APK 2105C Lecture Notes - Lecture 36: Carotid Sinus, Medulla Oblongata, Aortic Arch

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Chapter 14, Lecture 7
Vessels & Blood Pressure
MAP = CO x TPR
o Flow = pressure gradient / resistance
o Constant MAP = coming and going at the same rate
o Increased MAP = same resistance, more CO = more stretch in wall, more
pressure
Any increase in SV or HR
o Increased MAP = more CO, more resistance = more stretch, more pressure
o To increase MAP, increase CO or TPR
MAP = HR x SV x TPR
Regulation of MAP
o Only through extrinsic mechanisms
o Short term vs. long term regulation
Long term = blood volume regulation = minutes/hours/days
Short term = seconds/minutes
o Neural and hormonal changes
What is more associated with short vs. long term regulation?
Nervous = immediate responses
Hormonal = longer term
Neural control of MAP = arterial baroreceptors
Location
o Aortic arch
o Carotid artery bifurcation = carotid sinus (neck)
Detect changes in pressure in the wall
Stretch receptorssignaled when vessel wall stretches with more
blood volume
Always feeding information to CNS
o Increased pressure = increased AP frequency
o Decreased pressure = decreased AP frequency
o Change in pressure = change in signal to CNShave a
baseline AP frequency when things are normal
Major neural pathways in CV
control
o Medulla oblongata
CV control center
Used to
decide how
to control
CV
Sent out
using
autonomic
control
heart or
blood
vessels
Parasympathetic innervations
Innervates SA and AV nodes
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Document Summary

Vessels & blood pressure: flow = pressure gradient / resistance, constant map = coming and going at the same rate. Increased map = same resistance, more co = more stretch in wall, more pressure: any increase in sv or hr. Cv: sent out using autonomic control heart or blood vessels, parasympathetic innervations. Innervates sa and av nodes: baroreceptor reflex. Increase in hr and sv will increase co. Increased sympathetic tone: where is it released from, adrenal medulla, secreted in increased sympathetic tone, what receptors does it bind to, variable effect in vasculature, vasodilation in skeletal/cardiac muscle, vasoconstriction to all other organs, overall effect. Increase map: neg feed back, angiotensin ii, plasma protein derived from angiotensinogen, angiotensinogen +renin angiotensin i + ace angiotensin ii, long term basis, affects the kidneys more, adh secretion. Increase plasma volume increase pressure: vasopressor, neg feedback, vasopressin (adh) Immediate impact on vessels: long term impact to increase blood volume.

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