Approaches to

Understanding
Acid-Base Physiology
Dr A.Hadi Martakusumah SpPD-KGH
Sub Division of Nephrology and Hypertension
Department of Internal Medicine
Padjadjaran University/Hasan Sadikin General Hospital

"Acid/base homeostasis is arguably one of the most

difficult of the subdisciplines of physiology for medical
students to master. There are several reasons for this
understanding the data in a blood gas panel requires an
appreciation for not only acids and bases, but also
ventilation, gas exchange, dynamics of electrolyte and
water movement, plasma composition, respiratory
control, and renal mechanisms of hydrogen ion,
electrolyte, and water excretion.
from: Rawson RE & Quinlan KM, Adv Physiol Educ 2002; 26: 85-97
2

Approaches to Understanding AcidBase Physiology

Traditional Approach

The discussion of acid-base physiology outlined in most

of this lecture is the traditional empirical approach.
The concepts and explanations of this approach are still
the most common way that acid-base physiology is
taught and understood by many clinicians to some extent

Physico-chemical Approach

An alternative approach derived from physico-chemical

principles was proposed by Stewart in 1981
3

Physico-chemical Approach

Basic Principles of the Various

Theories of Acids & Bases
Acid: a substance that has certain
Traditional
properties (eg sour taste, turns litmus
red)
approach
+
Acid
:
H
in aqueous solution
Arrhenius
Bronsted-Lowry

Base : OH- in aqueous solution

At neutrality: [H+] = [OH-]
Acid : H+ donor
Base : H+ acceptor
Conjugate acid-base pairs

Lewis
Usanovich

Acid : a potential electron-pair acceptor

Base : a potential electron-pair donor
Acid: a substance that donates a
cation, or accepts an anion or an
electron
5
Base: a substance that donates an
anion, or accepts a cation.

Water

60-90% of body weight for most life forms

Essential nutrient to sustain life

often neglected

Good solvent

NaCl

attraction of ions (Na+ and Cl-) to water > attraction to

each other

Cohesion

one water molecule capable of bonding with 4

others

Water

Highly reactive

disassociation of water

H+

mass of H is small = proton jumping

H+

O-

H+

H+

O-

OH- + H3O+
8

The Composition of the Human Body

9
Figure 27.1a

Strong Ions

Cations

Na+
K+
Ca++
Mg++

Anions

ClSO4Lactic acid

Disassociate into ions in solution

10

Strong Ions and Water

Water disassociates to counter-balance the
charges of the ions

OH

OH

H+

H+

H+

O-

Na
H

OH
-

H+

OH+

O-

H+

H+

O-

H+

H+

H+

H+

H+

Cl-

H+

H+

O
OH
-

H+

O-

H+
H+

H+

O11

H+

Strong Ions and Plasma

Strong ions disassociate in plasma

Na

Cl-

Plasma

Na+

Cl12

Hydrogen Ion in Solution

Bare protons (ie H+) do not exist in solution

Protons are associated and react with
surrounding water molecules.
This is sometimes represented as H3O+ (the
hydronium ion) but this one-to-one relationship
is also inaccurate.
Stewart suggests that the most accurate
representation is {H:(H2O)n}+
This would be extremely inconvenient to use
clinically so we continue to speak of the
hydrogen ion (H+) simply out of convenience.
13

pH

The term pH was coined by the Danish

chemist, Soren Peter Sorensen in 1909 to
refer to the negative log of hydrogen ion
concentration
the symbol pH meaning potenz (power) of
Hydrogen.

pH = -log [H3O+]

H3O+ > OH- = acidic

OH- > H3O+ = basic

pH = - log10 aH+ (or: aH+ = 10

where aH+ is activity of H+

(-pH)

)
14

Which is Best: pH or [H+] ?

The advantages of pH compared to [H+]

are:

It is the traditional symbol and remains in wide

use
It is related to the activity of H+ (rather than
concentration) or more specifically the log of H+
activity and this is what physiological systems
seem to respond to.
It is what is measured by the pH electrode (ie
activity of H+)
The alternative [H+] is not correct because the
activity coefficient is ignored
Free H+ (ie bare protons) are not the form really
present in solution anyway
15

Which is Best: pH or [H+] ?

The disdvantages of pH compared

to [H+] are:

It is a contrived symbol which represents

a double non-linear transformation of
[H+]
It is difficult to learn and understand
It disguises the magnitude of changes in
[H+]

16

Relationship between pH & [H+]

pH

[H+]
(nanomoles/l)

6.8

158

6.9

125

7.0

100

7.1

79

7.2

63

7.3

50

7.4

40

7.5

31

7.6

25

7.7

20

7.8

15

17

Cations and Anions in Body Fluids

18
Figure 27.2

Normal
Kation (mEq/L)

Anion (mEq/L)

Na+

140

Cl

103

K+

HCO 3

25

Ca + +

Protein

16

Mg + +

Organic

H+

0.000040
Other
(40 nmol/L) Inorganic

3
19

H+ and the Potential

Threat to survival

The free [H + ] is tiny and must be kept so for

survival
A very large accumulation of [H + ] may kill
by binding to proteins in cells and changing
their charge ,shape and possibly their function

20

Why is pH so important?

The Davis Hypothesis

He found that nearly every biosynthetic

intermediate has at least one group that would be
largely ionised at physiological pH, whether it is
an acid or a base.

21

22

Acid-Base Balance

Each day there is always a net production of

acid by the bodys metabolic processes
To maintain balance, these acids need to be
excreted.
The acids produced by the body are classified
as :

respiratory (or volatile) acids

metabolic (or fixed) acids.
23

Respiratory Acid

The acid is carbonic acid (H2CO3) but the term

respiratory acid is usually used to mean carbon
dioxide.
CO2 is not a Bronsted-Lowry acid as it does not
contain a hydrogen so cannot be a proton donor, but
instead can be thought of as representing a potential to
create an equivalent amount of carbonic acid.
It is called a volatile acid meaning in this context it
can be excreted via the lungs
24

Basal Carbon Dioxide Production

Consider a resting adult with an oxygen

consumption of 250 mls/min and a CO2
production of 200 mls/min (Respiratory
quotient 0.8):
Daily CO2 production
= 0.2 x 60 x 24 l/day divided by 22.4 l/mole
= 12,857 mmoles/day.
25

Metabolic or Fixed Acids

This term covers all the acids the body produces which
are non-volatile.
Because they are not excreted by the lungs they are
said to be fixed in the body.
All acids other then H2CO3 are fixed acids.
These acids are usually referred to by their anion (eg
lactate, phosphate, sulphate, acetoacetate or bhydroxybutyrate).
Net production of fixed acids is about 1 to 1.5 mmoles
of H+ per kilogram per day:
About 70 to 100 mmoles of H+ per day in an adult.
This non-volatile acid load is excreted by the kidney
26

Dietary acid-base Impact

Nutrient

Product

[H + ] (mmol/day )

Reactions generating [H + ]
Sulfur-containing amino acid
-Cysteine/cystinine,methionine

[H + ]

70

-Lysine,arginine,histidine

[H + ]

140

Organic phosphates

HPO42- +[H + ] 30

Cathionic amino acids

Reactions removing [H + ]
Anionic amino acid
-Glutamate ,aspartate

HCO3-

-110

Organic anions eg citrate

HCO3-

-60

Organic phosphate excretion

with [H + ]

H2PO42-

-30

NET TOTAL [H + ] to be excreted as NH4+

40

27

DAILY PHYSIOLOGY
of [H + ]
[H+]

FUEL

BODY

H 2O + CO2

HCO3-

28

Role of the Kidneys

The lungs are important for excretion of carbon dioxide (the

respiratory acid) and there is a huge amount of this to be excreted: at
least 12,000 to 13,000 mmols/day.
In contrast the kidneys are responsible for excretion of the fixed acids
and this is also a critical role even though the amounts involved (70100 mmols/day) are much smaller.
The main reason for this renal importance is because there is no other
way to excrete these acids and it should be appreciated that the
amounts involved are still very large when compared to the plasma
[H+] of only 40 nanomoles/litre.
There is a second extremely important role that the kidneys play in
acid-base balance, namely the reabsorption of the filtered bicarbonate.
29

Role of the Kidneys

In acid-base balance, the kidney is responsible for 2

major activities:

Reabsorption of filtered bicarbonate: 4,000 to 5,000

mmol/day
Excretion of the fixed acids (acid anion and associated
H+): about 1 mmol/kg/day.

30

Terminology of Acid-Base Disorders

Acidosis
an abnormal process or condition which would lower arterial pH if
there were no secondary changes in response to the primary aetiological
factor.
Alkalosis
an abnormal process or condition which would raise arterial pH if there
were no secondary changes in response to the primary aetiological
factor.
Simple Disorders
are those in which there is a single primary aetiological acid-base
disorder.
Mixed Disorders
are those in which two or more primary aetiological disorders are
present simultaneously.
Acidaemia - Arterial pH < 7.36 (ie [H+] > 44 nM )
Alkalaemia - Arterial pH > 7.44 (ie [H+] < 36 nM )
31

The Anion Gap

Anion gap = [Na+] - [Cl-] - [HCO3-]

Reference range is 8 to 16 mmol/l.
An alternative formula which includes K+
is :

AG = [Na+] + [K+] - [Cl-] - [HCO3-].

32

Other Cations
Other Anions

AHCO325
Na +
140

Cl 103

Unmeasured Anions
Proteins (15 mEq/L)
Organic Acids (5 mEq/L
Phosphates (2 mEq/L)
Sulfates (1mEq/L)
UA = 23 mEq/L

Unmeasured Cations
Calcium (5 mEq/L)
Potassium (4.5 mEq/L)
Magnesium (1.5
mEq/L)
UC = 11 mEq/L

Anion gap = [Na+] - [Cl-] - [HCO3-]

33

Other Cations
Other Anions

AL-

Added Anions

HCO3Na +
140

Cl -

When an
acid such
lactic
acid is
added
The
HCO3will fall
and
replaced
by
lactate
anion

103

Metabolic Acidosis with increased anion gap

34

Other Cations

Other Anions

A-

Other Anions

AAHCO3-

L-

Added Anions

HCO3-

25
Na +
140

Cl 103

Normal AG

Increased AG

35

Other Cations
Other Anions

A-

HCO3-

Note that
with a loss
of
NaHCO3
HCO3- will
fall but no
new anions
will be
added

Na +
140

Cl -

Metabolic Acidosis with normal anion gap

36

Other Cations
Other Anions

A-

Other Anions

AHCO325

L-

AAdded Anions

Other Anions

AHCO3-

HCO3-

Na +
140

Cl -

Cl -

Cl -

103

Normal AG

Increased AG

Normal AG

37

The Basic Relationship between PCO2 and Plasma pH

38
Figure 27.6

Mechanisms of pH control

Buffer system consists of a weak acid and its anion

Three major buffering systems:
1.
Protein buffer system

Amino acid

H+ are buffered by hemoglobin buffer system

2.
Carbonic acid-bicarbonate

Buffer changes caused by organic and fixed acids

3.
Phosphate

Buffer pH in the ICF

39

Protein buffer system

If pH climbs, the carboxyl group of amino acid

acts as a weak acid
If the pH drops, the amino group acts as a weak
base
Hemoglobin buffer system

Prevents pH changes when PCO2 is rising or falling

40

Figure 27.8 Amino Acid Buffers

41
Figure 27.8

Carbonic Acid-Bicarbonate
Buffering System

Carbonic acid-bicarbonate buffer system

CO2 + H2O H2CO3 H+ + CO3

Has the following limitations:

Cannot protect the ECF from pH changes due to

increased or depressed CO2 levels
Only functions when respiratory system and control
centers are working normally
It is limited by availability of bicarbonate ions
(bicarbonate reserve)
42

The Carbonic Acid-Bicarbonate Buffer System

43
Figure 27.9a, b

Maintenance of acid-base
balance

Lungs help regulate pH through carbonic acid bicarbonate buffer system

Changing respiratory rates changes PCO2

Respiratory compensation

Kidneys help regulate pH through renal

compensation

44

Kidney tubules and pH Regulation

45
Figure 27.10a, b

Kidney tubules and pH Regulation

46
Figure 27.10c

The Central Role of the Carbonic AcidBicarbonate Buffer System in the Regulation of
Plasma pH

47
Figure 27.11a

The Central Role of the Carbonic AcidBicarbonate Buffer System in the Regulation of
Plasma pH

48
Figure 27.11b

Rates of correction

Buffers function almost instantaneously

Respiratory mechanisms take several minutes
to hours
Renal mechanisms may take several hours to
days

49

50

51

Acid-Base Disorders

Respiratory acid-base disorders

Result when abnormal respiratory function causes

rise or fall in CO2 in ECF

Metabolic acid-base disorders

Generation of organic or fixed acids

Anything affecting concentration of bicarbonate ions
in ECF
52

Respiratory acid-base disorders

Respiratory acidosis

Results from excessive levels of CO2 in body fluids

Respiratory alkalosis

Relatively rare condition

Associated with hyperventilation

53

Respiratory Acid-Base Regulation

54
Figure 27.12a

Respiratory Acid-Base Regulation

55
Figure 27.12b

Metabolic acid-base disorders

Major causes of metabolic acidosis are:

Depletion of bicarbonate reserve

Inability to excrete hydrogen ions at kidneys
Production of large numbers of fixed / organic acids
Bicarbonate loss due to chronic diarrhea

Metabolic alkalosis

Occurs when HCO3- concentrations become elevated

Caused by repeated vomiting

56

The Response to Metabolic Acidosis

57
Figure 27.13

Metabolic Alkalosis

58
Figure 27.14

Detection of acidosis and

alkalosis

Diagnostic blood tests

Blood pH
PCO2
Bicarbonate levels

Distinguish between respiratory and metabolic

59

A Diagnostic Chart for Acid-Base Disorders

60
Figure 27.15

Clinical Acid Base Problem Solving

Langkah Pertama :

Harus tahu harga normal parameter yang akan digunakan untuk

menganalisis kelainan asam basa :
a. pH 7.40 atau [H+ ] 40 nmol/L

Cara merubah pH kedalam [H+ ] :

Buang angka tujuh dan desimalnya jadi misal pH 7.26 didapat 26
Kurangi 40 dengan nilai tersebut jadi 40 26 = 14
Tambahkan 40 kedalam harga tersebut : 40 + 14 = 54 nmol/

b. pCO2 = 40 mm Hg
c. [HCO3 ] = 25 mmol/L
d. Anion gap plasma Na-Cl-[HCO3 ] = 12 mEq/L jika kadar
albumin normal yaitu 4 gr% . Setiap penurunan albumin 1 gram
% dari harga normal maka kadar AG dikurangi 4
61

Clinical Acid Base Problem Solving

Langkah Kedua :
Apakah ada Lab Error ?
Cara mengetahuinya adalah masukkan harga PH ,
pCO2 dan [HCO3 ] kedalam persamaan Henderson di
bawah ini : [H+ ] = pCO2 X 24/ [HCO3 ]
Jika penderita tidak demam dan harga [HCO ] yang
3
dihitung dan yang diukur berbeda lebih dari 10%
maka ada lab error .
Kita harus mengulangi pemeriksaan. Kita tidak ingin
menganalisis hasil AGD berdasarkan hasil
laboratorium yang salah .

62

Clinical Acid Base Problem Solving

Langkah Ketiga :
Tetapkan hasil pH :
Acidemia jika kurang dari 7.36
Alkalemia jika lebih dari 7.44

63

Clinical Acid Base Problem Solving

Langkah Keempat :
Tentukan apakah kelainan primernya
respiratorik atau metabolik
Alkalemia :
Respiratory Alkalemia jika pCO2 kurang dari 38
Metabolic Alkalemia jika [HCO ] lebih dari 25
3

Acidemia :
Respiratory Acidemia jika pCO2 lebih dari 44
Metabolic Acidemia jika [HCO ] kurang 25
3

64

Clinical Acid Base Problem Solving

Langkah Kelima :
Hitung anion gap (AG) serum yaitu :
Kadar Na serum ( Cl
+ [HCO3 ] serum
Jika AG > 10 ada kemungkinan
metabolic acidemia
Jika AG > 20 dapat dipastikan
ada metabolic acidemia

Jangan lupa factor albumin !

Other
Cation

A-

Na+
(140)

Other
Anion

HCO3(25)

Cl(103)
65

Clinical Acid Base Problem Solving

Langkah Keenam :
Check derajat kompensasi tubuh :

Metabolic Acidemia :

Metabolic Alkalemia :

Setiap pCO2 naik 10 mmHg = [HCO3 ] naik 4 mEq/L

Respiratory Alkalemia :
Akut :

Setiap pCO2 naik 10 mmHg = [HCO3 ] naik 1 mEq/L

Kronik :

Setiap kenaikan pCO2 = 0.6 X kenaikan [HCO3 ]

Respiratory Acidemia :
Akut :

pCO2 (Predicted) = [(1.5X [HCO3 ]+8] 2 (Winter Formula)

Setiap pCO2 turun 10 mmHg = [HCO3 ] turun 2 mEq/L

Kronik :

Setiap pCO2 turun 10 mmHg = [HCO ] turun 5 mEq/L

66

Clinical Acid Base Problem Solving

Langkah Ketujuh :

Determine Delta ratio (Delta gap) =

(Increase in anion gap / Decrease in
bicarbonate)

67

Guidelines for Use of the Delta Ratio in Metabolic

Acid-Base Disorders
Delta Ratio

Assessment Guideline

< 0.4

Hyperchloraemic normal anion gap acidosis

0.4 - 0.8

Consider combined high AG & normal AG

acidosis Ratio often <1 in acidosis assoc.
with renal failure
Usual for uncomplicated high-AG acidosis
Lactic acidosis: average value 1.6
DKA more likely to have a ratio closer to 1
due to urine ketone loss (esp if patient not
dehydrated)
Suggests pre-existing elevated HCO3 level:
consider a concurrent metabolic alkalosis
or a pre-existing compensated respiratory
68

1 to 2

>2

Other parameter to consider

The Urinary Anion Gap

The cations normally present in urine are Na+,

K+, NH4+, Ca++ and Mg++.
The anions normally present are Cl-, HCO3-,
sulphate, phosphate and some organic
anions.
Only Na+, K+ and Cl- are commonly measured
in urine so the other charged species are the
unmeasured anions (UA) and cations (UC).
Cl- + UA = Na+ + K+ + UC
Urinary Anion Gap =
( UA - UC ) = [Na+]+ [K+] - [Cl-]
69

Urinary Anion Gap

Clinical Use

Key Fact: The urinary anion gap can

help to differentiate between GIT and
renal causes of a hyperchloraemic
metabolic acidosis.
It has been found experimentally
that the Urinary Anion Gap (UAG)
provides a rough index of
urinary ammonium excretion.
70

Urinary Anion Gap

Clinical Use
In a patient with a hyperchloraemic
metabolic acidosis:

A negative UAG suggests GIT loss of

bicarbonate (eg diarrhoea)
A positive UAG suggests impaired renal
distal acidification (ie renal tubular
acidosis).
As a memory aid, remember neGUTive
- negative UAG in bowel causes

71

Osmolar Gap

Osmolar gap = (Measured osmolality) (Calculated osmolarity)

2 [Na+] + Glucose ( mmol/L) + Urea N (mmol/L)
0R
2 [Na+] + Glucose( mg% /18) + Urea N(mg% /2.8)
The osmolar gap can be very useful in assisting
diagnosis in metabolic acidosis due to toxic alcohols
& glycols (eg ethylene glycol, methanol).
72

Common Causes of Metabolic Acidosis

Increased Anion Gap
(ThinkMUDPILES)

Methanol intoxication*
Uremic acidosis (advanced renal failure)
Diabetic ketoacidosis*
Paraldehyde intoxication
INH
L-lactic acidosis*
Ethylene glycol intoxication*
Salicylate intoxication
D-lactic acidosis
Alcoholic ketoacidosis*
*Denotes most common

73

Non-anion gap Metabolic

Acidosis

USED CAR
U Uretero-Sigmoid Diversions

S
E

Accum of urine in colon reab chloride & water by intestine secretion of bicarb into intestine

Saline administration
Ethanol or Endocrinopathies
Addisons, Spirinolactone, Triamterene, Amiloride, Primary Hyperparathyroidism

Diarrhea

C
A
R

Carbonic Anhydrase Inhibitors

hyper-Alimentation
Renal Tubular Acidosis

Metabolic Acidosis
MUDPILES

Figure obtained from MKSAP Edition 14

USED CAR

Common Causes of Metabolic Acidosis

Normal anion gap

Mild to moderate renal failure*

Gastrointestinal loss of HCO3- (acute diarrhea)*
Type I (distal) renal tubular acidosis
Type II (proximal) renal tubular acidosis
Dilutional acidosis
Treatment of diabetic renal tubular acidosis*

Ketones lost in urine

*Denotes most common
76

Common causes of Metabolic

Alkalosis

Net loss of H+ from the ECF

G.I. Loss
Vomiting or nasogastric suctioning
Chloride losing diarrhea: chronic diarrhea/laxative
abuse

Renal loss
Loop or thiazide type diuretics esp. in CHF and
cirrhosis
Mineralocorticoid excess

Hyperaldosteronism
Cushings syndrome
77

Common causes of Metabolic

Alkalosis

Retention of HCO3

Excess administration of NaHCO3

Milk-alkali syndrome: antacids, milk, NaHCO3
Massive (>8 units) blood transfusion (citrate)
Posthypercapnia metabolic alkalosis (after
correction of chronic respiratory acidosis)

78

Four Main Acid-Base

Disorders

Disorde Primary
r
Alteration
Metaboli
c
Acidosis

in plasma
HCO3

Metaboli
c
Alkalosis

in
plasma HCO3

Respirato
ry
Acidosis

in plasma
pCO2

Respirato
ry
Alkalosis

in
plasma pCO2

Secondary
Response

Mechanism of
Response

in plasma Hyperventilation
pCO2
Hypoventilation
increase in pCO2
in plasma Increase in acid
HCO3 excretion; increase
in reabsorption of
HCO3
in plasma Suppression of
HCO3 acid excretion;
decrease in

Case 1

A 44 year old moderately dehydrated man was

admitted with a two day history of acute
severe diarrhea. Electrolyte results: Na+ 134,
K+ 2.9, Cl- 108, HCO3- 16, BUN 31, Cr 1.5.
ABG: pH 7.31 pCO2 33 mmHg
HCO3 16 pO2 93 mmHg
What is the acid base disorder?

80

Answer

1. History: Based on the clinical scenario,

likely acid base disorders in this patient are:
Normal anion gap acidosis from diarrhea or
Elevated anion gap acidosis secondary to lactic
acidosis as a result of hypovolemia and poor
perfusion.
2. Look at the pH.
The pH is low, (less than 7.35) therefore by
definition, patient is acidemic.

81

3. What is the process?

Look at the PCO2, HCO3- ,PCO2 and HCO3- are abnormal in

the same direction, therefore less likely a mixed acid base
disorder.
Need to distinguish the initial change from the compensatory
response.
A low PCO2 represents alkalosis and is not consistent with
the pH.
A low HCO3- represents acidosis and is consistent with the
pH, therefore it must be the initial change.
The low PCO2 must be the compensatory response. Since the
primary change involves HCO3-, this is a metabolic process,
i.e. Metabolic Acidosis.

82

4. Calculate the anion gap

The anion gap is Na - (Cl + HCO3-) = 134 -(108 + 16) = 10
Since gap is less than 16, it is therefore normal.
5. Is compensation adequate?
Calculate
the estimated PCO2.
Using Winter's formula; PCO2 = 1.5 [HCO3-]) + 8 2 =
1.5 16 + 8 2 = 30-34.
Since the actual PCO2 falls within the estimated range, we
can deduce that the compensation is adequate and there is
no seperate respiratory disorder present.
83

Assessment:

Normal anion gap acidosis with adequate

compensation most likely secondary to severe
diarrhea.

84

Case 2

A 22 year old female with type I DM, presents to the

emergency department with a 1 day history of nausea,
vomiting, polyuria, polydypsia and vague abdominal pain.
P.E. noted for deep sighing breathing, orthostatic
hypotension, and dry mucous membranes.
Labs: Na 132 , K 6.0, Cl 93, HCO3- 11 glucose 720, BUN
38, Cr 2.6.
UA: pH 5, SG 1.010, ketones negative, glucose positive .
Plasma ketones trace.
ABG: pH 7.27 HCO3- 10 PCO2 23
What is the acid base disorder?
85

1. History: Based on the clinical scenario, likely acid

base disorders in this patient are:

Elevated anion gap acidosis secondary to DKA, or

Elevated anion gap acidosis secondary to lactic acidosis in
the setting of vomiting and polyuria which may lead to
hypovolemia, and/or
Metabolic alkalosis in the setting of vomiting

2. Look at the pH.

The pH is low, (less than 7.35) therefore by
definition, patient is acidemic.
86

. What is the process?

3. Look at the PCO2, HCO3- . PCO2 and HCO3- are

abnormal in the same direction, therefore less likely a mixed
acid base disorder but not yet ruled out.
Again, need to distinguish the initial change from the
compensatory response.
A low HCO3- represents acidosis and is consistent with the pH,
therefore it must be the initial change.
To maintain the PCO2/HCO3-, the PCO2 is reduced in response.
The low PCO2 must be the compensatory response.
Since the primary change involves HCO3-, this is a metabolic
process, i.e. Metabolic Acidosis.
87

4. Calculate the anion gap

The anion gap is Na - (Cl + HCO3-) =
132 -(93 + 11) = 28
Since gap is greater than 16, it is therefore abnormal.
5. Is compensation adequate?
Calculate the estimated PCO2.
Using Winter's formula; PCO2 = 1.5 [HCO3-]) + 8
2 = 1.5 11 + 8 2 = 22.5 - 26.5.
Since the actual PCO2 falls within the estimated range,
we can deduce that the compensation is adequate and
there is no seperate respiratory disorder present.
88

6. Since anion gap elevated, calculate the

delta-ratio to rule out concurrent metabolic
alkalosis.
Delta ratio = (Increase in anion gap /
Decrease in bicarbonate) =(28-12)/(25-11)=1.2
Since the delta gap is between 1 and 2, we can
deduce that this is a pure metabolic acidosis.
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Assessment: Compensated elevated anion gap

acidosis most likely secondary to DKA.
Note the absence of ketones in the urine. This
is sometimes seen in early DKA due to the
predominance of beta-hydroxybutyrate. The
dipstick test for ketones detect acetoacetate but
not beta-hydroxybutyrate.

90