Cardiac Muscle; The Heart as a Pump

and Function of the Heart Valves:

Chapter:9
Introduction
 RIGHT HEART – pumps blood through the lungs
 LEFT HEART – pumps blood through the systemic circulation; provides -
 pulsatile, two-chamber pump composed of an -ATRIUM AND VENTRICLE
 The ventricles supply the main pumping force that propels the blood to lungs or system
 CARDIAC RHYTHMICITY – continuing succession of contractions; transmitting action
potentials throughout the cardiac muscle to cause the heart’s rhythmical beat

Physiology and anatomy of cardiac muscle

3 MAJOR TYPES:

1. ATRIAL MUSCLE
2. VENTRICULAR MUSCLE
3. SPECIALIZED EXCITATORY AND CONDUCTIVE MUSCLE – exhibit automatic rhythmical
electrical discharge in the form of action potentials or conduction of the action
potentials through the heart
Cardiac muscle as synctiyum

INTERCALATED DISCS – cell

membranes that separate
individual
cardiac muscle cells from one
another
- At each intercalated disc,
the cell membranes fuse with
one
another to form permeable
communicating junctions (gap
junctions) that allow rapid
diffusion of ions
- Cardiac muscle is a
syncytium of many heart muscle
cells in
which the cardiac cells are so
interconnected that when one
cell become excited, the action
potential rapidly spreads to all
of them
ATRIAL SYNYCTIUM – constitutes
the walls of the two atria
VENTRICULAR SYNCYTIUM –
constitutes the walls of the
two
ventricles
- The atria are separated from
the ventricles by fibrous tissue
that surrounds the
atrioventricular (A-V) valvular
openings
between the atria and ventricles
A-V BUNDLE – specialized
conductive system; bundle of
conductive
fibers several millimeters in
diameter
 INTERCALATED DISCS – cell membranes that separate individual cardiac muscle cells
from one another
 At each intercalated disc, the cell membranes fuse with one another to form permeable
communicating junctions (gap junctions) that allow rapid diffusion of ions - Cardiac muscle
is a syncytium of many heart muscle cells in which the cardiac cells are so interconnected
that when one cell become excited, the action potential rapidly spreads to all of them
Action potential in cardiac Muscle

Averages about 105 millivolts

o Intracellular potential rises
from a very negative value
to a slightly positive value (-85
mv to about +20mv)
o After the initial spike, the
membrane remains
depolarized for about 0.2
second = plateau (causes
ventricular contraction to last
as much as 15 times
longer in cardiac than in skeletal
muscle)
o Abrupt depolarization at the
end of plateau
 Averages about 105 millivolts
 Intracellular potential rises from a very negative value to a slightly positive value (-85 mv to
about +20mv)
 After the initial spike, the membrane remains depolarized for about 0.2 second =
plateau
 Abrupt depolarization at the end of plateau

Long Action potential and plateu

1. The action potential in cardiac muscle is caused by
 Voltage-activated fast sodium channels → allow tremendous numbers of Na+
ions to enter the skeletal muscle fiber from the ECF → remain open for only a few
thousandth of a second then abruptly close → repolarization occurs
  Calcium-sodium channels → slower to open & remain open for several tenths of a
second → large quantity of Ca2+ & Na+ ions flow to the interior of the fiber →
prolonged period of depolarization: PLATEAU
 Calcium ions that enter during this plateau phase activate the muscle
contractile process

 Immediately after the

onset of the action
potential, the
 permeability of the
cardiac muscle membrane
for potassium
 ions decreases about
fivefold (doesn’t occur in
skeletal m.)
 o May result from the
excess calcium influx
through the
 calcium channels
2. Immediately after the onset of the action potential, the permeability of the cardiac
muscle membrane for potassium ions decreases about fivefold
 May result from the excess calcium influx through the calcium channels

Phases of Cardiac Muscle action potential

PHASE 0 (DEPOLARIZATION):
FAST SODIUM CHANNELS OPEN
- Cardiac muscle stimulation
→ Fast sodium channels open →
rapid influx of sodium ions →
depolarization → membrane
potential becomes more positive
(about ±20 mV)
PHASE 1 (INITIAL
REPOLARIZATION): FAST
SODIUM CHANNELS
CLOSE
- Sodium channels close →
begin to repolarize →
potassium
ions leave the cell through open
potassium channels
PHASE 2 (PLATEAU): CALCIUM
CHANNELS OPEN AND FAST
POTASSIUM CHANNELS CLOSE
- Brief initial repolarization
→ action potential plateaus
(decreased potassium ion efflux:
↓ permeability & increased
calcium ion influx: ↑
permeability)
PHASE 3 (RAPID
REPOLARIZATION): CALCIUM
CHANNELS CLOSE
AND SLOW POTASSIUM
CHANNELS OPEN
- Calcium channels close &
increased potassium
permeability
→ potassium ions exit the cell
rapidly → plateau ends → cell
membrane potential returns to
resting level
PHASE 4 (RESTING MEMBRANE
POTENTIAL)
- Averages about -80 to -90
millivolts
 PHASE 0 (DEPOLARIZATION): FAST SODIUM CHANNELS OPEN - Cardiac muscle
stimulation → Fast sodium channels open → rapid influx of sodium ions →
depolarization → membrane potential becomes more positive (about ±20 mV)
 PHASE 1 (INITIAL REPOLARIZATION): FAST SODIUM CHANNELS CLOSE - Sodium
channels close → begin to repolarize → potassium ions leave the cell through
open potassium channels
 PHASE 2 (PLATEAU): CALCIUM CHANNELS OPEN AND FAST POTASSIUM
CHANNELS CLOSE - Brief initial repolarization → action potential plateaus
 (decreased potassium ion efflux: ↓ permeability & increased calcium ion influx: ↑
permeability)
 PHASE 3 (RAPID REPOLARIZATION): CALCIUM CHANNELS CLOSE AND SLOW
POTASSIUM CHANNELS OPEN - Calcium channels close & increased potassium
permeability → potassium ions exit the cell rapidly → plateau ends → cell
membrane potential returns to resting level
 PHASE 4 (RESTING MEMBRANE POTENTIAL) - Averages about -80 to -90 millivolts

Velocity of Signal conduction in Cardiac Muscle

 ATRIAL & VENTRICULAR MISCLE FIBERS = about 0.3 to 0.5 m/sec
 LARGE NERVE FIBERS = about 1/250
 SKELETAL MUSCLE FIBERS = about 1/10
 PURKINJE FIBERS (in the specialized heart conductive system) = 4 m/sec (rapid
conduction)

REFRACTORY PERIOD
 Interval of time during which a normal cardiac Impulse cannot re-excite an already excited
area of cardiac muscle

 NORMAL R.P. OF
VENTRICLE = 0.25 – 0.30 sec
 NORMAL R.P. OF ATRIAL
MUSCLE = 0.15 sec
 - There is an additional
relative refractive period of
about 0.05
 second during which the
muscle is more difficult to
excite
  than normal but can be
excited by a strong excitatory
signal
 NORMAL R.P. OF VENTRICLE = 0.25 – 0.30 sec ,NORMAL R.P. OF ATRIAL MUSCLE = 0.15 sec
 There is an additional relative refractive period of about 0.05 second during which the
muscle is more difficult to excite than normal but can be excited by a strong excitatory
signal

 EXCITATION-CONTRACTION
COUPLING-FUNCTION OF
CALCIUM
 IONS AND THE
TRANSVERSE TUBULES
EXCITATION-CONTRACTION COUPLING-FUNCTION OF CALCIUM IONS
AND THE TRANSVERSE TUBULES

EXCITATION-CONTRACTION
COUPLING – the action
potential that
causes the myofibrils of muscle
to contract
- When an action potential
passes over the cardiac
muscle
membrane, the action potential
spreads to the interior of the
cardiac muscle fiber along the
membranes of the transverse
(T) tubules
- The T tubule action
potentials then act on the
membranes of
the longitudinal sarcoplasmic
tubules to cause release of
calcium ions into the muscle
sarcoplasm from the
sarcoplasmic reticulum
- After, mag diffuse na ang
calcium ions sa myofibrils so
mapromote na ang interaction
sa actin & myosin (muscle
contraction)
- Calcium entering the cell
then activates calcium release
channels (ryanodine receptor
channels) in the sarcoplasmic
reticulum membrane,
triggering the release of
calcium into
the sarcoplasm
- In the sarcoplasm: Calcium
+ troponin = cross-bridge
formation & contraction
- Kung walay Calcium gikan
sa T tubules it means reduced
pud
ang strength of contraction
because mas less developed ang
sarcoplasmic reticulum sa
cardiac muscles compared sa
skeletal m. so dili siya maka
store enough Ca2+
- Also, inside the T tubules
is a large quantity of
mucopolysaccharides that are
electronegatively charged &
bind an abundant store of
calcium ions (keeping th
EXCITATION-CONTRACTION COUPLING

 the action potential that causes the myofibrils of muscle to contract - When an action
potential passes over the cardiac muscle membrane, the action potential spreads to the
interior of the cardiac muscle fiber along the membranes of the transverse tubules
 The T tubule action potentials then act on the membranes of the longitudinal sarcoplasmic
tubules to cause release of calcium ions into the muscle sarcoplasm from the
sarcoplasmic reticulum –
 After, interaction actin & myosin (muscle contraction) - Calcium entering the cell then
activates calcium release channels (ryanodine receptor channels) in the sarcoplasmic
reticulum membrane, triggering the release of calcium into the sarcoplasm
 In the sarcoplasm: Calcium + troponin = cross-bridge formation & contraction
 T tubules it means reduced strength of contraction because mas less developed
sarcoplasmic reticulum cardiac muscles compared sa skeletal m. so store enough Ca2+ -
Also, inside the T tubules is a large quantity of mucopolysaccharides that are
electronegatively charged & bind an abundant store of calcium ions (keeping th them
available for diffusion to the interior of the cardiac muscle fiber when a T tubule action
potential appears - THE STRENGTH OF CONTRACTION OF CARDIAC MUSCLE DEPENDS TO
A GREAT EXTENT ON THE CONCENTRATION OF CALCIUM IONS IN THE EXTRACELLULAR
FLUIDS (remember!) - THE QUANTITY OF CALCIUM IONS IN THE T TUBULE SYSTEM DEPENDS
TO A GREAT EXTENT ON THE EXTRACELLULAR FLUID CALCIUM ION CONCENTRATION
cardiac muscles, extracellular Ca2+ skeletal muscle)
 - Transport of calcium back into the sarcoplasmic reticulum is achieved with the help of a
calcium-adenosine triphosphatase (ATPase) pump or the sarcoplasmic endoplasmic
reticulum calcium ATPase (SERCA2) - Calcium ions are also removed from the cell by a
sodium-calcium exchanger
 Sodium: enters during the calcium-sodium exchange & exits by the sodium-potassium
ATPase pump

Duration of contraction

The duration of contraction of

cardiac muscle is mainly a
function of the duration of the
action potential including the
plateau
- About 0.2 second in atrial
muscle
- 0.3 second in ventricular
muscle
 The duration of contraction of cardiac muscle is mainly a function of the duration of the
action potential including the plateau
 About 0.2 second in atrial muscle - 0.3 second in ventricular muscle

Relationsahip of ecg to cardiac cycle

RELATIONSHIP OF THE
ELECTROCARDIOGRAM TO THE
CARDIAC
CYCLE
P WAVE – caused by the spread
of depolarization through the
atria
and is followed by atrial
contraction (slight increase in
atrial pressure
curve immediately after P wave)
Q R S WAVES – result of
electrical depolarization of the
ventricles;
initiates contraction of the
ventricles (ventricular pressure
begins to
rise) – begins slightly before
onset of ventricular systole
VENTRICULAR T WAVE – stage
of repolarization of the
ventricles
when the ventricular muscle
fibers begin to relax (occurs
before the
end of ventricular contraction
 P-wave -caused by the spread of depolarization through the atria and is followed by atrial
contraction (slight increase in atrial pressure curve immediately after P wave)
 Q R S WAVES – result of electrical depolarization of the ventricles; initiates contraction of
the ventricles (ventricular pressure begins to rise) – begins slightly before onset of
ventricular systole VENTRICULAR T WAVE – stage of repolarization of the ventricles
when the ventricular muscle fibers begin to relax (occurs before the end of ventricular
contraction