15. Baroreceptors and Control of Blood Pressure Flashcards

1
Q

What types of baroreceptor are there?

A

Baroreceptors are mechanoreceptors

that respond to stretch +

are also known as stretch or pressure receptors.

They are terminal myelinated nerve endings,

located within vessel walls
and the cardiac chambers.

Their action potential firing rate is altered
in response to changes in blood pressure,

which creates a negative feedback mechanism responsible for the autonomic regulation
of blood pressure.

They may be classified as
high- or low-pressure baroreceptors:

> High-pressure arterial baroreceptors:

Located within the walls of
the aortic arch

and carotid sinus
(a small dilatation of the internal carotid artery
just above its bifurcation).

Because of their proximity to blood leaving the heart,

these receptors are well positioned
to control perfusion pressures
to the coronary and cerebral circulations.

involved in the rapid short-term
control of blood pressure.

> Low-pressure baroreceptors:

Located in the chambers of the heart,
large systemic veins
and the pulmonary vasculature.

These receptors bring about changes
in blood volume and are involved in the slower and
sustained control of blood pressure.

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2
Q

How do the high-pressure baroreceptors work?

A

> The aortic arch - vagus
and
carotid sinus baroreceptors - glossopharyngeal nerves

discharge impulses to the
nucleus tractus solitarius in the medulla.

Here, the vasomotor and cardioinhibitory
centres modulate
sympathetic and parasympathetic outflow,

in turn restoring blood pressure towards normal.

> As blood pressure rises,
the rate of discharge increases,

leading to a reduction in sympathetic outflow
and increase in parasympathetic transmission.

The consequent reduction in 
blood vessel tone, 
heart rate and 
contractility leads 
to a reduction in blood pressure
(MAP = SV × HR × SVR). 

Conversely, the rate of discharge decreases
with reductions in blood pressure,

leading to increased sympathetic outflow.

> As this system relies on neural transmission,
it is extremely fast and is responsible
for the beat-to-beat control of blood pressure.

For example, these baroreceptors
mediate the bradycardia, 
which is sometimes observed in patients 
following administration of a bolus dose of
vasopressor such as phenylephrine.

> Although high-pressure baroreceptors
respond to both a rise and a fall
in blood pressure,

their most important role is in response to a fall
(e.g. haemorrhage, standing up).

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3
Q

What nerve innervates aortic arch

A

Vagus

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4
Q

What nerve innervates carotid sinus

A

Glossopharyngeal

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5
Q

What reflexes are elicited by a rapid fall in blood pressure,
e.g. sudden 2 L blood loss?

A
The physiological response involves 
cardiovascular, 
neurohumoral and 
renal
compensatory mechanisms
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6
Q

Baroreceptor reflex activation in response to blood loss

A

Baroreceptor reflex activation – immediate response

• Reduced baroreceptor 
(aortic arch and carotid sinus) input 
due to reduced vessel stretch 
leads to reduced afferent discharge
in glossopharyngeal and vagus nerves. 

Cardio-inhibitory centre is inhibited
while the vasomotor centre is activated,

leading to reduced parasympathetic activity and increased sympathetic activity,

resulting in
increased force of cardiac contraction,
tachycardia and
increased SVR.

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7
Q

> Cardiovascular response to blood loss

> Hypothalamic–Pituitary–Adrenal responses

A

• Redistribution of cardiac output from
skin, muscle and viscera to brain and heart.

> Hypothalamic–Pituitary–Adrenal responses
• Increased ADH secretion
from the posterior pituitary,
leading to water conservation

• Increased adrenal release of 
noradrenaline, 
adrenaline and 
cortisol via
sympathetic nervous system activation
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8
Q

> Starling’s forces Response to blood loss

A

> Starling’s forces

• Favour interstitial fluid movement
into the circulation through a
fall in intravascular hydrostatic pressure and a
rise in oncotic pressure

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9
Q

> Renin–Angiotensin–Aldosterone system in response to blood loss

A

> Renin–Angiotensin–Aldosterone system

• Fall in renal blood flow, 
detected by juxtaglomerular apparatus,
leads to release of renin, 
which converts 
angiotensinogen to angiotensin I. 

Angiotensin converting enzyme (ACE) secreted by the
lungs and kidneys converts this into
angiotensin 2,

which causes vasoconstriction
and stimulates the release of aldosterone.

• Aldosterone increases sodium and water
re-absorption at the distal convoluted tubules,
thereby expanding plasma volume.

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10
Q

What is the Bainbridge reflex?

A

Also known as the atrial reflex.
A rapid increase in venous return to the heart (
e.g. rapid IV fluid bolus) may lead
to activation of low-pressure atrial stretch receptors, resulting in an increase in heart rate.

The purpose of the tachycardia is to restore atrial
(and vena caval) pressures to normal
by removing blood volume
from the right atrium.

The Bainbridge reflex is involved in
respiratory sinus arrhythmia
where heart rate momentarily
increases with inspiration (lower intrathoracic pressure) due to increased venous return.

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11
Q

What is the Bezold–Jarisch reflex

A

Activation of left ventricular
chemo- and baroreceptors,
located in the left ventricle,

results in unopposed parasympathetic tone,
leading to the triad of
bradycardia, vasodilation and hypotension.

This is known synonymously as
vasovagal syncope,
neurocardiogenic syncope
or the Bezold–Jarisch reflex.

It is triggered by reduced venous return to the heart,

but may also have an affective component,
e.g. pain or fear.

Situations relevant to anaesthesia include regional

(spinal,
epidural
and interscalene blocks
where sympathetic output is blocked),

haemorrhage/hypovolaemia
and inferior vena cava compression
in supine pregnant patients.

Treatment is by restoring venous return

with fluids and administration of sympathomimetics,
in particular ephedrine.

This reflex may also explain the
bradycardia associated
with acute postero-inferior myocardial infarction, thrombolysis,
coronary angiography
and exertion syncope seen in aortic stenosis.

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12
Q

Describe the physiological control of blood pressure.

A

Blood pressure regulation occurs
not only from beat to beat
but also in the longer term over months to years.

Mean arterial pressure is the product of

cardiac output (heart rate × stroke volume)

and systemic vascular resistance.

MAP = CO × SVR

> Short-term regulation:

Mediated by the

arterial and cardiac baroreceptors

+ the vasomotor centre in
the nucleus tractus solitarius,

which ultimately alter the balance between parasympathetic and
sympathetic discharge, 
thereby altering heart rate, 
stroke volume and
systemic vascular resistance
.

> Long-term regulation:
Mediated by neurohumoral, renal, metabolic,
race and genetic factors.

The following factors may all affect long-term
blood pressure:
• Sodium intake
• Atrial natriuretic peptide
• Bradykinin
• Nitric oxide
• Glucocorticoids
• Renal function
• Psychological stress
• Obesity – with a possible link to insulin resistance
• Atherosclerosis
• Renin – angiotensin – aldosterone system
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