4.Action potential in cardiac muscle (1).pptx

Action potential in cardiac muscle

1. ACTION POTENTIAL IN CARDIAC MUSCLE /( SGD)

2. First year MBBS student were comparing the action potential between skeletal and cardiac muscles on frog. W hile performing their skill lab, they observed that there is a marked difference between action potential between these muscle fibers. CASE SCENARIO

3. Why there is a difference in duration of action potential between skeletal and cardiac muscles? What is the role of calcium ion cardiac muscle excitation and contraction? QUESTIONS

4. Learning Objectives At the end of skill lab/SGD, 1 st year MBBS students should be able to: Differentiate amongst various phases of action potential leading to excitation contraction coupling in cardiac muscle

5. A ction potential is the change from the normal resting negative membrane potential to a positive potential and ends with an almost equally rapid change back to the negative potential Action Potential

6. In cardiac muscle, the action potential is caused by opening of two types of channels: Voltage-activated fast sodium channels as those in skeletal muscle (2) L-type calcium channels (slow calcium channels), which are also called calcium-sodium channels, which are slower to open causing the plateau in the action potential Action Potential in Cardiac Muscles

7. Four stages: Depolarization stage (phase 0) Initial Repolarization stage (phase 1) Plateau (phase 2) Rapid Repolarization (phase 3) STAGES OF ACTION POTENTIAL

8. This phase occurs due to activation of voltage-gated Na + channels During this phase of the action potential, the membrane potential rapidly reverses to a positive value of about +20 mV to +30 mV Phase 0 Or Depolarization

9. I n activation of Na + channels contributes to rapid repolarization phase At peak potential , K + channels transiently opens The resultant limited efflux of K + through these channels brings about a brief, small repolarization as the membrane becomes slightly less positive Phase 1 or Initial Repolarization

10. Calcium channel opens and fast potassium channel closes Opening of the L-type Ca 2+ channels results in a slow, inward diffusion of Ca 2+ , This continued influx of Ca 2+ prolongs the positivity inside the cell This effect is enhanced by the concomitant decrease in K + permeability toward outside Phase 3 or Repolarization

11. The resultant reduction in outward movement of positively charged K + prevents rapid repolarization of the membrane and thus contributes to prolongation of the plateau phase

12. The rapid falling phase of the action potential results from: Inactivation of the Ca 2+ channels. D elayed activation of K + channels The decrease in Ca 2+ p ermeability diminishes the slow, inward movement of positive Ca 2 + The sudden increase in K + permeability simultaneously promotes rapid outward diffusion of positive K + Phase 3 or Repolarization

13. A s in other excitable cells, the cell returns to resting potential as K + leaves the cell At resting potential, the ordinary voltage-gated K + channels close and the leaky K + channels open once again Phase 4 or Resting Potential

14. The velocity of conduction of the excitatory action potential signal along both atrial and ventricular muscle fibers is about 0.3 to 0.5 m/sec, or about 1/250 the velocity in very large nerve fibers and about 1/10 the velocity in skeletal muscle fibers. The velocity of conduction in the specialized heart conductive system—in the Purkinje fibers—is as great as 4 m/sec in most parts of the system Velocity of Signal Conduction in Cardiac Muscle

15. A period immediately following stimulation during which a nerve or muscle is unresponsive to further stimulation The normal refractory period of the ventricle is 0.25 to 0.30 second There is an additional relative refractory period of about 0.05 second during which the muscle is more difficult to excite than normal but nevertheless can be excited by a very strong excitatory signal, as demonstrated by the early “premature” contraction Refractory Period of Cardiac Muscle

16. The refractory period of atrial muscle is much shorter than that for the ventricles (about 0.15 second for the atria compared with 0.25 to 0.30 second for the ventricles).

17. Excitation contraction coupling

18. Excitation contraction coupling refers to the series of events linking muscle excitation (the presence of an action potential) to muscle contraction ( crossbridge activity that causes the thin filaments to slide) Excitation Contraction Coupling

19. Rest of the mechanism is similar to that in skeletal muscles

20. T-tubules of cardiac muscle have a diameter 5 times as great as that of the skeletal muscle tubules, thus a volume 25 times as great Inside the tubules is a large quantity of mucopolysaccharides that are electronegatively charged and bind abundant calcium ions T tubules of cardiac muscles

21. There are fewer T-tubules in comparison with skeletal muscle

22. L-type Ca ++ channel acts as voltage gated channel Ca ++ enters in cytosol from T tubules Ca ++ from T tubules stimulates opening of Ryanodine receptor Ca ++ channels  contraction

23. Difference in Action Potential

24. A first year MBBS student was comparing the Action potential between skeletal and cardiac muscles on frog. He observed that there is a marked difference between action potential between these muscle fibers. Why there is a difference in duration of Action potential between skeletal and cardiac muscles? What is the role of calcium ion cardiac muscle excitation and contraction?