ARTERIAL BLOOD PRESSURE

It is the lateral pressure exerted by circulating blood on the walls of systemic arteries.

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

PHYSIOLOGICAL VARIATION IN B.P

1.AGE
B.P varies with age New born systolic B.P --40mm Hg After 06 months --70-80mm Hg 12 years --100 mm Hg Adolescence --120mm Hg Old Age --140mm Hg

2. DIURNAL VARIATION
Early morning minimum Late evening --increases in 5 10mm Hg

3.SEX
Before menopause B.P is lower in females as compared to males.
After menopause B.P is higher in females as compared to males. Cause: Estrogens lower plasma cholesterol level in female prevent atherosclerosis.

4.MEALS

5 mmHg of B.P can increased

5.POSTURE Highest Lowest Standing Lying down position

( In standing baroreceptors maintain B.P)

6.SLEEP
During deep sleep B.P Decreased B.P Increased

REM Sleep (terifying dreams) -

7.OBESITY
Obese Increased B.P

8.EMOTIONS
Anxiety B.P Increased

9.RACES
(In some races) Increased B.P

10.EXERCISE
B.P Increased

RECORDING OF BLOOD PRESSURE

BY SPHYGMOMANOMETER.
Principle: The air pressure outside artery is balanced against blood pressure inside the artery. When air pressure is increased the artery is compressed. When air pressure is released there is partial occlusion of artery. This produces sound below the cuff.

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.

REGULATION OF ARTERIAL BLOOD PRESSURE.

1. Short term regulation 2. Long term regulation

1. SHORT TERM REGULATION: This maintains B.P when there are rapid and momentary changes in B.P e.g during: Postural changes, Diurnal variation Sudden loss of blood from body.

 In short term regulation there are 3 types of mech.

Nervous mech. Hormonal mech. Miscellaneous mech.

1. Nervous mech:
They are rapidly acting. They are activated in seconds.

(a) Baroreceptor reflex mech:_

Baroreceptors remain functional when mean B.P changes between 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.

 Baroreceptors are only for short term regulation, undergo adaptation in 24 to 48 hours

So if a change in B.P persists for more then 48 hours baroreceptors do not remain effective,
As seen in hypertensive patients, in these patients baroreceptors reset at higher pressure.

 Baroreceptors maintain B.P during postural changes. Baroreceptors minimize diurnal variation in B.P. Baroreceptor mech is called pressure buffer system. Oppose changes in the B.P. The sensory nerves which carry impulse from baroreceptors are called pressure buffer nerves e.g hearing nerve and sensory nerve of vagi.

Baroreceptor reflex the response 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.

HIGH B.P

HIGH B.P BARORECEPTORS + V.M.C Less SYMP Negative feed back

PARASYM More A.Ch at muscarinic receptor Beta1 receptor Vent.myocar Less force of contr Less C.O

Less Nor-Adr released Alpha receptor ArterioS.M V.D Less TPR

SA Node
Less H.Rate

LOW B.P

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)

 Ischemia of neurons of vasomotor centre occurs From vasomotor centre discharge excessively occurs along sympathetic nerves this leads to
Tachycardia Vasoconstriction

Increased Blood Pressure

 This response is one the most powerful stimulant of the sympathetic vasoconstrictor nerves. This response is the last attempt of body to safe life, called last ditch response.

CUSHING REFLEX: Cushing reflex is a specialized CNS ischemic response . When intracranial pressure become so high compresses the cerebral arteries ischemia of brain ischemic neurons in vasomotor centre discharge excessively increased peripharal resistance ,increased B.P, increases the cerebral blood flow although intracranial pressure is high.

 It is a protective mech to maintain cerebral blood flow when intracranial pressure becomes very high. In cushings reflex intracranial pressure. stimulus is increased

When this reflex is initiated there will be tachycardia.

Normal intracranial pressure -10-12 cm of H2O When ICP is beyond 45cm of H2O cushing reflex is initiated.

CHEMORECEPTORS: The chemoreceptor helps to maintain blood pressure when its falls below 60mm Hg. When B.P is low the blood flow in body is sluggish: P02 decreased. PCO2 increased. Ph decreased.

 So the chemoreceptors in carotid and aortic bodies are stimulated impulses goes to vasomotor center tachycardica incr peripheral vasoconstriction incr B.P

VASOCONSTRICTION
When B.P falls there is symp. Stimulation. Veins are constricted mean systemic filling pressure & venouse return incr cardiac output incr B.P incr.

INCREASED CONTRACTION OF SKELETAL MUSCLES:When B.P falls symp stimulation incr force of skeletal muscle contraction including abdominal and thoracic muscles this leads to incr VENOUS RETURN incr CARDIAC OUTPUT incr B.P

HORMONAL MECHANISMS (Take minutes to activate)

Catecholamines:When B.P decreased symp stimulation large amount of catecholamines are released from adrenal medulla. Which produces same CVS effects as the effects produced by sympathetic stimulation increased peripheral resistance increased heart rate.

b) Renin angiotensin mechanism:When B.P falls to low value renal blood flow decr glomerular pressure decr ( normal is 60 mm Hg) conc. of Na+ and Cl at macula densa decr release of rennin from juxta glomerular cells.

Once released in blood persists for hour. Juxtaglomerular cells release RENNIN. Rennin acts on angiotensionogen to form angiotensen-I goes to lung capillaries angiotensen-II formed which remains for few minutes.

CONSTANTLY PRODUCES
LIVER

ANGIOTENSINOGEN IN PLASMA

J.G CELLS OF KIDNEY

B.P PRODUCE RENIN

ENDOTHELIAL CELLS OF LUNG CAPILLARIES

ANGIOTENSIN 1
DECAPEPTIDE IN PLASMA

CONTAIN ANGIOTENSIN-CONVERTING ENZYME (A.C.E) ANGIOTENSIN 2 OCTAPEPTIDE IN PLASMA CIRCULATES IN BLOOD FOR FEW MIN.

THEN DESTROYED BY ANGIOTENSINASE IN R.B.Cs etc

ROLE OF ANG2 IN SHORT+LONG TERM CONTROL OF B.P:(in 20 min)

ANG2
(Short-term) (LONG TERM )

Arterioles

VMC

Hypothalamus

Adrenal cortex
ALDOSTERONE

(cvs response) V.C Important in short term regulation only

ADH

THIRST

Na reabs

(VOL & OSMOLARITY)

B.P

3. MISCALLENEOUS MECHANISMIS 1. Capillary fluid shift When B.P incr CAPILLARY PRESSURE incr incr fluid passes from blood to interstitial spaces blood vol dec decr VENOUS RETURN decr B.P

 When B.P dec capillary pressure dec less fluid passed from blood to interstitial spaces blood volume incr incr venous return incr B.P.

STRESS RELAXATION:When the changes in B.P are due to changes in blood volume, there are changes in the size of blood 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

Stress Relaxation.
The smooth muscle in vessel wall undergo relaxation incr blood vol can be accomodated. B.P falls back to normal. This property of stress relaxation is property of smooth muscles.

 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.

Reverse stress relaxation

When B.P falls due to blood loss the smooth muscle in vessels wall contracts around the reduced blood vol decrease blood vol can adequately fill the vascular system. This reverse stress relaxation prevents development of circulatory shock.

IMPORTANT:
One factor for SHOCK development is disparity b/w blood vol. & capacity of vascular system.
In NEUROGENIC SHOCK, blood vol is same but because of loss of vasomotor tone disparity shock. In neurogenic shock reverse stress relaxation cant prevent shock because of loss of Vasomotor tone disparity b/w blood vol. & capacity of vascular system.

LONG TERM REGULATION OF B.P

This maintains B.P for days, weeks, months or even years. It involves renal body fluid pressure control mechanism.

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.

 When B.P falls renal blood flow dec GLOMERULAR PRESSURE dec GLOMERULAR FILTERATION RATE dec dec lost of salt and water or salt and water retension blood vol inc venous return & cardiac output inc B.P incr.

 When blood pressure changes there are marked changes in urinary output. Suppose B.P incr to 200 mmHg inc urinary output. When B.P is 60 mmHg Anuria

LOCAL BLOOD FLOW CONTROL MECHANISM:

Normally tissues are supplied by minimum amount of blood. When 2% in B.Vol & 5% in C.O there is autoregulation in tissues. Normally there is V.C in tissues (because tissues at rest do not require amount of blood) TPR. So due to C.O, TPR also due to autoregulatory V.C in tissues B.P (due to both in C.O & in TPR). So there will be 35-55% in B.P with only 2% in blood vol.

 This is the basis of giving diuretics in hypertensive patients.

 Renal body fluid pressure control mech.

It is assisted by 4 factors: SYMP IMPULSES to kidney RENNIN ANGIOTENSIN mech ADH mech ALDOSTERONE e.g

Suppose B.P ?
SYMP impulses to kidney are inhibited V.D in kidney salt & water loss. RENIN-ANGIOTENSIN will not be activated. ADH & ALDOSTERONE are not activated. Net effect: amount of salt & water loss in urine.

B.P decreased - Increased SYMP IMPULSES to kidney VASOCONSTRICTION More RENNIN ANGIOTENSINE
ADH mech( water reabsorbed)

ALDOSTERONE (water retentions)

Net result Increased salt & water retained in body Increased B.P