CVS reflexes Flashcards

1
Q

Pressor response

what kind of inputs are these?
name 2 examples
what happens when these are swtiched on?

A

Excitatory inputs e.g. Arterial chemoreceptors, Muscle metaboreceptors (Work)
When stimulated these receptors Switch ON reflexes to increase cardiac output/TPR/blood pressure

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2
Q

Depressor response

inputs are these?
name an example
what happens when these are swtiched on?

A

Inhibitory inputs e.g. Arterial baroreceptors

When stimulated these receptors Switch OFF reflexes to decrease cardiac output/TPR/blood pressure

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3
Q

aterial baro-receptors

where is blood flow vital?
how does body measure blood flow? why does the body measure it this way?
state the equation and importance of it

where are the sensory receptors? (2)
what do they detect?

A

Vital to maintain blood flow to brain and myocardium
But body has no blood flow sensors

Instead body monitors blood pressure, why?

Monitoring arterial BP tells us about blood flow from:

Blood flow (cardiac output, CO)  = BP / TPR     or     BP = CO x TPR	
CO = blood flow (both have units of volume/time)

Decrease in BP reflects a decrease in CO/TRP
Ultimately telling us about changes in blood flow

Blood pressure SENSORS found in walls of the carotid arteries and aorta

Allow specific sensing of blood flow to brain and heart

These sensors detect arterial wall stretch

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4
Q

Location of arterial baroreceptors

where are the two receptors? how do they send info?

how are the sensory nerve fibres placed? what happens when they detect a change?

A
aortic baroreceptors in ascending arch of aorta send info via the vagus nerve
carotid sinus (baroreceptors) at base of internal carotid send info via the IX, glossapharyngeal nerve

diffused, sprayed sensory nerve fibre endings with a flattened look which can sense pressure and changes in pressure which causes changing in firing of nerve terminals which means you can send info up the aortic baroreceptors through sensory nerves in the vagus nerve and send info up brainstem

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5
Q

How do baroreceptors respond to changes in pressure

what happens when pressure is increased? what happens to this response over time?

A

if you increase pressure and threshold is hit which indicates a change, there is a dynamic change so an increased firing of AP in nerve due to stimulation but over time it will adapt

if you decrease pressure, there will be a drop in firing of nerves due to less stimulation of baro receptors and it will adapt over time

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6
Q

what happens to baroreceptors if we have continued high or low pressure?

name this condition and the consequence

A

In the face of continued high or low pressure
the threshold for baroreceptor activation changes

e.g. Hypertension - baroreceptors are less activated
threshold becomes much greater
Consequently, we don’t regulate our BP as well

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7
Q

Effect of increased BP on baroreflex - termed Loading
e.g. Stress

what happens first? what detects this and what does this lead to?
what are the effects of this? (4)

A

Raising blood pressure, activate baroreceptors, stimulate carotid sinus nerve
Leads to BP falling (depressor reflex), HR slows (bradycardia) and pulse pressure falls (decrease SV)
Vasoldilation -> less tpr -> less BP
Alll due to a decrease Sympathetic activity and increased Parasympathetic (vagus) activity

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8
Q

Effect of decrease in BP on baroreflex – termed Unloading e.g. haemorrhage, standing up

what happens when bp drops?
what are the effects? (4)

what is the pressor reflex?

what haooebs with severe decrease in BP?
4 main effects?

A

More Sympathetic activity + less Vagus activity
More Heart rate and Force on contraction = More CO
Arteriolar constriction = More TPR
Venous constriction = More CVP = More SV = More CO (Starling’s law)

Pressor Reflex: Maintain blood pressure/blood flow to vital organs
BP = CO x TRP

With a severe decrease in BP, e.g. haemorrhage
Adrenaline secretion
Vasopressin (ADH) secretion
Stimulation of RAAS – Ang II production
Vasoconstriction - Less Capillary pressure -> absorption of interstitial fluid -> blood volume

Production of Ang II -> Aldosterone secretion
-> Na/H2O reabsorption in kidneys -> More blood volume

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9
Q

Cardiac receptors

name the two receptors
what do they both sense?
how and where do they feedback to?

explain how referred pain works
how does it feedback and what does it signal?

A

veno-atrial mechanorecptors
sense the return of blood to RS from great veins to RA hence signal CVP and filling of heart in diastole

Ventricular mechanoreceptors
sense over-distension

Both above feedback via cardiac vagal afferent fibres to the nucleus tractus solitarius

sympathetic afferents - nociceptors
feed back to spinal chord which go down the spinothalamic tract (signals from somatic afferent onto same spinal cord neurones - referred pain) to signal cardiac pain (agina, heart attacks)

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10
Q

Nociceptive sympathetic afferents

what are the fibres?
what are they stimulated by?
what do they mediate?
why is this called referred pain?

explain why it leads to acute pressor reflex

A

Chemo-sensitive ventricular afferent fibres
Stimulated by K+, H+ (lactate), bradykinin during ischaemia
Mediate pain/symptoms of angina & myocardial infarction
Fibres converge onto same neurones in spinal cord as somatic afferents –> basis of referred pain

Acute pressor reflex - More sympathetic: pale, sweaty, tachycardia (as it tries to increase heart function, increase HR/contractility and vasoconstriction)

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11
Q

Veno-atrial mechanoreceptors

what stimulates it?
what is the initial pressor reflex?
what is the bainbridge effect?

what happens in the long term?
how does it doe this? (3 ways)

A

Stimulated by increase in cardiac filling/CVP (stretch the SAN and leads to more work and tachycardia)

Initial pressor reflex -> More Sympathetic: tachycardia
Bainbridge effect – reflex tachycardia due to rapid infusion of volume into venous system (veno-atrial stretch receptors and pacemaker distension)

Longer term depressor reflex - More diuresis - Less Blood volume, feedback loop via changes in ADH, ANP, RAAS (try to decrease blood volume to decrease BP)

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12
Q

Ventricular mechanoreceptors

what stimulates this?
what kind of reflex does it set off?
what is it’s role? what reflex does it override?

A

Stimulated by over distension of ventricles
Depressor reflex
Role unclear - protective for heart – overrides veno-atrial reflex? (to reduce efforts of the heart to perform + contract against the volume (BP))

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13
Q

Location of chemoreceptors

A

found in similar areas to where barorecptors are

carotid body and aortic bodies

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14
Q

arterial chemorecptors

what stimulates them?
what does it regulate? and drive during which situations?

what is the pressor response?
what activity does it lead to?
what does it lead to? (4)

A

Located in CAROTID and AORTIC BODIES
(different to baroreceptors)

Stimulated by low O2 (hypoxia), High CO2 (hypercapnia)
H+ and K+

Very high blood flow – 20 ml g-1min-1

Regulate ventilation + 
Drive cardiac reflexes during:
Asphyxia (low O2/high CO2)
Shock (systemic hypotension)
Haemorrhage (when BP below range of baroreflex)

Pressor response
More Sympathetic activity
Tachycardia, More Selective arterial/venous constriction
More Cardiac Output/Blood pressure
Preservation of cerebral blood flow during low O2 (asphyxia/haemorrhage)

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15
Q

Muscle metaboreceptors (work receptors)

what type of fibres are they? located where? activated by?

what will the pressor response be? (3)

why is it important during isometric exercise? what is the issues with muscles here and how does the body bypass this probkem?

A

SENSORY FIBRES in Group IV motor fibres
located in SKELETAL MUSCLE
Activated via metabolites; ATP, K+, lactate, adenosine

Pressor response
More Sympathetic activity
Tachycardia, More arterial/venous constriction
More Cardiac Output/Blood pressure

Important during isometric exercise:
Joint angle and muscle length do not change
e.g. weight lifting / handgrip
(Coordination of CVS responses lecture)

Aids maintenance of blood perfusion to contracted muscle - contracted muscle causes mechanical interference to blood flow therefore tries to maintain enough BP to drive blood through contracted muscle therfore More global BP + inside muscle open up more blood vessels

These muscle undergoes metabolic hyperaemia allowing blood flow to the contracted tissue (to open up more vessels)

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16
Q

Human muscle metaboreceptors in static exercise

what will it produce and lead to?
how can this reflex be prevented?

A

4 seconds of hand gripping wil actively produce metabolites in muscles which stimulate the reflex and pressor response which increase HR and increase BP

(can be prevented by local anaesthetic which prevent APs being generated)

17
Q

How are sensory receptor signals coordinated in the brain?
Central role of the nucleus tractus solitarius (NTS)
and central pathways regulating outflow

where is info sent from baro/chemo/cardiac receptors?

what happens when increase activation of baro receptors? what does it lead to? what is the effect of this?

what happens when increase activation of chemo receptors? what does it lead to? what is the effect of this?

what else sends info to nts and where does this recieve info from?

A

baro + chemo + cardiac receptors will detect change and send the info via receptor afferent fibres to the NTS

Increase baroreceptors (Raised BP) – excitatory NTS – Increase CVLM (caudal ventrp-lateral medulla) -> Inhibition of RVLM(rostro ventro-lateral medulla) (acts as thermostat) – switch off sympathetic nerves - DEPRESSOR

Increase arterial chemoreceptor/muscle work receptors – inhibitory NTS - Inhibit CVLM -> Switch on RVLM and sympathetic nerves - PRESSOR

cerebral cortex sends and recieve info to hypothalamus, limbic and cerebellum which send ad recieve info from NTS to modulate these systems

18
Q

Central pathways regulating vagal parasympathetic outflow to SA and AV nodes in heart

what happens when baroreceptors excited? sequence of events?

significance of inapiratory centre?
hypothalamus/limbic system?

A
Increase baroreceptors (Raised BP) 
Excite NTS, Increase N. Ambiguous,  Switch on vagal nerve, Reduced Heart Rate

inapiratory centre can switch off vagus nerve (linked to sinus tachycardia)
NTS feedbacks back and forth with hypothalamus/limbic system which does the same with the cortex
Hupothalamus/limbic system can feedback to nucelus ambiguus alone during emotional faint too

19
Q

What is Sinus tachycardia (Sinus Arrhythmia)

what does inspiration stimulate? where does it send info and what does it switch off?

effect?

A

inspiration will stimulate the inspiration centre + send info to nucleus ambiguus to switch off vagus nerve

Breathe in – switch off vagal nerves
Speed up heart rate

20
Q

Central stimulation of cardiac vagal activity e.g. Limbic system (‘emotional centre’)

where does the info come from?
what kind of activity does it cause?
what can it lead to and why?

how does it lead to this effect? (3 ways)

A

excess vagal activity via higher centres
Fainting (syncope, vaso-vagal attack) – caused by less cerebral blood flow (reduced oxygen delivery) due to sudden drop in arterial blood pressure

Through:
Vagal bradycardia
decreased sympathetic activity – causing further decrease in heart rate
and also peripheral vasodilatation (lower TPR)

21
Q

overall affect of cvs reflexes

what is the main aim?
what happens if you remove reflexes?

A

keeps arterial pressure in a very precise control limit via reflexes

Remove CVS reflexes – less controlled and higher blood pressure
Reflexes stabilise blood pressure