3rd Lecture on Heart Physiology by Dr. Roomi

8/2/2019 3rd Lecture on Heart Physiology by Dr. Roomi

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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

3rd Lecture on Heart Physiology by Dr. Roomi

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