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Section VIII - Baroreflex and Cardiovascular Changes

I. Baroreceptor Reflex → decreased carotid sinus afferent nerve

A. Responds to changes in blood pressure to help firing → increased sympathetic response →
maintain a normotensive state vasoconstriction of arterioles and veins →
increased blood pressure
B. Composed of the carotid sinus (CN IX) and the
aortic arch (CN X). sympathetic
(T1-L2)

C. Considered upregulated when the efferent limb

of CN IX and X are inhibited (e.g. decreased
stimulation of CN X will increase heart rate and
contractility. This is considered initiation of the
baroreceptor reflex).
D. Increased blood pressure → increased firing of
the afferent limbs of CN IX and X → increased
stimulation of the nucleus tractus solitarius in
medulla of brain → increased efferent firing of II. Chemoreceptor Reflex
CN X → decreased sympathetic stimulation of A. Include central (ventrolateral medulla) and
the heart and vasculature throughout body peripheral (aortic and carotid) chemoreceptors
E. Decreased blood pressure → decreased B. Peripheral chemoreceptors
stretching of vessels → decreased firing rate
1. Stimulated by increased CO2, decreased O2,
of the afferent fibers of CN IX and CN X →
decreased pH → sympathetic stimulation of
decreased stimulation of the nucleus tractus
heart and vasculature (and lungs)
solitarius in the medulla of the brain →
decreased medullary stimulation of efferent CN C. Central chemoreceptors
X → increased sympathetic firing to the heart 1. Stimulated by increased CO2 and decreased
and vasculature throughout body pH → sympathetic stimulation of heart and
vasculature (and lungs)

sympathetic
(T1-L2)

F. Responses to the supine position

1. Blood pools in the veins due to their high
compliance. This increases the capillary
pressure which can lead to edema.
2. The relaxation of skeletal muscles decreases
the movement of blood from the venous
system to the heart → decreased preload
and cardiac output
G. Responses to standing
1. There will be a decrease in blood pressure
III. Cardiovascular Autonomics
A. Sympathetic
1. Heart: β1 receptors on SA and AV nodes →
increased heart rate and contractility
2. Arteries
a) Skeletal muscle arteries:
(1) α1 receptor stimulation →
vasoconstriction

(2) β2 receptors stimulation →
vasodilation
(3) At rest, α1 receptors dominate →
overall vasoconstriction
(4) During exercise, local metabolic
factors inhibit α1 receptors and
dilate local arteries → overall
vasodilation
b) Visceral arteries: α1 receptor stimulation
→ vasoconstriction
3. Veins: α1 receptor stimulation →
vasoconstriction → increased venous return
to right atrium
4. Visceral Vasculature and Skin: α1 receptor
stimulation → vasoconstriction → blood
shunted away from visceral organs and skin
5. Sympathetic stimulation of the adrenal
medulla → increased release of
catecholamines → increased sympathetic
response throughout body
6. Overall: increased total peripheral
resistance (TPR) and increased heart activity
B. Parasympathetic
1. Heart: M2 receptor stimulation → decreased
heart rate and contractility
2. Visceral Vasculature: M3 receptor
stimulation → increased blood flow to
internal organs
IV. Metabolic Demand
A. Increased metabolic demand
1. Means more ATP is being used up and
is converted to adenosine → increased
adenosine causes vasodilation
2. Lower levels of ATP → decreased Na+/K+
pump activity → increased extracellular K+,
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which causes vasodilation
3. Glucose is being used for energy → CO2 is
produced → CO2 then causes vasodilation
4. Insufficient O2 → more glucose shunted
to fermentation, producing lactate →
increased lactate → increased vasodilation
5. Adenosine, K+, CO2, and lactate will increase
vasodilation of surrounding vessels
→ more blood will flow to the tissue
(active hyperemia) → increased oxygen
consumption from tissues → cells able to
keep up with increased metabolic demand
V. Hyperemia
A. Increase in blood flow to an organ
1. There are two types
a) Active: the blood flow to a given organ
is determined by its metabolic demand
(CO2, adenosine, lactate, K+).
b) Reactive: the blood flow to an organ is
increased following an occlusive event
(e.g. ventricular systole, skeletal muscle
flexion).
VI. Circulations
A. Coronary circulation
1. Active hyperemia
a) Increased contractility → increased
metabolic demand of myocardium →
vasodilation of coronary arteries →
increased perfusion of myocardium,
especially in diastole when coronary
vessels are not compressed
b) Adenosine and CO2 are the most
important metabolic factors.
2. Reactive hyperemia
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a) Ventricular contraction during systole VII. Blood Alterations and Responses

→ increased ventricular pressure →
compression of coronary arteries →
decreased perfusion during systole →
reactive hyperemia during diastole

A. Exercise
B. Cerebral circulation
1. Hyperemia
1. Active hyperemia
a) Active
a) CO2 is the most important metabolic
factor. (1) Increased metabolic demand of
skeletal myofibers → increased
1. Decreased perfusion → syncope
K+, CO2, adenosine, and lactate →
vasodilation → increased perfusion
of skeletal muscle tissues and
greater filtration of blood into
lymph
b) Reactive
(1) During each contraction of the
skeletal muscle, arteries feeding the
C. Skeletal muscle
muscle are momentarily occluded
1. Active hyperemia. → reactive hyperemia
2. Reactive hyperemia. 2. Heart and vasculature
3. Sympathetic stimulation of α1 (constrict) and a) Increased sympathetic activity →
β2 (dilate) receptors. (1) β1 receptor stimulation of SA and AV
a) β2 receptor effect dominates during nodes → increased heart rate and
exercise → decreased TPR contractility
(2) α1 receptor stimulation of veins
→ vasoconstriction → increased
venous return to heart → increased
preload and cardiac output
(3) β2 receptor stimulation of arteries
in the skeletal muscle → arteriole
vasodilation → increased pressure
D. Skin reaches capillaries → increased
skeletal muscle perfusion
1. Sympathetic nerves play large role.
3. Hormonal changes
2. Trauma causes dilation from histamine
a) Hypoxia during exercise → upregulation
release.
of vascular endothelial growth factor
(VEGF) from the endothelial cells →
increased production of capillaries
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4. Overall, exercise causes vasodilation of stimulation of RAAS.

arteries feeding the skeletal muscles, which 2. Cardiogenic shock
decreases total peripheral resistance.
a) Decreased CO
B. Blood loss
(1) Decreased stretch on baroreceptors
1. Local changes decreased parasympathetic
a) At the site of vessel damage, endothelin action on heart increased
will be released → vasoconstriction to sympathetic action increased
prevent further blood loss at the site preload and afterload, venous
return and widespread arterial
2. Baroreceptor reflex
vasoconstriction
a) Hypovolemia → decreased stretch
(2) → stimulation of RAAS
on baroreceptor fibers → decreased
stimulation of CN X and increased
sympathetic firing to blood vessels and
heart
(1) → increased heart rate and
contractility (β1 receptors) →
increased CO
(2) → vasoconstriction of veins (α1
receptor) → increased venous
return
(3) → vasoconstriction of arteries (α1
receptor) → increased TPR and
more blood reserved for heart and
brain → decreased perfusion of skin
and visceral organs
3. RAAS
a) Increased activity of the Renin-
Angiotensin-Aldosterone System (RAAS)
→ increased H2O and Na+ reabsorption
→ increased blood pressure
b) Increased release of ADH → increased
H2O reabsorption from collecting duct
→ increased blood pressure
c) ADH also causes vasoconstriction →
increased blood pressure
C. Shock
1. Hypovolemic shock
a) Decreased blood pressure
(1) Decreased stretch on baroreceptors
decreased parasympathetic
action on heart increased
sympathetic action increased
CO, venous return and widespread
arterial vasoconstriction
(2) Decreased renal perfusion →
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1. What would happen to the baroreflex in a 4. What would aortic stenosis do to the
patient with acute decompensated heart failure? concentration of adenosine in the coronary
arteries?

5. How could severe vomiting cause syncope?

2. What would a carotid massage do to the
baroreflex?

3. During repetitive weight lifting, does the muscle 6. What would a large, rapid bolus of IV fluid do to
tissue receive blood from active or reactive heart rate? What would happen to HR if the IV
hyperemia? fluid was administered slowly?