Regulation of ABP magdi sasi 2018

REGULATION OF BLOOD PRESSURE
DR. MAGDI AWAD SASI
MAGDI AWAD SASI 2018 LIMU

Objectives

Blood Pressure
 Contraction of ventricles
generates blood pressure
 Systolic BP – highest pressure
attained in arteries during
systole
 Diastolic BP – lowest arterial
pressure during diastole
 Pressure falls progressively
with distance from left
ventricle
 Blood pressure also depends
on total volume of blood

Arterial blood pressure
It is the lateral pressure of the blood exerted on the arterial wall.
The systolic blood pressure is the maximum pressure reached during ventricular
systole ranges from 90 - 140 mmHg with average 120 mmHg.
the diastolic blood pressure is the minimal pressure reaches in the arteries during the cardiac
diastole, ranges from 60 - 90 mmHg with an average value of 80 mmHg.

Arterial Blood Pressure(continued)
■ Diastolic pressure is more important, because diastolic period is
longer than the systolic period in the cardiac cycle.
■ Pulse pressure = Systolic BP – Diastolic BP.
■ Mean arterial pressure = Diastolic BP + 1/3 Pulse press.
In normal adult  120/80 mmHg.

If the blood pressure drops suddenly, 2 problems confronts the pressure
control system :
1-The first if Survival :
To return the arterial pressure immediately to near a normal level that the
person can live trough the acute episode.
2-The second is to return the blood volume eventually to its normal level :
So that the circulatory system can re-establish full normality Including
return of the arterial pressure back to its normal value.

Control of blood pressure
 BP = CO x TPR (compare Ohm’s law)
 Cardiac output is controlled by sympathetic and para sympathetic
nerves which effect:
 heart rate
 force of contraction
 TPR controlled by nervous and chemical means to effect
constriction/dilatation of arterioles and venules

DETERMINANTS OF ARTERIAL BLOOD
PRESSURE

Q) What are the factors that maintain the ABP?
ABP = COP x TPR = SV x HR x TPR
 1. Stroke volume:
 2. Heart rate
 3. TPR
which depend on :
a-Arteriolar diameter.
b-The blood viscosity.
c-The blood volume .
d-Elasticity of aorta and big arteries which prevent excessive elevation of
the systolic pressure maintain the diastolic BP by its elastic recoil .

FACTORS CONTRIBUTING
TO BLOOD PRESSURE
1 Cardiac output-VR,HR,FOC—S.P
2. PERIPHERAL RESISTANCE
Elasticity
Viscosity
Velocity
Length of BV
Extra vascular
compression
Radius of BV
DP

REGULATION OF ARTERIAL BLOOD PRESSURE
Immediate mechanism
Short term mechanism
Long term mechanism

Immediate Regulatory Mechanisms:
Neural mechanisms
1. Baro-receptor reflexes
2. Chemo receptor reflexes
3. Cerebral ischemic response

VCC
(in M.O)
LHC
VMC
VDC
---
+++
Cardiac centres
CAC CIC
Heart
and
blood vessels

VCC
(in M.O)
LHC
VMC
VDC
---
+++
Cardiac centres
CAC CIC
Heart
and
blood vessels
sympathetic
Vagal stimulation
Pressor area
Depressor area

Brain stem cardiovascular centers
 Localized in reticular formation of medulla and lower 1/3 of the Pons.
 Information from IX and X nerves is integrated in nucleus tractus solitaries and
redirected to:
A. Cardiac accelerator center – SNS – SA node (increase heart rate, conduction
velocity through the AV node, contractility)
B. Cardiac decelerator center – PNS – n. vagus – SA node – decrease heart rate
C. Vasoconstrictor center – SNS – vasoconstriction of arterioles and venules

Role of cardiovascular center (CV)
 Site ---In medulla oblongata
 Action ---Helps regulate heart rate and stroke volume
 Divisions-----
a. Cardio-stimulatory and cardio-inhibitory centers
b. Vasomotor center control blood vessel diameter
 Contents---Groups of neurons regulate heart rate, contractility of
ventricles, and blood vessel diameter
 Also controls neural, hormonal, and local negative feedback systems that
regulate blood pressure and blood flow to specific tissues
 Receives input from both higher brain regions and sensory receptors

Brain stem regions of CV control
Area postrema
Nucleus tractus solitarius
Nucleus ambiguous
Cardiac decelerator center
Caudal ventrolateral Medulla
Fibers from this neurons project to the
vasoconstrictor area and inhibit it

CV Center

Control of blood pressure
Outline
 Short term control (baroreceptors)
 Location
 Types of baroreceptor
 Baroreceptor reflex
 Other stretch receptors
 Long-term control
 Renin/ angiotensin/ aldosterone system
 Vasopressin
 Atrial natiuretic peptide

Baroreceptors
• Baroreceptors are mechanoreceptors – sensitive to changes in pressure or
stretch
• located within the walls of the carotid sinus and the aortic arch
• Located in highly distensible regions of the circulation to maximise sensitivity
– Carotid sinus - afferent IX. C.N.
– Aorctic arch – (increase in arterial pressure) X. C.N.
– cardiovascular vasomotor centers in the brain stem
• Baroreflex - fast regulation – via changes in the output of sympathetic and
parasympathetic NS

Baroreceptors reflex:
 BP
+ Baroreceptors
= V.M.C ++ C.I.C
= Sympathetic
Vasodilatation &  TPR
+ Parasympathetic
Slowing of SA node ( HR)
&  CO

Increase
in ABP
decreased
sympathetic
outflow
Decrease
of heart rate
Increased
parasymp.
outflow
Stimulation
of NTS
Activation of
baroreceptors
Increase firing
rate in IX., X.
vasodilatation
decrease
of heart rate
contractility
Increased
activity
of NA
Decreased
activity
CAC
Decreased
activity
VC
CAC - cardiac accelerator center, VC – vasoconstrictor center
cardiac decelerator center

BARO RECEPTOR REFLEXES (MAREY’S REFLEXES)
BP

Stimulation of baroreceptors
(carotid sinus and aortic arch)

Tractus solitarius stimulation
Inhibition of VMC Stimulation of CIC
(nucleus ambiguous)
SNS Vagus
 Symp tone Vagal tone 
Blood Vessels Heart Rate Decreased
- Vasodilatation
- Venodilatation Bradycardia
BP

Net effect
 Peripheral resistance
 Myocardial contractility
 Heart rate (Bradycardia)
 Fall in BP
BARORECEPTOR REFLEX

Baroreceptor output
(from single fibres)
Rapid decrease in mean pressure
Rapid increase in mean pressure
Response to pulse pressure

Two types of baroreceptor
 Type A
 High sensitivity
 High firing rate
 Type C
 Lower sensitivity
 Lower firing rate
 Higher threshold (before firing starts)
 Therefore can deal with higher pressures
than type A which become “saturated”
From “An Introduction to Cardiovascular Physiology”
J.R. Levick

Baroreceptor reflex
Blood pressure falls
Aortic arch Carotid sinus
Constriction of veins
& arterioles
Increased stroke
volume
Increased heart
rate
Vasoconstriction Cardiac stimulation Cardiac inhibition
Increased peripheral
resistance
Increased cardiac
output
Increased blood pressure
Neural integration
Sensors
Effectors

Rapidly Acting Control Mechanisms:
Acts within. seconds / minutes. [ Fast Response ( S h o r t - T e r m ) ]
Concerned by regulating Cardiac output & Peripheral resistance.
Reflex mechanisms that act through autonomic nervous system:
Centers in medulla oblongata:
• Vasomotor Center (VMC) … Sympathetic nervous system.
• Cardiac Inhibitory Center (CIC) .. Parasympathetic nervous system

Effects of Rapidly Acting Pressure Control Mechanisms :
1. To cause constriction of the veins and provide transfer of blood into the heart.
2. To cause increased heart rate and contractility of the heart and provide greater
pumping capacity by the heart.
3. To cause constriction of the peripheral arterioles to impede the flow of the blood
out of the arteries.
All these effects occur almost instantly to raise the arterial pressure back into a survival
range

Other stretch receptors
 Coronary artery baroreceptors
 Respond to arterial pressure but more sensitive than carotid and aortic ones
 Veno-atrial mechanoreceptors
 Respond to changes in central blood volume
 Lie down, lift your legs and cause peripheral vasodilatation
 Unmyelinated mechanoreceptors
 Respond to distension of heart
 Ventricular ones during systole; atrial ones during inspiration

Location of receptors in and near the heart
From “An Introduction to Cardiovascular Physiology” J.R. Levick
Spinal cord
Baroreceptors in
coronary arteries and
aortic arch
Sympathetic afferents & unmyelinated nociceptors
Cardiac pain
Cardiac vagal afferents
unmyelinatedmyelinated

Overview of short-term control mechanisms
MAGDI AWAD SASI 2018 LIMUFrom: Introduction to Cardiovascular physiology. J.R. Levick. Arnold 4th edition

Importance of the baroreceptor reflex :
 To keep the arterial pressure relatively constant in the rang of (70 mmHg -150 mmHg ),
maintain the mean blood pressure at about 100 mmHg
 Pressure buffer system – reduce the blood fluctuation during the daily events, such as
changing of the posture
 Baroreceptor Resetting :
 Baroreceptor will adapt to the long term change of blood pressure.
 If the blood pressure is elevated for a long period of time, several days or years, the set
point will transfer to the elevated mean blood pressure.
 That makes the baroreceptor system unimportant for long-term regulation of arterial
pressure.

Baroreceptor Reflex Mechanism During
Changes in Body Posture
 Immediately on standing, Arterial pressure in the head & upper part of the
body tends to fall ,cause loss of consciousness.
 Falling pressure at the baroreceptors elicits an immediate reflex,resulting in
strong sympathetic discharge throughout the body.
 This minimizes the decrease in pressure in the head & upper body
 • Denervation of the baroreceptors can lead to paroxysmal hypertension. “

CHEMORECEPTORS
 Chemoreceptors reflex > work with baroreceptors only in
the situation of low blood pressure
 “it doesn’t work if the blood pressure is high” “in case of
emergency, such as hemorrhage , ischemia”

 BP <60 mm Hg
Hypoxia
Chemoreceptors
NTS Respiratory centre CIC
VMC stimulation N ambiguus
Vagus
SNS action  Vagaltone
Net effect  Pulmonary ventilation,  BP,  Heart rate
Chemo receptor reflexes

 Stimulation of chemoreceptors leads to a reflex increase in vasomotor tone
which causes generalized vasoconstriction and hence a rise in blood
pressure.
 Chemoreceptor mechanism is important in regulation of blood pressure
when it fall below the range in which baroreceptors act (70 mmHg).
 Chemoreceptor reflex is useful in regulation of blood pressure when it falls
to a level between (40 and 70 mmHg).
 But if the blood pressure below 40 mmHg, the last ray of hope for survival is
the central nervous system (CNS) ischemia response.
 • So it sometimes called the “last ditch stand” pressure control mechanism.

 CNS Ischemic Response “Last ditch stand” pressure control mechanism
 It is not one of the normal mechanisms for regulating ABP.
 It acts rapidly & very powerfully whenever blood flow to the brain ↓ dangerously
close to the lethal level.
 It operates principally as an emergency pressure control system to prevent further
decrease in arterial pressure.
 Local concentration of CO2 ↑ greatly.
 This has an extremely potent effect in stimulating the sympathetic vasomotor
nervous control areas in the brain’s medulla.

 BP < 40 mm Hg (or)
 Intracranial pressure
Cerebra ischaemia
Cerebral hypoxia
Direct effect on
VMC
SNS action 
Vasoconstriction
Cerebral Ischaemic Response
 BP with reflex
bradycardia
Cushing’s Reflex

Delayed or Intermediate Mechanism
Renin –Angiotensin System
Whenever there is a fall in B.P, there is a
decrease in the blood flow to the kidney.
This results is ischaemic kidney.
Renin is released from J.G. cells
Renin
Angiotensin Angiotensin I
ACE
Angiotensin I Angiotensin II
ACE - Angiotensin Converting Enzyme
( Present in the lungs)

Stress Relaxation Phenomenon:
BP
Blood vessels are stretched
Stress relaxation
Increased capacity
Decreased effective
blood volume
BP decreased
relaxation
BP MAGDI AWAD SASI 2018 LIMU

Long term Regulatory Mechanisms:
All the mechanisms
that tend to alter the
blood volume
participate in
Long term regulatory
mechanisms

Atrial natriuretic peptide (ANP)
 Released by cells of atria
 Released in response to stimulation of atrial receptors
 Increases salt excretion via kidneys
 By reducing water reabsorption in the collecting ducts
 relaxes renal arterioles
 inhibits sodium reabsorption in the distal tubule
 Lowers blood pressure by causing vasodilation and promoting
loss of salt and water in urine
 Reduces blood volume

Renal –body fluid system:
ECF or Blood volume
-  BP
B.P is brought back to
the normal level
ECF or Blood volume
- BP
B.P is slowly raised to
the normal level.
 GFR  urine output  GFR BP  urine output

HORMONAL REGULATIONS
1) Catecholamines
2) Mineralocorticocoid
3) Glucocorticoid
4) Thyroxine
5) ADH
6) Atrial Natriuretic Factor
7) Nitric Oxide
8) Histamine
9) Angiotensin
10) Serotonin

Autoregulation of blood pressure
 Ability of tissue to automatically adjust its blood flow to match metabolic
demands
 Demand of O2 and nutrients can rise tenfold during exercise in heart and
skeletal muscles
 Also controls regional blood flow in the brain during different mental and
physical activities
 2 general types of stimuli
1. Physical – temperature changes, myogenic response
2. Vasodilating and vasoconstricting chemicals alter blood vessel diameter

Relationship between Pressure,
Flow, and Resistance
F=ΔP/R
 Flow (F) through a blood vessel is determined by:
1) The pressure difference (Δ P) between the two ends of the
vessel
2) Resistance (R) of the vessel

Laplace’s Law: Myogenic mechanism
TENSION = PRESSURE X RADIUS
(dynes/cm) (dynes/cm2) (cm)
PRESSURE TENSION RADIUS
PRESSURE TENSION RADIUS
(to maintain tension constant)
(to maintain tension constant)

Vasodilator Theory for Blood Flow Control
 Local Vasodilators: Adenosine, CO2, Lactic acid, ADP compounds, Histamine,
K+ ions, H+ ions,
Prostacyclin, Bradykinin, and Nitrous oxid (NO)
TISSUE
METABOLISM
BLOOD
FLOW
ARTERIOLE
RESISTANCE
RELEASE OF
VASODILATORS

Arteriole Resistance: Control of Local Blood Flow

Humoral Regulation of Blood Flow
 Vasoconstrictors
Norepinephrine and epinephrine
Angiotensin
Vasopressin
Endothelin
 Vasodilator agents
Bradykinin
Serotonin
Histamine
Prostaglandins
Nitric oxideMAGDI AWAD SASI 2018 LIMU

Blood Flow: Brain
Blood flow to the brain is constant, as neurons are intolerant of ischemia
Metabolic controls – brain tissue is extremely sensitive to declines in pH,
and increased carbon dioxide causes marked vasodilation
Myogenic controls protect the brain from damaging changes in blood
pressure
Decreases in MAP cause cerebral vessels to dilate to insure adequate perfusion
Increases in MAP cause cerebral vessels to constrict

Regulation of ABP magdi sasi 2018

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Regulation of ABP magdi sasi 2018