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CVSBLOOD PRESSURE & ITS REGULATION

HYPERTENSIONDepartment of Physiology

Mahatma Gandhi Medical College & Hospitals, Jaipur

Blood pressure• Definition

• Systolic pressure

• Diastolic pressure

• Pulse pressure

• Mean arterial pressure

• MAP= diastolic pressure+1/3 pulse pre

Blood pressure

• Measurement:

• By catheterization

• Sphygmomanometer

• Mercury manometer

• Aneroid type

• Electronic ( digital)

• Automatic (ICU)

Sphygmomanometer

• Riva –Roci cuff. 1896- pediatrician

• Korotkoff(1905) by listening to sounds

Blood pressure

• Children 5 cm

• Adolescent 8 cm

• Adult 12 cm

Blood pressure

• Procedure

• Palpatary method

• Auscultatary method

• Korotkoff’s sounds – 1905

• Introduced auscultatory method – SBP-DBP

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• Other methods

• Oscillometric method

• Using doppler method

• Arterial tonometry

Blood pressure

• Determinants of BP

• Physical- blood volume

• vascular capacity

• Physiological- cardiac output

• peripheral resistance

Blood pressure

• Variations in BP

• Age

• Sex

• Meals

• Diurnal

• Pregnancy

• Posture

• Exercise

• Gravity

Gravity effect • Vasovagal syncope- emotional fainting

• Activation of muscle vasodilator system

• Activation of cardiac vagal activity

• Fall in BP

• Reduced cerebral blood flow

• Loss of conciousness

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at i Vasovagal syncope- emotional fainting s

vasovagal

Medulla

Arterial Pressure

Loss of Consciousness

Total Peripheral

Resistance

Venous Return

Cardiac Output

Emotional

Stress

Cerebral

blood flow

hypothalamusAVP

release

Decreased

Sympathetic Output

Increased

Vagal Ouput

Cortex

Regulation of BP

• Short term regulation

• Intermediate regulatory mechanisms

• Long term regulation

Regulation of BP• Vasomotor center

• Reticular formation of medulla and pons

• Affects activity of both symp. And parasymp.

• Vasoconstrictor area

• Vasodilator area- inhibit vasocons. area

• Sensory area – in tractus solitarius

• Receive information from IX & X nerve

The vasomotor centre

• The VMC transmits impulses downward through the cord to almost all blood vessels

• VMC is located bilaterally in the reticular substance of the medulla and the lower third of the pons

• The VMC is composed of a vasoconstrictor area, vasodilator area, and sensory area

Figure 18-3

Functions of The Vasomotor Center

• Vasoconstrictor area of VMC transmits signals continuously to sympathetic nerve fibers called sympathetic vasoconstrictor tone. These impulses maintain partial state of contraction in blood vessels called vasomotor tone

• Lateral portions of VMC controls heart activity by increasing heart rate

and contractility

• Medial portion of VMC transmits signals via vagus nerve to heart to decrease heart rate

Figure 18-4• Many higher centers of the brain such as the

hypothalamus can exert powerful excitatory or inhibitory effects on the VMC

Many higher centers of the braininfluence VMC

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Regulation of BP

• Sympathetic tone

• In heart

• In blood vessels

• Vagal tone

Regulation of BP

• Rapid control mechanisms

• Baro receptor reflex

• Location of receptors

• Type of receptors

• Nerve supply

• Response range- 0mm to 60mm Hg- no effect

• 60mm Hg to 150mmHg

• Normal operation – MAP of 100mmHg

• Resting discharge

Baro receptor location

fig 12-53

Baro receptors

Baro-receptors Baro receptors

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Blood pressure Blood pressure

Regulation of BP• Carotid v/s aortic baro receptors

• Response pattern when BP rises

• Response when BP falls

• Responds better to fluctuating pressure than static rise in pressure

• Response to change in posture

• Not good for long term regulation

• Due to Resetting

•Effect of posture

Decrease

Cardiac Output

Sensed By

Baroreceptors

Supine Standing

Decrease

Central

Blood Volume

Vasomotor

Center

Sympathetic

Nervous Activity

Decrease

Arterial Pressure

Baroreceptor response

fig 12-54

blood pressure → firing rate

fig 12-55

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Blood pressureResponse to hemorrhage

fig 12-56

hemorrhage → blood pressure

B.P. → baroreceptor response

fig 12-52

Response to standing up (from lying position)

fig 12-56 modified

standing

blood pools in legs

venous return

cardiac ouput

arterial pressure

after a few seconds, little

change in blood pressure

• Chemoreceptor reflex

• Location

• Innervations

• Stimulus

• Blood flow

• Responds better if MAP fall below 60mmHg

• Raises BP when stimulated -via VMC

Chemo receptors • Atrial and pulmonary artery reflexes

• Low pressure receptors

• Stretch receptors

• Responds to change in volume

• Infusion of 300ml fluid

• With intact receptors BP rises by 15mmHg

• With baroreceptor removed BP rises by 40mmHg

• With removal of low pressure receptors BP rises by 100mmHg

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• Atrial reflex- volume reflex

• Atrial stretch– ADH decrease

• Fluid loss

• ANP secretion increased

• Natriuresis and diuresis

• Atrial stretch– reflex renal vasodilation

• Bainbridge reflex and BP

• CNS ischemic response

• Fall in blood pressure

• Cerebral ischemia

• VMC strongly stimulated

• Vasoconstrictor area &cardio accelerator neurons activated

• Strong activation of heart and blood vessels

• Severe peripheral vasoconstriction

• Rise in systemic arterial pressure

CNS Ischemic Response

• CNS Ischemic response is activated in response to cerebral ischemia

• Reduced cerebral blood flow causes CO2 buildup which stimulates vasomotor center thereby increasing arterial pressure

• CNS Ischemic response is one of the most powerful activators of the sympathetic vasoconstrictor system

VasomotorCenter

CerebralIschemia

CO2 ArterialPressure

SympatheticActivity

Figure 18-3

• CNS ischemic response –most powerful of all activators of vasoconstriction

• Gets activated below MAP of 60mmHg

• Only emergency control mechanism

• Can elevate MAP to 250mmHg

• Last ditch stand

• Build up of CO2 in VMC

• Accumulation of lactic acid

• Other acid metaboites

• Cushing reaction:

• Special type of CNS ischemic response

• Increase pressure of CSF

• Compresses brain and cerebral vessels

• Cerebral ischemia

• CNS ischemic response

• Increased blood pressure

• Restoration of cerebral blood flow

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Intermediate/long term regulation

• Renin-Angiotension system

• JG cells ( modified smooth muscle cells)

• In afferent arteriole

• Fall in BP- pro renin –Renin

• Angiotensinogen ( 12 amino acids)

• renin

• Angiotensin I (deca peptide)

• Renin half life= 30 to 60 mnts

Renin-Angiotension system

• Angiotensin I

• ACE lungs, kidneys, blood vessels

• Angiotensin II ( octapeptide)

• Actions of angiotensin II

• Intra renal

• Extra renal

Renin-Angiotension system

• Extra renal effects

• Vascular

• Adrenal cortex

• Brain

Renin Angiotensin system

• Renin – proteolytic enzyme

• JG apparatus-

• JG cells

• Macula Densa cells

• Lacis cells( Polkissen cells)

• Messangial cells

Renin Angiotensin system

• Angiotensinogen

• Renin

• Angiotensin I Bradykinin

• ACE

• Angiotensin II Inactive metabolites

• Peptidases

• Angiotensin III & IV

& Inactive metabolites

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Renin Angiotensin system• Factors causing Renin release:

• Sympathetic stimulation

• Renal artery constriction

• Hyponatrimia

• Hypotension

• Hypovolemia

• Dehydration

• Cardiac failure

Renin Angiotensin system

• Upright posture

• Cirrhosis liver

• Catecholamine

• Prostaglandins

• Psychological stimuli

• Any factor associated with CVP

Renin Angiotensin system

• Decrease Renin release:

• Sodium & chloride absorption across macula densa

• Afferent arteriolar pressure

• Angiotensin II

• Vasopressin

Renin Angiotensin system

• Actions of Angiotensin II

• Receptors; AT I & AT II

• 1.Strong vasoconstriction—

• Effect is less potent in sodium depleted state-receptor down regulation

• 2. Aldosterone secretion

• 3. Release norepinephrine from symp. nerves

Renin Angiotensin system• 4. Contraction of Mesangial cells GFR

• 5. Tubular sodium absorption-direct action

• 6. Sensitivity of baro receptors reflex—

potentiates pressure effects of Ang. II

• Stimulates thirst center water intake

Renin Angiotensin system

➢Secretion of Vasopressin & ACTH- Ang. II-does

➢not cross BBB- acts via circumventricular organ

➢Area postrema– pressure response

➢OVLT & SFO-- water intake

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Renin Angiotensin system➢Angiotension III – strong Aldosterone secretion effect

➢Receptors - AT1 & AT2

➢AT1- coupled to G protein

➢ phospholipase C

➢ Cytosole Ca++

➢Activates Tyrosine Kinase

Intermediate/long term regulation• Aldosterone mechanism

• Anti diuretic hormone( vasopressin)

• Catecholamines

• Atrial natriuretic hormone

Long term regulation Long term regulation

• Two determinants:

• 1. renal output of salt and water

• 2. level of salt and water intake

• Long term basis – BP can be changed only by changing one of the above parameters

Renal output of salt and water

Equilibrium point

Change in renal output

curve

Change in salt and water intake

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Long term regulation

• Thus It is impossible to change the long term Mean arterial pressure level without changing one or both basic determinants of long term arterial pressure ie.

➢Level of salt and water intake

➢Change in renal output curve for salt and water

• If disturbed: pressure is regulated at new pressure level

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Long term regulation

• Capillary fluid shift mechanism

• Stress relaxation( delayed compliance)

Hypertension

• Definition

• Systolic hypertension

• Diastolic hypertension

• Both elevated

• Persistent SBP greater than or equal to 140 mmHg, & DBP greater than or equal to 90mmHg

Hypertension

• Pre hypertension :

• SBP- 120 to 139mmHg

• DBP – 80 to 89mmHg

• Hypertension stage 1- SBP- 140 to159mmHg,

• DBP – 90 to 99mmHg

Hypertension

• Hypertension stage 2

• SBP- 160mmHg or more

• DBP- 100mmHg or more

Hypertension

• Primary: Idiopathic, Essential hypertension

• 90 to 95% hypertension – primary

• Water & salt retention

• Altered Renin- Angiotension mechanism

• Stress & increased sympathetic activity

• Insulin resistance & hyper-insulinemia

• Endothelial cell dysfunction

• Nitric Oxide & Endothelins

Hypertension

• Changed baro-receptor sensitivity-

Results into:

• Resetting of baro-receptors

• Atherosclerosis

• Deranged renal functions

• Obesity , sedentary life style

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Hypertension

• Secondary:

• Chronic kidney disease

• Toxemia of pregnancy( endothelial dysfunction- decrease vasodilator release)

• thickning of glomerular membrane

• Neurogenic hypertension

• Coarctation of aorta( high BP in upper part of body)

Hypertension

• Cushing syndrome

• Conn’s disease

• Acromegaly & hypothyroidism

• Pheo chromo cytoma

• Iatrogenic:

• Oral contraceptives

• Prolonged use of NSAIDs

Goldblatt hypertension• One kidney Goldblatt hypertension:

• One kidney is removed

• Other kidney renal artery constricted

• Early rise in BP- renin-Angio. Mech.

• Delayed rise – retention of salt & water

• Due to angiotension II & Aldosterone

Goldblatt hypertension• Two kidney Goldblatt hypertension:

• One renal artery constricted, other normal

• Constricted kidney- secrete renin-Angio.

• Normal & constricted kidney retain salt and water--hypertension

Malignant hypertension

• Medical emergency

• Very high BP that occurs suddenly and quickly

• 1% of hypertensives

• Adults and children

• DBP may rise to 130 mmHg

Malignant hypertension

• Extremely high BP

• Swelling in lower limbs

• Abnormal heart sounds

• Pulmonary edema

• CNS changes

• Bleeding in retina

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To be continued

•Thank You!!