Reflex Control of the CVS Flashcards
What is the difference between exitatory and inhibitory inputs?
EXCITATORY INPUTS (eg. arterial chemoreceptors, muscle metaboreceptors) stimulate reflexes such as increasing CO, TPR and BP. It’s known as a pressor response.
INHIBITORY INPUTS (eg. arterial baroceptors, cardiac-pulmonary receptors) stimulate reflexes such as decreasing CO, TPR and BP. It’s known as a depressor response.
Describe arterial baroreceptors and their role in the body.
They’re vital for maintaining blood flow to the brain and myocardium.
However, there are no blood flow sensors, so the body monitors the blood pressure in the carotid and coronary arteries instead.
Monitoring the BP can tell us about blood flow from BP = CO x TPR. For example, a decrease in BP reflects a decrease in CO or TPR, which compromises blood flow to the brain and heart.
Blood pressure sensors in the walls of the carotid arteries/aorta inform the brain of pressure changes in these key feeder vessels.
These sensors, called baroreceptors, detect the arterial wall stretch.
Describe how baroreceptors respond to changes in pressure.
INCREASE IN PRESSURE:
There is not much firing at rest, then, as the pressure increases, there is fast firing which eventually slows down and becomes constant, but at a higher level than before. This is the adaptation to the 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 the baroreceptor activation can change (eg. long-term hypertension can lead to the baroreceptors being normalised at the new pressure and less activated).
Describe the effect of an increased BP on the baroreflex.
When there is an increase in blood pressure:
- the blood pressure falls (due to the depressor reflex)
- the pulse pressure falls
- vasodilation occurs, decreasing TPR and BP
- decreased sympathetic nerve activity
- increased Vagus nerve activity (Vagus nerve is not part of the sympathetic nervous system, so an increase in it’s activity will have a negative effect on the heart).
- heart rate is slowed down (bradycardia)
Describe the effect of a decreased BP on the baroreflex.
This is termed ‘unloading’, and can be caused by many things, such as a haemorrhage.
When there is a descrease in blood pressure:
- the blood pressure increases (due to the pressor reflex)
- the pulse pressure increases
- vasoconstriction occurs (to increase CVP, which increases SV, which increases CO)
- increased sympathetic nerve activity and decreased Vagus nerve activity (i.e. removal of the depressor)
- heart rate is increased (tachycardia)
Also:
- adrenaline secretion
- vasopressin (ADH) secretion
- stimulation of RAAS - Ang II production ~ Na/H2O reabsorption, increasing BP and maintain CO.
Describe the different cardiac receptors.
1) NOCICEPTIVE SYMPATHETIC AFFERENTS:
They are chemo-sensitive afferent fibres. They’re stimulated by K+, H+ (lactate) and bradykinin during ischaemia.
They mediate the pain of anginas and myocardial infarctions. The fibres converge onto the same neurones in the spinal cord as the somatic afferents - this is the basis of referred pain. The reflex increases sympathetic activity, causing paleness, sweatiness and tachycardia - angina and MI symptoms.
2) VENO-ATRIAL MECHANORECEPTORS:
They’re stimulated by increases in cardiac filling or CVP. They cause increased sympathetic activity, and thus tachycardia.
They also have the Bainbridge effect, which is where there is a reflex tachycardia due to the rapid infusion of volume into the venous system (sensed by veno-atrial stretch receptors and pacemaker distension).
Also, it increases diuresis, lowering blood volume via changes in ADH, ANP and RAAS. It switched off sympathetic activity to the kidneys and increases glomerular filtration.
It’s a mixed system, where the sympathetic stems can work independently; as one switches on, the other switches off.
3) VENTRICULAR MECHANORECEPTORS:
They’re stimulated by the overdistension of ventricles (depressor response). They’re a weak reflex, causing mild vasodilation and lowering blood pressure and preload.
Describe arterial chemoreceptors.
They are located in the carotid and aortic bodies. They’re stimulated by low O2 (hypoxia), high CO2 (hypercapnia), H+ and K+. They are well supplied with blood flow.
They regulate ventilation, as well as driving cardiac reflexes during asphyxia (low O2/ high CO2), shock (systemic hypotension) and heamorrhage.
When the BP is below the range of the baroreflex (maximally unloaded), the chemoreceptors are still active and may compensate.
They activate a pressor response.
Describe muscle metaboreceptors.
They’re sensory fibres located in the Group IV motor fibres located in skeletal muscle. They’re activated by metabolites, K+, lactate and adenosine.
They activate a pressor response.
They’re important during isometric exercise (ie. when you’re continuously contracting muscle, but the joint angle and muscle length do not change, such as in weightlifting).
The higher BP drives blood into the contracted muscle to maintain perfusion.
These muscles undergo metabolic hyperaemia, allowing blood flow to the contracted tissue.
Describe the central role of the nucleus tractus solitarius (NTS).
The baroreceptors (depressor) afferent fibres enter the nucleus tractus solitarius (NTS). This then sends information out to the caudal ventrolaterla medulla (CVLM).
The CVLM sends inhibitory information to the rostral ventrolateral medulla (RVLM).
This results in the inhibition of sympathetic efferent nerves to the heart and vessels.
Less sympathetic efferent signals results in the reduction of HR, vasoconstriction, BP, etc.
The situation is reversed when ‘unloading’ baroreceptors, in which case efferent sympathetic activity increases, increasing HR, vasoconstriction and BP.
Spinal injury can ablate this, so hypotension is a possibility when unloading.
In terms of the link between the CVLM and RVLM, describe the effects of iv. phenylephrine on the body.
1) Intravenous phenylephrine (α1 agonist) increases the TPR and BP
2) With the BP rising, the baroreceptors are loaded
3) There is a signal from the baroreceptors to the NTS, then to the CVLM
4) The CVLM signal inhibits the RVLM signals
5) Sympathetic activity to the heart and vessels decreases
6) The lower sympathetic signal gives us vasodilation and increased BP
Describe how baroreceptors affect the SA and AV nodes.
1) The loading of the baroreceptors also stimulates the vagus nerve, which again activates the NTS.
2) The signal from the NTS stimulates the vagal nuclei.
3) Vagal parasympathetic impulses (via the vagal parasympathetic fibres connected to the SA and AV node) are sent to the heart, and these have a depressor effect.
Describe how the NTS system receives signals from the inspiratory centre.
There is an inhibitory signal received from the inspiratory centre.
As we inspire, there is less vagal activity as each inhalation switches off the nucleus ambiguous (NAM) and our HR increases.
As we expire, the vagal activity recovers.
Describe the limbic stimulation of cardiac vagal activity.
For example, the limbic system (emotional centre) stimulates nucleus ambiguous, causing an increased activity of the vagus nerve and a depressor effect on the SA and AV nodes.
It can lead to fainting (syncope, vasovagal attack) caused by decreased cerebral blood flow (reduced oxygen delivery) due to the sudden drop in arterial cardiac output and blood pressure.
Describe how cardiovascular afferents help in stabilising blood pressure.
Normally, arterial pressure doesn’t really change much; it’s around 100mm Hg most of the time. A fall to 50mm Hg could cause insufficient perfusion to the end organs, whereas a rise to 150mm Hg could damage the cardiovascular system.
When afferent fibres from the baroreceptors are removed, arterial pressure varies enormously, though the means aren’t all that different.
When afferent fibres from cardiac receptors are also removed, the arterial pressure still varies, but the means have now become very different.
What is the pressor response?
If stimulated, they increase sympathetic nerve activity, which causes tachycardia. This causes selective arterial and venous constriction. This, in turn, increases CO/BP, thus preserving the cerebral blood flow.
