2. SESSION OBJECTIVES
Pacemakers of heart
Electrical conduction system of heart
Time delay in transmission
Conduction velocities of various conduction fibres
Innervation of heart
4. Heart has 2 special systems for
1. Cardiac impulse generation - pacemakers
2. Impulse conduction
This allows atria to contract 1/6th second
ahead of
ventricle
and all ventricle to contract simultaneously
5. Pacemaker
Generally S A node is pacemaker.
It is having highest rate of firing 70 -80 beats /min.
If SA node fails : Pacemakers are
Av node
(40-
60Beats/min)
Bundle of
his(about 40
beats/min)
Purkinje fibres
(15-40
beats/min)
6. SA node
Flattened ellipsoid specialized cardiac muscle
15mm long 3 mm wide 1mm thick.
Location : Immediately below and lateral to
opening of superior vena cava
Normal Pacemaker of heart.
It develops from right side of embryo and
innervated by right vagus
7. Av node
Shows AV nodal delay of 0.1 sec.
AV nodal delay has following
significance :
Preventing excess transmission
of impulses by SA node .
Gives time for atria to contract
fully before ventricular
depolarisation
Located near opening of
coronary sinus
Conducts Impulses from SA node
Defect in it’s conduction causes
heart blocks
8. Bundle of his and purkinje fibres
BUNDLE OF HIS
Derived from AV nodal cells
They divide into 2 segments and
lies on inter ventricular septum
They are isolated in a canal till
they form purkinje fibres
PURKINJE FIBRES
They penetrate the
ventricular wall
Their fast conduction
velocity allows ventricle to
contract almost altogether
13. SA NODE
INTERNODAL TRACTS
AV NODE
BUNDLE OF HIS
PURKINJE FIBRES
Special pathway in arterial wall that
transmit impulse from SA to AV node.
It has 3 parts
Anterior bachman
Middle wenckebach
Posterior thorel
Impulse from sa node can travel
directly to atrial muscle fibres
19. CONDUCTION RATE
TISSUE CONDUCTION SPEED (m/sec)
SAN 0.05
ATRIAL PATHWAY 1
AVN 0.02-0.05
BUNDLE OF HIS 1
PURKINJE SYSTEM 4
VENTRICULAR SYSTEM 1
CONDUCTION VELOCITY DEPENDS ON 1. Diameter of fibre
2. Number of gap junctions
21. VAGUS (Parasympathetic) effects
Acetylcholine released at vagal endings increases permeability of fibres to k+
ions.
This causes increased negativity inside the fibers called hyperpolarization
This makes tissue less excitable
Membrane potential of SA nodal fibers decreases to -65 to -75 mv from -55 to
-60mv.
Therefore initial rise of sinus nodal membrane potential caused by Na and Ca
leakage requires more time to reach threshold.
They are constantly active, producing a rhythm of 60 – 80 beats per minute. If
the vagus nerve was lesioned, the resting heart rate would be around 100
beats per minute.
Summary: acetylcholine binds on to M₂ receptors, which act to decrease the
slope of the pacemaker potential. This leads to a decrease in heart rate
negative chronotropic effect
22. SYMPATHETIC EFFECT
The sympathetic input into the heart is via the
postganglionic fibres from the sympathetic trunk which
innervate SA node AV NODE and ventricles mainly.
The postganglionic fibres release noradrenaline, which
acts on B₁ adrenoreceptors to increase the slope of the
pacemaker potential. By increasing permeability to na+
and ca++ ions.
This increases the heart rate (a positive chronotropic
effect by ca++), as well as the force of contraction
(positive inotropic effect).