of -60 (lower voltage than
typical Na channels) → only stay open long enough to bring
membrane potential to -50 (close) T (transient) type of calcium
channel - influx of Ca into cell until we hit threshold (-40) L type Ca
channels open → we get depolarizing current
● “Funny” Na channels open at -60mV, transient (close quickly)
○ Take from -60 to -50
● At -50, Ca channels open (t-type/transciet), close at -40
● At -40, L type Ca channels open
○ Depolarization: Contraction
■ Ca channels open during phase 2, comes into myocytes
■ Sarcoplasmic reticulum is reservoir for calcium
● Ryanodine receptors are ligand-gated ca receptors
● Ca is released into cell from SR (in addition to Ca channels)
● Increase Ca in contractile cell
■ Ca binds to troponin
● Troponin moves tropomyosin (rotates)
● Myosin heads interact with bind site on actin
● ATP activated, generates sliding of Actin and tropomyosin along
each other = ctx
■ ALL ABOUT GETTING CA TO CELL
2. Describe the features of the four major groups of antiarrhythmic drugs
● Sodium Channel Blockers (CLASS I) - most complex bc subtypes
○ Act on myocytes (not pacemakers cells)
○ Bind to sites in the subunit of the sodium channel
○ Effect on the action potential is to prolong depolarization (phase 0)
○ Are use dependent: block more channels at faster HR
■ Bind to preferentially to open or inactivated channels; more channels are
open when HR is fast
■ States of NA channels
● Resting state - closed but capable of opening (at resting potential
-70mV)
● Open (activated) from threshold to peak potential -50 - +50mV)
● Inactivated (Refractory to reaching threshold) - from peak to
resting potential +30 mV to -70
1. Describe ion transport during each phase of cardiac conduction
Action Potentials:
● Cardiac myocyte - much longer than nerve cell action potential
○ Can’t fire as strong as nerve bc life
● Five phases of non-pacemaker action potential (Myocyte = contractile cell)
○ Phase 0: depolarization
■ Depolarizing currents from adjacent cells - reach threshold (-70mV)
→ threshold opens voltage gated Na channels → K channels from
phase 4 close = rapid depolarization of this cell (fast channels) open for
almost no time (maybe millisecond or two)
■ Na channels open (at threshold = -70mV)
○ Phase 1: Partial Repolarization
■ Transient K+ channels open and K+ efflux (out of cell)
■ Na channels close; K channels open
○ Phase 2: Plateau
■ L = Long (L type channels open longer)
■ L type Ca channels open simultaneously with K channels → you get a
plateau (Ca into cell is + so it offset the K+ leaving the cell)
■ At end of phase 2: Ca channels close K stays open
● Ca channels open (flow in)
● K channels still open (flow out)
○ Phase 3: Repolarization
■ Ca channels close but K+ remains open → repolarizing back to RMP
● Moves closer to RMP
○ Phase 4: Resting Membrane Potential of -80 bw action potentials
■ -90mV (repolarized at below threshold) Na channels close (Na channels
responsible for repolarizing currents) K channels open (keep RPM at
-90 → K is leaving taking + charge and keeping cell at repolarization)
● K channels open, moving in both directions (mostly out)
● Na channels also open
● Refractory Period: in atria and myocytes (contractile cells)
○ During phases 0,1,2 and part of 3 the cell is refractory to the initiation of new
action potentials → cannot accept new PAs
○ Why do we have refractory pd?
■ Many antiarrhythmic drugs increase increase the Refractory Period
which reduces myocyte excitability (essentially elongate action
potentials)
● Limits the frequency of cardiac contractions
● Allows for adequate filling time
● Prevents sustained contractions
Pacemakers - SA node
● Cells within the sinoatrial (SA) node comprise the primary pacemaker site
● No true resting potential
○ Generate regular, spontaneous action potentials
● Depolarizing current is carried primarily by relatively slow, inward CA++ currents
○ No Na channels channels in SA nodes
● Three phases of pacemaker Action potential:
, ○ Phase 0: Rapid depolarization (no resting membrane potential)
■ Voltage gated Ca channels open, calcium moves in and we get
depolarization
■ Open voltage-gated L-type Ca channels
● Close at end of phase 0
● Stimulus that causes an opening of voltage gated calcium
channels
○ Phase 3: Repolarization
■ Open of K channels → in response to voltage that is achieved when
depolarize the cell → K efflux from the cell → membrane potential
down
● Open K channels
○ Phase 4: Slow depolarization
■ K channels close → at this voltage opening of unique voltage gated
Na channels (funny channels) open at mV of -60 (lower voltage than
typical Na channels) → only stay open long enough to bring
membrane potential to -50 (close) T (transient) type of calcium
channel - influx of Ca into cell until we hit threshold (-40) L type Ca
channels open → we get depolarizing current
● “Funny” Na channels open at -60mV, transient (close quickly)
○ Take from -60 to -50
● At -50, Ca channels open (t-type/transciet), close at -40
● At -40, L type Ca channels open
○ Depolarization: Contraction
■ Ca channels open during phase 2, comes into myocytes
■ Sarcoplasmic reticulum is reservoir for calcium
● Ryanodine receptors are ligand-gated ca receptors
● Ca is released into cell from SR (in addition to Ca channels)
● Increase Ca in contractile cell
■ Ca binds to troponin
● Troponin moves tropomyosin (rotates)
● Myosin heads interact with bind site on actin
● ATP activated, generates sliding of Actin and tropomyosin along
each other = ctx
■ ALL ABOUT GETTING CA TO CELL
2. Describe the features of the four major groups of antiarrhythmic drugs
● Sodium Channel Blockers (CLASS I) - most complex bc subtypes
○ Act on myocytes (not pacemakers cells)
○ Bind to sites in the subunit of the sodium channel
○ Effect on the action potential is to prolong depolarization (phase 0)
○ Are use dependent: block more channels at faster HR
■ Bind to preferentially to open or inactivated channels; more channels are
open when HR is fast
■ States of NA channels
● Resting state - closed but capable of opening (at resting potential
-70mV)
● Open (activated) from threshold to peak potential -50 - +50mV)
● Inactivated (Refractory to reaching threshold) - from peak to
resting potential +30 mV to -70
