II.

Blood vessels Physiology

By: Dr. Abdulrahman Aqra MD MSC
There are different types of blood vessels that form the containers, in which
blood circulates during each cardiac cycle. Arteries and arterioles form the
pressure reservoir of the circulatory system, while the veins form the volume
reservoir of the circulatory system.
Capillaries form the site of exchange of substances between the blood and
the interstitium.
Each blood vessel is composed of three layers:
Tunica adventitia; the outermost layer, which is composed of
connective tissue that involves elastin and collagen fibers. Elastin
serves for elasticity, while collagen serves for rigidity.
Tunica Media: composed of smooth muscle.
Tunica intima: composed of endothelial cells arranged on basement
membrane. Endothelial cells play important physiological role as they
respond to changes in blood flow and stretching in blood vessels. They
also respond to circulatory substances and inflammatory products. The
secretory activity of the endothelial cells has important regulatory roles
in regulation of blood flow and arterial blood pressure, as they release
vasoactive substances (vasoconstrictors and vasodilators).
Types of blood vessels:
1. Arteries: The wall of large arteries contain large amount of the elastic
fibers in its adventitia, because they stretch and recoil during the cardiac
cycle. There are large arteries with large diameter and small arteries with
lesser diameter in our organism. The arteries contain about 10% of blood
volume.
2. Arterioles: Their wall contains less elastic fibers but with much smooth
muscles, because they mostly act as sphincters. The smooth muscle fibers
have adrenergic innervation and in some locations have cholinergic
innervation. Arterioles are the major site of resistance, for that changing
their diameter has a distinguished influence on the total peripheral
resistance and the arterial blood pressure.
3. Capillaries: Arterioles are branched, and their branches, called
metarteriole will feed into capillaries. Capillaries are thin-walled blood
vessels with high total area may reach 6300 quadrant meters in adult
person. It is the major site for exchange of substances between blood and
interstitium. They are composed of endothelial cells arranged on basement
membrane. Depending on the function of the organ, within which given
capillaries are found, there will be fenestrae between endothelial cells. The
diameter of fenestrae is highly variable. Capillaries do not contain smooth
muscle in their wall except in the precapllary sphincter. Capillaries contain
about 5% of blood volume. In rest most of capillaries are closed.
4. Venules and veins: thin walled distended blood vessels with little smooth
muscles. The intima of the veins forms venous valves when it is folded.

Valves prevent blood retrograde and aid the venous return. Veins contain
about 54% of blood volume.

Arterial Blood Pressure

Definitions: Arterial blood pressure is the lateral force exerted by moving a
column of blood on the wall of lateral arteries. It is necessary to keep the
blood flowing, as it also provides enough hydrostatic pressure inside the
capillaries to helps the exchange of nutrients and vital gases as well as to
form the interstitial tissue, urine, etc.
ABP reaches its maximum during the systole (systolic pressure) and its
minimum during the diastole (diastolic pressure).
Systolic blood pressure: Is a result of rapid ejection of blood into the aorta. It
ranges between 90-140 mmHg. Two thirds of the ejected blood during the
cardiac cycle distends the arteries and raise the pressure, while only one
third leaves the arteries in blood flow.
The diastolic blood pressure is a result of recoiling of the stretched (during
systole) arterial walls; this will keep the blood pressure high enough to drive
the blood through the arterioles. It ranges between 60-90 mmHg.
Pulse pressure: is the difference between systolic and diastolic pressure.
Mean systemic pressure: Is the average pressure in the systemic arteries
throughout the cardiac cycle.
Mean systemic pressure = diastolic pressure + 1/3 pulse pressure.
It is about 93 mmHg.
Determinants of arterial blood pressure:
Blood pressure is directly proportional to cardiac output and total peripheral
resistance.
BP= CO X TPR
As we know Cardiac output is determined by heart rate and stroke volume ,
so any factors , affecting one or both of them , will affect the arterial blood
pressure.
Changes in stroke volume with heart rate kept constant, affect systolic more
than diastolic blood pressure.
The peripheral resistance is determined by many factors, including:
Diameter of blood vessels (especially the arterioles). It is inversely
proportional to the arteriolar diameter. Any factor that may cause
vasoconstriction or vasodilatation will affect the blood pressure by
increasing or decreasing it respectively.
Viscosity of blood: It is 5 times more than the viscosity of water. It is
due to plasma proteins, and the blood cells. Viscosity is increased by

dehydration and polycythemia, and decreased by anemia and

hypoproteinemia.
Length of blood vessels: It is constant in the human organism , so it
would not be involved in the determinants.
Physiologic Variations of blood pressure:
1. Age: ABP varies with age. In the newborn it is about 80/40 mmHg. At the
age of 5 years it is about 100/60 mmHg. At the age of 20 years it is about
120/80 mmHg.
By aging the ABP increases and at the age of 60 it is about 150/90 mmHg.
2- Gender: In female it is slightly lower under the age of 45 years.
3- Race: The BP of oriental people is lower than that of American and
European people due to different climate stress of life, and high cholesterol
diet of western people.
4- Body built: ABP is higher in obese people.
5- Meals: After meals, there is a vasodilatation in the splanchnic area ,
which will increase both the venous return and cardiac output , so it will
increase the ABP especially the systolic .
6. Gravity : Due to gravity when a person stand the blood pressure in any
vessel above the heart is decreased for 0.74 mm Hg for each one cm
distance , while the pressure in any vessel below the level of the heart is
increased for 0.74 mm Hg for each one cm distance.
This effect of gravity equals the weight of blood column.
e.g. The ABP in a large artery in the foot which is 100 cm below the level of
the heart will be 174 mm Hg . This is due to 74 mm Hg increase in arterial
blood pressure due to gravity in addition to 100 mm Hg mean arterial blood
pressure.
100+ (100x0.74) = 100+74=174 mmHg.
While the ABP in a large artery in the head, which is 50 cm above the level of
the heart will be:
100 - (50X0.74) = 100-37=63 mmHg.
7. Site of measurement: In recumbent position: the pressure in arteries
of the lower limb is higher due to the larger diameter and because they
constitute direct continuation of the aorta.
ABP is slightly higher in the right arm in right-handed people.
8. Emotions: Due to increased sympathetic activity, strong emotions
increase the ABP especially the systolic.
9. Exercise: The systolic is increased due to increased cardiac output and
vasoconstriction. The diastolic is firstly decreased due to the vasodilatation
of muscular arterioles in the active muscles, and then it may be increased
slightly.
10. Sleep: ABP is decreased during sleeping. In the stressful dreams it is
increased.
11. Respiration: In the respiratory cycle, the blood pressure is increased
during the late phase of inspiration and the initial phase of expiration. It is
decreased during the late phase of expiration and the initial of inspiration.
Explanation:

During the beginning of inspiration the intrathoracic pressure is

negative and this will increase the venous return , but the blood
returning to the left heart decreases due to the increasing of the
capacity of pulmonary circulation.
During the late inspiration the respiratory center stimulates the
vasomotor center in medulla oblongata, leading to increase in ABP.
During the beginning of expiration the pulmonary capacity decreases
due to the positive intrathoracic pressure, and increases blood
returning to the left heart.
In the late expiration the discharge from vasomotor center decreases
and consequently the blood pressure decreases.
Regulation of arterial blood pressure:
I. Short-term regulatory Mechanisms: Occurs through different
circulatory reflexes within few seconds after the change in arterial blood
pressure and lasts for few minutes to hours then declines.
These reflexes adjust the arterial blood pressure through adjustment of
vasomotor center and cardiac inhibitory centers from the following receptors:
1. Baroreceptors: They are found in carotid sinus and aortic arch. They are
normally stimulated by normal ABP.
These receptors discharge impulses via carotid sinus nerve (a branch of
Glossopharyngeal nerve ) and aortic nerve ( branch of Vagus nerve ) to
stimulate the cardioinhbitory center in medulla oblongata to cause vagal
tone .
When the pressure is increased , the response of the stimuli caused by these
receptor is: decrease in heart rate , vasodilatation of the arterioles in skeletal
muscles and venodilation ( cause decrease in venous return ) .The final result
of these responses is : decreasing cardiac output and decreasing of
peripheral resistance , and thus decreasing of arterial pressure.
When the Blood pressure is decreased, opposite effects occur: Increased
power of contraction, arteriolar vasoconstriction, venoconstriction, secretion
of Catecholamines: The final result: increasing both: cardiac output and
peripheral resistance, and thus increasing ABP.
The baroreceptors have the following properties:
* rapid response (within seconds), respond much more to rapid changes than
to gradually developing changes of BP.
* negative feedback mechanisms.
* stimulated at pressure levels of 50 mmHg up to 180 mm Hg.
* slowly adapting receptors.
2. The peripheral chemoreceptors:
They are also located on the carotid bodies and aorta. They are sensitive to
changes in blood gases especially the decrease pressure of O2.
When the BP drops below critical levels (below 60 mm Hg) they are
stimulated and send nerve impulses to both respiratory center and
vasomotor center in the medulla oblongata. This will lead to

vasoconstriction, increased heart rate, increased respiratory rate and

increased catecholamine concentration. The net result: returning of ABP
toward its normal level.
3. Atrial baroreceptors (low-pressure receptors):
They are stretch receptors found in the wall of atria and pulmonary arteries.
They are stimulated in response to changes in blood volume. When there is
an increased blood volume in the atria, the atrial baroreceptors are
stimulated and this leads to vasodilatation to decrease the ABP.
Vasodilatation of afferent arteriole in the kidney causes increase in
glomerular filtration rate, and the loss of fluid by the kidney .
Atrial baroreceptors also send impulses to the hypothalamus to decrease the
secretion of ADH and thus decrease the reabsorption of water from the renal
tubules and increase water loss by the kidney more and more.
Opposite response occur when the blood volume is decreased.
4. Ischemic response:
This response acts only at a very low level of ABP starts at 60 mm Hg and
reaches its highest degree of action at 20 mm Hg.
Its mechanism of action occurs as follows:
marked decrease in blood pressure, decreases the blood flow and causes
cerebral ischemia .Local ischemia causes strong stimulation of vasomotor
center and leads to vasoconstriction and tachycardia, and thus leads to
increased ABP.
* Cushing`s reaction: is a special type of ischemic response that results from
increased intracranial pressure (as a result of brain tumor or intracranial
hemorrhage). This will compress the intracranial vessels and thus causes
local ischemia that will causes severe vasoconstriction and then elevation of
ABP.
II. Intermediate-term regulatory mechanisms:
Start within few minutes and are effective for few hours to days. Most
important are:
1. Capillary fluid shift mechanism:
Correct the changes of blood pressure by shifting of fluid between the blood
plasma and interstitial fluid .
When there is an increase in blood volume, there is an increase in blood
pressure which will increase the capillary pressure at the arterial end (which
leads to increase the rate of fluid filtration), in the same time it will increase
the capillary pressure at the venous end and thus decrease the rate of the
fluid reabsorption. The net result: decrease the plasma volume and thus
decrease the arterial blood pressure.
When the blood volume is decreased, the opposite effect occurs:
Decrease blood volume will lead to a decrease in blood pressure, and
decrease pressure in the capillaries, and this will decrease rate of filtration at
the arterial end , and increase the rate of reabsorption at the venous end ,
and thus increase the blood volume and ABP.
2. Rennin -Angiotensin -aldosterone system:
When the blood pressure is decreased, this will decrease the renal blood

flow, and this will stimulate the juxtaglomerular apparatus in the kidney to
release Rennin (a proteolytic enzyme).
Rennin in blood acts on a plasma globulin called Angiotensinogen (inactive
protein) and activates it to Angiotensin I.
Angiotensin I is then activated by Angiotensin Converting Enzyme (ACE) in
the lungs by converting it to Angiotensin II.
Angiotensin II has the following effects:
* vasoconstriction (this will increase the peripheral resistance and thus
increase the arterial blood pressure).
* Stimulates the release of Aldosterone from the renal cortex. Aldosterone
acts on the distal renal tubule to enhance reabsorption of sodium .The water
will follow sodium as a result of osmosis and thus the blood volume will be
increased and thus the blood pressure.
* Stimulates the ADH release and thus increase water reabsorption in kidney.
This will lead to increase in blood volume.

3. Atrial Natriuretic peptide:

When arterial blood volume (and respectively blood pressure) is increased,
the bllod will stretch the atrial wall. This will release ANP.
* ANP acts on the kidney to increase excretion of sodium and water, which
will decrease the blood volume and thus return blood pressure to normal.
* ANP also promotes vasodilatations, and thus decreases the peripheral
resistance and returns the blood pressure to normal.
4. Stress- relaxation mechanism: When the pressure in blood vessels
becomes too high the vessels become stretched and keeping on stretching
more and more for minutes or hours, as a result the pressure in the vessels
falls toward normal.
On the other hand, when the pressure falls inside the vessels will decrease
the tension in its wall, the wall then will recoil and gradually contracts.
III. Long-term regulatory mechanisms

Slow mechanisms operate through the kidney. They start within hours and
last fully active as long as required. They regulate ABP by adjusting body
fluid volume.
They act via:
1. Renal- body fluid system: Increased blood pressure increases the rate at
which the kidney excretes water and salt. This is called pressure diuresis,
and pressure natriuresis .This cause marked loss of extracellular volume and
decrease arterial blood pressure.
2- Accessory mechanisms: enhancing water and salt excretion by: decrease
secretion of rennin , aldosterone and decreased sympathetic signals to the
kidney.
Clinical Physiology:
Pathologically increased arterial blood pressure is called hypertension, while
pathologically decreased blood pressure is called hypotension.
Hypertension is the pathologically increased blood pressure: It has two
forms:
1. Primary (Essential) hypertension : The most common (90%) : Without
known underlying cause , but probably due to atherosclerosis .
2. Secondary hypertension: due to underlying cause, which could be
* a tumor like Pheochromocytoma, a benign tumor in the chromaffin cells in
the adrenal medulla that secrete epinephrine and causes malignant
hypertension.
* Endocrine conditions
* renal disease: such as renal artery stenosis.
* Drugs and other factor.
When you start your clinical practice always return back to physiology of
blood pressure and review the determinant of ABP. Any pathological cause
that increases them may cause hypertension. The treatment of hypertension
will be much more understandable when you review the regulatory factors of
ABP.

Microcirculation
There are two types of circulation: Macro- and microcirculation:
1. Macrocirculation : circulation of blood from heart to organs and from
organs back to the heart.
2- Microcirculation: circulation of blood in the smallest blood vessels
embedded within the organ tissue, so they are also called (capillary
circulation).
In our organism, there are about 10 billion capillaries, which form a surface
area of 500-700 square meter. The total area of the capillaries` wall in the
body may reach 3600 quadrant meters.
The blood enters the capillaries through the arterioles and leaves them by
the way of venules. Arterioles act as sphincters as they are highly muscular
and their diameter can be changed many folds, and thus may resist the
blood flow.
From the arterioles, the blood pass into the terminal arterioles, which do not
have continuous muscle coat, but instead the smooth muscle fibers encircle
them at intermittent points.
From the terminal arterioles the blood passes into the capillaries and then
enters the venules.
Venules are larger than the arterioles and their muscle coat is much weaker
than that of the arterioles.
As we mentioned before , at anytime the blood content of the capillaries
does not exceed 5% of blood volume of the body. But this percentage is the
most important fraction of blood flow because it assures O2 and nutrients for
the cells and eliminates their metabolic west products.

Exchange of substances between the capillaries and interstitium occurs

thankful to what are known as Starling forces that involves hydrostatic

pressure of capillaries (Pc), oncotic pressure of the capillaries (c), and

hydrostatic pressure of the interstitial fluid (Pi), and oncotic pressure of the
interstitium (i). The struggle between these forces causes a net pressure
that favors filtration at the arteriolar end of the capillaries, and favors
reabsorption (oppose filtration) at the venular end of the capillaries.
The pressure in systemic capillaries at the arterial end is about 30-35 mm
Hg, while at the venous end it is about 15-20 mm Hg. The mean capillary
blood pressure is 25 mmHg.
Let`s now observe how Starling forces causes filtration versus reabsorption
at the different ends of the capillaries.
1. Capillary hydrostatic pressure (Pc): Tends to move fluid outward the
capillary membrane (promotes filtration). It is about 30-35 mm Hg at the
arterial end, 15-20 mm Hg at the venous end, and about 25 mm Hg in the
middle of the capillaries.
2. Interstitial fluid hydrostatic pressure (Pi): Tends to move fluid inward
across the cell membrane (opposes filtration) .It could be positive or
negative
3. The plasma colloid osmotic pressure (c): tends to cause osmosis of fluid
inward through the capillary membrane (opposes filtration). Its average is
about 28 mmHg.)19 mm Hg is caused by dissolved proteins and 9 mm Hg is
caused by cations).
4. The interstitial fluid osmotic pressure (i): tends to cause osmosis of fluid
outward through the capillary membrane. It is about 8 mm Hg.
At the arterial end the hydrostatic pressure is higher than both Pi and c
together compared that at the venous end of capillaries. So fluid filters out of
the capillaries.
The hydrostatic pressure is then increased because of the increasing filtered
fluid in the interstitium, which increases the interstitial hydrostatic pressure,
and the concentration of plasma proteins in capillaries increase due to
decreased fluid in the capillaries. As a result, the venous end of the
capillaries will reabsorb the fluid back.
As a conclusion: Fluid moves in capillaries affected by different pressure
forces that push it in different direction. At different moment the net pressure
either causes filtration or reabsorption. The blood flow in the capillaries is
slow, as it moves in velocity of 0.7 cm/s.
Fluid movement = k[(Pc Pi) (c i)]
K is the capillary filtration coefficient which mainly depends on the
capillary`s permeability.

Clinical Physiology:
Edema is developed either due to
Increase in capillary hydrostatic pressure as happens in hypertension
for example.
Decrease in capillary oncotic pressure, which may result from liver
diseases, comprising plasma protein production, or from kidney
diseases that causes loss of plasma proteins with urine.
Increased capillary permeability as in autoimmune leakage syndrome
Lymphatic obstruction or t salt and water retention .
Dehydration on the other hand may result from:
Increase capillary osmotic pressure as in diabetes mellitus (increased
glucose concentration)
Decreased hydrostatic pressure for any cause.
Coronary Circulation
The heart is supplied by two arteries:
1. Right coronary artery : supplies the right atrium , right ventricle , and the
posterior part of the interventricular septum .
2. Left coronary artery: supplies the left atrium, the left ventricle, and the
anterior part of the interventricular septum.
The two coronary arteries arise from the aorta after it just leaves the heart.
There are small anastomoses between them.

Coronary venous drainage: There are superficial and deep venous systems.
The superficial system is formed of the coronary sinus and the anterior
cardiac vein. The coronary sinus drains about 60% of the cardiac venous
blood.
Deep system: the most important is the thebesian veins that drain small
amount of the cardiac venous blood in the all chambers of the heart.
Coronary capillaries: There is about one capillary for each cardiac muscle
fiber. The capillaries run parallel to the cardiac muscle fibers.
Coronary blood flow is about 250 ml (5% of the cardiac output).
Note: In severe exercise the cardiac output is increased 7-8 folds, while the
coronary flow is increased only 3-4 fold.
This means that the ratio of coronary blood flow to the energy expenditure
by the heart decreases.
Note also: In resting state about 70% of the O2 in the coronary arterial blood
is removed as the blood passes through the heart ( On the other hand only
25% of O2 in the arterial blood in other tissue is removed ).
For that, in severe exercise the O2 consumption of the heart is increased by:
Increasing the coronary blood flow (not enough).
Increased efficiency of cardiac utilization of energy from glucose and
lactic acid by anaerobic oxidation.
Oxygen, delivered from myoglobin.
Specificity of coronary blood flow:
During systole: The coronary blood flow falls to a low value , which is
opposite to the flow in all other vascular beds in the body . This is due
to the strong compression of the ventricular muscle around the
intramuscular vessels during the systole. The lowest coronary flow
occurs during the Isovolumetric contraction phase of the cardiac cycle.
During diastole: The cardiac muscle relaxes completely and the blood
flows rapidly into the coronary arteries.

The most affected area is the subendocardial portion of the left

ventricle.
The highest flow occurs during Isovolumetric relaxation phase of the
cardiac cycle.

Note: Perfusion of right ventricle is much more sufficient because

pressure in the right ventricle is much lower than the pressure in the
aorta. For this reason Myocardial infarction affects mainly the left
ventricle (especially the subendocardial portion) rather than the right
ventricle.
Control of the coronary blood flow:
I. Intrinsic factors: (Most important): depends on the oxygen demand.
Oxygen lack is followed by coronary vasodilatation, due to:
1. Decreased O2 tension in the coronary blood has a direct relaxing
effect on the smooth muscles in the wall of the coronary arteries .
2- Oxygen lack causes release of vasodilative substances by tissue as:
adenosine, K+, Prostaglandins, Bradykinin..and others
II. Extrinsic factors:
1. sympathetic stimulation: has dual effect: direct vasoconstriction via
alpha receptors and mild vasodilatation via beta2 receptors.
Sympathetic also increase the metabolic activity and causes strong
vasodilatation (net effect: dilation).
2. Parasympathetic: direct vasodilatatory effect but due to heart rate
and then decreased metabolic activity the net result is
vasoconstriction.
Gastrocoronary reflex: Distention of stomach with heavy meal
produces reflective coronary vasoconstriction.
Clinical Physiology:
Coronary arteries disease (CAD) is the leading cause of death
everywhere. It may result from atherosclerosis.
Subendocardial portion of left ventricle is the most prone for
myocardial infarction region.
Aortic stenosis increases the risk for myocardial infarction, because the
intraventricular pressure is higher and thus contraction is more
powerful, which comprises the coronary arteries more and more.
Diastole is shorter than the systole (1/3), so the coronary flow is
decreased during tachycardia.
Heart failure decreases coronary flow because it decreases the
effective coronary perfusion pressure.