THE CARDIAC

CYCLE
One cardiac cycle consists of the atria and then
the ventricles contracting so that the blood that
has entered the heart is pumped out. This
occurs about 70 times every minute and is
continuous. The periods of contraction are
calledsystole. The periods of relaxation are
calleddiastole.
 We shall start when the atria and ventricles are in
diastole.

Blood at a low pressure in the veins flows into the

atria. This increases the pressure inside the
empty atria as they fill. Some of the blood trickles
through the openatrioventricularvalves into
the relaxed ventricles below.
When the atria are full, they go into atrial
systole, their walls contract and blood is
pushed through the valves into the ventricles.
The pressure in the atria is increased due to
the contractions and the pressure is increasing
in the ventricles as they fill with blood.
When the atria contract, blood cannot flow
back into the veins because the pressure of
the blood pushes on the valves in the veins
to shut them.
After a short delay the ventricles contract from
the apex (base) upwards. The pressure inside the
ventricles increases due to the ventricular
systole. As the pressure increases to a higher
level than the pressure in the atria, blood pushes
against the atrioventricular valves, shutting them
(the first heart sound) and preventing backflow.
 Thesemilunarvalves open under the
pressure and blood leaves the heart.
The ventricles relax - ventricular diastole - and
the semilunar valves snap shut behind the
blood (the second heart sound).
To work out from a graph what stage of the
cycle the heart is in, it is important to look at
the relative pressure of the atria and
ventricles.
Regulation of the cardiac cycle by the heart itself

The heartbeat is initiated in a specialised area of

muscle in the right atrium called thesinoatrial
node (SAN)or the pacemaker. The SAN starts
the waves of depolarisation, which results in
contraction.
The waves spread out over the 2 atrial walls so
that they contract. There is a band of fibres
between the atria and ventricles, which have a
high electrical resistance so the waves cannot
spread from the atria to the ventricles.
There is an area, however, which does conduct in
the septum, and the waves can pass from here
through the ventricles. This specialised area is
called theatrioventricular node (AVN)and will
pass on the waves of depolarization after about
0.1s.
It would be disastrous if the ventricles
contracted at the same time so that is why
there is a short period of delay before the
ventricles contract.
The AVN passes them on to thePurkinje(also
calledPurkyne)fibresin the inter-ventricular
septum. The excitation is passed to theapexof
the heart and then through the ventricle walls.
This causes the ventricles to contract from the
base upwards ensuring that the blood is forced
up and out in the vessels leaving the heart.
 The total amount of blood pumped by
the heart in lone minute = cardiac
output

Cardiac output = stroke volume x

number of beats per minute (Stroke
volume is the volume pumped in one
beat)
 Increasing the stroke volume therefore can increase
cardiac output. A larger volume might enter the atria
through the veins during exercise because the vessels
become dilated to enable more blood to flow to the
muscles to supply more oxygen and nutrients. The atria
are stretched more than normal; the heart detects this
and responds by beating faster and with more force.

Increasing the number of beats per minute can also

increase the cardiac output.
The effect of hormones.
This occurs whenadrenalineis released
from the adrenal medulla, flows in the blood
and affects the SAN. The SAN is stimulated,
works faster, increasing the heart rate.
The effect of nervous
stimulation.
One nerve, theaccelerator nerve, runs from
thecardioacceleratory centrein
themedullaof the brain to the SAN.

Another, thevagus nerves, runs from

thecardioinhibitory centrein the medulla of
the brain to the SAN.
 These nerves are stimulated in various situations, e.g.
during exercise, the accelerator nerve is stimulated. It
releasesnoradrenalineat the SAN resulting in the
heart rate increasing due to a decreased delay at the
AVN and increasing the force of the contractions.

If the vagus nerve is stimulated,acetylcholineis

released at the SAN. The delay at the AVN increases
and the cardiac output falls.
 Blood pressure also affects the cardiac
output. Some blood vessels (e.g. the aorta
and carotid arteries)
havebaroreceptors(also calledstretch
receptors) in their walls. These detect the
pressure and send impulses to the cardiac
centre in the medulla.
 If the pressure is too high: the cardioinhibitory centre
is stimulated, impulses are sent down the vagus
nerve, the heart rate is slowed and the pressure will
fall.

If the pressure is too low: the cardioacceleratory

centre is stimulated, impulses are sent down the
accelerator nerve, the heart rate is increased and the
pressure will rise.