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Flashcards in Cardiac action potential Deck (10):

Electrical activity of the heart

Action potential generated in the SAN
Atrial depolarisation
AP delayed at the AVN
AP travels down the septum and into he ventricles
Wave of AP causes wave of contraction
Wave of repolarisation follows wave of depolarisation


Basic ECG

P = atrial depolarisation
QRS = ventricular depolarisation
T = repolarisation
Delay between P and Q due to the delay of the action potential travelling through the AV node, allows atria to contract before the ventricles, blood is pumped into ventricles y the atria before they contract


Cardiac action potential

Phase 0- Sodium influx
Phase 1- Calcium influx, sodium inactivate, potassium efflux
Phase 2- plateau maintained by balance calcium vs potassium
Phase 3- Potassium efflux> calcium influx
Phase 4- Sodium inactive > closed


Mechanisms to change force of contraction

A: increased intracellular calcium concentration = increase in force of contraction
B: extracellular calcium influx triggers intracellular calcium release (CICR)
Contractile force proportional to calcium influx
Quantity of calcium influx dependent upon duration and size of plateau


Positive inotropy

Stimulation of B1 adrenoceptors causes activation of Gs
Activated Gs stimulates adenylyl cyclase to convert ATP to cyclic AMP
Increased cytosolic cAMP levels activates protein kinase G
PKG phosphorylates voltage sensitive calcium channels
Allows for a greater influx of calcium and a bigger contraction


Positive lusitropy

Stimulation of B1 adrenoceptors causes activation of Gs
Activated Gs stimulates adenylyl cyclase to convert ATP to cyclic AMP
Increased cytosolic cAMP levels activate protein kinase G
PKG phosphorylates phospholambin and voltage sensitive potassium channels
Level of free calcium decreases faster, allowing rate of relaxation to increase
Increased rate of potassium efflux causes a greater rate of repolarisation and faster relaxation


Negative inotropy

Stimulation of muscarinic receptors activates Gi which splits into subunits
Activated Gia inhibits adenylyl cyclase reducing the rate of cAMP production
As cAMP is main molecule driving increased force of contraction, reduced levels of cAMP reduce force of contraction
Gibg activates receptor operated potassium channel allowing extra potassium influx
The extra potassium influx decreases the duration of the plateau phase thereby reducing time for calcium entry leading to educed levels of intracellular free calcium reducing contractile force


Rhythmic generation of impulses in SAN

All cardiac cells can generate impulses
All cardiac cells possess If
Heart rate determined by dominant pacemaker
Few sodium channels in SAN, mostly inactivated at -60mV


Negative chronotropy (bradycardia)

Parasympathetic stimulation
ACh and muscarinic receptor
Gi activates Ikach
Increased potassium efflux opposes If



Sympathetic stimulation
NA and B adrenoceptor
Gs-alpha activates AC
cAMP increases If
Increases opening probability of voltage sensitive potassium channels
Increases rate of depolarisation and increase rate of repolarisation