Learning Objectives Heart - Dr Wus Learning Objectives...

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Dr. Wu’s Learning Objectives Cardiovascular Physiology Learning Objectives Lecture 14 (Cardiac Cells, Action potentials & excitation) 1. Describe function of intercalated discs . Specifically, discuss how gap junctions electrically connect cardiac myocytes and desmosomes physically connect cardiac myocytes. Discuss why this facilitates the myocardium working as a pump (functional syncytium = many cells working as one unit). Desmosomes allow force to be transferred and gap junctions provide electrical connection (permit local current flow). Allows coordinated contraction 2. Give an overview of the function of the organelles ( TTubules, SR, contractile apparatus ) and proteins ( voltage gated Ca 2+ channels and SR calcium release channels ) that are responsible for excitation contraction coupling in cardiac muscle ( i.e. calcium induced calcium release) . Remember that you have encountered some of these proteins in neurons and skeletal muscle cells. Build on your previous knowledge. Critical thinking: Building a myocyte 1. Action potential enters from adjacent cell 2. Voltage-gated calcium channels open 3. Calcium induces calcium release through ryanodine receptor channels 4. Local release causes calcium spark 5. Summed calcium sparks create calcium signal 6. Calcium ions bind to troponin to initiate contraction 7. Relaxation occurs when calcium unbinds troponin 8. Calcium pumped back into SR 9. Calcium is exchanged with Na+ by the NCX antiporter 10. Na+ gradient maintained by NaK ATPase **In cardiac muscle, the DHP receptor is a L-type voltage gated channel versus in skeletal muscle it is a sensor that mechanically gates calcium release from ryanodine receptor 3. Compare/contrast the action potentials and properties of the typical ventricular cardiac myocyte vs. the SA nodal cells. Discuss membrane potential stability/instability at rest. Compare the voltage gated channel (Na + , Ca 2+ and K + ) permeability to membrane potentials changes (depolarization, plateau and repolarization) during a typical cardiac myocyte AP and the SA node AP. Critical Thinking: Action potentials in myocytes versus nodal cells RMP of ventricular myocyte is much more negative (many K leak channels). Depolarization due to voltage gated Na channels, plateau due to voltage-gated calcium channels, repolarization via voltage-gated K channels. Special gating of funny channels in nodal cell, open with repolarization which starts depolarization for next action potential, RMP is unstable, superthreshold depolarization due to L type voltage gated calcium channel, repolarization via voltage gated potassium 4. Explain how the length of the refractory period prevents tetany in cardiac cells. (HINT: Think about what you have learned about skeletal muscle in CT 4.2. The short action potential and long twitch creates a situation where skeletal tetany can occur. What happens to the action potentials in cardiac tissue that prevents tetany in cardiac tissue?)
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Refractory period lasts almost as long as entire muscle twitch. Lengthened by L-type calcium current. Important so tetany does not occur in cardiac cells. If tetany occurred the heart
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