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HEART PHYSIOLOGY
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BYDR. MUDASSAR ALI ROOMI (MBBS, M. PHIL)
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Action Potential in the ventricularMuscle
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Ventricular Muscle Action Potential
-100
-80
-40
-60
+20
0
-20
2 3 40 1
MembranePotential
(mV
)
Seconds
Fast Na+
Channels Open
Slow Ca++Channels Open
0
1
2
3
4
p
hase
K+ ChannelsOpen
phase 0- Fast Na+ channels open then slow Ca++ channelsphase 1- K+ channels openphase 2- Ca++ channels open morephase 3- K+ channels open more
phase 4- Resting membrane potential
K+ ChannelsOpen More
Ca++Channels
Open More
Copyright 2006 by Elsevier, Inc.
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c on o en a a ong wionic basis) in the ventricular
MusclePhase 0: Initial upswing of action potential.o fast Na+ Channels open
Phase 1:The potential may repolarize slightly before startingthe plateau phase.
o Na+ Channels are inactivated.
o Outward Rectifier K+ Channels open transiently, causingslight repolarization.
o Membrane potential remains near zero.
Phase 2: Plateau Phase :This stage is responsible forprolonging the cardiac action potential, making it longer thana nerve action potential.
o Ca+2 Channels open, to keep the cells depolarized.
Phase 3: Repolarization
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Action Potential in theventricular Muscle
Some important notes:
plateau phase is not part of
reploarization rather It is sustaineddepolarization.
Duration of AP in ventricular muscle
is around 300 milli sec. most of thisis due to plateau phase.
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SA nodal action potential
Restingmembrane
potential of theSA nodal fiber is-55 to -60mvolts.
The cause ofthis lessernegativity is
that the cell4/25/12 66
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-100
-80
-40
-60
+20
0
-20
2 3 40 1
Seconds
Mem
branePotential(mV)
Threshold
Sinus NodalFiber
Na+Leak
Slow Ca++Channels Open
K+ ChannelsOpen more
VentricularMuscle fiber
}
Re
stingP
otenti
al
Rhythmical Discharge of Sinus Nodal Fiber
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SA nodal action potential At -55 mvolts, the fast Na+
channels becomeinactivated.
Therefore, only the slowsodium-calcium channels canopen and cause the
depolarization.
As a result, the SA nodalaction potential is slower todevelop than the that of theventricular muscle.
Therefore, the inherentleakiness of the sinusnodalfibers to Na+ and Ca++ ionscauses their self-excitation.*******
The slowly drifting restingmembrane potential which4/25/12 88
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SA nodal action potential
Note: There is no phase 1 and 2 inthe action potential of SA nodalfibers.
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THE MECHANISM OF PREPOTENTIAL 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 the
threshold of excitation
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WHAT DETERMINES THE HEARTRATE?
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 tosodium and calcium.
On vagal stimulation there is slowing of heart rate. Thereis release of acetylcholine which acts on SA nodal fibers toincrease its permeability for potassium. Which causeshyperpolarization and less steep of prepotential.
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Effect Of SympatheticAnd Parasympathetic
Stimulation On
Heart???
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Sympathetic Effects onHeart
Releases norepinephrine atsympathetic ending
Causes increased sinus nodedischarge with HR upto180-200 (+vechronotropic effect)
Norepinephrine increases thepermeability of SA nodal fibers tosodium and calcium which increasesthe slope of the pre-potential.
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Parasympathetic Effectson Heart
Parasympathetic (vagal) nerves, whichrelease acetylcholine at their endings,innervate SA node and A-V junctional
fibers proximal to A-V node.
Mechanism: Causeshyperpolarization because of
increased K+ permeability in responseto acetylcholine.
This causes decreased transmission of
impulses (-ve dromotropic effect) may4/25/12 1616
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