Physio_10.txt

• conduct AP generated at the SA node to the AV node bypassing the atrial muscle
• anterior, middle, and posterior

superior posterolateral wall of the right atrium, slightly below and lateral to the SVC

• -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

• it is slower to develop
• it is slower to return to its negative state

• 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

• 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

posterior wall of right ventricle behind the tricuspid valve

• 0.09 sec
• 0.13 if you combine the delY IN THE BUNDLE BRANCHES
• delay is causes by the lack of gap junctions

• 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

• SA node 70-80
• AV node 40-60
• Purkinje 15-40

its rite of rhythmic discharge is fastest

• anywhere that starts to fire faster then the SA node
• causes an abnormal sequence of contraction, causes significant debility of heart pumping

the atria continue to contract at a normal rate while the purkinje fibers take over in the ventricles and beat between 15 and 40

• 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

• 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

• 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

Pompe disease