CVS: Cardiac action potentials and conduction pathway Flashcards
How does initiation of heartbeat begin?
- SAN generates action potentials called pacemaker potentials, happens in absence of external stimulation (nerves, neurotransmitters, hormones)
- SAN located in upper wall of RA
- Firing rate of APs = Heart rate.
- Rhythm of APs = Heart rhythm
- SAN cell not contractile
How does the SAN produce pacemaker potentials?
SAN has unstable/ non-equilibrium resting membrane potential, it’s constantly trying to repolarise.
Phase 4 - Hyperpolarisation-activated Na+ channels (funny channels activated by hyper polarisation), Na+ influx produces depolarisation
Phase 0 - Depolarisation of Na reaches threshold value, opens VgCa, Ca influx, depolarisation
Phase 3 - VgK channels open, VgCa close, K+ efflux, repolarisation
Upward shows depolarisation
Downward slope shows repolarisation (hyperpolarisation)
Peaks show pacemaker potentials
Why are funny channels important in the SAN?
Allows for development of pacemaker potentials, and without these, external stimuli would be needed
Describe the conduction pathway beginning from the SAN
- Initiated at SAN
- Conducts across both atria to AVN
- AVN not contractile, so slows electric conduction b/w atria + ventricles
- Slows down as AVN is fatty tissue, insulating tissue → Acts as electrical insulator
- Allows for atrial ejection to correctly fill ventricles before electrical activity is conducted to ventricles and contraction occurs
- Low resistance pathways b/w aria and ventricular cells = Intercalated discs - allows for fast conduction
- Bundle of His to purkinje fibres is a fast conduction pathway which allows both ventricles to be stimulated and contracted together
What facilitates fast conduction to atria and ventricles?
- Intercalated discs
- There are branches/ connections b/w atria and ventricular cells
- There are many gap junctions which allow electrical activity to move quickly
Describe how the conduction pathway relates to the pattern seen on an ECG
P - Atrial depolarisation
QRS - Ventricular depolarisation
ST - Interval b/w ventricle depolarisation and repolarisation
T - Ventricle repolarisation
(ECG- Provides info on electrical conduction through heart, but not info on contraction)
Modulation of pacemaker potential frequency and conduction pathway have profound action on HR + rhythm
Describe electrical-contraction coupling in the heart
- Electrical activity generated in SAN, spreads out into atria to produce contraction
- Electrical activity then enters AVN which delays conduction before stimulating ventricles - allows ventricles to fill properly during atrial contraction-.
- Excitation conducts rapidly through bundle of His into purkinje fibres
- Excitation through purkinje fibres is conducted throughout ventricular contractile tissue producing contraction
Ventricular excitation and contraction begins at apex then spreads to base of heart.
How does an action potential induce contraction?
Action potentials in atrial/ventricular cells are ultimately generated from electrical activity arising in SAN.
Atrial/ventricular cells have a stable resting membrane potential, so they need to be stimulated e.g. from the SAN.
Phase 0:
- VgNa open, Na+ influx, depolarises cells, threshold value reached for AP firing
Phase 1:
- VgNa+ inactivating channels pull shut (as they’re positive so are attracted to less positive outside), VgNa channels inactivated.
Phase 2:
- VgCa opens as threshold reached, allows for sustained Ca2+ influx, therefore there’s sustained depolarisation
- This is the plateau phase - tissue is unexcitable or refractive -cannot fire more APs. VgNa channels inactivated. No twitching, 1 AP produces 1 contraction. This is essential for proper ejection of blood from heart.
- Lasts 200-400 ms
Phase 2 + 3:
- VgCa switch off, K+ channels open
Phase 3:
- VgK open, K+ exits cell, repolarising cell
Phase 4:
- Back to resting membrane potential
Where does ventricular contraction begin?
Begins at apex of heart, spreads to base of heart
How do atrial and ventricular action potentials couple to contraction?
- Contraction caused by an increase in cytosolic Ca2+ levels.
- AP opens VgCa channels on cardiac cell, induces calcium influx
- This calcium can bind to rynanidine receptors on SR for release of stored calcium to further increase calcium levels within cell
- Calcium binds to troponin C which allows troponin to undergo conformational change in shape, allows it to bind to tropomyosin on myosin head and remove it so that actin can bind, and then contraction can occur
