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
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 pre-
potential 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) Ions-
a) 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- 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 Middle bundle Posterior bundle

of bachman of wenkebach Of thorel

AV Node

Bundle of His

Right & left

bundle branches

Purkinje fibers
 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 delay-
i) smaller size of fibers
ii) smaller number of gap junctions
iii) more negative RMP
Significance-
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
 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 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
Velocity of shortening (mm/sec)

10

V max

0
5 10
Load (gm)
P0 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 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 :

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 period-
ARP- 250ms
RRP- 50ms
refractory period of atria-150ms
Significance of long refractory period-
• Cardiac muscle is non-tetanisable
• It is non-fatiguable