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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
Term used to describe acid exreted in urine
Fixed acid / metabolic
26
Major processes involved in renal a-b excretion
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
What is the source of H ion secreted into proximal tubule
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
Main function of secretion of H+ into prox tube
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
What is the effect of H ion secretion On Na reabs in prox tubule
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
Why is proxtimal tubular system for H - 'High capacity / low gradient sytem'
High capactiy - total daily secretion of H+ 5000 large low gradient - limitng pH prox tubule 7.0 so max gradient only 60nmole
31
What is source H ions ecretd into distal
Reaction CO2 & H20 - carbonic anhydrase Prod H & HCo3 H secreted tubule intercalated cell
32
Main function of the secretion of H ion into distal
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
Why is distal tubular low capacity high gradient
low gradient cause 70-100 mmmoles day High grad max h gradient about 3 pH units - high than prox tubuule
34
What is lowest urinary pH achievable
4.4
35
What is the gradient hion across the distal tubular cell
pH diff 3 - means max H gradient accross teh tidtal tubule cell
36
what are the buffers in the distal tubular fluid
Phosphate & ammonium
37
Where does the ammonia come from
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
Why doesnt ammonium ion contribute to titratable acidity
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
Creatine important urine buffer?
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
Total amount fixed acids per day = renal excretion
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
What is hyperncapnia
arterial pCo2 >44mhg =5.8kPa
42
Why does it cause physiological effects
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
cns effects of Hypercapnia
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
CVs hyperncapnia
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
Adverse effects of hyponcapnia
Ref range art pco236-44 pH 7.36-7.44 = [H+] - 44-36
46
Adverse effects of hypocapnia
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
Implication for CBF end of procedure
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
Main causes of hypoxaemia end of anaesthetic
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 9. lung collapse Low inspired pO2 hypovent shunt v/q diffusion Diffsuion hypoxia - outpouring insol NO into at end reduced alvoelar po2
49
interpreation of abg
Full interp - patient history speculation Acidosis - w/ acidaemia - low bic low
50
Alveolar gas equation
PaO2 = PiO2 - PaCo2/R
51
How could metabolic disorder quatnified
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
Is it a simple / mixed acid base disorder expected PCO2 formula
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
Further Invx metabolic acidosis
Urine test - glucose / ketons blood gucose Urea & creat Na * Cl - anion gap lactate
54
Common causes of HAGMA
Lactic acidosis ketoacidosis Renal failure Toxins
55
Normal anion gap acidosis
``` Loss of HCo3 from ec Chlroide excess addisons/acetozolamide Gi Extra ```
56
Infusion 1N HCL
1n HCL central line - load 100mmols of H+ Sufficent met acidosis Defence against change buffering compensation correction
57
Buffering
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
Compensation
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
Correction
Kidney excrete excess Acid anion Cl- equilvaent reabosprtion of bic & excretion acid - normal AB status restored - slower
60
Other physiological effects acid infusion
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
why is rep compesation 12h
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
Causes of normal anion gap acidosis
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
Infusion of 8.4% sodium bic what is its osmoliaty
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
Effects infusing 8.4% sodium bic
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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