3. Origin + spread of heartbeat Flashcards
Ohms Law
V=IR
Pressure
F x R (flow x resistance)
Systemic Pressure
CO x TPR
Cardiac Output
HR x SV
Sinoatrial (SA) node
100/min
Atrioventricular (AV) node
50/min
Bundle of His/Purkinje fibres
30/min
SA node AP
CaKNa
Phase 0 = Ca2+ influx
Phase3 = Ca2+ channels inactivate, Delayed K+ efflux
Phase 4 = Na+ influx, Ca2+ channels recover from inactivation, pumps restore ion gradients
Phase 4 SA Node
HCN-gated channels
mediates a ‘funny current’
simultaneous K+ efflux and Na+ influx
Na influx dominates and membrane slowly depolarises to threshold
Sympathetic change of HR
noradrenaline
acting on b1 adrenoceptors
·Increases opening of HCN channels
•Increase Na+ influx; If
·Opens Ca2+ channels
•Increased Ca2+ influx
·Increase in slope of prepotential hence HR
•Tachycardia
Parasympathetic change of HR
ach
muscarinic cholinergic receptors
·Decreases opening of HCN channels
•Decreased Na influx
·Slows opening of Ca2+ channels
- Decreased Ca2+ influx
- Increased K+ efflux
·reduces slope of prepotential hence, fall in HR
•Bradycardia
Ventricular Myocyte AP
NaKCa
Phase 0 = Na+ influx
Phase 1 = Na+ channels inactivate, fast K+ efflux
Phase 2 = Ca2+ influx
Phase 3 = Ca2+ channels inactivate, delayed K+ efflux
Phase 4 = Na+ and Ca2+ channels recover from inactivation, pumps restore ion gradients
Effect of ·High [K+] on heart
↓ K+ gradient across cell membrane
↓ K+ efflux
Cell initially more excitable
Closure of h gate
Conduction problems as Na channel cannot reset
Cannot generate another action potential upstroke
Arrest in diastole and death
Effect of low [Na+] on heart
Little effect on resting membrane potential
↓ Na+ concentration gradient
↓ Na+ influx
↓ Height of action potential, may not reach threshold
Conduction problems
Eventual arrest in diastole and death
Effect of ·High [Ca2+] on heart
↑ Ca2+ concentration gradient
↑ Ca2+ influx
Big force contraction
[Ca2+] too high to pump out enough to relax cell
Arrest in systole