Cardiac Action Potential Flashcards
Cardiomyocytes
contractile cells of heart - found in atria & ventricles
Pacemaker cells
only present in few areas of heart - mostly in SAN - cells in AVN take over when not working.
no sarcomeres - do not contribute to contractile nature.
set heart rate
Funny Current
slow depolarisation from -60mv to -40mv
Ectopic pacemaker
pacemaker cells not in SAN
Automaticity
pacemaker cells - self depolarisation
Role of PNS
reduce heart rate
Parasympathetic activity on heart
vagus nerve
3 main mechanisms of PNS action on heart rate
- lengthening funny current - longer for pacemaker cells to reach threshold potential = inhibition of HCN channel
- increasing threshold potential for activation of v- gated calcium channels
- decreasing maximum membrane potential the cell can achieve - longer to reach repolarisation potential - increased expression of potassium channels - HYPERPOLARISED MEMBRANE POTENTIAL
PNS activity on AV node
slow conduction from atria to ventricles
Ivabradine
blocks HCN channel - more time for ventricular filling
Verapamil
blocks action of v-gated calcium channels = reduces influx of calcium into cells = reduces contractile force of heart
SNS
increases heart rate
increased heart rate
- increases speed of funny current + threshold potential reached quicker
- increase calcium conduction through v-gated calcium channels - increases calcium induced calcium release from sarcoplasmic reticulum = MORE FORCEFUL CONTRACTIONS
gap junction
link pacemaker cells + cardiomyocytes = leads to localised depolarisation of the membrane
calcium diffuse through - leads to opening of sodium channels = RAPID DEPOLARISATION
plateau phase
influx of calcium channels
followed by rapid repolarisation - efflux of potassium
Cardiomyocyte action potential phases
depolarisation initial repolarisation plateau repolarisation resting membrane potential
stage 0
v - gated Na channels open = localised depolarisation - neighbouring channels open as well
fast depolarisation
stage 1
+20mV - v-gated Na channels close to an inactivated state = no stimulation will open
ABSOLUTE REFRACTORY PERIOD - no other action potential - prevents tetany
fast potassium channels open - repolarisation = EFLUX
stage 2
repolarisation is brief - potassium channels close - v gated Ca channels + delayed rectifier K channels open
MUSCLE CONTRACTION
stage 3
Ca channels close - slow K channels open = efflux of K -> RAPID REPOLARISATION
Na channels now closed in voltage dependent manner = no longer refractory state
stage 4
Na - K ATPase exchanges 2 extracellular K ions for 3 intracellular Na ions - drop of around 5mV in membrane potential
resting membrane potential mainly mediated by inwardly rectifying K channels - efflux of K
mainly mediated by K
Na - Ca exchanger - swaps intracellular Ca for Na
Absolute refractory period
180ms
Relative refractory period
membrane depolarises - v-gates Na channels become voltage sensitive
AP can be generated by requires greater stimulation
Electrical - Contraction coupling
Ca entry enters at T tubules - activates ryanodine receptor Ca channels = release of large amounts of Ca from sarcoplasmic reticulum
Ca interacts with actin and myosin = contraction
Ca removed from intracellular space through Ca ATPase and through Na-Ca exchanger