Recording of arterial blood pressure with special circulation - Coronary and cerebral circulation

1. RECORDING OF B.P
Direct method
Indirect method
METHODS
Indirect Methods
1. Palpatory method
2. Auscultatory method
3. Oscillatory method

2. Aneroid
sphygmomano
meter Simple mercury
sphygmomano
meter
Automated BP
device

3. 3
RECOMMENDED BLOOD PRESSURERECOMMENDED BLOOD PRESSURE
MEASUREMENT TECHNIQUEMEASUREMENT TECHNIQUE
2.
• The cuff must be level with heart.
• If arm circumference exceeds 33 cm,
a large cuff must be used.
• Place stethoscope diaphragm over
brachial artery.
2.2.
•• The cuff must be level with heart.The cuff must be level with heart.
•• If arm circumference exceeds 33 cm,If arm circumference exceeds 33 cm,
a large cuff must be used.a large cuff must be used.
•• Place stethoscope diaphragm overPlace stethoscope diaphragm over
brachial artery.brachial artery.
1.
• The patient should
be relaxed and the
arm must be
supported.
• Ensure no tight
clothing constricts
the arm.
1.1.
•• The patient shouldThe patient should
be relaxed and thebe relaxed and the
arm must bearm must be
supported.supported.
•• Ensure no tightEnsure no tight
clothing constrictsclothing constricts
the arm.the arm.
3.
• The column of
mercury must be
vertical.
• Inflate to occlude the
pulse. Deflate at 2 to
3 mm/s. Measure
systolic (first sound)
and diastolic
(disappearance) to
nearest 2 mm Hg.
3.3.
•• The column ofThe column of
mercury must bemercury must be
vertical.vertical.
•• Inflate to occlude theInflate to occlude the
pulse. Deflate at 2 topulse. Deflate at 2 to
3 mm/s. Measure3 mm/s. Measure
systolic (first sound)systolic (first sound)
and diastolicand diastolic
(disappearance) to(disappearance) to
nearest 2 mm Hg.nearest 2 mm Hg.
StethoscopeStethoscope
MercuryMercury
machinemachine

4. Palpatory methodPalpatory method
The radial pulse (the pulse at the radial artery in the
wrist) is palpated with the fingers of the left hand.

5. Auscultatory methodAuscultatory method
• The brachial pulse is palpated just above the
angle of the elbow (the "antecubital fossa").
• The diaphragm of stethoscope is placed over the
brachial artery in the space between the bottom
of the cuff and the crease of the elbow. At this
point no sounds should be heard

7. PRINCIPLE INVOLVED IN RECORDING
BLOOD PRESSURE

8. • At some point the personnel listening
with the stethoscope will begin to hear
sounds with each heartbeat. This point
marks the systolic pressure.
• The sounds are called “Korotkoff”
sounds.

10. Tapping sound 1SBP
110 mm Hg
Banging sound 3
Muffing sound 4
DBP-
95 mm Hg
85 mm Hg
120 mm Hg
Murmurish 2
80 mm Hg No sound 5
AUSCULTATORY METHOD (Korotkov sounds)
This method was introduced by a
Russian physician Korotkov

11. BASIS OF KOROTKOFF’SBASIS OF KOROTKOFF’S
SOUNDSOUND
Sounds are heard due to turbulenceSounds are heard due to turbulence
Cuff pressure > Systolic. P Lumen isCuff pressure > Systolic. P Lumen is
occluded No sounds are heard.occluded No sounds are heard.
Cuff pressure <just below> systolic .PCuff pressure <just below> systolic .P
Blood flow at height of systoleBlood flow at height of systole
Tapping soundTapping sound
Cuff pressure < diastolic.PCuff pressure < diastolic.P
Streamline flow No sounds.Streamline flow No sounds.

12. AUSCULTATORY GAPAUSCULTATORY GAP
A gap present afterA gap present after
tapping soundtapping sound
Seen in hypertensive patientsSeen in hypertensive patients..

13. Oscillometry methodOscillometry method

14. Invasive methodInvasive method
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15. PATHOLOGICAL VARIATION IN BP
1.Hypertension 2. Hypotension
Persistent
increase in
systemic arterial
B.P is known as
hypertension.
Normal - 120/80 mmHg.
Pre hypertension –
120-139/80-89mmHg
Stage I Hypertension-
140-159/90-99 mmHg
Stage II Hypertension-
>/160/100mmHg
Fall in B.P below
normal range is known
as hypotension.
Clinically, when
the
systolic blood
pressure is less
than 90 mm Hg, it
is considered
hypotension.

16. 04/15/1804/15/18
↑ BP is called Hypertension
(Above 140/90 mm of Hg )
Primary
(Essential 90%)
Secondary
(10%)

17. Hypertension
 Defined as an elevation of systolic
blood pressure
 Persistent hypertension very common
 30% of people over 50 are
hypertensive
 Never diagnosed on one reading
 Indication of cardiovascular disease
 Trauma
 Side effect of medication

18. Benign
Primary
Hypertension Malignant
Secondary
-Atherosclerosis
-Pheochromocytoma
-Cushing syndrome
-Glomerulonephritis
-Gestational
-Drug induced
White coat hypertension

19. Diseases Attributable to
Hypertension
Hypertension
Heart failure
Stroke
Coronary heart disease
Myocardial infarction
Left ventricular
hypertrophy
Aortic aneurysm
Retinopathy
Peripheral vascular disease
Hypertensive
encephalopathy
Chronic kidney failure
Cerebral hemorrhage
Adapted from: Arch Intern Med 1996; 156:1926-1935.
All
Vascular

20. 04/15/1804/15/18
Hypertension
Predisposing factors:
 Obesity
 Hereditary
 Alchoholism
 Stress
 Smoking
 Sedentary life

21. 04/15/1804/15/18
Secondary Hypertension
Causes:
 1.Renal-Acute & Chronic
Glomerulonephritis,Nephrotic syndrome
 2.Endocrine-
Cushings,Conns,Thyrotoxicosis,
Pheochromacytoma
 3.Vascular-Atherosclerosis
Arteriosclerosis

22. 04/15/1804/15/18
Secondary Hypertension
Causes:
 1.Renal-Acute & Chronic
Glomerulonephritis,Nephrotic syndrome
 2.Endocrine-
Cushings,Conns,Thyrotoxicosis,
Pheochromacytoma
 3.Vascular-Atherosclerosis
Arteriosclerosis

23. COMPLICATIONS OFCOMPLICATIONS OF
HYPERTENSIONHYPERTENSION
Renal failure
LVH
MI
Cerebral
haemorrhage
Retinal
haemorrhage

24. 04/15/1804/15/18
Treatment of Hypertension
Modification of lifestyle:
 Cessation of smoking.
 Moderation in alcohol intake.
 Weight reduction.
 Programmed exercise.
 Reduction in Na+
intake.
 Diet high in K+
.
 Relaxation technique – Yoga, TM

25. 04/15/1804/15/18
Treatment of Hypertension
 Medications:
 Diuretics:
 Increase urine volume.
 Beta-blockers:
 Decrease HR.
 Calcium antagonists:
 Block Ca2+
channels.
 ACE inhibitors:
 Inhibit conversion to angiotensin II.
 Angiotension II-receptor antagonists:
 Block receptors.

26. MANAGEMENT OFMANAGEMENT OF
HYPERTENSIONHYPERTENSION
Non drug therapy
Stop smoking
Control obesity
Regular exercise
Decrease salt
intake
Drug therapy
Beta blockers
Calcium channel
blockers
Vasodialators
Diuretics
ACE inhibitors
VMC depressors

27. HYPOTENSIONHYPOTENSION
Fall in B.P below normal range is known as
hypotension.
TYPES
Primary/Essential hypotension.
Secondary hypotension.
-MI
-Hypoactivity of pituitary gland
-Hypoactivity of adrenal gland
-Tuberculosis
Orthostatic hypotension

28. Hypotension
 Defined in adults as a
systolic pressure below
100mm Hg
 Rarely treated in this
country

29. 04/15/1804/15/18
↓ BP is called Hypotension
(Below 90/60 mm of Hg)
1. Hemorrhage
2. Dehydration
3. Vomiting
4. Diarrhea
5. Excessive
sweating
6.Adissons disease
7.Hypothyroidism

30. Prevention
 Reduce the risk of developing High Blood
Pressure by making lifestyle changes…..
 Eat a healthy , well balanced diet
 Reduce salt and fat intake
 Exercise regularly
 Stop smoking
 Reduce alcohol and caffeine consumption to
recommended levels
 Reduce weight

31. TREATMENT OFTREATMENT OF
HYPOTENSIONHYPOTENSION
Correct the underlying etiology.
Orthostatic hypotension
Change to supine position with head
below the heart level & leg raised.

32. 04/15/1804/15/18
Treatment of Hypotension
Treat the cause
Blood transfusion
I.V. Fluids
Vasoconstrictors

33. 04/15/1804/15/18
RECAP
At the end of this class, you should able to
recall.
1. Definition of Blood Pressure
2. Its variations.
3. Measurement - Korotkov sound
4. Factors contributing to B.P
5. Peripheral resistance
6. Regulation of BP
7. Immediate regulation
8. Short term regulation
9. Long term regulation.
10. Applied - Hypertension - Hypotension

35. The blood flow to individual organs must vary
to meet the needs of the particular organ as
well as of the whole body

36. Neural, myogenic, metabolic, and
endothelial
mechanisms control regional blood flow
Local or regional circulation of tissue blood flow is
controlled in two phases
Acute and chronic
1. Vasodilator theory-
special role of
adenosine
2. Oxygen lack
theory/ nutrient lack
theory
1. Autoregulation
2. Endothelial derived
relaxing (NO)and
constricting
factors(endothelin)
1. Change in tissue vascularity
2. role of oxygen
3. endothelial derived vascular
growth factors

37. Coronary Circulation

43. RCA
→ post. Interventricular branch
→ marginal br..
.LCA
→ Ant. Interventricular branch
→ circumflex

44. Two coronary arteries(Rt & Lt)
Arises from the root of aorta Supply blood to myocardium.

52. Phasic changes in coronary blood flow
Myocardial blood flow depends upon
- pressure head i.e. aortic pressure
- resistance offered to blood flow during
various phases of cardiac cycle.

53. Characteristics of coronary Circulation
O2 consumption of myocardium
• Very high - @ 8 ml / 100 gm / mt at rest
• Other tissues extract 25% O2/ unit of blood
• But myocardium extract 70-80% O2/ unit of
blood
• During exercise O2extraction reaches to 100 %
& B. flow also increases.

54. Coronary circulation cont…..

55. Two coronary arteries(Rt & Lt)
Arises from the root of aorta Supply blood to myocardium.

58. Perfusion of cardiac muscle from
epicardium –endocardium

65. Heart utilize varieties of substances for
metabolism
Free fatty acid, pyruvates, glucose,
lactate, ketone bodies and amino acids.
More than 60% of myocardial O2 consumption in the
fasting state is due to the oxidation of fatty acids.
When the O2 supply is adequate, the heart takes up and
oxidizes both lactate and pyruvate, as do red (i.e.,
oxidative) skeletal muscle fibers, although the arterial
concentration of pyruvate is usually low.

66. Characteristics of coronary Circulation
1-Blood flow variations in coronaries
- In 50% individuals RCA has greater flow
- In 20% LCA, &
- In 30% flow is equal in both LCA &RCA
• Normal blood flow at rest – 250 ml ( 70ml / 100 gm / mt )
– @ 5% of CO
• During exercise – 3-6 fold increase in flow
• LV blood flow – 80 ml / 100 gm / mt
• RV blood flow – 40 ml / 100 gm / mt
• LA blood flow – 20 ml / 100 gm / mt
• RA blood flow – 10 ml / 100 gm / mt

68. Comparison of oxygen supply & consumption by
myocardium and other body tissues
Oxygen content Other tissues Myocardium
- Arterial 19 ml % 19 ml %
- Venous 14 ml % 06 ml %
AV Difference 05 ml % 13 ml %
Coefficient of O2 utilization 5/19 x100 13/19 x 100
= 26 % = 69%
O2 saturation of venous blood 14/19 x100 06/19 x 100
= 74 % = 31 %
pO2 40 mm Hg < 20 mm Hg

69. 2- Phasic Changes in coronary
blood flow

70. 2-Phasic changes in coronary blood flow
Myocardial blood flow depends upon
- pressure head i.e. aortic pressure
- resistance offered to blood flow during
various phases of cardiac cycle.

73. Systolic compression has more effect on BF in the endocardial layer
CBF is 10-30% of that during Cardiac diastole

74. Blood flow to LV during systole
• Like sk. Muscle myocardium
compresses coronary vessels
during systole.
• LV pressure (121) > aortic pr.
(120).
• So LV blood flow practically
ceases to LV (max during
isovolumetric contraction
phase) especially in
subendocardial portion. So this
part is prone to ISCHEMIC
changes.
• Epicardial parts do receive some
B. flow during systole.

75. Blood flow to LV during diastole
• Myocardial
muscles relax
during diastole &
B.flow rises(max
during
isovolumetric
relaxation phase)
• Aortic pr. > LV pr.
so blood flow rises

76. Right coronary blood flow
Left coronary blood flow
* The peak left coronary flow
occurs at the end of isovolumetric
relaxation
*

78. Blood flow to RV, RA & LA
• Rt. coronary blood flow shows similar phasic
changes as in Lt. coronary A.
• Pressure in aorta > RV & in aorta > RA during
systole so coronary flow in these three parts
is not appreciably reduced.
• Thus blood flow to RV, RA & LA occurs both
during systole & diastole.

86. Applied aspects
• Subendocardial parts are more prone to ischemic
changes as during systole blood flow ceases to LV
• In AS (aortic stenosis) LV pressure > aorta causing
severe compression of coronaries.during systole
leading to ischemic changes.
• In CHF, venous pr. > aortic pr. In diastole causing
decreased coronary perfusion pr. & low coronary
blood flow.

89. Regulation of coronary blood flow
Three mechanisms
. Local control mechanism
2.Nervous control mechanism
3. Neuro - hormonal control
ANS control CBF

90. 1. Local control mechanism
 a. Autoregulation
 b. Role of local metabolites
 c. Role of endothelial cells

92. a. Autoregulation
It is the ability of tissues/organ to maintain a
relatively constant blood flow over a wide
range of arterial blood pressure.
By
Adjusting vascular resistance according to
changes in arterial pressure.

93. Autoregulation
Autoregulation is well developed in –
- Kidney
- Heart
- Brain
- Sk. Muscles & mesentary

95. a. Autoregulation
Two mechanisms –
(i) Metabolic theory
↓ BP → ↓ B. flow → ↑ local accumulation of
vasodilator subs. e.g.CO2,
B.flow comes H+, adenosine, NO, PG,
to normal K+, PO4--, ↑ O2
↓ resistance art. dilatation

96. a. Autoregulation
(ii) Myogenic theory
Vascular smooth muscles respond to wall
tension depends on art. Pressure & radius.
↑ BP → ↑ stretching of wall → VSM contracts
↓
↓ BP ← ↓ B. flow ← narrowing of lumen

97. Reactive hyperemia
 Defined as increased blood flow to the
organ/tissues after the removal of blockage
in a previously blocked artery.
 Magnitude of reactive hyperemia depends
on – duration of occlusion
 Cause of R. hyperemia – adenosine
release

98. b. Role of local metabolites
 At rest myocardium extracts 60 - 70 % O2
from Hb.
 So not much additional O2 can be provided to
myocardium unless blood flow increase due to
vasodilation.
 Cause of vasodilation – Adenosine release in
hypoxic states. Most imp. factor
 B. flow ↑ ― myocardial O2 consumption ↑(linear
relation)

99. b. Role of local metabolites
 Direct effect of ↓ pO2 on arterioles
vasodilation
 Role of other metabolites - H+
, NO, PG,
adenosine, CO2 etc. are vasodilators.

101. c.Role of endothelial cells
 Endo. Cells release several vasodilators
e.g. EDRF, prostacyclin (PGI2) & EDHF
 Endo. Cells also release several
vasoconstrictors e.g. endothelin-1(ET-1),
Angiotensin II, EDCF.

102. 2. Nervous control
 ANS control CBF –
a. Directly
b. Indirectly
a. Direct nervous control is exerted via
symp. & parasymp effects on coronary
vessels.
b. Indirect nervous control is exerted via
symp. & parasymp effects on heart.

103. Direct nervous control
 Parasymp.nerves to coronaries are too less there
fore have a negligible effect.
 Symp. Nerves extensively innervates coronary
vessels.
 Receptors – α- present mainly on epicardial vessels
β- present mainly on intramuscular
vessels
 NT - NE reacts with α → vasoconstriction
- E reacts with β → vasodilation
 Net effect is vasodilatation

104. Indirect Nervous control
 Through action on heart
 Symp. Stimulation → ↑ HR & force of contr
↓
↑B. flow ← ADP cause ← ADP ← ATP
vasodilation conversion
 Parasymp. Stimulation produce opp. effect

105. 3. Neuro – hormonal control
 ATP → vasoconstriction (P1 receptors)
→ vasodilation (P2 receptors)
 NPY (neuropeptide Y) → vasoconstriction
 CGRP (calcitonin gene related peptide)
&
 Substance P → vasodilation

109. Special Features of coronary Circulation
1. Receive -5 % of C.O i.e. 225ml/min.
2. Distribution of coronary arteries blood flow varies
3. Heart receives major blood supply during diastole
4. the coronary arteries are end arteries i.e. phasic blood flow
5. Metabolic regulation is well developed and show autoregulation
6. There is adequate coronary blood flow reserve
7. Major source of energy is free fatty acids (1/3)
8. Heart muscles extract about 80 % of oxygen from arterial blood, AV
difference is high even at rest.

111. Coronary Artery Disease
blood flow Myocardial ischemia
(“angina pectoris” means chest pain)
Accumulation of ‘P’ factor
If myocardial ischemia prolong and severe, results in
myocardial infarction (Heart Attack)
main factors coronary atherosclerosis
Fatty deposits build up in blood vessel walls and
narrow the passageway for the movement of blood.
The resulting condition, called atherosclerosis often leads
to eventual blockage of the coronary arteries and a “heart
attack”.

113. Risk factors for CAD include:
Coronary artery disease is one of the most common -
 Serious effects of aging,
 Gender,
 Haemostatic factors,
 Diabetes,
 Alcohol intake,
 Hypertension ,
 Family history,
 Hypercholesterolemia,
 Stress
 Homocysteine etc.

114. Coronary Artery Disease

116. Myocardial Infarction (Heart Attack)
Blockage more then 75%
Results in Cell death or infarction occurs
Fig:-
Acute
Myocardial
Infarction
(AMI )

117. Acute Myocardial
Infarction
(AMI )
Severe Chest pain
That radiates along
the ulnar border of
the upper arm, arm
and hand
With
excessive
sweating

118. 15/04/18 118
Diagnosis
Acute Myocardial Infarction (AMI )
ECG- Elevated ST segment
Plasma enzymes- elevated levels of enzymes –
Creatine kinase (CK-MB) and Lactate
dehydrogenase (fraction 1 of LDH)
 Typical clinical presentation –
Severe Chest pain With excessive sweating

119. Treatment-
Vasodilators -Nitrates (Nitroglycerine)
Streptokinase, TPA
Coronary angioplasty
Calcium channel blockers (Verapamil)
Antiplatelet aggregating agents- Low dose of aspirin
Folic acid and Vitamin B12- inhibits homocysteine
and convert it methionine a non toxic agent
 surgical by coronary artery bypass graft (Aortic
CABG)

121. Important notes of Cerebral blood flow and metabolism
Brain tissue is highly sensitive to hypoxia- Brain need
continuous blood flow.
Interruption of blood flow only for 5-20 seconds causes a
loss of consciousness.
Circulatory arrest for only 3-4 minutes results in
irreversible brain damage.
 utilizes glucose as main fuel which is independent of
insulin
(except ventro-medial hypothalamus)

122. SPECIAL FEATURES OF
CEREBRAL BLOOD FLOW:
Brain has a very rich blood supply.
Normal blood flow to brain (less than 2% of the body
weight) 15% of the CO (750 mL/min) or 50–55 mL
blood/100 g tissue/min.
 When cerebral blood flow falls below 18 mL/100 g
tissue/ min (critical flow level), there occurs
unconsciousness.

123. 
 Total O2 consumption of the brain is
40-50 mL/min (3.3 mL/100 g tissue/min), i.e.
20% of the whole body at rest.
 O2 consumption of grey matter (GM) is
much more than the white matter, possible
because of high density of capillary network.
SPECIAL FEATURES
conti…

124.  Cerebral arteries are end arteries and
 Brain present in rigid cage so intracranial
content is incompressible therefore increase
cerebral blood flow associated with
comparable increase in venous outflow
 Volume of fluid and ECF remains constant
Monrokellie Doctrine
At any given time total blood volume, CSF voume and
brain tissue in the cranial cavity remains constant
SPECIAL
FEATURES
conti…

125.  Capillaries are non - fenestrated and surrounded by
end feet process of astrocytes forming BBB.
 Very tight junction between endothelial cells of
capillaries.
SPECIAL FEATURES conti…

126. Cerebral blood vessels and
circulations

127. Arterial supply - 3 Pairs of cerebral arteries

128. Circle Of Willis

129. Arteries to the
Brain
“Putting it all
Together”
Arteries to the
Brain
“Putting it all
Together”
CEREBRAL BLOOD VESSELS
Arterial supply -3 Pairs of cerebral arteries
CAROTID
SYSTEM
Two internal carotid a.
CAROTID
SYSTEM
Two internal carotid a.
VERTEBROBASILAR
SYSTEM
2 vertebral a.
VERTEBROBASILAR
SYSTEM
2 vertebral a.

130. Overview of arterial cerebral circulationOverview of arterial cerebral circulation
CAROTID SYSTEM
70%
CAROTID SYSTEM
70%
VERTEBROBASILAR
SYSTEM 30%
VERTEBROBASILAR
SYSTEM 30%

131. Overview of cerebral circulation

132. Each artery give rise to two set of branches
Cortical branches
Ramify on the surface of the
Cerebral hemisphere and
Supply the cortex.
Central or perforating branches
Pass deep into the substance of
the cerebral hemisphere to
supply the structure within it.
Consist of six main groups.

133. Deep brain structures
Arteries of cerebral
haemorrhage

134. VENOUS DRAINAGEVENOUS DRAINAGE

135. Cerebral VeinsCerebral Veins
• Drain the cortex
and subcortical
white matter.
• Drain the substance
of the brain including
basal ganglia,and
diencephalon.
Both superficial and deep veins communicate by
anastomotic veins.
Both superficial and deep veins communicate by
anastomotic veins.
Superficial veins :
(sinuses)
Superficial veins :
(sinuses)
Deep veins:Deep veins:

136. Venous drainage at a glanceVenous drainage at a glance

137. Innervation of cerebral blood vessels
• arteries & arterioles supplied with
• Sympathetic fibers . (superior Cervical Ganglia)
NT is NE,NeuropeptideY.
• Para sympathetic fibres- (Sphenoplantine ganglia)
Cholinergic neurons. NT is
Ach,VIP,PHM27.
• Sensory fibers (trigeminal ganglia) are also
present in distal arteries
• Touch & pull of these vessels cause pain (no pain
fibers)
• arteries & arterioles supplied with
• Sympathetic fibers . (superior Cervical Ganglia)
NT is NE,NeuropeptideY.
• Para sympathetic fibres- (Sphenoplantine ganglia)
Cholinergic neurons. NT is
Ach,VIP,PHM27.
• Sensory fibers (trigeminal ganglia) are also
present in distal arteries
• Touch & pull of these vessels cause pain (no pain
fibers)

138. REGULATION OF
CEREBRAL BLOOD
FLOW

139. Cerebral blood flow depends on
REGULATION OF CEREBRAL BLOOD FLOW
The perfusion pressure
which determines cerebral
blood flow
is the difference between
the mean arterial pressure
at the head level and the
internal jugular pressure
(cerebral venous pressure).

140. Phenomenon of Auto regulation
• Between MAP 65-140mm Hg blood flow of
brain remain constant

141. • If BP<60mmHg cerebral blood flow is
extremely compromised syncope.
• If BP>140mm Hg disruption of blood
brain barrier, cerebral edema or Hemorrhage
may result
• Both Metabolic theory & Myogenic theory of
autoregulation are considered.
• In metabolic theory main regulating substance
of cerebral blood flow is pco2
• If BP<60mmHg cerebral blood flow is
extremely compromised syncope.
• If BP>140mm Hg disruption of blood
brain barrier, cerebral edema or Hemorrhage
may result
• Both Metabolic theory & Myogenic theory of
autoregulation are considered.
• In metabolic theory main regulating substance
of cerebral blood flow is pco2

142. Intrinsic Regulation of Blood Flow
(Autoregulation)
Intrinsic Regulation of Blood Flow
(Autoregulation)
• Maintains fairly constant blood flow despite BP
variation
• Myogenic control mechanisms occur in some
tissues because vascular smooth muscle contracts
when stretched & relaxes when not stretched
– E.g. decreased arterial pressure causes cerebral vessels
to dilate & vice versa
• Maintains fairly constant blood flow despite BP
variation
• Myogenic control mechanisms occur in some
tissues because vascular smooth muscle contracts
when stretched & relaxes when not stretched
– E.g. decreased arterial pressure causes cerebral vessels
to dilate & vice versa

143. Intrinsic Regulation of Blood Flow (Autoregulation) continued
• Metabolic control mechanism matches blood
flow to local tissue needs
• Low O2 or pH or high CO2, adenosine, or K+
from high metabolism cause vasodilation
which increases blood flow
• Metabolic control mechanism matches blood
flow to local tissue needs
• Low O2 or pH or high CO2, adenosine, or K+
from high metabolism cause vasodilation
which increases blood flow
14-40

144. The auto regulation of cerebral blood flow is seen only when the
arterial pco2 & po2 are maintained at their normal values
The auto regulation of cerebral blood flow is seen only when the
arterial pco2 & po2 are maintained at their normal values

145. Effect of Pco2
Effect of Pco2
• Physiologically partial pressure of co2 is most
potent vasodilator of cerebral blood vessels.
• With in arterial Pco2there occurs a linear in
cerebral blood flow.
• However when Pco2 increases above 80mmHg
no further in cerebral blood flow (due to
max. dilatation)
• When Pco2 is below 20mmHg no further
in cerebral blood flow
(due to vasoconstriction)
• Physiologically partial pressure of co2 is most
potent vasodilator of cerebral blood vessels.
• With in arterial Pco2there occurs a linear in
cerebral blood flow.
• However when Pco2 increases above 80mmHg
no further in cerebral blood flow (due to
max. dilatation)
• When Pco2 is below 20mmHg no further
in cerebral blood flow
(due to vasoconstriction)

146. Effect of Pco2
Effect of Pco2
• A rise of Pco2 of 1mmHg above normal range,
increases cerebral blood flow by 3ml/100gm/min
• A fall of Pco2 of 1mmHg below normal range
decreases cerebral blood flow by 1.5ml/100gm/min
• Effect of Co2 is mediated via change in Ph.
• A rise of Pco2 of 1mmHg above normal range,
increases cerebral blood flow by 3ml/100gm/min
• A fall of Pco2 of 1mmHg below normal range
decreases cerebral blood flow by 1.5ml/100gm/min
• Effect of Co2 is mediated via change in Ph.

147. Maintaining cerebral blood flow
CBF regulated by levels of CO2 and H+
in arterial
blood
Increase in CO2 / H+
/ decrease O2 :
- vasodilation occurs
- increases blood flow
Normally CBF constant
More active regions of brain receive increased
blood flow
E.g. during exercise motor areas receive increased
blood flow at expense of other areas
Why? Because of increase in levels of CO2 / H+
and decrease in O2 in those areas.
Maintaining cerebral blood flow
CBF regulated by levels of CO2 and H+
in arterial
blood
Increase in CO2 / H+
/ decrease O2 :
- vasodilation occurs
- increases blood flow
Normally CBF constant
More active regions of brain receive increased
blood flow
E.g. during exercise motor areas receive increased
blood flow at expense of other areas
Why? Because of increase in levels of CO2 / H+
and decrease in O2 in those areas.

150. Increased Intracranial Pressure
The effects of an increase in ICP can be more
serious than condition causing it.
An increase in ICP can:
- disrupt blood supply
- distort shape of brain
Causes of increased ICP:
- Expanding lesions, e.g haematoma, tumour
-Hydrocephalus,
-i.e. accumulation of excess CSF
Increased Intracranial Pressure
The effects of an increase in ICP can be more
serious than condition causing it.
An increase in ICP can:
- disrupt blood supply
- distort shape of brain
Causes of increased ICP:
- Expanding lesions, e.g haematoma, tumour
-Hydrocephalus,
-i.e. accumulation of excess CSF
Role of Intracranial Pressure

151. Effect of intracranial pressure changesEffect of intracranial pressure changes
ICP – Intracranial pressure
CPP- effective cerebral perfusion pressure
• Any change in ICP causes change in venous pressure

154. Clinical importance
Stroke - Two types
Ischemic Hemorrhagic
Blockage Rupture
mainly branch of Thromboembolism
middle Cerebral a.
Treatment- Fibrinolytic drugs
- Antiexitotoxic drugs Decrease glutamate
conc. locally

155. Cause- arteriosclerotic plaques in
arteries in brain
Clotting mechanism
Clot formation
Block artery
Acute loss of brain function in a
localized area

156. Rupture of
branch of
cerebral
artery

157. Effect of negative gEffect of negative g
• If the body is accelerated downwards, force
acting towards the head increases arterial
pressure at head level
• ICP also rises, so the vessels are supported
and do not rupture
• If the body is accelerated downwards, force
acting towards the head increases arterial
pressure at head level
• ICP also rises, so the vessels are supported
and do not rupture

158. CSF occupies @ 10% of the intracranial volume with a pressure between 0 to
7mmHg .when CSF volume
CSF occupies @ 10% of the intracranial volume with a pressure between 0 to
7mmHg .when CSF volume
• CSF gets displaced into the
spinal canal. This mechanism
provides @ 65% of
compensatory capacity of the
rigid skull.
• Beyond this even small increase
in CSF volume causes marked
in ICP
• CSF gets displaced into the
spinal canal. This mechanism
provides @ 65% of
compensatory capacity of the
rigid skull.
• Beyond this even small increase
in CSF volume causes marked
in ICP