Physiology 3120 Lecture Notes - Lecture 30: Intercalated Disc, Cardiac Muscle Cell, Tetanic Contraction
15 May 2018
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Lecture 30 – Action Potentials in the Heart
SA node - Characteristics responsible for self-excitation:
- To cause a slow depolarization to threshold to fire AP:
o Greater Na+ and Ca++ permeability (positive inward current) – leak into the cell
o K+ permeability declines during diastole (relaxation phase)
Conduction system of the heart
- AP spreads through the heart
- Contractile cells are joined by intercalated disks that contain gap junctions, so the AP can
jump from cell to cell and spreads as a wave in the contractile cells
- There is a functional syncytium: atria contract all at once and ventricles contract as well
- VS. SKELETAL MUSCLE:
o To contract, need motor nerves and motor units
o To increase the force of a muscle contraction, recruit more motor units
o This does not occur in cardiac contractile cells
o When one cell fires, they all fire and the wave propagates through gap junctions
causing all the cells to contract in a syncytium
o It is possible to sum muscle twitches together in skeletal muscle to form a smooth,
tetanic contraction
o DO NOT recruit motor units in a cardiac muscle cell
Action potentials in ventricular contractile cells
- Duration for contractile cells ≈ 300 ms (longer than neural)
- Membrane potential: -90 mV → +20 mV (different than SA nodal which starts at -60 mV)
- Permeability’s of ions:
o Chloride plays a small role in the action potential
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Phases:
(0) Depolarization
- AP starts in the SA node and propagates outward from there
- Action potential propagates from ventricular cell to ventricular cell through intercalated
disks which contain gap junctions (there are no nerves here)
- Current from neighboring cells depolarizes a cell (gap junctions)
- There is a depolarizing wave coming from the adjacent cell
- Depolarizing wave opens fast VG sodium channels (similar to VG channels in neuronal APs)
- Opens fast VG Na+ channels and Na+ enters very rapidly (= fast inward current)
- Membrane potential reaches, and depolarizes to +20 mV very rapidly
- Does not last very long but there is a rapid increase in the permeability of sodium
(1) Rapid repolarization
- Sodium VG channels are fast – open and close (inactivate) very quickly
- Na+ permeability decreases rapidly (fast Na+ channels close)
- Sodium stops flowing into the cell
- Cl- channels open and Cl- flows in (only briefly)
o There is a brief period of chloride movement – it is very short
o This contributes to the rapid repolarization of the membrane
- VG K+ channels open (increase permeability) and K+ begins moving out = repolarize
membrane
- Repolarization phase does not last very long because the chloride channels close but the
potassium channels are still open (potassium is still leaving)
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(2) Plateau phase
- AP triggers opening of slow (L type) Ca++ VG channels → Ca++ moves in slowly causing slow
inward current
o Channels are slow to respond to the depolarization
o L-type: long-lasting
o There channels are the ones seen in the depolarizing phase of the SA nodal AP
▪ When threshold is reached, slow L type calcium channels open
▪ SAME CHANNEL – used in different place for a different function
- This inward Ca++ current almost balances the outward K+ current
- It is not perfect – which is why there is a slight decline in the plateau phase
- = there is more potassium leaving than there is calcium coming in
- This results in a very long duration action potential – want it to last a long time
- Result is a relatively stable membrane potential plateau phase
(3) Restoration of resting potential
- Slow (L-type) Ca++ channels begin closing
- Potassium channels are still open
- Inward movement of Ca++ decreases while K+ continues to move outwards
- Potassium continuing to flow out causes the membrane potential to repolarize to resting
(4) Resting potential
- Membrane potential returns to -90mV
Refractory periods
- Effective (absolute) refractory period (BOX A)
o Due to inactivation of fast Na+ channels (and possibly inactivation of Ca++ VG
channels)
o CANNOT fire another action potential during this period (cannot be summed)
o It is a long period and lasts majority of the AP
- Relative refractory period (BOX B)
o Lasts the rest of the AP
o Caused mainly by K+ efflux (leaving the cell)
o Similar to the neural AP
o Can still fire another AP but the stimulus must be stronger
- Refractory periods occupy the entire AP
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find more resources at oneclass.com
Document Summary
Lecture 30 action potentials in the heart. To cause a slow depolarization to threshold to fire ap: greater na+ and ca++ permeability (positive inward current) leak into the cell, k+ permeability declines during diastole (relaxation phase) Contractile cells are joined by intercalated disks that contain gap junctions, so the ap can jump from cell to cell and spreads as a wave in the contractile cells. There is a functional syncytium: atria contract all at once and ventricles contract as well. It is possible to sum muscle twitches together in skeletal muscle to form a smooth, tetanic contraction: do not recruit motor units in a cardiac muscle cell. Membrane potential: -90 mv +20 mv (different than sa nodal which starts at -60 mv) Duration for contractile cells 300 ms (longer than neural) Permeability"s of ions: chloride plays a small role in the action potential. Ap starts in the sa node and propagates outward from there.
