11) Reflex control of circulation Flashcards

1
Q

What are the two types of reflex inputs?

A
  • Excitatory inputs: Stimulation of these reflexes increases cardiac output, TPR and blood pressure. They are known as a Pressor response. It involves arterial chemoreceptors and muscle metaboreceptors
  • Inhibitory inputs: Stimulation of these reflexes decreases cardiac output, TPR and blood pressure. It is known as a Depressor response. It involves arterial baroreceptors and cardiac-pulmonary receptors
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2
Q

What part of the brain deals with the reflexive inputs?

A
  • The medulla
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3
Q

What are arterial baroreceptors?

A
  • They maintain blood flow to the brain and myocardium
  • They monitor blood pressure in carotid and coronary arteries
  • By monitoring the blood pressure we can deduce what the flow is like as we do not have flow censors in the body
  • They do this by detecting arterial wall stretch
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4
Q

What is the relationship between blood flow (CO), pressure (Pa) and Total Peripheral Resistance (TPR)?

A
  • CO = Pa/ TPR
  • A fall in Pa means either a decrease in CO or a decrease in TPR (if CO remains the same)
  • Both of these reduce blood flow to the heart and brain
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5
Q

How do baroreceptors respond to changes in pressure?

A
  • At rest pressure is low so the amount of pulses fired is low
  • However as pressure starts to increase we have a fast firing of pulses as it reaches the threshold
  • Upon reaching the threshold the pulses fired starts to slow down and remains at a level that is faster and higher than at rest.
  • It has adapted to a new normal
  • When there is a decrease in pressure the firing slows down proportionately
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6
Q

What happens to baroreceptors when we experience a continued high/low pressure?

A
  • The threshold for baroreceptors activation can change
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7
Q

What are the effects of increased blood pressure on baroreceptors?

A
  • When exercising there is an increase in blood pressure (called loading)
  • Pulse pressure falls which means stroke volume is reduced
  • Vasodilation occurs (which causes a decrease in TPR and blood pressure) along with decreased sympathetic nerve activity
  • Finally activity of the vagus nerve is increased
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8
Q

What are the effects of decreased blood pressure on baroreceptors?

A
  • When haemorrhaging there is a decrease in blood pressure (called unloading)
  • As a result there is increased sympathetic activity and decreased vagus activity
  • Heart rate and force of contraction also increases to increase cardiac output
  • Arterioles constrict to give increased TPR
  • Venous constriction increases central venous pressure and so stroke volume and cardiac output increases (due to Starling’s law)
  • There is also the release of adrenaline, ADH and activation of RAAS
  • This causes constriction which will increase blood pressure and decrease capillary pressure
  • Hence there is a decrease in hydrostatic pressure (so less filtration and more reabsorption)
  • These effects maintain blood pressure and blood flow to vital organs
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9
Q

What are the different cardiac stretch receptors?

A
  • Veno-atrial mechanoreceptors: They are stimulated by increased cardiac filling/ CVP. When stretched they switch off ADH and RAAS which reduces the sympathetic activity to kidneys to increase filtration at capillaries. They also secrete atrial natriuretic peptide which increases Na+ secretion. This reduces blood volume and pressure
  • Ventricular mechanoreceptors: They are stimulated by stretching of ventricles and deliver a depression response. There is a weak reflex as they cause mild vasodilation which lowers blood pressure and preload which play a protective role for vessels
  • Nociceptive sympathetic afferents: Stimulated by K+, H+ and bradykinin during ischeamia. They mediate pain of angina and myocardial infarction. They cause increased sympathetic activity which results in a person turning pale, sweaty and tachycardia of angina. This allows less blood to the skin and more blood to the heart
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10
Q

Why are baroreflex so important?

A
  • When afferent baroreflex fibres are removed, arterial pressure varies enormously however the means were not too different
  • When afferent cardiac receptor fibres are also removed atrial pressure still varies greatly however the means become different too
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11
Q

What are arterial chemoreceptors?

A
  • They regulate ventilation and also drive cardiac reflexes during asphyxia, shock and haemorrhage.
  • They are stimulated by low O2 (hypoxia), high CO2 (hypercapnia), H+ and K+
  • They are well perfused
  • When blood pressure is below the range of baroreflex (maximally unloaded) the chemoreceptors are still active and may compensate
  • They produce a pressor response. This means that there is increased sympathetic activity, tachycardia, increased arterial/venous constriction and increased cardiac output and blood pressure
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12
Q

What is a pressor response?

A
  • Occurs when atrial chemoreceptors are stimulated
  • We experience increased sympathetic activity
  • There is also Tachycardia along with increased selective arterial/venous constriction
  • There is increased cardiac output and blood pressure (especially in the preservation of cerebral blood flow)
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13
Q

What does the vagus parasympathetic nerve do?

A
  • Slows down heart rate
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14
Q

What are the different parts of the medulla?

A
  • Nucleus Tractus Solitarius (NTS)
  • Nucleus Ambiguous (NA)
  • Caudal Ventrolateral Medulla (CVLM)
  • Rostral Ventrolateral Medulla (RVLM)
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15
Q

What are muscle metaboreceptors?

A
  • They are sensory fibres in skeletal muscle that are activated by metabolites such as K+, lactate and adenosine
  • They also produce a pressor response. This means that there is increased sympathetic activity, tachycardia, increased arterial/venous constriction and increased cardiac output and blood pressure
  • This is important during isometric exercise (exercise where muscle is continually contracted but joint angle and muscle length doesn’t change). This produces a higher blood pressure which drives blood into contracted muscles to maintain perfusion. These muscles undergo metabolic hyperaemia allowing blood flow to contracted tissue.
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16
Q

How does the interaction between the nucleus tractus solitarius (NTS) and the RVLM occur?

A
  • They are found in the medulla and receive signals from stretched baroreceptors via afferent fibres.
  • They send messages to the Caudal Ventrolateral Medulla (CVLM) which sends information to the Rostral Ventrolateral Medulla (RVLM).
  • This is an inhibitory signal as it causes the inhibition of sympathetic efferent nerves to the heart and vessels
  • As a result we receive less sympathetic efferent signals which means less heart rate, less vasoconstriction and lower blood pressure
17
Q

How does the interaction between the nucleus tractus solitarius (NTS) and the NA occur?

A
  • Loading of baroreceptors stimulates the vagus nerve which activates the NTS
  • The signal from the NTS stimulates the Nucleus Ambiguous (NA)
  • The NA sends vagal parasympathetic impulses to the heart which have a depressor effect
18
Q

What happens at the NTS during sinus tachycardia?

A
  • First an inhibitory input is sent from the inspiratory centre
  • This causes every inhalation to switch off the Nucleus Ambiguous (NA)
  • Hence the inhibitory parasympathetic signal to the vagus nerve decreases and heart rate increases slightly
  • This means heart rate is slightly quicker when we inhale compared to when we exhale
19
Q

How does an emotional reaction affect the Nucleus Tractus Solitarius (NTS)?

A
  • The limbic centre (the emotional centre) stimulates NTS which stimulates the Nucleus Ambiguous (NA)
  • This causes increased activity of the vagus nerve and a depressor effect on the AV and SA nodes
  • This can lead to fainting (syncope), called a vasovagal attack, caused by decreased cerebral blood flow due to sudden drop in arterial cardiac output and blood pressure