1. How may myocardial ischaemia lead to poor electrical coupling through connexons
2. What are the two functionally distinct regions of SR
3. What are calcium concentrations in skeletal and cardiac muscle during excitation and so how sub maximal is cardiac contraction
4. How does the inward rectifier potassium channel conserve potassium during the AP
5. Under which circumstances may NcX enter reverse mode
6. What are the two functions of the transient outward current
7. What causes inward rectification
8. In which cells is the late plateau exchanger current most marked
9. Why is it important that the long refractory period means that tension development is completed before the myocyte becomes reexcitable
10. How do adrenaline and intracellular Ca affect Ltype Ca channel inactivation
11. Why is Katp channel opening during ischaemia helpful
12. What did Fabiato and Fabiato 1975 show
13. What proportion of Ca transient is Ca-L or CICR
14. What is the cluster bomb model of CICR which reconciles all or none CICR with grades CICR
15. What are the two ways ischaemia increases intracellular Na and thus reduces NCX
16. Why can the Purkinje fibres conduct much faster than the AVN fibres 5vs0.05
17. Which 5 channels influence the decay of the pacemaker potential
18. Why are nore action potentials slow
19. How does adrenaline affect the RyR