regulation of Blood pressure through different mechanism and its applied aspect

1. REGULATION OF
BLOOD PRESSURE
Presented by:
Shilpa Arora
PG 1st year
Department of Public Health Dentistry
1

2. Contents
• Introduction
• Terms related to BP
• Classification
• Factors determining blood pressure
• Regulatory mechanisms
– Local
• Short term
• Long term
– Systemic
• Hormonal control
• Nervous control
2

3. • Reflex mechanisms for maintaining blood
pressure
– Baroreceptor
– Chemoreceptor
– Atrial and pulmonary artery reflex
– Central nervous system ischemic response.
• Role of skeletal nerves and skeletal muscles in
increasing cardiac output and arterial pressure.
• Role of kidneys in long term regulation of
arterial pressure
3

4. • Renin- angiotensin system
• Applied aspect
• Management in clinical dental situations
• References
4

5. Introduction
• Blood pressure is defined as the lateral
pressure exerted by flowing blood on the walls
of the arteries. It is measured as mm of Hg.
• It is one of the principal vital sign and
generated by cardiac contraction against the
vascular resistance.
5

6. • Changes in pressure are the driving force
that moves blood through the circulatory
system.
• Blood pressure is of two varieties:
- Total BP
- Lateral BP
6

7. • Total pressure (TP)is the total pressure
exerted by the blood at any given instance.
• Lateral pressure (LP)is the pressure
exerted by the blood on the walls of the
vessel.
Blood pressure basically means lateral pressure in the
systemic arteries.
7

8. • The blood pressure is
easily measured with a
sphygmomanometer.
• Since the blood
pressure increases with
anxiety, measurements
should be made with
the patient relaxed and
fully at rest.
8

9. IBP Measurement
9

10. • To ensure the blood flow to various organs
• Play an important role in exchange of
nutrients and gases across the capillaries
• Affects urine formation
• Required for the circulation of lymph
Significance
10

11. Terms related to BP
• Systolic blood pressure (SBP):
- Highest arterial pressure during a cardiac
cycle
- Is measured after the heart contracts and
blood is ejected into the arterial system
11

12. • Diastolic pressure (DBP):
- Lowest arterial pressure during a
cardiac cycle
- Is measured when the heart is relaxed
and blood is returning to the heart via
veins
12

13. • In a cardiac cycle of average duration,
the systole lasts for about 0.3 sec and
diastole lasts for 0.5 sec.
• Diastolic pressure is more important,
because diastolic period is longer than
the systolic period in the cardiac
cycle.
13

14. • Pulse pressure:
- Difference between systolic and
diastolic pressure.
- PP = SBP-DBP
- It represents the force that the heart
generates each time it contracts
14

15. • Mean Arterial Blood Pressure –The
lateral pressure force generated by the
pumping action of the heart on the wall of
aorta & arterial blood vessels per unit area.
• Mean Arterial BP = DBP+ 1/3 pulse
pressure
• Pulsatile
• Not constant during a cardiac cycle
15

16. • Casual BP –
- Means the BP recorded at an unspecified
time in ordinary conditions in our life.
• Basal BP –
- Means BP recorded when the conditions are
basal (complete mental and physical rest,
room temperature 250 C and some hours after
meal.
16

17. Blood Pressure Category
Chart
17

18. 18

19. Factors determining BP:
• Blood Pressure = Cardiac Output (CO) X
Peripheral Resistance (PR)
• Cardiac Output (CO) = Heart rate x Stroke
volume.
- Heart rate is the number of beat / minute
- Stroke volume is the amount of blood
ejected by ventricle/beat.
19

20. • Cardiac output depends upon:
- Contractility of the myocardium
- Preload
- Heart rate
Peripheral resistance = 8ηl / r4
• Peripheral resistance depends upon:
- viscosity(η)
- radius of blood vessel(r)
- length of vascular tree(l)
20

21. LOCAL FACTORS DETERMINIG
THE ARTERIAL BLOOD
PRESSURE:
Arterial pressure Factors
Arterial blood pressure is
directly proportional to
1. Cardiac output
2. Heart rate
3. Peripheral resistance
4. Blood volume
5. Venous return
6. Viscosity of blood
Inversely proportional to 1. Elasticity of blood vessels
2. Diameter of blood vessels
21

22. Regulatory Mechanisms
22

23. LOCAL REGULATORY
MECHANISMS
23

24. SHORT TERM BLOOD FLOW
REGULATION
Auto-regulation:
• The capacity of tissues to regulate their
own blood flow is referred to as Auto-
regulation.
• Most vascular beds have an intrinsic
capacity to compensate for moderate
changes in perfusion pressure by changes
in vascular resistance so that blood flow
remains relatively constant.
24

25. • Two theories have been put forth for auto-
regulation:
• Myogenic theory
• Metabolic theory
25

26. Myogenic theory
• Sudden stretch of small blood vessels
causes the smooth muscle of the vessel
wall to contract for a few seconds.
• Thus, when high arterial pressure stretches
the vessel, this in turn causes reactive
vascular constriction that reduces blood
flow nearly back to normal.
26

27. • Conversely, at low pressures, the degree of
stretch of the vessel is less, so that the
smooth muscle relaxes and allows
increased flow.
27

28. Metabolic theory
• When the arterial pressure becomes too
great, the excess flow provides too
much oxygen and too many other
nutrients to the tissues.
• These nutrients (especially oxygen)
then cause the blood vessels to constrict
and the flow to return nearly to normal
despite the increased pressure.
28

29. Vasodilator metabolites include:
• Decreased oxygen tension
• Decreased pH
• Increased CO2
• Temperature rise in tissues
• Local accumulation of potassium
• Lactate
• Adenosine in the cardiac muscles.
29

30. Vasoconstrictor like
• Serotonin
• Drop in temperature
Vasoactive substances include
- Prostacyclins
- Thromboxanes
- Nitric oxide also called EDRF
(endothelium derived relaxing factor)
- Endothelins
30

31. Prostacyclins and Thromboxane
A2
• Prostacyclins are produced by
endothelial cells and Thromboxane A2
by platelets via the cyclo-oxygenase
pathway.
• Thromboxane A2 promotes
vasoconstriction
• Prostacyclins promote vasodilatation.
31

32. • It is now known as Nitric Oxide (NO) and
is synthesized by Arginine.
• The NO diffuses to smooth muscle cells
where it activates soluble Guanylyl cyclase
producing cGMP which in turn mediated
the relaxation of vascular smooth muscle.
EDRF (endothelium derived
relaxing factor)
32

33. Endothelins
• Endothelial cells produce Endothelin 1, the
most potent vasoconstrictor agent yet
isolated.
• The cardiovascular effects include
- it evokes positive ionotropic and
chronotropic effects on myocardium
- stimulates intense vasoconstriction of
coronary arteries.
33

34. • LONG TERM BLOOD FLOW
REGULATION:
34

35. • Most of the mechanisms for local blood
flow regulation act within a few seconds to
few minutes after local tissue conditions
have changed.
• Yet even after full function of these acute
mechanisms the blood flow usually is
adjusted only about 3/4th of the way to the
exact requirement of the tissues.
35

36. • However over a period of hours, days
and weeks a long term type of local
blood flow regulation develops in
addition to the acute regulation.
• This long term regulation gives far
more complete regulation than the acute
mechanism.
36

37. Change in tissue vascularity:
• If the arterial pressure falls to 60mm Hg
and remains at this level for many weeks,
the physical structure sizes of the vessels
in the tissue increases, and under some
conditions even the number of vessels
increases.
• On the other hand if the pressure rises to
very high level, the number and size of
vessels decreases.
37

38. • Similarly if the metabolism in a given
tissue is increased for a prolonged period
vascularity increases and if metabolism is
decreased vascularity decreases.
38

39. Role of oxygen in long term
regulation:
• Oxygen is important both for acute and
long term control of blood flow e.g.
increase in vascularity of tissues in
animals that live at high altitudes,
where the atmospheric oxygen is low
and excess of oxygen causes almost
immediate cessation of new vascular
growth.
39

40. Growth of new vessels-
(Angiogenesis)
• Many angiogenic factors are known, the
important among them being:
- Endothelial cell growth factor
- Fibroblast growth factor
- Angiogenin
- Deficiency of tissue oxygen.
40

41. Development of Collateral
Circulation
• Phenomenon of long term local blood flow
regulation.
• When an artery or a vein is blocked in
virtually any tissue of the body, a new
vascular channel usually develops around
the blockage and allows at least partial
resupply of blood to the affected tissue
41

42. SYSTEMIC REGULATION
Systemic regulation can be achieved by two
methods:-
- Control by hormones
- Nervous regulation
42

43. HORMONAL REGULATION:
• Hormonal regulation means regulation by
substances secreted or absorbed into the
body fluids such as hormones and ions.
• These substances may be vasodilators or
vasoconstrictors.
Vasodilators
Kinin
Serotonin
Histamine
Prostaglandins
VIP (vasoactive
intestinal peptide)
ANP (Atrial
Natriuretic peptide)
Vasoconstrictors
-Norepinephrine
and Epinephrine
-Vasopressin or
ADH( anti diuretic
hormone)
-Angiotensin
-Endothelin
Ions:
-Calcium
-Potassium
-Magnesium
-Sodium
-Anions like
acetate and citrate
-Hydrogen ions
43

44. NERVOUS REGULATION:
• The nervous control of circulation is
almost entirely through the ANS
(Autonomic Nervous System) and the most
important part of the ANS in regulation is
the sympathetic nervous system.
• Sympathetic innervation of heart:
- Sympathetic stimulation of heart markedly
increases the activity of the heart both
increasing the heart rate and enhancing the
strength of pumping.
44

45. Sympathetic innervations of the
blood vessels:
- All the vessels except capillaries, pre-
capillary sphincters are innervated by
sympathetic nerves.
- The innervation of small arteries and
arterioles allows sympathetic stimulation
to increase the resistance and thereby to
decrease the rate of blood flow through the
tissues.
45

46. • The innervation of large vessels
particularly of the veins makes it possible
for sympathetic stimulation to decrease the
volume of these vessels and thereby to
alter the volume of peripheral circulatory
system.
46

47. • For regulation of the BP, the entire
vasoconstrictor and cardiovascular
function of the sympathetic nervous
system are stimulated as a unit.
• At the same time there is reciprocal
inhibition of the parasympathetic vagal
inhibitory signals to the heart.
Role of the nervous system for
rapid control of arterial pressure
47

48. • In consequence three major changes
occur simultaneously each of which
helps to increase arterial pressure:
1) Almost all arterioles of the body are
constricted. This increases the total
peripheral resistance and thus
increasing BP.
48

49. 2) The veins and other large vessels towards
the heart, thus increasing the volume of
blood in the heart chambers. This then
causes the heart to beat with far greater
force and therefore to pump increased
quantity of blood, thus increasing the BP.
3) Finally the heart itself is directly
stimulated by the ANS further enhancing
the cardiac pumping. This increases the
heart rate as well as the force of
contraction.
49

50. Reflex mechanisms for
maintaining normal arterial
pressure
• Aside from the exercise and stress
functions of the ANS to raise the arterial
pressure there are multiple subconscious
special nervous control mechanisms that
operate all the time to maintain the arterial
pressure at or near normal operating level.
Almost all of them are negative reflex
mechanisms.
50

51. • These include
i) Baroreceptor reflex
ii) Chemo receptor reflex
iii) Atrial and pulmonary artery reflex
iv)Central nervous system ischemic response.
51

52. Baroreceptors
• They are stretch receptors in the walls of
heart and blood vessels. They are spray
type nerve endings.
• Few baroreceptors are located in the wall
of almost all large artery of the thoracic
and neck regions but they are abundant in
the wall of each internal carotid artery
slightly above the carotid bifurcation, an
area known as Carotid sinus and in the
wall of aortic arch.
52

53. • The signals are transmitted from each
carotid sinus through the very small
Hering’s nerve to the glossopharyngeal
nerve and then to the tractus solitarius in
the medullary area of the brain stem.
Signals from the arch of aorta are
transmitted through the vagus nerve to the
same area of the medulla.
53

54. 54

55. • Thus excitation of baroreceptors by
pressure in the arteries causes arterial
pressure to decrease because of both a
decrease in peripheral resistance and
decrease in cardiac output. Conversely
low pressure has opposite effect.
55

56. Chemoreceptors
• Chemoreceptor reflex that operates in
much the same way except that the
chemoreceptor cells are chemosensitive
cells (sensitive to oxygen lack, carbon
dioxide excess or hydrogen ion excess).
• They are located in several small organs 1-
2 mm in size.
56

57. • Two carotid bodies one of which lies in the
bifurcation of each common carotid artery
and several aortic bundles adjacent to the
aorta.
• The chemoreceptors excite nerve fibres
that along with the baroreceptor fibers pass
through Hering’s nerves and the vagus
nerve to the vasomotor center.
57

58. Decrease BP
Decrease oxygen, Increase Carbon dioxide,
Increase Hydrogen ions
Chemoreceptors
Excitation of vasomotor centre
Increase arterial BP
58

59. • The chemoreceptor reflex is not a powerful
arterial pressure controller in the normal
pressure range because the chemoreceptors
themselves are not stimulated strongly by
pressure changes until the pressure falls
below 80mm Hg.
59

60. Atrial and Pulmonary artery
reflex
• Both the atria and pulmonary arteries have
stretch receptors called low pressure receptors.
• These low pressure receptors play an
important role to minimize arterial pressure
changes in response to changes in blood
volume. Thus although the low pressure
receptors in the pulmonary artery and the atria
cannot detect the simultaneous increase in
pressure in the low pressure areas of the
circulation caused by an increase in volume.
60

61. Central nervous system ischemic
response:
• Most nervous control of BP is achieved by
reflexes that originate in the baroreceptors,
Chemoreceptors and low pressure
receptors all of which are located in the
peripheral circulation outside the brain.
• It is possible that other factors such as
buildup of lactic acid and other acidic
substances also contribute to marked
stimulation of vasomotor center.
61

62. Decrease blood flow to vasomotor centre in
lower brain stem (cerebral ischemia)
Failure of removal of CO2 from slowly flowing
blood
Stimulation of sympathetic nervous system
Excitation of neurons
Increase systemic arterial pressure to a very high
level 62

63. Importance of CNS ischemic
response as regulator of BP
• Despite the powerful nature of CNS
ischemic response it does not become
significant until the arterial pressure falls
far below normal down to 60mm Hg.
63

64. 64

65. Cushing reaction
Increased pressure of cerebrospinal fluid
(cranial vault)
Increased intracranial tension
Compress whole brain & arteries in the brain
Cut off blood supply to brain
65

66. • CNS ischemic response initiated & arterial
pressure rises
• Then it will relieve the brain ischemia.
• The cushing reaction helps to protect the vital
centers of the brain from loss of nutrition if
ever the CSF pressure rises high enough to
compress cerebral arteries. 66

67. Role of skeletal nerves and skeletal muscles
in increasing cardiac output and arterial
pressure:
• Abdominal compression reflex:
whenever the sympathetic vasoconstrictor
system is stimulated, nerve signals are also
transmitted simultaneously through
skeletal nerves to skeletal muscles of the
body, particularly abdominal muscles.
67

68. • This increases the basal tone of these
muscles which compress all the venous
reservoir of the abdomen helping to
translocate blood out of the abdominal
vascular reservoirs towards the heart.
• As a result increased quantities of blood
are available to the heart to be pumped.
• This overall response is called ‘abdominal
compression reflex’.
68

69. Arterial pressure during exercise
• When skeletal muscles contract during
exercise, they compress blood vessels
throughout the body.
• The resulting effect is to translocate large
quantities of blood from the peripheral
vessels into the heart and lungs and
therefore increase the cardiac output.
69

70. • The increase in carbon monoxide in
turn is an essential ingredient in
increasing the arterial pressure during
exercise.
70

71. Role of kidneys in long term regulation
of arterial pressure
• The renal body fluid system for arterial
pressure control is a simple one.
• When the body contains too much
extracellular fluid, the arterial pressure
rises.
• The rising pressure in turn has a direct
effect to cause the kidneys to excrete the
excess extracellular fluid, thus returning
the pressure back to normal.
71

72. • The renal body fluid system is very
sensitive to even slight changes in arterial
pressure such that an increase in arterial
pressure by only a few millimeters of
mercury can double the renal output of
water, called pressure diuresis and even
that of salts called pressure natriuresis.
72

73. Renin- Angiotensin system
• Aside from the capability of kidney to
control arterial pressure through changes in
extracellular fluid volume, the kidneys
have another powerful mechanism for
controlling pressure – Renin Angiotensin
system.
• Renin is a small protein enzyme released
by kidneys when arterial pressure falls too
low.
73

74. 74

75. • Angiotensin II is an extremely powerful
vasoconstrictor.
• It persists in blood only for 1-2 minutes
because it is rapidly inactivated by blood
and tissue enzymes collectively called
Angiotensinase.
75

76. Effect of Angiotensin II
1) Vasoconstriction – occurs intensely in
arterioles and to a less extent in the veins.
- Constriction of arterioles increases
peripheral resistance
- Constriction of veins promotes
increased venous return of blood to heart.
2) Angiotensin II acts by decreasing the
excretion of both salt and water from
kidneys. This increases the extracellular
fluid volume. 76

77. • The Angiotensin causes the kidneys to
retain both salt and water in two ways :
- It acts directly on the kidney to cause salt
and water retention by constricting renal
vessels thereby decreasing blood flow
through kidneys.
- Causes the adrenal gland to secrete
Aldosterone, this Aldosterone increases salt
and water resorption by kidney tubules.
77

78. • Role of Renin- Angiotensin
system in maintaining a normal
arterial pressure despite wide
variations in salt intake
78

79. Increased salt intake
increased extracellular volume
Increased arterial pressure
Decreased Renin and Angiotensin
Decreased renal retention of salt and water.
79

80. Return of extracellular volume almost to
normal
Return of arterial pressure almost to normal.
80

81. • Applied aspect
81

82. Hypertension
• “Silent killer”
• Characterized by the elevation of
systolic and/or diastolic arterial blood
pressures
• May be either primary or secondary
82

83. • Primary hypertension- Lack of identifiable
causative factors for elevated blood pressure.
• Secondary hypertension-
Identifiable cause like
- Chronic kidney disease
- Pregnancy
- Hyperparathyroidism
- Alcohol abuse
- Atherosclerosis
- Autoimmune disorders such as periarteritis
nodosa
83

84. Causes, incidence and risk factors
• Many factors can affect blood pressure,
including:
- How much water and salt we have in our body
- The condition of kidneys, nervous system, or
blood vessels
- The levels of different body hormones
84

85. • A person is more likely to be told that
blood pressure is too high as one gets
older.
• This is because blood vessels become
stiffer with age. When that happens, blood
pressure goes up.
• High blood pressure increases chances of
having a stroke, heart attack, heart failure,
kidney disease, and early death.
85

86. • Other risk factors may be if people :-
- Are African American
- Are obese
- Are often stressed or anxious
- Drink too much alcohol (more than one drink
per day for women and more than two drinks
per day for men)
- Eat too much salt in diet
- Have a family history of high blood pressure
- Have diabetes
- Smokers
86

87. Symptoms
• Most of the time, there are no symptoms.
For most patients, high blood pressure is
found when they visit their health care
provider or have it checked elsewhere.
• Because there are no symptoms, people
can develop heart disease and kidney
problems without knowing they have high
blood pressure.
87

88. Symptoms may be:
• Confusion
• Ear noise or buzzing
• Fatigue
• Headache
• Irregular heartbeat
• Nose bleed
• Vision changes
88

89. • These may be signs of a complication
or dangerously high blood pressure
called malignant hypertension.
89

90. Tests
• Blood pressure is checked several times
before diagnosing with high blood
pressure. It is normal for blood pressure to
be different depending on the time of day.
• Blood pressure readings taken at home
may be a better measure of current blood
pressure than those taken at doctor's office.
A physical exam to look for signs of heart
disease, damage to the eyes, and other
changes in the body is also needed.
90

91. • Tests may be done to look for:
- High cholesterol levels
- Heart disease, such as an echocardiogram
and electrocardiogram
- Kidney disease, such as a basic metabolic
panel and urine analysis
91

92. Treatment and Prevention
• The goal of treatment is to reduce blood
pressure so that there are a lower risk of
complications.
• There are many different medicines that can be
used to treat high blood pressure, including:
- Alpha blockers
- Angiotensin-converting enzyme (ACE)
inhibitors
- Angiotensin receptor blockers (ARBs)
92

93. - Beta blockers
- Calcium channel blockers
- Central alpha agonists
- Diuretics
- Renin inhibitors
- Vasodilators
• It is also recommended to exercise, lose
weight, and follow a healthier diet.
93

94. • In addition to taking
medicine, there are
many things to help
control blood pressure,
including:
• Take healthy diet,
including potassium
and fiber, and drink
plenty of water.
• Regular exercise -- at
least 30 minutes a day.
94

95. • Quit smoking.
• Limit how much
alcohol to drink -- 1
drink a day for
women, 2 a day for
men.
• Limit the amount of
sodium (salt) to eat -
aim for less than
1,500 mg per day.
95

96. • Reduce stress -- try to avoid things that
cause stress. Meditation or yoga can be
tried.
• Keep track of your blood pressure at
home and use a good quality, well-
fitting home device.
• Most of the time, high blood pressure
can be controlled with medicine and
lifestyle changes.
96

97. When blood pressure is not well controlled, a
person is at risk for:
Aortic dissection
Blood vessel damage
(arteriosclerosis)
Brain damage
Congestive heart
failure
Chronic kidney
disease
Heart attack
Peripheral artery
disease
Pregnancy
complications
Stroke
Vision loss
97

98. White-Coat Hypertension
• It is higher in-office blood
pressure reading than
ambulatory (out of office)
reading.
• ‘White Coat’ effect can
lead to dentist referring
patients for possible
hypertension to their
physicians, treating them
for high blood pressure.
98

99. MANAGEMENT IN CLINICAL
DENTAL SITUATIONS
• Dentists have a unique opportunity to detect
cases of hypertension.
• It is a professional responsibility of a dental
clinician to inform the patient of their
hypertensive state and to offer medical
advice, including appropriate referrals.
99

100. • There are no recognized oral
manifestations of hypertension but
antihypertensive drugs can often cause
side-effects, such as:
- Xerostomia
- Gingival overgrowth
- Lichenoid drug reactions
- Taste sense alteration
- Paresthesia.
100

101. • Dental clinician must focus on the actions,
interactions and adverse effects of the
antihypertensive medications, as well as
the overall management of blood pressure
of the patient in the dental chair.
• There are, however, several areas of
general dental management to be
considered in the hypertensive patients.
101

102. Anesthesia
Local Anesthesia
• Dental patients with hypertension are best
treated under local anesthesia being sure
that the anesthesia is complete so that no
anxiety induced elevation of blood
pressure occurs. The use of
vasoconstrictors such as epinephrine in
local anesthetic agents is known to have
negligible influences on blood pressure in
hypertensive patients.
102

103. • Blood pressure and heart rate are
minimally affected by the typically low
dose and short duration of the drug used
in dentistry, both in healthy and those
with existing cardiovascular conditions.
103

104. • Nonetheless, the use of epinephrine-
containing anesthetics in patients with
uncontrolled hypertension, and elective
dental procedures are contraindicated.
• The use of aspirating syringes in local
anesthetics is imperative to avoid
intravenous, intrarterial, intraligamentary
and intrabony injections, which could
potentially precipitate further anxiety and
thus rise in pressure and possible
arrhythmias.
104

105. B. General Anesthesia
• All antihypertensive drugs are potentiated by
general anesthetic agents, especially
barbiturates. General anesthesia tends to
cause vasodilation.
• In the hypertensive person with vascular
disease, there is greater risk as the tissues
have become adapted to a raised blood
pressure which is needed to overcome the
resistance of the vessels and maintain
adequate perfusion.
105

106. • A fall in blood pressure below the
critical level needed for adequate
perfusion of vital organs such as the
kidneys, can therefore be fatal.
• Hypokalemia as a result of diuretics
may be associated with arrhythmias.
106

107. Anxiety control
• The anxiety and stress associated with
dental treatment typically causes a rise in
blood pressure and may precipitate cardiac
arrest or a cerebrovascular accident.
• Preoperative reassurance and oral sedation
may help in alleviating anxiety related rise
in pressure. Use of sedatives the night
before a procedure may also be used.
107

108. • Relative analgesia technique using nitrous
oxide (N2O) can also reduce both systolic
and diastolic pressure by up to 10-15mm
Hg, after approximately 10 minutes of use,
preoperatively.
• Use of oral sedation or nitrous oxide
sedation may reduce blood pressure to
acceptable levels, allowing initiation of
local anesthesia (with or without
vasoconstrictor).
108

109. Timing of Dental appointments
• The increase of blood pressure in
hypertensive patient is associated with the
hours surrounding awakening that peaks
by morning.
• This fluctuation of blood pressure tends to
be less likely in the afternoon. Afternoon
appointments are recommended over
mornings for this reason.
109

110. Orthostatic hypotension
• Orthostatic hypotension may be a problem in
patients using antihypertensive agents that
reduce sympathetic outflow or peripheral
vasodilatory actions.
110

111. • Management of orthostatic hypotension
includes avoiding sudden postural changes,
such as return to sitting position from the
supine operating position.
• The patient should also be instructed to
stay seated for a short period until such
time that adequate cerebral perfusion has
occurred.
111

112. Other dental concerns
• Aspirin is commonly taken by patients
with hypertension to decrease associated
coronary or cerebral vascular thrombotic
disease, and aspirin may cause bleeding
problems.
112

113. • SELECTIVE DENTAL PROCEDURE
may include, but not limited to;
• dental prophylaxis
• restorative procedures
• nonsurgical periodontal therapy
• nonsurgical endodontic procedures
113

114. • EMERGENT NONSTRESSFUL DENTAL
PROCEDURE may include, but not limited
to dental procedures that may help alleviate
pain, infection or masticatory dysfunction.
e.g., simple incision and drainage of
intraoral fluctuant dental abscess.
• The medical benefits should outweigh the
risk of complications secondary to the
hypertensive state.
114

115. 115

116. 116

117. PRE OPERATIVE MEDICATION
& MANAGEMENT
• Patient BP should be monitored &
controlled within normal.
• To antihypertensive patient morning
dose of medication prior to surgery
must be given.
117

118. INTRAAND POST OPERATIVE
MANAGEMANT
• 1) Blood pressure should be monitored
continuously.
• 2) Patient cardiac status also monitored.
• 3) Antihypertensive must be continued.
• 4) If the procedure is performed under
local anesthesia , the local anesthetic
without adrenaline is to be used.
118

119. ORAL MEDICATIONS USED
FOR MANAGEMENT OF
HYPERTENSION
• Diuretics
• Beta-Adrenergic blockers
• Central acting adrenergic inhibitors
• Peripheral acting adrenergic inhibitors
• Non-selective alpha and beta adrenergic
blockers
• Vasodilators
• Angiotensin converting enzyme (ACE) 119

120. Diuretics
Thiazides and related sulfonamides
Mode of action:
- Increase the excretion of Na+, Cl-, and water by
interfering with the transport of sodium ions
across the renal tubular epithelium reduce
blood pressure by decreasing cardiac output
Representative agent:
- Hydrochlorothiazide
Side effects:
Xerostomia, increased thirst, orthostatic
hypotension, polyuria, dizzines 120

121. Loop diuretics (also called High-
efficiency diuretics)
Mode of action:
- Inhibit Na+ and Cl- reabsorption in the
descending limbs of the loop of Henle
- Enhance excretion of K+, Mg++, and Ca++.
- Reduce blood pressure by decreasing fluid
volume and thereby reducing cardiac output
121

122. Representative agents:
- Furosemide
- Ethacrynic acid
- Bumetanide
Side effects:
• Xerostomia, increased thirst, lichenoid drug
reaction, neutropenia, leukopenia, anemia,
orthostatic hypotension, renal failure
122

123. Potassium-sparing agents
Mode of action:
- Competitive antagonism of the endogenous
mineralocorticoid aldestrone change
- Reduce blood pressure by reducing total fluid
volume
Representative agents:
- Amiloride
- Spironolactone (Aldactone)
- Triamterene
123

124. Side effects:
• Xerostomia, increased thirst, gingival
bleeding (spironolactone) , lichenoid drug
reaction
124

125. Carbonic anhydrase inhibitors
Mode of action:
- inhibition of the enzyme carbonic anhydrase
in the proximal and distal segments of the
renal tubule so as to allow diuresis
- reduce blood pressure by decreasing fluid
volume and thereby reducing cardiac output
Representative agents:
- acetazolamide
- dichlorphenamide
- methazolamide
125

126. Side effects:
• Xerostomia, burning mouth, tongue,
lips, parasthesia, metallic taste, thirst
126

127. BETA-ADRENERGIC
BLOCKERS
Mode of action:
- Blocks beta-1 and beta-2 receptors
- By blocking beta-1 receptors, reduces rate of
SA node firing rate, slows the conduction
through AV node, and reduces contractile
strength and automaticity
- In the vascular system, reduce blood pressure
by reducing cardiac output and increasing
peripheral resistance
127

128. Representative agents:
• Acebutolol
• Atenolol
• Metoprolol
• Nadolol
• Penbutolol
• Pindolol
• Propranolol
• Timolol
128

129. Side effects:
• Orthostatic hypotension
• Xerostomia
• Sore throat
• Nasal stuffiness
• Asthma
• Drowsiness
• Depression
• Fluid retention
129

130. CENTRAL-ACTING
ADNERNERGIC INHIBITORS
Mode of action:
- Direct effect on alpha 2-adrenoceptor
(sympathetic vasomotor center in CNS), which
reduces impulses in sympathetic nervous
system
- Reduces blood pressure by decreasing
peripheral resistance and by decreasing plasma
renin levels
130

131. Representative agents:
• Clonidine (Catapres)
• Methldopa (Aldomet)
• Guanabenz
• Guanfacine
Side effects:
• Xerostomia, taste changes, salivary gland pain
or swelling, palpitation, ECG abnormalities,
insomnia, anxiety, drowsiness
131

132. PERIPHERAL-ACTING
ADRENERGIC INHIBITORS
Mode of action:
- Decrease total vascular resistance by
vasodilation of arterioles and veins, by
selective blocking of alpha 1-receptors on
vascular smooth muscle
Representative agents:
– Prazosin (Minipress)
– Terazosin (Hytrin)
132

133. Side effects:
• Xerostomia
• Orthostatic hypotension, postural dizziness
• Nausea, Gl upset
• Drowsiness, fatigue, weakness
• Anxiety, depression
133

134. NONSELECTIVE ALPHA- AND
BETA- ADRENERGIC
BLOCKERS
Mode of action:
- Competitive blocking of both α and ß-
adrenergic receptors (greater affinity for ß-
receptors) on vascular smooth muscle
- Decrease blood pressure by decreasing
peripheral vascular resistance
134

135. Representative agents:
• Labetalol
Side effects:
• Xerostomia, taste changes, orthostatic
hypotension, nausea, nervousness, anxiety,
depression, parasthesia, bronchospasm
135

136. VASODILATORS
Mode of action:
- Direct relaxation (vasodilation) of arteriolar
smooth muscle
- Decrease blood pressure by decreasing
peripheral vascular resistance
Representative agents:
• Hydralazine (Apresoline)
• Minoxidil (Loniten)
136

137. Side effects:
• Nasal congestion
• Lupus-like syndromes
• Leukopenia
137

138. ANGIOTENSIN-CONVERTING
ENZYME (ACE) INHIBITORS
Mode of action:
- Inhibits ACE preventing conversion of
angiotension I to angiotensin II, resulting in
dilation of arteriole, venous vessels
- Decrease blood pressure by removing the
vasoconstricting effect of ACE and thereby
decreasing peripheral vascular resistance
138

139. Representative agents:
• Captopril
• Enalapril
• Lisinopril
Side effects:
• Xerostomia, loss of taste, angiodema, glossitis,
oral ulceration (Stevens-Johnson syndrome -
captopril, enapril), lichenoid drug reaction,
renal insufficiency
139

140. Slow Channel Calcium-Entry
Blocking Agents
Mode of action:
- direct relaxation (vasodilation) of coronary
and peripheral arteriolar smooth muscles by
blocking Ca++ influx
Representative agents:
• Verapamil (Calan, Isoptin)
• Diltiazem
• Nifedipine
140

141. Side effects:
• Gingival hyperplasia, xerostomia,
orthostatic hypotension, light-
headedness, nausea, edema, flushing,
skin reactions, congestive heart failure
141

142. References
• Hall JE. Guyton And Hall Textbook Of Mrdical
Physiology. ELSEVIER, Inc. 13th edition.
Philadelphia; 2016
• JAIN AK. Human physiology for BDS,.
Avichal publishing company: 4th edition.
Delhi; 2010
• Barrett KE, Boitano S, Barman SM, Brooks
HL. Ganong’s Review of Medical Physiology.
The McGraw-Hill Companies Inc, : 23rd
edition; 2010
142

143. 143