BLOOD PRESSURE

By Dr. W.A. SAKA

BLOOD PRESSURE
 Blood Vessels
 The blood pumped out of the heart circulates all over the whole body
through blood vessels.
 Arteries convey blood to the pulmonary and systemic circulation.
 The main artery that carries blood out of the left ventricles is the aorta
while
 The pulmonary artery carries deoxygenated blood out of the right
ventricles
Blood Vessels contd.

 Veins bring blood back to the atria of the heart.

 The vena cava conveys deoxygenated blood from the systemic
circulation into the right atrium.
 The pulmonary vein conveys oxygenated blood from the lungs to the
left atrium.
 The aorta is about 2.5cm wide and divides into smaller branches.
 The diameter of the branches gets smaller until at the level of terminal
arterioles of just 10µm.
Blood Vessels contd.

 The arterial system which is composed of elastic conduit and high

resistance terminals constitutes a hydraulic filter.
 The hydraulic filter converts the intermittent output of the heart to a
steady flow through the capillaries.
 The highest pressure reached during systole is termed systolic arterial
pressure.
 The lowest pressure reached during diastole is termed diastolic
arterial pressure.
Blood Pressure
 Blood flows from regions of higher pressure to regions of lower
pressure.
 The greater the pressure difference, the greater the blood flow.
 Contraction of the ventricles generates blood pressure (BP), the
hydrostatic pressure exerted by blood on the walls of a blood vessel.
 BP is determined by cardiac output blood volume, and vascular
resistance
 BP is highest in the aorta and large systemic arteries
 In a resting, young adult, BP rises to about 110 mmHg during systole
(ventricular contraction) and drops to about 70 mmHg during diastole
(ventricular relaxation).
 CONTD.
 Although the systolic blood pressure of person below the age of 50 ranges
between 90 – 140mmHg.
 The diastolic pressure ranges from 60 – 90mmHg
 ↑age = ↑systolic and diastolic pressure.
 The average blood pressure is 120mmHg systolic and 80mmHg diastolic arterial
blood pressure.
 The pressure makes the aorta to stretch to accommodate about 50% of the SV
while the other 50% flows into the peripheral blood vessels.
 The kinetic energy of the liquid motion is converted to potential energy
 In diastole the elastic recoil converts the potential back to kinetic energy, thus the
aortic pressure does not drop to zero but to 80mmHg
Mean Arterial Pressure (MAP)
 MAP is the average blood pressure in arteries.
 It is roughly one-third of the way between the diastolic and systolic
pressures.
 It can be estimated as follows:
MAP = diastolic BP + 1/3 (systolic BP - diastolic BP).
 CO = HR × SV
 CO = MAP ÷ R
 MAP = CO × R
 ↑CO due to ↑SV or HR = ↑ MAP as long as resistance remains steady.
Mean Arterial Pressure (MAP)
 Likewise, ↓CO = ↓MAP if resistance does not change.
 Blood pressure also depends on the total volume of blood in the
cardiovascular system.
 The normal volume of blood in an adult is 5L which is responsible for
the amount of pressure in the body.
 Condition like hemorrhage decrease blood pressure, although can be
compensated for by the body’s hemostatic mechanism, if the loss of
blood is up to 10%.
 Conversely, anything that increases blood volume, such as water
retention in the body, tends to increase blood pressure.
Measurement of Arterial Blood Pressure (ABP)
 Measured directly by inserting a fluid-filled cannula into an artery and
recording the pressure with a manometer or an electrical transducer.

 This method is invasive and not suitable for man.

 Clinically, it is measured by a sphygmomanometer

 Method of measuring arterial blood pressure includes:

Palpation and
Auscultation
These two methods are combined in sphygmomanometer
 Regulation of ABP
 INTRODUCTION:
 Mediated by two types of Reponses, which includes:
Short term/rapid adjustments
Long term adjustments
 Short term is over minutes or hours and intended to correct temporary imbalances
caused by postural change, exercise or hemorrhage.
 Short term adjustments is usually a series of autonomic reflex responses mediated
via the cardiovascular centers.
 Long term adjustments is over weeks or month and usually concerned with the
balance between
Extracellar fluid on one hand and
The renal mechanisms which control urine output on the other hand
Simplified schema showing primary pathways for short-term regulation of arterial blood
pressure
Cerebral
cortex

hypothalamus

Medula CV
center

Lungs
Cardio
pulmonary Arterial Extrinsic
receptors Baroreceptors Reflexes –
pain cold…
Heart Cardiac
output
Arterial
Pressure
Peripheral Peripheral
vessels Resistance
 Short-term Adjustments
 The main neural control of the circulation is located in “centers” in the medulla
collectively known as cardiovascular centers (CVC).
 There are two major control in the cardiovascular control area:
 a) The cardiac center (concerned with neural control of the heart) and
 b) The Vasomotor center (concerned with neural control of the peripheral blood
vessels.
 These two centers overlap anatomically and functionally.
 The cardiac centers consists of;
 Cardio-inhibitory centers and
Cardio-stimulatory center
 Short-term Adjustments
 Vagal efferents from the cardioinhibitory center carry impulses to the heart which
causes ↓HR & ↓atrial contractility.
 The cardio-stimulatory center is believed to have sympathetic efferents to the
heart, which causes:
 ↑HR and ↑contractility
 ↓activity of the cardio-inhibitory center.
 The vasomotor center discharges synthetic efferents to the arterioles leading to:
 Vasoconstriction
 ↑BP
 ↓sympathetic discharge from these centers causes:
 Arteriolar dilation
 Reduced sympathetic tone and
 ↓BP
 Baroreceptors and Vasomotor center Activity (VMC)
 These are stretch receptors located in the carotid sinuses and the aortic arch.
 An increase in the transmural pressure enlarges the vessel and thereby deforms the
receptors.
 They are not really pressure sensitive but stretch sensitive.
 Direct stretching of the receptors caused an ↑firing of the baroreceptor’s sensory
nerve.
 Impulses arising in the carotid sinus travel up through afferent fibres in the sinus
nerve
 ↑BP = stretched baroreceptors and ↑discharge of afferent impulses through IX and
X cranial nerve to the VMC
 These afferent impulses are inhibitory to the tonic activity of the VMC, which
reduces the sympathetic effect of the arterioles.
Baroreceptors and Vasomotor center Activity (VMC)

 Afferent impulses from the baroreceptors stimulate the cardio-inhibitory

center.
 Efferent parasympathetic fibres are sent to the heart.
 The more the increase in blood pressure, the more is the rate of firing of
afferent baroreceptor nerves.
 The overall baroreceptor response to a pressure increase, does these things;
 Increases baroreceptor firing rate of active units and
 The recruitment of more units until a saturation level is reached at about 200mmHg
 Above the pressure of 200mmHg baroreceptor response no longer
increases.
Baroreceptors and Vasomotor center Activity (VMC)
 When there is a fall in BP the reverse of the above responses occur.
Reduced stretching of the baroreceptors
Less inhibitory afferent impulses are sent to the VMC and the cardiac
centers.
↑sympathetic discharge to the blood vessels = vasoconstriction and
↑peripheral resistance.
The response of baroreceptors to increased or decreased BP operates
on:
 Negative feedback mechanism and
 a careful adjustment of the responses to a rise or fall in BP helps in
maintaining a constant BP.
 Role of Hormones
 The short term response involves hormones of the adrenal gland and the renin-
angiotensin system.
 ↑ sympathetic discharge seen in conditions of lowered blood pressure simultaneously
stimulate the adrenal medulla resulting in a rise in blood adrenaline and noradrenaline
concentrations for between one and three minutes.
 The effect of these hormones is to intensify the rapid Cardiovascular responses induced
by neural stimulation.
 ↓renal blood flow (following ↓ arterial BP), results in the release of renin from the
juxtaglomerular cells of the afferent arterioles of the kidneys
 Renin persists in the circulation for about one hour and initiates the sequence of
changes resulting in the formation of angiotensin Il from its precursor in plasma,
angiotensinogen.
 Angiotensin ll is a powerful vasoconstrictor and therefore raises blood pressure.
 The maximal response takes about 20 minutes and so, it is slower to act than the
 Vascular endothelium
 The vascular endothelium has been observed to play a key role in vasodilation.
 Many different stimuli act on the endothelial cells to produce endothelium -
derived relaxing factor (EDRF), which is now known to be nitric oxide (NO).
 NO is synthetized from arginine in a reaction catalyzed by nitric oxide synthase
(NO synthase, NOS).
 Nitric oxide has a half-life of only six seconds in the blood.
 Three isoforms of NOS has been identified, they are numbered 1, 2 and 3.
NOS 1 is found in the nervous system.
NOS 2 is found in the macrophages and other immune cells and
NOS 3 is found in the endothelial cells.
 NOS 1 and NOS 3 are activated by agents that increase intracellular Ca
concentration, including the vasodilators acetylcholine and bradykinin
Vascular endothelium
• The NO that is formed in the endothelium diffuses to smooth muscle
cells, where it activates soluble guanylyl cyclase, producing cyclic
GMP.
• The cyclic GMP mediates the relaxation of vascular smooth muscle.
• NO is inactivated by hemoglobin.
• Rapid flow of blood through the arteries causes shear-stress on
endothelial cells and causes release of nitric oxide.
• The nitric oxide relaxes the arterial wall, causing it to dilate.
Endothelins
 Endothelial cells also produce endothelin 7(ET-1), which is the most
potent vasoconstrictor agent yet isolated.
 It is a 21 amino acids polypepteide.
 Other members of the same family, also with 21 - amino acids in the
polypeptide chain are othelin-2 (ET-2) and endothelin-3 (ET-3).
 Two differeent endothelin receptors, ET, and ETB, have been cloned.
 The ET, receptor, which is specific for endothelin 1 is found in many
tissues and mediates the vasoconstriction produced by endothelin-1.
 The ET, receptor responds to all three endothelins.
 It may mediate vasodilation and it appears to mediate the growth
effects of the endothelins
 Endothelins
 Endothelin is present in the endothelial cells of all or most blood vessels.
 The usual stimulus for its release is damage to the endothelium, such as
caused by crushing of the tissues or by injecting a traumatizing chemical
into the blood vessel.
 After severe blood vessel damage, it is probably the local release of
endothelin and subsequent vasoconstriction that prevents excessive bleeding
from arteries as large as 5mm in diameter that have been broken wide open
by crushing injury.
 Extrinsic reflexes
 Certain stimuli originating from outside the circulation may elicit cardiovascular
responses via somatic afferent pathways.
 The central connections of these extrinsic reflexes are not known.
 Among the more common of these extrinsic reflexes are those elicited by pain and
cold.
 Pain produces a rather variable hemodynamic response.
 Mild to moderate pain usually elicits increased arterial pressure and tachycardia.
 Severe pain, as might experienced by undue stretching of the gall bladder, intestine
or ureter may induce bradycardia, hypotension and sometimes circulatory collapse
and fainting.
 Cold causes afferent impulse to be sent to the hypothalmus and this reflexly induce
cutaneous vasoconstriction.
 Intense local cold will result in an increase in arterial pressure through stimulation of
 Higher Centre Influences
 Besides the afferents from the baroreceptors, the medullary cardiovascular center
receives afferents from the respiratory centers and from higher CNS centers, such
as the hypothalamus and the cerebral cortex.
 The hypothalamus is an important integrating center for the coordination of the
cardiovascular responses to emotion, exercise and temperature change.
 The cerebral cortex influences the hypothalamic integrating areas along both
excitatory and inhibitory pathways.
 A strong emotion can lead to a precipitous hypotension with fainting. It has been
suggested that in the face of severe stress, the cortico-hypothalamic depressor
response may offer, in addition to fight or flight, a third option which is fainting
and oblivion.
LONG-TERM REGULATION OF ARTERIAL BLOOD
PRESSURE
 The long-term regulation of blood pressure is believed to be dependent mainly on
the blood volume-urinary output balance which in turn is mainly influenced by the
renin - angiotensin - aldosterone system.
 For example, an increase in arterial blood pressure causes increased fluid output
through the kidneys and a reduction in the extracellular fluid volume, blood
volume and venous return.
 This will lead to a decreased in cardiac output which will result in blood pressure
decrease.
 It should be noted that blood volume itself depends on a balance between fluid
intake and fluid losses and that only very small changes in body fluid volume are
required to produce marked changes in arterial pressure
LONG-TERM REGULATION OF ARTERIAL BLOOD PRESSURE

 Thus, 2% increase in blood Volume can result in an increase in arterial pressure of

as much as 50%.
 Although the rapidly acting control system will serve to reduce this change, the
long-term adjustment will be by increased fluid loss by the kidneys.
 By reabsorbing 99% of the water and sodium filtered in the glomerulus per day,
the kidneys help in conserving body water and therefore maintaining blood
volume.
 This ensures a long-term maintenance of normal blood pressure.
 The baroreceptors located in the high pressure sites (i.e. aortic arch and carotid
sinus) are not the only stretch receptors involved in the feedback regulation of the
circulation and arterial blood pressure
 CONTD.
• There are low-pressure baroreceptors that respond to increased fullness of the
vascular system, triggering tachycardia, renal vasodilation and diuresis.
• The low-pressure baroreceptors are bare ends of myelinated nerve fibres located at
strategic low-pressure sites.
• The latter include the pulmonary artery, junction of the right atrium with the vena
cava, junction of the left atrium and pulmonary veins, the atria themselves and the
ventricles.
• Distension of these receptors depends largely on venous return to the heart. They
constitute part of the larger system of volume sensors that control the effective
circulating volume of blood.
• They also help in the control of cardiac output. Thus, by regulating the effective
circulating volume and cardiac output, they indirectly regulate mean arterial blood
pressure.