Blood pressure mechanism

BLOOD PRESSURE

MECHANISMSHORT 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 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 contractionThe 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

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.

Baroreceptors

Effect of BaroreceptorsBaroreceptors 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.

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 PressureBaroreceptors inhibited

Decreased impulses to the brain

Decreased parasympathetic activity, increased sympathetic activity

Effects

Heartincreased heart rate and

increased contractility

Vesselsincreased vasoconstriction

Adrenal gland release of epinephrine and

norepinephrine which enhance heart 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

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)

Chemoreceptor

CNS Ischemic ResponseSevere decrease blood flow to brain

Cerebral hypoxia

Vasomotor center stimulated – causes powerful vasoconstriction

( INCREASE SYMPATHETIC DISCHARGE – 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

Relieve brain ischemia

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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:

PonsMedulla

In the Medulla are the:

Cardiac Acceleratory CentreCardiac Inhibitory CentreVasomotor 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 pressureB. 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 ResponseSevere decrease blood flow to brain

Cerebral hypoxia

Vasomotor center stimulated – causes powerful vasoconstriction

( INCREASE SYMPATHETIC DISCHARGE – 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

Relieve brain ischemia

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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

transmissiono 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 tracto 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 calcium-binding protein

• 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

calcitonin

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.

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.

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

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.

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ELECTROCARDIOGRAM

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

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