Cardiovascular System Physiology Flashcards
Describe the sinoatrial node.
- The pacemaker
- Specialised cardiac muscle cells, continuous with atrial syncytium
- Generate spontaneous action potentials
- Action potentials pass to atrial muscle cells and to the AV node
Describe atrioventricular node.
- Action potentials conducted more slowly here
- Ensures ventricles receive signal to contract after atria have contracted
Describe the AV bundle
- Passes through hole in cardiac skeleton to reach interventricular septum
Describe right and left bundle branches.
- Extend beneath endocardium to apices of right and left ventricles
Describe the purkinje fibres
– Large diameter cardiac muscle cells with few myofibrils.
– Many gap junctions.
– Conduct action potential to ventricular muscle cells (myocardium)
Describe the conducting system of the heart. (8)
- Depolarisation from SA node across atria.
- Three tracts within atria conduct
depolarisation to AV node. - Conduction slows in AV node; allows atria
to empty into ventricles before vent.
systole. - Atrioventricular bundle (bundle of His)
connects AV to bundle branches - Purkinje Fibres = terminal bundle branches
- SA node generates impulses about 75x/min
- AV node delays the impulse approx. 0.1 secs
- Impulse passes from atria to ventricles via
bundle of His to the Purkinje fibres and finally
to the myocardial fibres
Describe cardiac muscle.
- Faintly striated
- Branched, mono-nucleated cells
- Connected by intercalated disc
- High conductance gap junctions
(connexons) - Desmosomes: cadherin
- Functional syncytium
- Continuous action potential
Compare cardiac muscle to skeletal muscle.
Cardiac: Action propagated from cell to
cell.
Skeletal: Action along length of single fibre
* Slow propagation in cardiac muscle
because of gap junctions and small
diameter of fibres.
* Faster in skeletal muscle due to larger
diameter fibres.
Describe the sliding filament theory (cardiomyocyte contraction)
- Ca2+ binds to TN-C on thin filaments
- Exposes site on actin which can bind to myosin head
- ATP hydrolysis supplies energy for actin-myosin conformational change
- ‘Ratcheting’ of actin-myosin and shortening of the sarcomere occurs
- Ca2+ dissociates from TN-C and myosin unbinds from actin with energy from ATP
- Cycle ends when ATP binds to myosin and the sarcomere returns to original length.
Describe cardiomyocyte contraction.
- Ca2+ enters through L-type channel
- Ca2+ -induced calcium release (CICR) occurs
- Stimulates Ca2+ release from SR
- Intracellular Ca2+ rises ~ 0.5-2μM
- Ca2+ interacts with troponin-C
- Myosin binding site on actin freed
- Actin moves over myosin causing myocyte contraction
- Intracellular Ca2+ reabsorbed into SR via the sarco-endoplasmic reticulum Ca
ATPase (SERCA) pump and removed from the cell via Na+/ Ca 2+ exchanger and
ATP-dependent Ca 2+ pump. - Ca2+ dissociates from TN-C and the binding site on actin is inhibited.
- ATP required to unbind myosin from actin and reset the sarcomere to normal length.
When does an action potential occur?
- When excitation depolarisation exceeds threshold of -70mV
- Na+ gates open
Describe Phase 0: rapid depolarisation.
- Na + permeability»_space; x100 fold
- Membrane potential rises to +20 to +30mV
- Na + gates ‘inactivated’; Na + permeability falls
Describe Phase 1: initial repolariastion
- K + permeability»_space; by conc. & elec. gradient
- Simultaneous opening of L-type voltage-gated Ca 2+ channels; inward flow Ca 2+
Describe Phase 2: Plateau phase
- K + balances Ca 2+ flow = plateau phase
- Generates cardiomyocyte contraction
- Ca 2+ channels inactivated
Describe Phase 3: Repolarisation
- K + channels remain open
- Membrane potential falls to ~ E K