for B.Sc nursing students

1. Blood vessels - physiology

2. Increased
EDV(stretches)
Increased
PRELOAD
Frank starling law
Positive inotropic
agents
Increased
CONTRACTILITY
Increase force of contraction
at physio. Level of stretch
Increased STROKE VOLUME
Decreased arterial BP
during diastole
Decreased
AFTERLOAD
SL valves open sooner when
BP in aorta and pul. Artery
is lower
Increased
CARDIAC
OUTPUT
NERVOUS: inputs from
Cortex, baro n
chemoreceptors, limbic
system, proprioceptors
Increased sympathetic
stimulation n
decreased parasym.
CHEMICALS
CA or thyroid hormones,
moderate increase in
extracellular Ca2+
Increased HEART RATE
OTHER FACTORS
Infants, elderly, females,
less fitness, increased
body temp.

4. capillary exchange:
• Mission of the entire CVS is to keep blood flowing
through capillaries to allow ‘capillary exchange’, the
movement of substances between blood and
interstitial fluid.
• 7% of blood in systemic capillaries at any given time is
continually exchanging materials with interstitial
fluid.
• Substances enter and leave capillaries by 3 basic
mechanisms:
• 1. diffusion.
• 2. transcytosis.
• 3. bulk flow.

5. Diffusion:
• Most important method.
• Many susbtances, such as O2, CO2, glucose,
aminoacids, and hormones, enter and leave capillaries
by simple diffusion.
• O2 and nutrients normally are present in higher
concentrations in blood, they diffuse down their
concentration gradients into interstitial fluid and then
into body cells.
• CO2 and other wastes released by body cells are
present in higher concentrations in interstitial fluid, so
they diffuse into blood.

7. • Substances in blood or interstitial fluid can cross the
walls of a capillary by diffusing through the
intercellular clefts or fenestrations or by diffusing
through the endothelial cells.
• Water-soluble subs., such as glucose and aminoacids
pass across capillary walls through intercellular clefts
or fenestrations.
• Lipid-soluble materials, such as O2, CO2 and steroid
hormones, may pass across capillary walls directly
through the lipid bilayer of endothelial cell plasma
membranes.
• Most plasma proteins and RBCs cannot pass through
capillary walls because they are too large to fit through
the intercellular clefts and fenestrations.

9. • In sinusoids, intercellular clefts are so large that they
allow even proteins and blood cells to pass through
their walls.
• E.g: hepatocytes synthesize and release many plasma
proteins, such as fibrinogen and albumin, which then
diffuse into the blood stream through sinusoids.
• In red bone marrow, blood cells are formed and then
enter the bloodstream through sinusoids
• Capillaries of the brain allow only a few substances to
move across their walls.
• Most areas of the brain contain continuous capillaries.
These are very ‘tight’.
• Endothelial cells of most brain capillaries are sealed
together by tight junctions.

10. • Results in blockade to movement of materials into and
out of brain capillaries – ‘blood-brain barrier’.
• In areas that lack BBB, hypothalamus, pineal gland,
and pituitary gland materials undergo capillary
exchange more freely.

11. Transcytosis:
• Substances in blood plasma become enclosed within
tiny pinocytic vesicles that first enter endothelial cells
by endocytosis, then move across the cell and exit on
the other side by exocytosis.
• Important mainly for large, lipid insoluble molecules
that cannot cross capillary walls in any other way.
• Ex: hormone insulin.
• Certain antibodies pass from the maternal circulation
into fetal circulation.

13. Bulk flow: filtration and reabsorption
• Bulk flow – passive process in which large no.of ions,
molecules or particles in a fluid move together in the
same direction.
• Substances move at rates far greater than can be
accounted for by diffusion alone.
• Occurs from an area of higher pressure to an area of
lower pressure, and it continues as long as a pressure
difference exists.
• Diffusion is more important for solute exchange
between blood and interstitial fluid, but bulk flow is
more imp. For regulation of the relative volumes of
blood and interstitial fluid.

14. • Pressure driven movement of fluid and solutes from
blood capillaries into interstitial fluid is called
‘filtration’.
• Pressure driven movement from interstitial fluid into
blood capillaries is called ‘reabsorption’.
• 2 pressures promote filtration:
• 1. blood hydrostatic pressure – generated by the
pumping action of the heart.
• 2. interstitial fluid osmotic pressure.
• Main pressure promoting reabsorption of fluid –
‘blood colloid osmotic pressure’.
• Balance of these pressures – ‘net filtration pressure’ –
determines the volumes of blood and interstitial fluid
to remain steady or change.

15. • Normally,
• Volume of fluid and solutes filtered = volume
reabsorbed. (almost equals).
• This near equilibrium – ‘starlings law of the
capillaries’.
• Within the vessels, the hydrostatic pressure is due to
the pressure that water in blood plasma exerts against
blood vessel walls.
• BHP = 35mmHg at the arterial end of capillary.
• = 16mmHg at the capillary venous end.
• BHP ‘pushes’ fluid out of capillaries into interstitial
fluid.

17. • The opposing pressure of the interstitial fluid, called
‘interstitial fluid hydrostatic pressure’ IFHP – pushes
fluid from interstitial spaces back into capillaries.
• However, IFHP is close to zero.
• For discussion, IFHP is assumed as 0mmHg all along
the capillaries.

18. • The differences in osmotic pressure across a capillary
wall is due almost entirely to the presence in blood of
plasma proteins, which are too large to pass through
either fenestrations or gaps between endothelial cells.
• ‘blood colloid osmotic pressure’ BCOP – force caused
by the colloidal suspension of these large proteins in
plasma.
• 26mmHg in most capillaries.
• Opposing BCOP, is ‘interstitial fluid osmotic pressure’,
IFOP – which pulls fluid out of capillaries into
interstitial fluid.
• Normally, IFOP is very small – 0.1-5mmHg – because
only tiny amounts of protein are present in interstitial
fluid.

19. • Small amount of protein that leaks from blood plasma
into interstitial fluid doesn’t accumulate there because
it enters lymphatic fluid and is returned to the blood.
• Consider IFOP – 1mmHg.
• Whether fluid leave or enter capillaries depends on
the balance of pressures.
• If the pressures that push fluid out of capillaries
exceed the pressures that pull fluid into capillaries,
fluid will move from capillaries into interstitial
spaces (filtration).
• If the pressures that push fluid out of interstitial
spaces into capillaries exceed the pressures that pull
fluid out of capillaries, then fluid will move from
interstitial spaces into capillaries (reabsorption).

20. • The net filtration pressure (NFP), which indicates the
direction of fluid movement, is calculated as follows:
• NFP = (BHP + IFOP) – (BCOP + IFHP).
• pressures that pressures that promote
promote filtration reabsorption.
• At the arterial end of a capillary,
• NFP = (35 + 1) - (26 + 0) mmHg.
= 36 – 26 = 10mmHg.
• Thus, at the arterial end of a capillary, there is a ‘net
outward pressure’ of 10mmHg, and fluid moves out of
the capillary into interstitial spaces (filtration).

21. • At the venous end of a capillary,
• NFP = (16 + 1) – (26 + 0)mmHg.
= 17 – 26
= -9mmHg.
• At the venous end of a capillary, the negative value
represents a ‘net inward pressure’, and fluid moves
into the capillary from tissue spaces (reabsorption).
• On average, about 85% of the fluid filtered out of
capillaries is reabsorbed.
• The excess filtered fluid and the few plasma proteins
that do escape from blood into interstitial fluid enter
lymphatic capillaries.

24. • As lymph drains into the junction of the jugular and
subclavian veins in the upper thorax, these materials
return to the blood.
• Every day about 20 liters of fluid filter out of
capillaries in tissues throughout the body.
• Of this fluid, 17 liters are reabsorbed and 3 liters enter
lymphatic capillaries.

25. Edema:
• If filtration greatly exceeds reabsorption, the result is
‘edema’, an abnormal increase in interstitial fluid
volume.
• Edema is not usually detectable in tissues until
interstitial fluid volume has risen 30% above normal.
• Edema can result from either excess filtration or
inadequate reabsorption.
• 2 situations may cause excess filtration:
• 1. increased capillary BP – causes more fluid to be
filtered from capillaries.

26. • 2. increased permeability of capillaries – raises
interstitial fluid osmotic capillaries by allowing some
plasma proteins to escape.
• Such leakiness may be caused by the destructive
effects of chemical, bacterial, thermal, or mechanical
agents on capillary walls.
• One situation commonly causes inadequate
reabsorption:
• Decreased conc. Of plasma proteins – lowers the
blood colloid osmotic pressure.
• Inadequate synthesis or loss of plasma proteins is
associated with liver disease, burns, malnutrition, and
kidney disease.

28. Hemodynamics:
factors affecting blood flow:
• Blood flow is the volume of blood that flows through
any tissue in a given time period.
• Total blood flow is cardiac output – the volume of
blood that circulates through systemic blood vessels
each minute.
• CO = SV x HR.
• CO is distributed into circulatory routes depends on
two or more factors:
• 1. the ‘pressure difference’ that drives the blood flow
through a tissue and
• 2. the ‘resistance’ to blood flow in specific BVs.

29. • Blood flows from regions of higher pressure to regions
of lower pressure, the greater the pressure difference,
the greater the blood flow.
• Higher the resistance, the smaller the blood flow.
• Blood pressure:
• Contraction of the ventricles generates blood
pressure, the hydrostatic pressure exerted by blood
on the walls of a blood vessel.
• BP is highest in the aorta and large systemic arteries,
in a resting young adult, BP rises to about 110mmHg
during systole and drops to about 70mmHg during
diastole.

31. • SBP is the highest pressure attained in arteries during
systole, and DBP is the lowest arterial pressure during
diastole.
• As blood leaves the aorta and flows through the
systemic circulation, its pressure falls progressively as
the distance from the left ventricle increases.
• BP decreases to about 35mmHg as blood passes from
systemic arteries through systemic arterioles and into
capillaries, where the pressure fluctuations disappear.
• At the venous end of capillaries, BP has dropped to
about 16mmHg.
• BP continues to drop as blood enters systemic venules
and then veins because these vessels are farthest from
the left ventricles.

32. • Finally, BP reaches 0mmHg as blood flows into the
right ventricles.
• Mean arterial pressure (MAP) – averages BP in
arteries - roughly one-third of the way between the
DBP and SBP.
• MAP = DBP + 1/3 (SBP-DBP).
• Calculate MAP for a BP of 110/70mmHg?
• Another way to calculate CO:
• CO = MAP/R.
• MAP = CO x Resistance.
• If CO rises due to an increase in SV or HR, then the
MAP rises as long as R remains steady.

34. • A decrease in CO causes a decrease in MAP if R
doesn’t change.
• BP also depends on the total volume of blood in the
CVS.
• Normal volume of blood in an adult is about 5L.
• Any decrease in this volume, as from h’gge, decreases
the amount of blood that is circulated through the
arteries each minute.
• A modest decrease can be compensated for by
homeostatic mechanisms that help maintain BP, but if
the decrease in blood volume is greater than 10% of
the total, BP drops.

35. • Conversely, anything that increases blood volume,
such as water retention in the body, tends to increase
BP.
• Resistance:
• Vascular resistance is the opposition to blood flow due
to friction between blood and the walls of blood
vessels.
• VR depends on:
• 1. size of the blood vessel lumen.
• 2. blood viscosity.
• 3. total blood vessel length.

37. • 1. size of the lumen:
• Smaller the lumen of a blood vessel, the greater its
resistance to blood flow.
• Resistance is inversely proportional to the fourth
power of the diameter (d) of the blood vessels lumen.
• R = 1/d4.
• Smaller the diameter of the blood vessel, the greater
the resistance it offers to blood flow.
• E.g: diameter of bv decreases by half, the R increases
16times.
• Moment-to-moment fluctuations in blood flow
through a given tissue are due to VC and VD of the
tissue’s arterioles.

39. • As arterioles dilate, R decreases, and BP falls.
• As arterioles constrict, R increases, and BP rises.
• 2. blood viscosity:
• Viscosity (thickness) of blood depends mostly on the
ratio of RBCs to plasma volume, and to a smaller
extent on the concentration of proteins in plasma.
• Higher the blood viscosity, the higher the resistance.
• Any condition that increases viscosity of blood, such as
dehydration or polycythemia, thus increases BP.
• Depletion on plasma proteins or RBCs, due to anaemia
or hgge, decreases viscosity, and thus decreases BP.

40. • 3. total blood vessel length:
• Resistance to blood flow through a vessel is directly
proportional to the length of the blood vessel.
• The longer a blood vessel, the greater the resistance.
• Obese people often have HTN because the additional
blood vessels in their adipose tissue increase their
total blood vessel length.
• An estimated 650km of additional blood vessels
develop for each extra kg of fat.

41. • Systemic vascular resistance (SVR):
• Also known as total peripheral resistance (TPR).
• Refers to all the vascular resistances offered by
systemic blood vessels.
• Diameters of arteries and veins are large, so their
resistance is very small because most of the blood
doesn’t come into physical contact with the walls of
the blood vessel.
• Smallest vessels – arterioles, capillaries, and venules –
contribute the most resistance.
• A major function of arterioles is to control SVR – and
therefore BP and blood flow to particular tissues – by
changing their diameters.

43. • Arterioles need to vasodilate or vasoconstrict only
slightly to have a large effect on SVR.
• Main center for regulation of SVR is the vasomotor
center in the brain stem.
• Venous return:
• Volume of blood flowing back to the heart through the
systemic veins, occurs due to the pressure generated
by contractions of the heart’s left ventricles.
• The pressure difference from venules to the right
ventricle, although small, normally is sufficient to
cause venous return to the heart.

44. • If pressure increases in the right atrium or ventricle,
venous return will decreases.
• One cause of increased pressure in the right atrium is
an incompetent tricuspid valve, which lets blood
regurgitate as the ventricles contract.
• The result is decreased venous return and buildup of
blood on the venous side of the systemic circulation.
• When a person stands up, the pressure pushing blood
up the veins in lower limbs is barely enough to
overcome the force of gravity pushing it back down.
• The other 2 mechanisms pump blood from the lower
body back to the heart: 1. skeletal muscle pump, 2.
respiratory pump.

45. • Both depends on the presence of valves in veins.
• Skeletal muscle pump operates as follows:
• 1. standing at rest: both the venous valve closer to the
heart (proximal valve) and the one farther from the
heart (distal valve) in this par of the leg are open, and
blood flows upward toward the heart.
• 2.contraction of leg muscles – compresses the vein.
• This compression pushes blood through the proximal
valve – ‘milking’.
• Distal valve in the uncompressed segment of the vein
closes as some blood is pushed against it.
• Immobilized people – VR is slower and they may
develop circulation problems.

47. • 3. after muscle relaxation – pressure fails in the
previously compressed section of vein, which causes
the proximal valve to close.
• Distal valve now opens because BP in the foot is higher
than in the leg, and the vein fills with blood from the
foot.
• Respiratory pump:
• Also based on alternating compression and
decompression of veins.
• During inhalation, the diaphragm moves downward,
which causes a decrease in pressure in the thoracic
cavity and increase in pressure in the abdominal
cavity.

48. • As a result, abdominal veins are compressed, and
greater volume of blood moves form the compressed
abdominal veins into the decompressed thoracic veins
and then into the right atrium.
• when the pressures reverse during exhalation, the
valves in the veins prevent backflow of blood from the
thoracic veins to the abdominal veins.

49. • Velocity of blood flow:
• Speed or velocity of blood flow is inversely related to
the cross-sectional area.
• Velocity is slowest where the total cross-sectional area
is greatest.
• Each time an artery branches, the total CSA of all its
branches is greater than the CSA of the original vessel,
so blood flow becomes slower and slower as blood
moves further away from the heart, and is slowest in
the capillaries.

50. • When venules unite to form veins, the total CSA
becomes smaller and flow becomes faster.
• CSA of the aorta: 3-5cm2; average velocity of the
blood: 40cm/sec.
• Capillaries: total CSA: 4500-6000cm2; velocity of
blood flow is less than 0.1cm/sec.
• 2 venae cavae combined, the CSA: 14cm2; velocity is
about 15cm/sec.
• The velocity of blood flow decreases as blood flows
from the aorta to arteries to arterioles to capillaries,
and increases as it leaves capillaries and returns to the
heart.

51. • Relatively slow rate of flow through capillaries aids the
exchange of materials between blood and interstitial
fluid.
• Circulation time: time required for a drop of blood to
pass from the right atrium, through the pulmonary
circulation, back to the left atrium, through the
systemic circulation down to the foot, and back again
to the right atrium.
• Resting person: circulation time: 1minute.

53. Syncope:
• Or fainting.
• Sudden, temporary loss of consciousness that is not
due to head trauma, followed by spontaneous
recovery.
• Most commonly due to cerebral ischemia, lack of
sufficient blood flow to the brain.
• Reasons:
• 1. vasodepressor syncope: due to sudden emotional
stress or real, threatened, or fantasized injury.
• 2. situational syncope: pressure stress associated with
urination, defecation, or severe coughing.

54. • 3. drug-induced syncope: caused by drugs such as
antihypertensives, diuretics, vasodilators, or severe
coughing.
• 4. orthostatic hypotension: excessive decrease in BP
that occurs upon standing up, may cause fainting.

55. Control of BP and BLOOD FLOW:
• Several interconnected negative feedback systems
control blood pressure by adjusting HR, SV, SVR, and
BV.
• Some allow rapid adjustments to cope with sudden
changes, such as drop in BP in the brain.
• Some act more slowly to provide long term regulation
of BP.
• Body may also require adjustments to the distribution
of blood flow.
• E.g: during exercise – greater % of total blood flow is
diverted to skeletal muscles.

56. Role of the cardiovascular center:
• CV center in medulla oblongata helps regulate HR and
SV.
• CV center also controls neural, hormonal, and local
negative feedback systems that regulate BP and blood
flow to specific tissues.
• Groups of neurons scattered within the CV center
regulate HR, contractility of the ventricles, and BV
diameter.
• Some neurons stimulate the heart (cardiostimulatory
center); others inhibit the heart (cardioinhibitory
center).

58. • Others control BV diameter by causing constriction
(vasoconstrictor center) or dilation (vasodilator
center) – these neurons are referred collectively as
‘vasomotor center’.

59. • Cardiovascular center:
• Receives input from higher brain regions and from
sensory receptors.
• Nerve impulses descend from the cerebral cortex,
limbic system, and hypothalamus to affect the CV
center.
• E.g: even before starting of exercise, HR increases coz
of nerve impulses conveyed from the limbic system.
• Increased body temp. – hypothalamus sends impulses.
• Resulting vasodilation of skin bv’s allows heat to
dissipate more rapidly from the surface of the skin

61. • 3 main types of sensory receptors that provide input to
the CV center are: proprioceptors, baro and chemo
receptors.
• Proprioceptors monitor movements of joints and
muscles and provide input to the CV center during
physical activity.
• Their activity accounts for the rapid increase in HR at
the beginning of exercise.
• Baroreceptors monitor changes in the pressure and
stretch in the walls of blood vessels.
• Chemoreceptors monitor the concentration of various
chemicals in the blood.

63. • Output from the CV center flows along sympathetic
and parasympathetic neurons of the ANS.
• Sympathetic impulses reach the heart via the ‘cardiac
accelerator’ nerves.
• An increase in sympathetic stimulation increases HR
and contractility; decrease in sympathetic stimulation
decreases HR and contractility.
• Parasympathetic stimulation, conveyed along ‘vagus
nerves’ decreases HR.

65. • CV center also continually sends impulses to smooth
muscle in blood vessel walls via ‘vasomotor nerves’.
• These sympathetic neurons exit the spinal cord
through all thoracic and the first one or 2 lumbar
spinal nerves and then pass into the sympathetic trunk
ganglia.
• From there, impulses propagate along sympathetic
neurons that innervate blood vessels in viscera and
peripheral areas.
• The vasomotor region of the CV center continually
sends impulses over these routes to arterioles
throughout the body, but especially to those in the
skin and abdominal viscera.

67. • Result: moderate state of tonic contraction or
vasoconstriction – ‘vasomotor tone’ – sets the
resting level of systemic vascular resistance.
• Sympathetic stimulation of most veins causes
constriction that moves blood out of venous
reservoirs and increases BP.

68. Neural regulation of BP:
• Nervous system regulates BP via negative feedback
loops that occur as 2 types of reflexes:
• Baroreceptor reflexes
• Chemoreceptor reflexes.
• Baroreceptor reflexes:
• Pressure sensitive sensory receptors.
• Located in the aorta, internal carotid arteries, and
other large arteries in neck and chest.
• Send impulses to the cardiovascular center to help
regulate BP.
• 2 most imp. Reflexes: carotid sinus reflex and
aortic reflex.

69. • Baroreceptors in the wall of the carotid sinuses initiate
the ‘carotid sinus reflex’, which helps regulate BP in
the brain.
• The ‘carotid sinuses’ are small widenings of the right
and left internal carotid arteries just above the point
where they branch form the common carotid arteries.
• BP stretches the wall of the carotid sinus, which
stimulates the baroreceptors.
• Nerve impulses propagate from the carotid sinus
baroreceptors over sensory axons in the
glossopharyngeal nerves to the cardiovascular center
in the medulla oblongata.

71. • Baroreceptors in the wall of the ascending aorta and
arch of aorta initiate the ‘aortic reflex’, which regulates
systemic BP.
• Nerve impulses from the aortic baroreceptors reach
CV center via sensory axons of the vagus nerves.
• When the BP falls, the baroreceptors are stretched
less, and they send nerve impulses at a slower rate to
the CV center.
• In response, CV center decreases parasympathetic
stimulation of the heart by way of motor axons of the
vagus nerves and increases sympathetic stimulation of
the heart via cardiac accelerator nerves.

73. • Another consequence of increased sympathetic
stimulation is increased secretion of E and NE by the
adrenal medulla.
• As the heart beats faster and more forcefully, and as
systemic vascular resistance increases, CO and
systemic vascular resistance rises, and BP increases to
normal level.
• When an increase in pressure is detected, the
baroreceptors send impulses at a faster rate.
• CV center responds by increasing parasympathetic
stimulation and decreases sympathetic stimulation.

75. • Result: decrease in HR and force of contraction reduce
the CO.
• CV center also slows the rate at which it sends
sympathetic impulses along vasomotor neurons that
normally causes vasoconstriction.
• This leads to vasodilation – lowers systemic vascular
resistance.
• Decreased CO and decreased systemic vascular
resistance both lower SBP to the normal level.
• Moving from prone to erect position decreases BP and
blood flow in the head and upper part of the body.
• BR reflexes quickly counteract the drop in pressure.

76. • Sometimes these reflexes operate more slowly than
normal, esp in the elderly.
• Person then can faint due to reduces brain blood flow
upon standing up too quickly.
• Carotid sinus massage:
• Carotid sinus is close to the anterior surface of the
neck, it is possible to stimulate the baroreceptors –
putting pressure on the neck.
• Massage is used sometimes by physicians to slow
heart HR in person who has paroxysmal
superventricular tachycardia.

77. • carotid sinus syncope:
• Anything that stretches or puts pressure on the carotid
sinus, such as hyperextension of the head, tight
collars, or carrying heavy shoulder loads, may also
slow HR and can cause ‘carotid sinus syncope’ –
fainting due to inappropriate stimulation of the
carotid sinus baroreceptors.

78. • Chemoreceptor reflexes:
• Chemoreceptors – monitor the chemical composition
of blood.
• Located close to the baroreceptors of the carotid sinus
and arch of aorta is small structures called carotid
bodies and aortic bodies respectively.
• Detect changes in blood level of O2, CO2, and H+.
• Hypoxia, acidosis, or hypercapnia stimulates the
chemoreceptors to send impulses to the CV center.
• In response, the CV center increases sympathetic
stimulation to arterioles and veins, producing
vasoconstriction and an increase in BP.
• Also provide input to the respiratory center in brain
stem to adjust the rate of breathing.

80. Hormonal regulation of BP:
• Several hormones help regulate BP and blood flow by
altering cardiac output, changing systemic vascular
resistance, or adjusting the total blood volume.
• 1. renin-angiotensin-aldosterone system:
• When blood volume falls or blood flow to the kidneys
decrease, juxtaglomerular cells in the kidneys secrete
renin into the blood-stream.
• Renin and ACE act on their substrates to produce the
active hormone AT-II – raises BP in 2 ways:
• 1. AT-II is a potent vasoconstrictor, it raises BP by
increasing systemic vascular resistance.

81. • 2. it stimulates secretion of aldosterone – increases
reabsorption of sodium ions and water by the kidneys.
• Water reabsorption increases total blood volume,
which increases BP.
• 2. E and NE:
• In response to sympathetic stimulation, the adrenal
medulla releases E and NE.
• These increase CO by increasing the rate and force of
heart contractions.
• Also causes vasoconstriction of arterioles and veins in
the skin and abdominal organs and vasodilation of
arterioles in cardiac and skeletal muscle – helps
increase blood flow to muscle during exercise.

84. • 3.antidiuretic hormone (ADH): is produced by the
hypothalamus and released from the posterior
pituitary in response to dehydration or decreased
blood volume.
• Causes vasoconstriction – increases BP.
• Also called as vasopressin.
• 4. atrial natriuretic peptide (ANP): released by cells in
the atria of the heart, ANP lowers BP by causing
vasodilation and by promoting the loss of salt and
water in the urine, which reduces blood volume.

86. Autoregulation of BP:
• In each capillary bed, local changes can regulate
vasomotion.
• When vasodilators produce local dilation of arterioles
and relaxation of precapillary sphincters, blood flow
into capillary networks is increased, which increases
O2 level.
• Vasoconstrictors have the opposite effect.
• Ability of a tissue to automatically adjust its blood
flow to match its metabolic demands –
‘autoregulation’.
• In tissue such as the heart and skeletal muscle, where
the demand for O2 and nutrients and for the removal
of wastes can increase as much as ten fold during
physical activity.

89. • Thus, autoregulation is an important contributor to
increase blood flow through the tissue.
• Autoregulation also controls regional blood flow in the
brain; blood distribution to various parts of the brain
changes dramatically for diff mental and physical
activities.
• During talking – blood flow increases to motor speech
areas; when listening – increases to the auditory areas.

90. • 2 stimuli which cause autoregulatory changes in blood
flow:
• 1. physical changes: warming promotes vasodilation,
and cooling causes vasoconstriction.
• In addition Smooth muscle in arteriole walls exhibits a
‘myogenic response’ – it contracts more forcefully
when it is stretched and relaxes when stretching
lessens.
• When blood flow through an arteriole decreases,
stretching of the arteriole walls decreases.
• Smooth muscle relaxes and produces vasodilation,
which increases blood flow.

93. • 2. vasodilating and vasoconstricting chemicals:
• Several types of cells – including WBC, platelets,
smooth muscle fibers, macrophages, and endothelial
cells – release a wide variety of chemicals that alter
blood vessel diameter.
• Vasodilating chemicals: K+, H+, lactic acid, and
adenosine, NO.
• Tissue trauma or inflammation causes release of
vasodilating kinins and histamine.
• Vasoconstrictors: thromboxanse A2, superoxide
radicals, serotonin, and endothelins.

95. • Diff b/n pulmonary and systemic circulation is their
autoregulatory response to changes in O2 level.
• Walls of blood vessels in the systemic circulation dilate
in response to low O2.
• With vasodilation, O2 delivery increases, which
restores the normal O2 level.
• Walls in pulmonary circulation constrict in response
to low levels of O2. this ensures that blood mostly
bypasses those alveoli in the lungs that are poorly
ventilated by fresh air and most blood flows to better
ventilated areas of the lung.

97. Checking circulation:
• Pulse:
• Alternate expansion and recoil of elastic arteries after
each systole of the left ventricle creates a travelling
pressure wave – pulse.
• Strongest in the arteries closest to the heart, becomes
weaker in the arterioles, and disappears altogether in
the capillaries.
• Pulse may be felt in any artery that lies near the
surface of the body that can be compressed against a
bone or other firm structure.

98. Structure: Location:
Superficial temporal artery Lateral to orbit of eye.
Facial artery Mandible on a line with the
corners of the mouth.
Common carotid artery Lateral to larynx.
Brachial artery Medial side of biceps branchii
muscle.
Radial artery Distal aspect of wrist.
Femoral artery Inferior to inguinal ligament
Popliteal artery Posterior to knee
Dorsal artery of the foot Superior to instep of foot

100. • Pulse that normally is the same as the heart rate
about 70-80 beats per minute at rest.
• Tachycardia: rapid resting heart or pulse rate,
over 100/minute.
• Bradycardia: slow resting heart or pulse rate
under 50 beats/minute.

101. Measuring BP:
• Blood pressure: refers to the pressure in arteries
generated by the left ventricle during systole and the
pressure remaining in the arteries when the ventricle
is in diastole.
• Usually measured in the brachial artery in the left arm.
• Device used to measure pressure:
sphygomomanometer.
• Consists of a rubber cuff connected to a rubber bulb
that is used to inflate the cuff and a meter that
registers the pressure in the cuff.
• With the arm resting on the table so that it is about the
same level as the heart, the cuff of
sphygmomanometer is wrapped around a bare arm.

103. • Cuff is inflated by squeezing the bulb until the brachial
artery is compressed and blood flow stops, about
30mmHg higher than the person’s usual systolic
pressure.
• Place a stethoscope below the cuff on the brachial
artery, and slowly deflates the cuff.
• When the cuff is deflated enough to allow the artery
open, a spurt of blood passes through, resulting in the
first sound heard through stethoscope.
• This sound corresponds to SYSTOLIC BLOOD
PRESSURE – the force of BP on arterial walls just
after ventricular contraction.
• As the cuff is deflated further, the sounds suddenly
become too faint to be heard through the stethoscope.

105. • This level, called the DIASTOLIC BP, represents the
force exerted by the blood remaining in arteries during
ventricular relaxation.
• At pressures below DBP, sounds disappear altogether.
• Various sounds that are heard while taking BP are
called ‘korotkoff sounds’.
• Normal BP of an adult male is less than 120mmHg
systolic and less than 80mmHg diastole.
• In young adult females, the pressures are 8 to
10mmHg less.
• People who exercise regularly and are in good physical
condition may have even lower BPs.
• BP slightly lower than 120/80 may be a sign of good
health and fitness.

106. • Difference between systolic and diastolic pressure is
called ‘pulse pressure’.
• This pressure, normally about 40mmHg – provides
info about the condition of the CVS.
• E.g: atherosclerosis and PDA greatly increase pulse
pressure.
• Normal ratio of systolic pressure to diastolic pressure
to pulse pressure is about 3:2:1.
•

107. Shock:
• Failure of the CVS to deliver enough O2 and nutrients
to meet cellular metabolic needs.
• Causes of shock are many and varied, but all are
characterized by inadequate blood flow to body
tissues.
• With inadequate O2 delivery, cells switch from aerobic
and anaerobic production of ATP, and lactic acid
accumulates in body fluids.
• If shock persists, cells and organs become damaged,
and cells may die unless proper treatment begins
quickly.

108. • Types of shock:
• Can be of 4 different types:
• 1. hypovolemic shock:
• due to decreased blood volume.
• 2. cardiogenic shock:
• due to poor heart function.
• 3. vascular shock:
• inappropriate vasodilation.
• 4. obstructive shock:
• obstruction of blood flow.

109. • Hypovolemic shock:
• Common cause – acute h’gge.
• Blood loss may be external, as occurs in trauma, or
internal, as in rupture of an aortic aneurysm.
• Loss of body fluids through excessive sweating,
diarrhea, or vomiting also can cause hypovolemic
shock.
• Other conditions – diabetes mellitus – cause excessive
loss of fluid in the urine.
• Sometimes it can due to inadequate intake of fluid.
• When the volume of body fluids falls, venous return to
the heart declines, filling of the heart lessens, SV
decreases, and CO decreases.

111. • Cardiogenic shock:
• Heart fails to pump adequately.
• Most often because of MI.
• Other causes: poor perfusion of the heart (ischemia),
heart valve problems, excessive preload or afterload,
impaired contractility of heart muscle fibers, and
arrythmias.

112. • Vascular shock:
• Normal blood volume and normal CO.
• Shock occurs coz BP drops due to a decrease in
systemic vascular resistance – inappropriate dilation
of arterioles or venules.
• Anaphylactic shock – severe allergic reaction – e.g:
bee sting – releases histamine and other mediators
that cause vasodilation.
• Neurogenic shock – vasodilation may occur following
trauma to the head that causes malfunction of the CVC
in the medulla.
• Septic shock: coz of certain bacterial toxins that
produce vasodilation.

114. • Obstructive shock:
• When blood flow through a portion of the
circulation is blocked.
• Most common cause: pulmonary embolism –
blood clot lodged in a blood vessel in the lungs.

115. • Homeostatic responses to shock:
• Major mechanisms of compensation in shock are
negative feedback systems – work to return CO and
arterial BP to normal.
• When shock is mild, compensation by homeostatic
mechanisms prevents serious damage.
• Normal healthy person can maintain adequate blood
flow and BP till acute blood loss of 10% of total
volume.
• 1. activation of the RAA system:
• Decreased blood flow to the kidneys causes the
kidneys to secrete renin and initiates the RAA system.
• AT-II – vasoconstriction and stimulates the adenal
cortex to secrete aldosterone.

116. • Increases reabsorption of Na+ and water by the
kidneys.
• Increase in systemic vascular resistance and blood
volume help raise BP.
• 2. secretion of antidiuretic hormone:
• In response to decreased BP, the posterior pituitary
releases more ADH.
• Enhances water reabsorption by the kidneys –
conserve remaining blood volume.
• Also causes VC – increases systemic vascular
resistance.

118. • 3. activation of the sympathetic division of the ANS:
• As BP decreases, the aortic and carotid baroreceptors
initiate powerful sympathetic responses throughout
the body.
• Result: marked VC of arterioles and veins of the skin,
kidneys and other abdominal viscera.
• Constriction of arterioles increases systemic vascular
resistance and the constriction of veins increases VR.
• Both effects help maintain an adequate BP.
• Sympathetic stimulation also increases HR and
contractility and increases secretion of E and NE by
the adrenal medulla.
• Intensify VC and increase HR and contractility – raise
BP.

120. • 4. release of local VDs:
• In response to hypoxia, cells liberate VDs – including
K+, H+, lactic acid, adenosine and NO – dilate
arterioles and relax precapillary sphincters.
• Such VD increases local blood flow and may restore 02
level to normal in part of the body.
• VD also has potentially harmful effect of decreasing
systemic vascular resistance and thus lowering the BP.
• If blood volume drops more than 10-20%, or if the
heart can’t bring BP up sufficiently, compensatory
mechanisms may fail to maintain adequate blood
flow to tissues.
• At this point, shock becomes life threatening as
damaged cells start to die.

122. • Signs and symptoms of shock:
• SBP <90mmHg.
• Resting HR – rapid due to sympathetic stimulation
and increased blood levels of E and NE.
• Pulse is weak and rapid due to reduced CO and fast
HR.
• Skin is cool, pale, and clammy due to sympathetic
constriction of skin blood vessels and sympathetic
stimulation of sweating.
• Mental state is altered due to reduced O2 supply to the
brain.
• Urine formation is reduced due to increased levels of
aldosterone and ADH.
• Thirsty due to loss of ECF.

123. • pH of blood is low (acidosis) due to buildup of lactic
acid.
• Person may have nausea due to impaired blood flow to
the digestive organs due to sympathetic VC.