The Circulatory

system in mammals
Mr. James
Objectives
1. Describe the structure of the heart, arteries, veins, capillaries, erythrocytes, and
leucocytes, relating their structures to functions.
2. Explain the cardiac cycle and its initiation.
3. Discuss the internal factors that control the heart action.
4. Discuss factors affecting blood pressure.
5. Explain the role of haemoglobin in oxygen and CO2 transport.
6. Describe O2 dissociation curves for adult haemoglobin.
7. Explain the significance of the effect of Co2 on the oxygen dissociation curves (Bohr
Effect).
Structure and
function of the
heart
The cardiac cycle
The heart continuously contracts and relaxes in a rhythmic cycle. As it contracts, the heart pumps blood; when it
relaxes, it fills with blood. One complete rhythmic cycle of pumping and filling is called the cardiac cycle. Each
heartbeat is a cardiac cycle. The contraction phase of the cardiac cycle is called systole and the relaxation phase is
called diastole.

The volume of blood that each ventricle pumps each minute is called the cardiac output. The heart rate or rate of
contraction of the heart is the number of beats per minute. Stroke volume is the amount of blood pumped by a
ventricle during a single contraction. Thus, cardiac output is given by heart rate multiplied by stroke volume. The
sequence of events in one cardiac cycle is as follows:

● Both the left and right atria contract - Atrial Systole

● The left and right ventricles contract - Ventricular systole
● Atria and ventricles rest - Ventricular diastole
Cont’d
● Atrial Systole - Muscles of the atrial walls contracts. The pressure developed by the contraction is not very great, because the
muscular walls of the atria are only thin, but it is enough to force the blood in the atria down through the atrioventricular valves
into the ventricles. The blood from the atria does not go back into the pulmonary veins or the vena cava because these have a
semilunar valves to prevent backflow. About 0.1s after the atria contract, the ventricles contract. This is called ventricular
systole. During atrial systole, the pressure of the blood is higher in the atrium than in the ventricle and so forces the valve open.
During ventricular systole, the pressure of the blood is higher in the ventricle than in the atrium. The pressure of the blood
pushes up against the cusps of the valve, pushing it shut. Contraction of the papillary muscles, attached to the valve by tendons,
prevents the valve from being forced inside-out.
● Ventricular systole - The ventricles contract. The thick, muscular walls of the ventricles squeeze inwards on the blood, increasing
its pressure and pushing it out of the heart. As soon as the pressure in the ventricles becomes greater than that in the atria, this
pressure difference forces the atrioventricular valves shut, preventing blood from going back into the atria. Instead, the blood
rushes upwards into the aorta and pulmonary artery, pushing open the semilunar valves in these vessels as it does so. Ventricular
systole lasts for 0.3s.
Cont’d
● Ventricular diastole - The muscles of the heart relax. The pressure in the ventricles drops. The high pressure
blood which has just been pushed into the arteries would flow back into the ventricles, but for the presence of
the semilunar valves, which snap shut as the blood fills their cusps. During diastole, as the whole of the heart
muscles relaxes, blood from the veins flows into the two atria. The blood is at a very low pressure, but the thin
walls of the atria are easily distended, providing very little resistance to the blood flow. Some of the blood
flows down into the ventricles. The atrial muscle then begins to contract, pushing blood forcefully down into
the ventricles, and the whole cycle begins again.

During ventricular systole, the pressure of the blood forces the valves open. During ventricular diastole, the
pressure of the blood in the arteries is higher than in the ventricles. The pressure of the blood pushes into the
cusps of the valves, squeezing them shut.
Control of the heart beat
Cardiac muscles are myogenic, meaning they automatically contracts and relaxes. The cardiac cycle is initiated in a
small patch of muscle in the wall of the right atrium, called the sinoatrial node or SAN (pacemaker). The muscle
cells in the SAN set the pace and rhythm for all the other cardiac muscle cells. Their natural rhythm of contraction
is slightly faster than the rest of the heart muscle. Each time they contract, they set up a wave of electrical activity,
which spreads out rapidly over the whole of the atrial walls. The cardiac muscle in the atrial walls responds to this
excitation wave by contracting, in the same rhythm as the SAN. Thus, all the muscle in both atria contracts almost
simultaneously.

The muscles of the ventricles do not contract until after the muscles of the atria. This delay is caused by a feature of
the heart that briefly delays the excitation wave in its passage from the atria to the ventricles.
Cont’d
There is a band of fibres between the atria and the ventricles which does not conduct the excitation wave. As the wave
spreads out from the SAN, it cannot pass through these fibres. The only route is through a small patch of conducting
fibres, known as the atrioventricular node AVN. The AVN picks up the excitation wave as it spreads across the atria
and, after a delay of about 0.1s, passes it on to a bunch of conducting fibres called the Purkyne tissue (Bundle of His)
which runs down the septum between the ventricles. This transmits the excitation wave very rapidly down to the base
of the septum, from where it spread outwards and upwards through the ventricle walls. As it does so, it causes the
cardiac muscle in these walls to contract, from the bottom up, squeezing blood upwards and into the arteries.
Regulation of Cardiac output
Increased volume of blood flowing in the heart increases the stroke volume. At the same time, the stretching of the muscle in the wall
directly stimulates the SAN, which responds by firing action potentials slightly faster than usual, slightly increasing heart rate. During
exercise more blood is returned to the heart. This happens because of the drop in oxygen in the blood within blood vessels in active
muscles. This drop in oxygen stimulates the cells lining the inside of the blood vessels, causing them to release nitric oxide. The nitric
oxide causes muscles to relax in the walls of the arterioles supplying blood to the exercising muscles (vasodilation). This increases the
rate at which blood is returned to the heart. INcreasing the rate of blood returning to the heart increases cardiac output, which results in
more oxygen being transported to the muscles.

This mechanism only works up to a certain maximum cardiac output. However, nervous stimulation can alter the range which the heart
can cope with the blood returning to it. The heart has 2 types of nerves running to it, the vagus and sympathetic nerves. These nerves
bring impulses from the cardiovascular centre in the medulla of the brain. The vagus nerve brings these impulses from the brain to the
SAN and AVN, while the sympathetic nerves bring impulses to many areas of the muscle in the heart walls. If action potentials arrive
along a sympathetic nerve, they speed up the heart rate and increase stroke volume. The vagus nerve has the opposite effect.
Cont’d
These nerves may also be affected by blood pressure. Inside the aorta, and also in the walls of the carotid arteries,
are nerve endings which are sensitive to stretching. They are called baroreceptors or stretch receptors. If blood
pressure rises, this stretches the artery walls, which stimulates these nerve endings. They fire off impulses to the
brain, which then sends impulses down the vagus nerve to the heart. This slows the heart rate and reduces stroke
volume, which can help to reduce the blood pressure. Low blood pressure has the opposite effect. In this case, the
baroreceptors are not stretched and do not send impulses to the brain. The cardiovascular centre in the brain then
send impulses along the sympathetic nerve, which increases cardiac output and thus blood pressure. Impulses are
also sent to muscles in the arteriole walls (vasoconstriction), so increasing blood pressure.

Another factor which can influence the rate of heart beat, through the action of nerves to the heart, is the
concentration of CO2 and O2 in the blood. These are monitored by chemoreceptors, some which are in the brain
and others in the walls of the carotid artery and aorta. Higher CO2 concentrations or low O2 can increase the rate of
heart beat. However, this is usually of little importance compared with other factors.
Measuring blood pressure
The doctor can measure your blood pressure by using a device called a sphygmomanometer. The artery that the
doctor selects is in the arm at the same height at the heart. For a healthy adult at rest, the average arterial blood
pressure is the systemic circuit is 120 mmHg at systole and 80 mmHg at diastole. Both systolic (maximum pressure
produced from the contraction of the left ventricle) and diastolic pressure (lowest pressure caused by the relaxation
of the ventricular muscle) are measured.

A persistently high diastolic pressure in a person at rest is known as hypertension (140/90 mmHg). High blood
pressure can cause atherosclerosis.Systolic pressure rises temporarily when we exercise or are excited. This is a
result of the secretion of adrenaline, or the stimulation of of the SAN by the sympathetic nerve, causing the heart to
beat more forcefully.
Components of Blood
HAemoglobin dissociation curve
To investigate how haemoglobin behaves in different conditions, samples are extracted from the blood and then
exposed to different concentrations, known as partial pressures (kPa), of oxygen. Each haemoglobin molecule can
carry 4 molecules of O2. In the lungs, there is a high kPa of O2, as each O2 binds to a haemoglobin subunit, the
other units change their shape slightly to allow the other O2 to bind. This is an example of an allosteric effect.
When blood enters the capillaries in the tissue, the haemoglobin molecules all have four O2 bound. Tissues have a
low KPa of O2 and as one haemoglobin subunit unloads its O2, the other 3 subunits become more ready to unload
their O2.
Cont’d
The O2 that enters the pulmonary capillaries combines with the haemoglobin in the RBCs to form oxyhaemoglobin.
When oxygen is unloaded in the tissues, the haemoglobin is called deoxyhaemoglobin. At the KPa of O2 in the
lungs, haemoglobin is saturated with O2 but in the tissues, the oxyhaemoglobin gives up O2 which diffuse into the
cells. Hb + O2 → HbO2.

A dissociation curve for O2 from haemoglobin that shows how O2 binds to and is released from haemoglobin at
different KPa. Imagine a Hb molecule with no O2 bound to it. It is actually quite hard for the first O2 molecule to
bind. The Hb molecule is in a tense state (T-state). In an O2 KPa of 1 KPa, the Hb molecules are combined with
only 7% of their full load. You have to increase the KPa to 2.2 KPa before reaching a stage where each Hb is
combined with one O2. The Hb molecules is now in a relaxed state (R-state).
Carbon dioxide transport
● 5% of the total CO2 diffuses in the plasma and carried by the blood
● Some of the CO2 diffuses into the erythrocytes. In the cytoplasm of the RBCs, there is an enzyme called
carbonic anhydrase. The enzyme catalyses the following reaction: CO2 + H2O → H2CO3. The carbonic acid
formed dissociates to form: H2CO3 → H+ + HCO3 ions. The H+ quickly combines with Hb inside the RBC.
This forms haemoglobinic acid, which makes Hb release the O2 that it is carrying. The HCO3 ions diffuse
out of the RBC and into the blood plasma They remain here in solution, and are carried to the lungs. About
85% of CO2 is transported this way.
● Some of the CO2 that diffuses into the RBCs escapes the attention of the carbonic anhydrase. Instead, it
combines directly with Hb, forming carbaminohaemoglobin. About 10% of the CO2 is transported in this
form.
The bohr shift
We have seen that, when there is a lot of CO2 around, the high concentration of CO2 causes events in the RBC that
make the Hb release some of its O2. This is called the Bohr effect. It is exactly what the body needs. High
concentrations of CO2 are found in respiring tissues, which need O2. These high CO2 concentrations cause Hb to
release its O2 even more readily than it would otherwise do.