The extrinsic regulation of blood pressure and cardiac output

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The extrinsic regulation of blood pressure and
cardiac output

• Lecture 7
• Chapter 22 BB
• All but pages 550-554

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Arterial Blood Pressure
Flow
Pressures
Aortic arch
Thoracic aorta
Flow changes b/c -resistance -compliance -inertia
Abdominal aorta
Femoral artery
120 systolic/80 diastolic
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Mean Arterial Blood Pressure (MAP)
average arterial blood pressure during a cardiac
cycle Perfusion pressure
MAP DP 1/3 (SP-DP)
For a BP of 120/80, MAP is 93.5 mmHg
A MAP of 60 mmHg is sufficient for end
organ perfusion.
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Baroreceptor Feedback Loop for the Regulation of
Mean Arterial Blood Pressure
stretch
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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Carotid and Aortic Baroreceptors
Fig 22-2
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Carotid nerve fires above and below normal
pressures. Aortic nerves are activated above
normal pressures.
Aortic sinus
MAP 93.5 mmHg
The aortic receptors help reinforce the carotid
activation above normal pressures.
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Medulla Oblongata
NTS
Vagal/glossopharyngeal AFFERENTS
Cardio-inhibitory area Vasomotor area
Increased firing of Baroreceptors by stretch
Sympathetic and Parasympathetic EFFERENTS
TARGET ORGANS -heart -blood vessels -adrenal
medulla -glands (skin/sweat)
MAP
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Medullary Cardiovascular Center
Nucleus of the Tractus Solitarius (NTS)

interneurons

-
Receives afferents from CN IX and X
Dorsal motor nucleus of X
Cardio-inhibitory Area
Increased MAP
Nucleus ambiguous of X and IX
Vasomotor area
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Coordination of Medullary Cardiovascular Inputs
Parasympathetic activation bradycardia
Dorsal motor nucleus of X
Cardio-inhibitory Area
To heart
Nucleus ambiguous of X and IX
Vasomotor area
To spinal cord
(tonic vasoconstriction)
Sympathetic activation of -Blood
vessels -Heart -Adrenal medulla
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afferents
efferents
Fig. 22-4
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Low Pressure Cardiac Baroreceptors
Bainbridge Reflex
Unlike activation of the high-pressure barorecepto
rs, activation of the A and B fibers will
INCREASE heart rate. (and also cause renal
vasodilation).
Respond to fullness or volume Located in Low
pressure sites Control the effective circulating
volume
Indirectly regulate MAP
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• The dependence of cardiac output on effective
• circulating volume is the result of the complex
• Interplay among three factors
• Bainbridge reflex
• Baroreceptor reflex
• Starlings Law

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Baroreceptor
Bainbridge
Cardiac Output
Stroke Volume
Heart rate increases under volume depletion and
loading
Heart rate
In volume loading conditions Bainbridge
response prevails
In volume depletion conditions Baroreceptor
response prevails
Bainbridge response only HR is affected
Baroreceptor -Increased stretch on high pressure
decreases stroke volume flattening the
Starling response.
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Sympathetic input - HEART

• ACTIONS
• Nerve fibers release NE
• SA, atria, and ventricles
• ? HR and contractility
• R side SA node
• L side contractility

• MECHANISM
• ß1 receptors pacemaker activity
• ß1 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)
• ß? subunit (HR)
• Nitric oxide (weak inotropic effect)

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Sympathetic input Blood vessels

• ACTIONS
• Activated -Vasoconstriction throughout body
• Skin/kidney BVs
• most abundant
• De-activated
• Vasodilation

• MECHANISM
• Norepinephrine
• a gt ß
• Epinephrine
• ß gt a
• Vasoconstriction a1
• Vasodilation ß2

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Parasympathetic input Blood 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 second messengers.

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Sympathetic activation of skeletal muscle

• Causes vasodilation
• 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 vasomotor area
• Exert a positive drive on cardio-inhibitory area
• Respond to a ?PaO2 , ? PaCO2, fall in pH
• Normal O2 changes 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 area causing
tachycardia
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Fight or Flight Reaction (Sudden Sympathetic
Drive)

• Skeletal muscle blood flow sympathetic
  cholinergic stimulation -
• vasodilation.
• Cutaneous blood flow sympathetic cholinergic
  response sweat
• glands.
• Adrenal medulla sympathetic stimulation release
  epinephrine
• causes vasodilation in muscle and
  vasoconstriction in kidney/splanchnic
• Vessels.
• Veins vasoconstriction (sympathetic)
• Heart Increased sympathetic stimulus
  increased HR and contractility
• MAP Overall output is an increase in blood
  pressure.

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Fight or Flight Response
Fig. 24-4
vasoconstriction
sweat
Heart rate contractility
vasodilation
epinephrine
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FAINTING (Massive Parasympathetic Response)
vasovagal syncope

• Massive vasodilation occurs removal of
  sympathetic tone causes
• a rapid fall in blood pressure.
• Decreased Cardiac output Increased vagal output
  to heart causes
• bradycardia and decreased stroke volume
• Decreased arterial blood pressure secondary to
  vasodilation and CO.
• Cerebral blood flow reduced (gt 10 seconds)
  fainting occurs

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FAINTING (Massive Parasympathetic Response)
Emotional stress
AVP release
vasodilation
Bradycardia Decreased MAP
Reduce cerebral blood flow
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Integrated Response to Massive Hemorrhage

• Baroreceptors high pressure decreased firing
  result is enhanced
• Sympathetic output and less vagal output
• ? tachycardia, contractility, vasoconstriction
  re-establish MAP

• Baroreceptors low pressure reduced VOLUME
  less activity of LPBs.
• Increased sympathetic output vasoconstriction
  particularly of kidney BVs
• Increased release of Anti-diuretic
  hormone/Arginine Vasopressin/Vasopressin
• Peripheral Chemoreceptors low MAP reduces
  perfusion of carotid/aortic bodies
• Local hypoxia increased firing of
  chemoreceptors vasoconstriction and
• changes in ventilation.
• Central Chemoreceptors fall in blood pH
  (acidosis) increased sympathetic
• Output vasoconstriction
• Adrenal medulla as a result of sympathetic
  stimulation increased
• Medullary secretion of epinephrine (a BP drop to
  40 mmHg - 50 fold increase in Epi)

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Hemorrhage
? blood volume
? Venous return
? Atrial volume
? SV and CO
? MAP
LP Baroreceptors
HP Baroreceptors
Central Chemoreceptors
Peripheral Chemoreceptors
Medullary Cardiovascular Control
Center SYMPATHETIC RESPONSE
Hormonal response -Angiotensin/Renin -ADH
release -ANP (decreased)
? Heart rate Contractility
Vasoconstriction (arteriole/venous)