Short term control of blood pressure Flashcards

1
Q

Equation of MAP?

A

MAP= CO X TPR
mean arterial pressure =cardiac output x total peripheral resistance

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2
Q

What is MAP?

A

MAP is the driving force pushing blood through the circulation

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3
Q

Too low MAP?

A

fainting (syncope)- removes effects of gravity on cardiovascular system and less pooling in legs and therefore EDV restored, preload and stroke volume also restored

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4
Q

Too high MAP?

A

hypertension

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5
Q

What is function of arterial baroreflex?

A

going to detect changes in MAP

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6
Q

What are the names of the two sets of baroreceptors- responsible for sensory side of arterial baroreflex?

A

aortic arch baroreceptors

Carotid sinus
baroreceptors- at bifurcation of internal and external carotid arteries

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7
Q

How do baroreceptors work?

A

stretch receptors

the walls are going to stretch and these baroreceptors detect that change in stretch and they increase the firing rate of action potentials

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8
Q

Where do the aortic arch baroreceptors send their signals up to?

A

vagus nerve

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9
Q

Where do the carotid sinus baroreceptors send their signal up to?

A

glossopharyngeal nerve

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10
Q

Integrating centre?

A

medullary oblongata- the most inferior part of the brainstem (medullary cardiovascular centres)

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11
Q

How do the aortic arch baroreceptors and the carotid sinus baroreceptors send their signals up?

A

aortic- vagus nerve
carotid- glossopharyngeal

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12
Q

What nerve does the parasympathetic outflow go through?

A

vagus nerve

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13
Q

What does the vagus nerve innervate?

A

sinoatrial node in the heart

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14
Q

What happens after sinoatrial node in heart is innervated?

A

neurotransmitter will be released, acetylcholine.
Will bind to cholinergic muscarinic receptors on the pacemaker cells.
Will cause them to hyperpolarise and they’ll take longer to get to threshold + that’s going to lead to decreased heart rate or bradycardia.

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15
Q

What does the sympathetic nervous system innervate?

A

sympathetic nerves innervate the sinoatrial nodes in the heart and will get the release of noradrenaline- which will bind to beta one receptors and will cause pacemaker cells to depolarise faster and it will therefore increase heart rate.

Sympathetic nerves also innervate the muscle of the ventricle and it causes increased contractility.
Increased release of calcium- which will cause more actin and myosin crossbridges to form and increase the strength of that excitation-contraction coupling.
Stronger force of contraction and increased stroke volume.

Additionally have release of adrenaline and some noradrenaline from the adrenal medulla into the blood that’s going to circulate and bind to beta one receptors, causing increased heart rate and increased contractility.

In addition will bind to alpha one receptors on smooth muscle of blood cells. Will cause smooth muscle to contract and we’ll get venoconstriction and arteriolar constriction

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16
Q

What does venoconstriction lead to?

A

push more blood back into heart and therefore increased EDV , increased preload and and stronger force of contraction and larger stroke volume.

That will increase cardiac output.

And increase MAP

17
Q

What does arteriolar constriction lead to?

A

arterioles are resistance vessels are if constricted then it is more difficult to push blood from arteries into arterioles.
This will tend to increase total peripheral resistance- increase MAP.

18
Q

What are the other inputs to the medullary cardiovascular centres and what do they detect?

A

Cardiopulmonary baroreceptors (found in atria and walls of the vessels in the lungs)-
Sensing central blood volume

Central chemoreceptors
Sensing arterial pCO2 and pO2- when activated stimulate respiratory drive +breathe faster and deeper.
Increase how much oxygen in lungs and they send info to medullary to increase MAP.

Chemoreceptors in muscle
Sensing metabolite concentrations and send signals for more blood

Joint receptors
Sensing joint movement and send signals for more blood

Higher centres
Hypothalamus (responsible for co-ordinating vascular responses for thermoregulation and coordinating fight or flight responses) and cerebral cortex (strong emotional stimuli can trigger cardiovascular responses)

19
Q

What is vasovagal syncope?

A

fainting due to strong emotional response

20
Q

What is valsalva manoeuvre?

A

forced expiration against a closed glottis- forcefully expire with mouth closed

21
Q

What happens in phase 1 of valsalva maoeuvre?

A

Increased thoracic pressure is transmitted through to aorta – hence increase in blood pressure

22
Q

What happens in phase 2 of valsalva maoeuvre?

A

Increased thoracic pressure makes it difficult for blood to get back to heart.
Venous return will fall.
EDV will fall in turn. Preload will fall.
Reduced preload and less efficient excitation-contraction coupling - fewer cross bridges forming and reduced force of contraction.
Stroke volume will also fall.
Your cardiac ouput will go down and if so- pumping less blood out the heart into arteries.
MAP will also go down.

23
Q

What happens in late phase 2?

A

Reduced MAP is detected by baroreceptors. They tell medullary cardiovascular centre to do something. Response is to increase sympathetic tone and you’ll get increased release of noradrenaline from sympathetic nerves, that’ll bind to beta one receptors on the sinoatrial node and we’ll get this increase in heart rate.
You’ll also get increase un contractility as well as vasoconstriction. (veins and venules are going to constrict - going to push more blood back to heart and increase EDV. Also get arteriolar constriction and will increase TPR)

Blood pressure increasing

24
Q

What happens in phase 3?

A

the person stops doing the valsalva manoeuvre and we get decrease in blood pressure. Decrease in thoracic pressure is transmitted through to heart and through to aorta- causing that decrease in blood pressure.

25
Q

What happens in phase 4?

A

massive increase in blood pressure
as blood was accumulating in the veins and venules.
When stopped doing valsalva manoeuvre- the blood comes flooding back.
Massive increase in stroke volume.
Baroreflex is still in effect and what it’s now going to do is decrease MAP- will increase vagal tone .
More acetylcholine being released from vagus nerve and acting on cholinergic muscarinic receptors and slow dow sinoatrial node.
This is why we get decrease in heart rate and that will lead to a decreased cardiac output.
Blood pressure eventually gets back to normal.

26
Q

Why is valsalva manoeuvre clinically relevant?

A

Used as a test of autonomic function

The baroreceptor reflex can be reduced in:
Older people
Autonomic neuropathy (autonomic nerves damaged)

Can increase risk of myocardial infarction (heart attack)

Control of supraventricular tachycardia