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Physiology Kerry > 3.2 Myocardium & Blood flows > Flashcards

3.2 Myocardium & Blood flows Flashcards

1
Q

What is Myocardial oxygen comsupmption

A

7-9 mls/100g/min 21-27mls normal heart 300g

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2
Q

Major determ myocardial oxygen consumption

Other factors

A

Myocardial wall tensions
Contractility
HR

Basal energy metabolism (25% total consump)
Energy work performed
Energy for electrical activation
- 0.5-1%

Work is mauresured as product of pressure & volume

Oxygen cost work - depenedent on way work performed - pressure work - requires high myocar than boule work
Increase afterload causes greater increase O2 than icrease Preload

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3
Q

What is tension time index

A

Are under systolic part of LV pressure curve

Correlate well w/ oxy consump when contractility not altered

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4
Q

What substrates metabolised

A
  1. Heart use whatever available
  2. Can metabolise glucose, lactate, keto FA

Amiunt each used - related arterial concntrations of subrate

40% carbs 60% other

Uptake gluc incrase insulin
brain diff - excluse use glucose

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5
Q

How measure myocard o2 consump

A

not practical - require meausre flow - sampl cor sinus

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6
Q

Valsava

A

Close off moutj nostrils strain
increas intrathoacic pressure

Every time strain -
fly pop ears
effects on CR - tidal ventail interptad
impercetible pulse

blow mercury column to ~40mmhg hold 10 sec

Essential ft - increase intrahtoracic pressure

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7
Q

Changes bp valsva

A

1 - increased pressure - pulse steady - intraopuilm vessel - increase VR
increase sv - starling
rise bp few beats

2 Strain - bp falls - decrase Co
Barrecpto - sense reflex compens 
symp stim - incrase HR
symp stim - vasoconstric
maintain bp - organ flow compromised low co

3 BP dips - after release straing
removes squeeze vessel - increase size - decrease return blood - drop co & BP

4 blood left increase normal - restore co deliver normal co - vasoconstrict bed - overshoot bp
barorecptor sense - vagal slowing hr - lower previous resting
periph relax - return normal

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8
Q

Valsalva ratio

A

Ratio between ongest RR interval phase 4 and shortest phase 2

haert response secpndary events - occur d/t cartoid barorecptor
nromally >1.5
Decrease incrasing age - less in elderly
d/t decrease baro responsivness

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9
Q

Main cause increase pressure

A

increase pulmonary bv - resoevor

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10
Q

significat beta block - how alter

A

small overshoot bp in phase 5 - absne hr response pahse 2 hr not eleavted at phase 4 so co and bp not increase rapidly

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11
Q

Alpha blocked

A

lower bp phase 2 - incrase bp overshoot phase 2

Hr increase - unoopsed beta stim abense vascons to increase bp

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12
Q

Clin uses valsalva

A

Reversion SVT
-increased vagal activity
Autonomic function testing
Aids murmurs - hocm mv prlaopse increase

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13
Q

CVS response to standing

A

Immed reponse - blood pooling lower extreme
= VR & CO decrease - BP drop

Sense carotid barorec - vasomotor & cardiac centre medulla stimulated

Sympathetic stim
1 Perip vasocon - incr svr
2 Periph venocon - inc vr
3 Incr HR
4 Incr Contract

Change - restore bp & maint CP

Hydro-static effect - decreasing CPP
D/t brain higher heart erect position 30 cm
arterial pressure brain lower aorta
MAP at brain level is less after change response

Acitivity after moving
-Moves briskly - msucle pump - prevent pooling

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14
Q

How is standing response different in elderly

A

Sympathtic response slower & less effective

Baroreceptors less responsive

Experince lighthead/faint - decr CPP

Autoreg doesnt have imeediate onset

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15
Q

Soldiers collapsing

A

Decrease CPP - Decre CO

Blood pools - exstemities decrease VR

Standing still remove muslce pump

Hot - veodilates

Cartoid sinus not as effective in venocontsiction

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16
Q

CVS response rapid loss 1000mls blood

A

Mjaor acute BLood loss

Decrease CO & Decrease ABP

Change detected
1 high pressure barorecptor in carotid sinus
2 Low pressure (Volume) in RA & great veins

Compensatory -

Minimise effective blood change
Venoconstriction
transfer ISF-> plasma
Decrease RBF
Decrease Urine volume
Mobilisation resevoir
restless - increase muscle pump activity

Maintian ABP
Peripheral vasocon
Tachy

Sense carotid sinus
Reflex sympathetic stim

Increase HR Contractility - vasocon & venocon

Blood lungs Liver - mobilised -

Redistr - CO
Peripheral vasocon - decrease muslce

Renal vcon
olugira - min fluid oloss

CVF
perferent maintain
craotid sinu, pressure autogerg, metabolic autoreg

Changes in starling forces accorss capil - net reabs ISF into blood -0 incrase blood vol
~~1000ml / hr - transferred

Drop BP - oliguria - retnet salt water
Increase ADH - voulme rec
Increase ang & aldo
Increase thirst

Rapid loss ~~>shock

CO insuff - meet tissue demand - neurohumora l decompensating large / rapid loss - limited capacity response

Lactic acidosis arryht hf - older depress function
Hypotensi may sevcere - decr CPP - ischameic cns response - msmyph outflow ischameia medulla - last dithc mainta CPP - adernline medulla

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17
Q

What are delayed repsonse to major losses

A

Plasma volume should return normal 12-72 hours

Increase in plasma proteins - synthesis liver
Days retun plasma proteins to onormal

Incrase RCC production
EPO increase - poiesis - retuc level peak 1- day - fully restore 4-8/5

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18
Q

What is a reticulocyte

A

Erythroycte at final stage maturation

Cells enter blood * basophlic cell debri (rna, mitochandria & oorganelle)
extruded in couple days

normally only 1%

Increase epoiesis - more reticulcytes - readily detced exam
fine retic basophil material
Increased- increase epoesis

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19
Q

What are the effects of transfusion 1l autologues blood into normvoemic health

A

Blood vol increase 20%

Circulation overfilled - mean systemic pressure increases 15mmhg
RAP increase
CO increase 10-15l min d/t preload (starling) & increased HR

SVR init normal - increase CO - increase ABP

Short lived -

Venous pooling

increase BP - sense carotid sinus - result increase inflow - sinus &
decreased outflow vasomotor - cardiac centre medulla = periph venodilation & decrease systemic pressure

Increased venous pooling decrease VR & CO - retunr bp normally
Sustain increase CO - not occur - pressure autoreg - meatolic autoreg - adjust vascular resistance - maintain cosntant blood flow

Marked in brain heart kidney

Increase capillary hdydrostati c- increase tissue fluid formation - limited d/t similar oncotic pressure

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20
Q

How is the extra fluid extra

A

Increase in BP - pressure Diuruesis & natiriresis - increase
Increase urine flow - bp elevated -

autog - various tissue mainta blood flow normal level - increase periphral vasocon - rise arterial art bp

Beneficial - promotes excretion fluid salt - renal body fluid mechanism - maintain ECF

20% increase in volume - above thresld stim low pressure / boulme receptor
ADH secretion decrease - diuresis

Osmorecpt in hypothal - not stimm plasma osmolal - not alter

Increase o2 carry capactiy - remove epo stimulus

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21
Q

Rapids infusion of litre 5% dextrose

A

Haemodynamic effect - increase blood volume

Mean systemic, rap, co bp

rapidly lost IV compartment- haemodymaic change limited speed
Inital changes - ltd speed loss occurs
Venous pooling occurs

At infuson 5% isosomolar
fluid oncotic pressure -
balannce starlings - alter lower onctoic fluid lost interstital flud
gluco taken up

net effect
distrib all fluid compration
proportion contrib total bod water

Ready mobilised fluid -
ratio ICF:ECF 2:1
ECF - approximate ratio:IV 3:1 
Distrib 1l 5% 
ICF - 660
ECF 340 - ISF 255 + IV 85

Final increase blood vol <2%
Not sufficent acti volurecports
not suffic cause hd change

plasma oncotic not altered - incrased not sufficnet adverse oefefct cell fxxn
Change ISF - no effects not suffic oedema

Osmolality decrease 287->280
2.56% osmolaity
Aobve threshold
hypothal osmorec - adh dcerease
short half life 15mions - 
effect 1h 
excess water excreted urine
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22
Q

What effects rapid transfusion 1l NS into patient

A

Acute haemodynamic - depend magnitude actue increase iv volume

speed transufion - rate fluid lost inv volume

rapid trfsion - incrase mean systmic pressure rap co incr incr hr svr normal - increase abp

[Na} ~~ ECF
no increase ICF volume

ECF 0 fluid distributed ISF &amp; IV - proprtion contriub ecf volume
fluid distirb 
Intracell - nil
ECf ISF 750 IV 250
explains why ~ 3l need for 1
?less- glycocaylx

Osmolaltiy not altered - no osmrecptor stimulation

IV voume increase 5% - below 10% voulume stim - no adh change

mechanism excretion fluid

Fluid & salt - d/t 2 factors
Floumerultoublar imbal
pressure volume control mech

Increase blood vol - saliene - small drop oncotic pressure
Gloerulotubular imbal - kidney & GFR increases slightly less fluid & na reab prox tube

Increase Urine flow 0 excertion excess fluid and salt
Immed - no lag 0 urine flow increase
no sense hormone level change / adh

Pressure volume - powerful but slow - onset reflex minmise effect saline loading

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23
Q

Rapid infusion 5% normal ablumin

A

Fluid IV compartment
Similar autologus blood
Incr CO + Bp
capactiance vessel relax -venous pooling increase loss ISF - increase capilalary hysdrstatic pressure

elevated abp - pressure natriuresis diuresis p renal volume control

osmalilty ecf not changfe osmrec hyptol not stim

low pressure baro stim
adh falls - favour ecretion

o2 carry capiacty decrease - hb decrease
tissue increase floow - meet req
1 autoreg - art vadola
2 decrease vlood biscotisty

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24
Q

Which fluid excreted quickest

A

N saline - gloerulotublar mbalnce - ovvurs immed renal exretion occurs

water 5% dex & abl - decrease adh - not immed

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25
Q

Cerebral blood flow what is it

A

750mls min
50mls 100g min
15% CO

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26
Q

CMRO - what
typical vale
significance

A

Cerebral metolbic rate o2 consumption
3-3.5mls o2 100g min
50mls in total
brain weight 1.4kg - use 20% basal o2 conspump

hgih level metbolic activty - not tolerate momentray o2

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27
Q

Is CBF alter in exercise

A

No -global flow ulatered

change distrib - motor cortex increase
flow small - other receive less

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28
Q

Factors involve in cotnol cbf

A

CPP / CVR

MAP-CPP

Factors affecting CVR
Metabolic autoreg
pressure autoreg
chemical factors
nervous system
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29
Q

Metabolic control -

draw cbf & metolic control

A

autoreg - ability tissue adjust blood supply - recive flow carry fxn

local vasodil metbolite
impratnat min min reg control cbf

exampls
admin indction tho- decrease cbf - decreae cmro2 cbf decrease
fitting causes incrase work - cbf increase

supply meets demand

metbolic regulation - moment moment reg cbf
glocal may reman constant

draw curtve metabolic ontrol cbf - page 63
flow metabolism coupling

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30
Q

Pressure autoreg

draw effect change mean bp - cbf

A

rel constant cbf - despite map 50-150

page 63

Myogenic theory
Pressure arteriole increase - increase stethc vessel

vascular sm responds -> stretch contract - resting tone higher
results decrease redius - increased resistance vells - return blood flow to normal
despite continuation pressure
quickly - seconds

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31
Q

what circumstance autoreg pressure shift ight

A

Chronic htn & acute sympathetic stim

Main point - lower limit shift to right
not tolerate drop bp - without decrease cbf

Low BP not tolerated espec i fealvated ICP

Neonates - pressure reg left shift platue anrrow 30-90 slopes upward to right
lower bp - phys approp left shift
decrease upper limit neonate less toerate higher bp

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32
Q

Curve art PCO2 & CBF

What is the shape of the curve
from what to what

A

page 64

Curve almost liner 2.6-10.6
CBF linear change over pco2 wide rang

Where is the normal Pco2

Decrease CB F - sustain hypocanpoa - dimish time - bic equil across bbb
brain ISF pH - normal thus so does CBF

Effect - advance 4-hours
Sudnden return normal art pco2 - excess CBF & Rise OCp

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33
Q

What is factor level curve lower limit curve

A

Cerbal vasoldtion in response hypoxia

low flow limits amount ocygen deliver - vasodilation causes prevent further decrease cbf- with decrease art pco2

Proven in hypernaric chamaber
Sifficenmt o2 dissovled - oxygne receive adeq o2 despite low cbf - acute hypocapnic vasoconsitrciton

counter ewffect hypox vosdil remoced
further decrease cbf

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34
Q

Daw arterial po2 & CBF

Why is it that shape

A

Page 65
CBF not affected until po2 <50mmhg 6.6kpa

Shape odc for hb
po2 falls o2 content not alter much upper part
as falls <60 oxy content falls rapidly - steep odc
not much decrease o2 supply in level reach
cerbrel arterioles - vasodialte cbf incrases to maint o2 delivery

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35
Q

Nervous control cbf

cartoid sinus cbf

A

SNS - not import chang cerebral circ - change CVR
autonomic stimulation allter cvr small amount

Improtant in CBF - effects on CPP
Barorecporor monitor mean carotid arterial pressure

BP falls - neuroanl firing cartoid sinus diecrase
reflex - rapid powerful sympathet stim - hr contract
vasocn attemp maintain map

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36
Q

Barorectpor

A

Stretch receptors walls heart blood vessel

Carotid sinus aortic arch

Arterial Ra LA Pulm veins
small dilation ICA - increase rate firing distention - decrease sympathehtic increase vagal response

Carotid aortic baro - end NTS at medulla - releaseglutamte, siognal go caudal ventrolaterral medulla

Carotid sinus reflex & pressure autoreg - aim mantain constant cbf - despite change map

Carotid sinus reflex - responds rapider - improtant moment moment activ - chjange positon
pressure autoreg - minutes

Under cond extreme hypoxia - ishaemic response - chusin reflex
Max sympathetitic stim - last ditch resore CBF & o2 2supply

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37
Q

What is the CPP - how measure

A

CPP CVR

CPP - driving flow blood

perfusion organs - diff map & venous draing tissue

added consideration brain - icp
icp higher cenous pres
then map - icp

type something occurs lungs heart - starling resistor

CPP i MAP minus greatr CVP or ICP

dterm - CPP require all three measure

38
Q

Pressure autoregulation - brain MAP x acis

A

Curve drawn map x and cbf y - reason MAP est CPP

larger than ICP & JVP
Easy measure
Meausre ICP - more incasive

Path condition ICP high - high map low

39
Q

Why would we want tor reduce CBF intraop

A

Decrease ICP

Mimise blood loss

40
Q

What is monro kellie doctine

A

Brain ecnlsoed righid bony skull

total volume conents fixed
attempt increase volume any conents - rapid icnrease pressure

Diagr pg 67
Presuure not rise much initally csf out ventricle into extracran SA space
vuffer exhausted - rise very abrupt

Intracrain coent normally - 85% brain 10% csf blood 5%

41
Q

What are methods manipulate CBF & ICP cranitomy

A

Head up tilt

No obstruction drainage

avoid vdilator cerebral

Hyperventilation

Mannitol

Contolled hypotension

42
Q

How head til & no ostruction alter CBF

A

Decrease CPP - hydrostitc effect

keep jug veinbs collapse - no congestion

Min venous bleeing

Addit - decre VR - pool blood extermity - hypotension activated carotid sinus - icrease bp
fianl efect perfusion - effectie pressure & metab autoreg

Idisag - increase risk venous air ebolism
drop cpp & cbf may not be warranted

43
Q

Why is hyperventilation beneficial on ICP

A

Rapidly reduce art pco2

Decrease 4% every mmHg decrease art pco2 from normal

intracerbral pressure decrease - desired effect

Advant -
rapid reliable
potent
easily control

disadv
not lasting
-less 4-12h -> decrease bic brain ECF - restores ecf pH to normal & vascon - decreased
allow art pco2 rise - tend excess increase cbf

44
Q

How does mannitol work reducing ICP

A

Hypertonic - not cross cell membrane
draws water all cells

doesnt direct affect CBF - does decrease intrcerbal
decrease volumes
- rapid

IV volume
expanded water ICF - osmotic diruesis - loss fluid & decreae IV fluid

benefical - not direct depend on diuresis

45
Q

Hypertonic urea also dcrease ICP

A

Urea less able cross bbb

hpyeronic urea - cause cerebral dehydr - reduce icp
rapid excrete kidney

46
Q

What inter jug vei n pressure in erect positon

A

RAP low & Vp in vein above RA falls - hdyrostic pressure effect -
pressure drops almost 0 & veins collaprse
jug vein in erect position normally collapse

47
Q

Jug veins collapse in sitting neurosurge

How at risk air ebolsim

A

Pressure grad - favours entry air cerbral dural sinus - despire fact jug vein distended

Dural sinus not collapse rigid walls
-presure can subatmopher - air can sucked in - during caniotomy in sitting

venous air embolism - large & rapid

48
Q

Coronary blood flow - what is normal

How does it relate to Cardiac cycle LV/RB

A

200- 250 mls/min 5% CO

Supply LV - predom diastole - subendo flow to LV cease to LV during systole (commonest site MI)

Lower pressure in RV - differences less

Draw flow curves related to cardiac cycle 69

49
Q

What is CPP

A

Driving pressure for coronoary circulation

Aortic diastolic pressure - larger of LVEDP or RAP (cor sinus pressure)

LV diastolic pressure & rap smaller than aortic - CPP is stating aortic diastolic

Intraop - peripheral arterial disatolic pressur - index co pp
Difficult acurate diastolic pressure peripher - niv & Invasive

50
Q

Why is CPP defined like this

A

Starling resistors

Three pressures i heart

Arterial pressure
IV pressure
Cor sinus / RAP

CPP - perfusion pressure during diastole - highest most flow - lv occurs

Exa,[;s

LVV - systole

Aort - intracetric pressure =120-120= 0

LV duastole Aorti diastolic - RAP 80-5=75

RV during systole = Aortic - intraventricular 120-25=95

RV during systole Aortic - RAp 80-5 =-5

LV larger flow - larger mass - effects improtant

Subendo vsesles - subject ffull impact iv pressure - ceases during systole maj artery epicardial surface

51
Q

How does venous drain heart return circ

What percet of cor flow returns via sinus

Po2 cor sinus blod

A

Cor sinus drain in RA 90%
Thebesian vessels

pO2 cor sinus blood 20mmHg

  • myocardium high extracion ratio 55-65%
52
Q

What is the myocardial extraction ratio

What is the significance

A

55-65

Blood supply low relative to oxygen conumsption

myodacridum extract a lot of oxygen for unit blood flow

Signif - heart requires more oxy

cor blood flow must increase

Extraction high - no reason extraction increase

Increased myocardial consumption must be acomp by increase flow

53
Q

What happens cor blood during exercise

Mechanism

A

Cor artery flow increases to supply oxygen to match demand

Normally high extraction increased - provide more oxygen

High extraction ratio remains high - rest exercise anaemia
Heart cant devleop oxygen debty

cor flow can increase 5 times
1250

Increase
metabolic autreg in arterioles

counteract symp med vasocon
- increase mostly during ddiastole

Hypox hypercarb increase h ion, lactate, k adenosine

54
Q

What is oxygen debt

A

During strenous exercise - energy skeltal muscle exceed supply atp - aerobic metbolism - o2 deilvery insufficient

energy atp anaerobic metab

Lactate prod

After exercise increased - increased o2 ptake
Metabolise excsess lactate & replace atp stoore

Size o2 determ measure excess o2 consumpt end exercise until basal levels

Myocardial cannot accum o2 debt - all aerobic

55
Q

Hepatic blood flow

What is blood supply to the liver
where is it derived

factors control hepatic flow

A

Total hepatic flow 1500mls/min 30%

Hepatic artery 300-500ml min press 90-100
Portal vein 1000-1200mls min - 10mmhg

Some autoreg in artery
portal - not autoreg

Recirpocal relationship -
increased sympathetic active - increase portal flow - decrease heptaic artery

liver reseovr - 500mls - deliver cirulation - vasocon

56
Q

How much oxygen from two liver sources

A

40-50 hep art

50-60 portal vein
Liver - cannot supply artery supply removed

57
Q

What is hepatic oxygen consumption

A

50mls o2 mn 20% o2 cinsumption

well maintained - increased extraction if blood supply changes

58
Q

How is blood flow measured in an adult

A

Fick prince - ICG - co also

Dye removed circ only in liver - total excr bile
doesnt have enterohepatic circulation

level blood spect 805nm

Dye given contatst infusion - steady concnetration - rate infusion = uptake

Hep arter conc - same as peripheral artery

Hep vein - determ sample catheter

59
Q

Why dont amnt oxygenation of hb interfere icg

does icg interfere pulse ox

A

measure 805 - isobest for hb - amount light absorb hb - not vary with oxygen

reduced o2 & oxy absorb same wwavelength

True sat not altered

60
Q

Renal blood flow

What is normal RBF

How is it distributed

How is it measure

A

1200-1300mls - 25% CO

Majority 95% flow - cortex 5% medulla

Measured clearance PAH - para aminohippurate

low plasma conc - renal blood almost completely cleared PAH - PAH equal renal plasma flow

RBF - can be calc if HCT known

61
Q

What are properties indicator measure RBF

A

Freely filtered at glomerulus & secreted - not reabsorbed

Indicator cleared from blood single circulation

Stable easy measure non toxic not cause alteration in flow
PAH has properties

also measure eceltromagnetic othery type flow meter

62
Q

How is this related to fick princeiple

A

Fick principle underly principle - application law conservation matter

Uptake substance tissue - difference amount entering = flow x art conc
amount leave tissue flow x venous

rearrangement

Flow = uptake / a-v conc diff

Kidney

Renal plasma

PAH uptake / renl art pah - ren ven pah

Pah totally cleared - renoul venous pah -
arterial not required - not taken up any tissue
venous pah should be idntical
Renal PAH uptake - urinary pah times volume produced

Effective renal = urinary pah xbol urine / periph venous pah

Insepction eqn reveals - same quation clearance UV/P

Low pAH conc - not all PAH removed

Correction factor convert effective renal plasma flow into renal plsam flow
divide by 0.9
above 90% extraction PAH

63
Q

Why does the euqation calculate renal palsma flow and not rbf

A

sing plasma conc and plasma cleared pah - follows it is plasma not blood filtered glomerulus

volume calculated is clearance volume PAH for PAH removed plasma

64
Q

What is renal oxygen consumption

Significance value

A

18mls/o2 min

Renal blood suppl 25% co
weight 0.5 body weight
Renal o2 consumo 7% total baody consumpiton
dont correalte

kidney very meatbolic active high o2 consump compared weight

RBF higher predicted oxygen consumtion
- o2 extraction ratio low

Tissues receive flow needed to carry out function

most - oxygen metbolite maginatue flow -

excretory & homestoatic functions - determine large blood rather than oxyegen consumption

65
Q

How is it autoregulated

A

MAP autoreg 75-105

Myogenic - glomerular arterioles
tubuloglomeural feedback - involving juxtglom app

Sitatuion

myogenic mech -intrinsic mechansim - primary control rbf

tubuloglomerular feedback - involved primary maintain constant filtration rate - effector vascon / vasodil afferent arteriole - assist maintain constancy of blood flow - indirect consqew

66
Q

What is tubuloglomerular feedback

A

Imporatnt feedback autoreg GFR - too much fluid or electrolyte reaches early distal tubule - sensed macula densa - feedback signal vasocon - glomerual afferent arteriole decrease rbf and gfr = decreased delivery fluid * electrolytes in distal tubule

Two componenets to tubuloglomerular feedback - feeedback signal cause
vasocon / dil

details - not fully elucidated

signal sense macula desna - change na flux accross membrane

change content early distal tubular fluid

macula densa cells - compound acts signal

vasoconstrictor mechanism act efferent arteriole - vasdil afferent - renin angII not fully workled

Mech effect gfr change - few percent between map 80-160

67
Q

Urine flow regulation

A

Pressure dependent

Mechnism

autoreg GFR not perfect
GFFR does increase little increase MAP

Small increase GFT - a/w larger increase urine flow

Estimated GFR - controlled controlle dfew percet maintain normal levels ater & solute reab / excretion

Nt apprecated how tight control GFR - minimise change water & solute excretion

Tight control GFR - water excretion vary w/ autoreg pressure rang

Outside range - extremely large incrase/ decrease urine flow occur

small perfect change is a lrage voulme change

5% increase gfr - 9L day
large volume - too much reabsorb mainta noirmal volume

Pressure diruesis - intrsice system control bp
presure volume control system

Effect change renal water na excrtetion response change art pressure

Most imporatnt mech control blood vol - vital part pressure depend urin e flow

autoreg urine flow - not consistent survival

68
Q

What is typical po2 renal medulla

A

20 mmHg similar coronary sinus

69
Q

Hormonal affects in kidney

Norad

AtII

Pg
ACh

A

Norad - contrict renal vessle - interlobaeral artery & aff aterioles

At II casocon - effect both aff + EFF arterioles

PG = Increase cortex flow decrease medullary flow

Ach - vasodilation

70
Q

Micorcirculation

A

Smallest blood vessels in body
smallest arterioles metaarteroles precap sphincter cap small venules

arterioles - vascular sm major site sttem vasc resist
many tissue remain closed wiout flow

reserve capacity - open quickly local don fall po2 when addit flow reqd

Some tissue - contaains direct av connex shunt
flow under great control nervous system

now partic tfer gas
skin - heat regulation

71
Q

Capilarry flow intermittent or contin

A

sm metart - precapp contract & relax - intermittent flow in capillary - vasomotion

local drop PO2 - impratnt factor rrelax precaiplly sphincter

intermitt cap flow - not cycliac rise bp - flucation smooth out arterioles

72
Q

What is the importance of micorciulation

How do dif substance cross cap wall

A

System cap 5% lbood vol extreme imporatn - exchange water electolyte gas waste nutrient cap membrnn

most drug need cross reach site action

intracsular volume contaact ISF - baths all cells body

transfer substance principl fucntion microcir

Movement water accross cap membrane - 2 proccess diffusion
filtration

water molecuesl smaller size of pores in capilalry -c ross wall easily

cross gap enotheilail cell

electrole small mol - cross membrane thru pores - via intercell gaps

lipidsouilbe sub - o2 co2
cross thin wall endothial cell

protein large do not easily cross
some transfer pinocytsosis

73
Q

What is the magnitude capilary fluid exhcnages

A

Water movement //t tow process

diffsuion
otal daily diffusion water across cap hgh 80000l day
larger total cap blood flow
co 8000l day

Diffusional movement water large both direction not result net movement across cap - no osmotic gradient

FIltration
Accross capillar also occurs - ultrafiltration plasma proteins do not cross
Imbalance hydrostitic & oncotiuc pressure - along capillary memnbrane - starlings hypotehsis

UF 20ml min - body whol
18mls reabs in capillary rest retuend as lymph 2ml min

No net movement water d/t diffsuion accross membrane net diffsuon depnd conc gradient - orinaryl no water cocn differece cap mebrane

Filtration does = net movement water d/t imbalance between force out and inward - different times tissue net move in or out

forces change in value along length capillary - typical sitaution net movement out at arterial end - net movement in at vbenous end

74
Q

Diffsuion

A

Large volume
bidirection whole length
concntration gradtion

hydrostaic oncotic pressure - not involve

reponso net movement gas nutrients waste - move down con grat

75
Q

Filtration

A

Ultrafiltration - protein not cross membrane

volume msaller

inward or outward at position along capillary

net movement gover starling forces

not important gas nutrient waste -
is improitant water

76
Q

Starlings hypothesis fluid exchange

A

Fluid movement d/t filtration accross wal cpaillary depend balance hydrostraic pressure gradient & oncotic pressure grdient across capillary

Pc Pi Tc Ti
hydrstrric capilary
oncotic interstitium

Net driving pressure =
Pc-Pi - Tc - Ti

Net fluid flux - proportional to net driving pressure

Reflection coeff
filtration coeff

Capillary hydrostatic pressure falls along legnth of arterial to venous end
driving pressure - decrease become neg

77
Q

Reflection coefficient

A

Correction factor - apply to measured oncotic pressure ghradient accross capillary wall

Small leak protein accross capillary membrane two improtant effect

Itnstertial fluid oncotic pressure higher than would be

Not all protein effective retain water effective capillary oncotic pressure lower measured oncotic presure

Both effect decrease pressure grad

Instit oncotic pressure - acount included cal grad

Used correct magnitaute of measuredgraident ake account ineffectives some of oncotic pressure grad 0-1

eg
CSF & GF - low protein - reflection coeff close 1

Prtein cross wall hepatic sinusiod - protein cocn lymph high
reflection coeff low - walls do not reflect all protein ack - formula for net driving pressure include reflection coeff

78
Q

Filtration coefficient

A

net flud flux d/t filtration across capillary wall - proportional to net drving pressure

fitlration coefficient k is contstaing of proortioanlity in flux starling equn

net flux = K x (net driving pressure)

K x {(Pc-Pi)-d(Tc-Ti)}
k fitlration coeff d reflection coeff

filtration coeff two compnents net fluid flux depned

area capillary walls where transfer occurs

permeability capilary wall to water -

K = area x hydraulic condcutivty

leaky cpailly - high filtration coeff

glomeuralr capilary all leaky naturally

Filtration coeff - leaky capil membrane h20

reflection coeff - protein

79
Q

Typical values for starlings forces

A

Art end Venous end

Pc 25 10

Pi -6 -6

Tc 25 25

Ti 5 5

Net driving pressure out at art end & ion venous end

Change in net driving pressure d/t decrease capillary hydrostatic pressure - asummes reflection coeff high

80
Q

How are forces diff glomeurulus

A

sitatuion different remarkable

body whole net uf reabso 2-4l day
net excess capil gfr - 180l

Gloemrueres

Filtration coeff hih - high perm water

reflection coeff high - 1
filtrate true ultrafiltre - essent imperprotein - oncotic pressure filtrate 0

hydrostat pressure in capill high - not decerase along legnth

large loss fluid & imperm to protein - onctoic pressure in capillary icnrease along length of capillary -

Net outward filtration along whole legth capilary

hydrostatic pressure gloermural capill affect balance aff & efferetn constriction

81
Q

How diff in pulm capilly

A

Balance twoard reabsoprtion cap hyrstic pressure lower - genreally lower pressure in PA

82
Q

Cerebral

A

Cap membrane in cerebral Relatively impermeable to most low molecular weigh solutes present in blood as well as plasma proteins
Ions N Cl make up most solutes

solutes effective exert osmotic force acrros menbrae

Starling force cerbral cap & hyydrstat pressure and osmotic pressure d/t effective solutes

oncotic pressure small vs high osmotic pressure effectgive samll solutes

small leak solutes - reflection ceoff - plasma & other cap bed

1 milosm increase icrease osmotic gad bl and brain exert 17-20mmhg

small change tonicity marked effect on cerebral vol

83
Q

Pulmonary microcirulation
What is lung main fxn
what is the role of the circulation of this fuxn

A

Gas exchange

Moves pulmonary blood flow close a/w alverolar gas at bl gas barrier - gas exchange facil
large amt of flow pulmonary = co

Membrane thin - Large surface area
1 Pul capil - thin wall

Alv wall - cap dense network - continous film blood - large cap surf area

pressure pulm lower - system -
pvr low - pressure sufficent perfuse apical areas - erect healthy adult

84
Q

Values for starlings in pulmonary

A

Cap hydrostat 13 art 6 venous - vary effects gravity erect lung

instital hydrostatic pressure - vary 0 to negative value

Cap oncotic pressure 25mmh

instital oncotic 17 - est collection lung lymph

Oncotic pressure grad - interstital - oncotic pressure high - signif protein leak - albumin - normal circ - refecltion coeff low - est 0.5

Considering typical value -e st net oncotic snmall - favours reabsorption

Hydrostatic press grad
capil - intra alv vessel [ presure expose close alv pressure - actual measure - slight neg - closer holum more neg - favour flow alverolar intestium into lymphatics

85
Q

Capillary hydrostatic pressure lung

A

Capillary hydrstatic pressure vary - effects gravity

erect lung - suspend gravitato field - pressure veseel high than apex
pressure difference - static water column

Distance 30cm 0 pressur diff 30
typical pa press 25/8
Pressure barely adeq - prefusion apex

low resistiance - half d/t capil - no muslce wall

cap hydrstoatic quicl;y affect change pap & lap without buffer

normal - smell net forward movement fluid
est = pulmonary flow rate
use 10-20mls hr

86
Q

How is it useful to patient care

A

not uself - not possible measure value

estimate - plasma protein as index cap oncotic
and pa cather

87
Q

How is excess fluid removed

A

Large surf area & thin walls - faciliatte filtration cap to interstitum

intertsil moves wtoward hilum along space beside vessel airway

hydrostaitc instet - more neg apporaching hilum - excess filtrate removed lymphatics

flow premoted vetilatiy cycle & 1 way valves

88
Q

What are factor protect lung from Pulmonary oedma

A

For it to occur - excess fluid accumulate in iterstitum - then move into alvoeli

lung resistant - usually absorbed

1 increase lymph flow - increase filt increase flow

2 decrease intertstitial oncotic pressure - oncotic buffering

filtration icnrease - albmuin loss in filtrate decrease -
combined increased flow 0- washses albumin out interstitum & interstitial oncotic pressure decrease

3 High interstitial compliance
Large volume fluid - acumulate gel intestium without much pressure rise
tissue full fluid - pressure rise - alveolar flooding
bathtub effect - analogy tub take lot fill - point full suddnely overlys

safety - effective
capillary hyosratic rise x3 before flooding

surfactant also has a protective role

89
Q

Autoreg
What is it
what are diffrent ways tissue blood supply autoreg

A

Tissue ability regulate own blod suplly - so recieved bloof flow requires for function

intrinsic & local - each tissue
eprate nervus/ humoral factors affect arterioal resistance

Heart brain kidney - low neurogenic control circ 45% co to them

Pressure autoreg
metabolic autoreg

90
Q

Pressure autoreg

What is the mechanism responsible pressure

anywhere it doesnt occur?

A

blodo - tissue cosntant despite change system art pressure

blood flow - most tissue require dont alter w/ rise fall pressure -

tissue arteriolar resitrance change to compenase & hold flow coontsant

  • effective wide range map - many tissues
    cerebral blow flow for 50-150 in carotid

Myogenic mech increase pressure - increased strethc walls - vascular SM - repond contract
increased tone locally l- increase resist -drop blood flow

Uterine cirulatuion during preg
vasc bed preg utereus flully dilate - autoreg not present
uter blood flow late preg pressure depenedent - anaethit implication
decrease half normal before oxygenation affect

Hepatic portal supply venous drain bowle - not autoreg liver- heaptic art supply autoreg

91
Q

Metabolic autoregulation

whats the mech responsible

A

Varies depending on metabolic needs of organ or tissue
active nearly all tissues all times-

vasoidlator mediator considered cause

identiy not est certrainty mos ttissue

possible
adnosie
nitric
h ion

increase demand blood 0- increased metabolic activity - local increase in mediator - causes local arteriolar vasodilation
increase blood flow

Physiology Kerry (17 decks)

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