Blood gas analysis evaluates gases in blood and acid-base content to diagnose respiratory, circulatory, and metabolic disorders. It is important for monitoring patients on oxygen therapy or intensive care, and those with blood loss, sepsis, or other conditions. Blood gas analysis measures pH, partial pressures of oxygen and carbon dioxide, and calculates bicarbonate and oxygen saturation. Interpreting the values helps establish diagnoses and treatment plans by indicating acid-base and gas exchange status. Disorders are classified as metabolic or respiratory based on the primary pH change. Compensation responses also provide insights.

2. DEFINITION
Blood gas analysis is a commonly used diagnostic tool to evaluate
the partial pressures of gas in blood and acid-base content.
Understanding and use of blood gas analysis enable providers to
interpret respiratory, circulatory, and metabolic disorders.

3. OTHER COMMON NAME
Blood gas test.
Arterial blood gases.
ABG.
Blood gas analysis.

4. AIM
• Important routine investigation to monitor :
The acid-base balance of patients
Effectiveness of gas exchange
• A vital role in monitoring of
Postoperative patients,
Patients receiving oxygen therapy,
Those on intensive support,
Patients with significant blood loss, sepsis, and comorbid conditions
like diabetes, kidney disorders,
Cardiovascular system (CVS) conditions

5. WHY TO ORDER A BLOOD GAS
ANALYSIS?
Aids in establishing diagnosis
Guides treatment plan
Improvement in the management of acid/base; allows for optimal
function of medications
Acid/base status may alter levels of electrolytes critical to the status
of a patient

6. ABG COMPONENTS:
pH = measured acid-base balance of the blood
PaO2 = measured the partial pressure of oxygen
PaCO2 = measured the partial pressure of carbon dioxide
HCO3 = calculated concentration of bicarbonate
Base excess/deficit = calculated relative excess or deficit of base in
blood
SaO2 = calculated arterial oxygen saturation unless a co-oximetry
is obtained, in which case it is measured

7. ACCEPTABLE NORMAL RANGE OF
ABG VALUES
pH (7.35-7.45)
PaO2 (75-100 mmHg)
PaCO2 (35-45 mmHg)
HCO3 (22-26 meq/L)
Base excess/deficit (-4 to +2)
SaO2 (95-100%)

8. ARTERIAL VS VENOUS BLOOD GAS
ANALYSIS

9. VENOUS
Venous blood gases in the assessment of patients in whom acid-base
balance is the only concern (e.g. in diabetic ketoacidosis)
• If the venous sample is obtained :Values compared and interpreted
keeping in consideration.

10. ARTERIO-VENOUS PH DIFFERENCE
IS BETWEEN 0.03-0.04

11. SHOCK AND THE VBG
Venous values will show an increased pCO2 and acidemia due to
increased production by the tissues and impaired removal.
Things that need to be addressed is whether or not the way VBGs are
drawn should be standardized across the hospital so that the values
obtained in the ED match ones drawn on the floor or ICU

12. MEASUREMENT INCLUDED IN ABG
ANALYSIS
Blood gas analysis (BGA) involves measurement of three parameters:
 The amount of free (unbound) oxygen (O2)
 Carbon dioxide (CO2) dissolved in blood,
 The pH (acidity/alkalinity) of blood.
 The partial pressure (p) exerted by the two gases is what is actually measured so
the three measured parameters are:
 pO2, pCO2and pH. A further parameter, bicarbonate (HCO3
-) concentration is
generated during blood gas analysis but this is calculated from pH and pCO2, rather
than directly measured.

13. THE PARTIAL PRESSURE (P) EXERTED BY THE
TWO GASES IS WHAT IS ACTUALLY MEASURED
SO THE THREE MEASURED PARAMETERS ARE:
The partial pressure (p) exerted by the two gases is what is actually
measured so the three measured parameters are:
 pO2, pCO2and pH. A further parameter, bicarbonate (HCO3
-) concentration is
generated during blood gas analysis but this is calculated from pH and pCO2, rather
than directly measured.
 pO2 is used to assess patient oxygenation status; pCO2 is used to assess
ventilation; and pH, pCO2 and HCO3
- results together allow assessment of acid-
base status.
 Another calculated parameter, base excess (BE), is also helpful, although often not
necessary in this regard. Clearly, if the pO2 of arterial blood were the same as
the pO2 of venous blood, then it would be immaterial which sample were used to
assess oxygenation.

17. ERRORS
Allow a steady state after initiation or change in oxygen therapy
before obtaining a sample
 a steady state is reached between 3 and 10 minutes.
 in patients with chronic airway obstruction, it takes about 20-30 minutes.
Always note the percentage of inspired air (FiO2 ) and condition of
the patient
Do not use excess heparin as
 it causes sample dilution
 Excess of heparin may affect the pH.

18. CONTINUE
Avoid air bubbles in syringe.
Avoid delay in sample processing.
 As blood is a living tissue, O2 is being consumed and CO2 is produced in the blood
sample.
 In case of delay, the sample should be placed in ice and such iced samples can be
processed for up to two hours without affecting the blood gas values.
Accidental venous sampling. The venous sample report should not be
discarded and can provide sufficient information.

19. CONDITIONS CAUSING ACID-BASE
IMBALANCE
•Respiratory acidosis
Any condition causing the
accumulation of CO2in the body.
Central nervous system (CNS)
depression due to head injury
Sedation, coma
Chest wall injury, flail chest
Respiratory obstruction/foreign
body
•Respiratory alkalosis
Due to decrease in CO2.
Hyperventilation occurs and
CO2is washed out causing
alkalosis.
Psychological: Anxiety, fear
Pain
Fever, sepsis, pregnancy, severe
anemia.

20. INTERPRETATION
The first step is to look at the pH and assess for the presence of acidemia (pH <
7.35) or alkalemia (pH > 7.45).
If the pH is in the normal range (7.35-7.45), use a pH of 7.40 as a cutoff point.
In other words, a pH of 7.37 would be categorized as acidosis, and a pH of 7.42
would be categorized as alkalemia.
Next, evaluate the respiratory and metabolic components of the ABG results, the
PaCO2 and HCO3, respectively.
The PaCO2 indicates whether the acidosis or alkalemia is primarily from a
respiratory or metabolic acidosis/alkalosis.
PaCO2 > 40 with a pH < 7.4 indicates a respiratory acidosis, while PaCO2 < 40 and
pH > 7.4 indicates a respiratory alkalosis (but is often from hyperventilation from
anxiety or compensation for a metabolic acidosis).
Next, assess for evidence of compensation for the primary acidosis or alkalosis by
looking for the value (PaCO2 or HCO3) that is not consistent with the pH.
Lastly, assess the PaO2 for any abnormalities in oxygenation.

21. CONTINUE
When evaluating a patient's acid-base status, it is important to
include an electrolyte imbalance or anion gap in your synthesis of the
information.
For example: In a patient who presents with Diabetic Ketoacidosis,
they will eliminate ketones, close the anion gap but have persistent
metabolic acidosis due to hyperchloremia. This is due to the strong
ionic effect,

22. STEPS OF INTERPRETATION
Step 1: Anticipate the disorder
keeping in mind the clinical settings and the condition of the patient
e.g., the patient may present with a history of insulin-dependent
diabetes mellitus (IDDM), which may contribute to a metabolic
acidosis
Step 2: Check the pH.
 pH < 7.35: Acidosis
 pH > 7.45: Alkalosis
 pH = 7.40: Normal/mixed disorder/fully compensated disorder
(Note: If mixed disorder, pH indicates stronger component)

23. CONTINUE
Step 3: Check SaO2 /paO2
SaO2 is a more reliable indicator as it depicts the saturation of hemoglobin
in arterial blood.
Note: Always compare the SaO2 with FiO2
The SaO2 could be within normal range but still much less than FiO2 if the
patient is on supplemental oxygen (difference should be less than 10)

24. CONTINUE
Step 4: Check CO2 and HCO3 -(bicarbonate) levels-Identify the
culprit
Is it a respiratory/metabolic/mixed disorder?

25. CONTINUE
Step 5: Check base excess (BE).
Defined as amount of base required to return the pH to a normal
range.
 If it is positive, the metabolic picture is of alkalosis.
 If it is negative, the metabolic picture is of acidosis.
Either of bicarbonate ions/base excess can be used to interpret
metabolic acidosis/alkalosis.

26. INTERPRETATION OF ARTERIAL BLOOD GAS REPORT ON
THE BASIS OF USING BE AS A METABOLIC INDEX

27. EXAMPLE-1
ABG : pH = 7.39, PaCO2 = 51 mm Hg, PaO2 = 59 mm Hg, HCO3 = 30
mEq/L and SaO2 = 90%, on room air.
pH is in the normal range, so use 7.40 as a cutoff point, in which case it is
<7.40, acidosis is present.
The PaCO2 is elevated, indicating respiratory acidosis, and the HCO3 is
elevated, indicating a metabolic alkalosis.
The value consistent with the pH is the PaCO2. Therefore, this is a primary
respiratory acidosis.
The acid-base that is inconsistent with the pH is the HCO3, as it is elevated,
indicating a metabolic alkalosis, so there is compensation signifying a non-
acute primary disorder because it takes days for metabolic compensation to
be effective
Last, the PaO2 is decreased, indicating an abnormality with oxygenation.
However, a history and physical will help delineate the severity and urgency
of required interventions, if any

28. EXAMPLE 2:
ABG : pH = 7.45, PaCO2 = 32 mm Hg, PaO2 = 138 mm Hg, HCO3 = 23
mEq/L, the base deficit = 1 mEq/L, and SaO2 is 92%, on room air.
pH is in the normal range. Using 7.40 as a cutoff point, it is >7.40, so
alkalemia is present.
The PaCO2 is decreased, indicating a respiratory alkalosis, and the HCO3 is
normal but on the low end of normal.
The value consistent with the pH is the PaCO2. Therefore, this is a primary
respiratory alkalosis.
The HCO3 is in the range of normal and, thus, not inconsistent with the pH,
so there is a lack of compensation.
Last, the PaO2 is within the normal range, so there is no abnormality in
oxygenation.

29. EXAMPLE: 3
If pH is 7.21, HCO3-is 14, and CO2is 40.
 CO2 is normal
 HCO3- decreased
A case of metabolic acidosis.
Expected compensation would be a decrease in CO2causing respiratory
alkalosis.
Now consider this table ---

30. EXAMPLE: 4
pH: 7.55, paCO2: 49.0, HCO3 : 48.2
 pH: 7.55 alkalosis
 paCO2: 49.0 increased
 HCO3: 48.2 increased
paCO2 is increased -retention of CO2 causes acidosis
HCO3 is increased -increased base causes alkalosis
 So, the primary disorder is metabolic alkalosis.
CO2 is being retained to compensate for the same-
The pH has still not returned to a normal range.
 So, the interpretation -Partially Compensated Metabolic Alkalosis

31. EXAMPLE 5
pH: 7.34, paCO2 40.3, HCO3 : 20.4.
 The pH is acidic
 paCO2 is normal
 Bicarbonate is decreased.
Primary disorder is metabolic acidosis
but no compensatory response as the paCO2 is normal.
Interpretation -Uncompensated Metabolic Acidosis

32. EXAMPLE 6
pH: 7.52, paCO2 : 31.0, HCO3 : 29.4
 pH is alkalotic
 paCO2 is decreased (alkalosis)
 Bicarbonate is increased (alkalosis).
As the directions of paCO2 and bicarbonate are opposite and both
are causing alkalosis.
The picture is suggestive of a mixed disorder.
•Interpretation -Combined Alkalosis

33. Disorder
Base
Acid

34. DEFINITION
Acid-base disorders are pathologic changes in carbon dioxide partial
pressure (PCO2) or serum bicarbonate (HCO3
−) that typically produce
abnormal arterial pH values.
Acidemia is serum pH < 7.35.
Alkalemia is serum pH > 7.45.

35. CONTINUE
Acidaemia
An arterial pH below the normal range
(pH<7.35).
Alkalaemia
An arterial pH above the normal range
(pH>7.45).
Acidosis
A process lowering pH. This may be
caused by a fall in serum bicarbonate
and/or a rise in the partial pressure of
carbon dioxide (PaCO2). Acidosis refers to
physiologic processes that cause acid
accumulation or alkali loss.
Alkalosis
A process raising pH. This may be caused
by a rise in serum bicarbonate and/or a
fall in PaCO2. Alkalosis refers to
physiologic processes that cause alkali

36. HOW TO UNDERSTAND ACID BASE
PROBLEM
pH
Bicarbonate
PaCO2
Anion gap

37. CLASSIFICATION
Primary acid-base disturbances are defined as metabolic or
respiratory based on clinical context and whether the primary change
in pH is due to an alteration in serum HCO3
− or in PCO2.

38. TYPES OF ACIDOSIS AND
ALKALOSIS
Acidosis and alkalosis are categorized depending on their primary
cause as
Metabolic
Respiratory
Metabolic acidosis and metabolic alkalosis are caused by an
imbalance in the production of acids or bases and their excretion by
the kidneys.
Respiratory acidosis and respiratory alkalosis are caused by changes
in carbon dioxide exhalation due to lung or breathing disorders.
People can have more than one acid-base disorder.

39. CLASSIFICATION, CHARACTERISTICS,
AND COMPENSATION OF SIMPLE ACID–
BASE DISORDERS

40. DISORDERS OF ACID–BASE BALANCE ARE
CLASSIFIED ACCORDING TO THEIR CAUSE, AND
THE DIRECTION OF THE PH CHANGE
Metabolic acidosis
Process that primarily reduces bicarbonate:
Excessive H+ formation e.g. lactic acidosis, ketoacidosis
Reduced H+ excretion e.g. renal failure
Excessive HCO3
- loss e.g. diarrhoea
Metabolic alkalosis
Process that primarily raises bicarbonate:
Extracellular fluid volume loss e.g. due to vomiting or
diuretics
Excessive potassium loss with subsequent
hyperaldosteronism
Respiratory acidosis
Process that primarily causes elevation in PaCO2:
Reduced effective ventilation e.g. many chronic respiratory
diseases or drugs depressing the respiratory centre
Respiratory alkalosis
Process that primarily causes reduction in PaCO2:
Increased ventilation e.g. in response to hypoxia or
secondary to a metabolic acidosis
Acid-base disorders are classified according to whether there is acidosis or alkalosis present and
whether the primary problem is metabolic or respiratory

41. ACID-BASE DISTURBANCES AND
THE BODY'S RESPONSE

42. METABOLIC ACIDOSIS :
IS SERUM HCO3
−< 24 MEQ/L (< 24
MMOL/L)
Metabolic acidosis is primary reduction in bicarbonate (HCO3
−), typically with
compensatory reduction in carbon dioxide partial pressure (PCO2)
pH may be markedly low or slightly subnormal. Metabolic acidoses are
categorized as high or normal anion gap based on the presence or absence
of unmeasured anions in serum.
Causes : Accumulation of ketones and lactic acid, renal failure, and drug or
toxin ingestion (high anion gap) and gastrointestinal or renal HCO3
− loss
(normal anion gap).
Symptoms and signs in severe cases : Include nausea and vomiting, lethargy,
and hyperpnea.
Diagnosis is clinical and with arterial blood gas (ABG) and serum electrolyte
measurement. The cause is treated; IV sodium bicarbonate may be indicated
when pH is very low.

43. CAUSES OFMETABOLIC ACIDOSIS

44. CONTINUE

45. ETIOLOGY
Metabolic acidosis is acid accumulation due to:
 Increased acid production or acid ingestion
 Decreased acid excretion
 Gastrointestinal or renal HCO3
− loss
 Acidemia (arterial pH < 7.35) results when acid load overwhelms respiratory
compensation. Causes are classified by their effect on the anion gap

46. HIGH ANION GAP ACIDOSIS
The most common causes of a high anion gap metabolic acidosis are:
Ketoacidosis
Lactic acidosis
Renal failure
Toxic ingestions

47. KETOACIDOSIS
Ketoacidosis is a common complication of type 1 diabetes mellitus .
Chronic alcohol use disorder ( alcoholic ketoacidosis), undernutrition,
and, to a lesser degree, fasting. In these conditions, the body
converts from glucose metabolism to free fatty acid (FFA)
metabolism; FFAs are converted by the liver into ketoacids,
acetoacetic acid, and beta-hydroxybutyrate (all unmeasured anions).
Ketoacidosis is also a rare manifestation of congenital isovaleric
acidemia or congenital methylmalonic acidemia.

48. DIABETIC KETOACIDOSIS
Diabetic ketoacidosis (DKA) is most common among patients with type 1
diabetes mellitus and develops when insulin levels are insufficient to meet
the body’s basic metabolic requirements
Diabetic ketoacidosis (DKA) is an acute metabolic complication of diabetes
characterized by hyperglycemia, hyperketonemia, and metabolic acidosis.
Hyperglycemia causes an osmotic diuresis with significant fluid and
electrolyte loss.
DKA occurs mostly in type 1 diabetes mellitus. It causes nausea, vomiting,
and abdominal pain and can progress to cerebral edema, coma, and death.
DKA is diagnosed by detection of hyperketonemia and anion gap metabolic
acidosis in the presence of hyperglycemia.

49. LACTIC ACIDOSIS
Lactic acidosis is a high anion gap metabolic acidosis due to elevated
blood lactate. Lactic acidosis results from overproduction of lactate,
decreased metabolism of lactate, or both.
Lactate is a normal by-product of glucose and amino acid
metabolism. There are 2 main types of lactic acidosis:
 Type A lactic acidosis
 Type B lactic acidosis
D-Lactic acidosis (D-lactate encephalopathy) is an unusual form of
lactic acidosis.
Diagnosis requires blood pH < 7.35 and serum lactate levels > 45 to
54 mg/dL (> 5 to 6 mmol/L).

50. RENAL FAILURE
Causes high anion gap acidosis by decreased acid excretion and
decreased HCO3
− reabsorption. Accumulation of sulfates,
phosphates, urate, and hippurate accounts for the high anion gap.

51. TOXIC INGESTIONS
Toxins may have acidic metabolites or trigger lactic
acidosis. Rhabdomyolysis is a rare cause of metabolic acidosis
thought to be due to release of protons and anions directly from
muscle.

52. NORMAL ANION GAP ACIDOSIS
The most common causes of normal anion gap acidosis are
 Gastrointestinal (GI) or renal HCO3
− loss
 Impaired renal acid excretion
Normal anion gap metabolic acidosis is also called hyperchloremic
acidosis because the kidneys reabsorb chloride (Cl−) instead of
reabsorbing HCO3
−.

53. SYMPTOMS AND SIGNS
Symptoms and signs ( Clinical Consequences of Acid-Base Disorders)
are primarily those of the cause. Mild acidemia is itself asymptomatic.
More severe acidemia (pH < 7.10) may cause nausea, vomiting, and
malaise. Symptoms may occur at higher pH if acidosis develops
rapidly.
The most characteristic sign is hyperpnea (long, deep breaths at a
normal rate), reflecting a compensatory increase in alveolar
ventilation; this hyperpnea is not accompanied by a feeling of
dyspnea.
Severe, acute acidemia predisposes to cardiac dysfunction with
hypotension and shock, ventricular arrhythmias, and coma. Chronic
acidemia causes bone demineralization disorders (eg,

54. DIAGNOSIS
Arterial blood gas (ABG) and serum electrolyte measurement
Anion gap and delta gap calculated
Winters formula for calculating compensatory changes
Testing for cause

55. THE CAUSE OF AN ELEVATED ANION GAP MAY BE CLINICALLY OBVIOUS (EG,
HYPOVOLEMIC SHOCK, MISSED HEMODIALYSIS), BUT IF NOT, BLOOD TESTING
SHOULD INCLUDE
BUN (blood urea nitrogen)
Creatinine
Glucose
Lactate
Possible toxins

56. CONTINUE
Calculated serum osmolarity (2
[sodium] + [glucose]/18 + BUN/2.8 + blood alcohol/5, based on
conventional units) is subtracted from measured osmolarity.
A difference > 10 implies the presence of an osmotically active
substance, which, in the case of a high anion gap acidosis, is
methanol or ethylene glycol. Although ingestion of ethanol may cause
an osmolar gap and a mild acidosis, it should never be considered the
sole cause of a significant metabolic acidosis
If the anion gap is normal and no cause is obvious (eg, marked
diarrhea), urinary electrolytes are measured and the urinary anion gap
is calculated as [sodium] + [potassium] – [chloride]. A normal urinary
anion gap (including in patients with gastrointestinal losses) is 30 to
50 mEq/L (30 to 50 mmol/L) ; an elevation suggests renal HCO3
− loss

57. CONTINUE
In addition, when metabolic acidosis is present, a delta gap is
calculated to identify concomitant metabolic alkalosis, and Winters
formula is applied to determine whether respiratory compensation is
appropriate or reflects a second acid-base disorder.