short term control of BP Flashcards
how is MAP calculated
MAP = CO x TPR
what can occur is MAP is too low
syncope
what can occur if MAP is too high
hypertension
where are the arterial baroreceptors located
aortic arch
carotid sinuses
carotid arteries
what type of receptors are the baroreceptors and what do they detect
mechanoreceptors
arterial wall stretch –> activation of receptors
which nerve to the carotid sinus baroreceptors travel in
glossopharyngeal
which nerve to the aortic arch baroreceptors travel in
vagus
where do the nerves in the baroreceptor reflex synapse and what happens in this area
medullary cardiovascular centre
looks at info from baroreceptors, MAP
controls firing rate of parasymp/symp nerves if MAP gets too high/low
parasympathetic aspect of baroreceptor reflex
via vagus nerve innervates SAN release of ACh to act on muscarinic receptors pacemaker cells reach threshold later reduced HR
sympathetic aspect of baroreceptor reflex (HR)
innervate SAN release of NA onto beta 1 receptors modification of ion channels quicker depolarisation of pacemaker cells increased HR
adrenal medulla involvement in baroreceptor reflex
release of adrenaline
binds to B1 receptors
increased HR
veno and arteriolar constriction in baroreceptor reflex
sympathetic innervation of vessels
NA acts on alpha 1 receptors
increased contraction of smooth muscles
altered TPR and VR to heart
sympathetic aspect of baroreceptor reflex (myocardium)
NA and adrenaline bind to B1 increased Ca coming in from outside and released from SR more cross bridges increased strength of contraction increased SV and BP
short term control of BP can be via
baroreceptor reflex
posture
valsalva manoeuvre
how is BP controlled in the long term
revolves around blood vol
sensed by cardiopulmonary baroreceptors
effects tend to be hormonal and act on blood vessels and kidneys
name 5 inputs to the medullary cardiovascular centres
cardiopulmonary baroreceptors arterial baroreceptors chemoreceptors in the muscle joint receptors higher centres
cardiopulmonary baroreceptors feedback effect
in the walls of the vessels in the heart and lungs
mainly in low pressure areas
activated by increased blood vol and increased BP
central chemoreceptors feedback effect
detect blood [CO2]
increase RR if CO2 conc becomes too high
stimulate increased SV and increased HR when activated
chemoreceptors in the muscle feedback effect
respond to [K] and low pH (increased metabolic rate)
stimulated during exercise
more blood sent to these areas
joint receptors feedback effect
detect movement in the joints and are activated
allows more blood to be sent to these areas
higher centres and medullary CV centre
feed forward effect
consciousness tells medullary CV centres to increase HR
what is the effect of standing on blood in the legs
increased hydrostatic pressure
pooling of blood in veins/venules of the feet/legs
what effect does posture have on MAP and why
reduced VR reduced EDV reduced preload reduced SV reduced CO reduced MAP (less efficient cross bridge formation, reduced strength of contraction, less blood in arteries)
what effect does posture have on baroreceptor firing
reduced MAP
reduced baroreceptor firing rate
lack of AP sent to medullary CV centre indicates reduced MAP
reflex response to posture
reduced vagal tone, increased HR and CO
increased sympathetic tone, increased HR and CO
increased contractility, increased SV and CO
increased venoconstriction, VR, EDV, SV, CO
increased arteriolar constriction, increased TPR
what is the valsalva manoeuvre
forced expiration against a closed glottis
how does the valsalva manoeuvre affect MAP
increased thoracic pressure transmitted through to aorta
increased thoracic pressure results in reduced VR, EDV, SV, CO, MAP
reduced MAP detected by baroreceptors (initiate reflex, increase CO, TPR)
how does MAP change when the valsalva manoeuvre is stopped
reduced thoracic pressure transmitted through to aorta
VR restored
increased SV
reflex effects not yet worn off
