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1. Cardiac Action Potentials
2. Reading: Klabunde, Cardiovascular Physiology Concepts
Chapter 2 (Electrical Activity of the Heart) pages 18-26
4. The Cardiac Action Potential Types Are Either Fast Or Slow Response Fast-response action potentials
Atrial myocardial fibers
Ventricular myocardial fibers
Purkinje fibers
Slow-response action potentials
Sinoatrial node
Atrioventricular node
5. Differences between fast and slow cardiac action potentials:
7. Fast Response Action Potential
8. Phases of the Fast Response Action Potential Phase 0 = Depolarization
Phase 1 = Partial Repolarization
Phase 2 = Plateau
Phase 3 = Repolarization
Phase 4 = Resting Membrane Potential
9. Phase 0 The characteristics of the upstroke of the action potential depend almost entirely on inward movement of Na+
10. Phase 0
11. Phase 1 Inactivation of Na+ channels ends
Transient outward K+ current
13. Phase 2 (Plateau) What produces the plateau?
Slow inward Ca++ currents (L-type calcium channels)
Counterbalanced by:
Outward K+ currents
14. Action potential and ionic fluxes
15. Phase 2 (Plateau) Ventricular contraction persists throughout the action potential, so the long plateau produces a long action potential to ensure forceful contraction of substantial duration
16. Calcium-Induced Calcium Release When the myocyte is depolarized calcium enters the cell via L-type calcium channels. The amount of calcium that enters the cell is small, but this triggers the release of a large amount of calcium into the cytosol from the sarcoplasmic reticulum which results in binding of myosin to actin and contraction of the myocyte.
17. Phase 3 Outward K+ current is mainly responsible for repolarization
Na+ channel recovery begins during Relative Refractory Period
20. Phase 4 Restoration of ionic concentrations
Na+,K+-ATPase
Na+-Ca++ Exchanger
ATP-driven Ca++ Pump
21. Restoration of Ionic Gradients
22. Na/Ca Exchanger
23. Resting Membrane Potential in Cardiac Cells
Depends mainly on the conductance of K+
Determined mainly by the ratio of intracellular to extracellular concentration of K+
Measured value is slightly less negative than predicted because of small but finite conductance of Na+
Na+,K+-ATPase
24. Slow Response Action Potentials
25. Slow Response Action Potential Phase 0
Phase 2
Very brief
Phase 3
Not separated clearly from phase 2
Phase 4
Note: Phase 1 is absent
26. Slow Response Action Potential: Phase 0 Depolarization is mainly by Ca++ influx
28. Refractory Periods:Effective (ERP) and Relative (RRP)
29. Automaticity (Pacemaker Cells) Diastolic Depolarization
Inward Na+ (not via typical Na+ channels)
Ca++ influx
K+ efflux (opposes effects of other ions)
30. Autonomic neurotransmitters
31. Autonomic neurotransmitters
33. Conduction System
34. Sinus Rhythm The SA (Sinus) Node is the hearts dominant pacemaker.
The ability of a focal area of the heart to generate pacemaking stimuli is known as Automaticity.
The depolarization wave flows from the SA Node in all directions.
35. Overdrive Suppression
36. Overdrive Suppression
37. Overdrive Suppression Automaticity of pacemaker cells becomes depressed after a period of excitation at a high frequency
Due to activity of Na+, K+-ATPase.
At higher heart rates more Na+ is extruded than K+ enters the cell > tends to hyperpolarize the cells
Slow diastolic depolarization requires more time to reach threshold
38. THE END