Lecture 7 - Regulation of Blood Pressure

8/12/2019 Lecture 7 - Regulation of Blood Pressure

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The extrinsic regulation of blood

pressure and cardiac output

Lecture 7

Chapter 22 B&BAll but pages 550-554


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Arterial Blood Pressure

Flow Pressures

Aortic arch

Thoracic aorta

Abdominal aorta

Femoral artery

~120 systolic/80 diastolic

Flow changes b/c

-resistance

-compliance

-inertia


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Mean Arterial Blood Pressure (MAP)

MAP = DP + 1/3 (SP-DP)

average arterial blood pressure

during a cardiac cycle

Perfusion pressure

A MAP of ~ 60 mmHg is

sufficient for end organ

perfusion.

For a BP of 120/80, MAP is

~ 93.5 mmHg


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stretch

Baroreceptor Feedback Loop for the Regulation of

Mean Arterial Blood Pressure

mechanoreceptors


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High pressure baroreceptors respond to stretch in

the aortic arch and carotid sinus.

sinus nerve

depressor nerve


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Fig 22-2

Carotid and Aortic Baroreceptors


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Aortic sinus

Carotid nerve fires above and belownormal pressures.

Aortic nerves are activated abovenormal pressures.

The aortic receptors help reinforce the carotid activation above normal

pressures.

MAP ~ 93.5 mmHg


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MAP

Increased firing ofBaroreceptors

by stretch

Medulla Oblongata

Sympathetic and

Parasympathetic

EFFERENTS

Vagal/glossopharyngeal

AFFERENTS

TARGET ORGANS

-heart

-blood vessels

-adrenal medulla

-glands (skin/sweat)

NTS

Cardio-inhibitory area

Vasomotor area


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Medullary

Cardiovascular Center

Nucleus

of the Tractus

Solitarius (NTS)

Vasomotor area

Receives

afferents from CN IX and X

interneurons

Dorsal motor nucleus of X

Nucleus ambiguous of

X and IX

Cardio-inhibitory

Area

+

+

-

Increased MAP


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Vasomotor area

Dorsal motor nucleus of X

Nucleus ambiguous of

X and IX

Cardio-inhibitoryArea

To spinal cord

Sympathetic activation of:

-Blood vessels

-Heart

-Adrenal medulla

To heart

Parasympathetic activation

bradycardia

(tonic vasoconstriction)

Coordination of Medullary Cardiovascular Inputs


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afferents efferents

Fig. 22-4


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Low Pressure Cardiac Baroreceptors

Respond to fullness or volume

Located in Low pressure sites

Control the effective circulating volume Indirect lyregulate MAP

Unlike activation of the high-pressure

baroreceptors, activation of the A and

B fibers will INCREASEheart rate.(and also cause renal vasodilation).

Bainbridge Reflex


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The dependence of cardiac output on effective

circulating volume is the result of the complex

Interplay among three factors :

1) Bainbridge reflex

2) Baroreceptor reflex

3) Starlings Law


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Cardiac Output

Stroke Volume

Heart rate

BainbridgeBaroreceptor

In volume loading

conditionsBainbridge

response prevails

In volume depletion

conditionsBaroreceptor

response prevails

Bainbridge responseonly HRis affected

Baroreceptor -Increased stretch on high

pressure decreases stroke

volumeflattening the Starling response.

Heart rateincreases under

volume depletion and

loading


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Sympathetic input - HEART

ACTIONS

Nerve fibers release

NE

SA, atria, andventricles

HR and contractility

R side SA node L side contractility

MECHANISM

1 receptors

pacemaker activity

1 myocardium

contraction


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Parasympathetic input - HEART

ACTIONS

Vagus nerve releases

ACH

SA and myocardium

HR and conduction

velocity

R side SA node (HR) L side contractility

(slight)

MECHANISM

Muscarinic receptors

(M2)

subunit (HR) Nitric oxide (weak

inotropic effect)


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Sympathetic inputBlood vessels

ACTIONS

Activated -

Vasoconstriction

throughout body Skin/kidney BVs

most abundant

De-activated

Vasodilation

MECHANISM

Norepinephrine

>

Epinephrine >

Vasoconstriction1Vasodilation2


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Parasympathetic inputBlood vessels

ACTIONS

Vasodilation of BVs

Less common than the

sympathetic activity Salivary glands, g.i.

glands, reproductive

tissues

MECHANISM

ACH increases

vasodilation indirectly

through other secondmessengers.


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Sympathetic activation of skeletal muscle

Causes vasodi lat ion

Release of ACH

Action is on pre-capillary sphincters

Vasoconstriction in all vascular beds except skeletal

muscle

Increased HR and contractility

Control center is not medulla but rather cerebral cortex

-fight or flight response

-Anticipatory response to exercise


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Adrenal medulla

Sympathetic release of epinephrine and

norepinephrine

Global effects on increasing arterial blood

pressure.


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Chemoreceptors

Exert a positive drive on vasomotorarea

Exert a positive drive on cardio-inhibitoryarea

Respond to a PaO2, PaCO2, fall in pH

Normal O2changes not significant stimulus

Severe hypoxia is potent stimulus Coordination of inputs to cardiovascular

centers and respiratory centers.

Vasoconstriction and Bradycardia


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Chemoreceptors

Peripheral (ventilation)

Sense low O2

Carotid and aortic (glomus cell)

Synapse with IX and X, respectively

Central (medulla/CNS)

Sense low pH primarily


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Net result of Chemoreceptor stimulus is an integration

of central and peripheral chemoreceptors

Stretch of pulmonary receptors

cancel peripheral stimulus on cardio-inhibitory areacausing tachycardia


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Fight or Flight Reaction

(Sudden Sympathetic Drive)

1. Skeletal muscle blood flowsympathetic cholinergic stimulation -

vasodilation.

2. Cutaneous blood flowsympathetic cholinergic responsesweat

glands.

3. Adrenal medullasympathetic stimulation release epinephrine

causes vasodilation in muscleand vasoconstriction in kidney/splanchnicVessels.

4. Veinsvasoconstriction (sympathetic)

5. HeartIncreased sympathetic stimulusincreased HR and contractility

6. MAPOverall output is an increase in blood pressure.


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Fight or Flight

Response

Fig. 24-4

vasodilation

sweat

epinephrine

vasoconstriction

Heart rate

contractility


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FAINTING

(Massive Parasympathetic Response)

vasovagal syncope

1. Massive vasodilation occursremoval of sympathetic tone causes

a rapid fall in blood pressure.

2. Decreased Cardiac outputIncreased vagal output to heart causes

bradycardia and decreased stroke volume

3. Decreased arterial blood pressuresecondary to vasodilation and CO.

4. Cerebral blood flowreduced (> 10 seconds)fainting occurs


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vasodilationBradycardia

Decreased MAP

AVP release

Reduce cerebral blood flow

Emotional stress

FAINTING

(Massive Parasympathetic Response)


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Integrated Response to Massive Hemorrhage

1. Baroreceptorshigh pressuredecreased firingresult is enhanced

Sympathetic output and less vagal output tachycardia, contractility, vasoconstrictionre-establish MAP

2. Baroreceptorslow pressurereduced VOLUMEless activity of LPBs.

Increased sympathetic outputvasoconstriction particularly of kidney BVs

Increased release of Anti-diuretic hormone/Arginine Vasopressin/Vasopressin

3. Peripheral Chemoreceptorslow MAP reduces perfusion of carotid/aortic bodies

Local hypoxiaincreased firing of chemoreceptorsvasoconstrictionand

changes in ventilation.

4. Central Chemoreceptorsfall in blood pH (acidosis)increased sympatheticOutputvasoconstriction

5. Adrenal medullaas a result of sympathetic stimulationincreased

Medullary secretion of epinephrine(a BP drop to 40 mmHg - 50 fold increase in Epi)


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Hemorrhage

Venous return blood volume

MAP

SV and CO Atrial volume

LP Baroreceptors

HP BaroreceptorsCentral

Chemoreceptors

Peripheral

Chemoreceptors

Medullary

Cardiovascular

Control CenterSYMPATHETIC RESPONSE

Heart rate

Contractility

Vasoconstriction

(arteriole/venous)

Hormonal response

-Angiotensin/Renin

-ADH release

-ANP (decreased)

Lecture 7 - Regulation of Blood Pressure

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