1. Internodal pathways
    • conduct AP generated at the SA node to the AV node bypassing the atrial muscle
    • anterior, middle, and posterior
  2. Location of the SA node
    superior posterolateral wall of the right atrium, slightly below and lateral to the SVC
  3. resting membrane potential of the SA node
    • -55 to -60 compared to ventricular muscle fiber at -85
    • cause is leaky sodium and calcium channels, neutralize the intracellular negativity
    • at -55 mv the fast sodium channels have become inactivated, the inactivation gates are closes and need to become more negative to reset
  4. Effect of loss of fast Na channels on SA node AP
    • it is slower to develop
    • it is slower to return to its negative state
  5. Ion flow between heart beats at the SA node
    • positive sodium ions from outside the fibers tend to leak inside
    • causes a slow rise in resting membrane potential until it reaches the threshold, ~-40mv
    • At the threshold the slow Na/Ca channels open
  6. Cause of depolarization
    • the Na/Ca channels close and K channels open allowing K to leak out
    • K channels stay open long enough for the fibers to hyperpolorize
  7. Location of AV node
    posterior wall of right ventricle behind the tricuspid valve
  8. Length of delay in the AV node
    • 0.09 sec
    • 0.13 if you combine the delY IN THE BUNDLE BRANCHES
    • delay is causes by the lack of gap junctions
  9. Purkinje system
    • large fibers
    • 1.5-4.0 m/sec conduction, 6x greater then ventricular muscle
    • allow the ventricles to function as a sanctum
    • 0.06 seconds for the AP to spread to the entire ventricle
    • very few myofibrils, lots of mitochondria and glycogen
  10. stimulation pace of different part of the heart
    • SA node 70-80
    • AV node 40-60
    • Purkinje 15-40
  11. Why is the SA node the pacemaker of the heart
    its rite of rhythmic discharge is fastest
  12. Ectopic pacemaker
    • anywhere that starts to fire faster then the SA node
    • causes an abnormal sequence of contraction, causes significant debility of heart pumping
  13. During AV block
    the atria continue to contract at a normal rate while the purkinje fibers take over in the ventricles and beat between 15 and 40
  14. Stokes-Adams syndrome
    • delayed pick up of rythem
    • after sudden AV block the purkinje system does not emit rhythmic impulses for 5-20 seconds, before the blockage these fibers where in overdrive by the rapid sinus rhythm. Now in a suppressed state.
    • Ventricular escape
    • can cause syncope and death depending on length of delay
  15. Parasympathetic nerves to the heart
    • release acetylcholine, muscurinic receptors on the heart
    • decreases rate of contraction, negative chronotropic effect. Decrease inward leak of Na, increased outward K.
    • hyperpolorization
    • decreases excitability of the AV node, negative dromotropic effect. Decrease inward Ca and increase outward K
  16. Sympathetic stimulation of the heart
    • releases norepinephrine, B1 receptors, increase permeability of Na and Ca channels
    • increase rate, positive chronotrpic effect, Na
    • Increases rate of conduction, positive dromotrpic effect, Ca
    • Increases force of contraction, positive ionotropic effect, Ca
  17. What lysosomal storage disorder affects the heart?
    Pompe disease
Card Set
Chapter 10 Rhythmical excitation