This PPT only for study purpose

1. Properties of Cardiac Muscle - 1
by
Dr. Pandian M
Assistant Professor
Dept. of Physiology

2. 2
Properties of Cardiac Muscle Fibers

3. Cardiac Muscle Properties
•Morphological properties
•Electrical Properties
•Mechanical properties
•Metabolic properties

4. • Exhibit branching
• Adjacent cardiac cells are joined end to end by
specialized structures known as intercalated
discs
• Within intercalated discs there are two types of
junctions
• Desmosomes
• Gap junctions..allow action potential to
spread from one cell to adjacent cells.
• Heart function as syncytium
when one cardiac cell undergoes an AP, the
electrical impulse spreads to all other cells that
are joined by gap junctions. So, they become
excited and contract as a single functional
syncytium.
Atrial syncytium and ventricular syncytium
4
Histological Properties of Cardiac Muscle Fibers

5. Properties of heart muscles can be divided
under major groups:
1. Mechanical properties: Contractile response.
2. Electrophysiological properties :
• Excitability (or) Bathmotrophism
• Contractility (or) Inotrophism
• Rhythmicity (or ) Chronotrophism
• Conductivity (or) Dromotrophism
• Distensibility (or) Tonus
3. Metabolic 6

6. 1. Resting membrane
potential
2. Action potential
3. Automaticity
4. Rhythmicity
5. Conductivity
6. Contractility
7. Long refractory period
8. Incomplete tetanus
9. Infatiguability
10. Extrasystole &
compensatory pause
11. All or none
phenomenon
12.Staircase

7. Electrical Properties
•Excitability- All or None law
•Long refractory period
•Automaticity
•Autorhythmiticity
•Conductivity

8. • The ability of a tissue to a stimulus is known as
excitability.
• In the case of muscle the response is shortening of its
fibers.
• In heart two types of tissues are present:
• Conducting tissue: its function predominantly to initiate and
conduct impulses from one end to other end of the heart.
• Contractile tissue: its function is predominantly to contract.
• Both these tissue show excitation.
A. Excitability

9. •RMP of mammalian CM cells is about -
90mV.(interior negative to exterior) (-85 to -95)Guyton.
•Stimulation propagated AP i.e. responsible for
initiating contraction.
•Depolarization proceeds rapidly, and an overshoot is
present, as skel mus & nerve, but this is followed by a
plateau before the MP returns to the baseline.

10. •In mammalian hearts, depol lasts about 2ms, but
the plateau and repol lasts 200ms or more.
•Parasympathetic nerve stimulation decreases
excitability
•Sympathetic stimulation increases excitability

11. - Ganong
•These are of two types in the
heart, the T (for transient)
channels and the L (for long-
lasting) channels

13. Cardiac Action Potential

15. Phases of A.P.- RMP -90mV
(-85 to -95)Guyton
•Phase 0- Rapid depolarization (+20 to +30 mV)
•Phase 1- Rapid initial repolarization. (-10mV)
•Phase 2- Plateau phase
•Phase 3- Rapid repolarization
•Phase 4- Terminal phase of repolarization

16. Phase 0 :
Depolarization (due to entry of Na+ into the cell down the electro-
chemical gradient) event lasts about 2ms, amplitude of potential reaches up
to +20 to +30 mV (positive interior with reference to exterior)
Ionic basis – initial and overshoot depol are due to rapid opening of
voltage-gated Na+ & rapid entry of Na+ similar to skel.mus and nerve.
Phase I :
 Rapid Repolarization (reduced permeability to K + & Na+ as the mem
resistance ↑se )
Ionic basis – initial rapid repol due to closure of Na+ channels & opening
of K+ channels result transient outward current.
Various phases of action potential and ion basis
conductance

17. Phase II
 Decrease permeability to K+ to moderate high Na+ permeability.
Ionic basis-
*Slow influx of Ca+ + from opening of sarcolemma L-type Ca+ +
channels.
*Closure of distinct set of K+ channels called inward rectifying K+
channels.
• Phase III = conductance of Na+ & K+ return to the resting levels.
(Ionic basis- slow repol due to closig of Ca+ + )
• Phase IV = due to steady K+ conductance on the resting potential
level. (the resting ionic composition is restored by Na+ - K+
pump).

19. So, why!?
•Duration of action potential :
•The duration of action potential is abt
250ms at a HR 75 beats/min.
• The duration of AP ↓ses and ↑sed HR
(e.g. 150ms at a HR of 200beats/min)
Parasympathetic nerve stimulation
decreases excitability.
Sympathetic stimulation increases
excitability

20. References
• Text book of Medical Physiology 14th edition
Guyton & Hall
• Ganong's Review of Medical Physiology, 26 edition.
• Human Physiology
• Vander
• Text book of Medical Physiology
• Indukurana
• Hutchinson Clinical Methods

21. THANK YOU . . .

22. Properties of Cardiac Muscle - 2
by
Dr. Pandian M
Assistant Professor
Dept. of Physiology

23. B. Intro to Automaticity & Autorhythmiticity
• Heart is having inherent property of spontaneous generation
of own A.P.( excitation)
• The conduction system (pacemaker tissue- SAN,AVN or
AV bundle purkinje fibres) are capable of generation of the
cardiac impulse
• SAN is pacemaker under physiological condition
•The pattern of A.P. is different from the pattern of A.P. of
cardiac muscle
• Under abnormal conditions the cardiac ms and atrial ms can
also generate A.P.

24. •Pacemaker tissue is unstable RMP bcoz of the continues
change in membrane permeability.
•This slow depolarization b/w AP called pre-potential &
pacemaker potential or diastolic depol
•The property of spontaneous pre potential followed by
AP called autorhythemicity

25. RATE OF GENERATION OF A.P. IS
1.70- 80/min in SAN
2.40-50/min AVN
3.40/min Bundle of His
4.25-30/min in Ventricular muscle
•Rate of generation of impulses is highest in SAN,
therefore SAN 1st pacemaker

26. •The ability to initiate a heart beat continuously and
regularly without external stimulation.
•The heart continues to beat quite some time even after cut
their innervated nerves or even cut them into pieces.
•Because of presence of the specialized “pacemaker” tissue
(Includes SAN & AVN; atrioventricular bundle; &
purkinje) in the heart which can initiate the AP.

29. Intro of pacemaker potential & prepotential
•The cells of pacemaker are modified are myocardial
cells
•There are capable of generating the impulses
•The A.P. of SAN is called Pacemaker potential
•This cells are having unstable resting membrane
potential
•RMP automatically rises towards the firing level
and impulse is generated

30. Continue………..SAN POTENTIAL
•During recovery from the A.P. K+ diffuses and
causes hyperpolarization (-60mV)
•Hyperpolarization activates h-channels/ funny
channels which causes entry of Na+ and K+ inside
rising slowly potential to -40mV
•This slow rise of potential/ depolarization is known
as Prepotential or Pacemaker Potential
•Last phase of prepotential is completed by activation
of transient Ca++ channels rising -55 mV (firing
level)

31. Continue………..SAN POTENTIAL
•At the threshold level the long acting Ca++
channel open up and A.P. develops.
•At the end of A.P. K+ diffusion channels are
open and Ca++ channels closed
•K+ diffusion from inside to outside the cell
causes repolarization and hyperpolaziation

33. a. Phase 0
• It’s the upstroke of the action potential.
•It’s caused by an increase in Ca2+ conductance.
• This increase causes an inward Ca2+ current that drives
the membrane potential toward the Ca2+ equilibrium
potential.
• The ionic basis for phase 0 in the SA node is different from
that in the ventricles, atria, and Purkinje fibers (where it is
the result of an inward Na+ current).

35. b. Phase 3
•Its repolarization.
•Its caused by an increase in K+
conductance.
•This increase results in an outward K+
current that causes repolarization of the
membrane potential.

36. c. Phase 4
• It’s slow depolarization.
•Accounts for the pacemaker activity of the SA node
(automaticity).
•It caused by an increase in Na+ conductance, which
results in an inward Na+ current called If.
•If is turned on by repolarization of the membrane
potential during the preceding action potential.
d. Phases 1 and 2
•Are not present in the SA node action potential.

37. Ionic basis of pacemaker potential and action
potential in SA node
1. At the peak of each impulse, IK begins and brings about
repolarization.
2. IK then declines, and a channel permeable to both Na+ and K+ is
activated.
3. Because this channel is activated following hyperpolarization, it is
referred to as an “h” channel; however, because of its unusual
(funny) activation it has also been dubbed an “f ” channel and the
current produced as “funny current.”
4. As Ih increases, the membrane begins to depolarize, forming the
first part of the prepotential.

38. KEY-
f- funny channel
T – transient type channel
L- long lasting channel

39. 5. Ca2+ channels then open. These are of two types in the heart,
the T (for transient) channels and the L (for long-lasting)
channels.
6. The calcium current (ICa
2+ ) due to opening of T channels
completes the prepotential, and ICa
2+ due to opening of L
channels produces the impulse.
7. Other ion channels are also involved, and there is evidence
that local Ca2+ release from the sarcoplasmic reticulum (Ca2+
sparks) occurs during the prepotential.

40. 8. The action potentials in the SA and AV nodes are largely due to
Ca2+, with no contribution by Na+ influx.
9. 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.
10. In addition, prepotentials are normally prominent only in the
SA and AV nodes.
11. 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.
12. Atrial and ventricular muscle fibers do not have prepotentials,
and they discharge spontaneously only when injured or abnormal.

42. • When the cholinergic vagal fibers to nodal tissue are stimulated, the
membrane becomes hyperpolarized and the slope of the prepotentials is
decreased below Figure mentioned
• because the Ach. released at the nerve endings increases the K +
conductance of nodal tissue.
• This action is mediated by M2 muscarinic receptors, which, via the βγ
subunit of a G protein, open a special set of K+ channels.
• The resulting IK Ach slows the depolarizing effect of Ih .

44. •In addition, activation of the M2 receptors decreases
cyclic adenosine 3',5'-monophosphate (cAMP) in the
cells, and this slows the opening of the Ca2+ channels.
•The result is a decrease in firing rate.
•Strong vagal stimulation may abolish spontaneous
discharge for some time.
•Conversely, stimulation of the sympathetic cardiac
nerves speeds the depolarizing effect of Ih , and the rate
of spontaneous discharge increases.
•Norepinephrine secreted by the sympathetic endings
binds to β1 receptors

45. •the resulting increase in intracellular cAMP facilitates
the opening of L channels, increasing ICa and the
rapidity of the depolarization phase of the impulse.
•The rate of discharge of the SA node and other nodal
tissue is influenced by temperature and by drugs.
•The discharge frequency is increased when the
temperature rises, and this may contribute to the
tachycardia associated with fever.
•Digitalis depresses nodal tissue and exerts an effect
like that of vagal stimulation, particularly on the AV
node.

46. Applied
•Latent pacemaker / Ectopic
pacemaker
•Various chemical agents which alter
the heart rate by changing the
prepotential.

47. Applied Aspect
(i) If the natural pacemaker of SAN is destroyed, then
the next fastest latent pacemaker, often the AVN takes
over.
•Rhythmic rate of AVN is 40-60 beats/min, and that of
purkinje fibers is 15-40 beats/min.
(ii) The various chemical agents which alter the heart
rate, do so by changing tile slope of pre-potential.
The steeper is slope of pre-potential, the faster is the rate
at which the pacemaker fires

49. Conductivity
conductivity is a property of whole heart muscle, but it is especially developed in
the bundle of His, its branches & purkinje’s tissue.

50. Conduction Pathway

51. •anterior interatrial band, passes through the
anterior walls of the atria to the left atrium.
•In addition, three other small bands curve
through the anterior, lateral, and posterior atrial
walls and terminate in the A-V node;
•These are called, respectively, the anterior
internodal pathway of Bachman, middle
internodal pathway of Wenckebach, and
posterior internodal pathway of Thorel.

52. • Rate of production of rhythmic impulses by different
• parts of the heart is:
• SA node: 70–80/min,
• AV node: 40–60/min,
• Atrial muscle: 40–60/min and
• Ventricular muscles: 20–40/min.

53. • After sudden A-V bundle block, the Purkinje system does not
begin to emit its intrinsic rhythmical impulses until 5 to 20
seconds later because,
• before the blockage, the Purkinje fibers had been “overdriven” by
the rapid sinus impulses and,
• consequently, are in a suppressed state. During these 5 to 20
seconds, the
• ventricles fail to pump blood, and the person faints after the first 4
to 5 seconds because of lack of blood flow to the brain.
• This delayed pickup of the heartbeat is called Stokes-Adams
syndrome. If the delay period is too long, it can lead to death.

54. Mechanical Properties
a. Contractility
b. All or none law
c. Rp
d. Staircase effects

55. • The heart contracts to the stimulus originated by its own rhythm or to
an external stimulus.
• Difference in Contractility B/W the Myocardium and the Skeletal Muscle.
• Certain features of excitability cum contractility of the cardiac muscles
are:
a) All or none law
b) Treppe
c) Summation or latent addition of sub minimal stimuli
d) Refractory period
e) Tetanus and
f) Circus phenomenon.
• Effects of pre load
- Length – Tension Relationship
• Effect After load
- Force Velocity Relationship
Contractility

56. • All or none law: ( Bowditch in 1871)
• States that the weakest stimulus that is capable of causing a contraction at all (
minimal or threshold stimulus) will produce the maximum contraction.
• Different B/W skeletal & cardiac muscle is due to the fact that the functionally
a continuous protoplasmic sheet & an impulse which causes contraction in one
part of atrial myocardium spreads under ordinary circumstances throughout.
• The individual fibres of skel.muscle on other hand are insulated from one
another.
• So, when its said that the cardiac muscle follows, “ all or non law” it applies
subject to the physiological conditions existing at the time, like the initial
length of the fibre, H- ion Conc, state of Nutrition, fatigue and electrolytes
Conc.*

57. • Treppe :-
• If a number of stimuli of the same threshold intensity (maximal in
case of skel.mus) be sent into the muscle after a resting period,
repeated approx every 10 / sec, the first few contractions of the series
↑se successively in amplitude.
• This ascent in magnitude of the response like rising steps of a
staircase.
• This is due to the greater contractility of the muscle, resulting from
beneficial effects of the previous contraction like the : rise in temp,
slight increase in H- ion Conc of the muscle; as a result of lactic acid
production and metabolites formed.

58. Summation or latent addition:
• If a series of suminimal are given to the heart muscle the effects of excitation
due to these stimuli fuse
• i.e. there is summation of excitation due to stimuli, resulting in a response in
the form of a visible contraction.
Refractory Period:
• Defined as the period during which a muscle doesn’t respond to a second
stimulus.
• RP of Skel.Mus is very small, less than 0.005 sec, and lies 1st half of the LP
• In the heart RP is very long and lasts throughout the contraction phase. Normal
RP of ventricle is 0.25 to 0.30 sec.
• During this period muscle not respond to a second stimulus, no matter how
strong, so long as its fibres are in the contracted state is known as ARP

59. Absolute Refractive Period:
• is seen from onset of AP until Repol progresses to a transmembrane
potential of about -55mV.
Cardiac Muscle –
ARP lasts throughout the period of systole
Relative Refractive Period lasts throughout period of Diastole
Relative Refractive Period- during relaxation the muscle regains its
excitability gradually. Means it is the period of AP in which a second
stronger stimulus may produce a response, it lasts for about 0.05 sec.

61. • Effective RP:
• Under certain conditions the ARP appears to be abnormally
prolonged.
• Due to contraction initiated by the second stimulus, but it does not
spread to whole of the muscle.
• This periods include ARP and so called ERP.
• Increase of ERP is seen when CM is subjected to cols, pressure,
acid solution- veratrine or quinidine.
• ARP is ↑sed by ;
• Exposure to cold and pressure, increase in acidity, and quinindine
• ARP is ↓sed by;
• ↑se in HR
• ↑se in temp
• Vagal stimulation

62. •If RP appears, like rhythmicity is inversely related to
the glycogen content of the different region of the
heart muscle.
•Thus, it is longest duration in the nodes than
ventricles, shorter in atria & shortest in spl
conducting tissues of heart namely bundle of His
and Purkinje fibre.

63. • When stimuli are applied at a higher frequency, each stimulus
applied during contraction period of previous response, it causes
tetanus and sustained contraction of the muscle called so.
• Tetanus produced experimentally or infection by clostridium
tetani is due to synchronous discharge from all the nerve fibers.
• When the muscle is stimulated repeatedly for prolonged periods,
the muscle goes into fatigue
Tetanus

64. •Circus Excitation or re-entry
phenomenon:
• It refers to which the wave of excitation
propagates repeatedly (continuously)
within a closed circuit.
• It’s more common in trachyarrhythmias.
• Circus excitation is known to occur under
two situations;
• 1. in the presence of transient block in
the conduction pathway
• 2. in the presence of an abnormal
extrabundle of conducting tissues called
bundle of kent.

66. •The force of contraction of cardiac muscle depends on
its preloading and after loading
•Effects of preload :
• a load which starts acting on a muscle before it starts to
contract is called.
•Effects of after load:
• After load refers to the load which acts on muscle after the
beginning of muscular contraction
•Starling’s law:
• The frank starling law of heart can be stated as, within
physiological limits the force of contraction is proportional
to its EDV.

67. Cardiac muscle Skeletal Muscle
Myocardium as whole obeys “ all or none
law”. i.e. contracts maximally with TH
stimulus.
Single muscle fibre obeys “ all or none law”
muscle as whole shows Quantal Summation
The active state and duration of contraction
are longer
Comparatively shorter
The RP is longer.
Summation and tetanus not possible.
RP shorter.
Summation and tetanus possible.
The Rate of force development during
contraction is slower
The Rate of force development during
contraction is faster
Velocity of shortening is slower Velocity of shortening is slower
Marked ability to alter contractility Little ability to alter contractility
The maximum tension developed per unit of
cross section of muscle in only 1/3 to 1/2 that
of skel.mus
The max tension developed per unit cross
section of mus is greater

68. • Term refers to the mechanism by which AP causes myofibrils of
muscle to contract
• When AP passes over the CM Memb, its spreads to interior of CM
fiber along the Memb of the T tubules.
• T tubule AP turn act on memb’s of longitudinal sarcoplasmic
tubules to cause release of Ca2+ ions into the muscle sarcoplasm
from SR.
• These Ca2+ ions diffuse into myofibrils & catalyze the chemical
rxn’s that promote sliding of actin and myosin filaments along one
another; this produce the muscle contraction.
Excitation-contraction coupling(function of
Ca2+ ions & T tubules)

69. • Quite different:
• A large quantity of extra Ca2+ ions also diffuse into sarcoplasm from T
tubules themselves at the time of AP.
• Indeed, Without extra Ca2+ from T tubules, the strength of CM contraction
would be reduced considerably because:
• SR less well developed that skel.mus.
• Does not store enough Ca2+ to provide full contraction
• T tubules of CM have a diameter 5 times greater than Skel.mus tubules, which means
a volume 25 times as great.
• Inside the tubules is large quantity of mucopolysaccharides its negatively charged &
bind an abundant store of Ca2+ ions, keep these always available for diffusion to the
interior of CM fibers, when T tubule AP appear.
• Strength of contraction depends to a greater extent on Conc. Of Ca2+ ions in
ECF.
• Duration of contraction – including the plateau- 0.2 sec in atrial muscle and
0.3 sec in ventricular muscle.

71. Metabolic properties
• Blood flow in myocardium is very high 80mL/100gm/min.
• In skeletal muscle is 3mL/100gm/min
• Presence of numerous mitochondria in Cardiac fibers
• High content of myoglobin, O2 storing muscle pigment
• Heart work under anaerobic condition with essentially no
accumulation of LA
• Under basal (resting)condition of the total caloric need of heart –
• 60% is provided by fat
• 35% by CHO
• 5% by ketones & Amino Acids

72. References
• Text book of Medical Physiology 14th edition
Guyton & Hall
• Ganong's Review of Medical Physiology, 26 edition.
• Human Physiology
• Vander
• Text book of Medical Physiology
• Indukurana
• Hutchinson Clinical Methods

73. THANK YOU . . .