1. Electrical Properties of the Heart Chapters 9 and 10

2. Review of Heart Muscle Has actin and myosin filaments
Cardiocytes, myocardium
Branched cells
Intercalated discs- (desmosomes) and electrical junctions (gap junctions).
Has actin and myosin filaments
Has low resistance (1/400 the resistance of cell membrane)
Atrial syncytium
Ventricular syncytium
Fibrous insulator exists between atrium and ventricle (what would this do to any electrical activity trying to go through?)
Figure 9-1; Guyton & Hall

3. If the electrical signals from the atria were conducted directly into the ventricles across the AV septum, the ventricles would start to contract at the top (base). Then the blood would be squeezed downward and trapped at the bottom of the ventricle.
The apex to base contraction squeezes blood toward the arterial opening at the base of the heart.
The AV node also delays the transmission of action potentials slightly, allowing the atria to complete their contraction before the ventricles begin their contraction. This AV nodal delay is accomplished by the naturally slow conduction through the AV node cells. (Why are they slow conductors? Small diameter cells, fewer channels. Refer to text)

4. Fibers within the heart
Specialized Fibers
are the fibers that can spontaneously initiate an AP all by themselves!
The AP will spread to all other fibers via gap junctions
AKA “leading cells”
But they are also muscle, so they do contract, albeit feebly!
They are not nerves!!!!
Contractile Fibers
These maintain their RMP forever, unless brought to threshold by some other cell
They cannot generate an AP by themselves
AKA “following cells”
But they do have gap junctions, so once they’re triggered, they will help spread the AP to neighbors.

5. Pathway of Heartbeat Begins in the sinoatrial (S-A) node
Internodal pathway to atrioventricular (A-V) node
Impulse delayed in A-V node (allows atria to contract before ventricles)
A-V bundle takes impulse into ventricles
Left and right bundles of Purkinje fibers take impulses to all parts of ventricles
KEY Red = specialized cells;
all else = contractile cells

6. Sinus Node Specialized cardiac muscle connected to atrial muscle.
Acts as pacemaker because membrane leaks Na+ and membrane potential is -55 to -60mV
When membrane potential reaches -40 mV, slow Ca++ channels open causing action potential.
After msec Ca++ channels close and K+channels open more thus returning membrane potential toward -55mV.

7. A-V Node Internodal Pathways Delays cardiac impulse
Transmits cardiac impulse throughout atria
Anterior, middle, and posterior internodal pathways
Anterior interatrial band carries impulses to left atrium.
A-V Node
Delays cardiac impulse
Most delay is in A-V node
Delay AV node sec.
Delay AV bundle sec.

8. Purkinje System A-V Bundles
Only conducting path between atria and ventricles
Divides into left and right bundles
Time delay of 0.04sec
Fast conduction; many gap junctions at intercalated disks

9. Time of Arrival of Cardiac Impulse
(0.22)
SA Node
AV Bundle H
(0.19)
(0.0) T
(0.03)
(0.12)
Left Bundle
Branch
(0.16)
(0.19)
(0.18)
AV Node
Right Bundle
Branch
(0.21)
Main Arrival Times
S-A Node sec
A-V Node sec
A-V Bundle sec
Ventricular Septum sec
Base sec
(0.17)
(0.18)
Copyright © 2006 by Elsevier, Inc.

10. How can these Specialized fibers spontaneously “fire?”
Can’t hold stable resting membrane potential
Potentials drift (gradual depolarization) –”prepotential” or “pacemaker potential”
During this time, they have a gradually increasing perm to Na+ and less leaky to K+ (more “+” inside causes cell to depolarize, remember?)
Na+

11. Specialized fibers Notice slow rise from rest to threshold.
This is called the “prepotential” or “pacemaker potential”
Only specialized fibers of the heart can do this.
This is what gives the heart it’s rhythm.

12. Membrane Potential (mV)
Rhythmical Discharge of Sinus Nodal Fiber
Slow Ca++
Channels Open
Sinus Nodal
Fiber
Ventricular
Muscle fiber
K+ Channels
Open more
+20
Threshold
-20
-40
Membrane Potential (mV) }
-60
“Pre- Potential”
-80
Na+ Leak
And less leaky to potassium
-100 1 2 3 4
Seconds

13. Specialized fibers of conductive system
Each region generates its own rhythm.
If cells didn’t touch, then….
Faster at SA vs AV node, etc.
SA is faster than AV- “pacemaker”
SA depol/min
AV depol/min
Purkinje depol/min
Draw it! SA AV
Pur
Because SA node has the highest intrinsic rhythm, it is called the cardiac pacemaker. What if damaged…?
Time (min)

14. Specialized fibers of conductive system
These rhythms can ALSO be modified by the ANS
NTS can change slope of prepotentials…faster or slower rise to threshold (bringing them closer or further from threshold.) by altering ion permeability.
ACh (psymp postganglionic); NE (symp postganglionic)
K+ efflux

15. Sympathetic and Parasympathetic
Sympathetic – speeds heart rate by  Ca++ & Na+ channel influx and  K+ permeability/efflux (positive chronotropy)
Parasympathetic – slows rate by  K+ efflux &  Ca++ influx (negative chronotropy)
Figure 14-17: Modulation of heart rate by the nervous system

16. Other effect of ANS
Symp (NE) also affects inotropy in ALL fibers, specialized and contractile
Inotropy is the “force of contraction” or the tension development in the muscle fiber (strength of the contraction.)
Sympathetic firing causes positive inotropy! (the pounding heart)
Parasympathetics have little effect on inotropy
Terminology: Chrono, Inotropy Symp (+,+) Parasym ( -, )

17. Regulators of the Heart: Reflex Controls of Rate
Your HR at any moment is the balance between symp and parasym discharge rates. (“tone”/ reserve)
Tonic discharge
How to speed up? Two ways (faucet analogy)
How to slow down? Two ways
Range: about 50 – near 200
Typical resting HR: near 70 --SA would normally beat at bpm- but vagal tone slows it down. Parasympathetic slows-down (20bpm or even stop)-
Sympathetic speeds-speed up (230bpm) K+

18. Contractile Fibers of Heart
Bulk of heart mass
Review APs
Still need calcium to initiate contraction
Differences from Skeletal Muscle and neurons
Nature of AP
Source of calcium (EC vs. SR)
Duration of contraction
Resting potential

19. EC Coupling – how it works (skeletal muscle) AP Sequence of Events:
AP moves along T-tubule
The voltage change is sensed by VONa+ Channels
Is communicated to the (VOCC) (voltage operated calcium channel; VOCR) how much calcium released depends on voltage
Contraction occurs.
Calcium is pumped back into SR. Calcium binds to calsequestrin to facilitate storage.
Contraction is terminated. AP
Ca2+ pump
calsequestrin

20. EC Coupling – Cardiac Muscle AP Sequence of Events: Ca2+/Na+ exchanger
(Ca2+ out / Na+ in)
Sequence of Events:
1. AP moves along T-tubule.
2. Activation – voltage sensors that release a small amount of
Ca into the fiber.
3. Ca then binds to a receptor which opens, releasing a large
amount of Ca. (Calcium Activated Calcium Release) How much calcium released depends on how much calcium gets through cell membrane
4. Calcium is pumped (a) back
into SR, and (b) back into T
tubule.
5. Contraction is terminated. AP
Ca2+ pump requires ATP
calsequestrin

21. Slow Ca++ Channels open and decreased K+ permeability
Ventricular Muscle Action Potential-RMP -85mV;
Slow Ca++ Channels open and decreased K+ permeability
Fast Na+ close
K+ Channels
Open 1 2 3 4
phase
+20
-20
Membrane Potential
(mV)
-40
-60
-80
Fast Na+
Channels Open
-100 1 2 3 4
phase 0- Fast Na+ channels open
phase 1- Fast Na+ channels close
phase 2- slow Ca++ open and decreased K+ permeability
phase 3- K+ channels open
phase 4- Resting membrane potential
Seconds
Copyright © 2006 by Elsevier, Inc.

22. Important things to consider
Cardiac muscle cells have a long absolute refractory period
Twitches can not summate
Tetanus not possible (this is good!)
If average heart beats 72bpm; what does the heart do for the rest of the time?
Answer : It “rests” and fills

23. Spread of Depolarization

24. Direction of Depol
Resting Cell

25. Direction of Depol
Stim microelectrode

26. Direction of Depol +
+ + +
Depolarizing Current!
Stim microelectrode

27. Direction of Depol + + +
Depolarizing Current!
Stim microelectrode

28. Direction of Depol + + +
Depolarizing Current!
Stim microelectrode

29. Direction of Depol
Stim microelectrode

30. Direction of Depol
Stim microelectrode

31. Direction of Depol
Stim microelectrode

32. Direction of Depol
Stim microelectrode

33. Direction of Depol
Stim microelectrode

34. Direction of Depol
Stim microelectrode

35. Direction of Depol
Stim microelectrode

36. Direction of Depol
Stim microelectrode

37. Direction of Depol
Stim microelectrode

38. Direction of Depol
Depol = spread of surface NEG charge
Stim microelectrode

39. Direction of Repolarization
Begin Repolarization
Stim microelectrode

40. Direction of Repolarization
- - -
Stim microelectrode

41. Direction of Repolarization
Stim microelectrode

42. Direction of Repolarization
Stim microelectrode

43. Direction of Repolarization
Stim microelectrode

44. Direction of Repolarization
Repolarization= spread of positive surface charge
Stim microelectrode

45. Direction of Repolarization
Stim microelectrode

46. Direction of Repolarization
Repolarization= spread of POS surface charge
Stim microelectrode

47. Depolarization/Repolarization Cycle in the Atria

48. Depolarization Begins
=Resting cell
=Depol cell

49. =Resting cell
=Depol cell

50. =Resting cell
=Depol cell

51. =Resting cell
=Depol cell

52. Depolarization Complete
=Resting cell
=Depol cell

53. Repolarization Begins
=Resting cell
=Depol cell

54. =Resting cell
=Depol cell

55. =Resting cell
=Depol cell

56. Repolarization Complete
=Resting cell
=Depol cell

57. Depolarization/Repolarization Cycle in the Ventricles

58. Depolarization Begins
=Resting cell
=Depol cell

59. =Resting cell
=Depol cell

60. =Resting cell
=Depol cell

61. =Resting cell
=Depol cell

62. Depolarization Complete
=Resting cell
=Depol cell

63. Repolarization Begins
=Resting cell
=Depol cell

64. =Resting cell
=Depol cell

65. =Resting cell
=Depol cell

66. Repolarization Complete
=Resting cell
=Depol cell