The document discusses arterial blood gas analysis and interpretation. It provides an overview of gas exchange, acid-base homeostasis, and the basics of acid-base balance. It describes how to interpret an arterial blood gas report, including how to diagnose acid-base disorders and examples. Technical aspects like sampling technique and potential errors or complications are covered. Compensation mechanisms in response to primary acid-base disturbances are explained.

1. ARTERIAL BLOOD GAS ANALYSIS
AND ITS INTERPRETATION
PRESENTED BY :
Dr. PRATAP SINGH CHAUHAN
RMO II YEAR
Dept. of Medicine
NSCB,MCH,Jabalpur

2. Overview of the
discussion
• ABG Sampling , Technical Errors and Complications
• Gas Exchange
• Regulation of acid-base homeostasis
• Basics of acid-base balance and Interpretation of ABG
• Step-wise approach in diagnosis of acid-base disorders
• Examples

3. Indications for performing an ABG
analysis
• To document respiratory failure and assess its severity.
• To assess acid base imbalance, oxygenation status and
the oxygen carrying capacity of blood in critical illness.
• To monitor patients on ventilators and assist in
weaning.
• To assess response to therapeutic interventions and
mechanical ventilation .

4. Why an ABG instead of Pulse
oximetry?
• Pulse oximetry does not assess ventilation (PaCO2)
or acid base status.
• Pulse oximetry becomes unreliable when saturations
fall below 70-80%.
• Technical sources of error (hypoperfusion, nail polish,
skin pigmentation)
• Pulse oximetry cannot interpret methemoglobin or
carboxyhemoglobin.

5. ABG Sampling ,Technical Errors and Complications
Site
Procedure
Pre analytical Error
 Complication
 Contraindication

6. Site & Procedure - RadialArtery (Ideally)
BrachialArtery
FemoralArtery
 Perform a modified allen’s test
 Pre-heparinised ABG syringes :
- Syringe should be FLUSHED with 0.5ml of
1:1000 Heparin solution and emptied.
DO NOT LEAVE EXCESSIVE HEPARIN IN
THE SYRINGE
HEPARIN DILUTIONAL
EFFECT
HCO3
PCO2
 Only small 0.5ml Heparin for flushing and discard it
 Syringes must have > 50% blood. Use only 2ml or less syringe
 Use Lignocaine

7.  AIR BUBBLES
1. PO2 150 mmHg & PCO2 0 mm Hg in air bubble
2. Mixing with sample lead to  PaO2 &  PaCO2
DELAYED ANALYSIS
• Consumption of O2 & Production of CO2 continues
after blood drawn into syringe
• Iced Sample maintains values for 1-2 hours
• Uniced sample quickly becomes invalid
PaCO2  3-10 mmHg/hour
PaO2  at a rate related to initial value & dependant on Hb Sat

8. • Complications :
1. Bleeding or bruising at the puncture site
2. Infection at the puncture site
3. Accmulation of blood under the skin
4. Feeling faint
• Contraindications :
1. Inadequate collateral circulation at the puncture site
2. Surgical shunt
3. Peripheral vascular disease distant to puncture site
4. Coagulopathy

9. Parameter 37 C (Change
every 10 min)
UNICED
4 C (Change
every 10 min)
ICED
 pH 0.01 0.001
 PCO2 1 mm Hg 0.1 mm Hg
EFFECT OF TEMPERATURE ON RATE OF
CHANGE IN ABG VALUES :

10. Gas exchange

11. Understanding Arterial Blood Gases
• PaCO2 & its determinants
• PaO2 & its determinants
• The determinants of the PAO2 and PaO2 (Alveolar
gas equation)
• PaO2/FiO2 ratio

12. Determinants of PaC02
• PaC02 is based on the production of CO2 (VC02) and on
alveolar Ventilation (VA)
• Alveolar Ventilation (VA) is defined as minute ventilation (VE)
minus dead space ventilation (VD)
• PaC02 = VC02 x 0.86 or VC02 x 0.86
VA VE – VD
• The decrease in (VA) may be due to a decrease in minute
ventilation (VE) or an increase in dead space ventilation (VD)
since VA = VE-VD
• PaC02 increases with increased production of C02
– Hypermetabolism , malignant hyperthermia, high
carbohydrate diet

13. • Examples of an inadequate minute ventilation (VE)
leading to hypercapnia include
• Sedative Drug Overdose
• Respiratory muscle paralysis
• Central hypoventilation
• Examples of increased dead space ventilation (VD)
leading to hypercapnia include
• COPD
• Severe restrictive lung disease with rapid shallow
breathing

14. Determination of PaO2
2PaO is dependant upon Age, FiO ,P2 atm
As Age the expected PaO2
• PaO2 = 109 - 0.4 (Age)
As FiO2 the expected PaO2
• Alveolar Gas Equation:
• PAO2= (PB-P h2o) x FiO2- pCO2/R
O
X
Y
G
E
N
A
T
I
O
N
A 2 BP O = partial pressure of oxygen in alveolargas, P = barometric pressure
(760mmHg), Ph2o = water vapor pressure (47 mm Hg), FiO2 = fraction of
inspired oxygen, PCO2 = partial pressure of CO2 in the ABG, R = respiratory
quotient (0.8)

15. Determination of the PaO2 / FiO2 ratio
Inspired Air FiO2 = 21%
PiO2 = 150 mmHg
PalvO2 = 100 mmHg
PaO2 = 90 mmHg
O2CO2
(along with other criteria)

16. PaO2/ FiO2 ratio( P:F Ratio )
 Gives understanding that the patients
OXYGENATION with respect to OXYGEN delivered
is more important than simply the PaO2 value.
Example,
Patient 1
On RoomAir
Patient 2
On MV
PaO2 60 90
FiO2 21% (0.21) 50% (0.50)
P:F
Ratio
285 180

17. Hypoxemia
o Normal PaO2 : 80 – 100 mm Hg
o Mild Hypoxemia : PaO2 60 – 79 mm Hg
o Moderate Hypoxemia : PaO2 40 – 59 mm Hg
o Severe Hypoxemia : PaO2 < 40 mm Hg

18. BASICS OF ACID-BASE
. pH – signifies free hydrogen ion concentration. pH is inversely
related to H+ ion concentration.
• Acid – a substance that can donate H+ ion, i.e. lowers pH.
• Base – a substance that can accept H+ ion, i.e. raises pH.
• Anion – an ion with negative charge.
• Cation – an ion with positive charge.
• Acidemia – blood pH< 7.35 with increased H+ concentration.
• Alkalemia – blood pH>7.45 with decreased H+ concentration.
• Acidosis – Abnormal process or disease which reduces pH due to
increase in acid or decrease in alkali.
• Alkalosis – Abnormal process or disease which increases pH due
to decrease in acid or increase in alkali.

19. Normal Values
Variable Normal Range
pH 7.35 - 7.45
H+ 35-45 nmol/Lt
pCO2 35-45 mm Hg
Bicarbonate 22-26 mmol/Lt
Anion gap 8-10 mmol/Lt
PaO2 80 - 100 mm Hg
SaO2 93 - 98%
Base excess -2.0 to 2.0 mEq/L

20. Regulation of acid base balance
Renal regulatory
responses
Respiratory
regulatory
responses
Chemical
Buffers

21. Buffers
• Buffers are chemical systems which either
release or accept H+ and minimize change in
pH induced by an acid or base load.
• First line of defense blunting the changes in
[H+]
• A buffer pair consists of: A base (H+ acceptor)
& An acid (H+ donor)
• Extracellular and Intracellular Buffer.

22. Intracellular Buffers
1. Proteins
2. Haemoglobin
3. Phosphate
Extracellular Buffers
1. Proteins
2. Bicarbonate
CO2 + H2O
carbonic anhydrase
H2CO3 H+ + HCO3
-
BUFFERS

23.  Respiratory Regulation of Acid Base
balance- (Second line of defense)
H+ PaCO2
H+ PaCO2
ALVEOLAR
VENTILATION
ALVEOLAR
VENTILATION

24. Renal Regulation
Kidneys control the acid-base balance by
excreting either a basic or an acidic urine
• Excretion of HCO3
-
• Regeneration of HCO3
-
with excretion of H+

25. Excretion of excess H+ & generation of new
HCO3
- : The Ammonia Buffer System
GLUTAMINE
HCO3
- NH3REABSORBED NH3 + H+ NH4
+
EXCRETED

26. Abnormal Values
pH < 7.35
• Acidosis (metabolic
and/or respiratory)
pH > 7.45
• Alkalosis (metabolic
and/or respiratory)
paCO2 > 45 mm Hg
• Respiratory acidosis
(alveolar hypoventilation)
paCO2 < 35 mm Hg
• Respiratory alkalosis
(alveolar hyperventilation)
HCO3
- < 22 meq/L
• Metabolic acidosis
HCO3
- > 26 meq/L
• Metabolic alkalosis

27. Simple Acid Base Disorder/ Primary Acid Base
disorder – a single primary process of acidosis or
alkalosis due to an initial change in PCO2 and HCO3.
Compensation - The normal response of
the respiratory system or kidneys to change in pH
induced by a primary acid-base disorder
 The Compensatory responses to a primary Acid Base
disturbance are never enough to correct the change in
pH , they only act to reduce the severity.
Mixed Acid Base Disorder – Presence of more than
one acid base disorder simultaneously .

28. •Metabolic
DisorderHCO3
•Respiratory
DisorderPaCO2
During compensation HCO3¯ & PaCO2 move in
the same direction

29. Characteristics of Primary ACID
BASE Disorders
PRIMARY
DISORDER
PRIMARY RESPONSES COMPENSATORY
RESPONSESH+ ion pH Primary
Conc. Defect
Metabolic
Acidosis H+ pH HCO3
PCO2
Alveolar Hyperventilation
Metabolic
Alkalosis H+ pH HCO3
PCO2
Alveolar
Hypoventilation
Respiratory
Acidosis H+ pH PCO2 HCO3
Respiratory
Alkalosis H+ pH PCO2 HCO3

30. Compensatory changes (Metabolic disorders)
Primary
disorder
Primary
defect
Compensatory
response
Expected Compensation
Metabolic
acidosis
↓ HCO3 ↓ PCO2 PCO2=1.5[HCO3] + 8 ± 2
PCO2= PaCO2 will ↓ 1.25 mmHg per mmol/L ↓ in
HCO3
PCO2= 15+ [HCO3]
Metabolic
Alkalosis
↑ HCO3 ↑ PCO2 PCO2=1.5[HCO3] + 8 ± 2
PCO2= PaCO2 will ↑ 0.75 mmHg per mmol/L↑
in HCO3
PCO2=15+ [HCO3]

31. Compensatory changes (Respiratory disorders)
Primary
disorder
Primary
defect
Compensatory
response
Expected Compensation
Respiratory
acidosis
↑ PCO2 ↑ HCO3 Acute:
HCO3 will ↑ + 1 Meq/L for each10mmHg ↑ in
PCO2
Chronic:
+4 Meq/L ↑ HCO3 for each ↑ PCO2 of 10mmHg
Respiratory
Alkalosis
↓ PCO2 ↓ HCO3 Acute:
-2Meq/l ↓ in HCO3 for each ↓ in PCO2 of
10mmHg
Chronic:
-4 Meq/L ↓ in HCO3 for each ↓ in PCO2 of
10mmHg

32. METABOLIC ACIDOSIS
Deficit in HCO3
- and decreased pH
ACID
(CO2)
BASE
(HCO3)
RESPIRATORY
COMPONENT
METABOLIC COMPONENT
7.8
7.4
7.0

33. Classification of Metabolic Acidosis
 High Anion gap Metabolic Acidosis
– Lactic Acidosis
– Ketoacidosis (Diabetes, Alcohol, Starvation)
– Renal Failure
– Toxic Ingestion
• Salicylates, Methanol, Ethylene Glycol, Paraldehyde, INH
 Non- anion gap (Hyperchloremic metabolic Acidosis)
– GI loss of HCO3 (Diarrhoea,Ureteral Diversion)
– Renal Loss of HCO3(Carbonic Anhydrase inhibitor)
– Renal Tubular Disease
– Drug induced Hyperkalemia (with Renal insufficiency)
– Acid Loads (ammonium chloride , hyperalimentation)

35. Clinical sign and symptoms
• Kussmaul’s Respirations – deep and rapid breathing
• Lethargy, confusion, headache, weakness
• Nausea and Vomiting
• Arrhythmias
• Suppressed myocardial contractility
• Right shift of the oxyhemoglobin dissociation curve
• Hyperkalemia
• Increased protein catabolism
• Insulin resistance

36. Treatment of Met Acidosis
 Rx Underlying Cause
 HCO3- Therapy
• Aim to bring up pH to 7.2 & HCO3-  10 meq/L
• Qty of HCO3 administration calculated:
0.2 x weight (kg) x HCO3 Deficit (meq/L)
•Most recommendations favour use of base when pH
< 7.15-7.2 or HCO3 < 8-10 meq/L.

37. Adverse Effects of HCO3- Therapy
•  CO2 production from HCO3 decomposition 
Hypercarbia especially when pulmonary ventilation is
impaired.
• Myocardial Hypercarbia  Myocardial acidosis
Impaired myocardial contractility &  C.O.
 SVR and Coronary A perfusion pressure 
Myocardial Ischemia especially in pts with HF.
• Hypernatremia & Hyperosmolarity  Vol expansion 
Fluid overload especially in pts with HF.
• Intracellular (paradoxical) acidosis especially in liver &
CNS ( CSF CO2).
• Stimulation of Phosphofructokinase activity enhances
lactate production and worsens acidosis.

38. METABOLIC ALKALOSIS
Primarily due to Increased HCO3
- , increased pH
ACID
(CO2)
BASE
(HCO3
)
RESPIRATORY COMPONENT METABOLIC COMPONENT
7.
0
7.
4
7.
8

39. Metabolic Alkalosis
Etiology pH > 7.45, HCO3
- > 26 Meq/l
 Exogenous HCO3
- loads (Milk Alkali Syndrome)
 Acid loss ( Vomiting, Gastric Aspiration)
 Diuretics,Cushing’s Disease, Bartter’s syndrome
 Primary Hyperaldosteronism
 Liddle’s Syndrome
 Low K+ and Mg2+

40.  Symptoms
– Mental Confusion, obtundation, seizure
– Aggravation of Arrhythmias, dizziness
– Paresthesia, numbness, tingling of extremities
– Tetany
 Treatment
– Correct the primary cause of disorder
– Correct the deficiency which impairing renal HCO3
Excretion (give Chloride, water and k+)
– Expand ECF Volume
– Acetazolamide
– Supportive Measure

41. RESPIRATORY ACIDOSIS
ACID
(CO2)
BASE
(HCO3
)RESPIRATORY
COMPONENT
METABOLIC
COMPONENT
7.8
7.4
7.0

42. RESPIRATORY ACIDOSIS
H2O + CO2  H2CO3  H+ + HCO3
-
Cause - hypoventilation
Retention of CO2
Drives equation rightward
Increases both [H+] and [HCO3
-]

43. Respiratory Acidosis
Etiology pH < 7.35, PaCO2 > 45mm Hg
• Central ( Drug, Stroke Infection)
• Airways ( Obstruction, Asthma)
• Parenchyma (Emphysema, Bronchitis ,ARDS ,Barotrauma )
• Neuromuscular (Poliomyelitis , Myasthenia, Muscular
Dystrophies )
• Miscellaneous (Obesity, Hypoventilation, Permissive
Hypercapnia )

44. • Sign and Symptoms
– Dyspnea, Confusion, Psychosis, Disorientation or
coma
– Impairment of Coordination , Sleep Disturbance
– Dysrhythmia
– Hyperkalemia or Hypoxemia
• Treatment
– Treat underlying cause
– Support ventilation
– Correct electrolyte imbalance
– IV Sodium Bicarbonate

45. RESPIRATORY ALKALOSIS
H2O + CO2  H2CO3  H+ + HCO3-
cause - hyperventilation
Blows off CO2
Drives equation leftward decreasing both [H+] and [HCO3
-]

46. RESPIRATORY ALKALOSIS
ACID
(CO2)
BASE
(HCO3)
7.
0
7.
4
7.
8
RESPIRATORY
COMPONENT
METABOLIC
COMPONENT

47. Respiratory Alkalosis
Etiology pH > 7.45, PaCO2 < 35mm Hg
 Central Nervous System Stimulation (Pain, Anxiety ,
Psychosis, Tumor, Trauma, Meningitis ,Encephalitis )
 Hypoxemia or Tissue Hypoxia ( High altitude, pneumonia
Pulmonary edema, Aspiration, severe Anemia )
 Drugs or Hormones (Progesterone, Salicylates)
 Stimulation of Chest Receptor (Flail Chest, Hemothorax )
 Miscellaneous (Septicemia, Hepatic Failure, recovery from
Metabolic Acidosis, Mechanical Hyperventilation )

48.  Symptoms
• Tachypnea
• Complaints of SOB, chest pain
• Light-headedness, syncope, coma, seizures
• Numbness and tingling of extremities
• Difficult concentrating, tremors, blurred vision
• Weakness, paresthesias, tetany
 Treatment
• Monitor Vital Signs and ABG’s
• Treat underlying disease
• Assist the patient to breathe more slowly
• Help the patient to breath in a paper bag
• Sedation

49. Mixed Disorder
Clues to the presence of a mixed disorder.
• Clinical history
• pH normal, abnormal PCO2 and HCO3
• PCO2 and HCO3 moving opposite directions
• Acid Base map (Flenley Nomogram)
• Degree of compensation for primary disorder is
inappropriate
• Find Delta Gap

50. STEP WISE APPROACH
to
Interpretation Of
ABG reports

51. 1. HISTORY AND PHYSICAL EXAMINATION
• Its gives an idea of what acid base disorder
might be present even before collecting the
Arterial Blood Gas sample
e.g. Diarrhoea  Bicarbonate loss  pH 
Metabolic Acidosis

52. 2.Look at the pH
 pH < 7.35 : Acidosis
 pH > 7.45 : Alkalosis
 pH 7.35 – 7.45 : Normal/Mixed Disorder
 Look at the pO2 (<80 mm Hg) and O2
saturation (<90%) for hypoxemia

53. 3. Look at pCO2 and HCO3
-
 pCO2 > 45 mm Hg : Increased (Acidosis)
 pCO2 < 35 mm Hg : Decreased (Alkalosis)
 HCO3
- > 26 mEq/L : Increased (Alkalosis)
 HCO3
- < 22 mEq/L : Decreased (Acidosis)

54. 4.Determine the Primary acid-base disorder
 IS PRIMARY DISTURBANCE RESPIRATORY OR
METABOLIC
 If the pH is low (acidosis), then look to see ↑ CO2 or ↓ HCO3
(which ever is acidosis will be primary)
 If the pH is high (alkalosis), then look to see ↓ CO2 or ↑ HCO3
(which ever is alkalosis is the primary).
 pH ↑ HCO3
- ↑ or pH ↓ HCO3
- ↓ METABOLIC
 pH ↑ PCO2 ↓ or pH ↓ PCO2 ↑ RESPIRATORY

55. • If trend of change in paCO2 and HCO3
- is the
same, check the percentage difference . The one
with greater % difference , between the two is
the one that is the dominant disorder
• Example pH= 7.25, HCO3
- =16, paCO2 =60
here pH is acidotic and both paCO2 and HCO3
- explain its
acidosis : so look at difference
% difference = (24-16)/24 = 0.33
% difference = (60-40)/40 = 0.50
Therefore, Respiratory acidosis as the dominant disorder

56. IF RESPIRATORY, IS IT ACUTE OR CHRONIC?
 Acute respiratory disorder -∆pH(e-acute) = 0.008x ∆pCO2
 Chronic respiratory disorder - ∆pH(e-chronic)= 0.003x ∆pCO2
 Compare, pHmeasured (pHm) v/s pHexpected (pHe)
pH(m) = pH(e- acute)
pH(m) =
between pH(e- acute) &
pH(e- chronic)
pH(m) = pH(e-chronic)
ACUTE RESPIRATORY
DISORDER
PARTIALLY COMPENSATED CHRONIC RESPIRATORY
DISORDER

57. 5. Compensation
Is the compensation adequate??
 METABOLIC DISORDER  PCO2 expected
• PCO2measured ≠ PCO2expected  MIXED
DISORDER
 RESPIRATORY DISORDER  HCO3 expected
• HCO3m ≠ HCO3e range  MIXED DISORDER

58. 6. If Metabolic Acidosis then Calculate
Anion Gap
 Total Serum Cations = Total Serum Anions
 M cations + U cations = M anions + U anions
 Na + (K + Ca + Mg) = HCO3 + Cl + (PO4 + SO4
+ Protein + Organic Acids)
 Na + UC = HCO3 + Cl + UA
 But in Blood, there is a relative abundance of Anions. hence
Anions > Cations
 Na – (HCO3 + Cl) = UA – UC
 Na - (HCO3 + Cl) = Anion Gap
 AG= Na⁺ – (Cl¯ + HCO3¯)
 Normal range is 10 ± 2 mEq /L
 It represents unmeasured anions. These unmeasured anions can be;
– Anionic proteins
– SO4, PO4, organic anions
– Acid anions (acetoacetate, lactate, uremic anions)

59. Anion gap may increase due to:
 Increase in the unmeasured anions(0rganic,
inorganic, exogenous and unidentified anion)
 Decrease in the unmeasured cations
(hypocalcimia, hypomagnesimia)
Anion gap may decrease due to:
 Increase in unmeasured cations (Ca, Mg, K)
 Addition of abnormal cations (Li)
 Decrease in albumin ( each 1g/dl decrease of
albumin decreases AG by 2.5 mEq/L)
 Hyperviscosity and severe Hyperlipidaemia
(underestimation of chloride and Na conc.)

60.  Osmolar Gap
• The Osmolar gap is used to detect the presence of ingested toxins
such as ethylene glycol, methanol or isopropyl alcohol
• These Toxins often cause an increased AG acidosis. The Osmolar gap
is the difference between the measured osmolality and the
calculated osmolality
• The calculated osmolality is determined by 2*[Na] + Serum
Glucose/18 + BUN/2.8
• An Osmolar gap >15mOsm suggests the presence of an ingested toxin
as a contributor to the anion gap acidosis
 Urinary Anion Gap
Used to differentiate between Renal and Extra-renal cause of
normal anion gap metabolic acidosis
It Represent unmeasured Anion in Urine like Sulfate,phosphate
Indirect estimation of Urinary Ammonium Excretion
Urinary Anion Gap = UNa + Uk-Ucl
Normal Value -10 to +10

61. 7. CO EXISTANT METABOLIC DISORDER
 HGAG METABOLIC ACIDOSIS,ANOTHER DISORDER?
 ∆ Anion Gap = Measured AG – Normal AG
Measured AG – 10
 ∆ HCO3 = Normal HCO3 – Measured HCO3
24 – Measured HCO3
 Ideally ∆Anion Gap = ∆HCO3
 For each 1 meq/L increase in AG, HCO3 will fall by 1 meq/L
∆AG/  HCO3
- = 1-2  Pure anion gap metabolic acidosis
 AG/ HCO3
- > 2  High anion gap acidosis with concurrent
metabolic alkalosis
 AG/ HCO3
- < 1  High anion gap & normal AG acidosis
Delta ratio =∆AG/ ∆HCO3
= (observed AG-10)/ (24- obs HCO3)

63. Acid-Base Normogram

64. EXAMPLEs

65. Case 1
 A 19 year old pregnant insulin dependent diabetic
patient was admitted with a history of polyuria and
thirst. She now felt ill and presented to hospital. There
was a history of poor compliance with medical therapy.
She was afebrile. Chest was clear. Circulation was
adequate. Urinalysis: 2+ ketones, 4+ glucose.
• Na+ 136, K+ 4.8, Cl- 101, pH 7.26, pCO2 16.5 mmHg,
pO2 128 mmHg, HCO3 7.1 mmol/l ,AG 28.1
• Describe its Acid Base Disorder.

66. • Clinical possibilities:
– Diabetic ketoacidosis
• Look at the pH: 7.26
• Then find the primary disorder: Low HCO3 along
with low pCO2 suggests a
METABOLIC disorder.
ACIDOSIS

67. • Check for compensation: compensation for
metabolic acidosis brings pCO2 to 16.5-20.6 mmHg.
PCO₂ = (1.5 ×HCO3 ) + 8 ±2) Thus the acidosis is
by respiratory regulation and there is
• Anion Gap= 136+4.8-(101+7.1)=32.7
• ∆AG=32.7-12=20.7, ∆HCO3=24-7.1=16.9
• Delta ratio=20.7/16.9=1.22
• ∆AG/  HCO3
- = 1-2  Pure anion gap metabolic
acidosis
• FINAL ABG DIAGNOSIS
PURE ANION GAP METABOLIC
ACIDOSIS (Etiology, DKA)
PURE ANION GAP
ACIDOSIS
HIGH ANION
GAP acidosis
NO MIXED disorder.
FULLY COMPENSATED

68. Case 2
 A known case of chronic kidney disease, discontinued
Maintenance Hemodialysis & presented to the emergency in an
altered state of sensorium. Attendants gave history of repeated
episodes of vomiting at home. Describe its Acid Base Disorder.
ABG results
pH 7.42
PCO₂ 40
HCO₃ 25
Na 140
K 3.0
Cl 95
AG 23

69. • Clinical possibilities:
– Uremia  Metabolic Acidosis
– Vomiting  Metabolic Alkalosis
• Look at the pH: 7.42
• Then find the primary disorder: HCO3 along with
pCO2 are WNL So it is
NORMAL/MIXED DISORDER
NORMAL

70. • Anion Gap= 140+3-(95+25)= 23
• ∆AG=23-12=11, ∆HCO3=24-25= 1
• Delta ratio= 11/ 1=11
• ∆AG/  HCO3
- = 11  High anion gap acidosis with
concurrent metabolic alkalosis
• FINAL ABG DIAGNOSIS
HIGH ANION GAP METABOLIC
ACIDOSIS WITH METABOLIC
ALKALOSIS
HIGH ANION GAP
MIXED disorder.

71. REFERENCES
• Rao SM, Nagendranath V. Arterial Blood Gas Monitoring:
Indian J Anaesth. 2002;46:289-97
• Marino PL. Arterial Blood Gas Interpretation 3rd edi.
• Harrison’s Principles of Internal Medicine, 19th edition,
Chap 66 – Acidosis and Alkalosis
• Guyton and Hall – Textbook of Medical Physiology, 12th
edition
• Davenport – The ABC of Acid Base Chemistry, 6th edition
• Cohen and Kassirer – Acid Base
• Hansen JE, Clinics in Chest medicine10(2), 1989, 227-37
• Williams AJ. ABC of oxygen: assessing and interpreting
arterial blood gases and acid base
balance.BMJ1998;317:1213-6