Understanding Acid Base Disorders

Dr George JohnCritical 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 UnderstandingThe Iceberg Phenomenon

Aetiology

Pathology

Anatomical Change

Clinical symptoms & signs

Biochem-Physio change

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 PO2 below 70 mm Hg with a sensitivity of 100% and a specificity of 54%.

Information from ABGs

OXYGENATION

VENTILATION & ACID BASE

OXYGENATIONFiO2

(0.21 – 1.0)

PaO2

P/F ratio

A-a gradient

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 [H3O+] = [OH-]) only when the temperature of water is 25oC. 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 [H3O+] concentration increases) while low temperature decreases dissociation (decreasing both [H3O+] and OH- in equal amounts thus maintaining neutrality but increasing pH as [H3O+] 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 25oC, 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 37oC (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 ([H3O+] < [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

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

Acidic: [H3O+] > [OH-]

Neutral: [H3O+] = [OH-]

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

RELATIONSHIPS - 1

1. H+ & pH

H +

pH+/- 0 .3

x/div 2

50

40

30

7.3

7.4

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 -22. 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 2Key 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 compensationChronic = 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 – 7.50Chronic – pH change is within limits but at end of range

Analysing Acid Base Disorders

STEWART APPROACH

Strong Ion Approach

CLASSICAL APPROACHES:

Boston Approach

HCO3

Copenhagen Approach

Base Excess

CLASSICAL APPROACHES

CO2 +H2O H2CO3 H+ + HCO3-

Expired CO2

Tissues

H+

Simple acid base disturbances

Condition Primary Secondarychange change

Resp acidosis Incr 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 DISORDERSKey concepts:

Boston (US) Approach: LIMITS OF

COMPENSATION

Copenhagen (Europe) Approach: BASE EXCESS

BOSTON APPROACH 1

Primary- Respiratory AcidosisIncreased Bicarbs/ 10 mm Hg increase in CO2Acute = 1meq/L; LIMIT = 30; Chronic=4meq/L; LIMIT = 45Primary – Respiratory AlkalosisDecreased bicarbs/ 10mm Hg decrease in CO2Acute = 2meq/L; LIMIT = 18Chronic = 5meq/L; LIMIT = 15

Boston Approach: A Summary for Respiratory DisordersExpected change of HCO3 with PCO2 change

 

Remember!Changes in Chronic are more than in AcuteChanges in Alkalosis (washing out CO2) are more than in Acidosis (CO2 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 – 20pH = 7. 55; expected PaC02 = 55 + 5 = 50 – 60If beyond expected range, there is a mixed disorder.Rule applicable between pH limits of 7.10 – 7.60There is no acute vs chronic for metabolic disorders

Copenhagen ApproachSeparate the respiratory and non respiratory components of HCO3

• Standard HCO3 :

HCO3 at a PaCO2 of 40 mm Hg

• Buffer Base: Total of all buffer anions in bloodwith 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 HCO3 :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 APPROACHQuery

Where is the pH center

?

??

???????

?????

What is the difference?

H+

H+

PCO2

HCO3

PCO2

AtotSID

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-

phosphatealbumin

• 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 AcidsHA H+ + A-

AH + A- = ATOT• Proteins – Albumin, Globulin• PhosphateA- 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 acidosisHowever, 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 ATOT 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:

STRONG CATIONS

STRONG ANIONS

WEAK IONS

SID - 4• Cations (positive ions):

Strong: Na, K, Ca, MgWeak: H

• Anions (negative ions):Strong:

Measured - ChlorideUnmeasured - lactate, acetoacetate, betahydroxybutyrate

Weak: Measured - HCO3 Unmeasured - albumin, inorganic phosphate

Strong Ion Approach - 5

A Schematic view (Gamblegram) :

STRONGNa, K, Ca, Mg

WEAK - H

STRONGMEASURED

Cl

STRONGUNMEASURED

ketoacids, lactate

WEAK MEASURED

HCO3

WEAKUNMEASURED

proteins, phosphorus

ANION GAPSTRONG

ION DIFFERENCE = buffer base

STRONG ION GAP

SID – 6

The “Fitting”

STRONGCATIONS

STRONG ANIONS

H

WEAK ANIONS

SID

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+

Normal SID Increased SIDLess H+ ionisation = ALKALOSIS

Decreased SIDMore H+ ionisation = ACIDOSIS

SID

SID

SID

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 factor2.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 buffers4.Use H+ concentration not pH5. 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 AnalysisConsider 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 / LIn 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 mmolNormal 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 ClOn 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 / LThe 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

1.00.6 2.0

PaCO2 = 40

Atot = 17.2

SID 32 – 42mEq / L

Acidity

Fraction of Normal Value

Bedside Approach Fencl - Stewart partitioning approach

Component due to SIDThe 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 albuminThe 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 ScenarioPatient 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 ApproachUsing 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 = -22On 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: Lactate, ketoacids

increases increases increases

Weak anions:IgA myeloma

increases increases increases

Strong cations: Li reduces reduces reduces

Weak cations: IgG myeloma

reduces reduces reduces

Albumin decrease increase

reducesincreases

no effect no effect

P decrease increase

reducesincreases

reducesincreases

no effect

Ca, Mg decrease increase

increasesreduces

increasesreduces

no effect

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

SIGStrong Ion Gap = SIDa – SIDe

It is:POSITIVE when unmeasured anions > unmeasured cations, NEGATIVE in the unmeasured anions < unmeasured cationsIt 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-

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