Guyton/Chapter 10/Rhythmical Excitation of the Heart

1. Special system of the heart is:

➢generating rhythmical impulses to cause rhythmical contraction of the heart muscle
➢conducting these impulses through the heart

2. Importance of the rhythmical conductive system of the heart:

➢atria contract one sixth of second ahead of ventricular contraction and this allows filling
ventricles before the heart pumps the blood to the lungs and peripheral circulation.
➢all parts of ventricles contract simultaneously so this allows pressure generation in ventricular
chambers.

3. Disadvantage of this system:

➢it is sensitive to damage by heart diseases, especially by ischemia of heart resultingfrom poor
coronary blood flow which can result as:
● bizarre heart rhythm
● abnormal sequence of contraction of heart chambers

4. SA/Sinoatrial Node: generates normal rhythmical impulse

5. Internodal Pathways: conduct impulse from sa to av node

6. AV/Atrioventricular Node: impulse from atria is delayed to allow blood to go into ventricles
before ventricular contraction.

7. AV Bundle/ Bundle of His: conducts impulse from atria into ventricles

8. Left & Right Branches of Purkinje Fibers: conduct impulse to all parts of ventricles.

9. AV
:➢on posterior wall of right atrium
➢Av node and its adjacent conductive fibers cause the delay before the ventricular contraction.

10. SA:
➢on the superior posterolateral wall of the right atrium
➢fibers have so little contractile muscle filaments
➢sa nodal fibers connect directly with atrial muscle so when the action potential is generated, it
immediately spreads to atrial muscle
➢sa nodal fibers have capability of self-excitation, leakiness of Na+ and Ca++cause self-
excitation -1.Self-excitation to cause AP-

11. Self-excitation: process to cause automatic rhythmical discharge and contraction

12. Resting membrane of the sinus nodal fiber: -55 to -60 → it is less negative because cell
membranes of sinus nodal fibers are naturally leaking Na+ and Ca++.Resting membrane of
ventricular muscle: -85 to -90

13. SA NODAL FIBER:

➢fast Na+ channels: are inactivated because of the positivity inside of the sa nodal fiber which
is caused by the natural leakage of Na+ and Ca++.
➢slow Na+-Ca++ channels: cause action potential, Na+ goes inside the fiber(this also cause
slow rise of membrane potential in positive way because it makes the inner side of the fiber
even more positive than when it was already leaking Na+ and Ca++)
➢K+ channels: they open after action potential is finished, slow Na+-Ca++channels close
and when K+ goes outside from inside of the fiber, it causes excess of negativity in the fiber
which causes hyperpolarization.-2.Recovering from action potential, 3.Hyperpolarization after
AP is over
● Depolarization by: slow Na+-Ca++ channels
● Repolarization by: K+ channels

14. VENTRICULAR MUSCLE FIBER:

➢fast Na+ channels: cause action potential
➢slow Na+-Ca++: cause the plateau which lasts 0.3 sec
➢K+ channels: cause K+ diffusion from inside to out to return membrane potential to its normal
value.
● Depolarization by: fast Na+ channels
● Plateau by: slow Na+-Ca++ channels
● Repolarization: K+ channels

15. There is a difference in the function of the channels

➢BECAUSE: resting membrane of sinus nodal fiber is less negative than resting membrane
potential of ventricular muscle due to sinus nodal fibers natural leakage to Na+ and Ca++.

16. Atrial nodal action potential is slower to develop

➢BECAUSE: fast Na+ channels are inactivates in sinus nodal fibers

17. Return of potential to its negative state occurs in sinus nodal fibers after action potential
occurs
➢BECAUSE: high concentration of Na+ out tends to leak inside of sinus nodal fiber membrane.

18. Leakiness of sinus nodal fibers to Na+ and Ca++ doesn’t cause depolarization all the time.
➢BECAUSE:
1. slow Na+-Ca++ channels are inactivated after opening
2. amount of K+ channels opened increases at the same time as slow Na+-Ca++ channels get
inactivated.
***These reduces intracellular membrane potential so its resting level stays negative***

19. Hyperpolarization does not maintain forever

➢BECAUSE: after opening, K+ channels close and more close after.

20. After K+ channels close completely, inward leaking of Na+ and Ca++overbalance the outflux
of K+. This causes drift up of resting membrane potential, one more time it reaches to threshold
of -40 mV. -4. Drift of RestingMembrane to Threshold-

21. -55 to -60 mV: goes to this level because of hyperpolarization

22. -40 mV: goes to this level by the overbalance of Na+ and Ca++ leakage

23. Entire process goes like this again and again:

➢-1.Self-excitation to cause AP-
➢-2.Recovering from action potential-
➢-3.Hyperpolarization after AP is over-
➢-4. Drift of Resting Membrane to Threshold-

24. Action potential generated in sinus nodal fibers conducts to atrial muscle mass at the
velocity of 0.3 m/sec, and then to the AV node.

25. Action potential going through AV node via internodal pathways (similar to Purkinjefibers of
ventricles) at the velocity of 1 m/sec, more rapidly than its in the atrial muscle.
➢1. Anterior internodal pathway
➢2. Middle internodal pathway
➢3. Posterior internodal pathway
➢*Anterior internodal band (passes through anterior wall of left atrium)

26. 1. 0,03 sec→ delay from SA to AV node through internodal pathways

2. 0,09sec → delay in AV node
3. 0,04 sec→ delay in penetrating part of the AV bundle to distal part of AV bundle
-Total delay: 0,16 sec (from SA node to distal part of AV bundle)
4. 0,03 sec→ from left and right branches of purkinje fibers to ventricular muscle endocardium
5. 0,03→ from endocardium to epicardium of the heart (through all ventricular muscle mass)
-Total: 0,16+0,06= 0,22 ( from SA node to epicardium of the heart)

27. Slow conduction occurs in

➢Transitional fibers
➢nodal fibers
➢penetrating av bundle fibers
➢BECAUSE: they have gap junctions between cells and they resist to conduct impulse from one to other

28. Special characteristics of AV Bundle:

➢allows only forward conduction of impulse from atria to ventricles and prevents re-entry
➢atrial muscle is separated from ventricular muscle by a fibrous barrier (exceptAV bundle)

29. Special Purkinje fibers:

➢Lead from AV node through AV bundle into the ventricles
➢Larger than ventricular muscle fibers, transmit AP at a velocity of 1,5-4 m/sec faster than ventricular
muscle (x6) and some AV nodal fibers (x150).(This allows instantaneous transmission of impulse through
entire ventricular muscle)
➢They have so many gap junctions (more than in the AV bundle fibers) at a-high level of permeability
between successive cells
➢They have few myofibrils so they contract so little or they don’t contract at all.30. When the impulse is
transmitted to ventricular muscle from Purkinje fibers, the velocity of conduction is 0.3-0.5 m/sec (one
sixth of velocity in Purkinje fibers)
31. Why does the sinus node control the heartbeat of the heart?
➢BECAUSE: its rate of discharge is faster than other part of the heart such asAV node or Purkinje fibers

32. Normal rate of SA node: 70-80 times per minRate of AV node: 40-50 times per minRate of Purkinje
fibers: 15-40 times per min

33. Causes for the shift of pacemaker:

➢developing excessive excitability in another place than SA node
➢blockage of transmission of cardiac impulse from SA node to other parts of heart

34. Ectopic pacemaker causes:

➢Abnormal sequence of contraction of of different parts of heart and cause weakness of pumping

35. New pacemaker can be:

➢AV node
➢Purkinje fibers

36. If AV node gets blocked:

➢impulse fails to pass from atria to ventricles through AV nodal bundle system.
➢Purkinje fibers become the new pacemaker (ventricular escape)BUT: Purkinje fibers cannot begin to
be the pacemaker before 15-20 sec passes BECAUSE: before the blockage, the pacemaker was SA node
and because its discharge rate is the fastest, it depressed the suppressed others

37. During those 15 to 20 sec, the person faints BECAUSE: ventricles fail to pump blood-in that period of
time. This is called ‘’Stokes-Adams Syndrome’’

38. For the effective pumping of 2 ventricular chambers at the same time, synchronous contraction is
needed.
➢If impulse travels the ventricles slowly, then much of ventricular muscle mass would contract before
the remaining parts do so the effective pumping would be decreased.

39. Parasympathetic Nerves:

➢distributed to SA and AV nodes, small amount to atria muscles, less amount to ventricular muscles
➢stimulation of parasympathetic nerves to heart (by vagus), causes releasing of ACETYLCHOLINE at
vagal endings.
➢Ach will :
1. decrease rate of rhythm of SA node
2. decrease transmission of blood into the ventricles by decreased excitability
3. decrease the rate of pumping in strong stimulation and can block the transmission causing ventricular
escape or can stop the rhythmical excitation completely
4. increase the permeability to K+ so negativity increases and it is harder to-reach to threshold and
that’s why it is slow.

40. Sympathetic Nerves:

➢distributed to all parts of the heart
➢stimulation of sympathetic sympathetic nerves to heart (by vagus) causesreleasing of
NOREPINEPHRINE at vagal endings
➢NE will cause:
1. increased frequency of heartbeat
2. increased force of contraction (because of the increased Ca++ permeability)
3. increased rate of sinus node discharge
4. increased excitability
5. increased the permeability to Na+ and Ca++ so negativity decreases and it’seasier to reach the
threshold