 Elongated, branching
cells containing 1-2
centrally located nuclei
 Contains actin and
myosin myofilaments
 Intercalated disks:
specialized cell-cell
contacts.
Cardiac
Muscle
 Cell membranes
interdigitate
 Desmosomes hold cells
together
 Gap junctions allow action
potentials to move from one
cell to the next.
 Electrically, cardiac
muscle of the atria and of
the ventricles behaves as
single unit
• Mitochondria comprise 30% of volume of the cell vs. 2% in skeletal
The Action Potential in Skeletal and Cardiac
Muscle
Figure 20.15
Cardiac Muscle Contraction
 Heart muscle:
 Is stimulated by nerves and is self-excitable
(automaticity)
 Contracts as a unit; no motor units
 Has a long (250 ms) absolute refractory period
 Cardiac muscle contraction is similar to skeletal
muscle contraction, i.e., sliding-filaments
Conductive System of Heart
Conduction System of the Heart
 SA node: sinoatrial node. The pacemaker.
 Specialized cardiac muscle cells.
 Generate spontaneous action potentials (autorhythmic tissue).
 Action potentials pass to atrial muscle cells and to the AV node
 AV node: atrioventricular node.
 Action potentials conducted more slowly here than in any other part of
system.
 Ensures ventricles receive signal to contract after atria have contracted
 AV bundle: passes through hole in cardiac skeleton to reach
interventricular septum
 Right and left bundle branches: extend beneath endocardium to apices
of right and left ventricles
 Purkinje fibers:
 Large diameter cardiac muscle cells with few myofibrils.
 Many gap junctions.
 Conduct action potential to ventricular muscle cells (myocardium)
 Autorhythmic cells:
 Initiate action potentials
 Have unstable resting potentials called pacemaker
potentials
 Use calcium influx (rather than sodium) for rising
phase of the action potential
Sequence of Excitation
 Sinoatrial (SA) node generates impulses about 75
times/minute
 Atrioventricular (AV) node delays the impulse
approximately 0.1 second
 Impulse passes from atria to ventricles via the
atrioventricular bundle (bundle of His) to the Purkinje
fibers and finally to the myocardial fibers
Impulse Conduction through
the Heart
Pacemaker and Action Potentials
of the Heart
Pacemaker potentials
 Rhythmically discharging cells have a membrane potential
that, after each impulse, declines to the firing level. Thus,
this Prepotential pacemaker potential triggers the next
impulse
 At the peak of each impulse, IK begins and brings about
repolarization. IK then declines, and a channel that can
pass both Na+ and K+ is activated. Because this channel is
activated following hyperpolarization, it is referred to as an
“h” channel; however, because of its unusual (funny)
activation this has also been dubbed an “f” channel
 As I h increases,the membrane begins to depolarize,
forming the first part of the prepotential. Ca2+ channels
then open
 These are of two types in the heart, the T(for
transient)channels and the L(for
longlasting)channels.
 The action potentials in the SA and AV nodes are
largely due to Ca2+ , with no contribution by Na+
influx. Consequently, there is no sharp, rapid
depolarizing spike before the plateau,as there is in
other parts of the conduction system and the atrial
and ventricular fibers
 In addition, prepotentials are normally prominent only
in the SA and AV nodes. However, “latent pacemakers”
are present in other portions of the conduction system
that can take over when the SA and AV nodes are
depressed or conduction from them is blocked. Atrial
and ventricular muscle fibers do not have
prepotentials, and they discharge spontaneously only
when injured or abnormal
Depolarization of SA Node
 SA node - no stable resting membrane potential
 Pacemaker potential
 gradual depolarization from -60 mV, slow influx of Na+
 Action potential
 occurs at threshold of -40 mV
 depolarizing phase to 0 mV

fast Ca2+ channels open, (Ca2+ in)
 repolarizing phase


K+ channels open, (K+ out)
at -60 mV K+ channels close, pacemaker potential starts over
 Each depolarization creates one heartbeat
 SA node at rest fires at 0.8 sec, about 75 bpm
 SA nodal fibers continuous with atrial fibers
 Three Inter-nodal Pathways
 Anterior: Bachmen
 Middle: Wenckebach
 Posterior: Thorel
 Contain fibers similar to purkinji fibers
 With rapid conduction
Av nodal delay
 Depolarization initiated in the SA node
 spreads radially through the atria,
 then converges on the AV node.
 Atrial depolarization is complete in about 0.1 s.
Because conduction in the AV node is slow (Table 30–
1), a delay of about 0.1 s(AV nodal delay)occurs before
excitation spreads to the ventricles
 The slow conduction in transitional nodal and
penetrating A-V bundle fibers which is caused by
lesser number of gap junctions between the cells in
conducting pathways result in great resistance to
conduction of excitatory ions from one fiber to next.
 Rapid transmission in ventricular purkenji system at a
velocity of 1.5 – 4 m/s.
 Rapid transmission in purkenji system is caused by
high level of permeability of gap junction between the
cells.
 One way conduction through A-V bundle.
 The A-V bundle passes downward in ventricular
septum from 5 -15 mm dividing into left and right
bundle branches.
 Left bundle branch gives of anterior fascicle and
posterior fascicle
 Purkenji fibers penetrate the ventricular muscle
 Velocity of transmission in ventricular m uscle 0.3- 0.5
m/s.
Ectopic Pace Makers
 SA node functions as pace maker of heart because its rate of







discharge is 70-80 times per minute
AV node discharges at 40 – 60 per minute
Purkenji system discharge at 15 – 40 per minute.
ectopic pace makers if any part of the heart devalops rhythmical
discharge that is more rapid than SA node
AV node or purkenji fibers some times become ectopic pace
maker
Atrial and ventricular muscle devalops excessive excitability to
and become the pace maker
The blockage of transmission from the SA node to other parts of
heart may result in ectopic focci.
Stokes Adams syndrome
An Electrocardiogram