BLOOD PRESSURE

MECHANISM

SHORT TERM CONTROL OF

BLOOD PRESSURE
 Introduction
• There are two basic mechanisms for regulating
blood pressure:
(1)short-term mechanisms.
regulate blood vessel diameter, heart rate
and contractility
(2)long-term mechanisms.
regulate blood volume
• Blood Pressure = cardiac output x peripheral
resistance
• Any change in cardiac output, blood volume or
peripheral resistance will lead to a change in blood
pressure.
• Short term control of Blood pressure is mediated by
the :

I. nervous system
II. Chemicals

• that control blood pressure by changing

peripheral resistance. ( in sec or minutes)
• Rapidity of response (beginning within seconds and
often increasing the pressure to 2X normal(5 to 10
seconds).
• Sudden inhibition of nervous cardiovascular
stimulation can decrease the arterial pressure (one
half normal)(10- 40 seconds).
 I. Nervous
• Control BP bySystem
changing blood distribution in the body and by
changing blood vessel diameter.
• Sympathetic & Parasympatheticactivity will affects
veins, arteries & heart to control HR and force of contraction
The vasomotor center
• cluster of sympathetic neurons found in the medulla.
• It sends efferent motor fibers that innervate smooth muscle
of blood vessels.
Sympathetic activity Sympathetic activity

VASOCONSTRICTION VASODILATATION
Short-term Regulation of Rising Blood Pressure

Rising blood pressure

Stretching of arterial walls

Stimulation of baroreceptors in
carotid sinus, aortic arch, and other
large arteries of the neck and thorax

Increased impulses to the brain

 Barorecepto
• The best rs
known of nervous mechanisms for
arterial pressure control (baroreceptor reflex)
• Baroreceptors are stretch receptors found in
the carotid body, aortic body and the wall of
all large arteries of the neck and thorax.
• Respond progressively at 60-180 mm Hg.
• Respond more to a rapidly changing pressure
than stationary pressure.
Baroreceptor
s
 Effect of
Baroreceptors
Baroreceptors entered the medulla (tractus solitarius)

Secondary signals inhibit the vasoconstrictor center of

medulla and excite the vagal parasympathetic
center

EFFEC
T DECREASED HEART RATE
VASODILATATION OF
AND STRENGTH OF HEART
THE VEINS AND
CONTRACTION
ARTERIOLES

Therefore, excitation of baroreceptors by high pressure in the arteries

reflexly causes arterial pressure to decrease (as decrease in PR and
CO)

NOTE : Conversely, low pressure has opposite effects,reflexly causing the pressure rise
back to normal.
 Increased Parasympathetic
Activity
Effect of increased parasympathetic and
decreased sympathetic activity on heart and
blood pressure:
• Increased activity of vagus (parasympathetic) nerve
• Decreased activity of sympathetic cardiac
Nerves
• Reduction of heart rate
• Lower cardiac output
• Lower blood pressure
 Decreased Sympathetic
Activity
Effect of decreased sympathetic activity
on arteries and blood pressure:
• Decreased activity of vasomotor fibers
(sympathetic nerve fibers)
• Relaxation of vascular smooth muscle
• Increased arterial diameter
• Lower blood pressure
 Short-term Regulation of Falling Blood
Pressure Baroreceptors inhibited

Decreased impulses to the brain

Decreased parasympathetic
activity, increased sympathetic
activity

Effect
s
Heart Vessels Adrenal gland
increased heart rate increased release of epinephrine and
and increased vasoconstriction norepinephrine which enhance heart
contractility rate

Contractility and vasoconstriction

Increased blood pressure

• Sympathetic Activity on Heart and Blood Pressure

Effect of Increased Sympathetic Activity on Heart

and Blood Pressure:
• Increased activity of sympathetic cardiac nerves
• Decreased activity of vagus (parasympathetic) nerve
• Increased heart rate and contractility
• Higher cardiac output
• Increased blood pressure
 Vasomotor
Fibers
• Effect of Increased Sympathetic Activity
on Arteries and Blood Pressure:
• Increased activity of vasomotor
fibers (sympathetic nerve fibers)
• Constriction of vascular smooth
muscle
• Decreased arterial diameter
• Increased blood pressure
Sympathetic Activity on Adrenal Gland
and Blood Pressure

Effect of increased sympathetic

activity on adrenal glands and blood
pressure:
• Increased sympathetic impulses to adrenal glands.
• Release of epinephrine and norepinephrine
to bloodstream.
• Hormones increase heart rate, contractility and
vasoconstriction. Effect is slower-acting and
more prolonged than nervous system control.
• Increased blood pressure.
II.
Chemoreceptor
 Chemorecepto
• Chemosensitivercells that respond to changes in pCO 2
and pO2 and pH levels (Hydrogen ion).

pO2 and pH
pCO2


Stimulation of
vasomotor
center

CO HR vasoconstriction


BP (speeding return of

blood to the heart and lungs)
Chemorecepto
r
 CNS Ischemic
Response
Severe decrease blood flow to brain

Cerebral hypoxia

Vasomotor center stimulated – causes

powerful vasoconstriction
( INCREASE SYMPATHETICDISCHARGE –
Norepinephrine)

Increase blood pressure & blood flow

 Cushing Reaction
- Special type of CNS Ischemic Response
Increased pressure of cerebrospinal fluid (cranial vault)

Increase intracranial tension

Compress whole brain & arteries in the

brain

Cuts off blood supply to brain

CNS Ischemic Response initiated &

arterial pressure rises
 SHORT TERM
REGULATION OF
BLOOD PRESSURE
Innervation of blood vessels
 Sympathetic
vasoconstrictor fiber
 Distribution: Almost all
segments of the circulation.
 The innervation is powerful
in the kidneys, gut, spleen
and skin
 is less potent in
both skeletal and cardiac
muscle and in the brain.
Innervation of blood vessels

Almost all vessels, such as arteries,

arterioles, venules and veins are innervated.
except the capillaries, precapillary sphincters and
most of the metarterioles.

Tone: Usually the sympathetic vasoconstrictor

fibers keep tonic.
 Parasympathetic nerve fiber to peripheral
vessels
 Parasympathetic nerve fibers innervate
vessels of the blood vessels in
 Meninges
 the salivary glands
 the liver
 the viscera in pelvis
 the external genitals
 Importance: Regulate the blood flow of
these organs in some special situations.
Cardiac Centres (Higher Centres)
-IN MEDULLA-

1. Cardio Acceleratory Centre sends sympathetic neurones down the spine to

between T1 and T5, where they exit to the periphery.

2.Cardio Inhibitory Centre originates with the Vagus Nucleus in the medulla
and this parasympathetic nerve leaves the cranium as the Vagus (X) Nerve.

3. Vasomotor Centre - is a cluster of sympathetic fibres in the Medulla.

- transmits impulses via sympathetic vasomotor
fibres from T1 to L2 to blood vessels (arterioles)

Vasoconstriction is caused by increased frequency of impulses (Noradrenaline)

Vasodilation is caused by decreased frequency of impulses.
Brainstem contains:

Pons
Medulla

In the
Medulla
are the:

Cardiac Acceleratory Centre

Cardiac Inhibitory Centre
Vasomotor Centre
 Short-Term Regulation
• Rapidly Acting Pressure Control Mechanisms, Acting
Within Seconds or Minutes.

A. Baroreceptor reflexes (60 – 100 mmHg)

Change peripheral resistance, heart rate, and stroke volume
in response to changes in blood pressure
B. Chemoreceptor reflexes (40 – 60 mmHg)
Sensory receptors sensitive to oxygen lack, carbon
dioxide excess, and low pH levels of blood
C. Central Nervous System ischemic response (< 40 mmHg)
Results from severe decrease blood flow to the brain
 Baroreceptor reflexes
Baroreceptors are found in :
• Carotid Sinuses (blood going to brain) by glossopharyngeal nerve
• Aortic Arch (systemic blood going to body) by vagus nerve

As MAP increases this stretches the receptors and they send a fast train
of impulses to the Vasomotor Centre. After the signals enter the tractus
solitarius, secondary signals inhibit vasoconstrictor centres and excite the
vagal parasympathetic center. This results in a decrease in the frequency
of impulses from the Vasomotor Centre and arterioles dilate. Final result
is vasodilation and decreases MAP.

*CIC activity increases (stimulating the Vagus nerve) - decreases HR and

SV.

* CAC activity decreases (inhibiting Sympathetic nerves) - decreases CO.

Chemoreceptor Reflex
 CNS Ischemic
Response
Severe decrease blood flow to brain

Cerebral hypoxia

Vasomotor center stimulated – causes

powerful vasoconstriction
( INCREASE SYMPATHETICDISCHARGE –
Norepinephrine)

Increase blood pressure & blood flow

 Cushing Reaction
- Special type of CNS Ischemic Response
Increased pressure of cerebrospinal fluid (cranial vault)

Increase intracranial tension

Compress whole brain & arteries in the

brain

Cuts off blood supply to brain

CNS Ischemic Response initiated &

arterial pressure rises
HORMONES INVOLVE
IN CALCIUM
METABOLISM
 Calcium
•
Regulation
Calcium plays an key role in many physiological
process include:
-Contraction of skeletal, cardiac and smooth muscle.
- Blood clotting and neuromuscular function
and transmission
o Important feature of extracellular calcium
regulation:
-0.1 % of total calcium in ECF
- 1 % in cell
- rest in bone(largest reservoirs)
- Total Ca concentration in blood in blood is normally
at 10mg/dl
- 40% bound to plasma protein
- 10% complexed to anion (phosphate, citrate, sulfate)
- 50%is free ionized(biologically active)
o Calcium homeostasis involves 3 sys
-Bone, kidney, GI tract
o Also involves 3 hormones
-PTH, Calcitonin, Vitamin D
 Relation of Calcium &
• Phosphate
The calcium and phosphate homeostasis
are linked together
• Calcium complexes with phosphate where
more phosphate present then more calcium
bind to it and reduce the free ionized calcium
fraction in ECF.
• The less phosphate present the less calcium
bind to it and this increase the free, ionized
calcium fraction
• Hence ,decrease phosphate level in blood
help plasma Ca level in blood.
 Parathyroid Hormone
(PTH)
• It is secreted when the blood plasma Ca 2+
is decreased
• Thus, it prevents hypocalcemia
• Also acts to decrease concentration
of phosphate in the plasma
• The action is direct in the bone and
kidney
• In the intestine, the action is indirect
 Action of PTH in
bone
• Increases bone resorption
• Ca and phosphate are released to the
ECF
• The concentration of Ca in the
serum increases
 Action of PTH in
kidney
• PTH promotes Ca reabsorption and inhibits
phosphate reabsorption in the kidney
tubules
• Inhibition of phosphate reabsorption causes
it to be excreted in the urine, a condition
named phosphaturia
• Since Ca is reabsorbed, its concentration
in the plasma is elevated.
 Action of PTH on
intestine
• PTH has no direct effect on the intestine
• It indirectly increases Ca and phosphate
absorption to the small intestine by
activating vitamin D
• Vitamin D will promote Ca uptake by
the intestine
 Action of Vitamin
D
• The active form of vitamin D,125-
dihydroxycholecalciferol has several effect
on
– Intestine
– Kidney
– Bone
• General function of vitamin D is increase
absorption of calcium and phosphate into the
ECF
 Effect on
intestine
• 1,25-Dihydroxycholecalciferol promote
absorption of calcium by formation of a
calcium- binding protein in the intestinal
epithelial cells.
• The functions of protein are transport the
calcium into the cytoplasm, then the
calcium move to basolateral membrane by
difussion.
• The rate of calcium absorption is directly
proportional to the quantity of this
• Other effect of 1,25
dihydroxycholecalciferol : The formation
of :-

1.a calcium stimulated ATPase in the brush

border of the epithelial cells

2.an alkaline phosphatase in the epithelial

cells
 Effect on
•
Intestine
Vitamin D also promote phosphate
absorption
• Usually phosphate absorb easily, phosphate
flux through the gastrointestinal epithelium
is enhance by vitamin D
• It is a direct effect of
1,25-
dihydroxycholecalciferol
• Action on calcium absorption : the calcium
in- turn acting as a transport mediator for
the phosphate
 Effect on renal
(kidney)
• Vitamin D also decrease renal calcium
and phosphate excretion.
• Also increases calcium and phosphate
absorption by the epithelial cells of the renal
tubules, thereby tending to decrease
excretion of this substances in the urine
 Effect on bone and it relation
to parathyroid hormone
• activity
Vitamin D play important role in both
bone absorption and deposition.
• Extreme quantities of vitamin D
causes absorption of bone.
• Absences of vitamin D, the effect of PTH in
causing bone absorption is greatly reduce or
even prevented.
• Vitamin D in small quantities promote bone
calcification which is vit D increase calcium
and phosphate absorption from intestine
 Effect on bone and it relation
to parathyroid hormone
• activity
Vitamin D play important role in both
bone absorption and deposition.
• Extreme quantities of vitamin D
causes absorption of bone.
• Absences of vitamin D, the effect of PTH in
causing bone absorption is greatly reduce or
even prevented.
• Vitamin D in small quantities promote bone
calcification which is vit D increase calcium
and phosphate absorption from intestine
calcitoni
n
 biosynthesi
s
• Calcitonin is formed by
the proteolytic cleavage of a
larger prepropeptide, which is the product of
the CALC1 gene (CALCA). The CALC1 gene
belongs to a superfamily of related protein
hormone precursors including islet amyloid
precursor protein, calcitonin gene-related
peptide, and the precursor of
adrenomedullin.
 physiolog
• y
The hormone participates in calcium (Ca ) and phosphorus
2+

metabolism. In many ways, calcitonin counteracts

parathyroid hormone(PTH).
• -To be specific, calcitonin affects blood Ca2+levels in four
ways:
• -Inhibits Ca2+absorption by the intestines
• -Inhibits osteoclast activity in bones
• -Inhibits phosphate reabsorption by the kidney tubules
• Increases absolute Ca2+and Mg2+ reabsorption by
the kidney tubules, calcitonin is a renal Ca-conserving
hormone.
• Secretion of calcitonin is stimulated by:
• -an increase in serum [Ca2+]
• --gastrin and pentagastrin.
 action
• s
this actions, in a broad sense, are:
• Bone mineral metabolism:
• - Protect against Ca2+loss from skeleton during
periods of Ca2+stress such as pregnancy and lactation
• Serum calcium level regulation
• - Prevent postprandial hypercalcemia resulting from
absorption of Ca2+from foods during a meal
-Vitamin D regulationA satiety hormone:
• - Inhibit food intake in rats and monkeys- May
have CNS action involving the regulation of feeding
and appetite
 recepto
r
• The calcitonin receptor, found primarily on
osteoclasts, is a G protein-coupled receptor,
which is coupled by Gsto adenylyl cyclase
and thereby to the generation of cAMP in
target cells. It also affect the ovaries in
women and the testes in men.
THANK
YOU
ELECTROCARDIOGRA
M
Normal ECG and
Leads
 What is
ECG?
• Transthoracic interpretation
of the electrical activity of
the heart over time captured and
externally recorded by skin electrodes.
• The sum of the electrical activity generated
by the heart.
 How do ECG
•
works?
It works by detecting and amplifying the tiny
electrical changes on the skin that are
caused when the heart muscle
"depolarises" during each heart beat.
• ECG is measured by placing skin electrodes
on the body surface at different locations.
• This electrodes are connected in different
configuration to a amplifier and a
recorder.
 Normal ECG
Character?
The ECG comprise of several
waves:
• P wave
• QRS complex
• T wave
 What is P
wave?
• Caused by the electrical potentials
generated when the atria depolarise before
the contractions begins.
• This is depolarization wave.
 What is QRS
complex?
• It is caused by potentials generated when
the ventricles depolarized before
contraction.
• This is depolarization wave.
 What is T
wave?
• It is caused by potential generated as
the ventricles recover from the state of
depolarization.
• It is known as repolarization wave.
 What is ECG
Leads?
• They are electrical cable attaching
the electrodes to the ECG
recorder.
• They also may refer to the tracing
of
the voltage difference between two of the
electrodes and is what is actually produced
by the ECG recorder.
 How many leads are
there?
There are 12 leads:
• 3 limbs lead (I, II, III)
• 3 Augmented leads (aVR, aVL,
aVF)
• 6 Precordial Leads (V1 – V6)
Limbs
lead
Precordial
Leads
Augmented
Leads
THANK
YOU