Cardiovascular System - Paper 2000
2000
– 2nd semester – Q1_Part_A
The
heart is invested in a pericardium which has two main layers. The fibrous
pericardium is made of irregular dense connective tissue is forms the outer
layer. The serous pericardium has two inner layers, namely the parietal layer
and the visceral layer. The parietal layer is fused with the fibrous pericardium
and the visceral layer is what forms the epicardium of the heart and contributes
to the heart wall structure.
Between
these two layers there is small space filled with pericardial fluid which acts
as a lubricant and this cavity is known as the pericardial cavity.
The
heart is constituted of three main layers namely: epicardium, myocardium and
endocardium. The epicardium is formed by the visceral layer of the serous
pericardium and is made of a thin mesothelium and loose connective tissue. The
middle layer is the myocardium which constitutes the most percentage of the
heart wall and contributes to the hearts main function which is to act as a
pump. The myocardium is made up of cardiac muscle, and microscopically is
evident as thick interlacing bundles of muscle fibres. These muscle fibres have
special properties which enable the heart to contract in synchrony and as a
whole. The bottom layer is the endocardium and this I made up of a simple
squamous epithelium and some loose connective tissue. The endocardium is continuous
with the endothelial lining of the blood vessels.
Major
points: Pericardium and the formation of the epicardium, three main layers
(identify), what constitutes each layer structurally and how this helps
functionally.
2000
– 2nd semester – Q1_Part_B
Cardiac
stroke volume can be altered by two major mechanisms. One is the action of
myocardial fibres and the other is independent of the fibre length. Preload and
afterload are associated with the length of the muscle fibres whereas the
phenomenon of contractility is associated with calcium entry into the muscle
cells.
Preload
is was first initiated by Frank Starling, and this incorporates the fact that
the myocardial fibres will contract more strongly if they are stretched more.
That is if more blood fills up the ventricles then, this would result in
myocardial fibre stretch and then will allow for greater strength of
contraction. After load is defined as the pressure which needs to be overcome by
the ventricles in order for blood to be ejected into the associated blood
vessels. That is, if the associated blood vessels display a great pressure then
the amount of ventricular contractile force required in order to over come this
force must be high too. Thus afterload has also increased.
The
other main mechanism is through the entry of calcium ions. An increase in entry
of calcium ions into the muscle fibres will allow for more cross bridges to be
formed and therefore will allow for stronger contraction of the myocardium and
hence more blood will be ejected therefore affecting stroke volume. One way of
increasing calcium entry is by exciting the cardiac accelerator nerves which act
via b1 noradrenergic receptors and reduce the threshold of the plasma membrane
of the cardiac muscle fibres and therefore allowing for greater contraction, as
threshold is reached more readily.
Major
points: Two main mechanisms &
identify
Q2_2000_2nd
Semester
A
sudden change in the systemic mean arterial pressure initiates short term
controls on blood pressure and if this situation persists, then long term
controls would also be involved. In an event of a sudden change in blood
pressure, the sensors will detect the change, send afferent signals via afferent
pathways to the integration center. Here the situation will be analyzed and a
response is mediated through efferent pathways and efferent signals to the
effector.
The
baroreceptor reflex is initiated in the event of a sudden change in systemic
arterial blood pressure. The baroreceptors are specialized stretch receptors and
significant amounts are located within walls of the large arteries and veins of
the neck and thorax. These act as the sensors of this mechanism. Two particular
areas identified are the carotid sinus and the within the walls of the aortic
arch.
In
the event of a sudden fall in the systemic arterial blood pressure, the
baroreceptors will detect this as they will not be stretched to an extent
expected. Thus, an afferent signal will be sent to the integration center which
is the cardiovascular center. The baroreceptors located within the carotid sinus
will send afferent signals via the carotid sinus nerve which is a branch of the
glossapharyngeal nerve. The baroreceptors located within the walls of the aortic
arch will send afferent signals via the branches of the vagus nerve. These
signals are monitored by the cardiovascular center located near the medulla
within the brain stem. There are three areas here: the cardio-inhibitory center,
cardio-excitatory center and the vasomotor areas.
In
the case of a sudden fall in arterial blood pressure the cardio-excitatory and
vasomotor centers will be activated and via nerve signals, an increase in firing
of the SA Node will be sent (via cardiac accelerator nerves) and also
sympathetic fibres innervating the smooth muscle of the arterioles will be
stimulated, the effectors. This will cause increased vasoconstriction along with
increased heart rate, therefore increasing Total Peripheral resistance.
Increased heart rate will increase the cardiac output and therefore consequently
will produce an increased mean systemic arterial blood pressure. Thus
homeostasis is once again achieved.
Major Points: Identify the major components of the reflex & sensor, afferent pathway, int center, eff. Pathway and then an effector, Identify the baroreceptor reflex, main components etc. Identify what happens in the event of low MAP, What are the effectors?