2
Pressure = force/unit area
Blood pressure =
pressure exerted by blood
on the walls of the
heart or
blood vessels
What is B.P.?
3
PRESSURE falls
e.g. haemorrhage
same container;
same capacity;
less content
same content;
greater capacity
as the container
expands
Container vs. Content example
PRESSURE falls
e.g. generalized
vasodilation
4
GREATER PRESSURE
Arterial BLOOD VOLUME ∞ Arterial BLOOD PRESSURE
Since the arterial system is not very distensible
More blood
7
Functions of BP
• Intraventricular BP ejection of blood (stroke volume)
• Systemic arterial BP blood flow to tissues (tissue
perfusion)
• Capillary hydrostatic pressure filtration (tissue fluid
formation)
• Systemic venous BP blood flow back to the heart
(venous return)
The unconditional term
BLOOD PRESSURE
refers to
SYSTEMIC ARTERIAL
BLOOD PRESSURE
10
Systemic arterial blood pressure
= Cardiac output x Total peripheral resistance (TPR) or Systemic vascular reistance (SVR)
The 2 Major Determinants of Arterial B.P.
The other Determinants of Arterial B.P.?
11
Ventricular contraction
Ventricular relaxation Aorta is the most
elastic artery
When aortic elasticity
decreases (ageing or
disease):
Less expansion during
systole Incr. SBP
Less elastic recoil
during diastole decr.
DBP
Pulse pressure ?
12
• Stroke volume
• Aortic distensibility (elasticity)
DBP
• SBP
• Aortic distensibility
(elasticity)
• TPR
SBP = CO x TPR
DBP = CO x TPR
SBP
The Determinants of Arterial B.P.
Physiological Variations in BP
• Age: – SBP and DBP gradually rise with age (after about 30 years), the
SBP more so and more sustained than the DBP
• Sex: – the rise in BP with age is greater in males
• Circadian variation (diurnal variation): – lowest during sleep (nocturnal dip) and highest in the mornings after
waking up
• Increased transiently during physical stress (e.g. muscular exercise), mental stress(anger, apprehension, resentment, mental concentration), emotional excitement
• The effect of Gravity: When erect, BP in any vessel varies in relation to the vertical distance from the heart level
Physiological Variations in BP
• Gravity – In an upright position, BP
in the arteries below the heart level is increased, and that in the arteries above the heart level is decreased by 0.77 mm Hg for each cm of vertical distance below or above the heart.
– Thus, routine measurement of BP should be performed with the artery at the heart level.
Effect of Gravity
• Pressure in large artery in the
foot 105 cm below the heart =
[0.77 mmHg/cm x 105 cm = 80
mm Hg)] +
• 100 mm Hg (Mean ABP at heart
level)
• = 180 mm Hg
• Pressure in vein in the foot 105
cm below the heart = [0.77
mmHg/cm x 105 cm = 80 mm
Hg)] +
• 4 mm Hg (right atrial pressure)
• = 84 mm Hg
16
REGULATION OF SYSTEMIC ARTERIAL B.P.
– MAINTENANCE OF RESTING B.P.
B.P. HOMEOSTASIS
• SITUATIONAL ADJUSTMENT OF B.P.
e.g. changes in B.P. during muscular exercise
18
Systemic arterial blood pressure
= Cardiac output x Total peripheral resistance (arteriolar tone)
More immediate
More efficient:
RESISTANCE = 1
Radius
More economical
4
19
BP REGULATORY MECHANISMS
NEURAL: CARDIOVASCULAR REFLEXES
Baroreceptor reflexes
Chemoreceptor reflexes
Brain(CNS) ischaemic response
HORMONAL
Catecholamines
Renin-angiotensin-aldosterone(RAA) system
Vasopressin
RENAL-BODY FLUID CONTROL SYSTEM
Short term:
Rapid
Short term:
Intermediate
Long term
20
Receptors
Brain stem: Medulla
Spinal cord:
SYMPATHETIC
NERVOUS
SYSTEM
Integrating centres
Effectors
Hypothalamus
Afferents Efferents
X
(Parasym)
Vasopressin
Sym .outflow
• Baroreceptors
• Chemoreceptors
IX, X
(Parasym)
• Heart, Blood vessels
• Adrenal medulla: Catecholamines
• Kidney: activation of RAA system
21
Sympathetic Nervous System
• Major effector system for BP control
• Increased sympathetic tone incr. BP
• decreased sympathetic tone decr. BP
• Sym.N.S. is under the control of vasomotor
centre (VMC) in the medulla
• Descending tracts from the VMC excites the
sympathetic nervous system
• Inputs from the broreceptors and other receptors
go to the VMC (the integrating centre)
22
How does sympathetic N.S. activity
increase BP?
• Direct cardiovascular effects
• Neuroendocrine effects: activation of
– adrenal medulla
– renin-angiotensin-aldosterone (RAA) system
23
SYMPATHETIC
OUTFLOW
Sympathetic tone
HR SV Venoconstrictn Arteriolar constrictn
Venous return
CARDIAC OUTPUT TPR
Capillary pressure
ISF formation
Plasma loss
BLOOD PRESSURE
DIRECT CARDIOVASCULAR EFFECTS
24
SYMPATHETIC
OUTFLOW
Sympathetic tone
ADRENAL MEDULLA
BLOOD PRESSURE
JG CELLS IN KIDNEY
Secretion of
CATECHOLAMINES
CARDIOVASCULAR EFFECTS
Activation of
RENIN- ANGIOTENSIN-
ALDOSTERONE SYSTEM
VOLUME EFFECTS
NEUROENDOCRINE EFFECTS
25 BLOOD PRESSURE
CATECHOLAMINES
Noradrenaline Adrenaline Dopamine
a- receptors b- receptors
Vasoconstriction Cardiostimulatory effects:
Automaticity (SANodal
discharge)
Conductivity
Excitability
Myocardial contractility
TPR Cardiac output
Heart Rate
Stroke volume
26
Sympathetic tone
Juxtaglomerular(JG) cells in
afferent arteriolar muscle coat in KIDNEY
RENIN- ANGIOTENSIN-ALDOSTERONE SYSTEM
BLOOD
VOLUME/PRESSURE
Renal perfusion pressure
Baroreceptor reflex
Angiotensinogen Angiotensin I
ANGIOTENSIN II
RENIN
LIVER
Angiotensin-
Converting
Enzyme
Endothelial cells of
pulmonary circulation
VASCULAR and VOLUME EFFECTS
27
ANGIOTENSIN II
Vascular smooth muscle VASOCONTRICTION
Sympathetic nerve endings
Adrenal cortex
Facilitates release of
NORADRENALINE
Secretion of ALDOSTERONE
Brain: Hypothalamus
Stimulation
of THIRST
Release of VASOPRESSIN
Water intake
Renal reabsorption of Sodium
Renal reabsorption of Water BLOOD VOLUME
TPR
28
THE BARORECEPTOR REFLEX
operates within seconds
for moment to moment, day to day control
of BP
for BP homeostasis in the face of
challenges such as blood loss
Afferents: Parasympathetic
Efferents: Sympathetic noradrenergic
29
Baroreceptors = stretch receptors in the walls of
• Heart
Atria
• Arteries (arterial baroreceptors)
Aortic arch
Carotid sinus
Volume receptors
Low pressure baroreceptors
High pressure baroreceptors
BP
Wall
Stretch on
the wall
Stimulation of Stretch
receptors in the wall
32
Incr. baroreceptor discharge
• Stimulates the Parasympathetic centres
(Dorsal motor nucleus of vagus) in the
medulla
• Inhibits the vasomotor centre (VMC) in the
medulla (through inhibitory interneurones)
– Decr. excitatory discharge from the VMC to
the Sympathetic Nervous System in the spinal
cord
– decr. sympathetic noradrenergic discharge
33
Inhibits VMC stimulates motor vagal
nuclei
Parasym. fibres in IX and
X cranial nerves
Carotid sinus, aortic arch
35
HYPOTHALAMUS
POSTERIOR
PITUITARY VASOPRESSIN
Generalized vasoconstriction
(V1 receptors) TPR
Renal reabsorption of water
(V2 receptors)
plasma volume CARDIAC OUTPUT
BP
36
Note
• BP may not fall with minor haemorrhage
• Fall in venous return is detected by low pressure baroreceptors increase in TPR compensates for fall in CO BP unchnaged
• When blood loss is >20% of circulating blood volume, the fall in CO is great enough to cause a fall in BP
• BP = CO x TPR
38
Neural regulation of B.P.
Baroreceptor reflex
Chemoreceptor reflex
CNS ischaemic
response
120
100
80
60
40
B.P.
mmHg
BP BLOOD FLOW STAGNATION
O2 delivery to tissues (stagnant hypoxia)
CO2 uptake from tissues
O2 CO2 (in tissues)
Stimulation of chemoreceptors
•Stimulation of medullary respiratory centre
•Stimulation of medullary VMC
sympathetic discharge BP
IX, X
nerves
42
Medulla oblongata
VASOMOTOR
CENTRE
Spinal Cord
SYMPATHETIC
OUTFLOW
(+)
(+)
Sympathetic tone
BLOOD
PRESSURE
CEREBRAL
BLOOD FLOW
PO2
Stagnant
hypoxia
PCO2
CNS ISCHAEMIA
The CNS ischaemic response
43
CUSHING’S
REFLEX
VMC
SYMPATHETIC
OUTFLOW
(+)
(+)
Sympathetic tone
BLOOD
PRESSURE
CEREBRAL
BLOOD FLOW
PO2
Stagnant
hypoxia
PCO2
CNS ISCHAEMIA
Increased intracranial pressure
Pressure on cerebral arteries
BARORECEPTOR REFLEX
VAGAL TONE
HEART RATE
HEAD INJURY
Normal
44
Head injury CNS ischaemia The rise in BP
• Baroreceptor reflex
– stimulation of vagus fall in HR (since
parasympathetic control of HR is dominant
over sympathetic control)
– but baroreflex-mediated inhibition of VMC
is counterbalanced by direct stimulation of
VMC by CNS ischaemia
– sympathetic-mediated generalized
vasoconstriction maintained Incr. in BP
Slow, full and bounding pulse CUSHING’S REFLEX
45
Cushing's reflex
• Because the skull is rigid after infancy, intracranial masses or swelling may increase intracranial pressure. When intracranial pressure is increased sufficiently, regardless of the cause, Cushing's reflex and other autonomic abnormalities can occur.
• Cushing's reflex includes systolic hypertension, increased pulse pressure, and bradycardia.
46
Renal regulation of B.P.
I. Physical : by variation of Glomerular
filtration pressure variation in urine
formation
II. Hormonal : by secretion of renin
• Renin-Angiotensin (AGII)-
Aldosterone system (RAAS)
47
Renal regulation of B.P.
When blood volume and BP is increased,
KIDNEYS excrete excess fluid by
• Pressure diuresis
• Pressure natriuresis
increased urine formation as a result of increased
glomerular filtration due to raised renal perfusion
pressure
increased urinary excretion of sodium as a
result of increased glomerular filtration of
sodium due to raised renal perfusion pressure
48
Renal regulation of B.P.
When blood volume and BP is decreased:
decr. glomerular capillary H.P. decr.GFR
• Oliguria (deceased urine formation)
• Anuria (renal shutdown – no urine formation)
Thus KIDNEYS conserve ECF Volume
50
Summary :Systemic Arterial
Blood Pressure • Varies with the amount of blood in the systemic
arterial system (begins at the aorta, ends at
arterioles in various tissues)
• This is because the systemic arteries are not
very distensible
• The greater the cardiac output, the greater the
inflow of blood into the systemic arterial system,
the higher is the BP
• The greater the TPR, the lesser the outflow of
blood out of the systemic arterial system, the
higher is the BP
51
Systemic Arterial Blood
Pressure • Sympathetic nervous system and the RAA
system are powerful systems that can increase BP
• Moment to moment control is by baroreceptor reflex.
• What is the use of increasing the BP when blood supply to almost all tissues are shut down by arteriolar constriction?
• Ans. Local vasodilatory mechanisms in the vital organs- the brain and the heart, will overcome the systemic vasoconstrictor effect– diverting blood flow to them at the expense of other organs and tissues End