Activity 1:

1. Explain why the larger waves seen on the oscilloscope represent the
ventricular contraction.
During ventricular contraction the force to pump the blood is greater compared
to atrial contraction. Therefore, a lot of force is needed in order to provide the
systemic circulation with blood that gets send throughout the entire body. The
smaller waves represent the contraction of the atria.
2. Explain why the amplitude of the wave did not change when you
increased the frequency of the stimulation. (Hint: relate your
response to the refractory period of the cardiac action potential.) How
well did the results compare with your prediction?
Due to a longer refractory period (unlike the skeletal muscles) the cardiac
muscle is incapable of wave summation. As a result the amplitude of the wave
did not change during the experiment although the frequency of the
stimulation was increased. The cardiac action potential is longer vs. the skeletal
muscle potential. The amplitude of the ventricular systole did not changed with
more frequent stimulation because a new contraction could not begin until the
relaxation phase. The results matched my prediction.
3. Why is it only possible to induce an extrasystole during relaxation?
Only until the resting membrane potential is again established in cardiac
muscle cells, and is maintained until the next depolarization arrives, only then
an induced extrasystole can occur, i.e. during relaxation. Only after
repolarization the depolarization of cardiac cells can occur. Cardiac muscle is
incapable of reacting to any stimulus before approximately the middle of phase
3, and will not respond to a normal cardiac stimulus before phase 4.
4. Explain why wave summation and tetanus are not possible in
cardiac muscle tissue. How well did the results compare with your
prediction?
Because the ventricles must contract and relax fully with each beat to pump
blood. Therefore the cardiac muscle cells have a longer refractory period and
are incapable of wave summation and tetanus. The prediction was matched by
the results of the experiment.
Activity 2:
1. Explain the effect that extreme vagus nerve stimulation had on the heart.
How well did the results compare with your prediction?

If vagal stimulation is excessive the heart will stop beating. After a short time
the heart resumed beating, and the heart rate increased to normal values. My
prediction matched the results.
2. Explain two ways that the heart can overcome excessive vagal
stimulation.
After excessive vagal stimulation, the ventricles resume their contraction after
a short period of time. This is known as vagal escape and is due to the
initiation of a rhythm by the Purkinje fibers or sympathetic reflexes.
3. Describe how the sympathetic and parasympathetic nervous
systems work together to regulate heart rate.
The sympathetic and parasympathetic nervous systems are part of the ANS.
The sympathetic nervous system is known as the fight of flight and the
parasympathetic nervous system is known as resting and digesting. Both
supply nerve impulses to the heart. Even when at rest both of the nervous
systems work, but the parasympathetic nervous system is more active. The
sympathetic nervous branch becomes more engaged when it is needed (ex:
exercise, danger). By stimulating the parasympathetic nervous system the
heart rate will decrease without directly changing the force of contraction. On
the opposite side, by stimulating sympathetic nervous system the rate and
force of contraction of the heart are increased.
4. What do you think would happen to the heart rate if the vagus
nerve was cut?
This will lead to an increase in the heart rate. The SA node will generate action
potentials 100 times per minute. Without the vagus nerve there will be no more
feedback from the parasympathetic nervous system. Both the
parasympathetic and sympathetic nervous systems form a checks-andbalances system that provides the right parameters so the heart functions in
an optimum way. If you eliminate one, then the balance is broken and the
heart will suffer damage.
Activity 3:
1. Explain the effect that decreasing the temperature had on the frog
heart. How do you think the human heart would respond? How well
did the results compare with your prediction?
By decreasing the temperature of the Ringers solution resulted in a decreased
heart rate for the frog. This is due to the fact that the frog is poikilothermic
animal it lacks an internal homeostatic regulatory mechanism, thus its

internal body temperature changes depending on the temperature of its

external environment. On the opposite side humans are homeothermic, even
when the external temperature fluctuates the bodys internal mechanism will
try to keep the internal temperature between 35.8-38.2 C. If the external
temperature drops then the heat promoting center in the hypothalamus gets
activated. To conserve energy the human heart will reduce its heart rate. In
extreme cases of low external temperatures the human body becomes
hypothermic. My predictions matched the results.
2. Describe why Ringer's solution is required to maintain heart
contractions.
The Ringers solution consists of essential electrolytes chloride, sodium,
potassium, calcium, and magnesium, and it provides the necessary
environment for the frogs heart so that spontaneous cardiac actions potentials
can occur. The Ringers solutions provide the means for the isolated intact
frogs heart to be viable.
3. Explain the effect that increasing the temperature had on the frog
heart. How do you think the human heart would respond? How well
did the results compare with your prediction?
By increasing the temperature of the Ringers solution resulted in an increased
heart rate for the frog. This is due to the fact that the frog is poikilothermic
animal it lacks an internal homeostatic regulatory mechanism, thus its
internal body temperature changes depending on the temperature of its
external environment. The human body is homeothermic, and an increase of
the external temperature triggers a response from the heat-loss center in the
hypothalamus. This is done in order to keep the internal body temperature
within the normal ranges. Also the heart rate will increase. In extreme high
temperatures the body becomes hyperthermic due to failed thermoregulation.
The results matched my prediction.
Activity 4:
1. Describe the effect that pilocarpine had on the heart and why it had
this effect. How well did the results compare with your prediction?
Pilocarpine is a cholinergic drug (an acetylcholine agonist). When administered,
the heart rate decreased from the base line of 61 to 46. Pilocarpine is a
chemical modifier that mimics the action of acetylcholine on muscarinic
receptors. It decreases the frequency of action potentials by binding to
muscarinic cholinergic receptors embedded in the plasma membrane of the SA
node cells. Indirectly the potassium channels are opened, and the calcium and

sodium channels are closed. As a result the heart rate decreases.

2. Atropine is an acetylcholine antagonist. Does atropine inhibit or
enhance the effects of acetylcholine? Describe your results and how
they correlate with how the drug works. How well did the results
compare with your prediction?
Atropine, a chemical modifier, inhibits the effects of acetylcholine. Atropine
antagonizes the muscarine-like actions of acetylcholine. During the
experiment, pilocarpine decreased the heart rate to 46. When atropine was
administered the heart rate increased to 71. The results matched my
prediction.
3. Describe the benefits of administering digitalis.
Digitalis increases the force of contraction and decreases the heart rate. This
chemical modifier can help those with weakened hearts that need to allow
maximum time for venous return and increased stroke volume. Those that
suffer from congestive heart failure are prescribed digitalis.
4. Distinguish between cholinergic and adrenergic chemical modifiers.
Include examples of each in your discussion.
Chemical modifiers that inhibit, mimic, or enhance the action of acetylcholine
in the body are labeled cholinergic (for ex. pilocarpine is an agonist and
atropine is an antagonist). Chemical modifiers that inhibit, mimic, or enhance
the action of epinephrine in the body are labeled adrenergic (for ex.
epinephrine is an agonist).
Activity 5:
1. Describe the effect that increasing the calcium ions had on the
heart in this activity. How well did the results compare with your
prediction?
An increase in calcium ions resulted in an increased heart rate from the
baseline of 59 to 69. The rate of depolarization and the force of contraction
both increased. The results did not match my prediction.
2. Describe the effect that increasing the potassium ions initially had
on the heart in this activity. Relate this to the resting membrane
potential of the cardiac muscle cell. How well did the results compare
with your prediction?
The potassium concentration is greater inside the cardiac muscle cell vs. the
outside of the cell. The resting membrane potential favors the movement of

potassium ions more than sodium or calcium ions. The ratio of extracellular and
intracellular concentrations of potassium determines mainly the resting
membrane potential of cardiac muscle cells. By increasing the potassium ions
initially the heart rate dropped to 28 and then it became erratic. Thus, the
resting membrane potential decreased and also the force of contraction by
increasing the potassium ions. The results matched my prediction.
3. Describe how calcium channel blockers are used to treat patients
and why?
Those that suffer from high blood pressure and abnormal heart rates can
benefit from calcium channel blockers. They block the movement of calcium
through the ion channels of the plasma membrane, throughout all the phases
of the cardiac action potentials. If less calcium gets through, then both the rate
of depolarization and the force of contraction are reduced.