Nervous Control of the CVS Flashcards
3 reasons why brain need to control its blood flow?
Neuronal cell bodies have no energy reserves + are intolerant to hypoxia
The brain has a very high O2 consumption, so constantly requires a controlled high BF
Local functioning within the brain also needs constant controlled BF changes
4 adaptations which help control cerebral BF?
Circle of Willis allows constant BF to brain
Capillary density + diffusion area is v high= high 02 delivery
Auto-regulation (myogenic response) + Local metabolic vasodilatation is well-developed !
What is the circle of Willis & why does this make it important?
It is an anastomosis ( streams of arteries that branch out and then reconnect with one another ) –> enables continuous blood flow even when a potential area of a blood vessel is compromised !
Describe what is meant by autoregulation
Autoregulation is a myogenic response which maintains cerebral blood flow relatively constant between 60 and 150 mmHg mean arterial pressure
Describe the nervous control of cerebral arteries inside vs outside the brain
Cerebral arteries ‘outside’ the brain get dense symp nerve innervation
Cerebral arterioles ‘within’ the brain have little symp innervation - this prevents too much vasoconstriction ( normally Constriction of blood vessels reduces inflammation-induced vasodilation - so its hard to reduce inflammation-induced vasodilation in brain! )
What do the perivascular nerves release and how can we control this pharmacologically?
In a migraine or vascular headache (ie stroke), there is vasodilation - in response to this C fibres & nociceptors (perivascular nerves) release 5HT + CGRP to help mediate this pain.
5HT causes vasoconstriction - however CGRP causes vasodilation!
therefore Sumatriptan (5-HT1B agonist) reduces inflammatory vasodilation, while Calcitonin gene-related peptide (CGRP) inhibitors reduces CGRP-mediated vasodilation
- Both are used for migraines
Brain controls the CVS and therefore safeguards it own blood supply by Reflexes
Which parts of the brain are esp important in controlling the CVS?
baro/chemo/cardiac receptors send info to the NTS (brainstem) –> can either send signals to:
the nucleus ambiguus of vagus ( parasymp nerve) –> vagal efferents in heart OR the CVLM
CVLM —> inhibits RVLM
RVLM sends excitatory impulses to symp pregang. neurones in spinal cord –> impulses to cardiac + vasomotor fibres
What type of receptors measure BF?
Where are they found?
Give equations for BP and explain the link between BP and BF
Arterial baroreceptors sense changes in (BP) to measure BF. They are found in carotid artery + aorta walls
NOTE - Chemoreceptor aortic bodies are NOT in the walls
BP = (CO) x (TPR)
CO = blood flow (both have units of volume/time)
Explain the effect of increased BP on the baroreflex
which nerve stimulated + what this nerve activates, effects etc
increased BP stimulates carotid sinus nerve - activates baroreceptors in carotid sinus walls –> depressor response:
Acts on the n.ambigus of vagus to increase vagal tone, reduced symp innervation –> reduced HR, BP, vasoconstriction which also decreases TPR.
= loading response
Explain 5 effects of decreased BP on baroreflex
Decreased BP on baroreflex (e.g. standing up, haemorrhage (hypovolemia)=unloading ) –> pressor response
Baroreceptor afferents are switched off –> Reduced vagal tone, increased SAN innervation increases HR, increased contractility, Venoconstriction ( prevent postural hypotension) + Resistance vessel contraction
in comparison, compare the pressor response in severe decreases in BP
With a severe decrease in BP, (e.g haemorrhage) the pressor response also leads to:
Adrenaline + ADH secretion
Stimulation of RAAS –> Ang II production
These all cause: vasoconstriction, decreasing capillary pa, increasing absorption of interstitial fluid –> increasing blood volume!
Describe arterial chemoreceptors and when they come into effect
location, 3 things they are stimulated by, 2 functions + 3 situations in which they are activated
Where do they travel upon activation, what effects do they have?
Located in CAROTID and AORTIC BODIES (unlike baroreceptors)
Stimulated by hypoxia, hypercapnia, H+
Regulate ventilation + drive cardiac reflexes in:
Asphyxia (low O2/high CO2)
Shock (systemic hypotension)
Haemorrhage (when BP below range of baroreflex, so baroreflexes cannot respond)
Travel along Vagus + Glossopharyngeal afferent nerves to brain –> pressor reflex
Effects: arterial/venous constriction, increased HR, also switches off baroreceptors
Describe an example of a cardiac reflex:
? are found in ventricles
They are stimulated by ? which ?
? send info to brain + ? –> ?
Mediate ?
Chemoreceptor Nociceptive sympathetic afferents are found in ventricles
They are stimulated by H+ (lactate) during ischaemia which activates C fibres
C fibres send info to brain + activates pressor reflex –> pale, sweaty, tachycardia
Mediate angina & MI symptoms
Compare baroreceptors in the depressor and chemoreceptors in the pressor reflex
Baroreceptors stimulate excitatory neurones in NTS to the CVLM.
CVLM inhibits RVLM, therefore symp outflow inhibited= Depressor reflex
Arterial chemoreceptors stimulate inhibitory neurones in NTS - inhibits CVLM -> therefore stimulates RVLM + symp nerves = PRESSOR reflex
compare 2 central pathways regulating vagal parasympathetic outflow to SA and AV nodes in heart
Activated baroreceptors -> NTS - excites n.ambiguus –> stimulates vagal parasymp fibres–> reduces HR + BP
Inhibitory input from inspiratory Centre inhibits N. Ambiguus–> switch off vagal nerve –> sinus tachycardia
Describe how the limbic system can cause vagovagal attack
Fainting (syncope) due to vasovagal attack - caused by decreased cerebral BF due to sudden arterial BP decrease.
Hypothalamus or limbic system stimulates N.ambiguus + increases vagal response excessively + Reduction in symp activity –> decrease in HR + peripheral vasodilatation (less TPR)
