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, passes 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

• Passes 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 SELF-EXCITATION

• 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 potential- i) due to ca2+ influx through Transient (T-type) of ca2+channels

ii) TMP changes from -60mv towards positivity

II) Spike potential- i) 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) Repolarisation-

i) due to closure of Ca2+ channels and opening of K+ channels

Significance of Pre-potential

a) It is characteristic of tissues with automaticity

b) It is prominent in SAN and AVN

c) 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 pre-

potential and reduces the rate of impulse generation

b) sympathetic stimulation increases the slope and increases the impulse rate

ii) Temperatureiii) Hormonesiv) Drugsv) Ions- a) K+ increased K+ in ecf decreased

RMPhyperpolarisationreduced heart rate diastolic arrest

Vagal stimulation

Release of acetylcholine

Ach binds to M2 muscarinic receptor

β subunit of G-protein act on K+ channels

Opening of K + channels

Reduced cAMP

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: -90mvPhase 0- rapid influx of Na+

rising TMP to +20mvPhase 1- closure of Na+

channelsPhase 2- plateau- opening of L-type Ca2+ channelsPhase 3- Repolarisation-

closure of Ca2+ channels & opening of K+ channels

Phase 4- RMP

FACTORS AFFECTING EXCITABILITY

1) Nervous factors

2) Hormones

3) Drugs

4) 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

Posterior bundle Of thorel

AV Node

Bundle of His

Right & left bundle branches

Purkinje fibers

0.00

0.03

0.09

0.16

0.17

0.18

0.19

0.20

0.21

0.22

0.21

0.18

0.19

CONDUCTION RATESTISSUE 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 delay- i) smaller size of fibers ii) smaller number of gap junctions iii) more negative RMPSignificance- a) 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

con trac tion

C a2 + in to sa rcop lasm

op en in g o f R yan od in e ch an n e ls in te rm in a l c is te rn ae

D H P recep to r ac ts as sen sor an d trig g er

op en in g o f vo ltag e-g a ted (D H P ) C a2 + ch an n e ls in T-tu b u les

ac tion p o ten tia l

FACTORS AFFECTING CONTRACTILITY

1) nervous factors- sympathetic acting via 1 receptor & cAMP

2) Drugs- digitalis- inhibits Na+-K+ pump

3) Ions-

* Ca2+- increases force of contraction- systolic 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

• Passive 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

FORCE TENSION RELATIONSHIP

0

5

10

5 10

P0 Maximum isometric forceLoad (gm)

Ve

loc

i ty

of

sho

rte

nin

g (

mm

/se

c)

V max

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 2V 3V 4V

subthreshold threshold 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 :

1) Increased accumulation of calcium

2) Increased temperature

3) Reduced viscosity

REFRACTORY PERIODDef: it is the duration during which an excitable tissue

will not respond to a second stimulus

Characteristics of cardiac refractory period:-

Long refractory period-

ARP- 250ms

RRP- 50ms

refractory period of atria-150ms

Significance of long refractory period-• Cardiac muscle is non-tetanisable• It is non-fatiguable