Conduction Physio

Question 1

Fast Cardiac AP
Slow Cardiac AP
Channels:
1.) Na1.5: Work how? Similar to?
2a.) CaL: Rapid response to?
2b.) CaT: Activated by? Expressed where?
3a.) Kt: Depol. causes? Slightly slower than?
3b.) Kr/Ks: Called what?
3c.) Ki: Gated? Sensative to? Purpose?
3d.) GIRK: Acts on? Purpose?
4.) Non-selective: HCN: Turned off by? Turned on by? Critical for?

Answer 1

1. ) Depol causes activity; neurons/SM
   2a. ) Voltage and Ca [ ]
   2b. ) Weaker depol than L type; SA node
   3a. ) Activ and deactiv; Na channel
   3b. ) Rapid and slow delayed rectifiers
   3c. ) No; Cytoplasm [ ]; Keep K+ conc. close to Ek
   3d. ) M2 receptors to slow SA
2. ) Depol; Hyperpol; automaticity

Question 2

• Pacemaker cells: Don’t require?
• Absolute refractory period?
• Relative refractory period?
• Overdrive suppression?
• Ventricular AP’s: R wave relates to? ST segment? T wave? Isoelectric after T wave?
• PR represents?
• QT represents?
• Tachyarrhythmias:
  1. ) How does reentry work?
  2. ) Etopic foci?
  3. ) Triggered after depolarizations: EAD? DAD?

Answer 2

• Neuronal control
• Second AP cannot be fired
• Threshold for AP is higher but possible
• Myocardial cells other than pacemaker SA are capable of spon activity but at decreased frequency of firing
• Phase 0; Phase 2; phase 3; Phase 4
• Depol. pause at Bundle of His; conduction time across AV
• Total duration of depol. and repol of ventricles
  1.) Unidirectional block; slow conduction speed through reentry pathway
  2.) Myocardium outside conduction system acquires automaticity and rate exceed SA and AV
  3.) EAD: Occurs before AP has fully repolarized
  DAD: Occurs after AP is complete and then triggers

Question 3

Arrhythmias:

• Ramono Ward syndrome: Inheritance? LQT1 Mutation? LQT2? LQT3?
• Jervell Syndrome: Inheritance? Mutation? Also suffer?
• Mutations to K cause? Type of mutation?
• Mutations to Na cause? Type of mutation?
• Class 1 drugs: Type? 1a effects? 1b effects? 1c effects?
• Class 1 use dependence?
• Class 1 alternative mechanism?

Answer 3

• AD; Ks channel; Kr; Na
• AR; Ks LQT2; deaf autistic
• Reduce number of expressed K+ channels taking longer to get back to resting potential; LOF
• Prevent Na channels from inactivating prolonging phase 2; GOF
• Na channel blockers; slow upstroke of phase 0, increase refractory period phase 4 and prolonged phase 2 (similar to class 3)
• Slow upstroke, mildly shorten phase 2, prolong phase 4
• Pronounced phase 0 slowing; mildly prolong phase 2
• Na channels must be open to block; similar to anesthetics; increased affinity for inactivated state
• 1a also blocks K+ which prolongs phase 2

Question 4

• Class 2 work how? Effects? Used for?
• Class 3 work how? Effects?
• Class 4 work how? Effects?
• Afterdepolarizations due to?
• Reentrant 2 conditions?
• How is reentrant suppressed? (2)
• How do you decrease automaticity? Drugs? (2)
• Adenosine: Class? Works how? Effects?
• Class 1a actions?

Answer 4

• BB; Decrease Ifunny; LTCC and K current in slow AP’s; Decrease diastolic depol, slow upstroke and slow repolar.; AV node reentry; A fib
• Block K+ on fast; Longer phase 2 and much longer refractory
• Ca blockers; Slow AP’s; slow Ca dependent upstroke and prolong refractory period
• Prolonged phase 2 with excessive Ca that is then NCX
• unidirectional block; conducation around > refractory
• Decrease conducting velocity (upstroke); prolonged refractory period
• Decrease rate; class 2 & 3
• Class X; Increase K+ and Decrease CaL and Ifunny in SA/AV; Decrease conduction rate; works on Gi
• 1 and 3 actions