Arterial blood gas Biochemistry U. Satyanaryana U. Chakrapani

1. ARTERIAL
BLOOD GAS

2. Content
BlOOD GAS ANALYSIS
ARTERIAL BLOOD GAS
COMPONENTS OF ARTERIAL BLOOD GAS
WHY ABG IS DONE
HOW ABG IS DONE
• Puncture sites
• Equipments
• Procedure
• Complications
ACID – BASE DISORDERS

3. BLOOD GAS ANALYSIS
• Our blood cells transports oxygen and carbon dioxide throughout the body in order to
carry out various metabolic activities .These are known as blood gases.
• 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.
• A blood gas analysis can be performed on blood obtained from anywhere in the
circulatory system (artery, vein, or capillary).
• Estimation of blood gases from arterial blood Arterial blood gas analysis [ABG]
• Estimation of blood gases from venous blood Venous blood gas analysis [VBG]

4. ARTERIAL BLOOD GAS
Arterial blood gases (ABG), a clinical test that involves measurement of the pH of arterial blood
and the amount of oxygen and carbon dioxide dissolved in arterial blood, is routinely used in the
diagnosis and monitoring of predominantly critically/acutely ill patients being cared for in
emergency rooms and intensive care units. Additionally, ABG is useful in delivery of clinical care
to some patients with acute and chronic respiratory disease in medical wards and outpatient
departments.
In broad terms the test allows assessment of two related physiological functions:-
• The facility of the lungs to simultaneously add oxygen to blood and remove carbon dioxide from
blood (the dual process called pulmonary gas exchange)
• The ability of the body to maintain the pH of blood within narrow healthy limits (acid-base
balance).

5. Imbalances in the oxygen, carbon dioxide, and pH levels of your blood can
indicate the presence of certain medical conditions. These may include:-
• Kidney failure
• Heart failure
• Uncontrolled diabetes
• Hemorrhage
• Chemical poisoning
• Drug overdose
• Shock etc.

6. COMPONENTS MEASURED IN ABG
Partial pressure of oxygen (PaO2).
• This measures the pressure of oxygen dissolved in the blood and how well oxygen is able
to move from the airspace of the lungs into the blood.
Partial pressure of carbon dioxide (PaCO2).
• This measures the pressure of carbon dioxide dissolved in the blood and how well carbon
dioxide is able to move out of the body.

7. pH.
• The pH measures hydrogen ions (H+) in blood. The pH of blood is usually between 7.35 and
7.45. A pH of less than 7.0 is called acid and a pH greater than 7.0 is called basic (alkaline).
So blood is slightly basic.
Bicarbonate (HCO3
-).
• Bicarbonate is a chemical (buffer) that keeps the pH of blood from becoming too acidic or
too basic.
Oxygen content (O2CT) and oxygen saturation (O2 Sat) values.
• O2 content measures the amount of oxygen in the blood. Oxygen saturation measures how
much of the hemoglobin in the red blood cells is carrying oxygen (O2).

8. WHY ABG IS DONE
Check for severe breathing problems and lung diseases, such as asthma, cystic fibrosis,
or chronic obstructive pulmonary disease (COPD).
See how well treatment for lung diseases is working.
Find out if you need extra oxygen or help with breathing (mechanical ventilation).
Find out if you are getting the right amount of oxygen when you are using oxygen in the
hospital.
Measure the acid-base level in the blood of people who have heart failure, kidney failure,
uncontrolled diabetes, sleep disorders, or severe infections or who have had a drug
overdose.

9. A sample of blood from an artery
is usually taken from the inside of
the wrist (radial artery). But it can
also be taken from an artery in
the groin (femoral artery) or on
the inside of the arm above the
elbow crease (brachial artery).

10. EQUIPMENTS
• 2ml heparinized syringe (23g needle)
• Gauze
• Gloves
• Alcohol wipe
• Mask
• Cotton Tape
• Local anaesthetia [usually avoided]
• If you are on oxygen therapy, the oxygen may be turned off for 20 minutes before the blood test. This is called
a room air test . But if you can't breathe without the oxygen, the oxygen won't be turned off.
ABG SYRINGE

11. PROCEDURE
• Position the patient’s arm preferably on a
pillow for comfort with the wrist extended
(20-30°)
• Wear gloves and Clean the site with an
alcohol wipe for 30 seconds and allow to
dry before proceeding
• Palpate the radial artery with your non-
dominant hand’s index finger around 1cm
proximal to the planned puncture site
(avoiding directly touching the planned
puncture site that you have just cleaned)

12. • Holding the ABG syringe like a dart insert
the ABG needle through the skin at an
angle of 45° over the point of maximal
radial artery pulsation (which you
identified during palpation)
• Advance the needle into the radial artery
until you observe blood flashback into the
ABG syringe
• The syringe should then begin to self-fill
in a pulsatile manner (do not pull back the
syringe plunger)

13. • Once the required amount of blood has been
collected remove the needle and apply immediate
firm pressure over the puncture site with some gauze
• Engage the needle safety guard.
• Remove the ABG needle from the syringe and discard
safely into a sharps bin.
• Place a cap onto the ABG syringe and label the
sample.
• Dress the puncture site.
• During the collection of arterial blood, air bubbles in
the syringe need to be expelled immediately to avoid
bias on the results. Expel air bubbles from a blood
gas sample by gently tapping on the side of the
syringe to bring the air bubbles to the top. Then expel
them by pressing the plunger.

14. COMPLICATIONS
Arterial blood sampling is a relatively safe procedure with a low risk of
complications. Some complications that may occur as a result of arterial blood
sampling include:-
▪ Bleeding from the arterial puncture site
▪ Bruising at the site of sample collection
▪ Infection
▪ Pain and tenderness around the site of sample collection
▪ Swelling the site of sample collection.
▪ Nerve damage

15. Take the ABG sample to be analysed
as soon as possible after being
taken as delays longer than 10
minutes can affect the accuracy of
results.

16. NORMAL VALUES
REFERENCE RANGE OF ABG
PARAMETER NON-SI UNITS SI UNITS
pH 7.35 – 7.45 7.35 – 7.45
[H+] 35 – 43 mEq /L 35 – 43 mmol/L
pCO2 35 – 45 mm Hg 4.5 – 6.0 kPa
pO2 85 – 100 mm Hg 10.5 – 13.5 kPa
HCO3
- 22 – 26 mEq /L 22 – 26 mmol/L

18. ACID-BASE DISORDERS
▪ For a better understanding of the disorders of acid-base balance, the
Henderson-Hasselbalch equation must be frequently consulted.
▪ It is evident from the above equation that the blood pH (H+ ion concentration) is
dependent on the relative concentration (ratio) of bicarbonate (HCO3
-) and
carbonic acid (H2CO3
-).

19. ACID-BASE DISORDERS
The acid-base disorders are mainly classified as
 Acidosis—a decline in blood pH
• Metabolic acidosis—due to a decrease in bicarbonate.
• Respiratory acidosis—due to an increase in carbonic acid.
 Alkalosis—a rise in blood pH
• Metabolic alkalosis—due to an increase in bicarbonate.
• Respiratory alkalosis—due to a decrease in carbonic acid.

20. ANION GAP
• For a better understanding of acid-base disorders, adequate knowledge of anion gap is
essential. The total concentration of cations and anions (expressed as mEq/l) is equal in
the body fluids. This is required to maintain electrical neutrality.
• Anion gap is defined as the difference between the total concentration of measured
cations (Na+ and K+) and that of measured anion (Cl- and HCO3
- ). The anion gap (A-) in
fact represents the unmeasured anions in the plasma which may be calculated as
follows, by substituting the normal concentration of electrolytes (mEq/l).
Na+ + K+ = Cl- + HCO3 - + A–
136 + 4 = 100 + 25 + A-
A- = 15 mEq/l
• The anion gap in a healthy individual is around 15 mEq/l (range 8-18 mEq/l).
• Acid-base disorders are often associated with alterations in the anion gap

21. METABOLIC ACIDOSIS
• The primary defect in metabolic acidosis is a reduction in bicarbonate concentration
which leads to a fall in blood pH . The bicarbonate concentration may be decreased
due to its utilization in buffering H+ ions, loss in urine or gastrointestinal tract or failure
to be regenerated. The most important cause of metabolic acidosis is due to an
excessive production of organic acids which combine with NaHCO3
- and deplete the
alkali reserve.
NaHCO3
- + Organic acids Na salts of organic acids + CO2
• Metabolic acidosis is commonly seen in severe uncontrolled diabetes mellitus which is
associated with excessive production of acetoacetic acid and E-hydroxybutyric acid
(both are organic acids).

22. • Anion gap and metabolic acidosis : Increased production and accumulation of
organic acids causes an elevation in the anion gap. This type of picture is seen in
metabolic acidosis associated with diabetes (ketoacidosis).
COMPENSATION
• The acute metabolic acidosis is usually compensated by hyperventilation of lungs.
This leads to an increased elimination of CO2 from the body (hence H2CO ) but
respiratory compensation is only short-lived. Renal compensation sets in within 3-
4 days and the H+ ions are excreted as NH4
+ ions.

23. RESPIRATORY ACIDOSIS
• The primary defect in respiratory acidosis is due to a retention of CO2 (H2CO3 ).
There may be several causes for respiratory acidosis which include depression of the
respiratory centre (overdose of drugs), pulmonary disorders (bronchopneumonia)
and breathing air with high content of CO2.
COMPENSATION
• The renal mechanism comes for the rescue to compensate respiratory acidosis.
More HCO3
- is generated and retained by the kidneys which adds up to the alkali
reserve of the body. The excretion of titratable acidity and NH4
+ is elevated in urine

24. METABOLIC ALKALOSIS
• The primary abnormality in metabolic alkalosis is an increase in HCO3-
concentration. This may occur due to excessive vomiting (resulting in loss of H+)
or an excessive intake of sodium bicarbonate for therapeutic purposes (e.g.
control of gastric acidity). Cushing’s syndrome (hypersecretion of aldosterone)
causes increased retention of Na+ and loss of K+ from the body. Metabolic
alkalosis is commonly associated with low K+ concentration (hypokalemia). In
severe K+ deficiency, H+ ions are retained inside the cells to replace missing K+
ions. In the renal tubular cells, H+ ions are exchanged (instead of K+) with the
reabsorbed Na+. Paradoxically, the patient excretes acid urine despite alkalosis
COMPENSATION
• The respiratory mechanism initiates the compensation by hypoventilation to
retain CO2 (hence H2CO3 ). This is slowly taken over by renal mechanism which
excretes more HCO3 - and retains H+.

25. RESPIRATORY ALKALOSIS
• The primary abnormality in respiratory alkalosis is a decrease in H2CO3
concentration. This may occur due to prolonged hyperventilation resulting in
increased exhalation of CO2 by the lungs. Hyperventilation is observed in
conditions such as hysteria, hypoxia, raised intracranial pressure, excessive
artificial ventilation and the action of certain drugs (salicylate) that stimulate
respiratory centre.
COMPENSATION
• The renal mechanism tries to compensate by increasing the urinary excretion of
HCO3
-

28. MIXED ACID-BASE DISORDER
• Sometimes, the patient may have two or more acid-base disturbances occurring
simultaneously. In such instances, both HCO3
- and H2CO3 are altered. In general,
if the biochemical data (of blood gas analysis) cannot be explained by a specific
acid-base disorder, it is assumed that a mixed disturbance is occurring.
• Many a times, compensatory mechanisms may lead to mixed acid-base disorders

29. ACID-BASE DISORDER AND PLASMA POTASSIUM
Plasma potassium concentration (normal 3.5-5.0 mEq /l) is very important as it
affects the contractility of the heart. Hyperkalemia (high plasma K+) or
hypokalemia (low plasma K+) can be life-threatening. The relevance of
potassium balance in certain acid-base disorders is discussed briefly.
▪ Potassium and diabetic ketoacidosis : The hormone insulin increases K+
uptake by cells (particularly from skeletal muscle). The patient of severe
uncontrolled diabetes (i.e. with metabolic acidosis) is usually with hypokalemia.
When such a patient is given insulin, it stimulates K+ entry into cells. The result
is that plasma K+ level is further depleted. Hypokalemia affects heart
functioning, and is life threatening. Therefore, in the treatment of diabetic
ketoacidosis, potassium has to be given (unless the patients have high plasma
K+ concentration).

30. • Potassium and alkalosis : Low plasma concentration of K+ (hypokalemia)
leads to an increased excretion of hydrogen ions, and thus may cause metabolic
alkalosis. Conversely ,metabolic alkalosis is associated with increased renal
excretion of K+. In view of the importance discussed above, the measurement of
plasma K+ concentration assumes significance in the acid-base disorders. In
cases of these disorders associated with hypokalemia, potassium
supplementation (with careful monitoring of plasma K+) needs to be considered.

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PREPARED BY :- BURHAN JAVAID