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BLOOD FLOW IN SPECIAL

AREAS
Blood flow through body tissues (tissue perfusion) is involved
in:
• Delivery of oxygen and nutrients to and removal of metabolic
wastes from tissue cells
• Gas exchange in the lungs
• Absorption of nutrients from the digestive tract
• Urine formation in the kidneys

The rate of blood flow to each tissue is regulated to ensure


proper function no more, no less.
THE CEREBRAL CIRCULATION
The brain is highly intolerant of ischaemia and 3 minutes of
interrupted blood flow could lead to irreparable damage of
neurons.
The brain receives its blood supply from the Circle of Willis which
is formed at the base of the brain by the anastomoses of terminal
branches of the internal carotid arteries and the basilar artery.
The basilar artery rises from the union of the two vertebral arteries.
The Circle of Willis is the origin of the 6 main arteries that supply
the cerebral cortex. Despite the anastomoses occlusion of one
carotid artery causes effects in the cerebral hemisphere of the same
side.
The veins drain into large venous sinuses located within the dura
mater and from there into the internal jugular vein.
right left
Peculiarities of cerebral blood vessels:
The vessel walls are very thin except for the venous sinuses
The veins have no valves and do not collapse when pressures fall b/c
their walls are held open by the dura mater. The result of this is that
when one changes from supine to erect posture pressures fall
markedly. In supine posture MAP is about 100mmHg and internal
jugular pressure is 10mmHg or less. In erect posture MAP drops to
70mmHg and jugular pressure drops to 0mmHg or less. Cerebral
blood flow is reduced by 15% in erect posture.
According to Monro – Kellie doctrine, since the brain and CSF are
not compressible, the volume of blood, CSF and brain must be
constant at all times. Any space occupying lesion will compress
blood vessels reducing blood flow and this will trigger the Cushing’s
CNS ischaemic reaction which causes a rise in blood pressure. The
increase in blood pressure increases blood flow to the brain and
raises the intracranial pressure some more setting up a vicious cycle.
If not relieved the medullary centers eventually become depressed
Endothelial cells of cerebral capillaries are continuous i.e. without slit
pores at the tight junctions. In addition the neuroglial cells (astrocytes)
have end foot processes that wrap around the capillaries further
restricting the passage of substances from blood into the CSF. This
constitutes a blood – brain barrier that protects the brain from toxins
in the blood and helps to preserve the composition of the CSF. The
barrier is absent in the newborn and develops in childhood, for this
reason kernicterus can occur in haemolytic disease of the newborn. Also
drug treatment of meningitis must be with drugs that cross this barrier.
The brain is exceptionally sensitive to declining pH and increase in
blood carbon dioxide levels and these cause marked vasodilation.
Oxygen deficit is a much less potent stimulus for auto regulation.
The brain is not subject to significant vasoconstriction during
sympathetic discharge which occurs for example in response to the
baroreceptor reflex; rather in such situations flow is redistributed to
ensure adequate supply to brain and heart.
MEASUREMENT OF CEREBRAL
BLOOD FLOW
The method for this employs the Fick principle and is called
Kety’s method. When a given amount (Q) of the anaesthetic
gas nitrous oxide is inhaled, it is taken up by the brain and
after about 10 minutes the N2O equilibrates between the brain
and the blood. The volume of cerebral flow is determined from
Q and its arteriovenous concentration difference.
Cerebral Blood Flow = Q/[A] – [V]
About 14 – 15% of cardiac output i.e. 750ml goes to the brain.
Oxygen utilization by the brain is very high – 20% of total body
consumption of oxygen though it constitutes only 2% of body
weight.
Rate of oxygen consumption and blood flow depends on
neuronal activity e. g. unilateral arm exercise causes an
increase in flow in the arm region of the contralateral motor
cortex only.
STROKE – cerebro vascular accident (CVA)
When blood supply to a part of the brain is interrupted
ischemia damages or kills the cells in the area producing
the signs and symptoms of a stroke. Generally there are
two types of stroke; a) hemorrhagic b) ischemic
Hemorrhagic stroke occurs when a cerebral artery or
arteriole ruptures. Sometimes this may occur at the site of
a small aneurysm.
Ischemic stroke occurs when flow in a vessel is obstructed
by atherosclerotic plaques on which thrombi form.
Thrombi may be formed elsewhere like in the atria and
pass to the brain as emboli.
CORONARY CIRCULATION
The myocardium is supplied with blood by the right
and left coronary arteries which arise from the aorta.
About 90% of venous return from both ventricles
empty into the right atrium through the coronary
sinus and the anterior cardiac vein.
 The rest of venous blood is drained by vessels that
empty directly into the cardiac chambers. (thebesian
veins and arterioluminal vessels)
The heart has a large capillary reserve; there are about
3500 capillaries per square millimeter of ventricular
cross section and only a third of this is utilized at rest.
At rest about 5% of cardiac output (250ml/min) flows
into the coronary arteries.
This can be measured by Kety’s N2O inhalation method.
 Blood flow in coronary arteries is phasic i.e. minimal
during systole and maximal during diastole. Systolic
compression affects the left coronary vessels more than
the right because of higher pressures in the left. The
compression is maximal in the subendocardium which
is therefore a common site for myocdardial infarction.
REGULATION OF CORONARY BLOOD FLOW
The rate of blood flow to the heart is dependent on rate of
metabolism of the heart.
The relationship between oxygen consumption of the heart and
blood flow is a linear one.
The heart extracts up to 75% of oxygen delivered to it at rest.
Heart tissue is highly intolerant of oxygen lack.
If arterial PO2 is reduced in a heart – lung preparation or a
coronary artery is occluded for 2 – 3 seconds marked increase in
blood flow occurs – this is reactive hyperemia. The increase in
flow is due to vasodilation which persists even after PO2 is
restored to normal and is most likely due to adenosine and not to
local effect of hypoxia. Other metabolites that might contribute
to the vasodilation include; CO2, H+, K+, lactate and
prostaglandins.
Regulation of coronary circulation contd.
Sympathetic innervation density in coronary vessels is
scanty. Sympathetic discharge causes increase in
coronary blood flow by two mechanisms:
The redistribution of blood flow from parts of the body
with high vasoconstrictor control (e.g. kidneys, gut and
skin) to heart and brain
An increase in myocardial metabolism with resultant
production of vasodilator metabolites. The vasodilation
complements the flow redistribution.
CORONARY ARTERY DISEASE (CAD)
When flow through a coronary artery is reduced to the point
that the myocardium becomes hypoxic angina pectoris
develops. If the ischemia is severe and prolonged irreversible
changes occur in the muscle and result in myocardial
infarction.
There is a positive correlation between atherosclerosis and the
following:
Hypercholesterolemia
Circulating levels of lipoprotein(a) – a substance which interferes
with fibrinolysis
Circulating levels of homocysteine which damages endothelial
cells. But is converted to non toxic methionine by folate and
vitamin B12
Levels of C- reactive protein and other inflammatory markers.
Circulating antibodies to Chlamydia Pneumoniae
Other risk factors for CAD include
Age above 45 years
Family history of CAD
Hypertension
Smoking
Diabetes mellitus
Sedentary lifestyle
obesity
FETAL CIRCULATION
The haemoglobin – oxygen saturation throughout the
fetal circulation is less than that of mixed venous
blood (70%) in extrauterine life.
This relatively hypoxic environment is the reason for
the high blood erythrocyte values of the fetus.
The fetal circulation has some peculiarities that
ensure sufficient oxygen supply to the brain and heart.
STRUCTURAL PECULIARITIES OF FETAL CIRCULATION

STRUCTURAL PECULIARITIES OF FETAL CIRCULATION


The placenta serves the function of the lungs. It is the source of
oxygen supply and route for CO2 excretion. It is the source of
nutrients and site for excretion of wastes. The fetus obtains
supplies from the placenta through the umbilical vein and
sends blood to it through the umbilical arteries.
The lungs of fetus are in a collapsed state so the blood vessels
are physically compressed. They are also constricted because of
hypoxia therefore pulmonary vessels offer a high resistance to
the flow of blood.
The fetal heart has a valve – like opening, the foramen ovale, in
the interatrial septum which permits blood flow from the right
atrium to the left atrium.
Peculiarities contd.
The two vascular connections that do not persist in
extrauterine life: a) between the pulmonary artery and
aorta known as the ductus arteriosus. It joins the aorta
at a point after it has given off the arteries that supply
the upper part of the body especially the brain and
heart. b) The other is the ductus venosus that conveys
blood from the umbilical and hepatic veins to the
inferior vena cava. It largely by - passes the liver
although it sends some oxygenated blood to it.
Fetal red cells contain fetal Hb which has a greater
affinity for oxygen than adult Hb.
The Circulation
The umbilical vein carries oxygenated blood from the
placenta with HbO2 saturation of about 80%.
 Some of the oxygenated blood flows to the liver through
a branch to the portal vein but most flow through the
ductus venosus to the inferior vena cava (IVC) where
it mixes with deoxygenated blood from lower limbs and
abdominal organs lowering the oxygen saturation of
blood entering the right atrium to 67%.
There is a preferential flow of this 67% oxygenated blood
through the foramen ovale into the left atrium and to
the left ventricle which pumps it into the aorta.
The circulation contd.
Deoxygenated blood from the head and upper limbs through the
superior vena cava (SVC) streams through the tricuspid valve
into the right ventricle from where it is pumped into the
pulmonary artery.
Because of high vascular resistance in the pulmonary vessels
blood from the right ventricle is diverted through the ductus
arteriosus to the aorta and only 5 – 10 per cent goes to the lungs.
 As a result of the point where ductus arteriosus joins the aorta
the coronary and carotid arteries receive 67% oxygenated blood
pumped from the left ventricle while the deoxygenated blood from
right ventricle supplies the lower parts of the body.
There is some admixture of blood from the IVC and SVC in both the
right atrium and aorta so that oxygen saturation of blood going to
the lower parts of the body is about 60% saturated with oxygen.
About 55% of the cardiac output leaves via the
umbilical arteries to be oxygenated in the placenta.
The right ventricle contributes more to cardiac output
so its wall is thicker than the left ventricle.
Circulatory Changes after Birth:
CHANGES AS A RESULT OF LUNG EXPANSION
CHANGES AS A RESULT OF CUTTING UMBILICAL
CORD
CONTRACTION AND OBLITERATION OF FETAL
VESSELS
Changes as a result of lung expansion:
 Lungs expand, resistance in pulmonary vessels fall so
blood flows from right ventricle to lungs, get oxygenated
and enter the left atrium increasing pressure in left
atrium.
 Also the expanding lungs draw off up to 50ml of blood
from the placenta into the infants’ circulation before the
umbilical cord is tied and cut.
Changes as a result of cutting the umbilical cord:
The low resistance flow through the placenta is removed
and all aortic flow is forced to flow through the systemic
circulation which has higher resistance.
This together with increased inflow from pulmonary
vein into left atrium causes pressure to rise in the left
atrium, ventricle and aorta.
 As left atrial pressure exceeds the right the foramen
ovale slams shut and gradually the septum fuses
permanently.
Contraction and Obliteration of fetal vessels:
Immediately after birth the ductus arteriosus contracts
to half its diameter.
The umbilical arteries contract and shut off completely.
 After several days or weeks the ductus arteriosus is
obliterated by endarteritis.
The umbilical vein closes by aseptic thrombosis leaving
a vestigial structure called the ligamentum teres.
The ductus venosus atrophies and disappears.

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