ch.10.6buffers in blood

7/25/2019 Ch.10.6buffers in Blood

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Buffers in Blood.

Acidosis and Alkalosis.

Chapter 10.



2

Buffers in the Blood The pH of blood is 7.35 – 7.45 Chanes in pH belo! ".# and abo$e #.0 %a& result in

death The %a'or buffer s&ste% in the bod& fluid is H(C)3*HC)3

+ ,o%e C)(- the end product of cellular %etabolis%- is

carried to the luns for eli%ination- and the rest dissol$esin bod& fluids- for%in carbonic acid that dissociates to

produce bicarbonate HC)3+/ and h&droniu% H3)0/ ions.

ore of the HC)3+ is supplied b& the kidne&s.

C)( H() ↔ H2CO3

H2CO3 + H() ↔ H3O+ + HCO3-



3

Carbonate buffer

H2CO3 + H() ↔ H3O+ + HCO3-

2cess acid H3)/ in the bod& is neutralied b& HC)3

+

H2CO3 + H() ← H3O+ + HCO3-

Equilibrium shifts left 2cess base )H+/ reacts !ith the carbonic

acid H(C)3/ H2CO3 + )H+ → H2O + HCO3

-

Equilibrium shifts right



4

pH of the blood buffer The concentrations in the blood of H(C)3 and

HC)3+ are 0.00(4 and 0.0(4 respecti$el&

H(C)3* HC)3+ 1*10 is needed to %aintain the

nor%al blood pH 7.35 – 7.45/

37.7/103.4lo

103.410.0103.40(4.0

00(4.0103.4

6

6

6

6

66

#

#77

3

3(

3

3(

33

=−=

===

==

=

−

−−−

−

+

−+

x pH

x x x x x

HCO

CO H

K O H

CO H

HCOO H K

a

a



6

>eulation of blood pH The luns and kidne&s pla& i%portant role in

reulatin blood pH.

The luns reulate pH throuh retention oreli%ination of C)( b& chanin the rate and

$olu%e of $entilation.

The kidne&s reulate pH b& ecretin acid-

pri%aril& in the a%%oniu% ion ?H4/- and b&

reclai%in HC)3+ fro% the lo%erular filtrate and

addin it back to the blood/.



8%portance of the bicarbonate+

carbonic acid bufferin s&ste%1. H(C)3 dissociates into C)( and H()-

allo!in H3)0 to be eli%inated as C)( b&

the luns

(. Chanes in @C)( %odif& the $entilation

rate

3. HC)3+ concentration can be altered b&

kidne&s



)ther i%portant buffers The phosphate buffer s&ste% H@)4

(+*H(@)4+/ pla&s

a role in plas%a and er&throc&tes.

H(@)4+ H() ↔ H3O+ + HPO42-

An& acid reacts !ith %onoh&droen phosphate tofor% dih&droen phosphate

dih&droen phosphate%onoh&droen phosphate

H2PO4-

+ H2O ← H@)4(+

H3)

he b!se is "eutr!li#e$ b% $ih%$r&ge" 'h&s'h!tedih&droen phosphate %onoh&droen phosphate

H2PO4- + OH- → H@)4

(+ H3)


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@roteins act as a third t&pe of blood

buffer @roteins contain – C))+ roups- !hich- like acetate ions

CH3C))+/- can act as proton acceptors.

@roteins also contain – ?H30 roups- !hich- like

a%%oniu% ions ?H40/- can donate protons.

8f acid co%es into blood- h&droniu% ions can beneutralied b& the – C))+ roups

+ C))+ H3)0 → - COOH + H2O

)f b!se is !$$e$* it !" be "eutr!li#e$ b% the , H3+

gr&u's - H3

+ + OH- → - H2 + H2O


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?or%al alues for Blood Buffer in

Arterial Blood. The follo!in $alues are deter%ined b&

blood as anal&er

pH 7.35 – 7.45

@C)( 35 – 45 %% H

H(C)3 (.4 %%oles*9 of plas%a

HC)3+ (4 %%oles*9 of plas%a

@)( #0 – 110 %% H



..

Blood Gases In the body, cells use up O2 and give o !O2"

O2 lo#s into the tissues because the partial

pressure o O2 is higher $100 mm %g& ino'ygenated blood, and lo#er $(30 mm %g& in

the tissues"

!O2

lo#s out o the tissues because thepartial pressure o !O2 is higher $)50 mm

%g& in the tissues and lo#er $*0 mm %g& in

the blood"



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Blood Gases In the lungs, O2

enters the blood,

#hile !O2 romthe blood is

released"

In the tissues, O2

enters the cells,

#hich release

!O2 into the

blood"



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8nterpretation of Clinical Blood as Data

H()

C)(

H(

) ↔ H2

CO3

↔ H3

O+ + HCO3

-

The concentration of carbonic acid in the bod& isassociated !ith the partial pressure of C)(.

<hen C)( le$el rises- producin %ore H(C)3- thee=uilibriu% produces %ore H3)- !hich lo!ers the pH – acidosis.

Decreasin of C)( le$el due to a h&per$entilation-!hich epels lare a%ounts of C)(- leads to a

lo!erin in the partial pressure of C)( belo!nor%al and the shift of the e=uilibriu% fro% H(C)3 to C)( and H(). This shift decreases H3) andraises blood pH – alkalosis.



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>espirator& Acidosis C)(E pH 0

,&%pto%s Failue to $entilate- suppression of

breathin- disorientation- !eakness- co%a

Causes 9un disease blockin as diffusion e..-e%ph&se%a- pneu%onia- bronchitis- and asth%a/G

depression of respirator& center b& drus-

cardiopul%onar& arrest- stroke- polio%&elitis- or

ner$ous s&ste% disorders Treat%ent Correction of disorder- infusion of

bicarbonate



.5

>espirator& Alkalosis C)( 0 'H 1 ,&%pto%s 8ncreased rate and depth of breathin-

nu%bness- liht+headedness- tetan&

Causes h&per$entilation due to aniet&- h&steria-fe$er- eerciseG reaction to drus such as salic&late-

=uinine- and antihista%inesG conditions causin

h&poia e..- pneu%onia- pul%onar& ede%a- and

heart disease/ Treat%ent 2li%ination of aniet& producin state-

rebreathin into a paper ba



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etabolic ?onrespirator&/

Acidosis H E pH 0 ,&%pto%s 8ncreased $entilation- fatiue-

confusion

Causes >enal disease- includin hepatitis andcirrhosisG increased acid production in diabetes%ellitus- h&perth&roidis%- alcoholis%- andstar$ationG loss of alkali in diarrheaG acid retentionin renal failure

Treat%ent ,odiu% bicarbonate i$en orall&-dial&sis for renal failure- insulin treat%ent fordiabetic ketosis



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etabolic ?onrespirator&/

Alkalosis H 0 'H E ,&%pto%s Depressed breathin- apath&-

confusion

Causes o%itin- diseases of the adrenal

lands- inestions of access alkali

Treat%ent 8nfusion of saline solution-

treat%ent of underl&in diseases

ch.10.6buffers in blood

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