DISCUSSION

Refractory Period
The cardiac refractory period is
related to the ion currents that flow
freely into and out of the cell. The
flow of ions translates into a change
in the voltage of the inside of the cell
relative to the extracellular space.
This change in voltage is referred to
as an action potential. After an action
potential initiates, the cardiac cell is
unable to initiate another action
potential for some duration of time.
This period of time is referred to as
the refractory period (Schimdt &
Thews, 1983).
The absolute refractory period is the
interval from the beginning of the
action potential until the fiber is able
to conduct another action potential.
The relative refractory period follows
and is the time period in which,
although the cell has not fully
recovered, a small, weak action
potential can be generated as the
result of a strong input stimulus
(Cannon, 1924).
The absolute refractory period of
cardiac muscle cells is much longer
compared to skeletal muscle cells
(250 ms vs. 2-3 ms), preventing
wave
summation
and
tetanic
contractions which would cause the
heart to stop pumping rhythmically. It
is the period during which the rapid
influx of Na+ rapidly decreases the
negativity of the cardiac cell. As the
membrane potential approaches
zero, the electrostatic force pulling
Na+ into the cell is neutralized. The
concentration gradient of Na+
however continues to push Na+ into

the cell and the cell begins to

hyperpolarize as the membrane
potential begins to become positive.
This closing of the Na+ channels
signals the beginning of the absolute
refractory period.
Once these
channels close, they cannot reopen
for a set period of time (Schimdt &
Thews, 1983).
When the membrane potential
becomes positive by about 20mV,
Na+ continues to to enter the cell
because the concentration gradient
overpowers the electrostatic forces.
The influx is slow however, and
many of the inactivation gates have
already closed. At about 30mV, Na+
influx ceases. The channels remain
closed until the first half of
repolarization, and thus the cell is
absolutely refractory during this
entire period. No action potential
can be generated by the cell during
this time, and the cell will not
respond to further excitation. This
mechanism
prevents
sustained,
tetanic contraction of cardiac muscle.
Tetanus will preclude the normal
intermittent pumping action of the
heart and interrupt the pattern of
electrical conduction throughout the
cardiac
muscle,
resulting
to
fibrulation (Randall et al. 2001).
The relative refractory period
immediately follows the absolute
refractory period, and is due to the
efflux of K+ ions. During the second
half of repolarization, the excitatory
Na+ channels are mostly ready to
open, and a small weak action
potential
can
be
generated.
However, it is better to wait until the
channels are fully ready before
continuing with the next excitation.

Full excitability is not regained until

the cardiac fiber has been fully
repolarized. In order for an action
potential to be generated during the
relative refractory period the stimulus
must be greater than that which
would normally elicit a response.
Unlike the absolute refractory period,
the duration of the relative refractory
period can change. As heart rate
increases, and systole decreases,
the
action
potential
becomes
narrower due to a decrease in
relative refractory period. At rest, the
heart rate slows, and the action
potential becomes wider as the
relative refractory period increases.
This allows greater oxygen supply to
reach needy areas during exercise
and other stress conditions (Wiener
& Rosenblueth, 1946).
These refractory periods are
important because during this time
the gradient concentrations of
important ions (Na+, K+) are
restored.
This allows further
excitation of the cardiac fiber. The
results of the refractory periods can
be seen in the plateau of the cardiac
fiber action potential (Randall et al.
2001).
In the experiment, the refractory
period was observed at early to
middle
diastole.
Premature
contractions
and
compensatory
pause were observed at late
diastole.
Vagal escape is stronger than an
ordinary heart contraction because it
happens when cardiac muscle
begins to contract after a brief period
of rest after vagal stimulation. Its
initial
strength
of
contraction

increases to a plateau by staircase

effect. The strong vagal stimulation
of the heart can stop the heartbeat
for a few seconds. Vagal separation
can cause sudden death in the
animal (Guyton, 2012).
Extrasystole is the premature
contraction of the heart that is
independent of the normal rhythm of
the heart and that arises in response
to an impulse in some part of the
heart other than the normal impulse
from the sinoatrial node. It is followed
by a pause, as the heart electrical
system "resets" itself and the
contraction following the pause is
usually more forceful than normal
(Guyton, 2012).
Changes in excitability during an
action potential from the beginning of
0 phase to 60mv of repolarization,
no action potential can be elicited, no
matter how strong the stimulus is.
This period is called effective
refractory period (ERP). This period
of the cardiac muscle is very long
which is different from skeletal
muscle. Therefore tetanus does not
occur in myocardial contraction. It is
very important for pumping blood to
arteries. After ERP, if there is an
extra stimulus that occurs before the
arrival of the normal impulse from the
sinoatrial
node,
a
premature
excitation and contraction may
happen. The premature excitation
also has its own refractory period. If
the next normal impulse from the
sinoatrial node arrives during the
refractory period of the premature
excitation,
it
cannot
cause
contraction. As a result, a prolonged
diastole is usually observed after the
premature
contraction.
This

prolonged diastole is also called

compensatory pause (Premature
Contraction
and
Compensatory
Pause, n.d.).
All-or-None Law
The all-or-none law is a principle
that the strength by which a muscle
fiber responds to a stimulus is
independent of the strength of the
stimulus. If the stimulus exceeded
the threshold potential, the muscle
fiber will give a complete response;
otherwise, there is no response.
(Cannon, 1924).
This principle happens due to the
presence of gap junstions in the
heart. Gap junctions allow all cardiac
muscle
cells
to
be
linked
electrochemically, so that activation
of a small group of cells spreads like
a wave throughout the entire heart.
This is essential for "synchronistic"
contraction of the heart as opposed
to skeletal muscle (Randall et al.
2001).
In the experiment, the threshold
stimulus was determined at 0.7 V.
Subsequent increases in electrical
intensity maintained the same wave
amplitude. There is no change in
wave amplitude, as the maximum
threshold will not change in cardiac
muscle cells (as with any other cells),
which is determined by the amount
of voltage needed for calcium
channels to open. After this point, no
additional voltage can cause the
channels to open more, or again,
prior to depolarization.
Effect of Inorganic ions
The fluids perfusing the heart must

contain a proper balance of three

essential ions. These are sodium
ions, potassium ions and calcium
ions. If these ions are in proper
proportions, the heart is able to
maintain its normal contraction for
hours in an oxygenated environment
(Randall et al. 2001).
If the concentration of these ions is
altered, then heart rate and rate of
contraction are changed. An excess
of potassium ions in the heart causes
the heart to become dilated, thereby
slowing the heart rate. This is due to
the potassium ions completely
blocking the conduction of impulse
from the atria to the ventricles
through the atrioventricular bundle
and may stop heart during diastole.
In contrast, an excess of sodium ions
depresses cardiac function, but for
an entirely different reason. These
ions compete with the calcium ions
at the same point in the excitatory or
contractile process of the heart
muscle in such a way that the
greater the sodium ion concentration
in the fluids, the less the
effectiveness of calcium ions in
causing
contraction.
Similarly,
excess calcium ions in the fluids
enhance myocardial contractility,
wherein a large amount of calcium
ions relaxes the heart less during
diastole and eventually stops in
systole. Contrastingly, a deficiency of
calcium
ions
causes
cardiac
flaccidity (Study of the Effects of
Inorganic ions on Heart Contractility,
n.d.).
In the experiment, the application of
the Ringers solution serves as a
control for the normal heart rate.
Upon adding 0.7% NaCl, the heart

rate increased. This is in contrast

with the theoretical results, wherein it
should slow down heart rate. Upon
washing with Ringers again, and
then adding 0.9% KCl, the heart rate
decreased. This is in line with the
theoretical
results,
wherein
potassium influx should slow heart
rate. Lastly, upon addition of
1%CaCl2, the heart rate increased,
but only by a very minimal amount.
This somehow agrees with the
theoretical results wherein calcium
ion influx enhances myocardial
contraction.

Randall, D., W. Burggren & K.

French.
2001.
Eckert
Animal
Physiology. ISBN: 0716738635.

Reference/s:

Online Reference/s:
Study of the Effects of Inorganic ions
on Heart Contractility. n.d. Web.
Retrieved
at:
http://www.physiology.sdu.edu.cn/jpk
c/5/5-2-14.htm. Accessed on 21 April
2015.

Cannon, Walter B. Biographical

Memoir, Henry Pickering Bowditch,
1840-1911.
Washington,
D.C.:
National Academy of Sciences,
Volume xvii, eighth memoir. 1924.
Guyton, Arthur C.. Textbook of
Medical Physiology, 11th Edition.
Saunders Book Company, 062005.
10.1.2

Schmidt, Robert F.; Thews, Gerhard

(1983). Human physiology. SpringerVerlag. p. 725.
Wiener, N.; Rosenblueth, A. (1946).
"The mathematical formulation of the
problem of conduction of impulses in
a network of connected exitable
elements, specifically in cardiac
muscle". Arch. Inst. Cardiologia de
Mexico (journal) 16 (34): 205265.

Premature
Contraction
and
Compensatory Pause. n.d. Web.
Retrieved
at:
http://www.physiology.sdu.edu.cn/jpk
c/5/5-2-12.htm. Accessed on 21 April
2015.