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1
AcidsandBases
Basics
Compoundsthatdissociateinsolution
Acidscanrelease hydrogenions(H
+
)
e.g.hydrochloricacid(HCl)
HCl H
+
+Cl

Basescanbind hydrogenions(H
+
)
e.g.sodiumhydroxide(NaOH)
NaOH Na
+
+OH

Natureofacids&bases
AcidityoralkalinityisbasedontheconcentrationofH
+
H
+
concentration([H
+
])goesfrom10
0
moles/L(=1mole/L
alotofH
+
)to10
14
moles/L(very,verylittleH
+
)
100,000,000,000,000xdifferencebetweeneachendofthe
scale!
ExpressedmoreeasilyonalogarithmicscaleasapHvalue
pH=log([H
+
])
Howisaciditymeasured?
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2
pHscale
pH=log([H
+
])
HighpH=Low [H
+
]
LowpH=High[H
+
]
Scaleislogarithmic
1pHunit=10xdifferencein[H
+
]
pH5has100xhigher[H
+
]thanpH7
RegulationofpH
ThebodymustmaintainplasmapHwithinan
incrediblynarrowrange(pH7.357.45)
AlteredpH(H
+
)affectshydrogenbonds
Profoundeffectsonahugenumberofbiological
molecules/reactions
AnypHoutsidethatrangedisruptscellular
processes
>pH6.8=coma,death
<pH7.8=convulsions,musclespasms,death
PlasmapH
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3
1.Chemical
buffers
2.Respiratory
Response
3.Renal
Response
H
+
concentration(pH)isregulatedby
Veryrapid
Fairlyrapid
Slow
RememberonlyfreeH
+
haveaneffectonpH
Strong acids/bases(i.e.HCl)dissociatecompletelyin
solution
allH
+
endupfreeinsolution
HaveabigeffectonpH
Weak acids/bases(i.e.H
2
CO
3
)dontcompletelydissociate
OnlysomeH+endsupfreeinsolution
MuchlesseffectonpH
Chemicalbuffersareweakacids/bases
ChemicalBufferSystems
If[H
+
]istoohigh(low pH):
HCO
3

bindstheexcessH
+
Morecarbonicacidformed
[H
+
]decreases(pHincreases)
pHreturnstonormal
If[H
+
]istoolow(high pH):
Carbonicaciddissociatesinto
HCO
3

andH
+
[H
+
]increases(pHdecreases)
pHreturnstonormal
Carbonicacid bicarbonatesystem
H
2
CO
3
HCO
3

+H
+
Carbonicacid
(weakacid)
H
+
donor
Bicarbonateion
(weakbase)
H
+
acceptor
proton
ResponsetoriseinpH
ResponsetodropinpH
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Otherbuffersystems:
Phosphatebuffersystem
NaH
2
PO
4
(weakacid) Na
2
HPO
4
(weakbase)
Notasimportantinblood/ECFasbicarbonatesystem
Moreimportantinurine&ICFduetohigherconcentrationsof
phosphatesinthesefluids
Plasmaproteins
RCOOH H
+
+RCOO

RNH
2
+H
+
RNH
3
+
ParticularlyimportantforcontrollingpHofintracellularcompartment
Otherchemicalbuffersystems
1.Chemical
buffers
2.Respiratory
Response
3.Renal
Response
H
+
concentration(pH)isregulatedby
If[H
+
]istoohigh(low pH):
venlaon=pCO
2
H
+
pH
If[H
+
]istoolow(high pH):
ventilation=pCO
2
H
+
pH
RespiratoryResponse
H
2
CO
3
HCO
3

+H
+
Carbonicacid Bicarbonateion proton
CO
2
+H
2
O
Carbonicanhydrase
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1.Chemical
buffers
2.Respiratory
Response
3.Renal
Response
H
+
concentration(pH)isregulatedby
Onlyway togetridofnonvolatileacidsproducedvia
cellularmetabolismeg.phosphoricacid,lacticacid,uric
acid,ketonebodies
Onlyway toregulatebloodlevelsofalkaline substances
Onlyway torenewchemicalbuffersthatareusedinup
regulatingH
+
levelsintheECF
Respondsslowly(effectively35days)BUTmosteffective
longtermregulatorofpH(byfarthebiggestbuffering
capacity)
RenalResponse
KidneysalterpHbyalteringexcretion&
reabsorptionofH
+
andHCO
3

IfpH([H
+
])inblood alkaline
LessH
+
isexcreted
LessHCO
3

isreabsorbed(moreexcreted)
H
+
+HCO
3

=pH
RenalResponse
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KidneysalterpHbyalteringexcretion&
reabsorptionofH
+
andHCO
3

IfpH([H
+
])inblood acidic
MoreH
+
isexcreted
MoreHCO
3

isreabsorbed(moreretained)
NewHCO
3

iscreated
H
+
+HCO
3

=pH
RenalResponse
RenalResponse
Reabsorption ofHCO
3

Remember:HCO
3

isfilteredbutcant
bereabsorbedfromlumen
1. Carbonicacidsplitsintubule
cell
2. H
+
tolumen(bindstofiltered
HCO
3

thenexcreted)
3. HCO
3

toblood
4. AllHCO
3

filteredarereplaced=
equivalentofbeingreabsorbed
RenalResponse
New HCO
3

formation
method#1
1. Carbonicacidsplitin
tubulecell
2. H
+
tolumen(bindsto
HPO
4
2
)
3. HCO
3

toblood
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RenalResponse
New HCO
3

formation
method#2
1. Glutaminemetabolised
intubulecell
2. NH
4
+
tolumen
3. HCO
3

toblood
Abnormalitiesin
Acid/BaseBalance
pHofarterialblood=7.4
pHabnormalitiesaredescribedasAcidosis (pH<
7.35)orAlkalosis (pH>7.45)
Acidosis/Alkalosiscanbeoftwotypes:
Respiratory
Metabolic
AbnormalitiesinAcidBaseBalance
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RespiratorypHimbalances arearesultofaltered
ventilationcausingchangesinCO
2
MetabolicpHimbalancesincludeallabnormalities
EXCEPT thosecausedbyCO
2
Usuallydirectloss/retentionofeitherH
+
orHCO
3

AbnormalitiesinAcidBaseBalance
Hypoventilation(underbreathing)
ventilation=pCO
2
H
+
formaon(pH)
Causes
impairedlungfunctione.g.CF,emphysema,chronicbronchitis
impairedventilatory movemente.g.chestinjury,dysfunctionofresp.
muscles
drugabuse(overdose)orinjurytobrainstem
RespiratoryAcidosis
H
2
CO
3
HCO
3

+H
+
Carbonicacid Bicarbonateion proton
CO
2
+H
2
O
Carbonicanhydrase
Hyperventilation(overbreathing)
ventilation= pCO
2
H
+
formation(pH)
Causes
strongemotione.g.anxiety,panicattack,fear
hypoxemia e.g.asthma,pneumonia,altitude
braintumourorinjurye.g.regulatorycentres
RespiratoryAlkalosis
H
2
CO
3
HCO
3

+H
+
Carbonicacid Bicarbonateion proton
CO
2
+H
2
O
Carbonicanhydrase
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RespiratoryAcidosis:
renalexcreonofH
+
renalreabsorponofHCO
3

renalcreationofnewHCO
3

RespiratoryAlkalosis:
renalexcreonofH
+
renalreabsorptionofHCO
3

Compensation=Kidney
BuildupofH
+
OR lossofHCO
3

Causes
ingestionoftoomuchalcohol(excessacidinblood)
lacticacidaccumulationinexercise
Starvation/diabetes e.g.keytone bodies
severediarrhoeae.g.lossofHCO
3

renaldysfunction
MetabolicAcidosis
H
2
CO
3
HCO
3

+H
+
Carbonicacid Bicarbonateion proton
CO
2
+H
2
O
Carbonicanhydrase
BuildupofHCO
3

orlossofH
+
muchlesscommonthanacidosis
Causes
vomiting,lossofstomachHCl
intakeofexcessivealkalinedrugse.g.excessantacidingestion
MetabolicAlkalosis
H
2
CO
3
HCO
3

+H
+
Carbonicacid Bicarbonateion proton
CO
2
+H
2
O
Carbonicanhydrase
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Metabolicacidosis
[H
+
]inECFstimulatesrespiratorycentres
respiratoryrateanddepth
blowoffCO
2
[H
+
]
Metabolicalkalosis
respiratoryrateanddepth,shallowbreathing
CO
2
accumulatesintheblood
[H
+
]
Compensation=Respiratory