Acidosis Alkalosis Biochemistry

8/9/2019 Acidosis Alkalosis Biochemistry

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Eric Niederhoffer, Ph.D.

SIU-SOM

Biochemical basis of acidosis and alkalosis:

evaluating acid base disorders


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Outline

• Approachhistory

physical examination

differentials

clinical and laboratory studies

compensation

• Respiratoryacidosis

alkalosis

•Metabolicacidosisalkalosis


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Approach

• History - subjective information concerning events,

environment, trauma, medications, poisons, toxins

• Physical examination - objective information

assessing organ system status and function• Differentials - potential reasons for presentation

• linical and laboratory studies - degree of changes

from normal

• ompensation - assessment of response to initial

problem


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1elta ratio

Delta ratio Assessment

0%!$ Hyperchloraemic normal anion gap acidosis

%!$ 2 %!*'ombined high A3 and normal A3 acidosis4ote that the ratio is often 0) in acidosis associated5ith renal failure

) - (

6ncomplicated high-A3 acidosis

.actic acidosis7 average value )!/

18A more likely to have a ratio closer to ) due to urine

ketone loss 9if patient not dehydrated:

;(

&re-existing increased


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'ompensationPrimaryDisturbance pH H!

"

#

P!$ ompensation

Respiratory acidosis 0!"# 'ompensatoryincrease

&rimaryincrease

Acute7 )-( m+. increase inH'O"

- for every )% mm Hg increase

in &'O('hronic7 "-$ m+. increase inH'O"

- for every )% mm Hg increase

in &'O(

Respiratory alkalosis ;!$# 'ompensatorydecrease

&rimarydecrease

Acute7 )-( m+. decrease inH'O"

- for every )% mm Hg

decrease in &'O('hronic7 $-# m+. decrease inH'O"

- for every )% mm Hg

decrease in &'O(

?etabolic acidosis 0!"# &rimarydecrease

'ompensatorydecrease

)!( mm Hg decrease in &'O( for

every ) m+. decrease in H'O"-

?etabolic alkalosis ;!$# &rimaryincrease

'ompensatoryincrease

%!/-%!# mm Hg increase in &'O(

for every ) m+. increase in H'O"-

, &'O( should not rise above ## mm

Hg in compensation


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Respiratory acidosis

&'O( greater than expected

Acute or chronic

'auses

excess 'O( in inspired air

9rebreathing of 'O(-containing expired air, addition of'O( to inspired air, insufflation of 'O( into body

cavity: decreased alveolar ventilation

9central respiratory depression @ other '4

problems, nerve or muscle disorders, lung or chest5all defects, air5ay disorders, external factors:

increased production of 'O(9hypercatabolic disorders:


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Racid acute

A /#-year-old man 5ith a history of emphysema comes to

the physician 5ith a "-hour history of shortness of breath!

pH !)*

&O( /) mm Hg

&'O( #* mm Hg

H'O"- (/ m+.

History suggests hypoventilation, supported by increased&'O( and lo5er than anticipated &O(!

Respiratory acidosis 9acute: due to no renal compensation!


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1escription

pH !)*

&O( /) mm Hg

&'O( #* mm Hg

H'O"- $% m+.

)-( m+. increase in H'O"- for every )% mm Hg increase

in &'O(!

&'O( increase > #*-$% > )* mm Hg!

H'O"- increase predicted > 9)-(: x 9)*)%: > (-$ m+.

add to ($ m+. 9reference point: > $%#$& m+.


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Racid chronic

A #/-year-old 5oman 5ith 'O&1 is brought to the physician

5ith a "-hour history of severe epigastric pain!

pH !"B

&O( /( mm Hg

&'O( #( mm Hg

H'O"- (B m+.

History suggests hypoventilation, supported by increased&'O(!

Respiratory acidosis 9chronic: 5ith renal compensation!


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1escription

pH !"B

&O( /( mm Hg

&'O( #( mm Hg

H'O"- $' m+.

"-$ m+. increase in H'O"- for every )% mm Hg increase

in &'O(!

&'O( increase > #(-$% > )( mm Hg!

H'O"- increase predicted > 9"-$: x 9)()%: > $-# m+.

add to ($ m+. 9reference point: > $$' m+.


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Respiratory alkalosis

&'O( less than expected

Acute or chronic

'auses

increased alveolar ventilation9central causes, direct action via respiratory centerC

hypoxaemia, act via peripheral chemoreceptorsC

pulmonary causes, act via intrapulmonary receptorsC

iatrogenic, act directly on ventilation:


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Ralk acute

A )-year-old 5oman is brought to the physician 5ith a "-hour history of epigastric pain and nausea! he admitstaking a large dose of aspirin! Her respirations are full andrapid!

pH !#&O( )%$ mm Hg

&'O( (# mm Hg

H'O"- (" m+.

History suggests hyperventilation, supported by decreased&'O(!

Respiratory alkalosis 9acute: due to no renal compensation!


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1escription

pH !#

&O( )%$ mm Hg

&'O( (# mm Hg

H'O"-

$" m+.)-( m+. decrease in H'O"

- for every )% mm Hg decrease

in &'O(!

&'O(

decrease > $%-(# > )# mm Hg!

H'O"- decrease predicted > 9)-(: x 9)#)%: > (-" m+.

subtract from ($ m+. 9reference point: > $(#$$ m+.


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Ralk chronic

A *)-year-old 5oman 5ith a history of anxiety is brought tothe physician 5ith a (-hour history of shortness of breath!he has been living at B,%%% ft elevation for the past )month! Her respirations are full at (%min!

pH !$$&O( /B mm Hg

&'O( ($ mm Hg

H'O"- )/ m+.

History suggests hyperventilation, supported by decreased&'O(!

Respiratory alkalosis 9chronic: 5ith renal compensation!


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1escription

pH !$$

&O( /B mm Hg

&'O( ($ mm Hg

H'O"-

(% m+.$-# m+. decrease in H'O"

- for every )% mm Hg decrease

in &'O(!

&'O(

decrease > $%-($ > )/ mm Hg!

H'O"- decrease predicted > 9$-#: x 9)/)%: > /-* m+.

subtract from ($ m+. 9reference point: > (%#(& m+.


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?etabolic acidosis

&lasma H'O"- less than expected

3ain of strong acid or loss of base

Alternatively, high anion gap or normal anion gap metabolic acidosis

'auses high anion-gap acidosis 9normochloremic:

9ketoacidosis, lactic acidosis, renal failure, toxins: normal anion-gap acidosis 9hyperchloremic:

9renal, gastrointestinal tract, other:


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?acid high A3

A #-year-old man 5ith severe congestive heart failure isbrought to the emergency department! He is on nomedication! His respirations are ($min and blood pressureis *%#% mm Hg! He has decreased urine outputC hisbaseline creatinine concentration has been )!/ mgd.!

pH !)B 4aD

)"# m+.&O( *% mm Hg 8

D $!% m+.

&'O( (% mm Hg 'l- B m+.

H'O"- * m+. 'O(, total * m+.

.actate (% m+. 6rea #$mgd.'reatinine (!# mgd.

History suggests congestive heart failure 9poor perfusion:!

?etabolic acidosis 5ith appropriate respiratory

compensation!


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1escription

pH !)B 4aD )"# m+.&O( *% mm Hg 8

D $!% m+.

&'O( $) mm Hg 'l- B m+.

H'O"- * m+. 'O(, total * m+.

.actate (% m+. 6rea #$ mgd. A3 > )"#-B-*>"% m+. 'reatinine (!# mgd.

1R > 9"%-)(:9($-*: > )!)

)!( mm Hg decrease in &'O( for every ) m+. decrease in

H'O"-

!H'O"

- decrease > ($-* > )/ m+.

&'O( decrease predicted > )!( x )/ > )B mm Hg!

subtract from $% mm Hg 9reference point: > $( mm Hg


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?acid normal A3

A (-year-old girl is brought to the physician because of poorgro5th! he is at the "rd centile for height and 5eight!&hysical examination sho5s no other abnormalities!.aboratory studies sho5 a fractional excretion of H'O"

- of(!#E!

pH !"$ 4aD )"B m+.&O( B/ mm Hg 8

D $!" m+.

&'O( (* mm Hg 'l- ))( m+.

H'O"- )# m+. 6rine pH #!%

History is non-contributory!

?etabolic acidosis 5ith respiratory compensation!


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1escription

pH !"$ 4aD )"B m+.&O( B/ mm Hg 8

D $!" m+.

&'O( $& mm Hg 'l- ))( m+.

H'O"- )# m+. 6rine pH #!%

A3 > )"B-))(-)#>)( m+. F+H'O"- (!#E

)!( mm Hg decrease in &'O( for every ) m+. decrease inH'O"

-!

H'O"- decrease > ($-)# > B m+.

&'O( decrease predicted > )!( x B > )) mm Hg!

subtract from $% mm Hg 9reference point: > $' mm Hg


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?etabolic alkalosis

&lasma H'O"- greater than expected

.oss of strong acid or gain of base

'auses 9( 5ays to organiGe:

loss of HD from +'F via kidneys 9diuretics: or gut 9vomiting: gain of alkali in +'F from exogenous source 9I 4aH'O"

infusion: or endogenous source 9metabolism of ketoanions:

or addition of base to +'F 9milk-alkali syndrome:

'l- depletion 9loss of acid gastric juice: 8D depletion 9primarysecondary hyperaldosteronism: Other disorders 9laxative abuse, severe hypoalbuminaemia:


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6rinary 'hloride

pot urine 'l- less than )% m+. often associated 5ith volume depletion respond to saline infusion common causes - previous thiaGide diuretic therapy,

vomiting 9B%E of cases:

pot urine 'l- greater than (% m+. often associated 5ith volume expansion and hypokalemia resistant to therapy 5ith saline infusion causes7 excess aldosterone, severe 8D deficiency, current

diuretic therapy, Jartter syndrome


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?alk lo5 6rine 'l-

An ($-year-old 5oman is brought to the physician 5ith a "-month history of 5eakness and fatigue! Jlood pressure isB%/% mm Hg!

pH !#( 4aD )" m+.&O

(* mm Hg 8D (!/ m+.

&'O( $B mm Hg 'l- B% m+.

H'O"- "B m+. 6rine 'l- # m+.

History and physical examination suggests bulimia!

?etabolic alkalosis 5ith respiratory compensation!Khe cause is most likely bulimia!


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1escription

pH !#( 4aD )" m+.&O( * mm Hg 8

D (!/ m+.

&'O( *' mm Hg 'l- B% m+.

H'O"- "B m+. 6rine 'l- # m+.

%!/-%!# mm Hg increase in &'O( for every ) m+.increase in H'O"

-!

H'O"- increase > "B-($ > )# m+.

&'O( increase predicted > %!/-%!# x )# > B-)( mm Hg!

add to $% mm Hg 9reference point: > *'#+$ mm Hg


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?alk high 6rine 'l-

An *"-year-old 5oman is brought to the physician 5ith a )-5eek history of 5eakness and poor appetite!

pH !#* 4aD )$# m+.&O( /% mm Hg 8

D )!B m+.

&'O( #/ mm Hg 'l-

*/ m+.H'O"

- #( m+. 6rine 'l- $ m+.

History is limited!

?etabolic alkalosis 5ith respiratory compensation!

Khe cause is unkno5n, most likely excess adrenocorticalactivity, current diuretic therapy, or idiopathic!


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1escription

pH !#* 4aD )$# m+.&O( /% mm Hg 8

D )!B m+.

&'O( +% mm Hg 'l- */ m+.

H'O"- #( m+. 6rine 'l- $ m+.

%!/-%!# mm Hg increase in &'O( for every ) m+.increase in H'O"

-!

H'O"- increase > #(-($ > (* m+.

&'O( increase predicted > %!/-%!# x (* > )-() mm Hg!

add to $% mm Hg 9reference point: > +,#%( mm Hg


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Revie5 Luestions

• What is an effective approach to acid base problems?• What are the normal ranges and reference points?

• What are the anion and osmolar gap?

• What is compensation?

• What are the characteristics of respiratory acidosis and

alkalosis?

• What are the characteristics of metabolic acidosis and

alkalosis?

• What is the utility of spot urine Cl-?

Documents

Acidosis Alkalosis Biochemistry