Properties of Cardiac Muscle and Conducting Systems
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Transcript of Properties of Cardiac Muscle and Conducting Systems
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PHYSIOLOGICAL ANATOMY• Mammalian Heart has
4 chambers- 2 atria and 2 ventricles
• Right side- pulmonary circulation
• Left side- systemic circulation
• Contraction is called systole and relaxation is called diastole
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• Two types of muscle fibers- contractile and conducting
• Contractile fibers in atria and ventricles- form two functional syncytia due to presence of gap junctions
• Conducting system includes SA Node, internodal tracts, AV Node, Bundle of His, Bundle branches and purkinje fibers
• Conducting system has-• i) less cross-striations• ii) less glycogen• iii) do not contract
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CONDUCTING SYSTEM• SA Node- • Small, flattened, ellipsoid strip of specialized
muscle • Size- 3x15x1mm• Situation- superior lateral wall of right atrium
below and lateral to opening of superior venacava
• Pacemaker of heart• P cells- primitive cells- pale- rhythm generators
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• Internodal pathway-• Connect SA Node and
AV Node• Faster rate of
conduction than Atrial muscles
• Anterior- Bachman’s bundle
• Middle- Wenkebach’s bundle
• Posterior- Thorell’s bundle
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• AV Node-• Only conducting pathway between atria
and ventricles normally• Situation- posterior septal wall of RA
immediately behind tricuspid valve• Has thinner fibers with more negative
RMP & fewer gap junctions causing conduction delay
• Velocity of conduction- 0.05m/sec• It acts as pacemaker when SA Node is
damaged
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• Bundle of His-
• It begins from AV Node, passes downwards in the intraventricular septum for 5-15mm
• Divides into right and left bundle branches
• Left branch divides into anterior and posterior fasciculus
• Both divide repeatedly and lie subendocardially
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• Purkinje fibers-
• Takes origin from terminal divisions of bundle branches
• Fastest conducting
• It is 1-2mm thick- largest conducting fiber
• Passes impulses to ventricular myocytes
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PROPERTIES OF CARDIAC MUSCLE
I) Electrical properties i) Autorhythmicity ii) Excitability iii) Conductivity II) Mechanical properties i) Contractility ii) All-or-none law iii) Staircase phenomenon iv) Refractory period
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I. AUTORHYTHMICITY
• All the cells of heart have an inherent ability to generate impulse
• SAN is the pacemaker of heart
• Rates of impulse generation-
• SAN- 70 to 80/min
• AVN- 40 to 60/min
• Purkinje fibers- 15 to 40/min
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Action potential in SAN
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MECHANISM OF SELF-EXCITATION
• RMP of SAN is -60mv (that of contractile cardiac fibers is –90mv)
• It has a pre-potential, a spike,& a repolarization phase.
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I) Pre-potential or pacemaker potential- i) due to ca2+ influx through Transient (T-type) of ca2+channels
ii) TMP changes from -60mv towards positivity
II) Spike potential- i) starts at threshold potential of -40mv ii) due to opening of voltage-gated Ca2+
channels (L-type or long-standing type) iii) potential peaks to +20mv
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III) Repolarisation-
i) due to closure of Ca2+ channels and opening of K+ channels
Significance of Pre-potential
a) It is characteristic of tissues with automaticity
b) It is prominent in SAN and AVN
c) Alterations in pre-potential will alter the rate of impulse generation
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FACTORS AFFECTING AUTORHYTHMICITY
i) Autonomic nerve stimulation a) vagal stimulation decreases the slope of pre-
potential and reduces the rate of impulse generation
b) sympathetic stimulation increases the slope and increases the impulse rate
ii) Temperatureiii) Hormonesiv) Drugsv) Ions- a) K+ increased K+ in ecf decreased
RMPhyperpolarisationreduced heart rate diastolic arrest
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Vagal stimulation
Release of acetylcholine
Ach binds to M2 muscarinic receptor
β subunit of G-protein act on K+ channels
Opening of K + channels
Reduced cAMP
Reduced Ca2+ influx
Decreased pre-potential slope
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Sympathetic stimulation
Release of noradrenaline
Binds to β1 receptors
Increased cAMP
Opening of L-type Ca2+ channels
Increased Ca2+ influx
Reduced pre-potential slope
Increased rate of impulse generation
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EXCITABILITY
• Ability Of excitable tissues to show change in potential when stimulated
• Chronaxie of cardiac muscle is 3-30ms
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ACTION POTENTIALS IN VARIOUS CARDIAC CELLS
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ACTION POTENTIAL IN VENTRICULAR MYOCYTE
RMP: -90mvPhase 0- rapid influx of Na+
rising TMP to +20mvPhase 1- closure of Na+
channelsPhase 2- plateau- opening of L-type Ca2+ channelsPhase 3- Repolarisation-
closure of Ca2+ channels & opening of K+ channels
Phase 4- RMP
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FACTORS AFFECTING EXCITABILITY
1) Nervous factors
2) Hormones
3) Drugs
4) Ions- K+ acts by altering RMP and Na+ acts on amplitude of AP
5) Temperature
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ORIGIN AND SPREAD OF IMPULSES
SA Node
Anterior bundle of bachman
Middle bundle of wenkebach
Posterior bundle Of thorel
AV Node
Bundle of His
Right & left bundle branches
Purkinje fibers
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0.00
0.03
0.09
0.16
0.17
0.18
0.19
0.20
0.21
0.22
0.21
0.18
0.19
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CONDUCTION RATESTISSUE m/sec
Atrial muscle 0.3
Internodal tract 1.0
AV Node 0.05
Purkinje fibers 1.5-4
Ventricle muscle 1.0
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AV Nodal delay
• Delay in transmission of impulses to ventricles by 0.13sec-( 0.09 at AVN & 0.04 at AV bundle)
Causes of delay- i) smaller size of fibers ii) smaller number of gap junctions iii) more negative RMPSignificance- a) atria contracts 0.1sec earlier than ventricle b) limits the number impulses transmitted to
ventricles- <230/min
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STOKES ADAMS SYNDROME
• Seen during acute complete AV block
• Ventricles stop beating due overdrive suppression
• Person faints due reduced blood supply to brain
• Ventricle recovers after few seconds & starts generating own impulses
• Rx- artificial pacemaker
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FACTORS AFFECTING CONDUCTIVITY
• 1) Nervous stimulation
• 2) Hormones
• 3) Drugs
• 4) Ions
• 5) temperature
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II.MECHANICAL PROPERTIES
I.CONTRACTILITY :-
# excitation-contraction coupling is almost similar to that of skeletal muscle
# it depends more on ECF Ca2+
# Ryanodine receptors are triggered open by DHP receptors
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con trac tion
C a2 + in to sa rcop lasm
op en in g o f R yan od in e ch an n e ls in te rm in a l c is te rn ae
D H P recep to r ac ts as sen sor an d trig g er
op en in g o f vo ltag e-g a ted (D H P ) C a2 + ch an n e ls in T-tu b u les
ac tion p o ten tia l
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FACTORS AFFECTING CONTRACTILITY
1) nervous factors- sympathetic acting via 1 receptor & cAMP
2) Drugs- digitalis- inhibits Na+-K+ pump
3) Ions-
* Ca2+- increases force of contraction- systolic arrest
4) temperature
5) load
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EFFECT OF LOAD ON CONTRACTILITY
• Pre-load: it is the load acting on heart before it starts contracting
• After-load: it is the load acting on heart after it starts contracting- resistance
• Frank starling’s law- the force of contraction is proportional to initial length of the muscle within the physiological limits
• Initial length depends on pre-load, i.e, end-diastolic volume(130ml).
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LENGTH-TENSION RELATIONSHIP
• As the preload increases the tension increases
• Passive tension is given by diastolic intraventricular pressure
• Total tension is indicated by systolic intraventricular pressure
• Descending limb at high degree of stretch is due to disruption of myocardial fibers
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FORCE TENSION RELATIONSHIP
0
5
10
5 10
P0 Maximum isometric forceLoad (gm)
Ve
loc
i ty
of
sho
rte
nin
g (
mm
/se
c)
V max
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ALL OR NONE LAW• Action potential fails to occur if the
stimulus is subthreshold in magnitude, and it occurs with constant amplitude and form regardless of the strength of the stimulus if the stimulus is at or above the threshold.
1V 2V 3V 4V
subthreshold threshold Maximal
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STAIRCASE PHENOMENON (TREPPE)
• after a brief rest, on stimulation at regular frequency the force of contraction increases progressively to a maximum and then is maintained at a plateau
2V 2V 2V 2V 2V 2V
>
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• Causes of staircase effect :
1) Increased accumulation of calcium
2) Increased temperature
3) Reduced viscosity
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REFRACTORY PERIODDef: it is the duration during which an excitable tissue
will not respond to a second stimulus
Characteristics of cardiac refractory period:-
Long refractory period-
ARP- 250ms
RRP- 50ms
refractory period of atria-150ms
Significance of long refractory period-• Cardiac muscle is non-tetanisable• It is non-fatiguable