Action potentials in the heart Flashcards
AP in the SAN - 1st step (depolarisation)
- AP is generated
- At -60mV it leads to the opening of HCN channels(hyperpolarisation gated cyclic nucleoside chanels)
- Opening of HCN alows Na+ ions to move in to the cell, causing depolarisation fom -60mV to -40mV
AP in the SAN - 2nd stage (2nd depolaristion)
- 1st stage caused depolarisation from -60mV to -40mV
- Voltage gated Ca2+ channels open and Ca2+ enters, causing further depolarisation of the cell to +20mV
AP in the SAN - 3rd stage (repolarisation)
- 2nd stage caused depolarisation to +20mV
- This results in the opening of K+ channels
- K+ moves out of the cell, loss of +ve charge causes repolarisation
- Hyperpolarisation threshold gets reached and HCN channels open again (cycle)
Effect of catecholamine on HR
- Has a positive chronotropic effect
- Leads to faster repolarisation, so reaches threshold faster, so increased HR
(has its effect on the SAN cycle)
Effect of acetylcholine on SAN cycle
Slows down the opening of HCN
Slows HR
Describe the 1st stage of a myocardial action potential
- Resting potential is -90mV
- Depolarisation of cell, reaches threshold of -70mV
- Sodium gated fast channels open, Na+ enters the cells and depolarises to +20mV
Describe 0st and 1st stage of myocardial action potential
- 1st stage causes depolarisation to +20mV
- K+ channels open, K+ leaves the cell and drops to -15mV (partial repolarisation). Na+ stops.
Describe 2nd stage of myocardial AP (after 2nd stage repolarised to -15mV)
- Voltage gated Ca2+ channels open, Ca2+ moves in and counters the K+ channels, resulting in a plateau for approx 200msec
What is the plateau stage in a myocardial AP?
Ca2+ and K+ channels balance out (Ca2+ moving in, K+ moving out)
Describe the 3rd stage of a myocardial AP (after plateuau)
- Entry of Ca2+ into the cell results in contraction of myocyte
- Ca2+ inflow stops, K+ outflow, repolarisation until -90mV
4th stage in myocardial AP
Resting potential maintained (K+ outflow)
Describe sympathetic control of HR
- Increase HR (positive chronotropic)
- Increase force of contraction (positive inotropic)
- Increase CO by 200%
- Controlled by adrenaline and noradrenaline - type 1 beta adrenoreceptors, increased adenyl cyclase and increased cAMP
Describe parasympathetic control of HR
Decrease HR by 30-40 bpm (negative chronotropic)
Decrease force of contraction (negative inotropic)
Decrease CO by 50%
Controlled by ACh - M2 receptors which inhibit adenyl cyclase so less cAMP