Properties Of Cardiac Muscle And Conducting Systems k14

PHYSIOLOGICAL ANATOMY • Mammalian Heart has 4 chambers- 2 atria and 2 ventricles • Right side- pulmonary circulation • Left side- systemic circulation • Contraction is called systole and relaxation is called diastole

• Two types of muscle fibers- contractile and conducting • Contractile fibers in atria and ventricles- form two functional syncytia due to presence of gap junctions • Conducting system includes SA Node, internodal tracts, AV Node, Bundle of His, Bundle branches and purkinje fibers • Conducting system has• i) less cross-striations • ii) less glycogen • iii) do not contract

CONDUCTING SYSTEM • SA Node• Small, flattened, ellipsoid strip of specialized muscle • Size- 3x15x1mm • Situation- superior lateral wall of right atrium below and lateral to opening of superior venacava • Pacemaker of heart • P cells- primitive cells- pale- rhythm generators

• Internodal pathway• Connect SA Node and AV Node • Faster rate of conduction than Atrial muscles • Anterior- Bachman’s bundle • Middle- Wenkebach’s bundle • Posterior- Thorell’s bundle

• AV Node• Only conducting pathway between atria and ventricles normally • Situation- posterior septal wall of RA immediately behind tricuspid valve • Has thinner fibers with more negative RMP & fewer gap junctions causing conduction delay • Velocity of conduction- 0.05m/sec • It acts as pacemaker when SA Node is damaged

• Bundle of His• It begins from AV Node, es downwards in the intraventricular septum for 5-15mm • Divides into right and left bundle branches • Left branch divides into anterior and posterior fasciculus • Both divide repeatedly and lie subendocardially

• Purkinje fibers• Takes origin from terminal divisions of bundle branches • Fastest conducting • It is 1-2mm thick- largest conducting fiber • es impulses to ventricular myocytes

PROPERTIES OF CARDIAC MUSCLE I) Electrical properties i) Autorhythmicity ii) Excitability iii) Conductivity II) Mechanical properties i) Contractility ii) All-or-none law iii) Staircase phenomenon iv) Refractory period

I. AUTORHYTHMICITY • All the cells of heart have an inherent ability to generate impulse • SAN is the pacemaker of heart • Rates of impulse generation• SAN- 70 to 80/min • AVN- 40 to 60/min • Purkinje fibers- 15 to 40/min

Action potential in SAN

MECHANISM OF SELFEXCITATION • RMP of SAN is -60mv (that of contractile cardiac fibers is –90mv) • It has a pre-potential, a spike,& a repolarization phase.

I) Pre-potential or pacemaker potentiali) due to ca2+ influx through Transient (T-type) of ca2+channels ii) TMP changes from -60mv towards positivity II) Spike potentiali) starts at threshold potential of -40mv ii) due to opening of voltage-gated Ca2+ channels (L-type or long-standing type) iii) potential peaks to +20mv

III) Repolarisationi) due to closure of Ca2+ channels and opening of K+ channels Significance of Pre-potential d) It is characteristic of tissues with automaticity e) It is prominent in SAN and AVN f) Alterations in pre-potential will alter the rate of impulse generation

FACTORS AFFECTING AUTORHYTHMICITY i) Autonomic nerve stimulation a) vagal stimulation decreases the slope of prepotential and reduces the rate of impulse generation b) sympathetic stimulation increases the slope and increases the impulse rate ii) Temperature iii) Hormones iv) Drugs v) Ionsa) K+ increased K+ in ecf decreased RMP hyperpolarisationreduced heart rate diastolic arrest

Vagal stimulation

Release of acetylcholine

Ach binds to M2 muscarinic receptor

βγ subunit of G-protein act on K+ channels

Reduced cAMP

Opening of K + channels

Reduced Ca2+ influx

Decreased pre-potential slope

Sympathetic stimulation Release of noradrenaline

Binds to β1 receptors Increased cAMP Opening of L-type Ca2+ channels

Increased Ca2+ influx Reduced pre-potential slope Increased rate of impulse generation

EXCITABILITY • Ability Of excitable tissues to show change in potential when stimulated • Chronaxie of cardiac muscle is 3-30ms

ACTION POTENTIALS IN VARIOUS CARDIAC CELLS

ACTION POTENTIAL IN VENTRICULAR MYOCYTE RMP: -90mv Phase 0- rapid influx of Na+ rising TMP to +20mv Phase 1- closure of Na+ channels Phase 2- plateau- opening of L-type Ca2+ channels Phase 3- Repolarisationclosure of Ca2+ channels & opening of K+ channels Phase 4- RMP

FACTORS AFFECTING EXCITABILITY 1) 2) 3) 4)

Nervous factors Hormones Drugs Ions- K+ acts by altering RMP and Na+ acts on amplitude of AP 5) Temperature

ORIGIN AND SPREAD OF IMPULSES SA Node Anterior bundle of bachman

Middle bundle of wenkebach AV Node Bundle of His Right & left bundle branches Purkinje fibers

Posterior bundle Of thorel

0.09

0.22

0.00 0.19 0.03

0.16

0.21 0.18

0.17 0.19 0.18 0.21

0.20

CONDUCTION RATES TISSUE

m/sec

Atrial muscle

0.3

Internodal tract

1.0

AV Node

0.05

Purkinje fibers

1.5-4

Ventricle muscle

1.0

AV Nodal delay • Delay in transmission of impulses to ventricles by 0.13sec-( 0.09 at AVN & 0.04 at AV bundle) Causes of delayi) smaller size of fibers ii) smaller number of gap junctions iii) more negative RMP Significancea) atria contracts 0.1sec earlier than ventricle b) limits the number impulses transmitted to ventricles- <230/min

STOKES ADAMS SYNDROME • Seen during acute complete AV block • Ventricles stop beating due overdrive suppression • Person faints due reduced blood supply to brain • Ventricle recovers after few seconds & starts generating own impulses • Rx- artificial pacemaker

FACTORS AFFECTING CONDUCTIVITY • • • • •

1) Nervous stimulation 2) Hormones 3) Drugs 4) Ions 5) temperature

II.MECHANICAL PROPERTIES I.CONTRACTILITY :# excitation-contraction coupling is almost similar to that of skeletal muscle # it depends more on ECF Ca2+ # Ryanodine receptors are triggered open by DHP receptors

a c t io n p o t e n t ia l o p e n in g o f v o lt a g e - g a t e d ( D H P ) C a 2 + c h a n n e ls in T - t u b u le s D H P r e c e p t o r a c t s a s s e n s o r a n d t r ig g e r o p e n in g o f R y a n o d in e c h a n n e ls in t e r m in a l c is t e r n a e C a 2 + in t o s a r c o p la s m c o n t r a c t io n

FACTORS AFFECTING CONTRACTILITY 1) nervous factors- sympathetic acting via β 1 receptor & cAMP 2) Drugs- digitalis- inhibits Na+-K+ pump 3) Ions* Ca2+- increases force of contractionsystolic arrest 4) temperature 5) load

EFFECT OF LOAD ON CONTRACTILITY • Pre-load: it is the load acting on heart before it starts contracting • After-load: it is the load acting on heart after it starts contracting- resistance • Frank starling’s law- the force of contraction is proportional to initial length of the muscle within the physiological limits • Initial length depends on pre-load, i.e, end-diastolic volume(130ml).

LENGTH-TENSION RELATIONSHIP • As the preload increases the tension increases • ive tension is given by diastolic intraventricular pressure • Total tension is indicated by systolic intraventricular pressure • Descending limb at high degree of stretch is due to disruption of myocardial fibers

Velocity of shortening (mm/sec)

FORCE TENSION RELATIONSHIP

10

V max 5

0

P0

5

10

Load (gm) Maximum isometric force

ALL OR NONE LAW • Action potential fails to occur if the stimulus is subthreshold in magnitude, and it occurs with constant amplitude and form regardless of the strength of the stimulus if the stimulus is at or above the threshold. 1V subthreshold

2V threshold

3V

4V Maximal

STAIRCASE PHENOMENON (TREPPE) • after a brief rest, on stimulation at regular frequency the force of contraction increases progressively to a maximum and then is maintained at a plateau >

2V

2V

2V

2V

2V

2V

•

Causes of staircase effect :

3) Increased accumulation of calcium 4) Increased temperature 5) Reduced viscosity

REFRACTORY PERIOD Def: it is the duration during which an excitable tissue will not respond to a second stimulus Characteristics of cardiac refractory period:Long refractory periodARP- 250ms RRP- 50ms refractory period of atria-150ms Significance of long refractory period• Cardiac muscle is non-tetanisable • It is non-fatiguable