Electrical activity of the Heart Flashcards
What produces electrical impulses in the heart
Pacemakers cells
Spontaneously depolarise and generate AP
Spread across myocardium to generate coordinated contraction in systole
Very different AP to muscle
What is cardiac muscle
Functional syncytium
Desmosomes make a strong connection between cells
Gap junctions electrically connect muscle cells
Where are pacemaker cells
SA node
If SA node damaged another takes over
AV node and Purkinje fibres can produce impulse but slower than SA so overidden
What is the flow from the SA node
SA node
Fire down to AV node which slows AP getting intro
ventricle
Annulus fibrosis = non-conducting region between atria and ventricle
Bundle of His
R and L bundle
Purjinke fibres = rapid conducting system in ventricle
Conduct down Bundle of His then split into R+L branch
Want ventricle to contract at same time
What is the pacemaker potential
Occurs at end of one AP and before the start of the next
Slow depolarisation of SA node towards threshold
Activation of HCN channels when RMP - allow Na to enter enabling slow depolarisation
Activated at around -50
Once threshold reached = AP
How is the AP formed
When at threshold
Voltage gated Ca open = faster
HCN inactivate
At peak Ca inactivate and K open
K = repolarise cell as move out so that HCN can be activated again
Unlike ventricular = Ca not sustained so no plateau
How is SA node controlled / HR
Para increase intervals by Arch acting on M2 receptor
Sympa decrease time between by NA acting on B1
What causes arrythmia
Disturbance to normal electrical activity
What happens to allow muscle to contract
AP enters contractile cell which sit at -90
Initial depolarisation = Na enter
Move cross sacrolema and enter T tubule
Voltage gated Ca channels open
Ca enters and AP in plateau
Induces Ca release from stores in sarcoplasmic reticulum
Ca binds to troponin on actin filament
Repolaries If Ca drops then will unbind Myosin releases actin Ca back to reticulum + removed from cell K open
What is the difference in AP in cardiac vs skeletal muscle
2ms in skeletal (short AP + refractory period so twitch contractions can produce sustained)
Contractions all or none
200ms in cardiac, long AP so long refractory (must repolarise before contracts)
Contractions graded by how much Ca enters cell
What modulates AP throughout contractile cell and pacemaker cells
Para + sympa CCB Cardiac glycoside - increase contraction Hyperkalaemia Hypokalaemia Hypercalcaemia Hypocalcaemia
How does K affect
If hyper (high plasma K) the K gradient is reduced and cell will depolarise spontaneously as Na forced in due to +K = fibrillation + heart block
If hypo (low plasma K) cell with hyperpolaries + channels open = depolarisation
How does Ca affect
If hyper Ca then Ca will flow in faster and increase contraction
