Reflex Control of the CVS Flashcards
How do the cardiovascular reflexes work?
CVS responds to change through sensory / afferent pathways
Give examples of excitatory inputs
arterial chemoreceptors
muscle metaboreceptors
What is the role of excitatory inputs?
Stimulation of reflexes that: - increase CO - increase TPR - increase BP => pressor response
Name some examples of inhibitory inputs
arterial baroreceptors
cardiopulmonary receptors
What is the effect of inhibitory input stimulation?
- decreased CO
- decreased TPR
- decreased BP
=> Depressor response
What is the role of arterial baroreceptors?
Vital to maintain blood flow to the brain and myocardium
Where does the body monitor BP?
As there are no blood flow sensors, the body monitors BP in the carotid and coronary arteries
What does a decrease in arterial pressure tell us?
Reflects a decrease in CO or TPR which compromises blood flow to the brain and heart
Where in the body are blood pressure sensors located?
Blood pressure sensors are in the walls of the carotid arteries and aorta
What is the role of aortic / arterial BP sensors ?
BP sensors inform the brain of pressure changes in the carotid arteries and aorta
What do baroreceptors detect?
Sensors detect arterial wall stretch
respond to changes in pressure
How do baroreceptors respond to an increase in pressure?
Not much firing at rest once threshold reached: - fast firing - eventually slows to become constant at a higher level than before
adaptation to a new normal
How do baroreceptors respond to a decrease in pressure?
Firing slows in proportion to the decrease in pressure
What is the effect of continued high / low pressure?
The threshold baroreceptor activation can change
What is the effect of long term hypertension?
Baroreceptors become normalised at the new pressure and less activated
Describe the effects of increased blood pressure on baroreflexes
- pulse pressure falls due to decreased SV
- vasodilation decreases TPR and BP
- decreased sympathetic nerve activity
- increased vagus nerve (p/s) activity
What are the effects of decreased BP on baroreflexes ?
- increased sympathetic activity & decreased vagus
activity - increased heart rate & contraction force
=> increased CO - Arteriolar constriction = increased TPR
- venous constriction increases CVP, CO & SV
What can cause a decrease in BP?
unloading - e.g. haemorrhage
What neuronal and hormonal secretions also aid BP maintenance?
Adrenaline secretion
Vasopressin (ADH)
RAAS stimulation
How does vasoconstriction decrease BP?
Vasoconstriction decreases capillary pressure, increasing absorption of interstitial tissue fluid to decrease blood volume = decreasing BP
How are ventricular mechanoceptors stimulated?
Stimulated by the over distension of ventricles
=> depressor response
this is a weak reflex causing mild vasodilation, lower BP and preload -> protective
How are Nociceptive sympathetic afferents stimulated?
Chemo-sensitive ventricular afferent fibres are stimulated by:
- K+
- H+
- lactate
- bradykinin during ischaemia
What is the role of nociceptive sympathetic afferents?
They mediate pain of angina and myocardial infarction, as fibres converge onto same neurones in the spinal cord as somatic afferents - basis of referred pain
What are the effects of reflex increased sympathetic activity?
pale, sweaty, tachycardia of angina / MI symptoms
How are venoatrial mechanoceptors stimulated?
Stimulated by the increase in cardiac filling / CVP
What is the result of an increase in sympathetic activity at the venoatrial mechanoceptors?
tachycardia
what is the Bainbridge effect?
Reflex tachycardia due to rapid infusion of volume into venous system
(venoatrial stretch receptors & pacemaker distension)
What causes increased diuresis?
Due to lower blood volume, feedback loop via changes in ADH, ANP and RAAS
What is the effect of increased diuresis on the kidneys?
- switches off the sympathetic activity to kidneys and
increases GFR - mixed system, sympathetic systems can work
independently as well
What is diuresis?
increased / excessive urine production
Where are atrial chemoreceptors located?
In the carotid and aortic bodies
What are atrial chemoreceptors stimulated by?
Hypoxia and hypercapnia as well as H+ and K+
How well perfused are the atrial chemoreceptors?
They are well supplied with blood flow around 20 ml/g/min
What is the role of atrial chemoreceptors?
They regulate ventilation and drive cardiac reflexes during asphyxia (low O₂ /CO₂ ), shock (systemic hypotension) and haemorrhage
What is the effect on atrial chemoreceptors during low BP?
When BP is below the range of baroreflex ( maximally unloaded), the chemoreceptors are still active and many compensate
What are the effects of the pressor response?
- increased sympathetic activity
- tachycardia, increase selective arterial / venous
constriction - increase CO & BP - especially preservation of cerebral blood flow
What is hypoxia?
low O₂ levels
What is hypercapnia?
high CO₂ levels
Where are muscle metaboreceptors found?
Sensory fibres in Group IV motor fibres located in skeletal muscle
How are muscle metaboreceptors stimulated?
Activated via metabolites K+, lactate and adenosine
When is the activation of metaboreceptors especially significant?
Important during isometric exercise
continually contracted muscle but joint angle doesn’t change
e.g. weight lifting / hand grip
How is perfusion maintained during exercise?
Higher BP drives blood into contracted muscle to maintain perfusion
These muscles undergo metabolic hyperaemia allowing blood flow to contracted tissue
Describe what happens to muscle metaboreceptors during static exercise?
(e.g. maintaining hand grip exercise)
metaboreceptor afferent fibres blocked by local anaesthetic injected into muscle to prevent pressor response
increasing arterial BP, drives blood into contracted muscle, bringing in O₂ and glucose, removing CO₂
What is the NTS?
nucleus tractus solitaris
How is the depressor effect created via the NTS?
- Baroreceptor (depressor) afferent fibres enter NTS
- Info sent from NTS to CVLM
- CVLM sends inhibitory info to RVLM
=> inhibition of sympathetic effect nerves, to heart and vessels
less sympathetic signals results in reduction in HR, BP, vasoconstriction etc.
What happens when ‘unloading’ baroreceptors enter NTS?
Efferent sympathetic activity increases, increasing HR, BP and vasoconstriction
What is the effect of a spinal injury on unloading baroreceptors?
Spinal injury can ablate the pressor response so hypotension is a possibility when unloading
Outline how the link between CVLM and RVLM can be seen experimentally
- IV phenylephrine (alpha-1 agonist increases TPR & BP)
- BP rises & loads baroreceptors
- baroreceptor signal -> NTS -> CVLM
- CVLM inhibitory signals, RVLM signals
- Decreased sympathetic activity to heart & vessels
- Lower sympathetic gives vasodilation & BP
How does the CVLM lower BP?
Electrical stimulation of CVLM lowers BP coupled to decreased RVLM activity
Describe the vagal parasympathetic outflow (SA and AV nodes)
loading of baroreceptors also stimulates the vagus nerve which activates the NTS
signals from the NTS stimulates the vagal nuclei
vagal p/s impulses are sent to the heart
=> depressor effect
Describe how sinus tachycardia is a result of vagal parasympathetic outflow
Inhibitory input from inspiratory centre cases each inhalation to switch of nucleus ambiguus, increases HR
=> sinus tachycardia
Describe sinus tachycardia
Breathing in switches off vagal nerves - speeding up heart - increased HR
Explain the role of the limbic system on the SA and AV nodes
Limbic system (emotional centre) stimulates the nucleus ambiguus causing increased vagal nerve activity causing a depressor effect on the SA and AV nodes
What is a possible consequence of a limbic depressor effect ?
Can lead to fainting (syncope. vagovagal attacks) caused by decreased cerebral blood flow (reduced O₂ delivery) due to a sudden drop in arterial CO and BP
Describe the effect of removing afferent fibres from baroreceptors
Arterial pressures vary enormously although means aren’t that different
