Gross structure of the heart

The four cardiac chambers are built upon a ring o fibrous fatty tissue called the
annulus fibrosus. The annulus fibrosus acts as a base for the atria and ventricles. It
also insulates the atria from the ventricles.

The cardiac chambers are internally lined with endocardium. Endocardium consists
of a thin sheet of flattened endothelial cells over connective tissue (and smooth
muscle cells in some places). The outer surface of the heart is covered by the
epicardium (epi=outside) a thin layer of flattened mesothelial cells over connective
tissue. The entire heart is enclosed in a fibrous sac called the pericardium. The lower
surface of the pericardium is fused to the diaphragm. So each time to diaphragm
moves, the heart moves in the same direction.

Roles of the heart

Receives blood from the veins at low pressure and raises the blood to a higher
pressure. Then ejects blood into the arteries.

Right atrium and tricuspid valve

The right atrium receives deoxygenated blood from the two vena cavae and the
coronary sinus. The tricuspid valve has three cusps and connects the right atrium to
the right ventricle. Each cusp is thin and consists of connective tissue and is
covered by endothelium. Each cusp is tethered to the papillary muscles by chordae
tendineae. As pressure builds up in the ventricles, the papillary muscles contract
which tenses the chordae tendineae and prevents the valve from inverting into the
atrium.

Right ventricle and pulmonary valve

The pulmonary valve has three cusps

Left atrium and mitral valve

The left atrium receives oxygenated blood from the four ( 2 left and 2 right)
pulmonary veins and transmits It into the left ventricle through the bicuspid valve. Th
bicuspid valve has two cusps.

Left ventricle, apex beat and aortic valve

The left ventricle wall is 3X thicker than the right ventricle because the left side has
to generate higher pressure. When left ventricle contracts, the apex taps against the
chest wall which produces. Palpable apex beat.

The cardiac cycle

One cardiac cycle is one complete contraction and relaxation of the heart (systole
and diastole).

Diastole (filling phase) consists of

Passive filing of the ventricles

Atrial systole
(ESV)

Diastole: rapid filling phase

In diastole the atria and ventricles are relaxing. Blood flows from the great veins
(vena cavae and pulmonary veins) through the tricuspid and bicuspid valves into the
ventricles. Initially, the pressure in the ventricles falls despite blood volume
increasing because the relaxing ventricles recoil from its end systolic shape. Once
the ventricles are completely relaxed, their pressure begins to rise as they fill.

Diastole: filling slows down (diastasis)

In diastasis, the passive filling of the ventricles slows down. The ventricles become
less compliant (stiffer) which causes the pressure in the ventricles to rise. Increased
pressure in the ventricles reduces the pressure gradient across the AV valves so that
the rate of filling decreases. The pressure in the atria increases due to venous blood
flowing into the atria.

Diastole: atrial systole

Contraction of the atria pumps extra blood into the ventricles.

End diastolic volume and end diastolic pressure

The volume of blood in a ventricle at the end of the filling phase (diastole) is called
end diastolic volume. End diastolic pressure is a little higher on the left than the right
because the thicker left ventricle requires a higher pressure to distend it.

Ventricular systole consists of

Isovolumetric contraction (brief)
Ejection phase (longer)

Isovolumetric contraction
The pressure in the ventricles rises above pressure in the atria so tricuspid and
bicuspid valves close. The AV valves are closed and the ventricles are temporarily
closed so the pressure of the rapped blood rises very quickly.
Ejection: rapid ejection phase
The pressure in the ventricles is greater than the pressure in the atria so pulmonary
and aortic valve open. ¾ of the stroke volume is ejected in the first half of the
ejection so this is called the rapid ejection phase.

Blood is ejected faster than it drain/move away so most of the stroke volume is
temporarily stored in elastic arteries i.e aorta.

Ejection: slows down

Relaxation of the ventricles begins so the rate of ejection slows down. So the rate at
which blood drains away now exceeds the rate of ejection so pressure in elastic
arteries falls. The pressure in the ventricles falls below pressure in the major arteries,
but the kinetic energy of the blood propels blood into the aorta and pulmonary artery.
However, blood flow slows down until backflow closes the aortic and pulmonary
valve.

Isovolumetric relaxation
As the ventricles relax and pressure in the ventricles fall below atria, the aortic and
pulmonary valves close so the ventricles briefly become a closed chamber. The
deformed, relaxing ventricle causes blood pressure in the ventricles to fall rapidly
(ESV). When pressure in the ventricle falls below pressure in the atria, the AV valves
are pushed open which indicates the end of isovolumetric relaxation.

NOTE: During ventricular systole, the atria have been filling up.

Cardiac cycle (Changes in pressure)

Isovolumetric
Isovolumetric relaxation
contraction
Closure of the aortic and pulmonary valves creates a notch called the incisura.

End systolic volume and ejection fraction

End systolic volume is the volume of blood that remains in the ventricles after
ejection. The ESV is a reserve of blood that can be used to raise the stoke volume
and ejection fraction during exercise. Ejection fraction is the proportion of blood
ejected (SV/EDV).
Left ventricular volume changes

The ventricular pressure volume loop

The pressure-volume loop is derived from
plotting left ventricular volume against left
ventricular pressure. Stroke work is the
work done by the ventricle to eject a
volume of blood (SV). So, the force
applied to the volume of blood in the
ventricles.
Stroke work=volume of fluid (SV) x
pressure required to move fluid (Mean
aortic pressure)
The mean aortic pressure is the average
pressure in the aorta during 1 cardiac
cycle.
The right atrial cycle
Changes in right atrial pressure creates a jugular venous pulse

The A wave is the increase

is pressure caused by atrial
systole. The ‘A’ stands for
atrial.

Atrial systole causes a

slight backflow of blood into
the vena cavae which do
not have valves. This raises
the central venous pressure
to its maximum point in the
cardiac cycle.

The C wave is caused by

bulging of the cusps of the
tricuspid or mitral valves
into the atrium as the valves
close (during ventricular systole). The C wave is also partly caused by expansion of
the carotid artery (which is adjacent to the jugular vein) during systole. The ‘C’
stands for carotid.

The X descent is caused by

the atria relaxing and the
downwards movement of the
base of the ventricles as they
contract. The downwards
movement of the base of the
ventricles stretches the atria
which sucks blood into the
ventricles.

The V wave is caused by the

atrial filling and the rise in
pressure as a consequence.
‘V’ refers to ventricular
systole which occurs at the
same time as atrial filling.

The Y descent is caused by the AV valves opening and blood from the atria draining
into the ventricles which produces a sharp drop in pressure.

The eye particular notices the X and Y descents.

Altered phase durations when heart rate increases

When heart rate increases the cardiac cycle shortens. So, each phase of the cycle
shortens. The different phases do not shorten by the same amount. Diastole doesn’t
shorten too much because it sets a limit to the maximum useful heart rate.

Heart sounds

When a cardiac valve closes, the cusps bulge back to check the momentum of the
blood which causes a vibration that is transmitted through the tissues to the chest
wall.

S1 – “Lub”
 Closure of tricuspid and mitral values at beginning of ventricular systole.

S2 – “Dub”
 Closure of aortic and pulmonary valves (semilunar valves) at end of
ventricular systole.
 The second heart sound is sometimes split into 2 sounds: closure of the aortic
valve and pulmonary valve.

Splitting is more recognisable during inspiration. Why? Increasing the rate and depth
of inspiration increases the filling of the right ventricle. This lengthens right
ventricular ejection time and slows the closing of the pulmonary valve.
Inspiration expands the lung blood vessels which slows the return of blood to the left
ventricle. This reduces stroke volume of the left ventricle, shortens ejection time and
speeds up closure of the aortic valve.

S3 – Occasional (common in young people)

 Turbulent blood flow into dialated ventricles during early diastole. Detected
near end of first 1/3 diastole, especially in older people.
 Normal in children

S4 - Pathological in adults

 Occurs just before the first heart sound

 Blood rapidly enters a stiff ventricle

Valve abnormalities cause cardiac murmurs

There are two types of valve abnormalities: incompetence and stenosis.
Incompetence is failure of the valve to close properly which allows blood to
regurgitate through the valve. Stenosis is when an open valve narrows so a high
blood pressure gradient is needed to drive blood through the valve. In aortic valve
stenosis, high pressure is needed in the left ventricle to force blood through the
narrowed valve. Blood flow through the stenosed or incompetent valve is turbulent
which causes vibration called a murmur.

Aortic pressure is reduced which decreases the oxygen supply to the coronary
arteries, causing angina during exercise.