Reflex control of the Circulation Flashcards
What are examples of excitatory inputs?
Arterial chemoreceptors, muscle metaboreceptors
Stimulation of reflexes- increase cardiac output, TPR, and blood pressure Pressor response
What are examples of inhibitory outputs?
Arterial baroreceptors, cardiac-pulmonary receptors
Stimulation of reflexes- decrease cardiac output, TPR and blood pressure depressor response
What are arterial baroreceptors?
Vital to maintaining blood flow to brain and myocardium
There are no blood flow sensors, the body monitors blood pressure in carotid and coronary arteries
Blood pressure sensors in walls of the carotid arteries/aorta inform the brain of pressure changes in these key feeder vessels
Sensors detect arterial wall stretch- baroreceptors
Why do we monitor blood pressure?
Monitoring BP tells us about blood flow from:
Blood flow (CO)= Pa/TPR or Pa= CO x TPR
Decrease in Pa reflects a decrease in either CO or TPR which compromises blood flow to the brain and heart
Blood pressure sensors in walls of the carotid arteries/aorta inform the brain of pressure changes in these key feeder vessels
Sensors detect arterial wall stretch- baroreceptors
How do baroreceptors adapt to chronic changes in blood pressure?
Baroreceptors respond to changes in pressure
Increase in pressure:
Not much firing at rest then as pressure increases fast firing which eventually slows down and becomes constant, but at a higher level than before
Adaptation to a new normal
Decrease in pressure
For a decrease in pressure the firing slows down proportionately
In the face of continued high or continued low pressure the threshold for baroreceptor activation can change e.g. long term hypertension- baroreceptors become normalised at the new pressure and less activated
What is the effect of increased BP on baroreflex?
Increase in BP is termed loading (e.g. stress or exercise)
Pulse pressure falls (decreased stroke volume)
Vasodilation decreases TPR and BP
Decreased sympathetic nerve activity
Increased Vagus nerve activity
What is the effect of decreased BP on baroreflex?
Decrease in BP is termed unloading (e.g. haemorrhage)
Increased sympathetic activity and decreased Vagus activity
Increased HR and force of constriction so increased cardiac output
Arteriole constriction gives increased TPR
Venous constriction increases central venous pressure and so by Starling’s law increases stroke volume and cardiac output
This all maintains blood pressure therefore blood flow to vital organs
Also adrenaline secretion, vasopressin (ADH) secretion and stimulation of RAAS (i.e. Angiotensin II increases Na+/H2O absorption in kidneys raising blood volume)
Vasoconstriction decreases capillary pressure which increases absorption of interstitial fluid which also increases blood volume
What are two different mechanoreceptors in the heart and what do each signal?
There are some other receptors which send their signal to a place in the medulla called the nucleus tractus solitarius (NTS)
The veno-atrial mechanoreceptor- on the veins (vena cava) and atria, connected to vagus afferents
If these are getting stretched that means you blood pressure is too high
Ventricular mechanoreceptor- stimulated by over distention of the ventricles
Nociceptive sympathetic afferents- these signal pain
If we are not perfusing the heart enough these nerves are triggered and simulate pain through the spinal cord then brain
They converge onto some neurons on the spinal cord that come from other parts of the body such as the shoulder or the jaw and sometimes the brain makes you feel pain in those places
What does each of the vagus afferents signals?
Ventricular mechanoreceptors- Stimulated by overdistension of ventricles- depressor response
Weak reflex- mild vasodilatation, lower blood pressure and preload, protective
veno-atrial mechanoreceptors- stimulated by an increase in cardiac filling/CVP
Increased diuresis switches off ADH and RAAS- reduces sympathetic activity to kidneys increasing glomerular filtration.
Secretes atrial natriuretic peptide (increasing Na+ excretion)
Nociceptive sympathetic afferents- Stimulated by K+, H+ (lactate), bradykinin during ischaemia
Converge onto same neurones in spinal cord as somatic afferents- referred pain
Mediate pain of angina and myocardial infarction
reflex increased sympathetic activity- pale, sweaty, tachycardia of angina/MI symptoms
Why is the baroreflex so important?
- When afferent fibres from baroreceptors are removed arterial pressure varies enormously, though the means aren’t all that different
- When afferent fibres from cardiac receptors are also removed arterial pressure still varies and the means have now become very different
Normally, arterial pressure doesn’t change much it is around 100mmHg most of the time. A fall to 50mmHg could cause insufficient perfusion to end organs whereas rise to 150mmHg could damage the cardiovascular system.
- When afferent fibres from cardiac receptors are also removed arterial pressure still varies and the means have now become very different
Where are arterial chemoreceptors located and what do they do?
Located in carotid and aortic bodies:
Stimulated by low O2 (hypoxia), high CO2 (hypercapnia),high H+ and high K+
They are well supplied with blood flow around 20ml/g/min
Regulate ventilation and also drive cardiac reflexes during asphyxia (low O2/high CO2) shock (systemic hypotension) and haemorrhage
When BP below the range of baroreflex (maximally and unloaded) the chemoreceptors are still active and may compensate
What is the pressor response of the arterial chemoreceptors?
Pressor response:
Increased sympathetic activity
Tachycardia, increased selective arterial/venous constriction
Increased cardiac output and blood pressure- especially preservation of cerebral blood flow
Where are the muscle metaboreceptors (work receptors) located and what do they do?
Sensory fibres in Group IV motor fibres located in skeletal muscle:
Activated via metabolites K+, lactate, adenosine
Pressor response:
Increase sympathetic activity
Tachycardia, increase arterial/venous constriction
Increase cardiac out/blood pressure
Important during isometric exercise:
Continually contracted muscle but joint angle and muscle length do not change e.g. weight lifting/handgrip
Higher BP drives blood into the contracted muscle to maintain perfusion
These muscles undergo metabolic hyperaemia allowing blood flow to the contracted tissue
What is the central role of the nucleus tractus solitarius?
Loading of the baroreceptors also stimulates the vagus nerve which again activates the NTS
The signal from the NTS stimulates the nucleus ambiguous (vagal nuclei)
Vagal parasympathetic impulses are sent to the heart and these have a depressor effect
What is the vasovagal syncope?
Vagal parasympathetic outflow
Limbic system (emotional centre) stimulates NTS which in turn stimulates the nucleus ambiguous causing increased activity of the vagal nerve and depressor effect on the AV and SA nodes
Can lead to fainting (syncope)- vasovagal attack
Syncope caused by decreased cerebral blood flow due to sudden drop in arterial cardiac output and blood pressure
