The document describes the conducting system of the heart, which generates electrical impulses that cause rhythmic heart contractions. It has specialized tissues that conduct electrical impulses, including the sinoatrial node, atrioventricular node, bundle of His, and Purkinje fibers. The sinoatrial node acts as the primary pacemaker and initiates impulses that spread to the atria. The atrioventricular node delays conduction to allow for proper atrial filling of the ventricles before their contraction. The Purkinje fibers rapidly conduct impulses throughout the ventricles. This specialized conduction system ensures coordinated heart contractions and blood flow.
Cardiac muscle has three types of membrane ion channels that play important roles in causing the voltage changes of the action potential. They are (1) fast sodium channels, (2) slow sodium-calcium channels, and (3) potassium channels
Depolarization: First, the action potential of cardiac muscle is caused almost entirely by sudden opening of large numbers of so-called fast sodium channels that allow tremendous numbers of sodium ions to enter the cardiac muscle fiber from the extracellular fluid. These channels are called “fast” channels because they remain open for only a few thousandths of a second and then abruptly close. After depolarization, there's a brief repolarization that takes place with the efflux of potassium through fast acting potassium channels.
Plateau: Secondly, another entirely different population of slow calcium channels, which are also called calcium-sodium channels. This second population of channels differs from the fast sodium channels in that they are slower to open and, even more important, remain open for several tenths of a second. During this time, a large quantity of both calcium and sodium ions flows through these channels to the interior of the cardiac muscle fiber, and this maintains a prolonged period of depolarization, causing the plateau in the action potential.
Repolarization: When the slow calcium-sodium channels do close at the end of 0.2 to 0.3 second and the influx of calcium and sodium ions ceases, the membrane permeability for potassium ions also increases rapidly; this rapid loss of potassium from the fiber immediately returns the membrane potential to its resting level, thus ending the action potential.
Cardiac muscle has three types of membrane ion channels that play important roles in causing the voltage changes of the action potential. They are (1) fast sodium channels, (2) slow sodium-calcium channels, and (3) potassium channels
Depolarization: First, the action potential of cardiac muscle is caused almost entirely by sudden opening of large numbers of so-called fast sodium channels that allow tremendous numbers of sodium ions to enter the cardiac muscle fiber from the extracellular fluid. These channels are called “fast” channels because they remain open for only a few thousandths of a second and then abruptly close. After depolarization, there's a brief repolarization that takes place with the efflux of potassium through fast acting potassium channels.
Plateau: Secondly, another entirely different population of slow calcium channels, which are also called calcium-sodium channels. This second population of channels differs from the fast sodium channels in that they are slower to open and, even more important, remain open for several tenths of a second. During this time, a large quantity of both calcium and sodium ions flows through these channels to the interior of the cardiac muscle fiber, and this maintains a prolonged period of depolarization, causing the plateau in the action potential.
Repolarization: When the slow calcium-sodium channels do close at the end of 0.2 to 0.3 second and the influx of calcium and sodium ions ceases, the membrane permeability for potassium ions also increases rapidly; this rapid loss of potassium from the fiber immediately returns the membrane potential to its resting level, thus ending the action potential.
How to Make a Field invisible in Odoo 17Celine George
It is possible to hide or invisible some fields in odoo. Commonly using “invisible” attribute in the field definition to invisible the fields. This slide will show how to make a field invisible in odoo 17.
Macroeconomics- Movie Location
This will be used as part of your Personal Professional Portfolio once graded.
Objective:
Prepare a presentation or a paper using research, basic comparative analysis, data organization and application of economic information. You will make an informed assessment of an economic climate outside of the United States to accomplish an entertainment industry objective.
Unit 8 - Information and Communication Technology (Paper I).pdfThiyagu K
This slides describes the basic concepts of ICT, basics of Email, Emerging Technology and Digital Initiatives in Education. This presentations aligns with the UGC Paper I syllabus.
Synthetic Fiber Construction in lab .pptxPavel ( NSTU)
Synthetic fiber production is a fascinating and complex field that blends chemistry, engineering, and environmental science. By understanding these aspects, students can gain a comprehensive view of synthetic fiber production, its impact on society and the environment, and the potential for future innovations. Synthetic fibers play a crucial role in modern society, impacting various aspects of daily life, industry, and the environment. ynthetic fibers are integral to modern life, offering a range of benefits from cost-effectiveness and versatility to innovative applications and performance characteristics. While they pose environmental challenges, ongoing research and development aim to create more sustainable and eco-friendly alternatives. Understanding the importance of synthetic fibers helps in appreciating their role in the economy, industry, and daily life, while also emphasizing the need for sustainable practices and innovation.
Francesca Gottschalk - How can education support child empowerment.pptxEduSkills OECD
Francesca Gottschalk from the OECD’s Centre for Educational Research and Innovation presents at the Ask an Expert Webinar: How can education support child empowerment?
1. Conducting System of the Heart
(Junctional Tissue)
Dr.Viral I. Champaneri, MD
Assistant Professor
Department of Physiology
1
2. Conducting System of the Heart
• Heart has Special system
• That Generates Electrical impulses
• To Cause Rhythmic Contractions
2
3. Conducting System of the Heart
• Heart
• Specialized pathway
• Conducts Electrical impulses
3
4. Electrical impulses
• Allow the atria to contract
• Before ventricles
• Proper filling of the ventricles
• Ventricles pumps the
• Blood to the various parts of the body
4
5. Conducting System of the Heart
• This special system which is
• Combination of
• Specialized excitable tissues & Pathway
• Conducting system & Junctional tissue
5
6. Conducting System of the Heart
1. Sinoatrial node (SA node)
2. Atrioventricular node (AV node)
3. Bundle of His
4. Right & Left Bundle branches (RBB & LBB)
5. Purkinje fibers
6
7. SA node (Sinoatrial node)
• Small
• Flattened
• Ellipsoid strip of Specialized cardiac tissue
7
9. SA node Location
• Superior Posterolateral wall of the Right atrium
• Immediately below and
• Slightly lateral to the
• Opening of the Superior vena cava (SVC)
9
10. SA node Location
• At the junction of the
• Superior vena cava (SVC) and
• The Right atrium (RA)
10
11. SA node (Sinoatrial node)
• Fibers No contractile muscle filaments
• In diameter 3 to 5 micrometers
• Diameter of 10 to 15 micrometers
• For the surrounding Atrial muscle fibers
11
13. SA node Innervation
• The Right Vagus
• Right Xth CN Parasympathetic
• Mainly distributed to SA node
13
14. SA node Pacemaker
• Primary (Normal) pacemaker
• Generates Maximum number of impulses
• 70-80 / minute
• Sets the pace of the heartbeat Pacemaker
14
15. Automatic Electrical Rhythmicity of the
Sinus Fibers
• Some Cardiac fibers have the capability of
• “Self-excitation”
• A process that can cause Automatic
• Rhythmical discharge and contraction
15
16. Automatic Electrical Rhythmicity
• Capability Automatic Rhythmical discharge and
contraction
• Is especially true of the fibers of
• The heart’s specialized conducting system
16
17. Automatic Electrical Rhythmicity of the
Sinus Fibers
• The Fibers of the sinus node (SA node)
• For this reason...
• The sinus node ordinarily
• Controls the rate of beat of the entire heart
17
18. Self excitation of SA nodal Fibers
1. Action potential
2. Recovery from the action potential
3. Hyperpolarization After the action potential
is over
18
19. Self excitation of SA nodal Fibers
4. Drift of the “Resting” potential to Threshold
5. Finally re-excitation to elicit another cycle
• Process continues throughout a person’s life
19
21. Pacemaker Potential
• The cells of the SA node
• Do not maintain a
• Resting Membrane Potential (RMP)
• In the manner of
• Resting neurons or skeletal muscle cells
21
22. Pacemaker Potential / Prepotential
• During the period of Diastole (Relaxation)
• The SA node exhibit
• Slow Spontaneous depolarization
• Called the Pacemaker potential / Prepotential
22
23. Resting Membrane Potential of SA node
• “Resting membrane potential”
• Of the Sinus nodal (SA) fiber
• Between discharges
• − 55 mV to − 60 millivolts
23
24. RMP of SA node : − 55 to − 60 mV
• In comparison with
• − 85 to − 90 millivolts
• Of the ventricular muscle fiber
24
25. Cause of this Lesser Negativity
• Cell membranes of the sinus fibers
• Naturally leaky to Na+ and Ca2+ ions
• Positive charges of the entering Na+ and Ca2+ ions
• Neutralize some of the intracellular negativity
25
26. Self excitation of Sinus Nodal fibers
• High sodium ion concentration [Na+]
• In the ECF outside SA nodal fiber
• Moderate number of already open Na+ channels
• Na+ from outside
• Normally tend to leak to the Inside (Influx)
26
27. Inherent leakiness to Na+ & Ca2+
• SA nodal fibers
• To Na+ and Ca2+ ions
• Causes Self-excitation Autorythmicity
27
28. Between Heartbeats
• Influx of positively charged Na+ ions
• Causes Slow rise in the RMP
• In the Positive direction
• Become Less negative
28
29. Potential Reaches Threshold voltage
• −40 millivolts
• L-type calcium channels become “Activated”
• Causing the action potential
29
30. SA nodal fibers Not depolarized all the time
• 2 events occur
• During the course of the action potential
• To prevent such a constant state of depolarization
30
32. 1st Event Closure of L –Type Ca2+ channel
• Slow sodium-calcium channel
• L-type calcium channels become Inactivated
• Closes Within about 100 to 150 milliseconds
• After opening
32
33. 1st Event Closure of L –Type Ca2+ channel
• Influx of
• Positive Calcium (Ca2+) and Sodium (Na+) ions
• Through the L-type calcium channels Ceases
33
34. 2nd Event K+ Channels Open
• At about the same time,
• Greatly Increased numbers of
• Potassium (K+) channels Open
34
35. 2nd Event K+ Channels Open
• Potassium (K+) channels Open
• Large quantities of Positive Potassium ions
• Diffuse out Of the fibre
35
36. 2nd Event K+ Channels Open
• Remain open for another Few 10th of a second
• Temporarily continuing movement of
• Positive charges (K+) out of the cell
36
37. Both these 2 events
• Reduce intracellular potential
• Back to Negative resting level (-55 to -60 mV)
• Terminate SA nodal action potential
37
38. Hyperpolarization State
• Excess negativity inside the fiber
• Initially carries
• The “Resting” membrane potential
• Down to about − 65 mV to − 75 mV
• At the termination of the action potential
38
39. Hyperpolarization Not maintained forever
• The next few 10th of a second
• After the Action potential is over
• Progressively
• More and More potassium (K+) channels Close
39
40. Inward – Leaking Na+and Ca2+ ions
• Once again overbalance
• Outward flux of K+ions
• Causes the “Resting” potential
• To drift upward once more
40
41. Again RMP reach Threshold level − 40 mV
• Finally reaching the Threshold level
• For discharge
• At a potential of about − 40 millivolts
41
42. Secondary Pacemaker Regions
• Two potential or secondary pacemaker regions
• The AV node and Purkinje fibers are
• Normally suppressed by….
• Action potentials originating in the SA node
potential
42
44. AP From SA node AV Node
• Sinus nodal fibers
• Connect directly with the atrial muscle fibers
• Action potential that begins in the sinus node
• Spreads immediately into the Atrial muscle wall
44
45. Internodal & Interatrial Pathways
• Ends of the sinus nodal (SA) fibers
• Connect directly
• With surrounding Atrial muscle fibers
45
46. Internodal & Interatrial Pathways
• Action potentials originating
• In the Sinus node (SA node)
• Travel outward into Atrial muscle fibers
46
47. Internodal & Interatrial Pathways
• The Action potential
• Spreads through the entire Atrial muscle mass
• Eventually To the A-V node
47
49. Anterior Interatrial Band
• Passes through Anterior walls of the atria
• To the Left atrium
• Conduction is more rapid About 1 m/sec
49
50. 3 Internodal Atrial Pathways
• 3 other small bands
• Curve through
• The Anterior, Lateral, Posterior Atrial walls
• Terminate in the A-V node
50
51. 3 Internodal Atrial Pathways
1. Anterior bundle of Bachmann
2. Middle bundle of Wenckebach
3. Posterior bundle of Thorel
51
52. 3 Internodal Atrial Pathways
• Fibers are similar to
• Even more rapidly conducting
• “Purkinje fibers” of the ventricle
52
53. 3 Internodal Atrial Pathways
• Cause of more rapid velocity of conduction in
these 3 bands
• Presence of Specialized conduction fibers
53
54. AV node delays impulse : Atria Ventricles
• Atrial conductive system is organized such
• The cardiac impulse Does not travel
• From the atria into The ventricles too rapidly
54
55. Importance of A-V nodal delay
• Allows time For the atria
• To empty their blood into the ventricle
• Before Ventricular contraction begins
55
56. A-V node & Adjacent conductive fibers
• Delay this transmission into the ventricles
56
57. A-V node Location
• In the
• Posterior wall of the Right atrium (RA)
• Immediately
• Behind the tricuspid valve (RA RV)
57
58. A-V node Development
• Develops from
• Left-sided embryonic structures
• Between Atrium and Ventricle
• Closed to the AV opening
58
60. A-V node Produce Impulse
• Can produce impulses at rate
• 50-60 / min
60
61. Penetrating A-V bundle
• Composed of multiple small fascicles
• Passing through The fibrous tissue
• Separating the atria from the ventricles
61
62. Interval of time taken by Cardiac Impulse to travel
Origin of
Impulse
(From)
Reaches
Time taken
(Seconds)
Delay
(Seconds)
Total Delay
(Seconds)
SA node A-V node 0.03 sec 0.03 sec 0.03 sec
A-V node
Penetrating
Portion of
A-V bundle
0.12 sec 0.09 sec 0.12 sec
Penetrating
Portion of
A-V bundle
Contracting
muscles of
Ventricles
0.16 sec 0.04 sec 0.16 sec
62
63. Cause of Slow Conduction
• Transitional, Nodal, and Penetrating A-V bundle
fibers mainly by...
• Diminished numbers of gap junctions
• Between Successive cells
• In the conducting pathways
63
64. Cause of Slow Conduction
• Diminished numbers of gap junctions
• In the conducting pathways
• So, Great resistance to conduction of
• Excitatory ions
• From one conducting fibre to the next
64
65. Bundle of His (Hiss)
• Beginning
• At the top of the interventricular septum.
• Pierces
• The fibrous skeleton of the heart
• Continues
• To descend along the interventricular septum
65
66. Right & Left Bundle Branch
• The Atrioventricular Bundle of Hiss divides
• Into
• Right (RBB) and Left (LBB) bundle branches
66
67. One way conduction through A-V bundle
• A-V bundle is Unable to travel
• Action potentials
• Backward from The Ventricles to The Atria
• Except In abnormal states
67
68. One way conduction through A-V bundle
• Prevents re-entry of cardiac impulses
• By this route from the ventricles to the atria
• Allowing Only forward conduction
• From the atria to the ventricles
68
69. Continuous Fibrous Barrier
• The Atrial muscle
• Is separated from the Ventricular muscle
• By a Continuous fibrous barrier
• Except At the A-V bundle
69
70. Continuous Fibrous Barrier Function
• Normally acts as an Insulator
• To prevent passage of the cardiac impulse
• Between atrial and ventricular muscle
• Through any other route
70
71. Re-entry of Cardiac impulsePrevented
1. Forward conduction through the A-V bundle
2. Insulator continuous fibrous barrier
71
72. Rare instances Abnormal Muscle Bridge
• Penetrate the fibrous barrier elsewhere
• Besides at the A-V bundle
• Cardiac impulse can Re-enter the atria
• From the ventricles
• Serious cardiac arrhythmias
72
73. Ventricular Purkinje System
• Special Purkinje fibers
• Lead from the A-V node
• Through The A-V bundle into Ventricles
• Generate impulse at 15-40 impulses / min
73
74. Initial Portion of Purkinje System
• Where They penetrate the A-V fibrous barrier
• They have Functional characteristics
• Quite the opposite of those of the A-V nodal fibers
74
75. Purkinje System :1.5 to 4.0 m/sec
• Very large fibers
• Even larger than the normal ventricular muscle
fibers
• Transmit action potentials at a velocity of
• 1.5 to 4.0 m/sec
75
76. Purkinje System : Velocity of conduction
• 6 times that in the usual ventricular muscle
• 150 times that in some of the A-V nodal fibers
• Instantaneous transmission of the cardiac impulse
• Throughout the entire remainder of the
ventricular muscle
76
77. Rapid Transmission of AP by Purkinje fibers
• Very high level of permeability of the gap
junctions
• At the intercalated discs
• Between the successive cells make Purkinje fibers
77
78. Rapid Transmission of AP by Purkinje fibers
• High level of permeability of the gap junctions
• Ions are transmitted
• Easily from one cell to the next
• Enhancing the velocity of transmission
78
79. Ventricular Purkinje System
• Contain Very few myofibrils
• They contract little or not at all
• During the course of impulse transmission
79
80. Distribution of Purkinje fibers in ventricles
• After penetrating
• The continuous fibrous tissue
• Between the Atrial and Ventricular muscle
80
81. Distribution of Purkinje fibers in Ventricles
• The distal portion of the A-V bundle
• Passes downward in the ventricular septum
• For 5 to 15 millimeters
• Toward the apex of the heart
81
82. Right & Left Bundle Branch
• The Atrioventricular bundle divides...
• Into
• Right and Left bundle branches
82
83. Distribution of Purkinje fibers in ventricles
• The A-V bundle divides
• Into Left and Right bundle branches
• Lie beneath the Endocardium
• On the two respective
• Sides of the ventricular septum
83
84. Left and Right Bundle Branch
• Each branch spreads
• Downward toward the apex of the ventricle
• Progressively dividing Into smaller branches
84
85. Smaller branches
• In turn course
• Sidewise around each ventricular chamber
• Left & Right Ventricular Chamber
85
87. End of Purkinje Fibers Penetrate
• About one third (1/3rd) of the way
• Into the muscle mass
• And finally become
• Continuous with The cardiac muscle fibers
87
88. Total elapsed Time Avg. 0.03 sec
• From The time the cardiac impulse Enters
• The bundle branches in the ventricular septum
• Until
• It reaches the terminations of the Purkinje fibers
88
89. Once Cardiac Impulse Enters Purkinje system
• It spreads Almost Immediately
• To the entire ventricular muscle mass
89
90. Transmission of Cardiac Impulse in
Ventricular muscle
• Once the impulse
• Reaches the ends of the Purkinje fibers
• It is transmitted through the ventricular muscle
mass by the ventricular muscle fibers themselves
90
91. Velocity of Transmission in Ventricular Muscle
• 0.3 to 0.5 m/sec
• One sixth (1/6th)
• That in the Purkinje fibers
91
92. Cardiac Muscle Wraps the Heart
• In a double spiral
• With Fibrous septa
• Between the Spiraling layers
92
93. Cardiac Muscle Wraps the Heart
• Directly
• Outward toward the surface of the heart
93
94. Cardiac Impulse Angulates
• Instead Angulates
• Toward the surface
• Along the directions of the spirals
94
95. Because of Angulation
• Transmission
• From Endocardial surface
• To Epicardial surface of the ventricle
• Requires Another 0.03 second
95
96. 0.03 sec Approximately equal to the time
• Required for transmission through
• The entire ventricular portion of the purkinje
system
96
97. Total time 0.06 sec
• For transmission of the cardiac impulse
• From The initial bundle branches
• To The last of the ventricular muscle fibers
• In the Normal heart is about 0.06 second
97
98. Summary of Spread of Cardiac Impulse
• Origin of the cardiac impulse in Sinus node
• Impulse spreads
• At moderate velocity through the atria
• Atrial depolarization is complete in about 0.1 s
98
99. Summary of Spread of Cardiac Impulse
• Delayed > 0.1 second in A-V nodal region
• Before
• Appearing in the ventricular septal A-V bundle
99
100. Summary of Spread of Cardiac Impulse
• Because conduction in the AV node is slow
• A delay of about 0.1 s (AV nodal delay)
• Occurs before excitation spreads to the ventricles
100
101. AV Nodal Delay
• When there is a lack of contribution of INa
• In the depolarization (phase 0) of the action
potential
• A marked loss of conduction is observed
101
102. AV Nodal Delay (0.1 s) Shortened
• Stimulation of
• The sympathetic nerves to the heart
102
103. AV Nodal Delay (0.1 s) Lengthened
• Stimulation of
• The Vagi ( Xth - CN Parasympathetic
103
104. Impulse enter in Bundle of His
• Once it has entered this bundle,
• It spreads very rapidly
• Through the Purkinje fibers
• To the entire endocardial surfaces of the ventricles
104
105. Impulse enter in Bundle of His
• From the top of the septum
• The wave of depolarization spreads
• In the rapidly conducting Purkinje fibers
105
106. Purkinje fiber Ventricles
• To all parts of ventricles
• Impulse spreads 0.08 – 0.1 sec
106
107. In Humans Direction of Spread of Impulse
• Depolarization of the ventricular muscle
• Starts
• At the Left side of the interventricular septum
107
108. In humans Direction of Spread of Impulse
• Moves First to the right
• Across the mid portion of the interventricular
septum
108
109. In humans Direction of Spread of Impulse
• The wave of depolarization then
• Spreads down the septum
• To the apex of the heart
109
110. In humans Direction of Spread of Impulse
• Returns along the ventricular walls
• To the AV groove
• Proceeding
• From the Endocardial to the Epicardial surface
110
111. Last portion of Heart to be Depolarized
1. Posterobasal portion of the left ventricle
2. Pulmonary conus
3. Uppermost portion of the septum
111