so here we have the cardiac septum and
this will be the right ventricular wall
here the right ventricular myocardium
and the left ventricular myocardium and
here we're looking at the heart around
about the time of birth or late fetal
life and before birth the right
ventricle pump blood into the fetal
systemic circulation just as the left
ventricle did and this means that both
the right and the left ventricle had a
similar workload during fetal life and
we can see this on this diagram we
looked at previously when we considered
the fetal circulation in more detail so
in fetal life the left ventricle here
was pumping blood into the aorta as you
would expect and that was going off into
the fetal systemic circulation but as
well as that in fetal life the right
ventricle is pumping blood out into the
pulmonary artery as you would expect but
then there's this shortcut called the
ductus arteriosus which is taking the
blood through to join the aorta also
going into the systemic circulation and
this is necessary because here we have
the placenta this is the placenta and
going through the umbilical cord as well
as the umbilical arteries of course
which aren't illustrated here we have
the umbilical vein carrying highly
oxygenated blood back from the placenta
derived from the mother's circulation
and that Bloods going into the inferior
vena cava and the inferior vena cava is
carrying on all the way up here to the
right side of the heart
so this blood that's going from the
right atrium to the right ventricle into
the pulmonary artery highly oxygenated
blood but it's going into the systemic
arterial circulation so what we see is
both the right ventricle and the left
ventricle are pumping blood into the
systemic circulation in the fetal
circulation
and it's that when the baby is first
born so the right ventricular wall and
the left ventricular wall are going to
be about the same thickness representing
the same amount of muscle mass and at
birth the thickness of both ventricles
it is round about five millimeters but
with the establishment of the pulmonary
circulation in postnatal life the
workload of the right ventricle is going
to decrease so because it's not as far
for the right ventricle to braum pump
blood into the lungs the workload of the
right ventricle is going to decrease but
the left ventricle and we can consider
the cardiac septum as functionally part
of the left ventricle is now pumping
blood into the systemic circulation so
it has a higher workload and we can just
remind ourselves of what this looks like
in the adult heart so here we notice
that the left ventricular myocardium
here because of its higher workload and
we're including the cardiac septum as a
functional part of the left ventricle
it's quite a bit thicker than the right
ventricular wall and that's reflected in
the blood pressure the blood pressure in
the pulmonary arterial system is going
to be significantly lower than the blood
pressure in the in the aorta into the
systemic arterial system so as soon as
the pulmonary circulation is established
just after birth when PUD blood is being
now pumped to the lungs there's going to
be a reduction in right ventricular
workload but an increase in left
ventricular workload and this is
necessary to support the activity of the
growing baby of course we need a a more
effective systemic circulation to put
blood to all parts of the growing body
from the head to the ears to the toes
there's a consequence of this after
birth there's rapid growth of the left
ventricle to meet the increased systemic
metabolic demand an increased
development of the left ventricle and
the cardiac septum continues and by the
end of this
second year of life the left ventricle
weighs twice as much as the right and
that's a ratio that continues into adult
life so the mass of the two ventricles
the ventricular myocardium is that the
adult ratio by the age of about two
so here we see a group of individual
myocytes in the heart the individual
cells that compose the contractile
myocardium and these are the cardiac
muscle fibers that they're slightly
shorter than skeletal muscle fibers that
the length from here to here would be
about fifty to a hundred micrometers and
we noticed that they are branching they
branch and connect with each other and
we also noticed that in between the
individual fibers in between the
individual myocytes we have these
junctions here and these junctions
between the cells are the intercalated
discs the intercalated discs between
individual myocytes between individual
fibers and these are actually held
together by proteinaceous desmosomes so
they're well held together so it's a
very strong tissue the myocardium and
they also have small gap junctions
between the two and basically this
allows the whole myocardium to function
as a single unit with electrical
currents able to pass across the
myocardium in different directions and
that's true whether we're talking about
the atrial myocardium or the ventricular
myocardium as you would expect the cells
are very rich in mitochondria there's
actually relatively more mitochondria in
cardiac muscle cells than in normally
Tomas ourselves about 25 percent of the
space in here 25% of the cytosol volume
is actually mitochondria and that's
compared to about 2% in in ordinary
tissues because of course this has to
keep contracting it doesn't get a rest
it needs to continuously produce energy
usually there's one nuclei per cell but
occasionally there that there might be
two and the contractile filaments inside
the meijer sites are the same as in
skeletal muscle so there's the actin and
the myosin the actual contractile fibers
are the same the fibers that will
contract together to shorten the muscle
and that will relax as the
expands in the case that the heart it
will contract during systole and there
will be relaxation during die systole
extraction as the heart chambers filled
with blood prior to the next contraction
now birth the neonatal Maya sites are
not fully developed the Maya sites these
contractile cells in the myocardium are
not fully developed at birth and in
addition this is the main point
these Maya sites at birth have a higher
proportion of fibrous tissue to contract
our tissue so at birth there is more
fibrous tissue which is good because it
gives them a lot of strength but it
means there's less contractile force and
it means it's also somewhat harder for
the myocardium to expand as well because
the normal actin and myosin thick and
thin fibers are very stretchy as well as
having contractile strength they are
they are stretching but because there's
a high proportion of fibrous tissue in
the neonatal Maya sites the heart is not
able to expand as readily so in adults
the relatively stretchy Maya sites will
stretch as the heart fills during die
systole and if there's increased
myocardial stretching if there's more
stretching of the myocardium during die
systole that will automatically increase
the strength of the next muscle
contraction of the next cardiac
contraction because in the adult there's
a well fixed relationship the degree of
stretching the more stretching there is
the stronger the next myocardial
contraction is going to be so if it
stretches more of there's more filling
then the next contraction is going to be
more vigorous and this is necessary to
enter the increased volume of blood from
the heart and this of course is called
the frank-starling law of the heart
which represents the relationship
between a stroke volume and end
diastolic volume so the end diastolic
volume is higher
because there's more stretching then the
next stroke volume is going to be more
vigorous more blood will be pumped out
during that particular cardiac
contraction so the frank-starling law
states that the stroke volume of the
heart increases in response to an
increase in the volume of blood in the
ventricles before contraction but we've
said that the neonatal heart or the
neonatal myocytes contains more fibrous
tissue compared to contract our tissue
so the neonatal myocardium is unable to
perform in the same way and this results
in the heart being less able to respond
to volume loading which increases venous
return
so if venous return is increased the
neonatal heart can't stretch as much as
an adult heart and is not going to
contract as efficiently as an adult
heart either so this means that neonates
unlike adults possess a limited ability
to increase cardiac output by increasing
stroke volume instead neonatal cardiac
output is significantly dependent on the
heart rate rather than increasing stroke
volume and it's important to remember
that neonatal oxygen requirements are
also much greater than the adult and
actually what this means is that the
neonatal heart is functioning at near
maximum capacity as it is so given that
the neonatal heart current increases
stroke volume it could only compensate
with increasing heart rates and this is
why relative reduction in heart rates
are such an important and potentially
dangerous clinical observation in
children so they give children too much
fluid the heart is essentially acting as
a bottleneck for that fluid it can't get
through the heart quickly enough
therefore there's going to be fluid
damming back in the venous circulation
and that's what leads to edema and
pulmonary edema and we'll also see in a
minute that that can cause further
damage to the blood vessels which can be
life-threatening
now it's interesting to know that in a
full-term neonate the heart is located
midway between the crown of the head and
the lower level of the buttocks and the
heart is well you could say relatively
large at birth it weighs about 20 grams
and Grey's Anatomy informs us that the
normal blood pressure of a neonate is 80
millimeters of mercury systolic and 46
millimeters of mercury diastolic now
when we're thinking about the physiology
of the heart there's really two things
to consider in terms of cardiac output
the first is the stroke volume
now the stroke volume is the amount of
blood pumped out per cardiac contraction
so the stroke volume is going to be the
volume of blood in the ventricle
immediately prior to systole to the
point where is pumped out that will be
the stroke volume and of course it's
going to be the same on the the right
side of the heart as well so we have
stroke volume so that's one parameter to
take into account that's a stroke volume
and the other parameter we want to think
about is is heart rate so the number of
times that the heart is contracting per
a minute that's heart rate and if we
multiply heart rate and stroke volume
together that equals what we call
cardiac output so cardiac output his
heart rate multiplied by the stroke
volume so the cardiac output is a figure
it's mils of blood per a minute being
discharged in this case we're thinking
about into the systemic circulation so
let's try and work out what this would
be for a child that a neonate has
recently been born so the question is
what is the the cardiac output
and we know it's light rate times stroke
volume and let's suppose the heart rate
in this baby is 120 beats per minute
hundred 2231 being all I suppose a
surgeon 20 now the pediatric advanced
life support documentation tells us that
neonatal cardiac output is one point
five mils per kilogram so one point five
mils per kilogram so to work out stroke
volume that will be one point five mils
times the weight of the child let's say
an Aborigine NH is three point five so
that would give us a stroke volume of
one point five times three point five so
that means the cardiac output is going
to equal 120 and one point five times
3.5 if you're anything like me you get
your calculator out that equals five
point two five so cardiac output in the
neonate with a heart rate of 120 it's
going to be 120 times five point two
five and that equals 630 mils according
to my calculations so the cardiac output
in a neonate should be roundabout 630
mils of blood being pumped out per
minute and this is very important
because children have a high oxygen
demand especially me and ACE and infants
they have a high oxygen demand high
oxygen requirement because their tissues
are metabolizing very rapidly so we've
seen that the heart in children is
relatively small birth we've got a
cardiac output of 630 mils but only a
stroke volume of about five five and a
quarter mils so it's a fairly small
stroke volume being ejected per
contraction we've also seen that the
contractility in the stretch ability of
the myocardium is much less than in
older children and adults and this means
that the cardiac output in young
children is very dependent on the heart
rate because they can't significantly
modify their stroke volume if there was
increased cardiac stretching they could
modify the stroke volume whatever the
heart was bigger they could modify the
stroke volume but they can't so the
stroke volume is relatively constant
this is why young children are dependent
on a high heart rate heart rate is so
important so a reduction in heart rate
means by definition in young children
that there's going to be a reduction in
cardiac output which of course is
significant for the oxygenation of the
whole body so what we would say is
children lack I know trophic capacity
infants especially lack I know tripping
capacity they can't increase their
stroke volume significantly that they're
dependent on their chrono tropic output
the the actual rate of the heart is
beating out for their cardiac output and
this explains why the high rated
children is going to be relatively
faster than adults so here I have my a
pediatric early warning system chart and
this is for children under 1 so under 1
the parameters that we accept as normal
for heart rate are between 110 and 116
110 to 160 under the age of 1 now this
is the chart we use for 1 to 5 year olds
so 1 to 5 year olds we're accepting 90
to 150 without scoring on the pews
five to twelve year olds we are
accepting 80 to 120 as being normal
without scrolling on the pews and over
the age of 12
we accept sixty to a hundred which is
the same as the iPod race essentially as
being the normal acceptable rate without
scoring for being tachycardic or
bradycardic
now this physiology where children can
significantly or younger children can't
increase their stroke volume has also
got great significance for giving fluids
because if we give too much fluids the
heart essentially acts as a bottleneck
because it can't increase the stroke
volume so if we give too much fluids to
children there's going to be fluid
overload but only so much blood can go
through the ventricle at any time
because of the restricted stroke volume
that means if we give too much fluid
they can be more fluid coming into the
atrium and that fluid is unable to get
through to the ventricle because of the
ventricles limited output capacity so
that means that blood can dam back into
the atria and from there blood can dam
back into the pulmonary circulation
because these of course are the
pulmonary veins if the blood is damming
back in the pulmonary veins that's going
to increase the pressure in the
pulmonary capillaries and that's going
to make it harder for fluid to be
reabsorbed from the pulmonary
interstitial spaces back into the
pulmonary capillaries so what we have
here have we notice on this diagram we
can see that as well in terms of the
circulatory system so if the left
ventricle here is acting as a bit of a
bottle leg and we've got more fluid
coming in here that fluids going to down
back to the left atrium that fluids
going to down back in the pulmonary
veins
and you're going to get a pulmonary
venous hypertension so that means the
pressure in the lungs is going to be
higher the fluid is not going to
efficiently reabsorb from the
interstitial spaces in the lungs into
the pulmonary capillaries where the
pressure is now higher that's going to
reduce the reabsorption of tissue from
the lungs and that means fluid is going
to be accumulating in the lungs and in
the alveolar spaces and of course that
is the life threatening condition of
pulmonary edema so we've got the
relatively small size of the heart we've
got the hearts inability to increase
stroke volume and there's another reason
why I flew it over though this is a
particular problem in children and we're
going to look at that in the next video
clip now there's another factor I would
like to discuss when we're thinking
about fluid resuscitation and fluid
overload in children now here we have
the cells of the capillary the vascular
endothelial cells that we know and on
the outside of that as of know again
there is a basement membrane on the
outside facing the tissue spaces and the
endothelial capillary cells sit on that
basement membrane but what is less
well-known is there's another layer
inside called the endothelial glycocalyx
layer so there's another layer here
lining the vasculature lining the
capillaries but this one is facing in
the way this is facing in to the lumen
so this is the lumen in here and as
we've said this is the endothelial
glycocalyx layer and it's made of
glycoproteins and proteoglycans
it's carbohydrate rich but it contains
proteins and this layer is actually a
large molecule
proof layer it's what actually keeps the
plasma proteins inside so as we know
this plasma proteins particularly
albumin these large molecules that
generate the oncotic pressure the
osmotic pressure in the capillary in the
blood and these are actually kept in by
this glycocalyx layer so this glycocalyx
layer is essentially or theoretically at
least impervious to these large protein
molecules and that's very good of course
because it means that the oncotic
pressure is maintained exactly what we
want
but we now know is this there of
glycocalyx that's keeping this capillary
protein proof stopping the protein
getting out but what has been discovered
recently is that there can be insults to
this glycocalyx layer such as sepsis so
you've probably like me nurse patients
with their sepsis and they can become
massively ademma tests they can blow up
like balloons and even blood blood can
escape and they can get bruising and and
ecchymotic features out as blood can
escape out into the tissue spaces
because of the breakdown or it's now
believed because of the breakdown of
this glycocalyx layer and this might be
one reason that shock can become
irreversible so when a patient has gone
from progressive into irreversible shock
even if we correct the intravascular
status the patient will still go on to
die of shock and that may be partly at
least because of the breakdown and the
damage to this glycocalyx layer lining
the inside of the blood vessels surgery
can also damage this this layer post
ischemic changes can can result in
damage to the layer hyperglycemia is
another one the high blood sugar levels
can damage the glycocalyx layer but it's
also now believed by many workers in
this field
that fluid overload can damage this
layer as well
and it's also believed that children are
particularly prone to fluid overload
damaging the glycocalyx layer and if the
glycocalyx layer is damaged that means
that the proteins can escape out into
the tissue spaces because they're no
longer being maintained by this protein
poof glycocalyx layer and obviously that
means that water's going to be
automatically sucked out and water will
leak out anyway because it's going to
increase the permeability of the
capillary and the patient will become
Adam mattes and of course when we when
we look at fluid overload in the
clinical situation very often the first
thing we see is the effect of the
pulmonary edema particularly this
orthopnea where the patients have great
difficulty breathing when lying flat
because of the accumulation of fluid in
the lungs the pulmonary edema so very
important not to fluid overload because
this can be any reversible condition in
children and of course it's an example
of yatra Genesis a condition caused by
our interventions which is exactly what
we don't want so another reason to very
carefully monitor the amounts of
intravenous fluid therapy that we give
to children