Reflex control of the circulation Flashcards
Arterial baroreceptors
Arterial baroreceptors are vital to maintain blood flow to brain and myocardium.
The body monitors blood pressure in carotid and coronary arteries - there are no blood flow sensors.
Monitoring BP = Blood flow
- Blood Flow (CO) = Pa/TPR or Pa = CO x TPR
- Decrease in Pa reflects a decrease in eitehr CO or TPR which compromises blood flow to brain and heart.
BARORECEPTORS = DETECT ARTERIAL WALL STRETCH.
Baroreceptors respond to changes in pressure
- See diagram first.
Continued high or low pressure = threshold can eventually change –> long term hypertension - Baroreceptors become normalised at new pressure so they get less activated.
Baroreceptros respond to changes in pressure
Effect of increased BP on baroreflex
Increase in BP is termed loading - stress or excercise.
* Pulse pressure falls - decreased stroke volume.
* Vasodilation decreases TPR & BP.
* Decreased sympathetic nerve activity.
* Increased Vagus nerve activity.
Effect of decreased BP on baroreflex
Decrease in BP is termed unloading - Haemorrhage.
* Increased sympathetic activity and decreased Vagus activity.
* Increased HR and force of contraction 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.
^^^^ All this maintains blood pressure and blood flow to vital organs
Haemorrhage and the Baroreceptor reflex Diagrams
Cardiac receptors and efferent nerves
Veno-atrial mechanoreceptors:
* Stimulated by increase in cardiac filling.
* Reduces sympathetic activity to renal arteries increasing glomerular filtration - also secretes atrial natriuretic peptide increasing Na+ excretion all of which lowers blood volume reducing ADH and RAAS
Ventricular mechanoreceptors:
* Stimulated by over distension of ventricles - depressor response.
* Weak reflex - mild vasodilatation, lower blood pressure and preload, protective.
Nociceptive sympathetic afferents:
* Stimulated by K+, H+ (lactate), bradykinin during ischaemia.
* Mediate pain of angina and myocardial infraction.
* Reflex increased sympathetic activity - pale, sweaty, tachycardia of angina/MI symptoms.
Cardiovascular afferents - stabilising blood pressure
- When afferent fibres from baroreceptors are removed, arterial pressure varies enormously.
- When afferent fibres from cardiac receptors are also removed, arterial pressure still varies.
Arterial chemoreceptors
Located in carotid and aortic bodies.
* Stimulated by low O2 - hypocia, High CO2 - hypercapnia, H+ and K+.
* Regulate ventilation and also drive cardiac reflexes during asphyxia - low O2/high CO2, shock and haemorrhage.
When BP below the range of baroreflex, the the chemoreceptors are still active and may compensate.
Pressor response (raising of blood pressure)
* Increased sympathetic activity.
* Tachycardia, increased selective arterial/venous constriction.
* increased cardiac output and blood pressure - especially preservation of cerebral blood flow.
Muscle metaboreceptors (work receptors)
Sensory fibres in Group IV motor fibres located in skeletal:
-Activated via metabolites K+, lactate, adenosine.
Pressor response:
- Increase sympathetic activity.
- Tachycatdia, increase arterial/venous constriction.
- Increase cardiac output/blood pressure.
Important durinf isometric exercise:
-Continually contracted muscle but joint angle and muscle length do not change - EG weight lifting/handgrip.
-Higher BP drives blood into the contracted muscle to maintain perfusion.
These muscles undergo metabolic hyperaemia allowing bllod to flow to the contracted tissue.
Central role of the nucleus tractus solitarius
- signal from stretched baroreceptor sent via afferent fibres enter NTS.
- Then info sent out to the caudal ventrolateral medulla (CVLM).
- The CVLM sends info to the rostral ventrolateral medulle (RVLM).
- Results in inhibition of sympathetic efferent nerves to heart and vessels.
- Less sympathetic efferent signals result in reduction of HR, less vasoconstriction and lower BP.
Vagus parasympathetic Impulses to the heart
- loading of the baroreceptors also stimulates the vagus nerve which activates the NTS.
- the signal from NTS stimulates the nucleus ambiguous (vagal nuclei).
- Vagal parasympathetic impulses are sent to the heart and these have a depressor effect.
Vagal parasympathetic outflow - sinus tachycardia
Sinus tachycardia:
* Inhibitory input from inspiratory centre.
* Each inhalation switches off nucleus ambiguous.
* the inhibitory parasympathetic signal to the vagus decreases and heart rate increases slightly.
Your heart rate is slightly quicker when you inhale compared to exhaling.
Vagal parasympathetic outflow - vasovagal syncope
Limbic system –>stimulates NTS –> stimulates nucleus ambiguus –> increased activity of vagal nerve and depressor effect om 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.
Medulla oblongata summary
