properties of cardiac muscle.pdf

8/16/2019 Properties of cardiac muscle.pdf

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PROPERTIES OF

CARDIAC MUSCLE

NZD


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Objectives2

Prior Knowledge :External and internal features of heart

By the end of your learning, you should be able to :Describe the cardiac muscle and their significanceExplain the action potential for myocardial and pacemaker.

Describe the ionic basis of different phases ofmyocardial and pace maker action potential.Describe the physiological basis of cardiac muscleproperties.


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Cardiac muscle and their significance (Pg : 2)

Intercalated discs contain two junctions;desmosomes

gap junctions.

Desmosomes , which contain strong protein

fibers (keratin), act like spot-welds thatstrongly anchor one myocardial cell toanother. (the heart puts tremendous physicalstrain on the connections between cells).

Gap junctions link the cytoplasm of one cell

with that of an adjacent cell via smallconnecting tunnels called connexons .Small molecules and ions can readily pass from onemyocardial cell to another through the connexons.

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Cardiac muscle and their significance (Pg : 3)5

Myocardial cells are electrically excitable cells,capable of initiating and propagating actionpotentials.

The propagation of an action potential from onemyocardial cell to another occurs by the movement ofions through the gap junction.

Therefore ,the gap junction is an electrical synapse.


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Cardiac muscle and their significance (Pg : 4)6

All of the myocardial cells connected through gap junctions arecollectively called a myocardium .

A myocardium functions as a single unit i.e when stimulated, theentire myocardium contracts simultaneously.

The two ventricles form a myocardium and the two atria form a secondmyocardium.

The synchronous contraction of myocardial cells that make upthe myocardium is required to produce the force necessary topump blood


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Action potential for myocardial andpace maker.

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ACTION POTENTIAL IN MYOCARDIAL TISSUE

Divided into FIVE phases :

Phase 0:Opening of Na + channels cause sharp depolarisation due torapid entry of Na +.

Phase 1:a notch due to closure of Na + channels

repolarisation is caused by the opening of K+ channel.Cl- ions move across the membrane due the change in membranepotential, from K + efflux, and is not a contributory factor to the“notch”.

Phase 2 :plateau due to the opening of L-type Ca 2+ channels

(depolarisation) again repolarisation (by opening of K+ channel)

Phase 3 :abrupt repolarisation due to the closure of L- type Ca 2+ channels(no more depolarisation) and opening of K+ channels.

Phase 4 :

attainment of resting potential due to closure of K+

channels.

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4

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Myocardial: Effective Refractory Period (ERP)

also known as Absolute Refractory Period(ARP)

a period of time comprising phases 0, 1,2, and part of phase 3 that a new action

potential cannot be initiated.a protective mechanism in the heart bypreventing multiple, compounded actionpotentials from occurring i.e., it limits thefrequency of depolarization and

therefore heart rate.This is important because at very high heartrates, the heart would be unable to adequatelyfill with blood.

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ACTION POTENTIAL IN PACE MAKER TISSUE

Divided into THREEphases :Phase 4:

Begin at the end of repolarization (about -60 mV),

depolarisation due to opening of Na + gate channel andslow entry of Na + known as "funny" currents

At AP about -50 mV, another type of channel o penscalled transient or T-type Ca 2+ channel .

Phase 0:depolarisation due to opening of L-type Ca 2+ channel.

closure of Na + and T-type Ca 2+ channel

Phase 3 :Repolarisation due to opening of K+ channels

closure of L-type Ca2 + channel

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Ionic basis of different phases of myocardial andpace maker action potential.

Myocardial

1. Have a true restingpotential

2. depolarizing current

primarily by relatively fastNa 2+ produce rapiddepolarisation

3. Referred as "fast response"action potentials

Pace Maker

1. no true resting potential

2. depolarizing currentprimarily by relatively

slow T-type Ca2+

produce slowerdepolarisation

3. Referred as "slowresponse" action potentials.

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Is it normal for the heart rate toincrease during fever


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Physiological Basis of CardiacMuscle Properties .

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1. Rhythmicity2. Contractibility3. Excitability4. Conductivity


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1. RHYTHMICITY14

The heart generates its own rhythm.

The SA node is the pace maker, but the other parts of the conductingsystem are also capable of generating their own rhythm.

All parts of the heart beats at the same rate because an impulseoriginating from SA node spreads throughout the heart atrium beforeAV node or any other part of the conduction system.


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Factors that influence cardiac rhythmicityinclude (pg.1):

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1.Sympathetic StimulationIncreases permeability of the membrane to sodium thusdepolarising rate increases

2.Parasympathetic StimulationIncreases permeability of the membrane to potassium thushyperpolarising the membrane with the result thatdepolarisation takes longer to occur. This results in a slowerrate.


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Factors that influence cardiac rhythmicityinclude (Pg.2):

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3.IonsSodium

A decrease in extracellular sodium concentration causes a decrease in theheart rate - less sodium leaking inAn increase in extracellular sodium concentration has little or no effect.

PotassiumA mild increase in extracellular potassium concentration causes partialdepolarisation and thus increases the heart rate.A marked increase in extracellular potassium concentration causesmarked depolarisation and the heart stops in diastole.

CalciumA decrease in extracellular calcium concentration causes an increase inthe heart rate - less compettion with sodium, resulting in more sodiumleaking in.An increase in extracellular calcium concentration causes a decrease inthe heart rate - more compettion with sodium, resulting in less sodiumleaking in.


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Factors that influence cardiac rhythmicityinclude (Pg.3):

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4.TemperatureAn increase in body temperature, increases the heart rate as the permeability of sodiumincreases - one of the reasons that patients have an increased heart rate when running afever.

5.HypoxiaMild Results inpartial depolarisation - increase in the heart rateSevere Depression of metabolism - decrease in heart rate

6.pHAcid Decreases heart rate - probably due to a decrease in the entry of sodium due to a higher

competition of calciumAlkali Initially increases heart rate (opposite reason of above) but finally decreases it.

7.Drugs and ToxinsAdrenaline

Same as sympathetic system - increases heart rate.Acetyl choline Diphteria Toxin

Decrease heart rate - in the case of diphteria - patient with fever but heart rate notelevated.


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Mechanism Producing Abnormal Rhythms19

Under normal conditions, when the cardiac impulse has travelledthroughout the muscle it just dies away.This occurs as the depolarising wave would meet tissues that arein the Absolute Refractory Period ( ARP -zero excitability)

Under certain conditions, the normal sequence of events does notoccur and the depolarising wave meets tissues that has alreadyrepolarised and hence able to be depolarised again.In these conditions, the impulse travels around and around in a

Circus or Re-entry way.


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Conditions that can give rise to CircusMovement:

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Length of Pathway - if the impulse has to take alonger pathway than normal , the impulsereturns back to the origin and finds the musclein the resting phase.A Decrease in the Velocity of the Impulse -results in a similar scenario

Shortening of the Refractory Period.


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2. Contractility21

Contraction of the heart is called systole whilst relaxationof the heart is called diastole.

As the function of the heart is that of a pump, both actions

are important - a pump has to fill up with fluid before it canpump it out. The filling process occurs during diastole.

One systole and its following diastole is called one cardiaccycle .


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Factors that influence cardiac contractilityinclude:

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CONTRACTILITY AND ALL OR NONE LAW23

If a stimulus is applied, either the tissue will not respond at all;if it responds, it will respond maximally.This means,

i) if the strength of the stimulus is below threshold, the tissue will notrespond;ii)when the stimulus strength is threshold the tissue will respond readilyiii) further increase in the strength of stimulus (how strong it might be) willnot increase the response.

This is becausei) action potential is an all and none phenomenon,ii) impulse generated in any part of the heart spreads to other parts(syncytium) and gives a uniform response.


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CONTRACTILITY AND STAIRCASE PHENOMENON24

If ventricle is stimulated repeatedly (stimuli is less than 10 s), the first 3-4contractions are progressively more forceful.

This is known as staircase phenomenon.

Reason :Large amount of calcium ions is released during each contraction, the pumping backof calcium into the sarcotubular system may not be complete within 10 seconds .Hence the second stimulus operates under the beneficial effect of higher calcium ionconcentration.


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CONTRACTILITY AND REFRACTORY PERIOD25

Refractory period can be divided into two phases:

i) absolute refractory period :the phase during which no stimuluscan produce any contraction.

ii) Relative refractory period : following contraction, when themuscle starts relaxing, the excitability of the muscle graduallyreturns towards normal. During this phase, a stimulusconsiderably stronger than the threshold stimulus may lead to aresponse.


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CONTRACTILITY27

Long refractory period : Refractory period is theperiod during which a stimulus fails to evoke aresponse.

The long absolute refractory period in cardiac musclelasts throughout its contraction phase and initial partof the relaxation phase. Therefore, cardiac musclecan not be tetanised and therefore can not befatigued.


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LENGTH-TENSION RELATIONSHIP30

The force of contraction of cardiac muscle is directlyproportional to the initial length of the muscle fibers.This is known as the Starling’s law of heart.

In practice, the length of the cardiac muscle fibersincreases when the venous return increases. Hence,increase in venous return increases the force ofcontraction of the ventricle.


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3. Excitability31

Excitability : The ability to respond to a stimulus iscalled excitability.

The excitability of cardiac muscle is less than theneurons and skeletal muscles.


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Excitability and Plateau phase32

In common with other muscle tissue, the heart musclecell membrane is an excitable membrane i.e

it is capable of transmitting an action potential andthe depolarisation is due to the opening of the fastsodium channels.

The unique characteristic of cardiac muscle action

potential is the plateau phase i.e. the maintenanceof the potential at a positive level.

The plateau is ensuring that the heart muscle cell can

never be tetanised .


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Factors that increase excitability:33

Sympathetic stimulation - Lowers the restingmembrane potential - becoming more positive.Mild Hyperkaleamia (increase in potassiumconcentration) - partial depolarisationHypocalcaemia (decrease in calcium concentration) -partial depolarisationAdrenaline - similar to sympathetic stimulation

Digitalis - increase atrial muscle excitabilityMild Hypoxia - Partial depolarisationIschaemia - Partial depolarisation


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4.Conductivity35

Specialised conducting system to ensure that excitation travels to all theheart muscle fibres and in a certain pre-defined pattern .

Conducting Pathways include:1. Anterior, Middle and Posterior Internodal Atrial bundles2. A-V node - only pathway from atria to AV bundle; slow conduction and

a long absolute refractory period3. A-V bundle

4. Right and Left Bundle Branch5. Purkinje Fibres


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QUIZ

Why the velocity of conduction is different inatrial , ventricular and purkinje fibers (i. e 0.3ms -1 ,1ms-1 and 4.0ms -1 respectively) and the AV node

impulse conduction is very slow (0.05 ms-1

).Answer :

To allows a delay of conduction of atrialdepolarization to the ventricles and ensures thatventricular contraction always occurs after thecompletion of the atrial contraction.

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Summary38

Cardiac muscle and their significanceDifferences between myocardial and pace makeraction potential.

Rhythmicity ,Contractibility ,Excitability andConductivity of cardiac muscle.

properties of cardiac muscle.pdf

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