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78 Cards in this Set
- Front
- Back
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what is the most important control mech for coronary vessels
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local metabolites
*hypoxia: decreased O2 will increase BF *Adenosine: dilate *NO *H+ *CO2 *SNS is least importatn |
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is SNS important for coronaries?
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not really
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what mechanical forces work on coronary circulation
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vessels are compressed during systole
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what is the most important control mech for cerebral circulation
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local metabolites
*CO2 *H+ *SNS is least important |
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does SNS matter for cerebral circulation
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not really
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what mechanical mech works when intracranial pressure increases
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increased pressure will increase cerebral BF
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what is the most important control mech for sk mm exercise, at rest
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local metabolites
*Lactate *K+ *adenosine REST: SNS a1: constricts B2: dilates |
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what happens to BF when mm contract
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temporary decrease
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when are local metabolites importatn during exercise? what about at rest?
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Metabolites:
Exercise: lactate, K+, Adenosine Rest: SNS a1: constrict B2: dilate |
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what is the most importatn control mech in skin
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SNS. temp regulation
Cold will vasoconstrict Hot will vasodilate |
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what intrinsic local control mechs does the heart do?
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all
1. autoregulation 2. active hyperemia 3. reactive hyperemia **the heart relies on local metabolites for control, hypoxia, adenosine, NO, H+, CO2 |
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explain hyperemia and reactive hyperemia in heart
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Active:
contractility increases so local O2 decreases and demand increases, coronaries dilate and BF increases Reactive: During contraction coronaries are compressed and BF is interrupted, during diastole coronaries dilate to increase BF to pay the O2 debt |
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what is the main control for cerebral circulation? why types of intrinsic control does it exhibit?
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local metabolites: CO2, H+, adenosine, K+, NO
ALL: Autoreg, active & reactive hyperemia |
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at rest how is sk mm controlled?
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SNS:
a1: constricts b2: dilates **constriction increases TPR |
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do mm do reactive hyperemia
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you bet ya
when mm contract compress arteries and decrease flow, after occlusion BF increases to pay the O2 debt |
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what do lactate, K+, and adenosine do?
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vasodilate sk mm during exercise
**at exercise local metabolites play the biggest role in regulation. Sk mm do autoregulation, when demand increases the BF increases |
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is cutenaous BF under intrinsic or extrinsic control
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extrinsic, recall extrinsic controls BP and Flow (intrinsic meets metabolic needs)
**relies on SNS, will constrict when cold (preserve heat) and dilate when hot (get rid of heat) |
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if there is a slow forming occlusion in a coronary what happens
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collateral circulation
**preexisting collateral vessels will enlarge |
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if your heart beats faster what happens
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active hyperemia:
increased metabolic demand, adenosine is released to vasodilate the coronaries and supply the heart with more blood *O2 demand now matches O2 supply |
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if a coronary vessel is occluded for a great length of time what happens
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Reactive Hyperemia: there is a larger O2 debt to pay so there is a longer increase in BF to make up the difference
**magnitude and duration of increased flow due to duration of occlusion **occlusion of coronaries occurs in systole |
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when does BF decrease in the coronaries
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occlusion due to compression during diastole
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what side of the heart displays the greatest effects of reactive hyperemia
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left
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what percent of coronary flow occurs in systole
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20%
systole is shorter AND compression of coronaries |
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what is the sympathetic stim of the ARTERIES of the heart?
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a1: NE constriction (overcome by other factors)
b2: EPI dilation |
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what is the sympathetic stim of the HEART itself? how does this in turn affect local metabolites
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B1: increased HR, increased contractility
**this increases the workload of the heart and increases vadodilation |
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so in the heart we have vasodilators and vasoconstrictors, who wins
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the dilators
Arteries: B2 dilates Arteries: a1 constricts, out numbered |
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how do parasymp affect the heart? net effect?
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well, it will cause coronaries to dilate via NO BUT...
it also will decrease the activity of the heart, decreased HR and decreased O2 consumption NET: decreased coronary flow |
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the B1 receptors in the heart are stim by what branch of ANS? what other branch is out competed
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the B1 in the heart itself increase metabolic demands by SNS
**the a1 in the vessels also are stimulated but to constrict, this is overcome by the effects of B1 |
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the coronaries are dilated by PNS by what mech? is this the only factor at play
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PNS dilates coronaries by cholinergic, to increase flow
***BUT... at the heart cholinergic PNS decreases HR and contractility which decreases the hearts O2 needs and will decrease flow NET: decreased flow by PNS |
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can the brain survive without O2? do you think it exhibits reactive hyperemia
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no
no |
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what implication does the skull have in cerebral circulation?
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constant volume
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the brain is incompressible, what implication does this have on flow
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flow in MUST equal flow out
increase in arterial flow is met by an increase in venous flow |
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what prevents vasoactive substances from acting on the brain?
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tight junction btwn endothelial cells
**prevents circulating substances from affecting cerebral blood flow |
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how is cerebral circulation controlled?
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local metabolites, same as heart and exercising sk mm
CO2, H+, adenosine, K, NO |
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metabolites affecting cerebral and coronary.. 4 are the same and one is different
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SAME:
CO2 Adenosine H+ NO Heart: Decreased O2 Brain: K+ |
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what is the MOST important vasodilator for the brain
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CO2 (H+)
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what is the MOST important metabolic factor for the heart
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adenosine
NO |
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what happens to cerebral BF when CO2 decreases
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vessels constrict
**when CO2 increases the vessels dilate |
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how are CO2 and H+ related with cerebral BF
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CO2 produced H+ so when CO2 is high so is H+
* an increase in either one causes dilation |
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what does K+ released by active neurons do to cerebral BF
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dilates coronaries, increases BF
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name 3 dilators of cerebral BF
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NO
K Adenosine |
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does the SNS have a strong effect on cerebral circulation?
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nope
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what is the cushing reflex
(where is P high?) |
increased P in the head! can be due to hemmorage
increased P leads to increased hydrostatic P of CSF, it eventually exceeds MAP Vessels AND brainstem become compressed wich leads to ischemia **ischemia leads to increased SNS to constrict vessels, to increase TPR to increase MAP and Increase cerebral blood flow *baroreceptor mediated bradycardia |
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wht does a hemmorage do in the brain
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well, pressure increases, CSF hydrostatic pressure increases and exceeds MAP such that blood flow is inhibited. This causes ischemia, the ischemia then causes the SNS to vasoconstrict everything else to restore BF to the brain
**baroreceptor mediated reflex by bradycardia |
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what happens to cerebral BF when systemic pressure drops WAY low
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ischemia
Vasomotor neurons become stimulated SNS increases systemic constriction, TPR increases, MAP increases, cerebral BF increases |
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what is the ischemic response
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when the brain gets no O2 bc the systemic BP is SO low
the vasomotor neurons are excited SNS induced systemic constriction TPR increased MAP increased cerebral BF increased |
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what determines TPR
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the degree of vasoconstriction in sk mm
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a1 predominates in sk mm when...
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rest! causes constriction
*the sk mm is largely under SNS control at rest a1: activated by NE increases resistance, decreases BF b2: dilates, activated by EPI from adrenal gland, decreases resistance, increases BF |
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what does EPI do?
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acts on B2 in sk mm to dilate them and increase BF
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withdraw of SNS on sk mm does what
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passive dilation
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at rest in sk mm high resistance is caused by...
at exercise in sk mm low resistance is cause by |
rest: a1 constriction by NE
exercise: dilation by lactate, K+, adenosine, AND b2 dilation by epinepherine from adrenal medulla |
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adenosine, K and lactate do what
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dilate sk mm during exercise, autoreg, active/reactive hyperemia
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what causes hyperemia in sk mm? what does this do to venous return
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mm contraction. decreased BF will increase lactate, K, adenosine to increase BF
**the compression also increases venous return |
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at 30% contraction of sk mm what happens to bf? 70%
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30%: flow interrupted
70% flow stopped |
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muscle pump does what
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increased sk mm perfusion
*contraction/relaxation cycle creates intermettient BF **decreases venous Pressure which increases the pressure gradient and increases flow |
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what happens to BF in the calf during rhythemic contractions
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BF increases
**venous return increases, venous pressure decreases, change in P increases, larger driving force for flow, flow increases |
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at low conc what does epi do?
high conc? |
Low: dilate, B2
High: constricts a1 |
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what does vasopressin and angiotensin do?
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constriction
**when BP deceases these are released and BP is restored |
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what is the main fx of skin
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BP reg: major resevoir for blood
Heat loss: major fx Nutrients: necessary but monimal |
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when there is in an increase in bloodvolume what happens (hypervolumia)
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some blood enters cutaneous circulation to try to decreased the volume
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what happens when there is a decrease in blood volume (hypovolumia)
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blood is taken from the skin
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where does blood flow directly from an artery to a vein? why?
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in thte skin, arteriovenous anastamose
allows blood to bypass capillary beds |
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where are arteriovenous anastamoses located
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cutaneous circulation, direct a to v path
Finger, Lips, Toes, Ears, Nose |
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when are AVA (aretriovenous anastamoses) open
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open when its hot, (SNS is removed)
also open during prolonged cold exposure **open by decreasing sympathetic tone Closed with sympathetic tone |
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are AVA's regulated by intrinsic or extrinsic factors
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NO intrinsic: no metabolic factors, active/reactive hyperemia
**tonic symp tone keeps constricted |
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how do AVA's open?
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passive dilation by removing SNS
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arterioles in the cutaneous circulation have what receptors
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lots of a
NO b2 **remember a1 constrict and b2 dilate so it makes sense |
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where in the skin do we have sympathetic cholinergic receptors
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sweat glands
dilation via brady kinin |
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how is brady kinin made? what does it do?
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from symp cholinergic receptors to the sweat glands, activation makes bradykinin
**brady kinin mediates dilation |
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we know AVA's dont do intrinisic regulation (autoreg, re/active hyperemis) so arterioles in the skin?
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yep!
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where in the skin is the greatest blood resevoir
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venous plexus in the skin
**important for heat transfer **constriction via SNS |
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how is heat conserved
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the skin has SNS that clamps down on its AVA's and arterioles to reduce heat transfer to environment
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how is heat lost
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SNS is reduced to allow vasodilation in the skin and heat is transfered to the environemnt via venous plexus
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what does local cooling/heat do to cutaneous circulation
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cool: constrict
heat: dilate **due to direct effects of vasculature, and CNS reflex center |
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if one part of the body is exposed to cold what happens to the other part
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the part exposed will constrict immediatly, that info goes to brain and makes the rest of the body regulated to the cold temp
**a spinal cord injury leave an individual with poor temp control. we need the CNS integration center for temp regulation |
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explain how skin does reactive hyperemia
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sitting leads to compression, accumulation of metabolites, this activates nocireceptors which makes it pain ful and you shitf to let blood flow back
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explain cold induced vasodilation,
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when its SO cold the SM freezes and cant constrict, so we get passive dilation
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in the skin what does....do?
epi antiotensin II vasopressin |
epi: constriction
angiotenisn II: constriction vasopressin: constriction |
