Arterial Blood Gas

Analysis …..1
SAMIR EL ANSARY
ICU PROFESSOR
AIN SHAMS
CAIRO
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 Existing approaches to acid No click

base balance:

Henderson-Hasselbalch Equation
Copenhagen approach
Boston approach
Stewart approach

To provide Bedside approach to

ABG analysis
Copenhagen approach
No click

Acid-base disorders are classified as

being of
Respiratory origin
(primary change in pCO2)
or of
Metabolic origin
(primary change in fixed acids)
 No click

Copenhagen approach
•Respiratory disorders are quantified by
pCO2

•Metabolic disorders are quantified by the

amount of excess fixed acids (the ‘metabolic
acids’)
Often there may be more than one type involved.
It is difficult to predict which one it is and it is not feasible to
measure all of them.
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Copenhagen approach

The magnitude of the metabolic

disorder (in the ECF)
can be quantified indirectly by
the amount of change in the
[HCO3]
 No click

Boston Approach

This approach is based on actual whole body

titrations rather than on blood samples in a
machine.

The aim has been to determine the magnitude

of the compensation that occurs to graded
degrees of acid-base disturbance.
 Stewart’s physicochemical
approach 1970

• Henderson–Hasselbalch equation fails to

consider all the factors influencing
hydrogen ion concentration

• And is insufficient to explain complex

metabolic abnormalities of acid–base
physiology
 Stewart’s physicochemical
approach 1970

Based on 3 principles:
• Electrochemical neutrality
• Conservation of mass
• Law of mass action
Stewart Equation

pH is dependent on other ions in solution not

just H+ and HCO3-
- There are dependent and independent variables :
Dependent:
-H+ - OH- - HCO3- - CO32-
Independent:
-PaCO2
Total of weak non-volatile acids
SID {Strong Ion Difference }
 A strong ion = an ion that totally
dissociates at a given pH
SID = strong cations – strong anions

SID = (Na+ + K+ + Ca2+ +Mg2+) – (Cl- -

other anions)

Modified SID
(Na+ + K+) – Cl-
 Henderson-Hasselbalch No click

Equation
The starting point is the Henderson
Equation

Based on application of law of mass

action on reaction of CO2 with
water

[H+] x [HCO3-] = K x [CO2] x [H2O]

Hasselbalch modified No click

Henderson's elegant idea

Regarding the water concentration as

constant and taking logarithms of the
remaining components.
This resulted in the Henderson-Hasselbalch
Equation:

pH = pK + log ( [HCO3-] / [CO2] )

 No click

Kassirer-Bleich equation

H+ = 24 × Pco2/HCO3 −

This equation illustrates that acid-base balance

depends on the ratio of Pco2 and HCO3 −
Not on the absolute value of either one alone.
 ABG Interpretation
1. Is patient acidemic or alkalemic?
2. Is primary disorder respiratory or
metabolic?
3. If respiratory, is it acute or chronic?
4. If metabolic acidosis is there an anion
gap? is there an osmolar gap?
 ABG Interpretation
5. Is there appropriate compensation?
if no, what is the second disorder?

6. IN THE SETTING OF AG
METABOLIC ACIDOSIS, is there
another problem? what is the delta gap?
 Are the data consistent?

The Henderson Equation

[ H ] = 24 × HCO
+ PaCO2
−
3
 Convert [H+] to pH
• Subtract calculated [H+] from 80; this gives the last
two digits of a pH beginning with 7
• example: calculated [H+] of 24 converts to pH
of (80-24)~7.56

• example: calculated [H+] of 53 converts to pH

of (80-53)~7.27
• Refer to table for more precise conversion, or if
Calculated [H+] exceeds 80
Relationship between [H+] & pH

pH [H+] pH [H+]
7.80 16 7.30 50
7.75 18 7.25 56
7.70 20 7.20 63
7.65 22 7.15 71
7.60 25 7.10 79
7.55 28 7.00 89
7.50 32 6.95 100
7.45 35 6.90 112
7.40 40 6.85 141
7.35 45 6.80 159
 HCO3 (bicarbonate)
-

SB (standard bicarbonate)
AB (actual bicarbonate)

SB
The contents of HCO3- of serum of arterial
blood
{ at 37℃, PaCO2 40mmHg, SaO2 100%.}

Normal: 22-27mmol/L
Mean: 24mmol/L
 AB
The contents of HCO3- in actual
condition.

In normal person
AB=SB
 AB and SB are parameters to
reflect
metabolism, regulated by kidney

Difference of AB-SB can reflect the

respiratory affection on serum HCO3-
Respiratory acidosis: AB > SB
Respiratory alkalosis: AB < SB

Metabolic acidosis
AB ＝ SB < Normal

Metabolic alkalosis
AB = SB > Normal
 Base Excess

∆base to normalise HCO3 (to 24)

with PaCO2 at 40 mm Hg
Buffer bases （ BB)
Buffer base is a measure of the concentration of all the
buffers present in either plasma or blood.

HCO3-
Hemoglobin
Plasma proteins
HPO42- (phosphate)
Buffer bases （ BB)

Normal: 45-55mmol/L
mean: 50mmol/L
Significance
Metabolic acidosis: BB
Metabolic alkalosis: BB
 Regulation of Acid-basic
Balance
Chemical buffer
Dielectric changes of incells and
excells
H+---K+ HCO3- ---Cl-
Physiology regulation through

lung and kidney

Classification of Acid-basic
Disorder
Complementary: PH is
normal
Dis-complementary: PH is
abnormal.
 Oxygenation parameters

PaO2
Normal: 95-100mmHg
PaO2=100mmHg - (age×0.33)
±5mmHg
Hypoxia
Mild: 80-60mmHg
MODERATE
60-40mmHg
Severe: <40mmHg
 SaO2
0.95-0.98
Not sensitive
PaCO2
35-45mmHg (4.7-6.0kPa)
Mean:
 PA-aO2
Gas exchange
Normal: 15-20mmHg
(<30mmHg in the old)

CaO2
19-21 mmol/L
 PvO2
Mixed venous oxygen pressure
35-45mmHg
Mean: 40mmHg
Significance
Pa-vO2 is to reflect the tissue absorbing oxygen
Oxygenation
Indices
O2 Content of blood:
Hb. x O2 Sat + Dissolved O2
(Don’t forget hemoglobin)

Oxygen Saturation: reported as ABG report

( Derived from oxygen dis. curve
not a measured value )

Alveolar / arterial gradient:

( Useful … to classify respiratory failure )
 Normal arterio/venous difference No click

0 10 20 30 40 50 60 70 80 90 100 PaO2

100

80 Rt. Shift Oxygen delivered

to tissues
with normally placed curve
60
Delivered oxygen
with Rt. Shift curve
40

Normal
20

Shift of the curve ……changes saturation for a given PaO2

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Alveolar-arterial Difference
Inspired O2 = 21 %
piO2 = (760-45) x . 21 = 150 mmHg

palvO2 = piO2 – pCO2 / RQ

O2 = 150 – 40 / 0.8
CO2 = 150 – 50 = 100 mm Hg

PaO2 = 90 mmHg

One click and wait

palvO2 – partO2 = 10 mmHg
 Alveolar- arterial Difference No click

Oxygenation Failure Ventilation Failure

WIDE GAP NORMAL GAP
piO2 = 150 piO2 = 150
pCO2 = 40
pCO2 = 80
palvO2= 150 – 40/.8
palvO2= 150-80/.8
=150-50
O2 =150-100
=100 CO2 = 50
PaO2 = 45 PaO2 = 45
 = 100 - 45 = 55  = 50 - 45 = 5
PAO2 (partial pres. of O2. in the alveolus.)
760 – 45 = 715 : 21 % of 715 = 150 = 150 - ( PaCO2 / .8 )
 No click

Expected PaO2
Normal situation

FiO2 × 5 = PaO2

20 × 5 = 100
 No click

The essentials
The Blood Gas
Report: normals…

pH 7.40 + 0.05
PaCO 2 40 + 5 mm
HCO3 Hg
PaO 2 80 - 100 mm Hg

HCO 3 24 + 4 mmol/L

O2 Sat >95
Always mention and see
The
No click

5
Steps for
Successful
Blood Gas
Analysis
Step 1
Look at the pH
Is the patient acidemic pH < 7.40
or alkalemic pH > 7.40

Step 2
Who is responsible for this change in pH ( culprit )?
 CO 2 will change pH in opposite direction
 Bicarb. will change pH in same direction
Acidemia: With HCO 3 < 24 mmol/L = metabolic
With PCO 2 >40 mm hg = respiratory

Alkalemia: With HCO 3 >24 mmol/L = metabolic

With PCO 2 <40 mm Hg = respiratory
Step 3
If there is a primary respiratory
disturbance, is it acute ?

10 mm
Change = .08 change in pH ( Acute )
.03 change in pH ( Chronic )
PaCO2
 Three clicks

pH HYPER VENTILATION

PaCO2
BICARB CHANGES
pH in same direction

Compensation

Bicarbonate

Low Primary lesion

Alkali
METABOLIC ACIDOSIS
 Three clicks

pH HYPO VENTILATION

PaCO2

BICARB CHANGES
pH in same direction
Compensation

Bicarbonate

High
Primary lesion
Alkali METABOLIC ALKALOSIS
 Three clicks
Wait for red circle
pH
CO 2 CHANGES
pH in opposite direction

BICARB

compensation
PaCO 2

High
CO2 Primary lesion Respiratory acidosis
 Three clicks
Wait for red circle
pH PaCO 2 CHANGES
pH in opposite direction

BICARB

compensation

PaCO 2

Primary lesion
Low
PaCO2 Respiratory alkalosis
Step 4 : Degree of compensation
Primary disorder Formula
Metabolic acidosis ↓PCO2 = 1.2 x ↓[HCO3-]
Metabolic alkalosis ↑PCO2 = 0.7 x ↑[HCO3-]
Respiratory acidosis
Acute ↑[HCO3-] = 0.1 x ↑PCO2
Chronic ↑[HCO3-] = 0.4 x ↑PCO2
Respiratory alkalosis
Acute ↓[HCO3-] = 0.2 x ↓ PCO2
Chronic ↓[HCO3-] = 0.5 x ↓ PCO2
Suspect if .............
actual PaCO 2 is more than
expected : additional …
respiratory acidosis

actual PaCO 2 is less than

expected : additional …respiratory
alkalosis
Step 4 : cont.
If there is metabolic acidosis, is there a wide anion gap ?

- -
Na - (Cl + HCO 3 ) = Anion Gap usually < 12

If >12, Anion Gap Acidosis :

M ethanol
U remia
Common pediatric D iabetic Ketoacidosis
causes P araldehyde
1) Lactic acidosis I nfection (lactic acid)
2) Metabolic E thylene Glycol
disorders S alicylate
3) Renal failure
Step 4: Which type?
• Check anion gap (AG): If AG is high
• High AG metabolic acidosis is present
• If metabolic acidosis is diagnosed:
Check ↑AG / ↓[HCO3-]
• <1 : High AG Met. Acid + normal AG Met. Acid.
• 1-2 : High AG Met. Acid
• >2 : High AG Met. Acid. + Met. Alk.
• If metabolic acidosis is not diagnosed:
• High AG Met. Acid. + Met. Alk.
Metabolic acidosis and the anion gap
1. Normal gap 2. Increased gap

2. GI “HCO3” 1. ↑ Acid prod

losses 2. ↓ Acid elimination
1. Renal “HCO3”
losses

Lactate Renal disease

DKA
Proximal RTA Diarrhea Ketosis
Distal RTA Toxins
Alcohols
Salicylates
Iron
 No click

5 th step

Clinical correlation
 No click
Same direction
HCO3 pH META.
Same direction

PaCO2 pH RESP.

Opposite direction
PaCO of 10
2 pH

Acute change .08

Chronic change .03

Compensation No click

Considered complete
when the pH returns
to normal range
COMPENSATION LIMITS
METABLIC ACIDOSIS
PaCO2 = Down to 10 ?

METABOLIC ALKALOSIS
PaCO2 = Maximum 6O

RESPIRATORY ACIDOSIS
BICARB = Maximum 40

RESPIRATORY ALKALOSIS
BICARB = Down to 10
 Case 1
Blood Gas Report
o 16 year old female with
Measured 37.0 C
pH 7.523 sudden onset of dyspnea.
PaCO2 30.1 mm Hg
PaO2 105.3 mm Hg No Cough or Chest Pain
Calculated Data
HCO3 act 22 mmol / L Vitals normal but RR 56,
O2 Sat 98.3 % anxious.
PO2 (A - a) 8 mm Hg ∆
PO2 (a / A) 0.93

Entered Data Acute respiratory alkalosis

FiO2 21.0 % And why acute ?
Case 2 Five clicks
6 year old male with progressive respiratory distress
Muscular dystrophy .
pH <7.35 :acidemia
Blood Gas Report
o Res. Acidemia : High PaCO2 and low pH
Measured 37.0 C
pH 7.301  CO2 =76-40=36
PaCO2 76.2 mm Hg Expected  pH for ( Acute ) = .08 for 10
PaO2 45.5 mm Hg Expected ( Acute ) pH = 7.40 - 0.29=7.11

Calculated Data Chronic resp. acidosis

HCO3 act 35.1 mmol / L

O2 Sat 78 %
PO2 (A - a) 9.5 mm Hg ∆
PO2 (a / A) 0.83

Entered Data
FiO2 21 %
Chronic respiratory acidosis
Hypoxemia
Normal A-a gradient With hypoxia due to hypoventilation
Hypoventilation
8-year-old male asthmatic with resp. distress Six clicks

Case 3
pH <7.35 ; acidemia

PaCO28-year-old
>45; respiratory acidemia
male asthmatic;
3 -days
 CO2 = 49 40 = 9of cough, dyspnea
Expectedand
 pH orthopnea
( Acute ) = 9/10not
x 0.08 = 0.072
Expectedresponding to usual
pH ( Acute ) = 7.40 - 0.072 = 7.328
Acute resp. acidosis
bronchodilators.
WITH INCREASE IN CO2 BICARB MUST RISE ?
30 × = 150 O/E:
5Bicarbonate Respiratory distress;
is low………
suprasternal
Metabolic acidosis andacidosis
+ respiratory
intercostal retraction;
tired looking; on 4 L NC.
Hypoxia
piO2 = 715x.3=214.5 / palvO2 = 214-49/.8=153 Wide A / a gradient
Case 4 8 year old diabetic with respi. distress fatigue and loss of appetite.
Three clicks

pH <7.35 ; acidemia
Blood Gas Report

Measured
o
37.0 C Last two digits of pH
pH 7.23 Correspond with co2
PaCO2 23 mm Hg
PaO2 110.5 mm Hg
Calculated Data
HCO3 act 14 mmol / L
HCO3 <22; metabolic acidemia
O2 Sat %
PO2 (A - a) mm Hg ∆
PO2 (a / A)
If Na = 130,
Entered Data Cl = 90
FiO2 21.0 %
Anion Gap = 130 - (90 + 14)
= 130 – 104 = 26
Case 5 : 10 year old child with encephalitis
Four clicks

Blood Gas Report

Measured
o
37.0 C pH almost within normal range
pH 7.46 Mild alkalosis
PaCO2 28.1 mm Hg
PaO2 55.3 mm Hg PaCO2 is low , respiratory
Calculated Data low by around 10
HCO3 act 19.2 mmol / L ( Acute ) by .08
(Chronic ) by .03
O2 Sat %
PO2 (A - a) mm Hg ∆ Bicarb looks low ?
PO2 (a / A) Is it expected ?
Entered Data
FiO2 24.0 %

BICARBINATURIA
Case #6:
• A 4 year old with chronic renal failure
presents to the pedes ER with history of
increasing azotemia, weakness, and
lethargy.
• Exam reveals the patient to be modestly
hypertensive, and tachypneic. Labs reveal
BUN=100, and Creatinine=8.
• How can we tell if an acid-base disorder is
present?
Case #6:
• Steps 1&2: must know pH, PaCO2, HCO3
• pH=7.37, PaCO2=22, and HCO3=12
• Step 3: are the available data consistent?

[ H ] = 24 × HCO
+ PaCO2
−
3
Case #6:
• [H+]=44, equates to pH~7.36; data are
thus consistent
• What is the primary disorder?
• “_________Acidosis”
• Which variable (PaCO2, HCO3) is
deranged in a direction consistent with
acidosis?
• Primary disorder is “Metabolic Acidosis”
Is compensation appropriate?
• HCO3 is decreased by 12 mmoles/l
• PaCO2 should decrease by 1 to 1.5 times the
fall in HCO3; expect PaCO2 to decrease by
12-18 mm Hg or be between 22-28 mm Hg
• Since PaCO2 is 22 mm Hg, compensation is
appropriate, and the data are consistent with
a simple metabolic acidosis with respiratory
compensation
• If the data are consistent with a simple disorder,
it does not guarantee that a simple disorder
exists; need to examine the patient’s history

• When compensatory responses do not lie within

the accepted range, by definition a
combined disorder exists.
Case #7:

• A 15 year old female is brought to the

pedes ER in an obtunded state.

• Per her family, patient history is

notable for progressive weakness over
two months.
Case #7:

• A recent “complete physical”

demonstrated decreased DTRs
symmetrically, without other
abnormal findings.
• Exam shows shallow, tachypneic
respiratory effort.
Case #7: Steps 1, 2, and 3
• What baseline information is required?
• PaCO2=40 mm Hg, HCO3=7, pH=6.88
• Are the data internally consistent?

[ H ] = 24 × HCO
+ PaCO2
−
3
Case #7:

• [H+]~140, which equates to a pH~6.85, so

data are internally consistent
• What is the primary disturbance?
• “___________ Acidosis”
• Which variable is deranged in a direction
which is consistent with acidosis?
• PaCO2 WNL, “Metabolic Acidosis”
 Is compensation appropriate?
• Metabolic Acidosis
• PaCO2 should fall by 1 to 1.5 mm Hg x the fall
in plasma [HCO3]
• HCO3 decreased by 17, so we expect PaCO2
to be decreased by 17-26
• PaCO2 WNL; since PaCO2 inappropriately
high, there is a combined metabolic acidosis
and respiratory acidosis
Case #8:
• A 16 year old male with sickle cell
anemia, hemochromatosis, & subsequent
cirrhosis, presents with a several day
history of emesis.
• At presentation to the pedes ER, he is
hypotensive, orthostatic, and confused.
• What acid-base disorders might be
anticipated based on the above
information?
Case #8:

• 16 yo male with sickle cell anemia, hemo-

chromatosis, & subsequent cirrhosis, and
several days of emesis. In the pedes ER,
he is hypotensive, orthostatic, and
confused.
• Emesis-loss of H+ (HCl)-metabolic
alkalosis
Case #8:

• Orthostatic hypotension-?

• lactic acidosis
Case #8:

• SCD-decreased O2 delivery-?

• Lactic acidosis
Case #8:

• Cirrhosis

Decreased lactate metabolism

Case #8:
• What baseline information is available?
• pH=7.55, PaCO2=66
• ‘lytes: Na+=166, K+=3.0, Cl-=90, HCO3=56
• Are the data internally consistent?

[ H ] = 24 × HCO
+ PaCO2
−
3
Case #8:
• [H+]~28, equates to pH~7.55; consistent
• What is the primary abnormality?
• “_________ Alkalosis”
• PaCO2↑ed, HCO3 ↑ed, therefore…….
• “Metabolic Alkalosis” presumed due to
emesis
• Is compensation appropriate?
Case #8:
• Metabolic Alkalosis
• PaCO2 should rise by .25 to 1 mm Hg x the
rise in plasma [HCO3]
• HCO3 ↑ed by 32; PaCO2 should ↑ by 8-32
• PaCO2 ↑ed by 26, so compensation
appears appropriate
• What about multiple risk factors for
lactic acidosis?
Case #8:
• Could there be a concealed lactic acidosis?
• What is the anion gap?
• Na+- (Cl- + HCO3), normally 12-14
• Anion gap here is 166 - (90 + 56) = 20
∀ ↑ed anion gap implies metabolic acidosis
• Combined metabolic alkalosis & metabolic
acidosis therefore present
• Always calculate the anion gap
• Often it is the only sign of an occult
metabolic acidosis

IN

• Acidotic patients partially treated

with HCO3
• Acidotic patients with emesis
• Always calculate the anion gap

May be the only sign of metabolic

acidosis “concealed” by concomitant
acid-base disorders
Occult metabolic acidosis post-Rx:

Normal Ketoacidosis Post-RX

Na+ 140 140 148
Cl- 105 105 98
HCO3 25 10 25
ketones 0 15 15
AG 10 25 25
pH 7.40 7.30 7.40
PaCO2 40 31 40
Causes of Anion Gap Acidosis
• Endogenous acidosis
• Uremia (uncleared organic acids)
• Ketoacidosis, Lactic acidosis (increased
organic acid production), Rhabdomyolosis
• Exogenous acidosis
• Ingestions: salicylate, iron; paraldehyde
use
• Other Ingestions
• Methanol toxicity, Ethylene Glycol toxicity
Anion Gap:
Based on the concept of
electroneutrality

Available cations
=
Available anions
Anion Gap:
UA-UC
Anion Gap

Na - (Cl +HCO3-)
+ -

12 to 14
Anion Gap:

Serum albumin
contributes ~1/2 of the
total anion “UA” pool
Anion Gap:

1gm/dl in serum
albumin
Anion gap by
3 mEq/L
Anion Gap:

• Therefore an anion gap of

12 mEq/L is corrected to
17-18 mEq/L when the
serum albumin is half of
normal
 Case #9:

• A 3 year old is brought to the pedes

ER at ~3am, stuporous and
tachypneic. History is remarkable
for his parents having cleaned out
their medicine cabinet earlier that
day.
Case #9:

• An ABG and electrolytes have

been

• Accidentally drawn
by the nurse.
Case #9:
• Available data: pH=7.53, PaCO2=12;
Na+=140, K+=3.0, Cl-=106, HCO3=10
• Are the data internally consistent?

[H ] +
= 24 ×
PaCO2
HCO3−
Case #9:
• [H+]~29, so pH~7.51; data consistent
• What is the primary disturbance?
• “__________ Alkalosis”
• Which variable (PaCO2, HCO3) is deranged
in a direction consistent with alkalosis?
∀ ↓ed PaCO2, ↓ed HCO3; so “Respiratory
Alkalosis”
Case #9:
• Is compensation appropriate?
• Acute respiratory alkalosis
• Plasma [HCO3] should fall by ~1-3
mmole/l for each 10 mm Hg decrement in
PaCO2, usually not to less than 18 mmoles/l
• PaCO2 ↓ed by ~30 mm Hg; HCO3 should fall
by 3-9 mmole/l; HCO3 ↓ is too great, so
superimposed metabolic acidosis
 Case #9:
• What is the anion gap?
• 140 - (106 + 10) = 24; elevated anion
gap consistent with metabolic acidosis
• What is the differential diagnosis?
• Combined (true) respiratory alkalosis
and metabolic acidosis seen in sepsis,
or salicylate intoxication
 Case #10:
• A 5 year old with Bartter’s Syndrome is
brought to clinic, where she collapsed.
• She has recently been febrile, but
history is otherwise unremarkable.

• pH=6.9, PaCO2=81; Na+=142, K+=2.8, Cl-

=87, HCO3=16
Case #10:
• Are the data consistent?

[H ] +
= 24 ×
PaCO2
HCO3−

• [H+]=122, pH~6.9; data are consistent

Case #10:
• What is the primary disturbance?
• “_________ Acidosis”
• Which variable (PaCO2, HCO3) is
deranged in a direction consistent with
acidosis?
• Both; pick most abnormal value--
• “Respiratory Acidosis”
• Is compensation appropriate?
 Case #10:
• Acute Respiratory Acidosis
• Plasma [HCO3] should rise by ~1mmole/ for each
10 mm Hg increment in PaCO2
• Since HCO3 is inappropriately depressed,
compensation is not appropriate, and there is
a concomitant metabolic acidosis as well
• What is the anion gap?
• AG=39, confirms metabolic acidosis
 Case #10:
• Combined Respiratory Acidosis and
Metabolic Acidosis; are there other disorders
present?
• What about the dx of Bartter’s Syndrome?
• Bartter’s Syndrome characterized by
hypokalemic metabolic alkalosis
• Does this patient have a concealed metabolic
alkalosis?
 Case #10:
• Anion gap is 39, or 25-27 greater than
normal
• Typically, increases in anion gap correlate
with decreases in HCO3
• Assuming a 1:1 relationship, as anion gap
increases by 25, HCO3 should fall by 25
• Starting HCO3 must have been 16 + 25 = 41
 Case #10:
• Therefore, starting HCO3 was ~41 mmol/l,
consistent with expected chronic metabolic
alkalosis.

• This metabolic alkalosis was “concealed” by

the supervening profound metabolic and
respiratory acidoses
Case #10:

• Final diagnosis

Metabolic alkalosis, metabolic

acidosis, & respiratory acidosis
Rule

Mixed Acid-Base Disorders

Coexistant metabolic acidosis and

metabolic alkalosis may occur.
Always check the change in the anion gap
vs. decrement in bicarbonate to rule out
a concealed metabolic disorder.
Delta Ratio

• The increase in Anion Gap /

the decrease in HCO3-

• Indicates what has happen to

the denominator (HCO3-)
Delta Ratio

• Used in RAGMA to see whether

change in HCO3- is appropriate
• Normal value = 1 to 1.5

• If normal there is only one pathology

(uncomplicated RAGMA)
Delta Ratio

• Interpretation
• < 0.4 - hyperchloraemic normal anion
gap acidosis
• 0.4 - 0.8 - consider combined high AG &
normal AG acidosis
• BUT note that the ratio is often < 1 in
acidosis associated with renal failure
Delta Ratio

• 1 – 2 - usual for uncomplicated high-AG

acidosis (lactic acidosis: average value 1.6
) { DKA: around 1 }
• > 2 - a high delta ratio an elevated
bicarbonate at onset of the metabolic
acidosis pre-existing metabolic
alkalosis or compensated respiratory
acidosis.
 Case #11:
• A 3 year old toddler is brought to the ER at 3
am after being found unarousable on his
bedroom floor, with urinary incontinence,
bradycardiac.
• One amp of D50W and 0.1 mg of naloxone
were given IV without response.
• Vital signs are stable; respiratory effort is
regular, but tachypneic.
• He is acyanotic.
 Case #11:
• Initial lab studies (lytes, ABG & urine tox
screen) are sent. Initial dextrostick is >800.
• Initial available data are:
• Na+=154, K=5.6, Cl=106, HCO3=5, BUN=6
creatinine=1.7, glucose=804, PO4=12.3, Ca+
+
=9.8, NH4=160, serum osms=517
• pH=6.80, PaCO2=33, PaO2=298
 Case #11:
• What is the primary disturbance?
• ________ Acidosis
• Metabolic Acidosis
• Is compensation appropriate?
• No; PaCO2 level is inappropriately high
• Are other disorders present?
• Respiratory acidosis (due to evolving coma)
 Case #11:
• What is our differential thus far?
• Anion gap vs. non-anion gap metabolic acidosis
• DKA, lactic acidosis, renal failure, ingestion
• The urine tox screen comes back negative
• What does urine tox screen actually screen for?
• The patient’s IV falls out.
• He then has a seizure, is incontinent of urine.
Case #11:

• What is the calculated serum osmolality,

and does an osmolal gap exist?
• 2(Na) + BUN/2.8 + Glucose/18
• Calculated=355, Measured=517
• What is the most likely diagnosis?
• How can this be confirmed definitively?
• Review of urinanalysis
• Serum ethylene glycol level
Case #11:
Methanol, ethylene glycol
ethyl alcohol, isopropyl alcohol

Anion gap metabolic

acidosis

Osmolal gap
You CAN have a respiratory problem and
a metabolic problem (and even a secondary
metabolic problem on top of that)

look at delta gap

Anion gap delta versus Bicarb delta
 Normally in AG Met Acidosis
the number of anions above 14 should
equal the number of bicarb below 24

(Calculated anion gap - 14) versus (24 -

measured HCO3)
If Bicarb delta is less than the Anion
gap delta

Metabolic alkalosis as well

 If Bicarb delta is more than the
Anion gap delta

Non AG metabolic acidosis as well

 Most common AG met acidosis:
ketoacidosis, lactic acidosis, ASA
(IF ruled out investigate toxic alcohols)

ASA not only results in AG met

acidosis but also Resp alkalosis
A low glucose does not rule
out ketoacidosis
Look out for starvation, dehydration,
alcohol
 Consider cyanide and carbon
monoxide in inhalation and burn
victims

Don’t be fooled by normal Osat and

PaO2 - Carbon monoxide needs
Carboxyhemoglobin
Isoniazid antidote is vit b6...think
about it in refractory seizures (esp
high risk TB populations)

Reduced arterial-venous oxygen sat

difference (<10%) suggests cyanide
toxicity

Cyanide antidote is induced

methemaglobinemia
Ethylene glycol or methanol antidote
is etoh or Fomepizole

Ethylene glycol in urine will

fluoresce using a Wood’s lamp

Calcium oxalate crystals in urine are

sign of possible ethylene glycol
ingestion
 Most common loss of bicarb
by GI {Diarrhea}

or kidneys
{ Tubular acidosis or renal failure }
Metabolic Alkalosis - Saline
Responsive
Either loss of H+ or contraction (volume contraction
around constant HCO3)

Urine Cl <10
Gastric suction
Vomiting
Diuretics
Give Saline, gets better
Metabolic Alkalosis - Non Saline
Responsive
Retention of HCO3 associated with
mineralcorticoid excess
Urine Cl >20
Hyper aldosteronism
Exogenous steroids
Adenocarcinomoa
Bartter’s syndrome
Cushing’s syndrome
 When to calculate what ?

RAGMA
{Raised anion gap metabolic acidosis }

look for lactate, calculate Delta ratio,

Stewart Equation
 When to calculate what ?
NAGMA
{Normal anion gap metabolic acidosis }

Calculate Urinary anion gap

Stewart Equation
Osmolar gap
 Osmolar Gap
The osmolality is measured in lab

Calculated osmolarity
(2 x [Na+]) + [glucose]/18 + [urea]/2.8

Osmolality {from lab.} – Osmolarity {calculated}

An osmolar gap > 10 mOsm/l is often stated to
be abnormal
 Osmolar Gap
Significance
Indirect evidence for the presence of an
abnormal solute which is present in significant
amounts.

Ethanol, methanol & ethylene glycol -> will

cause an elevated osmolar gap.
 Urinary Anion Gap {UAG}
[Na+]+ [K+] - [Cl-]
Clinical Use
Differentiate between GIT and renal
causes of a hyperchloraemic metabolic
acidosis
 Blood Gas values { High altitudes }
The decreased PaO2 causes us to increase our
minute ventilation resulting in a lower PaCO 2.

In order that pH remain within normal limits,

the kidneys excrete HCO3- to compensate for
the low PaCO2

So ABG values are slightly different than

textbook sea level values
 In a code situation

The pH may be very low, i.e. < 7.00

Since both a metabolic acidemia
(anaerobic metabolism, lactic acidemia)

And a respiratory acidemia (inadequate

ventilation) will be causing the pH to fall.
 No click

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 Remember that COPD patients may
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SAMIR EL ANSARY
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