characteristic of cardiac muscle cells_cvsk4

7/31/2019 Characteristic of Cardiac Muscle Cells_CVSK4

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Characteristic of

Cardiac musce cells

Departemen Fisiologi

Fakultas Kedokteran

Universitas Sumatera Utara


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Difference between cardiac

muscle and skeletal muscle (1) they can be self-generating;

(2) they can be conducted directly from cell

to cell; and

(3) they have long durations, which

preclude fusion of individual twitch

contractions.


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The heart contracts, or beats,rhythmically as a result of actionpotential that it generate by itself

autorhythmicity.


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Cardiac muscle cells

Two classes of cardiac muscle cells

1) Auto rhythmic cells : Specialized muscle

cells of conducting system

2) Contractile cells


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ELECTRICAL

PROPERTIES

The resting membranepotential -90 mV


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Conducting System of the Heart

AV Node

Posterior Inferior Fascicle

Anterior Superior Fascicle

Septal Depolarization Fibers

Purkinjie Fibers

Inter- nodal Tracts

Bundle of HIS

Left Bundle

Branch

Right Bundle

Branch

SA Node


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Pacemaker potential ~ slow response action potentialPacemaker potential ~ slow response action potential


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Intercalated disks

(1)firm mechanical attachments between

adjacent cell membranes by proteins called

adherins in structures called desmosomesand

(2) low resistance electrical connections

between adjacent cells through channelsformed by protein called connexin in

structures called gap junctions.


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Conduction velocity depends on:

Diameter of muscle fiber involved

Intensity of the local depolarizing current ~

rate of rise of action potential

Capacitive and/or resistive properties of the

cell membranes, gap junctions, and

cytoplasm


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Action potential conduction is greatly slowed as

it passes through the AV node. because of thesmall size of AV nodal cells and the slow rate of

rise of their action potentials.

Since the AV node delays the transfer of the

cardiac excitation from the atria to the

ventricles, atrial contraction can contribute to

ventricular filling just before the ventricles

contract


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Control of Heart Beating Rate

Normal rhythmic contractions of the heart

occur because of spontaneous electrical

pacemaker activity (automaticity) of cells inthe SA node.

The SA nodal cells fire at a spontaneous or

intrinsic rate (100 beats per minute) in theabsence of any outside influences.


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Cardiac parasympathetic fibers Via vagus nerves, release acetylcholine on SA

nodal cells. increases permeability of resting

membrane to K+ and decreases diastolic

permeability to Na+.

two effects on cardiac pacemaker cells:

(1)initial hyperpolarization of resting membrane

potential by bringing it closer to K+ equilibrium

potential and

(2)Slow rate of spontaneous depolarization of

resting membrane.


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increase the time between beats by

prolonging the time required for the restingmembrane to depolarize to the threshold

level.

Since there is normally some continuous

tonic activity of cardiac parasympathetic

nerves, the normal resting heart rate is

approximately 70 beats per minute.

increases in parasympathetic activity

decrease conduction velocity (have a

negative dromotropic effect).


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Acetylcholine interacts with a muscarinic

receptor on the SA nodal cell membrane

which in turn is linked to an inhibitory Gprotein, Gi. The activation of Gi has two

effects: (1) an increase in K+ conductance

resulting from an increased opening of theKAch channels and (2) a suppression of

adenylate cyclase leading to a fall in

intracellular cyclic adenosinemonophosphate (cAMP) which reduces the

inward-going pacemaker current carried by

Na+

(if).


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Sympathetic nerves

Release norepinephrine on cardiac cells.

increases the inward currents carried by Na+

(if) and by Ca2+ during the diastolic interval.

increase heart rate by increasing the rate of

diastolic depolarization

Increases in sympathetic activity increase

conduction velocity (have apositive

dromotropic effect),


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Sympathetic speeds heart rate byCa++ & I-f

channel flow Parasympathetic slows rate byK+ efflux &

Ca++ influx

Sympathetic and ParasympatheticSympathetic and Parasympathetic

Rate of discharge SA node and other nodal tissue is influenced by:

Temperature; fever -> tachycardia

Drugs; digitalis -> effect like vagal stimulation


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An abnormally high concentration of Ca2+

in the extracellular fluid, for example, tends

to decrease heart rate by shifting thethreshold potential.

Factors that increase heart rate are said to

have apositive chronotropic effect. Thosethat decrease heart rate have a negative

chronotropic effect.


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Norepinephrine interacts with 1-adrenergic

receptors on the SA nodal cell membrane

which in turn are linked to stimulatory Gproteins, Gs. The activation of Gs increases

adenylate cyclase, leading to an increase in

intracellular cyclic AMP which increasesthe open-state probability of the pacemaker

Na+ current channel (if).


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Mechanical Activity of the Heart

excitation-contraction coupling is a

dramatic rise in the intracellular free Ca2+

concentration. The "resting" intracellular free Ca2+

concentration is less than 0.1M, during

maximum activation of the contractileapparatus, the intracellular free Ca2+

concentration reaches nearly 100M.


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Action potential in cardiac contractilecell Travels down T tubules Entryof small amount of Ca2+ from ECF

Release of large amount of Ca2+ fromsarcoplasmic reticulum Troponin -tropomyosin complex in thin filaments

pulled aside Cross-bridge cyclingbetween thick and thin filaments

Thin filaments slide inward between

thick filaments

Contraction

Mechanical Activity of the Heart


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Excitation (Depolarization of plasma membrane)

Opening of voltage-sensitive plasma membrane Ca2+ channels in T tubules

Flow of Ca2+ into cytosol

Ca2+ binds to Ca2+ receptor on the external

surface of the sarcoplasmic reticulum

Opening Ca2+ channels intrinsic

to these receptors

Flow of Ca2+

into cytosol

Cytosol Ca2+ concentration

Contraction


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Spread of cardiacexcitation

Depolarization inSA node spreadsradially through theatria, thenconverges on theAV node.

Atrialdepolarization iscomplete in about

0.1


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Conduction in AVnode is slow, about0.1 s (AV nodaldelay) beforeexcitation spreads

to ventricles. From top of

septum,

depolarizationspreads conductingPurkinje

fibers to all parts of


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Activation anteroseptal regionventricular myocardium

Activation major portion

ventricular myocardium fromendocardial surfaces

Late activation posterobasal left

ventricle and pulmonary conus


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Spread of cardiac excitation


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Physiological regulation of

contractile force

(1) length tension relation

(2) chemically induced rises in thecalcium store leading to highersarcoplasmic Ca2+ concentration

in systole; sympatheticneurotransmitter andcathecholamine.


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Relation of Tension to Length in Cardiac

Muscle

Starling's law of the heartorFrank-

Starling law = "energy of contraction is

proportional to the initial length of cardiacmuscle fiber."

= relation between ventricular stroke

volume and end-diastolic volume


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Relation of Tension to Lengthin Cardiac Muscle

The length-tension relationship in cardiac muscle issimilar to that in skeletal muscle as the muscle isstretched, the developed tension increases to a

maximum and then declines as stretch becomesmore extreme.


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Factors that normally increase ordecrease the length of ventricular


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= Length of muscle fiber = preload


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Kurva Frank Starling

Strokevo

lum

e

End Diastolic Volume

Normal

Stimulasi

Adrenergik

Fungsi jantung

Syok

Kardiogenik


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Myocardial Contractility


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Let it

b t!

characteristic of cardiac muscle cells_cvsk4

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