physiology- rhythmical excitation of heart by dr. mudassar ali roomi

7/31/2019 Physiology- Rhythmical Excitation of Heart by Dr. Mudassar Ali Roomi

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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

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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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physiology- rhythmical excitation of heart by dr. mudassar ali roomi

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