Characteristic of Cardiac musce cells

Departemen Fisiologi Fakultas Kedokteran Universitas Sumatera Utara

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.

 The heart contracts, or beats, rhythmically as a result of action potential that it generate by itself autorhythmicity.

Cardiac muscle cells

Two classes of cardiac muscle cells 1) Auto rhythmic cells : Specialized muscle cells of conducting system 2) Contractile cells

ELECTRICAL PROPERTIES

The resting membrane potential -90 mV

Conducting System of the Heart

Inter- nodal Tracts SA Node AV Node

Left Bundle Branch

Anterior Superior Fascicle

Bundle of HIS

Posterior Inferior Fascicle Septal Depolarization Fibers

Purkinjie Fibers

Right Bundle Branch

Pacemaker potential ~ slow response action potential

Intercalated disks
(1) firm mechanical attachments between adjacent cell membranes by proteins called adherins in structures called desmosomes and (2) low resistance electrical connections between adjacent cells through channels formed by protein called connexin in structures called gap junctions.

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

 Action potential conduction is greatly slowed as it passes through the AV node. because of the small 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

Control of Heart Beating Rate

Normal rhythmic contractions of the heart occur because of spontaneous electrical pacemaker activity (automaticity) of cells in the SA node. The SA nodal cells fire at a spontaneous or intrinsic rate (100 beats per minute) in the absence of any outside influences.

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.

 increase the time between beats by prolonging the time required for the resting membrane 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).

 Acetylcholine interacts with a muscarinic receptor on the SA nodal cell membrane which in turn is linked to an inhibitory G protein, Gi. The activation of Gi has two effects: (1) an increase in K+ conductance resulting from an increased opening of the KAch channels and (2) a suppression of adenylate cyclase leading to a fall in intracellular cyclic adenosine monophosphate (cAMP) which reduces the inward-going pacemaker current carried by Na+ (if).

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 a positive dromotropic effect),

Sympathetic and Parasympathetic Sympathetic speeds heart rate by Ca++ & I-f channel flow Parasympathetic slows rate by K+ efflux & Ca++ influx

Rate of discharge SA node and other nodal tissue is influenced by: Temperature; fever -> tachycardia Drugs; digitalis -> effect like vagal stimulation

 An abnormally high concentration of Ca2+ in the extracellular fluid, for example, tends to decrease heart rate by shifting the threshold potential. Factors that increase heart rate are said to have a positive chronotropic effect. Those that decrease heart rate have a negative chronotropic effect.

 Norepinephrine interacts with 1-adrenergic receptors on the SA nodal cell membrane which in turn are linked to stimulatory G proteins, Gs. The activation of Gs increases adenylate cyclase, leading to an increase in intracellular cyclic AMP which increases the open-state probability of the pacemaker Na+ current channel (if).

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 0.1 M, during maximum activation of the contractile apparatus, the intracellular free Ca2+ concentration reaches nearly 100 M.

Mechanical Activity of the Heart

Action potential in cardiac contractile cell Travels down T tubules Entry of small amount of Ca2+ from ECF Release of large amount of Ca2+ from sarcoplasmic reticulum Troponin tropomyosin complex in thin filaments pulled aside Cross-bridge cycling between thick and thin filaments Thin filaments slide inward between thick filaments Contraction

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

Spread of cardiac excitation

Depolarization in SA node spreads radially through the atria, then converges on the AV node. Atrial depolarization is complete in about 0.1

 Conduction in AV node is slow, about 0.1 s (AV nodal delay) before excitation spreads to ventricles. From top of septum, depolarization spreads conducting Purkinje fibers to all parts of

 Activation anteroseptal region ventricular myocardium Activation major portion ventricular myocardium from endocardial surfaces Late activation posterobasal left ventricle and pulmonary conus

Spread of cardiac excitation

Physiological regulation of contractile force

(1) length tension relation (2) chemically induced rises in the calcium store leading to higher sarcoplasmic Ca2+ concentration in systole; sympathetic neurotransmitter and cathecholamine.

Relation of Tension to Length in Cardiac Muscle Starling's law of the heart or FrankStarling law = "energy of contraction is proportional to the initial length of cardiac muscle fiber." = relation between ventricular stroke volume and end-diastolic volume

Relation of Tension to Length in Cardiac Muscle

The length-tension relationship in cardiac muscle is similar to that in skeletal muscle as the muscle is stretched, the developed tension increases to a maximum and then declines as stretch becomes more extreme.

Factors that normally increase or decrease the length of ventricular

= Length of muscle fiber = preload

Kurva Frank Starling

Stimulasi Adrenergik Normal Fungsi jantung Syok Kardiogenik

e m l ov e kort S u

End Diastolic Volume

Myocardial Contractility

Let it beat!