Understanding Acid Base Disorders

Dr George John
Critical Care
CMC
 CONCEPTS
• Normal and Acceptable
• The Hydrogen Ion, Acidosis & Alkalosis
• Compensation
• Acute vs Chronic
• Diagnosis
 Concept of ‘NORMAL’
• Statistical
• Benefit – quantity / quality of life
• Benefit versus therapeutic harm

Mean +/- 2SD

 Concept of ‘ACCEPTABLE’
• pH = 7.30 – 7.50 (Textbook = 7.35 – 7.45)

• pCO2 = 30 – 50 (Textbook 35 – 45)

• pO2 (on air) = >80

(on ventilator) = 60-90

• HCO3 = 24-28
Dx: Levels of Understanding
The Iceberg Phenomenon

Clinical
symptoms & signs
Biochem-Physio change
Anatomical Change

Pathology

Aetiology
 SAMPLING
If you cannot get an arterial sample use, VENOUS
 ARTERIAL vs VENOUS

Arterial and venous blood gas samples were strongly correlated in normal individuals, and there with only small
differences between them.
 
 VBG- 1
• Decreased pain for the patient. A double-blinded study found that pain scale
ratings were reduced by almost half with VBG compared to ABG. There was
no significant difference in the ratings when a local anesthetic had been
used prior to an arterial blood draw, but this is not always done.

• VBG sample can be drawn using the same intravenous line that is used to
draw blood for other lab tests, thus necessitating only one puncture. This
translates into decreased costs, labor, and risk of needle stick injury to the
health care provider.

• Complications such as arterial laceration, hematoma, and thrombosis are

non existent with venous blood sampling.
 VBG - 2
• Venous pH values closely mirror arterial values for several metabolic conditions, including diabetic ketoacidosis
(DKA) and uremia. However, they do not correlate in a cardiac arrest. it has also been shown that as cardiac
output declines, the differences between arterial and venous measurements increase. VBG analysis in cardiac
arrest provides values more indicative of the true cellular environment. In clinical practice, however,
knowledge of either the arterial or venous pH or PCO2 during cardiac arrest does not alter management.
•  An abnormally elevated venous lactate level (1.6 mmol/L or greater) was 100% sensitive and 89% specific in
predicting elevated arterial lactate levels. There is a close correlation between arterial and venous lactate
levels. A venous lactate level above 2 mmol/L predicts an elevated injury severity score, ICU admission, and
length of stay. The bottom line is that venous lactate levels are similar to those found in arterial samples. A
normal venous lactate measurement predicts a normal arterial lactate reading, precluding the need to perform
an arterial puncture.
• A close correlation between arterial and venous PCO2 that would decrease dependency on an ABG does NOT
exist in critically ill patients. However, a venous PCO2 value that predicts significant arterial hypercarbia is
available. In a study published in 2002 , a venous PCO2 level above 45 mm Hg predicted an arterial PCO2 above
50 mm Hg (the designated value for significant hypercarbia) with a sensitivity of 100% and specificity of 57%. In
this study, a venous PCO2 value above 45 mm Hg detected all cases of significant arterial hypercarbia (negative
predictive value, 100%) and reduced the requirement for arterial blood sampling in 41% of cases.
•  Venous PO2 values do not provide any significant reflection of arterial PO2 levels and are therefore a poor
surrogate to quantify oxygen delivery to target tissues. However, the widespread availability of pulse oximetry
makes it an attractive alternative. A 2001 study of more than 700 emergency department patients showed
that an oxygen saturation level of 96% or less on room air predicted a PO 2 below 70 mm Hg with a sensitivity of
100% and a specificity of 54%.
 Information from ABGs

OXYGENATION

VENTILATION & ACID BASE

OXYGENATION
FiO2
(0.21 – 1.0)
P/F ratio

A-a gradient

PaO2
 Understanding the terms
• Acidic: [H3O+] > [OH-]

• Neutral: [H3O+] = [OH-]

• Basic / Alkaline: [H3O+] < [OH-]

• In order to obtain insight into acid base chemistry, you must understand the fact that the
following terms do not mean the same.
• A solution is neutral if it contains equal concentrations of H+ and OH- ions. It is not the same as
pH = 7.0
• pH measures the hydrogen ion activity in a solution.
 The Hydrogen Ion
• The word “acid” is derived from “acere” (Latin) which means “sour” as acids are
sour to taste. Bases / alkalies were those which destroyed / neutralized acid.

• “Acidity” is easured by a pH meter and refers to the hydrogen ion activity not the
hydrogen ion concentration. On a linear scale this is expressed as nM.

• Water is amphoteric meaning that it can act as an acid by donating a proton

NH3 + H2O = NH4+ + OH¯ or
as a base by accepting a proton
HCN + H2O = H3O+ + CN¯.
In the presence of an acid it acts as a base (accepts a proton) while in the presence
of a base it acts as an acid (donates a proton).

• It can even react with itself (autoprotolysis). In water, one molecule can donate a
proton while another can receive it:
H2O + H2O H3O+ + OH-
 Insight!
• Source of hydrogen ion is: WATER
• One liter of water contains hydrogen ions:
= 55 x 6,023 x 1023
The quantity of hydrogen ions released from
water depends on the three Stewart
independent variables.
At 25oC, one in 1014 water molecules are
dissociated
 Insights about pH & H+
• The concentration of H+ in water has been found to be 1.0 x 10 -7 M at 298K (25oC). As dissociation of water
produces equal numbers of the two ions, it is neutral.
• The common (mis)understanding is that an aqueous solution with pH of 7.0 is neutral while a solution with a
value below this is acidic and those with a value more than this is basic. However, this popular perception ignores
the fact that a pH of 7 is neutral (which means that [H 3O+] = [OH-]) only when the temperature of water is 25 oC. At
other temperatures, it changes.
• The dissociation reaction given above indicates that pure water dissociates into one positive and one negative ion
in a 1:1 ratio. In pure water, because the only source of H + ( =[H3O+] )and OH- is water, pure water is always acid
base neutral. In other words, for pure water, [H3O+] = OH- , under all circumstances . The extent to which pure
water dissociates depends on its temperature. High temperature increases dissociation (increasing both [H 3O+]
and OH- in equal amounts thus maintaining neutrality, but decreasing pH as the [H 3O+] concentration increases)
while low temperature decreases dissociation (decreasing both [H 3O+] and OH- in equal amounts thus
maintaining neutrality but increasing pH as [H 3O+] concentration decreases).
• Thus the pH (hydrogen ion concentration) of pure water changes with temperature but neutrality is maintained.
Hence water does not have a single pH but a range of pHs depending on the temperature. Since pure water is
always neutral, this means that pure water has a range of “neutral pHs” depending on the temperature.
• These values apply only to pure water. Addition of ions (electrolyte solutions) and solutes will cause the
dissociation to increase slightly.
• The above understanding implies that at temperatures other than 25 oC, if pH of water is recorded as 7.0, it is not
neutral (neutral implying [H3O+] = OH). if pure water is taken at a temperature of 37 oC (normal body
temperature), the [H3O+] = [OH] = 10-6.8 moles per liter. This means that the pH (measure of hydrogen ion
concentration) at which water is neutral ( [H3O+] = [OH] ) at body temperature is 6.8! In fact, if the pH recorded
is 7.0 at this temperature, the aqueous solution is slightly alkaline ([H 3O+] < [OH-]) and it is not pure water. From a
clinical perspective, as the pH of plasma is 7.4, this is, in reality, 0.6 units (alkaline) above the neutral pH for the
body temperature (and not just 0.4 units above the “neutral”, as per popular perception).
 Temperature & pH of water

Acidic: [H3O+] > [OH-]

Neutral: [H3O+] = [OH-]

Basic /
Alkaline: [H3O+] < [OH-]

http://www.chembuddy.com/?left=pH-calculation&right=water-ion-product
 RELATIONSHIPS - 1

1. H+ & pH

x/div 2
H +

+/- 0 .3
50 7.3
40 7.4 pH
30 7.5
 pH vs H +

pH H+
7.00 100
7.10 80
7.20 60
7.30 50
7.40 40
7.50 30
7.60 25
7.70 20
7.80 15
7.90 12.5
8.00 10
 RELATIONSHIPS -2
2. Hydrogen ion activity, Carbon Dioxide
& Bicarbonate

• The ratio of carbon dioxide to bicarbonate

determines the H+ activity
• In the body, the numerator is regulated by the
lungs (change in ventilation) and the denominator
by the kidneys to fine tune the pH.
The H-H Equation
The H Equation
 Compensation 1
• Changes in PaCO2/ HCO3 occurring due
to changes in respiratory / renal
function in response to the primary
event, tending to return the pH to near
normal.
 Compensation 2
Key Concept
Compensatory mechanisms do not correct the
pH to the MIDDLE of the acceptable range as
the drive for correction reduces as the
acceptable levels are reached (as in any
feedback loop).
Compensatory mechanism:s
NEVER OVERCORRECT!!
 Respiratory
? Acute vs Chronic
Acute = inadequate time for compensation
Chronic = adequate time for compensation

The key point in deciding is whether there is a change

in the pH:

Acute – Change in pH present beyond 7.30 – 7.50

Chronic – pH change is within limits but at end of range
 Analysing Acid Base Disorders

CLASSICAL APPROACHES: STEWART APPROACH

Boston Approach Strong Ion Approach

HCO3

Copenhagen Approach
Base Excess
 CLASSICAL APPROACHES

CO2 +H2O H2CO3 H+ + HCO3-

Tissues

Expired CO2 H+
 Simple acid base disturbances
Condition Primary Secondary
change change
Resp acidosisIncr CO2 Incr HCO3
Resp Alkalosis Decr CO2 Decr HCO3
Metab Acidosis Incr H+ / Decr CO2
DecrHCO3
Metab Alkalosis Decr H+ / Incr CO2
incr HCO3
 Respiratory Acidosis
• In Respiratory Failure
• CO2 retention
• Causes – from cerebral cortex to the
peripheral nerve innervating respiratory
muscle; from large airway to pleura..
• Treatment – mechanical ventilation, cause.
 Respiratory Alkalosis
• As in Hyperventilation
• Results in Hypocarbia
• Causes- Anxiety, cerebral stimulation,
sepsis, drugs, hypoxia.
• Treatment - Cause, rebreathing
 Metabolic Acidosis-
• Check too much Heparin ??
• Increased Anion gap – Sepsis, renal Failure,
Ketoacidosis, Drugs and Poisons
• Normal Anion Gap – GI-loss, Renal tubular
acidosis, Endocrine (steroid def, renin def) Drugs
( Spironolactone, Amiloride, Triamterene )
• Treatment – Cause, Bicarb to replace buffer.
 Metabolic Alkalosis
• Causes –
- Vomiting as in Gastric outlet obstruction; loss of HCl
acid,
- Renal with increased steroids,
- K+ depletion as with loop diuretics,
- Iatrogenic as with bicarbonate therapy.
Treatment – correct perpetuating cause(s):
volume depletion, potassium correction
 MIXED DISORDERS
Key concepts:

Boston (US) Approach: LIMITS OF COMPENSATION

Copenhagen (Europe) Approach: BASE EXCESS

 BOSTON APPROACH 1

Primary- Respiratory Acidosis

Increased Bicarbs/ 10 mm Hg increase in CO2
Acute = 1meq/L; LIMIT = 30;
Chronic=4meq/L; LIMIT = 45
Primary – Respiratory Alkalosis
Decreased bicarbs/ 10mm Hg decrease in CO2
Acute = 2meq/L; LIMIT = 18
Chronic = 5meq/L; LIMIT = 15
 Boston Approach: A Summary for Respiratory Disorders
Expected change of HCO3 with PCO2 change

Remember!
Changes in Chronic are more than in Acute
Changes in Alkalosis (washing out CO2) are more than in Acidosis (CO 2 retention)
 BOSTON APPROACH - FOR METABOLIC DISORDERS

Primary- METABOLIC ACIDOSIS:

Expected decrease in CO2 = (0.7 x HCO3) + (21+2)

Primary – METABOLIC ALKALOSIS:

Expected increase in CO2= (1.5 x HCO3) + (8+2)
 Bedside Rules for Metabolic Disorders
In a simple metabolic disorder,
The PaCO2 should be within + 5 of the 2 digits of the
pH after the decimal point:
pH = 7.15; expected PaC02 = 15 + 5 = 10 – 20
pH = 7. 55; expected PaC02 = 55 + 5 = 50 – 60
If beyond expected range, there is a mixed disorder.
Rule applicable between pH limits of 7.10 – 7.60
There is no acute vs chronic for metabolic disorders
 Copenhagen Approach
Separate the respiratory and non respiratory components of HCO 3

• Standard HCO3 :
HCO3 at a PaCO2 of 40 mm Hg

• Buffer Base: Total of all buffer anions in blood

with a Hb of 15g%,the BB is 48mEq/l
with the Hb is 8g%,then BB is about 45mEq/l
HCO3 is about half the total BB.
 Base Excess / Deficit
• It is the difference between the patient’s normal BB and the actual BB. It
was originally based on actual measurement by titration but in a modern
ABG lab it is a CALCULATED value.
• BE = CALCULATED BB - NORMAL BB
• As BE takes into account all the buffer base, the relationship between BE
& HCO3 is not linear. Normal values are -2 to +2 mM/L
• The Base Excess (BE) is a calculated value which estimates the metabolic
(non respiratory) component of an acid base abnormality. It is an estimate
of the amount of strong acid or base needed to correct the metabolic
component of an acid base disorder. It is the amount of acid / base
needed to titrate blood to restore normal values:
plasma pH to 7.40
at a PaCO2 of 40 mm Hg, at 37oC.
 Base Excess
• Actual
• Standard

If BE is calculated for a haemoglobin concentration of 30 or 50 g/l instead of the

actual haemoglobin, the differences between in vitro and in vivo behaviour
can be mostly eliminated. This lower [Hb] is considered to be the ‘effective
[Hb]’ of the whole ECF (ie what the [Hb] would be if the haemoglobin was
distributed throughout the whole ECF rather than just the intravascular
compartment). This is Standard Base Excess .
(always check with the ABG manual as to what the manufacturing
company actually means by the various terms they use)
 ANION GAP - 1

CORRECTED ANION GAP:

In critically ill patients, the normal range for anion gap is different due to changes in
albumin and phosphate. It has been suggested that as a correction, the expected Anion
Gap is as follows:
Expected AG = 2(albumin in g%) + 0.5 (phosphate in mg%)
(twice albumin plus half phosphorus).
= 0.2 (albumin in g/liter) + 1.5 (phosphate in mmol / l)

If the phosphate has not significantly changed,

Expected AG = 2.5 x Albumin (g%)
= 0.25 x Albumin ( g/liter )

The anion gap thus allows for the differentiation of 2 groups of metabolic acidosis.
Metabolic acidosis with a high AG is associated with the addition of endogenously or
exogenously generated acids. Metabolic acidosis with a normal AG is associated with the
loss of HCO3 from the kidney or GI tract, or the failure of the kidney to excrete H +.
 Using the AG - 2

The change in Anion Gap should be equal to change in HCO 3 :

Δ anion gap = Δ HCO3
The delta/delta concept allows for the partitioning of metabolic acidosis into an anion
gap and a non-anion gap component, which can occur together. The concept behind
delta/delta is based on the assumption that for every increase in anion gap of 1 mmol/L
above normal (12 mmol), serum HCO3- will drop by an equal amount.
If the delta HCO3- is greater than the delta anion gap, then a concomitant non-anion gap
acidosis must exist along side the anion gap acidosis. 
 STEWART APPROACH
Query
Where is the pH center

??
????
???

?????
 What is the difference?

PCO2

PCO2

H+

SID Atot

HCO3
H+

Change of Focus!
Does the sun go around the earth or vice versa ????
 Basic Principles
Principle of Electroneutrality:
The concentration of all cations must equal the
concentration of all anions as the human body is
not electrically charged
Principle of Conservation of Mass:
The amount of any substance remains constant
unless it is added, generated or removed.
 Determinants of H+
• PaCO2

• Weak Acids (source of weak anions)

HA H+ + A-
phosphate
albumin

• SID (strong ion difference)

 PaCO2
A rise in PaCO2 results in compensation by the
body by altering another independent
determinant of pH – the SID

There is no change to the evaluation of

respiratory acid base abnormalities
 Weak Acids
HA H+ + A-
AH + A- = ATOT
• Proteins – Albumin, Globulin
• Phosphate
A- by itself is not an independent variable as it changes with SID & PCO2.
However, ATOT (= HA + A-) is an independent variable.
Sudden decrease in ATOT causes alkalosis
Sudden increase in ATOT causes acidosis
However, the body does not regulate ATOT to maintain pH – there is no “proteinaceous”
acidosis / alkalosis.
ATOT = 0.25 x albumin (g/L) + 0.09 x globulin (g/L) + 2 (phosphate in mmol/L).
The Anion Gap includes strong unmeasured and weak unmeasured anions. In the absence of strong unmeasured
anions (lactate, ketoacids) the A TOT is equal to the Anion Gap

Estimation of normal AG:

A- = 2(albumin in g %) + 0.5 (phosphate in mg%)
If the measurements are in international units:
 A-    = 0.2(albumin in g / L) + 1.5 (phosphate in mmol / L).

 
 Strong Ion Difference (SID) - 1
• A strong ion is defined as one whose charge does not
depend on the concentration of other ions.

• Since the human body is electrically neutral, it

follows that the net difference in charges between
the strong cations and anions determines the
amount of ionization of the other ions – the “weak”
ions. The weak ions become ionized or non ionized
to maintain electroneutrality.
 SID - 2

Just as a fluid changes shape to mould itself to

the shape of its container, the “weak” ions
must change their “charged concentrations”
( = dissociation) to confirm to the “available
space” ( the strong ion difference = SID )
 SID - 3
Strong and Weak ions:

WEAK IONS

STRONG CATIONS
STRONG ANIONS
 SID - 4
• Cations (positive ions):
Strong: Na, K, Ca, Mg
Weak: H

• Anions (negative ions):

Strong:
Measured - Chloride
Unmeasured - lactate, acetoacetate, betahydroxybutyrate
Weak:
Measured - HCO3
Unmeasured - albumin, inorganic phosphate
 Strong Ion Approach - 5
A Schematic view (Gamblegram) :

STRONG
STRONG
UNMEASURED
WEAK - H ION GAP ketoacids, lactate
WEAK
UNMEASURED
ANION GAP
STRONG proteins, phosphorus
ION WEAK
DIFFERENCE MEASURED
STRONG = buffer base HCO3
Na, K,
Ca, Mg STRONG
MEASURED
Cl
 SID – 6
The “Fitting”

WEAK
ANIONS

STRONG SID
CATIONS
STRONG
ANIONS
 SID - 7

• As the SID falls (increase in strong negative or

decrease in strong positive), the H+ increases
• Lactate is a strong ion as it is almost
completely dissociated at a pH of 7.40
The most important weak acids are albumin
and phosphate
• The above 3 independent factors control all
other factors
 Change in SID & pH – A visual aid

H+ H+
H+

SID
SID
SID

+ + +
-
-
-

Normal SID Increased SID Decreased SID

Less H+ ionisation More H+ ionisation
= ALKALOSIS = ACIDOSIS
 Causes of Changes
Increase in SID – less ionisation of H (ALKALOSIS)
- Decrease in anions
loss of chloride (vomiting, diuresis)
- Increase in cations (rare)
Decrease in SID – more ionisation of H (ACIDOSIS)
- Increase in anions
generation of organic anions – lactate, ketones
exogenous - excess chloride administration,
- hypoproteinemia (Cl retention)
- Decrease in cations
- diarrrhoea
- renal tubular acidosis
 SID in the Critically ill

• In critically ill patients, the SID is reduced

• The value of SID in the critically ill is 30 – 35
mEq / liter (healthy 40 – 42 mEq / liter)
 Paradigm Shift - 1 !

1.Bicarbonate not a controlling factor

2.Vital role for strong ions – specially chloride
(HCl increases acidity because of strong anion
without strong cation – not because of the H)
3.Weak acids – not buffers
4.Use H+ concentration not pH
5. Definition of acid = that which increases H+
concentration
 Paradigm Shift - 2
• SID (plasma) is almost equivalent to Buffer
Base (whole blood)
• Standard Base Excess = amount of change in
SID needed to restore pH to 7.40 at a PaCO2
of 40mm Hg
• Negative SBE = amount SID must increase
• SBE better than BE as it is standardised for
invivo invitro differences
 What is the difference?

Explains more in metabolic disorders!

• Role of albumin
• Role of chloride
 Role of albumin - 1
Albumin behaves as a weak acid and thus hpoalbuminemia has an alkalinizing effect.
However, hypoalbuminemia does not necessarily lead to a disorder of acid base balance.
Critically ill patients are often hypoalbuminemic but are not always alkalemic as their SID
is reduced. A loss of weak acid secondary to hypoproteinemia leads to a renal
mediated increase in chloride so that the SID decreases without any changes in H +
and HCO3-
It has also been shown that hypoalbuminemia is strongly associated with a low serum
sodium. Correction of the hypoalbuminemia with albumin infusion results in a
significant increase in serum sodium without much change in urine osmolality. Thus
the change in serum sodium is likely to be due to a shift in the distribution of sodium
between plasma and interstitial fluid resulting from the Gibbs-Donnan effect. A
hyponatremia in a hypoalbuminemic person does not necessarily indicate fluid
overload or water excess. Consequently, when sodium concentration rises in
hypoalbuminemia, strong anions (Cl and XA) will need to increase to preserve
electroneutrality.
 Role of albumin - 2
• Reduction in albumin reduces ATOT & A-
• This alkanising effect of reduced serum
albumin can be adjusted for by altering PCO2
or SIG – the body prefers to decrease SID.
 Role of Chloride
• NaCl – Na regulated for tonicity, Cl can be changed to
alter SID
• Increase in Na relative to Cl (or a drop in Cl relative
to Na) increases SID
• Loss or addition of HCl has an effect on
pH because chloride change is unaccompanied by a
strong cation.
• Addition of normal saline – Cl increases relatively as
difference between Na and Cl not same as serum
(SID in normal saline = 0 and in serum = 28mEq/l;
Addition of KCl – K moves into cell, leaving Cl outside
 Effect of addition of Normal Saline – An Analysis
Consider what happens when ten liters of normal saline is infused in a person with normal electrolytes:
Weight of person = 50 kg; Body water = 50 x 0.6 = 30 liters;
Serum Na = 140 mmol / L; Serum Chloride 100 mmol / L
The difference in the concentrations = Strong Ion Difference = 40 mmol / L
In actual fact, the potassium, calcium, magnesium also has to be considered in the calculation but as these are
relatively small and not present in the normal saline being added, we will ignore it for this calculation to
keep it simple.
Total Na = 140 x 30 = 4200 mmol; Total Chloride = 100 x 30 = 3000 mmol
Normal Saline has 154 mmol of Na and the same amount of Cl per liter of fluid.
Hence 10 liters will have 1540 mmol of Na and 1540 mmol of Cl
On adding 10 liters of normal saline,
• Body sodium becomes = 4200 + 1540 = 5740mmol
• Boy Chloride becomes = 3000 + 1540 = 4540 mmol
• Body water goes up by 10 liters = 30 + 10 = 40 liters.
• Final concentration of Na = 5740 / 40 = 143 .5 mmol / L
• Final concentration of Cl = 4540 / 40 = 113.5 mmol / L
The new Strong Ion Difference = 143.5 – 113.5 = 30 mmol / L

In other words, although the added normal saline has equal concentrations of sodium and chloride, since
the serum chloride is lower than serum sodium, the relative rise in chloride concentration is more than
that of serum sodium. This reduces the Strong Ion Difference and causes more dissociation of hydrogen
ions - explaining the acidifying effect of normal saline.
 Another Perspective

Acidity

PaCO2 = 40

Atot = 17.2

SID 32 – 42mEq / L

0.6 1.0 2.0

Fraction of Normal Value
 Bedside Approach
Fencl - Stewart partitioning approach

Component due to SID

The SID is calculated from the difference of serum Na and serum Cl. In the original article which described this simplified
approach, the mean difference in their lab between normal serum Na and Cl was 38. Hence the amount by which the
actual gap between serum Na and Cl differed from the average difference was considered the base excess
attributable to SID.
BE Na – Cl = [Na] – [Cl] – 38
If the mean difference in the lab between normal serum Na and normal serum Cl is a number other than 38, that should
be used.

Component due to albumin

The normal albumin was taken as 42g/l in the published study and the component of Base Excess due to albumin was
taken as 0.25 of the difference between actual and normal serum albumin.
BE alb = 0.25 (Normal serum albumin – actual serum albumin)

 
Component due to unmeasured anions (UMA):
This is the remaining Base Excess: 
BEUMA = BE TOT – (BE Na – Cl - BE alb )
 Application Scenario
Patient in septic shock:
Serum Na 140mmol /L ; K 5.5mmol/L; Cl 95mmol/L;
Total protein 6g% Albumin 2.2g%
ABG: PO2 60mm Hg; PaCO2 30mm Hg; pH 7.30;
SaO2 90%;HCO3 15mmol/L; Base Excess - 10mmol/L

Given 13 liters of normal saline over 24 hours for resuscitation:

Serum Na 145mmol / L; K 5.0mmol/L; Cl 110mmol/L;

Total protein 6g% Albumin 2.2g%
PaO2 200mm Hg; PaCO2 20mm Hg; pH 7.00;
SaO2 90%;HCO3 5mmol/L; Base Excess - 20mmol/L;
 Applied Stewart Approach
Using the bedside partitioning approach:
BE = SID + Alb + UMA

On the first day,

-10 = [(140 – 95) – 38] + [(42 – 22) /4] + UMA;
-10 = 7 + 5 + UMA; UMA = -22
On the second day,
-20 = [(145 – 110) – 38] + [(42 – 22) /4] + UMA;
-20 = -3 + 5 + UMA; UMA = -22

The UMA is the same for the two days but the change in Na/Cl
(SID) has caused the change in pH and Base Excess.
 A Comparison - 2
Anion Gap AGc SIG
Strong anions: increases increases increases
Lactate, ketoacids
Weak anions: increases increases increases
IgA myeloma
Strong cations: Li reduces reduces reduces
Weak cations: reduces reduces reduces
IgG myeloma
Albumin decrease reduces no effect no effect
increase increases

P decrease reduces reduces no effect

increase increases increases
Ca, Mg decrease increases increases no effect
increase reduces reduces
 SID & SIG
• SID apparent = (Na + K + Ca + Mg) – (Cl + Lact)
= Strong Cations – Strong Anions
= “Difference of the strongs” (Indirect estimation)
• SID effective = CO2 + A-
= “Sum of the weaks” (Direct calculation)

In health, SIDa = SIDe

Apparent SID may be wrong an excess of unmeasured weak ANIONS (proteins) as they are
not included in the equation.
Effective SID may be erroneous a lot of unmeasured strong ANIONS (ketones,sulphate)
as they are not in the calculation.

The gap between the two is known as the Strong Ion Gap (SIG).
 
SIG = Apparent minus Effective (Indirect minus Direct)
= SIDa – SIDe
 SIG
Strong Ion Gap = SIDa – SIDe
It is:
POSITIVE when unmeasured anions > unmeasured cations,
NEGATIVE in the unmeasured anions < unmeasured cations
It is important to be aware that SIG is not the same as the anion gap (AG).
Classical Anion Gap = (Na + K) – (HCO3 + Cl)
Strong Ion Gap = (Na + K + Ca + Mg) – (A- + HCO3- + Cl + Lactate + Urate )

The difference is that the SIG has a smaller unmeasured list as compared to the
classical AG. Hence the value of SIG is almost zero while the value of the Classical
Anion Gap is 8-12mEq/litre.

From the above,

Classical Anion Gap = SIG + A-
1.
References
Adrogue HJ, et al.: Assessing acid-base status in circulatory failure: differences between arterial and central venous
blood. N Engl J Med 1989; 320:1312.
2. Brandenburg MA and Dire DJ: Comparison of arterial and venous blood gas values in the initial emergency
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19. http://www.emedmag.com/html/pre/fea/features/038120044.asp
20. http://www.acidbase.org/index.php?show=sb
21. http://www. ccm.upmc.edu/education/resources/phorum.html
22. http://www.anaesthesiamcq.com/AcidBaseBook/ab9_5.php
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