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HEART PHYSIOLOGY
RHYTHMICAL EXCITATION OF HEART
By
Dr. Mudassar Ali Roomi (M.B;B.S, M.PHIL.)
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CONDUCTION SYSTEM OF HEART
SA node
Internodal pathways
AV node
AV bundle of His
Right and left bundle
branches
Purkinje fibers
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Conduction System of the Heart
SA node: sinoatrial node. The pacemaker. Specialized cardiac muscle cells. Generate spontaneous action potentials
(autorhythmic tissue). Action potentials pass to atrial muscle cells
and to the AV node
AV node: atrioventricular node. Action potentials conducted more slowly
here than in any other part of system. Ensures ventricles receive signal to
contract after atria have contracted
AV bundle: passes through hole in cardiacC.T. skeleton to reach interventricularseptum
Right and left bundle branches: extendbeneath endocardium to apices of rightand left ventricles
Purkinje fibers: Large diameter cardiac muscle cells with
few myofibrils. Many gap junctions. Conduct action potential to ventricular
muscle cells (myocardium) very rapidly
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SA nodal action potential
Resting membranepotential of the SA nodalfiber is -55 to -60 mvolts.
The cause of this lessernegativity is that the cellmembranes of the sinusfibers are naturally leakyto Na+ and Ca++ ions andentry of these ionsneutralize much of theintracellular negativity.
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-100
-80
-40
-60
+20
0
-20
2 3 40 1
Seconds
Mem
branePotential(mV)
Threshold
Sinus Nodal
Fiber
Na+
Leak
Slow Ca++Channels Open
K+ Channels
Open more
Ventricular
Muscle fiber
SA NODAL AND VENTRICULAR MUSCLE ACTION POTENTIALUS
NODAL FIBER
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SA nodal action potential At -55 mvolts, the fast Na+ channels
become inactivated.
Therefore, only the slow sodium-
calcium channels can open and cause
the depolarization.
As a result, the SA nodal action
potential is slower to develop thanthe that of the ventricular muscle.
Therefore, the inherent leakiness of
the sinusnodal fibers to Na+ and
Ca++ ions causes their self-
excitation.*******
The slowly drifting resting membrane
potential which reaches to threshold
by itself is also called as pre-potential
or pacemaker potential.
The early part of the prepotential is
because ofJune 4, 2012 6
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SA nodal action potential
Note: There is no phase 1 and 2 in the action
potential of SA nodal fibers.
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THE MECHANISM OF PRE POTENTIAL SLOPE:
SA Nodal fibers membrane isnaturally more leaky to sodium andcalcium
As soon as the membrane potentialreaches to the Resting value, themembrane becomes immediately
less permeable to potassium. Thisallows the negativity of membranepotential to decrease towards thethreshold of excitation
The last of portion of pre potential isdue to activation of (transient) T -Type of slow calcium sodiumchannels. At -40 mV there is openingof L- type of calcium sodiumchannels. L = Transient Type
T= Lasting type
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WHAT DETERMINES THE HEART RATE?
Slope of pre potential determines the heart rate.
More steep- increased heart rate.
Less steep- decreased heart rate.
On sympathetic stimulation, there is increase in heart rate.
Norepinephrine released from sympathetic fibers, increases the
permeability of SA nodal fibers membrane to sodium and calcium.
On vagal stimulation there is slowing of heart rate. There is release of
acetylcholine which acts on SA nodal fibers to increase its permeability for
potassium. Which causes hyperpolarization and less steep of prepotential.
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Rate of impulse generation in heart:
SA NODE: 70-80/min
AV NODE: 40-60/min
AV BUNDLE,BRANCHES & VENTRICLES: 15-40/min
SA NODEPACEMAKER
OTHERS ECTOPIC FOCI
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AV Node, and Delay of Impulse Conduction from the
Atria to the Ventricles
Locationof the A-V node:in the posterior wall of theright atrium immediatelybehind the tricuspid valve
there is a delay of 0.09second in the A-V node
A delayof another 0.04second occurs mainly in A-Vbundle
Thus, the total delay in theA-V nodal and A-V bundlesystem is about 0.13second.
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AV Node, and Delay of Impulse Conduction
from the Atria to the Ventricles
Cause of the Slow Conduction:
caused mainly bydiminished numbers of gapjunctions b/w successivecells in the conductingpathways
Importance of AV nodal delay:
this delay allows time forthe atria to empty theirblood into the ventriclesbefore ventricularcontraction begins
One-Way ConductionThrough the A-V Bundle?
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Rapid Transmission in the Ventricular
Purkinje System They are very large fibers, even larger
than the normal ventricular muscle fibers
and they transmit action potentials at a
velocity of 1.5 to 4.0 m/sec, a velocity
about 6 times that in the usual ventricular
muscle and 150 times that in some of the
A-V nodal fibers.
Cause of rapid transmission:
The rapid transmission of action potentials
by Purkinje fibers is believed to be caused
by a very high level of permeability of the
gap junctions at the intercalated discs
between the successive cells that make upthe Purkinje fibers.
FUNCTION: rapid transmission in Purkinje
fibers is responsible for synchronous
contraction of ventricular muscle.
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Conduction velocities of hearttissues:
ATRIAL MUSCLE= 0.3m/sec
INTERNODAL PATHWAYS=
1m/sec AV NODE: slowest 0.05-
0.1m/sec
AV BUNDLE &BRANCHES/PURKINJE SYSTEM:
Maximum velocity= 1.5-4m/sec
VENTRICULAR MUSCLE=0.5m/sec
SUMMARY OF SPREAD OF THE CARDIAC IMPULSE THROUGH
THE HERAT
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Effect Of Sympathetic And Parasympathetic
Stimulation On Heart???
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Parasympathetic Effectson Heart
Parasympathetic (vagal) nerves,which release acetylcholine at theirendings, innervate SA node and A-V
junctional fibers proximal to A-Vnode.
Mechanism: Causeshyperpolarization because of
increased K+ permeability in responseto acetylcholine.
This causes decreased transmissionof impulses (-ve dromotropic effect)may be temporarily stopping heartrate.
Decreased heart rate by decreasing
the frequency of impulse generation(-ve chronotropic effect) Minimal decrease of force of
contraction. decreased excitability of heart (-ve
bathmotropic effect)
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