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Physiology Kerry > 2. Acid-Base Physiology > Flashcards

2. Acid-Base Physiology Flashcards

1
Q

What is a buffer

A

Solution to minimise changes in H+ concentration - when acid or base added

Physicochem process test tube / body

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2
Q

How does a buffer system work

A

Solution contains weak acid - HA mixed w/ salt of acid & strong base NaA

Salt provides a reservoir - A to replenish A- when removed by reaction with H+

Majority - capacity is maximal at pKa of weak acid

Majority buffering range pKa +-1

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3
Q

What is buffer power

A

effectiveness of diff buffer compared how much acid or base needs to be added to cause unit change in pH

Buffer power D[B+] / dpH

d{B+] - change conc base
dpH -refers to change pH

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4
Q

Major buffer systems

Extracellular

x 7

A

Extracellular -

  1. bicarbonate - highest conc
    major ECF buffer
  2. Hb - major buffer H= - prod red cell when HCO3 formed from Co2 & H20
  3. Deoxy hb >powerful buffer
    o2 unloading assist increasing carriage of Co2 - Haldane effect
  4. Plasma proteins - excell buffer - phosphate not important - low conc plasma
  5. ISF & CSF - low conc buffer
  6. Calcium bic in bone - signif excell buffer - prolonged disorder
  7. Urine - Phosphate concentrations are much high
    Phos buffer - major titratable acidity urine - protein conc urine low &; protein non important
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5
Q

Intracellular

A

Proteins & phospates - signif conc & important

hb - intracelll

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6
Q

pKa of phosphate buffer

A

~~6.8 - very effective buffers - because
total con phos is significant
intracell ph is lower 6.8-7.1 - than excell pH - closer to pka

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7
Q

Why is bic effective buffer in plsam despite pKa far from physiological pH

A

pKa - bic 6.1 excell ph 7.4 - >1 pH away

‘Open at both ends

Both pCo2 & HCO3 - can be altered - minimising change HCO3/PCO2- henderson hasselbach

excretion Co2 - lungs mainta constant Paco2 - increases effective as a buffer -change co2 can occur rapidly

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8
Q

Why is Hb a more imporant

A

Hb 6x more important quantitatively
1. Conc x2 - proteins 150g v 70

  1. Each hb contains x3 histidine residues than acg plasma
    imidazole group is the only AA provides buffering at phys Ph - average pKa 6.8 present proteins

Note bic cant act effective buffer H ion formed during formation of bic - hb predom buffer H= from source
Hb& bic can occur red cell

Bic aids vuffer metabolic acid ecf - transfer of bic out necessary Rc

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9
Q

Affects buffering capactiy hb

A
  1. pH solution
  2. state oxygenation - haldane
  3. Hb concentration higher Hb - more buffering capactiy per unit volume

More reduced Hb on venous circ - more buffering capacity - required increased H formed Co2 - bic carbino

Reduced hb is weaker acid

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10
Q

Deoxy hb 3.5 times more effective than oxyhb - formation carbamino compounds - increased formation of carbamino comp increased capacity buffer

A

No - carbamino compounds produced reaction Co2 - terminal amine groups each hb chanin
result production carbamic acid ;pw pka - plsam ph intracell ph - acid almost complete dissoc

form carb - small net increase H= - H= require buffering
Formation carbamino not affect buffering capacity Hb - a/w increase H+ conc

Carriage Co2 - bic & carbamino increase H+ - buffered histidine

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11
Q

Define pH

A

Negative log H+ conc

effective concentration or activity -

pH glass electrode - respond activity rather than concentrations

pH -Log 10 aH+
AH+ activity hydrogen ion

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12
Q

pKa

A

Ka - equil dissoc conc for dissoc acid Ha prod H= & acid anion A- {HA<=> H+A-]

pKa neg log to base 1- of dissoc constant
ph equal to pKa - acid is 5-% dissoc
ie equal amount Ha & A

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13
Q

Why is Hb > important carry co2 than plasma protein

A
  1. Concentration 150 v 70
  2. Mol wt alb & hb close - hb treramer each mol con 4N term groups - compare 1 alb
    carbamino compound form w/ N terminal
  3. Abil Hb form carbamino compound increased 3.5 times becomes deoxygenated - situation peripheral capillary
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14
Q

Volatile acid

A

carbon dioxide which can be excreted by the lungs - ketones -> excreted partly lungs - volatiles amount small

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15
Q

Fixed acids

A

Fixed or metabolic acids - excreted kidneys phosp/sulphuric or metab body - lactic

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16
Q

Carbon dioxide an acid

A

Not -bronsted lowry a/b system

Molecule Co2 can be converetred to carbonic - co2 repesenting portenial produce equal amount acid

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17
Q

what is a bronsted lowry acid

A

acid donate hydrogen ion to another sub

donor - conjugate acid - acceptor conjugate base

more comple than arrhenius sytem - acid defined capable H ion aqeuous soltuin
CO2 not acid - doesnt cotain H

Co2 - acidic propertys not H
Lewis - anycompund that was a potential elctor pair acceptor

Bronsted lowry - carbonic acid is the acid & not CO2
a-b discussions co2 - acid when dissolced exhibt acidic proerty

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18
Q

Resp excretion dffierent to renal excertion

A

Excretion via lung more rapid - amount acid deal lung 20000mmol day large v fix acid load kidney 70mmpol day

Co2 only acid excrete lung
excretion co2 rapid
system high capicty

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19
Q

Respiratory regulation of AB balance

A

Ventilation - rapidly - cause pH change all compartment co2 cross membranes easily

change ventilation alters paCo2
Change Paco2 alter pH

Change alveolar ventilation inversely related to change in art PCO2:

PaCO2 = K x Co2/Ca

Art partial pressure co2 paco2, vco2 - co2 production, va - alveolar vent k - propor constan

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20
Q

Change alveolar ventilation inversely related to change in art PCO2:

equation

A

PaCO2 = K x Co2/Ca

Art partial pressure co2 paco2, vco2 - co2 production, va - alveolar vent k - propor constant

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21
Q

Change in arterial pco2 cause change in pH

A

pH = pKa + log [HCO3] . .03 x pco2

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22
Q

How does the body sense & respond to change in arterial pco2

A

Central chemo rec
Medulla - sep resp centre
change H+ conc - adjacent brain ecf
Co2 - x bbb - immed change in brain [H+]
Stim resp centre increase ventilation - H+ rises

Systemic metabolic acidosis - not cause immed stim of central chemo - neither H+ nor acid anion can x bbb
equilib of hc03 - slowly - metabolic will eventually csf h change - central stim

Peripheral chemo
aortic carotid body - respond change art po2 pco2 ph

Ventilatory response to increase in art pco2 - 80% central 20% periph

Periph more important - may respond more rapidly to acute changes

Overall ventilatory respond to change in arterial pco2 - rapid & effective under normal circumstances
Ventilation increase - 2l/,in for mmHg rise art pco2
size increase - vary

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23
Q

cartoid sinus is a

carotid body is a

A

sinus = baroreceptor

Body = chemoreceptor

Carotid body IX - sensitive O2 Co2 & pH

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24
Q

What are the major routes excretion for acid from body

A

lungs gas

kidney urine

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25
Q

Term used to describe acid exreted in urine

A

Fixed acid / metabolic

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26
Q

Major processes involved in renal a-b excretion

A

Reabsorption of bic

Net excretion H and acid anion body

Processes
Secretion of H+ in prox tubule - respons reab 90% filtered bic

Secretion of H+ into distal tubule - H+ mostly buffered by phospahte buffer =- responisble for some bic reabs

Secretion of NH4 into prox & dist

27
Q

What is the source of H ion secreted into proximal tubule

A

H+ is produced from hydration of Co2 in reaction catalysed by carbonic anhydrase
present in cytoplasm of prox tub cell & brush boreder of mminal membrane
H+ actively transpiorted into prox tubular lumen

28
Q

Main function of secretion of H+ into prox tube

A

Reabs filtered bic - filter bic 4-5000 mmol/day

Calc as product of GFR & plsam HCo3 conc - 180l day x 24mmols

Filtered bic - reacts w/ secreted H+ in presence brush border carbonic anyhdratse - co2 & water co2 lipid solbue - diffuse into prox tubular cell

Filtered bic - elim & replaced by bic produced in cell in reaction which genereation H- secreted into lumen

bic aenter blood stream across BLmembrane
large secretion Hion not lead net exretion H body - net effect prevent acidfiyin effect loss of bic

29
Q

What is the effect of H ion secretion On Na reabs in prox tubule

A

Na cross luminal membrane into prox tubule - x2 ways

  1. Diffusion thru Na channel
  2. Carried mediated facilitated diffusion thru luminal membrane
    cotransport - glucose & AA
    countertport against H secretion

Na moves down electrical & concentration gradient to enter cell

Active tport Na out - BL membrane - energy drives reabsorptionNa @ luminal membrane - secondary active transport - water reabsorption here & thru kidney passive in response to osmotic gradient

65% filtered Na load reabs in prox tubule

90% hco3 reab prox tubule

Prox tub tport H a/w 1/4 Na reabs
Exchange H & Na - electoneutrality - net effect section 1 mol H tfre 1 mol Na & 1 mol Hco3 peritubular

30
Q

Why is proxtimal tubular system for H - ‘High capacity / low gradient sytem’

A

High capactiy - total daily secretion of H+ 5000 large

low gradient - limitng pH prox tubule 7.0 so max gradient only 60nmole

31
Q

What is source H ions ecretd into distal

A

Reaction CO2 & H20 - carbonic anhydrase

Prod H & HCo3

H secreted tubule intercalated cell

32
Q

Main function of the secretion of H ion into distal

A

Net acid excretion

High rate secretion H - nearly all converted water - no net excrretion urine from site

Distal tubule - lower rate secretion ~70 - this account nearly all H excreted

33
Q

Why is distal tubular low capacity high gradient

A

low gradient cause 70-100 mmmoles day

High grad max h gradient about 3 pH units - high than prox tubuule

34
Q

What is lowest urinary pH achievable

A

4.4

35
Q

What is the gradient hion across the distal tubular cell

A

pH diff 3 - means max H gradient accross teh tidtal tubule cell

36
Q

what are the buffers in the distal tubular fluid

A

Phosphate & ammonium

37
Q

Where does the ammonia come from

A

Glutamine & gultamate

Ammonia split from gulatmine - rxn catlyse gyltaminse
Mostly proximal tubule

Ammonia total present as ion Nh4 as pKa very high

Mostl removed LO
if pH low in ditsal tubule - augment trasnfer meddulary interstitum into dital tubular fluid

Mostly produced prox tubule cell

Medullary cycling proccess - removed LOH enter medulla - some renter late prox tubule - some enter medullary collecting duct

38
Q

Why doesnt ammonium ion contribute to titratable acidity

A

Ammonium ion charged Nh4 - water soulbe
not lip solube

trapped in tubule lumen

pKa - high - enterile ionised almost

titrating urine pH 7.4 - not release any H from NH4

Contribution - determined only measuring amount ammonium present

39
Q

Creatine important urine buffer?

A

Normally no
pK 4.97 - so low urinary pH higher

Diff if pH low - max acidity 4.4 - can 1/4 titratable acidity

dKa beta hydorxybutyrate 0 excreted large amount in acid urine - large part titratable

40
Q

Total amount fixed acids per day = renal excretion

A

Body produce 1-1.5 `mosm / kg/ day 70-100 of fixxed acids require renal excretion

normal circmstances - acid involed mostly phos & suplhate

Lactate is higher 1500 metabolised or converted back to gluc and not excreted

41
Q

What is hyperncapnia

A

arterial pCo2 >44mhg =5.8kPa

42
Q

Why does it cause physiological effects

A
  1. Co2 crosses lipid barriers - ease obtains rapid entry all cell
  2. Rapidly reacts with water - intracellular acidosis
  3. Intracellular acidosis - adverse effects on enz/metab
    - buffering minimise change pH

Due to hypoventilation normally - typically a/w hypoxia - exerts effects

43
Q

cns effects of Hypercapnia

A

Co2 cross membrane - intracellular acidosis

Affects all cell - nervous cvs 8 resp predom clinically

Cerebra;

  1. Increased CBF
  2. Increased ICP
  3. Potent stimulation of ventilation
  4. . Sympathetic stim
  5. central depress very high >100mmHg
  6. A/w hypoxia - also effects

for ever 1 rise in mmHg - CBF increase 4% -
MV increase 1-3l.min

Stim - correction
if its a compensatory to met alk - cent depressed
inadeq alveolar vent - most causes

44
Q

CVs hyperncapnia

A

Indirect effets

  1. Sympathetic stimulation]
  2. Coexistent hypoxia
  3. Underlying illness medication
Direct 1. 
Increased BF
2.general peripheral vdiln
3. depression myocardium
4. Increased arrytyhmia

CVs effects - balance by direct and inderect

warm flushedsweaty tachy w/ boundy pulse

45
Q

Adverse effects of hyponcapnia

A

Ref range art pco236-44

pH 7.36-7.44 = [H+] - 44-36

46
Q

Adverse effects of hypocapnia

A
  1. Shift oxyhb dissoc curve left
    - increase iaffinity - impair delivery
  2. Decrease Serum - acute alk - small decrease
  3. Decrease CO -
    myo contract decrease slightly w/ acute alk
  4. Decr CBF (desired neuro_
    Decrease 4% mmHg - decrease art pCo2 - down to 15
  5. Resp depression
    Intraop hypocapnia - obligatory hypoventilatiion @ end-
47
Q

Implication for CBF end of procedure

A

Hypoventilation - allow pco2 - rise - increase cbf - exceed preop

Continued hypocania - decrease cbf dimin time

Circ d/t ISF pH rather than Pco2 - 6-8h hypocap - bic almost requil bbb increase brain ISF conc -
restore isf pH normal - cbf normal

Rise art Pco2 - increase CBF hgiher than normal

ICP increase - exacreb depression of ventiolaion - opoiod

48
Q

Main causes of hypoxaemia end of anaesthetic

A
  1. Hypocapnia - resp depression

central depressin agents

resp centre depress - narctic

diffusion hypoxia

Redduced FRC d/t aneaes

upper airway obstruction

resp musle weak - inadeq reversal

bronchospasm - aspiration

  1. lung collapse

Low inspired pO2 hypovent shunt v/q diffusion

Diffsuion hypoxia - outpouring insol NO into at end reduced alvoelar po2

49
Q

interpreation of abg

A

Full interp - patient history

speculation

Acidosis - w/ acidaemia - low bic low

50
Q

Alveolar gas equation

A

PaO2 = PiO2 - PaCo2/R

51
Q

How could metabolic disorder quatnified

A

Use of base excess

comparing actual & expected PCo2

How much vic decrease normal - most excell buffer bic - fall hco3 = equivalent amount acid hidden

Altered bic
1 compensatory change pco2 - cause change measure bic
2 if pre exist met acidosis - measured bic metraolic acidosis can be higher than 24

uncomplicated metabolic acidosis - measure value plasma bic - simple approach

52
Q

Is it a simple / mixed acid base disorder

expected PCO2 formula

A

Mixed - 2/+ disorders

Resp disorder on top?
Determ ventilatory compensation appropriate
- if compensation maximal - expected pco2

exp pco2 = 1.5 x bic + 8
mmHg

actual pco2 - same - suggest max compenation no respiratory compenent

Resp compensation can take 12h

Combo met acidosis - dka+lactic

53
Q

Further Invx metabolic acidosis

A

Urine test - glucose / ketons

blood gucose

Urea & creat

Na * Cl - anion gap

lactate

54
Q

Common causes of HAGMA

A

Lactic acidosis
ketoacidosis
Renal failure
Toxins

55
Q

Normal anion gap acidosis

A 
Loss of HCo3 from ec
Chlroide excess
addisons/acetozolamide
Gi
Extra
56
Q

Infusion 1N HCL

A

1n HCL central line - load 100mmols of H+

Sufficent met acidosis

Defence against change
buffering
compensation
correction

57
Q

Buffering

A

Rapid process - titration body acid ecf buffer - bic

biv 24 ecf vol 19 - pool 450
acid load 100 titral bic buffer to 18.7
assume all vuffer aecf - by bic

58
Q

Compensation

A

met acidos - periperhal chemo = Inc ventilation
hypocapnia - phys compesn response - cant take 24h reach max

Comepnsation not return ph complete normal

Expected pco2 = 1.5 X[HCO3] + 8

Pco2 is arterial pco2 and bic mmol abg

59
Q

Correction

A

Kidney excrete excess Acid anion Cl- equilvaent reabosprtion of bic & excretion acid - normal AB status restored - slower

60
Q

Other physiological effects acid infusion

A

right shift o2 dissoc - o2 unload

aAG - unchgen acidos hypercholaemic

Met acids - not x bbb - brain non signaif - perph chemo for resp

Hyper H -K exhchange across membrane - urine K loss increased

Hypcapn - intracell alkaosis - depress cell activityy

61
Q

why is rep compesation 12h

A

Perpheral chemo - hypercent

Result decrease H around central chemo as Co2 can diffsue

Central - medaited injuib limit rise vent

bic equilivrates slowly across bbb & H increase & removed central inhibition

62
Q

Causes of normal anion gap acidosis

A

Hyperchloraemic

GIT
acute severe diarrhyo
admin acid salt
obstruct ileal conduit
ureteroenterostomy
drain panc / biliary secretion

RTA
carbonic anhyudrase inhib
isterstil renal
recov DKA

63
Q

Infusion of 8.4% sodium bic

what is its osmoliaty

A

2 osm/kg 2000 mOsm kg
7x plsama osmalilty

8.4NaHCO3 - one molar solution
each molecule dissoc into two particles - in soltuion so osmolality is double the molality

64
Q

Effects infusing 8.4% sodium bic

A

Hypertonic
alkanising

Na restrict distrib of admin solution

hypertonic nautre - draw water out cells until ecf icf equal- increase ecf volume greater than vol admin

ECF Na conc - increase dep amount of solution admin
water drawn will minimise increase

Na bic - occasionaly recommend actue hypo

ECF [HCo3] incrase - exog admin base 0 met alk
K move intracell ecf K decrease
Basis rx hyperkalameia

Normally - plasma bic>27 - hco3 rapdiyl exccrete urine - actue met alkalosis - rapidly correct unless additioanl factor maintais

ADH levels increase 0if tonicty 1-2 rise
sense hypotahlamic osmorectpor

incrase blood bol - 10
5 - low pressure barorcep inhib adh rel - net result balance on effects

Increase blood vol d/t infusion fall in pslam oncotic pressure & h2o reabs in prox tubule decrease slihgly d/t glom tub imbal - small percent decrease in proc tubule - large increase urine flow

Physiology Kerry (17 decks)

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