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Blood Pressure Regulation Nyunt Wai
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Blood pressure regulation 2013

May 07, 2015

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Health & Medicine

VNyunt Wai

Blood pressure variation and homeostasis - physiological basis for medical and health sciences students and professionals
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Page 1: Blood pressure regulation 2013

Blood Pressure Regulation

Nyunt Wai

Page 2: Blood pressure regulation 2013

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Pressure = force/unit area

Blood pressure =

pressure exerted by blood

on the walls of the

heart or

blood vessels

What is B.P.?

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PRESSURE falls

e.g. haemorrhage

same container;

same capacity;

less content

same content;

greater capacity

as the container

expands

Container vs. Content example

PRESSURE falls

e.g. generalized

vasodilation

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GREATER PRESSURE

Arterial BLOOD VOLUME ∞ Arterial BLOOD PRESSURE

Since the arterial system is not very distensible

More blood

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GREATER PRESSURE LESSER PRESSURE

PRESSURE creates FLOW

PRESSURE ∞ FLOW

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Functions of BP

• Intraventricular BP ejection of blood (stroke volume)

• Systemic arterial BP blood flow to tissues (tissue

perfusion)

• Capillary hydrostatic pressure filtration (tissue fluid

formation)

• Systemic venous BP blood flow back to the heart

(venous return)

The unconditional term

BLOOD PRESSURE

refers to

SYSTEMIC ARTERIAL

BLOOD PRESSURE

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blood pressure ∞ cardiac output

The determinants of BP

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Blood pressure ∞ Total Peripheral Resistance(TPR)

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Systemic arterial blood pressure

= Cardiac output x Total peripheral resistance (TPR) or Systemic vascular reistance (SVR)

The 2 Major Determinants of Arterial B.P.

The other Determinants of Arterial B.P.?

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Ventricular contraction

Ventricular relaxation Aorta is the most

elastic artery

When aortic elasticity

decreases (ageing or

disease):

Less expansion during

systole Incr. SBP

Less elastic recoil

during diastole decr.

DBP

Pulse pressure ?

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• Stroke volume

• Aortic distensibility (elasticity)

DBP

• SBP

• Aortic distensibility

(elasticity)

• TPR

SBP = CO x TPR

DBP = CO x TPR

SBP

The Determinants of Arterial B.P.

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Physiological Variations in BP

• Age: – SBP and DBP gradually rise with age (after about 30 years), the

SBP more so and more sustained than the DBP

• Sex: – the rise in BP with age is greater in males

• Circadian variation (diurnal variation): – lowest during sleep (nocturnal dip) and highest in the mornings after

waking up

• Increased transiently during physical stress (e.g. muscular exercise), mental stress(anger, apprehension, resentment, mental concentration), emotional excitement

• The effect of Gravity: When erect, BP in any vessel varies in relation to the vertical distance from the heart level

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Physiological Variations in BP

• Gravity – In an upright position, BP

in the arteries below the heart level is increased, and that in the arteries above the heart level is decreased by 0.77 mm Hg for each cm of vertical distance below or above the heart.

– Thus, routine measurement of BP should be performed with the artery at the heart level.

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Effect of Gravity

• Pressure in large artery in the

foot 105 cm below the heart =

[0.77 mmHg/cm x 105 cm = 80

mm Hg)] +

• 100 mm Hg (Mean ABP at heart

level)

• = 180 mm Hg

• Pressure in vein in the foot 105

cm below the heart = [0.77

mmHg/cm x 105 cm = 80 mm

Hg)] +

• 4 mm Hg (right atrial pressure)

• = 84 mm Hg

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REGULATION OF SYSTEMIC ARTERIAL B.P.

– MAINTENANCE OF RESTING B.P.

B.P. HOMEOSTASIS

• SITUATIONAL ADJUSTMENT OF B.P.

e.g. changes in B.P. during muscular exercise

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Regulation of

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Systemic arterial blood pressure

= Cardiac output x Total peripheral resistance (arteriolar tone)

More immediate

More efficient:

RESISTANCE = 1

Radius

More economical

4

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BP REGULATORY MECHANISMS

NEURAL: CARDIOVASCULAR REFLEXES

Baroreceptor reflexes

Chemoreceptor reflexes

Brain(CNS) ischaemic response

HORMONAL

Catecholamines

Renin-angiotensin-aldosterone(RAA) system

Vasopressin

RENAL-BODY FLUID CONTROL SYSTEM

Short term:

Rapid

Short term:

Intermediate

Long term

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Receptors

Brain stem: Medulla

Spinal cord:

SYMPATHETIC

NERVOUS

SYSTEM

Integrating centres

Effectors

Hypothalamus

Afferents Efferents

X

(Parasym)

Vasopressin

Sym .outflow

• Baroreceptors

• Chemoreceptors

IX, X

(Parasym)

• Heart, Blood vessels

• Adrenal medulla: Catecholamines

• Kidney: activation of RAA system

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Sympathetic Nervous System

• Major effector system for BP control

• Increased sympathetic tone incr. BP

• decreased sympathetic tone decr. BP

• Sym.N.S. is under the control of vasomotor

centre (VMC) in the medulla

• Descending tracts from the VMC excites the

sympathetic nervous system

• Inputs from the broreceptors and other receptors

go to the VMC (the integrating centre)

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How does sympathetic N.S. activity

increase BP?

• Direct cardiovascular effects

• Neuroendocrine effects: activation of

– adrenal medulla

– renin-angiotensin-aldosterone (RAA) system

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SYMPATHETIC

OUTFLOW

Sympathetic tone

HR SV Venoconstrictn Arteriolar constrictn

Venous return

CARDIAC OUTPUT TPR

Capillary pressure

ISF formation

Plasma loss

BLOOD PRESSURE

DIRECT CARDIOVASCULAR EFFECTS

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SYMPATHETIC

OUTFLOW

Sympathetic tone

ADRENAL MEDULLA

BLOOD PRESSURE

JG CELLS IN KIDNEY

Secretion of

CATECHOLAMINES

CARDIOVASCULAR EFFECTS

Activation of

RENIN- ANGIOTENSIN-

ALDOSTERONE SYSTEM

VOLUME EFFECTS

NEUROENDOCRINE EFFECTS

Page 25: Blood pressure regulation 2013

25 BLOOD PRESSURE

CATECHOLAMINES

Noradrenaline Adrenaline Dopamine

a- receptors b- receptors

Vasoconstriction Cardiostimulatory effects:

Automaticity (SANodal

discharge)

Conductivity

Excitability

Myocardial contractility

TPR Cardiac output

Heart Rate

Stroke volume

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Sympathetic tone

Juxtaglomerular(JG) cells in

afferent arteriolar muscle coat in KIDNEY

RENIN- ANGIOTENSIN-ALDOSTERONE SYSTEM

BLOOD

VOLUME/PRESSURE

Renal perfusion pressure

Baroreceptor reflex

Angiotensinogen Angiotensin I

ANGIOTENSIN II

RENIN

LIVER

Angiotensin-

Converting

Enzyme

Endothelial cells of

pulmonary circulation

VASCULAR and VOLUME EFFECTS

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ANGIOTENSIN II

Vascular smooth muscle VASOCONTRICTION

Sympathetic nerve endings

Adrenal cortex

Facilitates release of

NORADRENALINE

Secretion of ALDOSTERONE

Brain: Hypothalamus

Stimulation

of THIRST

Release of VASOPRESSIN

Water intake

Renal reabsorption of Sodium

Renal reabsorption of Water BLOOD VOLUME

TPR

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THE BARORECEPTOR REFLEX

operates within seconds

for moment to moment, day to day control

of BP

for BP homeostasis in the face of

challenges such as blood loss

Afferents: Parasympathetic

Efferents: Sympathetic noradrenergic

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Baroreceptors = stretch receptors in the walls of

• Heart

Atria

• Arteries (arterial baroreceptors)

Aortic arch

Carotid sinus

Volume receptors

Low pressure baroreceptors

High pressure baroreceptors

BP

Wall

Stretch on

the wall

Stimulation of Stretch

receptors in the wall

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Arterial baroreceptors

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Basic network

How the baroreceptor reflex works

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Incr. baroreceptor discharge

• Stimulates the Parasympathetic centres

(Dorsal motor nucleus of vagus) in the

medulla

• Inhibits the vasomotor centre (VMC) in the

medulla (through inhibitory interneurones)

– Decr. excitatory discharge from the VMC to

the Sympathetic Nervous System in the spinal

cord

– decr. sympathetic noradrenergic discharge

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Inhibits VMC stimulates motor vagal

nuclei

Parasym. fibres in IX and

X cranial nerves

Carotid sinus, aortic arch

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•Adrenal

medulla

•RAA system

•Hypothalamus

•Posterior pituitary

•Vasopressin (ADH)

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HYPOTHALAMUS

POSTERIOR

PITUITARY VASOPRESSIN

Generalized vasoconstriction

(V1 receptors) TPR

Renal reabsorption of water

(V2 receptors)

plasma volume CARDIAC OUTPUT

BP

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Note

• BP may not fall with minor haemorrhage

• Fall in venous return is detected by low pressure baroreceptors increase in TPR compensates for fall in CO BP unchnaged

• When blood loss is >20% of circulating blood volume, the fall in CO is great enough to cause a fall in BP

• BP = CO x TPR

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50 110 mm Hg

MEAN ARTERIAL B.P.

CHEMO-

RECEPTORS

BARORECEPTORS

S E

N S

I T

I V

I T

Y

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Neural regulation of B.P.

Baroreceptor reflex

Chemoreceptor reflex

CNS ischaemic

response

120

100

80

60

40

B.P.

mmHg

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The chemoreceptor reflex

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CAROTID BODIES

AORTIC BODIES

ARTERIAL

CHEMORECEPTORS

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BP BLOOD FLOW STAGNATION

O2 delivery to tissues (stagnant hypoxia)

CO2 uptake from tissues

O2 CO2 (in tissues)

Stimulation of chemoreceptors

•Stimulation of medullary respiratory centre

•Stimulation of medullary VMC

sympathetic discharge BP

IX, X

nerves

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Medulla oblongata

VASOMOTOR

CENTRE

Spinal Cord

SYMPATHETIC

OUTFLOW

(+)

(+)

Sympathetic tone

BLOOD

PRESSURE

CEREBRAL

BLOOD FLOW

PO2

Stagnant

hypoxia

PCO2

CNS ISCHAEMIA

The CNS ischaemic response

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CUSHING’S

REFLEX

VMC

SYMPATHETIC

OUTFLOW

(+)

(+)

Sympathetic tone

BLOOD

PRESSURE

CEREBRAL

BLOOD FLOW

PO2

Stagnant

hypoxia

PCO2

CNS ISCHAEMIA

Increased intracranial pressure

Pressure on cerebral arteries

BARORECEPTOR REFLEX

VAGAL TONE

HEART RATE

HEAD INJURY

Normal

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Head injury CNS ischaemia The rise in BP

• Baroreceptor reflex

– stimulation of vagus fall in HR (since

parasympathetic control of HR is dominant

over sympathetic control)

– but baroreflex-mediated inhibition of VMC

is counterbalanced by direct stimulation of

VMC by CNS ischaemia

– sympathetic-mediated generalized

vasoconstriction maintained Incr. in BP

Slow, full and bounding pulse CUSHING’S REFLEX

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Cushing's reflex

• Because the skull is rigid after infancy, intracranial masses or swelling may increase intracranial pressure. When intracranial pressure is increased sufficiently, regardless of the cause, Cushing's reflex and other autonomic abnormalities can occur.

• Cushing's reflex includes systolic hypertension, increased pulse pressure, and bradycardia.

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Renal regulation of B.P.

I. Physical : by variation of Glomerular

filtration pressure variation in urine

formation

II. Hormonal : by secretion of renin

• Renin-Angiotensin (AGII)-

Aldosterone system (RAAS)

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Renal regulation of B.P.

When blood volume and BP is increased,

KIDNEYS excrete excess fluid by

• Pressure diuresis

• Pressure natriuresis

increased urine formation as a result of increased

glomerular filtration due to raised renal perfusion

pressure

increased urinary excretion of sodium as a

result of increased glomerular filtration of

sodium due to raised renal perfusion pressure

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Renal regulation of B.P.

When blood volume and BP is decreased:

decr. glomerular capillary H.P. decr.GFR

• Oliguria (deceased urine formation)

• Anuria (renal shutdown – no urine formation)

Thus KIDNEYS conserve ECF Volume

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Anuria

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Summary :Systemic Arterial

Blood Pressure • Varies with the amount of blood in the systemic

arterial system (begins at the aorta, ends at

arterioles in various tissues)

• This is because the systemic arteries are not

very distensible

• The greater the cardiac output, the greater the

inflow of blood into the systemic arterial system,

the higher is the BP

• The greater the TPR, the lesser the outflow of

blood out of the systemic arterial system, the

higher is the BP

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Systemic Arterial Blood

Pressure • Sympathetic nervous system and the RAA

system are powerful systems that can increase BP

• Moment to moment control is by baroreceptor reflex.

• What is the use of increasing the BP when blood supply to almost all tissues are shut down by arteriolar constriction?

• Ans. Local vasodilatory mechanisms in the vital organs- the brain and the heart, will overcome the systemic vasoconstrictor effect– diverting blood flow to them at the expense of other organs and tissues End