Short-term control of blood pressure is mediated by the nervous system and chemicals that regulate peripheral resistance within seconds or minutes. The baroreceptor reflex detects changes in blood pressure and regulates heart rate, stroke volume, and vascular tone to maintain pressure. Chemoreceptors sense oxygen and carbon dioxide levels and stimulate the vasomotor center. If blood flow to the brain decreases severely, the CNS ischemic response triggers powerful vasoconstriction to increase pressure.

1. BLOOD PRESSURE
MECHANISM
SHORT TERM CONTROL OF BLOOD
PRESSURE

2. 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.

3. • 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).

4. I. Nervous System
• Control BP by changing blood distribution in the body and by
changing blood vessel diameter.
• Sympathetic & Parasympathetic activity 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

5. 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

6. Baroreceptors
• The best 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.

7. Baroreceptors

8. Effect of Baroreceptors
Baroreceptors entered the medulla (tractus solitarius)
Secondary signals inhibit the vasoconstrictor center of medulla
and excite the vagal parasympathetic center
VASODILATATION OF THE
VEINS AND ARTERIOLES
Therefore, excitation of baroreceptors by high pressure in the arteries
reflexly causes arterial pressure to decrease (as decrease in PR and CO)
DECREASED HEART RATE AND
STRENGTH OF HEART
CONTRACTION
EFFECT
NOTE : Conversely, low pressure has opposite effects,reflexly causing the pressure rise
back to normal.

9. 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

10. 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

11. Short-term Regulation of Falling Blood Pressure
Baroreceptors inhibited
Decreased impulses to the brain
Decreased parasympathetic activity,
increased sympathetic activity
Effects
Heart
increased heart rate and
increased contractility
Vessels
increased vasoconstriction
Adrenal gland
release of epinephrine and
norepinephrine which enhance heart rate
Contractility and vasoconstriction
Increased blood pressure

12. • 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

13. 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

14. 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.

16. II. Chemoreceptor

17. Chemoreceptor
• Chemosensitive cells that respond to changes in pCO2 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)

18. Chemoreceptor

19. CNS Ischemic Response
Severe decrease blood flow to brain
Cerebral hypoxia
Vasomotor center stimulated – causes powerful
vasoconstriction
( INCREASE SYMPATHETIC DISCHARGE – Norepinephrine)
Increase blood pressure & blood flow

20. 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
Relieve brain ischemia

22. SHORT TERM
REGULATION OF
BLOOD PRESSURE

23. 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.

24. 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.

26.  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.

27. 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.

28. Brainstem contains:
Pons
Medulla
In the Medulla are the:
Cardiac Acceleratory Centre
Cardiac Inhibitory Centre
Vasomotor Centre

29. 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

30. 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.

33. Chemoreceptor Reflex

34. CNS Ischemic Response
Severe decrease blood flow to brain
Cerebral hypoxia
Vasomotor center stimulated – causes powerful
vasoconstriction
( INCREASE SYMPATHETIC DISCHARGE – Norepinephrine)
Increase blood pressure & blood flow

35. 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
Relieve brain ischemia

37. HORMONES INVOLVE IN
CALCIUM METABOLISM

38. 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)

39. - 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

40. 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.

41. 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

42. Action of PTH in bone
• Increases bone resorption
• Ca and phosphate are released to the ECF
• The concentration of Ca in the serum
increases

43. 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.

44. 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

45. 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

46. 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 calcium-
binding protein

47. • 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

48. 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

49. 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

50. 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

51. 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

52. calcitonin

53. biosynthesis
• 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.

54. physiology
• The hormone participates in calcium (Ca2+) and phosphorus
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.

55. actions
• 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

56. receptor
• The calcitonin receptor, found primarily on
osteoclasts, is a G protein-coupled receptor,
which is coupled by Gs to adenylyl cyclase and
thereby to the generation of cAMP in target
cells. It also affect the ovaries in women and
the testes in men.

57. THANK YOU

58. ELECTROCARDIOGRAM
Normal ECG and Leads

59. 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.

60. 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.

61. Normal ECG Character?
The ECG comprise of several waves:
• P wave
• QRS complex
• T wave

63. What is P wave?
• Caused by the electrical potentials generated
when the atria depolarise before the
contractions begins.
• This is depolarization wave.

65. What is QRS complex?
• It is caused by potentials generated when the
ventricles depolarized before contraction.
• This is depolarization wave.

67. 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.

70. 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.

71. 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)

72. Limbs lead

73. Precordial Leads

74. Augmented Leads

75. THANK YOU