Arterial b.p by Dr Sadia Zafar

7/28/2019 Arterial b.p by Dr Sadia Zafar

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ARTERIAL BLOOD

PRESSURE

It is the lateral pressure exerted by

circulating blood on the walls of systemicarteries.


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MEAN BLOOD

PRESSURE It is the average pressure in systemic arteries

present through out cardiac cycle .

It is the physiological mean blood pressure .

Mean B.P = Diastolic B.P + 1/3 Pulse pressure . = 80 +1/3 x 45

= 80 + 15= 95 mmHg


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PHYSIOLOGICAL VARIATION

IN B.P


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1.AGEB.P varies with ageNew born systolic B.P --40mm Hg

After 06 months --70-80mm Hg12 years --100 mm Hg

Adolescence --120mm Hg

Old Age --140mm Hg


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2. DIURNAL

VARIATION

Early morning minimum

Late evening --increases in 5 10mm Hg


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3.SEX Before menopause B.P is lower infemales as compared to males.

After menopause B.P is higher infemales as compared to males.

Cause: Estrogens lower plasmacholesterol level in female preventatherosclerosis.


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4.MEALS

5 mmHg of B.P can increased

5.POSTURE

Highest - Standing

Lowest - Lying down position

( In standing baroreceptors maintain B.P)


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6.SLEEP

During deep sleep - B.P Decreased

REM Sleep (terifying dreams) - B.P Increased

7.OBESITY

Obese - Increased B.P


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8.EMOTIONS

Anxiety - B.P Increased

9.RACES

(In some races) Increased B.P

10.EXERCISE

B.P Increased


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RECORDING OF

BLOOD PRESSURE


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BY SPHYGMOMANOMETER.

Principle:- The air pressure outside artery is balanced against

blood pressure inside the artery.

When air pressure is increased the artery iscompressed.

When air pressure is released there is partialocclusion of artery. This produces sound below thecuff.


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RATE OF LOWERING OF

AIR PRESSURE.

2 -3 mm Hg per sec. air pressure

should be lowered in the cuff.

B.P = c.output + Peripheral

resistance.


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REGULATION OF ARTERIAL BLOODPRESSURE.

1. Short term regulation

2. Long term regulation


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1. SHORT TERM

REGULATION:- This maintains B.P when there arerapid and momentary changes in B.P

e.g during: Postural changes, Diurnal variation

Sudden loss of blood from body.


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In short term regulation there are 3 typesof mech.

Nervous mech.

Hormonal mech.

Miscellaneous mech.


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1. Nervous mech:-

They are rapidly acting. They are activated in seconds.

(a) Baroreceptor reflex mech:_

Baroreceptors remain functional when mean B.P changesbetween 60 180 or upto 210 mm Hg.

when mean B.P falls below 60mmHg Baroreceptors are

not functional.

when B.P rises beyond 180mm Hg there is no additional stimulation of baroreceptors.


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B t l f h t


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Baroreceptors are only for shortterm regulation, undergoadaptation in 24 to 48 hours

So if a change in B.P persists formore then 48 hours baroreceptors

do not remain effective,

As seen in hypertensive patients, inthese patients baroreceptors resetat higher pressure.


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Baroreceptors maintain B.P during posturalchanges.

Baroreceptors minimize diurnal variationin B.P.

Baroreceptor mech is called pressurebuffer system.

Oppose changes in the B.P. The sensory nerves which carry impulse

from baroreceptors are called pressurebuffer nerves

e.g hearing nerve and sensory nerve ofvagi.


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Baroreceptor reflex theresponse to B.P:

B.P Firing of Baroreceptors in carotid artery & aorta

sensory neurons stimulate V.M.C (Cardiovascular control

centre in medulla) sympathetic part &

parasympathetic part.


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HIGH B.P


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PARASYM

Less Nor-Adr released More A.Ch at muscarinic receptor

Alpha receptor Beta1 receptor

SA NodeVent.myocarArterioS.M

V.D Less force of contr Less H.Rate

Less TPRLess C.O

LOW B.P

Less SYMP

V.M.C

BARORECEPTORS

HIGH B.P

Negative feed back

+


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CNS ISCHAEMIC RESPONSE

It is activated when mean B.P falls below 60 mmHg

Blood flow to the brain decreases ischemia of brain( including vasomotor centre)


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Ischemia of neurons of vasomotor centreoccurs

From vasomotor centre dischargeexcessively occurs along sympatheticnerves this leads to

Tachycardia

Vasoconstriction

Increased Blood Pressure


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This response is one the mostpowerful stimulant of the

sympathetic vasoconstrictornerves. This response is the last attempt

of body to safe life, called lastditch response.


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CUSHING REFLEX:- Cushing reflex is a specialized CNS ischemic

response

. When intracranial pressure become so high compresses the cerebral arteries ischemiaof brain

ischemic neurons in vasomotor centredischarge excessively increased peripharal

resistance ,increased B.P, increasesthe cerebral blood flow although

intracranial pressure is high.


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It is a protective mech to maintain cerebralblood flow when intracranial pressure becomes

very high.

In cushings reflex stimulus is increasedintracranial pressure.

When this reflex is initiated there will betachycardia.

Normal intracranial pressure -10-12 cm ofH2O When ICP is beyond 45cm of H2O cushing

reflex is initiated.


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CHEMORECEPTORS:-

The chemoreceptor helps tomaintain blood pressure when its fallsbelow 60mm Hg.

When B.P is low the blood flow inbody is sluggish:

P02 decreased.

PCO2 increased.

Ph decreased.


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So the chemoreceptors in carotidand aortic bodies are stimulated

impulses goes to vasomotor center tachycardica incr peripheralvasoconstriction incr B.P


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INCREASED CONTRACTION

OF SKELETAL MUSCLES:- When B.P falls symp stimulation

incr force of skeletal musclecontraction including abdominal andthoracic muscles this leads to

incr VENOUS RETURN incr CARDIAC OUTPUT

incr B.P


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HORMONAL MECHANISMS(Take minutes to

activate)


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Catecholamines:-

When B.P decreased symp stimulation large amount of catecholamines are

released from adrenal medulla.

Which produces same CVS effects as theeffects produced by sympathetic

stimulation increased peripheralresistance increased heart rate.


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b) Renin angiotensin

mechanism:-When B.P falls to low value renal bloodflow decr glomerular pressure decr (normal is 60 mm Hg) conc. of Na+ andCl at macula densa decr release ofrennin from juxta glomerular cells.


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Once released in blood persists for hour.

Juxtaglomerular cells release RENNIN.

Rennin acts on angiotensionogen to

form angiotensen-I

goes to lungcapillaries angiotensen-II formed whichremains for few minutes.


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LIVER

CONSTANTLY PRODUCESANGIOTENSINOGEN

IN PLASMA

B.P

J.G CELLS OF KIDNEY

PRODUCE

RENIN

ANGIOTENSIN 1

DECAPEPTIDE IN PLASMA

ANGIOTENSIN 2

OCTAPEPTIDE IN PLASMA

ENDOTHELIAL CELLS OF LUNG CAPILLARIES

CONTAIN ANGIOTENSIN-CONVERTING ENZYME (A.C.E)

CIRCULATES IN BLOOD FOR FEW MIN.

THEN DESTROYED BY ANGIOTENSINASE IN R.B.Cs etc


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ROLE OF ANG2 IN SHORT+LONGTERM CONTROL OF B.P:(in 20

min)

Arterioles

ANG2

VMC Hypothalamus Adrenal cortex

(Short-term) (LONG TERM )

V.C

Important in short term regulation only

(cvs response)ADH THIRST

(VOL & OSMOLARITY)

ALDOSTERONE

Na reabs

B.P


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3 MISCALLENEOUS


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3. MISCALLENEOUS

MECHANISMIS

1. Capillary fluid shiftWhen B.P incr CAPILLARYPRESSURE incr incr fluid passes

from blood to interstitial spaces blood vol dec decr VENOUSRETURN decr B.P


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When B.P dec capillary pressuredec less fluid passed from bloodto interstitial spaces blood volume

incr

incr venous return

incr B.P.


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STRESS RELAXATION:-

When the changes in B.P are due to changes inblood volume, there are changes in the size ofblood vessels so that B.P is regulated.e.g A pt. receives 2 liter of blood

transfusion B.P increased within 01 hour it comes back to normal

Mechanism involved

STRESS RELAXATION

Brings B.P back to normal


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Stress Relaxation. The smooth muscle in vessel wallundergo relaxation incr

blood vol can be accomodated. B.P falls back to normal.

This property of stress relaxation

is property of smooth muscles.


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Smooth muscle can change its size

without change in pressure. e.g smooth muscle in stomach wall

relaxes to allow extra food volume

without increase pressure.


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Reverse stress

relaxation When B.P falls due to blood loss thesmooth muscle in vessels wall contractsaround the reduced blood vol decrease

blood vol can adequately fill the vascularsystem. This reverse stress relaxation prevents

development of circulatory shock.


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IMPORTANT: One factor for SHOCK development is disparityb/w blood vol. & capacity of vascular system.

In NEUROGENIC SHOCK, blood vol is same butbecause of loss of vasomotor tone disparityshock.

In neurogenic shock reverse stress relaxation

cant prevent shock because of loss of Vasomotortone disparity b/w blood vol. & capacity ofvascular system.


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LONG TERM REGULATION

OF B.PThis maintains B.P for days, weeks,months or even years. It involves

renal body fluid pressure controlmechanism.


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Renal body fluid pressure control

mech.When B.P incr renal blood flow incr GLOMERULAR PRESSURE incr GLOMERULAR FILTERATION RATE incr

incr salt and water excreation in urine dec blood vol dec VENOUS RETURN dec CARDIAC OUTPUT decr B.P.


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When B.P falls renal blood flowdec GLOMERULAR PRESSURE dec GLOMERULAR FILTERATION

RATE dec dec lost of salt andwater or salt and water retension blood vol inc venous return &cardiac output inc B.P incr.


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When blood pressure changes thereare marked changes in urinary output.

Suppose B.P incr to 200 mmHg incurinary output.

When B.P is 60 mmHg Anuria

LOCAL BLOOD FLOW


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LOCAL BLOOD FLOWCONTROL MECHANISM:

Normally tissues are supplied by minimum amountof blood.

When 2% in B.Vol & 5% in C.Othere is autoregulation in tissues. Normally thereis V.C in tissues (because tissues at rest do notrequire amount of blood) TPR.

So due to C.O,TPR also due to autoregulatory V.C in tissuesB.P (due to both in C.O & in TPR).

So there will be 35-55% in B.P with only 2%

in blood vol.


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This is the basis of giving

diuretics in hypertensivepatients.


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Renal body fluid pressurecontrol mech.

It is assisted by 4 factors:

SYMP IMPULSES to kidney

RENNIN ANGIOTENSIN mech

ADH mech

ALDOSTERONE

e.g


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Suppose B.P

? SYMP impulses to kidney are inhibited V.D in kidney salt & water loss.

RENIN-ANGIOTENSIN will not beactivated.

ADH & ALDOSTERONE are not activated.

Net effect: amount of salt & water

loss in urine.


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B.P decreased - Increased SYMP IMPULSES tokidney

VASOCONSTRICTION

More RENNIN ANGIOTENSINE

ADH mech( water reabsorbed)

ALDOSTERONE (water retentions)

Net resultIncreased salt & water retained in

body

Increased B.P

Date post:	03-Apr-2018
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Arterial b.p by Dr Sadia Zafar

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