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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!!