BLOOD PRESSURE AND ITS
REGULATION
DR.V. ANEBARACY MBBS,MD
PROFESSOR,PHYSIOLOGY
ARUNAI MEDICAL COLLEGE & HOSPITAL
BLOOD PRESSURE DEFINITION
Blood pressure is defined as the
lateral pressure exerted by the
column of blood on the walls of
the arteries.
• Systolic blood pressure is defined as the
maximum pressure exerted during [Link]
depends upon cardiac output.
• Diastolic blood pressure is defined as the
minimum pressure exerted during [Link]
depends upon peripheral resistance.
• Pulse pressure is the difference between the
systolic and diastolic blood pressure.
PP=SBP-DBP
• Mean arterial pressure is the average pressure
throughout the cardiac cycle.
MAP = DBP + 1 / 3 PP
NORMAL VALUES
• SBP: 100 - 120 mmHg
• DBP : 60 - 80 mmHg
• PP : 20 - 50 mm Hg
• MAP : 75 - 105 mm Hg
FACTORS AFFECTING BP :
Blood pressure = cardiac output x peripheral
resistance ( COPR)
FACTORS AFFECTING CARDIAC OUTPUT
Cardiac output = stroke volume x Heart rate
The stroke volume is affected by preload,afterload
and myocardial contractility
Heart rate is mainly affected by parasympathetic
and sympathetic activities.
PRELOAD
• Preload is the end diastolic volume , that is
the amount of blood present in the ventricle
at the end of the diastole.
• When the EDV increases , the cardiac output
increases and when EDV decreases , the
cardiac output decreases .
• This occurs due to the operation of the Frank
– starling mechanism.
AFTERLOAD
• After load is the peripheral resistance that the
heart has to overcome in order to eject blood.
• Cardiac output is inversely proportional to
peripheral resistance
• Increase in peripheral resistance
(vasoconstriction) decreases the cardiac output
• Decrease in peripheral resistance
(vasodilatation) increases the cardiac output
MYOCARDIAL CONTRACTILITY
• The contractility of the myocardium exerts a
major influence on the cardiac output (↑C.O)
FACTORS THAT ARE POSITIVELY INOTROPIC:
• Sympathetic Stimulation
• Digitalis
FACTORS ARE NEGATIVELY INOTROPIC:
• Parasympathetic Stimulation
• Hypoxia , Hypercapnia And Acidosis
HEART RATE
• Increase in heart rate increases cardiac
output
• Decrease in heart rate decreases cardiac
output.
FACTORS AFFECTING PERPHERAL RESISTANCE
DIAMETER OF BLOOD VESSELS:
• The decrease in vessel diameter
(vasoconstriction) increases peripheral resistance
and increases blood pressure .
• Vasodilatation , on the other hand , decreases
peripheral resistance and decreases blood
pressure.
VISCOSITY:
• Viscosity of blood depends on the composition
of plasma ie. total number of cells in the blood.
Increased viscosity increases the BP.
FACTORS THAT INCREASE VISCOSITY:
• Polycythemia
• Hyperproteinemia
FACTORS THAT DECREASE VISCOSITY:
• Anemia
• Hypoproteinemia
Physiological variations
1. Age
2. Gender
3. Eating
4. Sleep
5. Emotion & excitement
6. Exercise
7. Posture
8. Climate
9. Pregnancy
Importance of blood pressure:
Blood pressure is the driving force for blood flow
and its maintenance is necessary for adequate
perfusion of vital organs.
Fall in BP(hypotension) if severe leads to death
due to shock and damage of heart, brain and
other organs.
High blood pressure can lead to hemorrhage,
stroke, retinopathy, nephropathy etc.
Hence blood pressure has to be regulated and
maintained within normal limits.
Regulation of blood pressure
VASOMOTOR AREA IN MEDULLA
Sensory area
Vasoconstric Vasodilator ( Nucleus
tor area area tractus
solitarius)
NTS (Nucleus tractus
solitarius)Sensory center) (glutamine)
VASOMOTOR CENTER Cardiac vagal center (Cardiac
RVLM CVLM (vasodilator inhibitory center) nucleus
(vasoconstrictor − area,
area, depressor area)
ambiguous , Dorsal motor
Pressor area) GABA nucleus of vagus
glutamine
↓Sympathetic Activation of parasympathetic
↑Sympathetic activity activity (VAGUS)
activity
1. ↓Heart rate
1. ↓Heart rate
1. ↑Heart rate 2. ↓ Myocardial
2. ↓ Myocardial
2. ↑ Myocardial contractility
contractility
contractility 3. ↓ Cardiac output
3. ↓ Cardiac output
3. ↑ Cardiac output 4. Vasodilatation
4. Fall in BP
4. Vasoconstriction 5. Fall in BP
5. Increase in BP
Short-term mechanism of BP
Regulation
Short-term mechanism of blood pressure
regulation occurs within few seconds to
few minutes.
Mechanisms involved:
1. Baroreceptor reflex
2. Chemoreceptor reflex
3. CNS ischemic reflex/Cushing reflex
BARORECEPTOR REFLEX
• Most important of all reflexes since it regulates BP
within seconds and hence it is a life saving reflex.
• It is also called as sinoaortic reflex
• This is the first and foremost reflex for regulation
of BP
• It regulates BP when the mean arterial pressure is
in the range of 60 to 180 mmHg
• Carotid baroreceptors are located at carotid sinus
(dilated initial part of internal carotid artery) and
aortic arch.
• Receptors : Baroreceptors present in
the carotid sinus and aortic arch.
• Stimulus : Responds to change in
pressure
• Afferent: 9th cranial nerve
(glossopharyngeal nerve)carries
information from the carotid sinus
and 10th cranial nerve (vagus nerve)
from aortic arch
Center: Cardiovascular regulatory
centers in the medulla (NTS,
Vasomotor center,Cardiac vagal
center)
Efferent: Sympathetic nerves from
VMC & Parasympathetic nerve
(Vagus) nerve from Cardiac vagal
center.
Effector organs: Heart & Blood vessels
[Link] in BP
2. Stretching of carotid sinus & aortic arch and activation
of BARORECEPTORS
[Link] discharge in 9th and 10th cranial nerve
4. Stimulation of Nucleus tractus solitarius (glutamine)
VASOMOTOR CENTER
[Link] of [Link] of Cardiac vagal
− [Link] of
vasoconstrictor
vasodilator area,
Center/Cardiac inhibitory
area, Center
(depressor area)
(Pressor area)
↓ Sympathetic ↑Parasympathetic activity (VAGUS)
activity
a. ↓Heart rate
a. ↓Heart rate
b. ↓ Myocardial
b. ↓ Myocardial contractility
contractility
c. ↓ Cardiac output
c. ↓ Cardiac output
d. Vasodilatation
DECREASE IN BP OCCURS INORDER TO
RESTORE BP TO NORMAL
[Link] in BP
[Link] Stretching of carotid sinus &aortic arch and no
activation of BARORECEPTORS
[Link] discharge in 9th and 10th cranial nerve
4. No stimulation of Nucleus tractus solitarius
VASOMOTOR CENTER
[Link] of Cardiac vagal
[Link] of − [Link] of
vasoconstrictor center /Cardiac inhibitory
vasodilator area,
area,
(depressor area) Center
(Pressor area)
↑Sympathetic
↓Parasympathetic activity (VAGUS)
activity
1. ↑Heart rate 1. ↑ Heart rate
2. ↑ Myocardial contractility 2. ↑ Myocardial
3. ↑ Cardiac output contractility
4. Vasoconstriction 3. ↑ Cardiac output
INCREASE IN BP OCCURS INORDER TO
RESTORE BP TO NORMAL
CHEMORECEPTOR REFLEX
• Chemoreceptors are the aortic and carotid bodies.
• Carotid bodies are located at the bifurcation of the
common carotid artery and the aortic bodies are
located at the arch of aorta.
• They respond to changes in the chemical composition
of blood like changes in pO2,pCO2,H+ ion
concentration (hypoxia, hypercapnia, acidosis)
• Chemoreceptor reflex regulates BP when the mean
arterial pressure is in the range of 40 to 60 mmHg
• These reflexes plays an important role in the regulation
of respiration and also helps in regulation of BP.
• Receptors : Chemoreceptors are present
in the carotid body and aortic body.
• Stimulus : ↓pO2 ,↑pCO2,↑H+ ion
concentration
• Afferent: 9th cranial nerve
(glossopharyngeal nerve)carries
information from the carotid sinus and
10th cranial nerve (vagus nerve) from
aortic arch
Center: Respiratory center, Vasomotor
Center, Cardiac vagal center.
Efferent: Sympathetic nerve from VMC
& & Parasympathetic nerve (Vagus)
from Cardiac vagal center.
Effector organs: Heart & Blood vessels
& Inspiratory muscles of respiration.
[Link],Hypercapnia,Acidosis
[Link] of chemoreceptors
[Link] of Respiratory center
[Link] of vasomotor center (vasoconstrictor area) &
Inhibition of cardiovagal center
[Link] in sympathetic activity &Increase in Rate and Depth of
breathing
INCREASE IN BP & ↑PULMONARY VENTILATION
CNS ISCHEMIC RESPONSE
[Link] BP falls below 40mmHg as seen in acute severe
hemorrhage
2. Decreased cerebral blood flow produces CNS ischemia (hypoxia
and hypercapnia of vasomotor center)
3. Direct stimulation of VMC (vasoconstrictor area) causes
intense sympathetic discharge and BP ↑
This is the last physiological reflex to correct the BP
and is referred to as last ditch effort/stand to
prevent the death of a person.
Cushing’s reflex
One of the CNS ischemic response which occurs
when intracranial pressure increases as in
brain tumors.
Raised ICP, decreased blood flow
to the VMC
Hypoxia and hypercapnia at VMC,
Strong stimulation of VMC
(vasoconstrictor area)
Intense sympathetic discharge
and BP ↑
Increased pressure at the carotid
sinus and aortic arch
Activation of baroreceptor reflex (activation
of vagus and inhibition of VMC
(Vasoconstrictor area)
Reflex Bradycardia (outstanding
feature of brain tumours)
Intermediate mechanism BP
regulation
a. Capillary fluid-shift mechanism
b. Stress relaxation & inverse
Stress relaxation mechanism
It takes few minutes to few hours
to act.
Capillary fluid-shift mechanism
Increase in BP
↓
Mean capillary pressure↑
↓
Shift of fluid from the capillaries into the interstitial
space
↓
Blood volume decreases
↓
Blood pressure decreases.
Capillary fluid shift is 2 to 3 times more potent than
Baroreceptor mechanism but it takes few minutes to
hours to act
Capillary fluid-shift mechanism
Decrease in BP
↓
Mean capillary pressure↓
↓
Shift of fluid from the interstitial space into the
capillaries
↓
Blood volume increases
↓
Blood pressure increases.
Stress relaxation and Reverse stress
relaxation mechanisms
• When BP increases suddenly, stretching
of the blood vessel occurs. The smooth
muscles of the blood vessels relax and
vasodilatation [Link] BP ↓
• Reverse stress relaxation occurs when
the BP decreases.
Long term mechanism of BP regulation
Long term regulation of BP are slow and sustained
mechanisms that take several days for the complete
restoration of BP.
[Link] Renal mechanism
a. Renal- Body fluid mechanism/Extracellular fluid
mechanism
b. Renin Angiotensin Aldosterone System (RAAS)
2. By Hormonal mechanism
c. ADH (antidiuretic hormone )mechanism
d. ANP (atrial natriuretic peptide) mechanism
[Link]- body fluid feedback mechanism:
When ECF ↑,BP ↑,RBF ↑,GFR ↑,
kidneys excrete large amounts of sodium
& water by pressure natriuresis and
pressure diuresis.
Hence the ECF volume ↓ BP ↓.
When the ECF volume ↓ BP ↓, RBF
↓,GFR ↓, reabsorption of more sodium
& water from renal tubules occurs.
Hence the ECF volume ↑ and BP ↑.
[Link]-Angiotensin-Aldosterone System
a) ADH (antidiuretic hormone) is release during
decreased BP-↑water reabsorption from
kidneys,↑blood volume,↑BP
b) ANP (atrial natriuretic peptide) from atrial
myocytes - Released in response to increase in
BP -causes Natriuresis and diuresis ,↓BP