Functional anatomy and physiology of cardiac muscle

DR NILESH KATE
MBBS,MD
PROFESSOR
DEPT. OF PHYSIOLOGY
FUNCTIONAL
ANATOMY AND
PHYSIOLOGY OF
CARDIAC MUSCLE

OBJECTIVES.
 FUNCTIONAL ANATOMY OF HEART
 Chambers of heart
 Valves of heart
 Structure of walls
 PHYSIOLOGY OF CARDIAC MUSCLE
 Structural organization
 Structure of cardiac muscle fibre
 Sarcotubular system.
 Process of excitability & contractility.
 Properties of cardiac muscle.

FUNCTIONAL ANATOMY OF
HEART
 Muscular pump
 Wt – 300 gms
 2 halves
 Right – pumps blood to
lungs for oxygenation
 Left – Pump blood to
systemic circulation.
Monday, August 31, 2020

CHAMBERS OF HEART
 Atria
 Right atrium – receives
venous blood through
superior & inferior venacava.
 Atrioventricular orifice guided
by tricuspid valve
 Left atrium – receives blood
from pulmonary veins & give
to left ventricle throgh mitral
valve.
 Interatrial septum.

CHAMBERS OF HEART
 Ventricles
 Left ventricle – receives blood
from left atrium & give blood
top systemic circulation
through aorta.
 Right ventricle-receives blood
from right atrium & give blood
top pulmonary circulation
through pulmonary artery.
 Interventricular septum.

VALVES OF HEART
 Atrioventricular
valves.
 Right – tricuspid
 Left – bicuspid/mitral
 At the periphery cusps
are attached to
atrioventicular rings &
free edges attached to
papillary muscles.

VALVES OF HEART
 Semilunar valves
 Open away from
ventricles & close
towards ventricles.
 Closes when ventricles
relax & prevent
backflow of blood into
ventricles.

STRUCTURE OF WALLS
 Pericardium
 Myocardium
 Endocardium.

PERICARDIUM
 Heart & root of great
vessels enclosed by
fibroserous sac
 Has 2 layers
 Fibrous
 Serous – has parietal &
visceral layers.
 Between this is
pericardial cavity filled
with pericardial fluid.

MYOCARDIUM
 Main tissue
constituting walls
 3 types
 Cardiac muscle –
forming walls of atria &
ventricles
 Pacemakers
 Conducting system

ENDOCARDIUM.
 Thin, smooth &
glistening membrane
lining myocardium
internally.
 The endocardium
continues as the
endothelium of great
vessels opening in the
heart

PHYSIOLOGY OF CARDIAC
MUSCLE
 STRUCTURAL
ORGANIZATION
 Fibres are striated &
involuntary
 Ribbon-like & branched &
at junction 2 fibers are
fused & form
Intercalated disc –
important during
contraction.

PHYSIOLOGY OF CARDIAC
MUSCLE
 Along the sides fibers
connected through Gap
juctions which provide
low resistance bridges &
acts as a functional
syncytium.
 Fibres are richly supplied
by the capillaries (one
capillary/fibre).

STRUCTURE OF CARDIAC
MUSCLE FIBRE
 80–100 μm long and 15
μm broad.
 Cell membrane –
sarcolemma & cytoplasm
called sarcoplasm.
 Myofibril – each muscle
fibre ( 2µm diameter)
 Made up of thick & thin
filaments.

SARCOTUBULAR SYSTEM.
 Well developed like that
of the skeletal muscle
 The tubules of the T-
system penetrate the
sarcomere at Z-line.
 So in cardiac muscles,
there is only one triad per
sarcomere as compared
to two in skeletal muscle

PROCESS OF EXCITABILITY &
CONTRACTILITY.
 The events which link
the electrical
phenomenon with
mechanical
phenomenon constitute
the Excitation–
Contraction Coupling
phenomenon.

ELECTRICAL POTENTIAL IN
CARDIAC MUSCLE
 Resting membrane
potential
 Is −85 to −95 mV
(negative interior with
reference to exterior).

ELECTRICAL POTENTIAL IN
CARDIAC MUSCLE
 Action potential.
 Divided into five
distinct phases.
 Phase 0: Rapid
depolarization
 Phase 1: Initial rapid
repolarization
 Phase 2: Plateau
 Phase 3: Repolarization
 Phase 4: Resting potential

Phase 0: Rapid depolarization
 The depolarization which
proceeds rapidly, an
overshoot is present, as in
skeletal muscle and nerve.
 Amplitude of potential
reaches up to +20 to +30 Mv.

Ionic basis
 Due to the rapid opening of voltage-gated Na+ channels
and rapid influx of Na+ ions.
 At -30 to -40 mV membrane potential the calcium
channels also open up and influx of Ca2+ ions also
contributes in this phase.

Phase 1: Initial rapid
repolarization
 Rapid depolarization is
followed by a very short-lived
slight rapid repolarization.
 The membrane potential
reaches from +30 mV to -10 Mv
during this phase.

Phase 1: Initial rapid
repolarization
 Ionic basis. The initial rapid
repolarization is due to closure
of Na+ channels and opening of
K+ channels resulting in
transient outward current.

Phase 2: Plateau
 The membrane potential
falls very slowly only to -
40 mV during this phase.
 The plateau lasts for about
100-200 ms.

Ionic basis.
 Very slow repolarization
during the plateau phase is
due to:
 Slow influx of Ca2+ ions
resulting from opening of
sarcolemmal L-type Ca2+
channels.
 Closure of a distinct set of
K+ channels called the
inward rectifying K+
channels.

Phase 3: Repolarization
 complete repolarization
occurs and the membrane
potential falls to the
approximate resting value.
 This phase lasts for about
50 ms.

Ionic basis.
 Results from the closing of Ca2+ channels and opening of
following two types of
 K+ channels: Delayed outward rectifying K+ channels,
which are voltage-gated and are activated slowly.
 Ca2+ activated channels which are activated by the
elevated sarcoplasmic Ca2+ levels.

Phase 4: Resting potential
 The potential is maintained
at −90 mV
 Ionic basis. The resting
membrane potential is
maintained by a resting K+
current, the largest
contributor to which is the
inward rectifying K+ current.
 The resting ionic
composition is restored by
Na+−K+ ATPase pump

DURATION OF ACTION
POTENTIAL.
 Is about 250 ms at a heart
rate 75 beats/min.

SPREAD OF AP THROUGH
CARDIAC MUSCLE.
 The cardiac muscle acts as
a physiological
syncytium due to the
presence of gap junctions
amongst the cardiac
muscle fibres.

EXCITATION-CONTRACTION
COUPLING
 Refers to the sequence of
events by which an
excited plasma membrane
of a muscle fibre leads to
cross-bridge activity by
increasing sarcoplasmic
calcium concentration.

EXCITATION-CONTRACTION
COUPLING
 The sequence of events
during excitation–
contraction coupling in the
cardiac muscle is similar to
those observed in a skeletal
muscle with the following
exceptions -

Exceptions
 In cardiac muscle extra
calcium ions diffuse into the
sarcoplasm from T-tubules
without which the
contraction strength would
be considerably reduced.

Exceptions
 The T-tubules of cardiac
muscle contain
mucopolysaccharides,
which are negatively
charged and bind an
abundant store of calcium
ions.Monday, August 31, 2020

Exceptions
 T-tubules open directly to
the exterior and therefore,
Ca2+ ions in them directly
come from the
extracellular fluid (ECF).
 Because of this, strength of
cardiac muscle contraction
depends to a great extent
on Ca2+ concentration in
the ECF.

PROCESS OF CARDIAC MUSCLE
CONTRACTION.
 The molecular mechanism of cardiac muscles contraction
similar to that of skeletal muscles & smooth muscles.
However, ………

PROCESS OF CARDIAC MUSCLE
CONTRACTION.
 Troponin–tropomyosin complex controls the onset and
offset of cross-bridge cycling, similar to that in the skeletal
muscles.
 Like smooth muscles, the contractility of cardiac muscle is
sensitive to phosphorylation.

RELAXATION OF CARDIAC
MUSCLE
 Relaxation of cardiac muscle (diastole) occurs when levels
of Ca2+ ions fall in the cardiac muscle fibres.
 During diastole, the Ca2+ ions are extruded out of the
cardiac muscle fibre by a carrier system operating at the
sarcolemma in which two Na+ ions are exchanged for each
Ca2+ ion extruded

PROPERTIES OF CARDIAC
MUSCLE.
 Automaticity.
 Rhythmicity
 Conductivity.
 Excitability.
 Contractility.

EXCITABILITY
 The cardiac muscle responds by the development
of action potential.

REFRACTORY PERIOD
 Refractory period refers to the
period following action potential
during which the cardiac muscle
does not respond to a stimulus.
 Cardiac muscle has a long
refractory period (250−300 ms in
ventricles and about 150 ms in
atria

TYPES
 Absolute
 Relative.

ABSOLUTE.
 During this period, the cardiac
muscle does not show any
response at all.
 It extends from phase 0 to half
of phase 3 of action potential.
 Normal duration of ARP in the
ventricles is about 180-200 ms.

RELATIVE.
 During this period, the
muscle shows response if
the strength of stimulus is
increased to maximum.
 It extends from second
half of the phase 3 to
phase 4 of the action
potential.
 Normal duration of relative
refractory period in
ventricles is about 50 ms

SIGNIFICANCE OF LONG
REFRATORY PERIOD
 The complete summation of contractions and thus tetanus
cannot be produced in the cardiac muscle.
 Since the heart has to function as a pump, it must relax, get
filled up with blood and then contract to pump out the
blood.
 A tetanized heart would be useless as a pump.

CONTRACTILITY.
 The ability of the cardiac muscle to actively generate force
to shorten and thicken to do work when sufficient
stimulus is applied.

CHARACTERISTIC FEATURES
 All or None law
 Staircase phenomenon
 Summation
 Effect of preload
 Effect of afterload
 Effect of ions
 Effect of temperature.

ALL OR NONE LAW
 when a stimulus is applied either the heart does not
contract at all (none response), or contracts to its
maximum ability (all response).
 This is because of the syncytial arrangement of the
cardiac muscle fibres

STAIRCASE PHENOMENON
 The successive increase
in the force of cardiac
contractions in first few
(4−5) contractions after
the quiescent heart starts
beating. This is because of
the beneficial effect.

Cause of beneficial effect
When the heart stops, there occurs increase
in Na+ and decrease in K+ concentration
inside the cell, this increases Ca2+ influx.
Progressive increase in the Ca2+
concentration in the sarcoplasm due to
increase in Ca2+ influx with each action
potential.
This produces a progressive increase in
strength of the few (4-5) cardiac muscle
contractions.

SUMMATION
When a
subthreshold
stimulus is
applied to the
quiescent heart,
there occurs no
response.
However, when
subthreshold
stimuli are
applied
repeatedly at an
interval of one
half to one second,
there occurs a
contraction of the
heart after about
10-20 stimuli.
This phenomenon
is called temporal
summation of
subminimal
stimuli

EFFECT OF PRELOAD
 A load which starts acting on a muscle before it starts
to contract is called preload.
 In the case of heart muscle, the end diastolic volume forms
the preload.
 The Frank–Starling law of heart states that within
physiological limits the force of cardiac contraction is
proportional to its end diastolic volume.

Length–tension relationship
 Length–tension relationship, i.e.
the relation between the initial
fibre length and total tension in
cardiac muscle.
 Diastolic intraventricular
pressure represents the passive
tension and it increases with the
increase in end diastolic volume.

Length–tension relationship
 Systolic ventricular pressure
represents the active tension
developed (isometric tension)
which is proportionate to the
degree of diastolic filling of the
heart (initial length of muscle
fibres).

EFFECT OF AFTERLOAD
 Afterload refers to the
load which acts on the
muscle after the beginning
of muscular contraction.

Force–velocity relationship
 The force–velocity curve
is plotted by noting the
velocity of muscle
contraction with
progressively increasing
load on the muscle.

 In the heart, load is
represented by the
resistance against which the
ventricles pump the blood
and velocity of muscle
contraction is represented
by the stroke output.

 Effects of change in initial
length on force–velocity
relationship curve.
 An increase in change in
the initial length. (within
physiological limits)
increases the force of
contraction (Po) without
changing the velocity
(Vmax), i.e. the relationship
shifts to the right.

 Effect of catecholamines or
increased calcium
concentration in ECF.
 The catecholamines or
increased Ca2+
concentration in ECF, both
cause an increase in Po as
well as Vmax.

Functional anatomy and physiology of cardiac muscle

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