Regulation of BP Flashcards

1
Q

SNS and MAP

A

increases TPR, HR, SV

therefore increases MAP via vasoconstriction
also causes release of Epi from adrenal medulla which amplifies the effects of NE

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2
Q

SNS and TPR

A

increases TPR through vasoconstriction (pressor effect) NE/Epi—>VC in smooth muscles

-exceptions include skeletal and cardiac m (Epi—>B2—>VD)

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3
Q

Exercising vs. resting skeletal muscle and SNS

A

Resting skeletal muscle: neural control dominates—>VC

exercising: intrinsic regulation dominates—>VD
* *local metabolic effect overrides SNS output

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4
Q

PSNS and MAP

A

indirect (think NO) promotion of VD—>decreased TPR (minimal effect due to lack of receptors)

decreases HR
Decreases contractility
*decreases MAP

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5
Q

Medulla Oblongata

A
  • *Major CV integrating center: vasomotor area
  • regulates MAP
  • mediates SNS and PSNS outputs
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6
Q

Input to MO

A

Baroreceptors, chemoreceptors, cortex, skin, local Co2 and O2

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7
Q

High pressure baroreceptors

A

Located at aortic arch and carotid sinus
inc MAP—>inc stretch—>inc receptor depol—>decrease SNS—>VD and bradycardia

rate(graded upon degree of stretch)
-respond to change in pressure:respond more to increased pulse pressure-not mean pressure

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8
Q

Increased MAP on high pressure Baroreceptors

A

inhibition of vasomotor area—>dec SNS–>dec VC—>VD

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9
Q

Impact of inc HR on baroreceptors

A

excitation of interneurons in cardioinhibitory area—>increases PSNS output—> dec HR

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10
Q

Low pressure baroreceptors

A

located in cardiac chambers (RA) and large pulmonary vessels (IVC) (in low pressure regions)

inc filling pressure/stretch—>increase FR
—>monitor blood volume (atrial filling) —> inc HR and dec renal VC–>inc urine output—>decreased effective circulating volume

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11
Q

Brainbridge reflex

A

increase VR/RAP–>inc HR (want to move extra blood volume through more quickly)

wins out over HPB response during times of high volume

counterbalance High pressure baros (which slow HR to compensate high pressure)

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12
Q

SV and HPB

A

–>inc MAP—>activates HPB—>decrease SNS—>dec contractility and flattening (plateau) of starling releationship

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13
Q

SV and LBP

A

activates LBP—>inc SNS output—>increase contractility and slope of Starling curve

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14
Q

Peripheral chemoreceptors

A

located at the carotid bodies or aortic arch near HPB
**detect inc CO2 and dec pH (some dec O2

increase rate and depth of respiration, some influence of vascular tone, and HR

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15
Q

Central chemoreceptors

A

in the MO
detect changes in central CO and decreased pH (indirect)

inc CO2—>stim vasomotor area—>VC—>increased TPR (in hopes of increasing MAP which maintains adequate driving force to supply the brain)

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16
Q

Net effect of chemoreceptor activation

A

inc HR, inc TPR, inc MAP (thru inc SNS)

17
Q

Baroreceptor vs Chemoreceptor response

A

if there is a increase pCO2 and increase in MAP, both would be stimulated, but baro-mediated inhibition of VC wins out

18
Q

Epinephrine

A

from adrenal gland
VC (a1)
VD (B2)

19
Q

ANG II

A

converted from ANG I by ACE (lungs)

VC (from renin in Kidneys during blood loss and exercise )

20
Q

ADH/AVP

A

from posterior pituitary gland

—>VC, released during hemorrhagic shock

21
Q

Histamine

A

response to tissue trauma

Vasodilation and Venoconstriction

22
Q

ANP

A

from atrial myocytes (LPB receptors)—>VD

**causes increase Na excretion (H20 follows)

opposes ADH in RAS system in order to decrease MAP

23
Q

long term regulation of BP

A

done by non-vasoactive factors thru regulation of blood volume

**kidney is key

24
Q

RAAS

A

main function is to maintain Na reabsorption —>increase MAP

occur in response to dec blood volume

25
Q

Ortostasis

A

Gravity effects upon standing

from pooling in large veins—>dec VR–>dec CO—>Dec MAP

stimulates HPB—>inc SNS and inc muscle pump

26
Q

Vasovagal syncope

A

common response to emotional response

dramatic increase in PSNS (dec SNS)—>dec HR, CO, MAP (bradycardia, hypotension, apnea)—>causes dizziness/faintness or LOC, skin pallor, blurred vision, nausea

27
Q

FIght or Flight

A

Stress induced response from the CNS ONLY—>inc SNS—> inc skeletal m. flow (via B2 vasodilation) and generalized vaso and venoconstriction (via a1—>dec renal and splanchnic flow)

inc CO,
inc ADH—>inc blood volume
Inc MAP

28
Q

Exercise

A

inc CO and HR and SV
distribute blood flow based upon metabolic demand
Net decrease in TPR

29
Q

Early response to exercise

A

higher CNS activity

anticipation—>SNS
Inc CO (HR, contractility)
inc VC to non-essential areas (including skin)—>more blood to muscles

30
Q

Delayed response to execise

A

Mechanical (inc venous return)

Chemical (increased autoregulation in exercising muscles, overall VD—>dec TPR)

31
Q

Effects of exercise on muscles

A

Inc Pc
inc O2 delivery (dec Hb affinity for O2)
Inc O2 consumption

32
Q

Exercise pressor reflex

A

reflex originates in muscle—>neural drive

sustains SNS output

33
Q

Arterial baroreflex and exercise

A

re-set sensitivity by CNS (inc set-point)

—>maintains SNS output even with high MAP

34
Q

Epi and exercise

A

exercise increases adrenal medulla produciton of epi—>B1

35
Q

temperature regulation

A

inc metablism—>inc CBT–>cutaneous heat loss–> inhibits SNS VC to skin (from early response)—>inc cutaneous flow

SNS cholinergic fibers activate sweat glands

36
Q

MAP and Power relationship

A

has a small increase that CO does, due to dramatic decrease in TPR (due to VD to skeletal muscles)