Post on 03-Apr-2018
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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