Flashcards in 9/ short term control of blood pressure Deck (25):
what is MAP? why is it important?
- mean arterial pressure, the driving force pushing blood through the circulation - has to be regulated as too low may lead to syncope (fainting) and too high leads to hypertension
where are the main arterial baroreflex? where do they send their signal to?
- on the aortic arch (aortic arch baroreceptor)
- on the carotid sinus of the internal carotid arteries (carotid sinus baroreceptors)
- signals from baroreceptors are sent to the brain
which nerve receives the signal from the aortic arch baroreceptor?
which nerve receives the signal from the carotid sinus baroreceptors?
where in the brain are these signals sent?
medullary cardiovascular centres
which nerve leads the response signal from medullary CV centres to right heart?
parasympathetic of vagus nerve
which nerve leads the response signal from medullary CV centres to left heart?
sympathetic nerves (stops at the adrenal medulla to get the adrenaline)
what are the possible responses from the sympathetic system?
increases contraction, venoconstriction and arteriolar constriction (in the systemic circulation)
what are the possible response from the parasympathetic system?
increased or decreased contraction into the respiratory circulation
what other inputs are there to the medullary CV centres?
- cardiopulmonary baroreceptors
- central chemoreceptors
- chemoreceptors in muscle
- joint receptors
- higher centres
what are the major inputs for the long term regulation of blood pressure?
- cannot be arterial baroreceptors (they would eventually re-program to higher threshold)
- revolves around blood volume
- main sensors are the cardio-pulmonary baroreceptors
- effects tend to be hormonal and tend to act on blood vessels and kidneys
what are the different inputs for hormonal long term regulation of blood pressure?
- renin, angiotensin, aldosterone system:
- vasopressin (= antidiuretic hormone)
- atrial natriuretic peptide & brain natriuretic peptide
characteristics of renin - angiotensin - aldosterone system
- angiotensin II causes arteriolar constriction and increase in TPR
- aldosterone increases Na+ reabsorption, and increases plasma volume
characteristics of vasopressin (= antidiuretic hormone)
- vasopressin causes arteriolar constriction, increase in TPR, increase in water permeability of collecting duct and increase in plasma volume
characteristics of atrial natriuretic peptide & brain natriuretic peptide
- causes arteriolar dilation and decrease in TPR
- increase Na+ excretion (natriuresis) and decrease in blood volume
what do the effects of standing have to do with venous pressure?
effects of standing: increased hydrostatic pressure causes pooling of blood in veins/ venules of feet/ legs
how does the body deal with the effects of standing on venous pressure?
- decreased venous return, decreased EDV, decreased preload, decreased stroke volume, decreased cardiac output, decreased mean arterial pressure
- decreased baroreceptor firing rate
how is the reflex response adapted to this?
- decreased vagal tone when standing (increased HR and CO)
- increased sympathetic tone (increased HR + CO, increased contractility (increased SV, CO) increase venoconstriction (increased VR, EDV, SV, CO), increased arteriolar constriction (increased TPR))
what is the valsalva manoeuvre?
forced expiration against a closed glottis
what is the effect of the valsalva manoeuvre on thoracic pressure (first part of the manoeuvre)?
increase in thoracic pressure
what is the effect of increase in thoracic pressure?
decrease in VR, EDV, SV, CO, MAP
what is triggered because of the decrease in MAP? what then?
baroreceptors initiates reflex to increase CO and TPR
what is the effect of the valsalva manoeuvre on thoracic pressure (second part of the manoeuvre)?
decrease in thoracic pressure transmitted through the aorta
what happens when thoracic pressure normalises?
VR is restored so SV increases, but the reflex effects have not worn off yet
then eventual back to normal