Atriovetricular valve : Tricuspid & Bicuspid valves hold the valves in closed postion

when ventricles contract, to prevent back flow of blood to atria (right and left)

Tricuspid valve - consists of three

Flaps, present between right
atrium and right ventricle. Flaps are
connected to chordae tendineae.
Bicuspid valve – consists to two flaps,
present between left atrium
and left ventricle. Flaps
are also connected to
chordae tendineae.

Chordae tendineae are

attached to the inner walls
of ventricles
Atherosclerosis - Causes and consequences of occlusion of the coronary arteries.

• Atherosclerosis is the development of fatty tissue in arteries called atheroma.

• Atheroma is the degeneration of the walls of the arteries caused by accumulated fatty deposits and scar tissue, and leading
to restriction of the circulation and a risk of thrombosis.
• Thrombosis is the formation of a blood clot, known as a thrombus, within a blood vessel. It prevents blood from flowing
normally through the circulatory system.
• Low density lipoproteins (LDL) containing fats
and cholesterol accumulate and phagocytes are
then attracted by signals from endothelium cells
and smooth muscle.
• The phagocytes engulf the fats and cholesterol by
endocytosis and grow very large to form foam cells.
• Smooth muscle cells migrate to form a tough cap
over the atheroma.
•The artery wall bulges into the lumen narrowing it and thus
impeding blood flow.
•Coronary occlusion (blockage) is a narrowing of the arteries
that supply blood containing oxygen and nutrients to the
heart muscle (cardiac muscle).
•Lack of oxygen (anoxia) causes pain, known as angina, and weakens the muscle’s ability to contract, so the heart
beats faster to supply oxygen and nutrients to its non-functioning muscle.
•The fibrous cap covering atheromas sometimes ruptures, which stimulates the formation of blood clots that can block
arteries supplying blood to the heart muscles.
•The causes of atherosclerosis are not yet fully understood. Various factors are associated with an increased risk of
atheroma but are not the sole causes of the condition:
1.high blood concentrations of LDL (low density lipoprotein)
2.chronic high blood glucose concentrations, due to overeating, obesity or diabetes
3.chronic high blood pressure due to smoking, stress or any other cause
4.consumption of trans fats, which damage the endothelium of the artery.
There are also some more recent theories that include microbes:
5.infection of the artery wall with Chlamydia pneumoniae (bacterium that can cause
respiratory tract infections)
2. production of trimethylamine N-oxide (TMAO) by microbes (bacteria) in the intestine.
 The sinoatrial node - The heartbeat is initiated by a group of specialized muscle cells in the
right atrium called the sinoatrial node.

• The heart muscles (cardiac muscles) can contract without stimulation from motor neurons.
• The contraction is called myogenic, meaning that it is generated in the muscle itself.
• The membrane of a heart muscle cell depolarizes (develops electrical signal as charges) when the
cell contracts and this activates adjacent cells, so they also contract.
• A group of heart muscle cells therefore contracts almost simultaneously at the rate of the fastest.
• There is a small group of special muscle cells in the wall of the
right atrium, called the sinoatrial node.
• These cells have some proteins that cause contraction in other
muscle cells.
• The sinoatrial node therefore initiates each heartbeat,
because the membranes of its cells are the first to depolarize
(develop electrical signal as a charge) in each cardiac cycle
(one complete heart beat).
SA node controls atrial systole & AV node controls ventricular systole
Initiating the heartbeat -The sinoatrial node acts as a pacemaker.

• Because the sinoatrial node initiates each heartbeat, it sets the pace (consistent rate) for the
beating of the heart and is often called the pacemaker.
• If it becomes defective, its output may be regulated or even replaced entirely by an artificial
pacemaker.
• This is an electronic device, placed under the skin with electrodes implanted in the wall of the
heart that initiate each heartbeat in place of the sinoatrial node.
Atrial and ventricular contraction (Systole) -The sinoatrial node sends out an
electrical signal that stimulates contraction as it is propagated through the walls of
the atria and then the walls of the ventricles.
• The sinoatrial node initiates a heartbeat by contracting and simultaneously sends out an electrical signal that
spreads throughout the walls of the atria.
• This can happen because there are interconnections between adjacent cardiac muscle fibres
across which the electrical signal can be propagated or move forward.
• Also the cardiac muscle fibres are branched so each fibre passes the signal on to several fibres.
• It takes less than a tenth of a second for all cells in the atria to receive the signal.
• This propagation of the electrical signal causes the whole of both left and right atria to contract.
• After a time delay of about 0.1 seconds, the electrical signal is conveyed
to the ventricles.
• The time delay allows time for the atria to pump the blood into the
respective ventricles.
• The signal is then propagated throughout the walls of the ventricles,
stimulating them to contract and pump blood out into the arteries
(pulmonary artery and aorta).
The sinoatrial node - Signals from the sinoatrial node that cause contraction cannot pass directly
from atria to ventricles.

• The SA node spreads very rapidly across the entire atrium as if it were one cell. This causes the atria to
undergo systole, i.e. they contract.
• Signals from the sinoatrial node that cause contraction within the atria cannot pass directly from the atria to
ventricles.
• Instead the signal from the SA node reaches the atrioventricular (AV) node.
• From there the signal spreads throughout the heart via specialized heart muscle tissue called Purkinje fibres.
• This signal causes the ventricles to undergo systole.
• This snaps the atrioventricular valves shut.
• After the ventricles are emptied the semilunar valves close.
• The ventricles begin diastole, the atrioventricular valves open
and the ventricles start filling with blood. Finally, all four
chambers are in diastole and filling. When the atria are filled
and the ventricles are 70 per cent filled, the cycle has ended.
The atrioventricular node - There is a delay between the arrival and passing on of a stimulus at the atrioventricular
node.

• The mechanism of contraction of the atria and the ventricle take place in different ways.
• The fibres which connect the SA node to the AV node carry the action potential (electical impulse as a change) relatively
slowly.
• There is a delay of approximately 0.12 second between arrival of the stimulus from the SA node and initiation of the
impulse with the ventricles.
• The cells of the AV node take longer to become excited than the cells of the SA node.
There are a number of features of the AV node that lead to the delayed initiation of contraction of ventricles by the AV node.
• The AV node cells have a smaller diameter and do not conduct as quickly.
Atrioventricular node (continues)
● There is a relatively reduced number of Na+ channels in the cell membranes of AV node cells as
Na+ ions help in creating impulses as electrical charges.
Atrioventricular node (continues)
• A more negative resting potential and a prolonged refractory period within the cells of the AV
node
Resting potential = Inside charges on membrane are
negative while outside positive. No impulse is passing.
Action potential = Inside charges on membrane
become positive while outside become negative.
Impulse is passing.
Refractory period = The period from the initiation to the
action potential
• There are fewer gap junctions between the cells of the
AV node.
• There is relatively more non-conductive connective tissue
in the node.
The delay in conduction - This delay allows time for atrial systole before the
atrioventricular valves close.

• The delay in the initiation of contraction caused by the AV node is important

because it ensures that the atria contract and empty the blood they contain into
the ventricles first before the ventricles contract.
• The contraction of ventricles causes the atrioventricular valves (ticuspid &
bicuspid valves) to snap shut.
• The delay in conduction prevents the early contraction of the ventricles which
would lead to too small a volume of blood entering the ventricles.
• This allows the ventricles to receive maximum amount of blood from the atria.
Coordination of contraction - Conducting fibres ensure coordinated contraction of the
entire ventricle wall.
• The bundle of His receives the impulse from the AV node and conducts the signal rapidly to a point (Bundle of His) where it
splits into the right and left bundle branches.
• The bundle branches conduct the impulses through the wall between
the two ventricles called inter-ventricular septum.
• At the base, or apex of the heart, the bundle branches connect to
the Purkinje fibres which conduct the signal even more rapidly to
the ventricles.
• These Purkinje fibres have a number of modifications that facilitate
them conducting signals at such a high speed:

● They have relatively fewer myofibrils (actin & myosin).

● They have a bigger diameter.
● They have higher densities of voltage-gated sodium channels.
● They have high numbers of mitochondria and high glycogen stores.

• The contraction of the ventricle begins at the apex.

Causes of the sound of the heartbeat - Normal heart sounds are caused by the atrioventricular
valves and semilunar valves closing causing changes in blood flow.

• A normal heartbeat has two sounds, both of which are caused by the closing of valves.
• When the atrioventricular valves snap shut, there is a “lub” sound. This happens when the
ventricles contract (vetricular systole)
• After the ventricles are emptied the semilunar valves close, causing the second sound, the “dub”
sound. This happend when the heart undergoes diastole (Relax)
• The above actions happen to prevent the backflow of blood.
Changing the heart rate - The heart rate can be increased or decreased by
impulses brought to the heart through two nerves from the medulla of the brain.

Medulla – Cardiovascular centre

Epinephrine - Epinephrine increases the heart rate to prepare for vigorous physical activity.

• The sinoatrial node also responds to epinephrine in the blood, by increasing the heart
rate.
• This hormone is also sometimes called adrenalin and is produced by the adrenal
glands.
• The secretion of epinephrine is controlled by the brain and rises when vigorous
physical activity may be necessary because of a threat or opportunity. 
• So epinephrine has the nickname “fight or flight hormone”.
• In the past when humans were hunters rather than farmers, epinephrine would have
been secreted when humans were hunting for prey or when threatened by a predator.
• In the modern world athletes often use pre-race routines to stimulate adrenalin
secretion so that their heart rate is already increased when vigorous physical activity
begins.