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19 Cards in this Set

  • Front
  • Back
What structure allows signal to travel through the myocardium and allow unanimous contraction?
Intercalated discs
What molecules make up the thin filament?
G and F actin that make up actin filaments
Tropomyosin
Troponin T, I and C
Where does Troponin T bind? Troponin I? Troponin C?
Troponin T binds to tropomyosin.
Troponin I binds to the actin chain and blocks the active sites.
Troponin C binds to calcium to cause confomational change.
How does myosin binding protein C regulate myosin protein?
MyBPC covers myosin heads at regular intervals. It prevents the myosin from contracting too far. Phosphorylation allows the muscle to relax quickly.
Defects cause diastolic heart failure.
How does ATP regulate cardiac muscle contraction?
ATP is bound and hydrolized by myosin, allowing weak attachment to actin. When the phosphate is lost, the myosin binds strong.
Release of ADP causes conformational change to generate the power stroke.
Another ATP is required for detachment of the myosin head.
What are the two types of myocardial cells? What are the unique features to each?
Electrical cells- automaticity, excitability, conductivity.
Conractile cells- contractility and extensibility
What are the types of electrical cells? What is the function?
Pacemaker cells- initiate impulses
Transitional cells- connect pacemaker with other cells.
Purkinje- connects transitional cell with a myocardial cell
Which area of heart conduction is the slowest? Which is the fastest?
AV node is the slowest; Purkinje fibers are the fastest.
Why do conduction velocities differ in the myocardium?
Action potentials are slower with fewer Na channels.
Increased branching causes slower velocity.
Fewer gap junctions result in less junction.
Type of connexins.
Which connexins are fast? Which are slow? Where are they located?
CX40 are fast- located in the atria, purkinje fibers, bundle branches.
CX30.2 are slow- located in SA and AV node.
What are the phases of pacemaker action potentials? Which channels are associated?
Phase 4- continuous movement toward depolarization by funny sodium channels.
Phase 0- depolarization phase due to opening of calcium channels.
Phase 3- repolarization due to closing of calcium channels and opening of potassium channels.
What are the phases of ventricular action potentials? What channels are associated?
Phase 0- rapid depolarization due to opening of fast sodium channels.
Phase 1- repolarization due to opening of transient potassium channels.
Phase 2- plateau phase due to opening of slow calcium channels.
Phase 3- repolarization due to opening of potassium channels.
Phase 4- resting state due to sodium/potassium ATPase
What is the absolute refractory period?
Myocardial cells will not respond to stimulation because sodium channels have not been restored.
What is the effective refractory period?
Time including ARP and a little after when the cell is still unable to respond.
What is the relative refractory period?
Cardiac cells will respond to stimulus, but to a lesser degree.
How does calcium transfer from a voltage to muscle contraction?
Current carried through the cell by calcium influx at the T tubules.
Calcium stimulates ryanodine receptors to release sarcolemmal calcium.
Release of calcium causes increased intracellular calcium to induce tropomyosin translocation adn myosin contraction.
Lowering of calcium levels by SERCA pump and Na/Ca exchangers causes relaxation
What are the effects of parasympathetic stimulation on the heart? How does it produce these effects?
Negative chronotropy
Negative dromotropy
Inhibition of cAMP production.
Activates potassium channels to cause hyperpolarization, reduces funny current and reduces calcium influs.
What are the heart effects of sympathetic stimulation? How does it produce these effects?
Positive chronotropy.
Positive inotropy
Positive dromotropy.
Activates funny current and increases calcium influx.
What are the effects on cardiac conduction by hyperkalemia?
Increased resting potential.
Increased phase 0 slope.
Decreased action potential amplitude.