seminar on blood presure

2. Blood pressure
PRESENTER:- DR. JAYESH
1° YR MDS
DEPTOF ORALAND MAXILLOFACIALSURGERY

3. 1. BLOOD
2. FUNCTION OF BLOOD
3. COMPOSITION
4. BLOOD PRESSURE
5. SYSTOLE AND DIASTOLE
6. CARDIAC CYCLE
7. NORMAL BLOOD PRESSURE (B.P)
8. FUNCTIONS OF B.P
9. SIGNIFICANCE OF B.P
10. MEASUREMENT OF B.P
11. FACTORS CONTROLLING B.P
12. REGULATION OF B.P
13. HYPERTENSION
14. HYPOTENSION
15. PULSE
16. BIBLIOGRAPHY
CONTENTS

4. BLOOD
 It can be described as a specialized connective
tissue in which there is liquid intercellular substance
known as plasma and formed elements , the red
blood cells (RBC), the white blood cells platelets
and ions suspended in plasma

5. Blood
 It is the fluid that circulates through the heart,
arteries, capillaries, and veins and is the chief
means of transport within the body. It
transports oxygen
from the lungs to the body tissues, and carbon dioxide
from the tissues to the lungs. It transports
nutritive substances and metabolites to the
tissues and removes waste products to the
kidneys and other organs of excretion. It has an
essential role in the maintenance of fluid balance

6. Function of blood
 Transport of respiratory gases
 Transport of nutrients
 Acts as a vehicle for hormones and other chemicals
 Drainage of waste products
 Maintainence of water balance
 Maintainence of acid base equilibrium
 Maintainence of ion balance
 Regulation of body temperature
 Defensive action
 Protect against hemorrhage by coagulative properties
 Regulation of blood pressure

7. Composition of blood
 Formed
 Cells.- RBC , WBC, PLATELETS
 Plasma
water-91-92%
solids- 8-9%
inorganic constituents-.9% like NaCl, K,ca
organic - albumin, fibrinigen, globulins etc
proteins
urea creatininie etc
fats, carbohydrates, bile etc

8. BLOOD PRESSURE
 It is defined as the lateral pressure exerted by the
blood on the vessel walls while flowing through it.

9. CARDIAC CYCLE
Systole -
.3sec
Diastole -
.5sec
Total - .8 sec

10. Systole and Diastole

11. Significance
 Systolic pressure – it undergoes considerable
fluctuations. It indicates. 1. extent of work.2.
force with which heart is working. 3. degree of
pressure the arterial walls have to with stand
 Diastolic pressure- undergoes less fluctuations.
It is a measure of peripheral resistance. Ie the
load against which heart has to work

12. Cardiac cycle

13. Certain terms
 Systolic pressure-maximum pressure during
systole
 Diastolic pressure- minimum pressure during
diastole
 Pulse pressure-differenc between systolic and
diastolic pressure
 Mean pressure-the arithematic mean of systolic
and diastolic pressure
 S.P/D.P/P.P =3/2/1 in normal adults

14. Normal Blood pressure
 In average adult the normal blood pressure is 120/80
+/- 15
PHYSIOLOGICAL VARIATIONS
 Age
 Gender
 Build
 Exercise
 Posture
 Sleep
 After meals
 Emotional state

15. Normal function of B.P
1. To maintain sufficient presure to keep the
blood flowing.
2. To provide for the motive force of filtration at
the capillary bed- thus ensuring supplies to all
the cells and tissues, formation of lymph ,
urine and so on

16. Measurement of blood pressure
 ARTERIAL BLOOD PRESSURE
 A. Direct method- a canula is placed directly into lumen of a
exposed artery. Other end is inserted into a U shaped
mercury manometer.

17.  B. Indirect method:- 1896 Riva-Roci introduced .
 Kortkoff in 1905 introduced measurement of B.P by
listening to sounds. There are 4 sounds called as Kortkoffs
sounds.

18. Kortkoffs sounds
PHASE NATURE OF
SOUND
DURATION
I Tapping
sound
10 mmHg
II Murmer 20 mmHg
III Gong sound 5 mmHg
IV Muffled Rest
V Dissappear
s

19. Production of kortkoff’s sound

20. Measurement of B.P
COMMONEST METHOD – pressure is measured at
brachial artery by the use of sphygomamometer

21. Method to measure B.P
 1. Oscillatory method

22. Methods to measure B.P cont.....
 Palpatory method

23. Methods to measure B.P cont.....
 Ausculatatory

24. VENOUS BLOOD PRESSURE

25. Factors controllling the B.P
 Depends on
 1. Pumping action of the heart
 2. Cardiac output
 3. Peripheral resistance
 4. Elasticity of arterial wall
 5. Blood volume
 6. Viscosity of blood

26. REGULATION OFARTERIALBLOOD PRESSURE
 BODY HAS 4 MECHANISM TO CONTROL THE BLOOD
PRESSURE
A. NERVOUS CONTROL- by vasomotor centres and impulses
from periphery
B. RENAL MECHANISM- by regulation of ECF and renin-
angiotensis system
C. HORMONAL SYSTEM- hormones causing vasoconstriction and
vasodilation
D. LOCAL MECHANISM- local vasoconstrictors and vasodilators

28. Nervous control
 Adjustment of blood pressure depending on need of body is carried out
by various complex reflexes whose centres are lying in
 Cerebral cortex,
 Formatio reticularis
 Hypothalamus
 Medullary and spinal vasomotor centres
The a) efferent (motor) and afferent(sensory)
pathways constituting the reflexes are lying
withing the sympathetic and parasymathetic
nervous system and the activites are modiefied by
hypothalamus and other centres

29. Efferentpathway
 Consists of A. Vagi ,B. Sympathetic nerves
 It controls the B.P by
 a. Modifying cardiac activity
 b. Altering the cardiac output
 c. Altering the lumen of the blood vessels
control of vasomotor system
VASOMOTOR SYSTEM =
1. VASOMOTOR CENTRE
2. VASOCONSTRICTOR NERVES
3. VASODILATOR NERVES

30. VASOMOTOR CENTRE
 Situated in the floor of the 4 th ventricle in the reticular
formation.
 There are 2 areas in the reticular formation.
a. Pressor centre, b. Depressor centre
Pressor causes rise in blood pressure . The depressor causes
inhibition of vasoconstrictore tone and not by vasodilation. It
relays inhibitory impulses to pressor centre.
They form one unit and are called as vasomotoer centre.
Vasomotor centre discharges the impulse down the lateral
white column of the spinal cord in the cerviccal, thoracic and
lumbar segmetns of the spinal cord and form sypanptic
connections with lateral horn cells of spinal cord

31. VASOMOTOR REFLEX
 Consists of : A.Depressor, B. Pressor reflex
 A. Depressor reflex:- blood pressure reduces due to diffuse
dilation of arterioles. Rise of blood pressure stimulates the
baroreceptors of carotid sinus and aortic arch , and causes
slowing of heart and arteriole dilation. The vasodialtion is due to
inhibition of vasoconstrictor effect of sympatheic system
 B. Pressor reflex:- B.P rises due to diffuse constriction of
arterioles. Diminution of B.P fails to stimulate the baroreceptors
of the carotid sinuses and aortic arch , and parasympathetic
inhibition on heart and arterioles is withdrawn. B.P is rasied due
to overactivity of sympathetic system.
 Reflex vasoconstriction also occurs due to chemoreceptors during
fall of B.P

32. Control of V.M.C(vasomotor centre)
 1. Higher centres (including hypothalamus)
 2. Respiration
 3. CO2 excess
 4.O2 lack
 5.Sino- aortic nerves
 6.other afferent

33. VASOMOTOR NERVES
 Vasoconstrictor nerves :-The fibres pass along
the sympathetic outflow from 1 st thoracic to 2 nd
lumbar segment.
 1. to skin and muscle
 2.To head and neck
 3.to the forelimbs
 4.to the hind limbs
 5.to abdominal viscera
 6.to thoracic viscera

34.  Vasodilator Nerves :-3 types of
 1. Parasympathetic (craniosacral)
 2.Sympathetic
 3.Antidromic fibres of posterior spinal root

35. . Parasympathetic vasodilators
 A. Cranial:-
 i. Chorda tympani- to submaxillary or
submandibular glands
 ii.lesser superficial petrosal- to parotid
 B. Sacral- to vessels of genitalia

36. Sympathetic
vasodilators
 They are mostly vasoconstrictors but some are
vasodialtors also.
 A. Dilator fibres of coronary vessels comes thru
sympathetic
 B. Sympathetic dilator fibres have been
demonstrated in peripheral nerves in humans
 C. Stimulation of last anterior thoracic root
produces dilation of Kidney vessels
 D. Stimulation of the right splanchnic nerve
sometimes causes vasodilation and fall of blood
pressure

37. Antidromic vasodilators
 In the post spinal root
 When the posterior spinal root is cut, Distal to
the ganglion and peripheral end is stimulated –
although the nerve is afferent, yet the vessels in
the periphery- both skin and muscles-
dilates(axon relfex).
 In skin is due to liberation of histamin, in
muscles it liberates acetylcholine and then
vasodilation

38. AFFERNTPATHWAY
 They are lying in two sets of receptors that carry the
information of instantaneous circulatory system.
 These receptors are
 A. Baroreceptors
 B. Chemoreceptors
 The B.P is controlled thru different afferent pathways viz.
 ! Sino-aortic mechanism
 !! Vascular receptors other than sino aortic pathways

40. Sino aortic mechanism in regulation of
normal B.P
It regulates B.P by regulating the heart rate,
vasomotor centre, secretions of Adrenaline and
nor adrenaline. It also adjusts the respiratory
centre in such a way that it run parallel to heart

41. Sino aortic mechanism
A. BARORECEPTORS:- It includes carotid
sinus and aortic arch
!. Carotid sinus:- is a dilation at root of internal
carotid artery often involving common carotid.
Wall is thinner. Deeper part of advetitia layer is a
extensive network of nerve, the fibers end in free
nerve terminal and hava charesteristic minisci.
These pressor receptor are sensitive to stretch
(distortion effect) being stimulated by rise of B.P.
The sinus nerve(afferent) arises from carotid sinus and
body, passes along the glossopharyngeal nerve in close
relation with respiratory, cardiac and vasomotor centre

42.  Aortic Arch- Afferent nerves and stretch
receptors similar to the carotid sinus are also
present in the adventia of the aortuc archm
the roots of the great vessels and even the
adjoining parts of the left venticle,
 Aortic nerve- arises from aortic body, arch
and basal partu of left ventricle . Purely
afferent.
 It mostly passes in the vagus.
 Ends in medulla and closely related to
cardiac, vasomotor , and respiratory centres

43.  B. CHEMORECEPTORS - includes carotid
body and aortic body
 CAROTID BODY:- is a small nodule situated
close on the occipital artery, branch of external
carotid artery. Close to carotid sinus. It consist of
clumps of large polyhedral cells(Glomus cells). Is
rochly supplied with blood and nerves.
Numerous nerve fibres surround the cell clumps
and cells and terminate in special
chemoreceptors,

44.  AORTIC BODY :-
 4 groups of aortic bodies are seen. Small
nodular structures, supplied by special blood
vessels and are situated in
 A. Thorax between pulmonary trunk
andascending aorta
 B. Ventral surface of root of the righ subclavian
artery
 C.on the ventral surface of root of the left
subclavian artery
 D. Ventral surface of aortic arch


46. RENAL MECHANISMB.PCONTROL
 The renal–body fluid system for arterial
pressure control is a simple one: When the body
contains too much extracellular fluid, the blood
volume and arterial pressure rise. The rising
pressure in turn has a direct effect to cause the
kidneys to excrete the excess extracellular fluid,
thus returning the pressure back toward normal.

47.  Increased Fluid Volume Can Elevate Arterial Pressure
by Increasing Cardiac Output or Total Peripheral
Resistance

48. Importance of Salt (NaCl) in the Renal–Body Fluid
Scheme for Arterial Pressure Regulation
 1. When there is excess salt in the extracellular
fluid, the osmolality of the fluid increases, and
this in turn stimulates the thirst center in the
brain, making the person drink extra amounts
of water to return the extracellular salt
concentration to normal. This increases the
extracellular fluid volume.
 .

49.  2. The increase in osmolality caused by the excess
salt in the extracellular fluid also stimulates the
hypothalamic-posterior pituitary gland secretory
mechanism to secrete increased quantities of
antidiuretic hormone. The antidiuretic hormone then
causes the kidneys to reabsorb greatly increased
quantities of water from the renal tubular fluid,
thereby diminishing the excreted volume of urine
but increasing the extracellular fluid volume

50.  The graph shows an extreme capability of the
kidneys to eliminate fluid volume from the body in
response to high arterial pressure and in so doing to
return the arterial pressure back to normal

51. Analysisof arterialpressureregulationbyequatingthe“renaloutputcurve”withthe
“saltandwaterintakecurve.”Theequilibriumpoint describestheleveltowhichthe
arterialpressurewill be regulated.

52. The Renin-Angiotensin
System
 Renin is a protein enzyme released by the
kidneys when the arterial pressure falls too low.
In turn, it raises the arterial pressure in several
ways, thus helping to correct the initial fall in
pressure.

54.  Renin is synthesized and stored in an inactive
form called prorenin in the juxtaglomerular cells (JG
cells) of the kidneys.
 When the arterial pressure falls, intrinsic
reactions in the kidneys themselves cause many
of the prorenin molecules in the JG cells to split
and release renin. Most of the renin enters the
renal blood and then passes out of the kidneys
to circulate throughout the entire body

55.  Renin acts enzymatically on another plasma
protein, a globulin called renin substrate (or
angiotensinogen), to release a 10-amino acid
peptide, angiotensin I. Angiotensin I has mild
vasoconstrictor properties but not enough to
cause significant changes in circulatory function.
The renin persists in the blood for 30 minutes
to 1 hour and continues to cause formation of
still more angiotensin I during this entire time.

56.  Within a few seconds to minutes after formation of
angiotensin I, two additional amino acids are split
from the angiotensin I to form the 8-amino acid peptide
angiotensin II. This conversion occurs almost entirely
in the lungs while the blood flows through the small
vessels of the lungs, catalyzed by an enzyme called
converting enzyme that is present in the endothelium of the
lung vessels. Angiotensin II is an extremely powerful
vasoconstrictor, and it also affects circulatory function in
other ways as well. However, it persists in the blood only
for 1 or 2 minutes because it is rapidly inactivated by
multiple blood and tissue enzymes collectively called
angiotensinases

57.  Angiotensin II has 3 principal effects
 1. vasoconstriction in many areas of the body, occurs
rapidly
 2. decrease excretion of both salt and water by the
kidneys.
 3. is also one of the most powerful stimulators of
aldosterone secretion by the adrenal glands.
Aldosterone cause marked increase in sodium
reabsorption by the kidney tubules, thus increasing
the total body extracellular fluid sodium. This
increased sodium then causes water retention

59. HORMONALMECHANISM FOR
REGULATION OFBLOOD PRESSURE
Hormones which increase arterial blood
pressure
Hormones which decrease arterial
blood pressure
1. Adrenaline
2. Noradrenaline
3. Thyroxine
4. Aldosterone
5. Vasopressin
6. Angiotensin
7. Serotonin
1. Vasoactive intestinal
polypeptide (VIP)
2. Bradykinin
3. Prostaglandin
4. Histamine
5. Acetylcholine
6. Atrial natriuretic peptide
7. Brain natriuretic peptide
8. C type natriuretic peptide
Inc. systolic
Dec. diastolicActs mainly through alpha recp.
General vasoconstrictor effect
Inc. in rate & force of contraction
Inc. in C.O
SBP inc. & DBP dec.
Dec. in DBP is due to release of
metabolites due to inc. metabolic
activity & dec. TPR
Causes retention of salt & water
Inc. ECF vol. & blood vol.
Retn. Of water
Vasopressor actn.
Constriction of systemic arterioles
Secreted in stomach
Vasodilatn.
During inflammation
vasodilator
Allergic condn, inflammation or
damage
Produced by atrial
musculature of
heart

60. HYPERTENSION
 hypertension in adults is defined clinically as
persistently elevated systolic blood pressure of
140-159 mmHg, or diastolic pressure of 90-99
mmHg as stage 1 hypertension, and corresponding
values above 160 or above 100 mmHg as stage 2
hypertension

61. CLASSIFICATION
 1. Primary or essential hypertension in which the
cause of increase in blood pressure is unknown.
Essential hypertension constitutes about 80-95%
patients of hypertension.
 2. Secondary hypertension, in which the increase
in blood pressure is caused by diseases of the
kidneys, endocrines or some other organs.
Secondary hypertension comprises remaining 5-
20% cases of hypertension.

62.  According to the clinical course, both essential and secondary
hypertension may be benign or malignant.
 1.Benign hypertension is moderate elevation of blood
pressure and the rise is slow over the years. About 90-95%
patients of hypertension have benign hypertension.
 2.Malignant hypertension is marked and sudden increase of
blood pressure to 200/140 mmHg or more in a known case of
hypertension or in a previously normotensive individual; the
patients develop papilloedema, retinal haemorrhages and
hypertensive encephalopathy. Less than 5% of hypertensive
patients develop malignant hypertension

64. EFFECTS OF HYPERTENSION
 hypertension causes major effects in four main
organs
1.Heart and its blood vessels
2.Nervous system
3.Kidneys
4.Eyes

65. EFFECTS OF HYPERTENSION
on KIDNEYS
 The renal effects in the form of benign and
malignant nephrosclerosis
 Benign Nephrosclerosis:-
 C/f- There is variable elevation of the blood
pressure with headache, dizziness, palpitation
and nervousness. Eye ground changes may be
found but papilloedema is absent. Renal
function tests and urine examination are normal
in early stage. In long-standing cases, there may
be mild proteinuria with some hyaline or
granular casts. Rarely, renal failure and uraemia
may occur.

66.  Malignant Nephrosclerosis:-
 The patients of malignant nephrosclerosis have
malignant or accelerated hypertension with
blood pressure of 200/140 mmHg or higher.
Headache, dizziness and impaired vision are
commonly found. The presence of
papilloedema distinguishes malignant from
benign phase of hypertension. The urine
frequently shows haematuria and proteinuria.
Renal function tests show deterioration during
the course of the illness. Azotaemia (high BUN
and serum creatinine) and uraemia develop soon
if malignant hypertension is not treated
aggressively.

67. EFFECTS OF HYPERTENSION
on EYE
 HYPERTENSIVE RETINOPATHY:-
 In hypertensive retinopathy, the retinal arterioles are reduced
in their diameter leading to retinal ischaemia
 Malignant hypertension is characterised by necrotising
arteriolitis and fibrinoid necrosis of retinal arterioles.

68. EFFECTS OF HYPERTENSION
on HEART
 HYPERTENSIVE HEART DISEASE:-
 The stress of pressure on the ventricular wall
causes increased production of myofilaments,
myofibrils, other cell organelles and nuclear
enlargement. Since the adult myocardial fibres
do not divide, the fibres are hypertrophied

69. EFFECTS OF HYPERTENSION
on nervous system
 INTRACRANIAL HAEMORRHAGE:-
 a. Intracerebral Haemorrhage
 b. Subarachnoid Haemorrhage

70. INVESTIGATIONS OF
HYPERTENSION

71. Treatment

73. Dental aspect

74. Hypotension

75. Pulse
 Pulse :expansion and elongation of arterial
walls passively produced by pressure changes
during systole and diastole of heart.
 By convention the right radial pulse is assessed .
 It is assesed for a. Rate in bpm. b. Rhythm. c.character(as
volume and waveform of the pulse. Evaluted at right carotid
artery). d. Symmetery (at radial,carotid, femoral, popliteal,
and pedal pulses)

76.  Radial pulse The most common places to measure heart rate using the
palpation method is at the wrist (radial artery) and the neck (carotid artery).
 Other places sometimes used are the elbow (brachial artery) and the groin
(femoral artery).

77. Types of pulse
1. Sinus arrhythmia- frequency increases during inspiration and
decreases during expiration. (alteration of vagal tone)
2. Water hammer pulse- rise and fall are steep
3. Pulsus alterans–alt large and small. (myocardial infarctions)
4. Weak pulse- amount of blood ejected bty left ventricle to arteries is
less than normal
5. Pulsus paradoxicus –reverse of sinus arrhythmia.

78. BIBLIOGRAPHY

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