ARTERIAL BLOOD GAS ANALYSIS IS A ROUTINELY USED PRACTICE IN CRITICAL CARE UNIT. UNDERSTANDING OF ABGA IS BETTER FOR IMPROVING OUR DAY TO DAY PRACTISE.

1. ARTERIAL BLOOD GAS
ANALYSIS
Dr KEYUR ZATAKIYA
MBBS MD IDCCM
CONSULTANT CRITICAL CARE
INTENSIVIST

2. Definitions
Indications And contraindications
Procedure
Technical Errors
Stepwise approach in Acid- Base
interpretation
Management

3. Negative logarithm of the hydrogen ion [H+ ]
concentration in the blood, used as a positive
number.
The negative logarithm of water 1×10-7.
pH of water is 7
(7) represents the midpoint of the pH scale.
Normal range 7.35 to 7.45

4. PCo2 is a measurement of the partial
pressure exerted by CO2 in solution in the
blood.
Normal range for PCo2 in arterial blood is 35
to 45 mmHg.

5. Po2 measures the partial pressure exerted by
oxygen (O2) dissolved in the blood.
Normal range for arterial Po2 is 70 to100
mmHg

6. The pH of arterial blood is related to the
PaCo2 by the Henderson-Hasselbalch
equation:
o Correlates metabolic & respiratory
regulations
-
HCO3
pH = pK + log -------------
0.03 x[PaCO2]

7. Age, FiO2, Patm
 Determination of PaO2
PaO2 is dependantupon
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
PAO2 = partial pressure of oxygen in alveolar gas, PB = 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)

8.  Aids in establishing a diagnosis.
 Helps guide treatment plan.
 Aids in ventilator management.
 Improvement in acid/base management allows for optimal
function of medications.
 Acid/base status may alter electrolyte levels critical to patient
status/care.
 Pre operative fitness.

9.  Site- (Ideally) RadialArtery
BrachialArtery
FemoralArtery
 Ideally - 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.

10.  Ensure No Air Bubbles. Syringe must be sealed immediately
after withdrawing sample.
◦ Contact with AIR BUBBLES
Air bubble = PO2 150 mm Hg , PCO2 0 mm Hg
Air Bubble + Blood = PO2 PCO2
 ABG Syringe must be transported at the earliest to the
laboratory for EARLY analysis via COLD CHAIN

11.  Patients Body Temperature affects the values of PCO2
and HCO3.
ABG Analyser is controlled for Normal Body temperatures
Any change in body temp at the time of sampling leads to
alteration in values detected by the electrodes
 Cell count in PO2
 ABG Sample should always be sent with relevant
information regarding O2, FiO2 status and Temp.

12. A. pH (Sanz Electrode)
Measures H+ ion concentration of sample against a known pH
in a reference electrode, hence potential difference. Calibration
with solutions of known pH (6.384 to 7.384)
B. PCO2 (Severinghaus Electrode)
 CO2 reacts with solution to produceH+
higher C02 more H+  higher P CO2 measured
C. P02 (Clark Electrode)
 02 diffuses across membrane producing an electricalcurrent
measured as P 02.

14. CONTRAINDICATIONS COMPLICATIONS
 Bleeding diathesis
 AV fistula
 Severe peripheral
vascular disease,
absence of an arterial
pulse
 Infection over site.
 Abnormal Allens test.
 Severe coagulopathy.
 Use of thrombolytic
agents.
Pain and discomfort
Hematoma
Vasovagal response
Thrombosis and
embolism
Infection or
contamination
Inadvertent needle
stick
Vascular trauma or
occlusion
Arterial spasm

16. Wash your hands, introduce yourself to the
patient and clarify their identity.
Explain what you would like to do and obtain
consent.
This is a slightly uncomfortable procedure so
you should let the patient know this.
16

17. Position the patient’s arm with the wrist
extended.
Locate the radial artery with your index and
middle fingers.
17

19. Take the cap off the needle, flush the heparin through the
syringe and again locate the radial artery using your
non-dominant hand.
Insert the needle at 45 degrees to the skin at the point
of maximum pulsation of the radial artery
Advance the needle until arterial blood flushes into the
syringe.
The arterial pressure will cause the blood to fill the
syringe.
19

20. Remove the needle/syringe placing the needle into the
bung. Press firmly over the puncture site with the gauze
to halt the bleeding. Remain pressed for 5 minutes.
20

21. Cap the syringe, push out any air within it, and
send immediately for analysis ensuring that the
sample is packed in ice. Remove your gloves
and dispose them in the clinical waste
bin. Wash your hands and thank the patient.
21

22.  Before attempting to interpret the
results you should know whether the
patient was on room air or on oxygen
when the sample was taken, and if on
oxygen, what concentration.
22

23. 1. Was the blood gas specimen obtained
acceptably? Free of air bubbles and
clots?Analyzed promptly and/ or iced
appropriately?
2. Did the blood gas analyzer function
properly? Was there a recent acceptable
calibration of all electrodes or sensors?
Was analyzer function validated by
appropriate quality controls?

24. 3. Is pH within the normal limits (7.35 to 7.45)?
If so, go to Step 4.
If below 7.35, acidosis is present;
If above 7.45, alkalosis is present.
Otherwise, look for compensatory changes or
combined disorders.
4. Calculate the anion gap. Is it within the
normal range?

25. Anion Gap
AG = [Na+
] - [Cl-
+HCO3
-
]
• Elevated anion gap represents
metabolic acidosis
• Normal value: 3 – 11 mEq/L
• Major unmeasured anions
– albumin
– phosphates
– sulfates
– organic anions

26. 5. Is Pco2 within normal limits (35 to 45 mm
Hg)?
If so, go to Step 6.
If Pco2 > 45 and pH < 7.35, then respiratory
acidosis is present.
If Pco2 > 45 and pH > 7.35, then
compensated
respiratory acidosis is present.

27. If Pco2 < 35 and pH > 7.45, then respiratory
alkalosis is present.
If Pco2 < 35 and pH < 7.45, then compensated
respiratory alkalosis is present.

28. RESPIRATORY
ACIDOSIS

29. EXCRETORYCOMPONENTPROBLEMS:
1. Perfusion:
Massive PTE
Cardiac Arrest
2.Ventilation:
Severe pulmonary edema
Severe pneumonia
ARDS
Airway obstruction
3.Restriction of lung/thorax:
Flail chest
Pneumothorax
Hemothorax

30. 4. Muscular defects:
Severe hypokalemia
Myasthenic crisis
5. Failure of Mechanical Ventilator
CONTROL COMPONENT PROBLEMS:
1. CNS:
Drugs (Anesthetics, Sedatives)
Trauma
Stroke
2. Spinal Cord & Peripheral Nerves:
Cervical Cord injury
Neurotoxins
(Botulism,Tetanus)
Drugs causing Skeletal muscle
paralysis (SCh, Curare, Pancuronium,
aminoglycosides)

31. EXCRETORY COMPONENT PROBLEMS:
1. Ventilation:
COPD
Advanced ILD
2. Restriction of thorax/chest wall:
Kyphoscoliosis
Arthritis
Fibrothorax
Hydrothorax
Muscular dystrophy
Polymyositis

32. CONTROL COMPONENT PROBLEMS:
1. CNS:
Obesity Hypoventilation Syndrome
Tumors
Brainstem infarcts
Myxedema
Chronic sedative abuse
Bulbar Poliomyelitis
2. Spinal Cord & Peripheral Nerves:
Poliomyelitis
Multiple Sclerosis
ALS
Diaphragmatic paralysis

33. A) CARDIOVASCULAR:
Related to coronary vasodilation
1. Tachycardia
2. Ventricular arrythmias
B) BIOCHEMICALABNORMALITIES:
 CO2
 Cl-
 PO4
3-

34. C) NEUROMUSCULAR: Related to cerebral Artery
vasodilatation &  Cerebral BF
1. Anxiety
2. Asterixis
3. Headache
4. Papilledema
5. Focal Paresis
6. Tremors, myoclonus
7. Seizures
8. Delirium
9. Lethargy, Stupor, Coma

35.  In response to rise in CO2 (& H2CO3)  blood
and tissue buffers take up H+ ions, H2CO3
dissociates and HCO3- increases with rise in pH.
 Steady state reached in 10 min & lasts for 8
hours.
 PCO2 of CSFchanges rapidly to match PaCO2.
 Hypercapnia that persists > few hours induces
an increase in CSF HCO3- that reaches max by
24 hr and partly restores the CSFpH.
 After 8 hrs, kidneys generate HCO3-
 Steady state reached in 3-5 d

36. Ensure adequate oxygenation - care to avoid
inadequate oxygenation while preventing
worsening of hypercapnia due to supression
of hypoxemic respiratory drive
Correct underlying disorder if possible

37.  Alkali (HCO3) therapy rarely in acute and
never in chronic respiratory acidosis
 Problems with alkali therapy:
1)Decreased alveolar ventilation by decrease in
pH mediated ventilatory drive
2)Enhanced carbon dioxide production from
bicarbonate decomposition

38. RESPIRATORY
ALKALOSIS

39. NEUROMUSCULAR: Related to cerebral artery
vasoconstriction &  Cerebral BF
1. Lightheadedness
2. Decreased intellectual function
3. Paraesthesias (circumoral, extremities)
4. Muscle twitching, cramps, tetany
5. Hyperreflexia
6. Strokes in pts with sickle cell disease
7. Seizures
8. Confusion
9. Syncope

40. CENTRAL RESPIRATORY STIMULATION
(Direct Stimulation of Respiratory Center):
Structural Causes Non Structural
Causes
• Head trauma Pain
• Brain tumor Anxiety
• CVA Fever
• Voluntary
PERIPHERALRESPIRATORYSTIMULATION
(Hypoxemia  Reflex Stimulation of Respiratory
Center via Peripheral Chemoreceptors)
• Pul V/Q imbalance
• Pul Diffusion Defects Hypotension
• Pul Shunts High Altitude

41. INTRATHORACIC STRUCTURAL CAUSES:
1. Reduced movement of chest wall & diaphragm
2. Reduced compliance of lungs
3. Irritative lesions of conducting airways.
MIXED/UNKNOWN MECHANISMS:
1. Drugs – Salicylates Nicotine
Progesterone Thyroid hormone
Catecholamines
Xanthines (Aminophylline & related compounds)
1. Cirrhosis
2. Gram –ve Sepsis
3. Pregnancy
4. Heat exposure
5. Mechanical Ventilation

42. CARDIOVASCULAR: Related to coronary
vasoconstriction
1. Tachycardia
2. Angina
3. ECGchanges (ST depression)
4. Ventricular arrythmias
GASTROINTESTINAL: Nausea & Vomitting
BIOCHEMICAL ABNORMALITIES:
4
 CO2 PO 3 -
Cl-  Ca2+

43.  In response to fall in CO2 (& H2CO3)  release of
H+ by blood and tissue buffers  react with
HCO3-  fall in HCO3- (usually not less than 18)
and fall in pH
 Cellular uptake of HCO3- in exchange for Cl-
 Steady state in 15 min - persists for 6 hrs
 After 6 hrs kidneys increase excretion of HCO3-
(usually not less than 12-14)
 Steady state reached in 11/2 to 3 days.

44.  Respiratory alkalosis by itself not a cause of
respiratory failure unless work of increased
breathing not sustained by respiratory muscles.
 Rx underlying cause
 Usually extent of alkalemia produced not
dangerous.
 Admn of O2 if hypoxaemia
 If pH>7.55 pt may be sedated/anesthetised/
paralysed and/or put on Mechanical Ventilation.

45. 6. Is calculated HCO3
 within the normal limits(22 to 27 mEq/L)? If so,
the acid-base status is probably normal; go to
Step 7.
 If HCO3 < 22 and pH < 7.35, then metabolic
acidosis is present.
 If HCO3 < 22 and pH > 7.35, then
compensated metabolic acidosis is present.
 If HCO3 >27 and pH > 7.45, then metabolic
alkalosis is present.
 If HCO3 >27 and pH < 7.45, then compensated
metabolic alkalosis is present

46. METABOLIC ACIDOSIS

47. Metabolic Anion Gap
Acidosis
◦ M - Methanol
◦ U - Uremia
◦ D - DKA
◦ P - Paraldehyde
◦ L - LacticAcidosis
◦ E - Ehylene Glycol
◦ S - Salicylate
Non Gap Metabolic
Acidosis
Hyperalimentation
Acetazolamide
RTA (Calculate
urine anion gap)
Diarrhea
Pancreatic Fistula

48. When to treat?
 Severe acidemia  Effect on Cardiac function
most important factor for pt survival since rarely
lethal in absence of cardiac dysfunction.
• Contractile force of LV  as pH  from 7.4 to 7.2
• However when pH < 7.2, profound reduction in
cardiac function occurs and LV pressure falls by 15-
30%
 Most recommendations favour use of base when
pH < 7.15-7.20 or HCO3 < 8-10 meq/L.

49. Rx Undelying Cause
HCO3- Therapy
Aim to bring up pH to 7.2 & HCO3-  10 meq/L
Qty of HCO3 admn calculated:
0.5 x LBW(kg) x HCO3 Deficity (meq/L)

50. METABOLIC ALKALOSIS

51.  Metabolic alkalosis common (upto 50%
of all disorders)
• pH, HCO3
• PCO2 by 0.7 for every 1mEq/L  in HCO3
 Severe met alkalosis associated with significant
mortality
• Arterial Blood pH of 7.55  Mortality rate of45%
• Arterial Blood pH of 7.65  Mortality rate of 80%

52. H+ loss:
GIT : Chloride Losing Diarrhoeal Disease
Removal of Gastric Secretions (Vomitting,
NG suction)
Renal: Diuretics (Loop/Thiazide)
Mineralocorticoid excess
Hypercalcemia
High dose i/v penicillin

53. HCO3- Retention:
Massive Blood Transfusion
Ingestion (Milk-Alkali Syndrome)
Admn of large amounts of HCO3
H+ movement into cells
Hypokalemia

54. • Rx underlying cause
• While replacing Cl- deficit, selection of
accompanying cation (Na/K/H)
dependent on:Assessment of ECFvol
status
• Presence & degree of associated K
depletion
• Pts with vol depletion usually require
replacement of both NaCl & KCl

55. Dialysis
In presence of renal failure or severe fluid
overload state in CHF, dialysis + / - UF may
be required to exchange HCO3 for Cl &
correct metabolic alkalosis.
Adjunct Therapy
PPIcan be administered to  gastric acid
production in cases of Cl-depletion met
alkalosis resulting from loss of gastric
H+/Cl- (e.g. pernicious vomiting, req for
continual removal of gastric secretions.

56. MILK-ALKALI SYNDROME & OTHER
HYPERCALCEMIC STATES
Cessation of alkali ingestion & Ca sources
(often milk and calcium carbonate)
Treatment of underlying cause of hypercalcemia
Cl- and Volume repletion for commonly
associated vomiting

58. In the presence of acidosis or alkalosis, regulatory mechanismsoccur
which attempt to maintain the arterial pH in the physiologic range.
Disturbances in HCO3- (metabolic acidosis or alkalosis) resultin
respiratory compensation while changes in CO2 (respiratory
acidosis/alkalosis) are counteracted by renal compensation
a. Renal compensation – kidneys adapt to alterations in pH by
changing the amount of HCO3- generated/excreted. Full renal
compensation takes 2-5 days
b. Respiratory compensation – alteration in ventilation allow
immediate compensation for metabolic acid-base disorders
59

59. 1)Acute Respiratory Acidosis
For every 10 mmHg increase in PaCO2, the
HCO3
- will rise by 1 mmol/L
Expected HCO3 = 24 + (PaCO2-40) / 10)
2) Chronic Respiratory Acidosis
For every 10 mmHg increase in PaCO2, the
HCO3
- will rise by 4 mmol/L
Expected HCO3 = 24 + (4 × (PaCO2-40) / 10)

60. 3)Acute Respiratory Alkalosis
For every 10 mmHg increase in PaCO2, the
HCO3
- will fall by 2 mmol/L
Expected HCO3 = 24 - (2 ×(PaCO2-40) / 10)
4)Chronic Respiratory Alkalosis
For every 10 mmHg increase in PaCO2, the
HCO3
- will fall by 5 mmol/L
Expected HCO3 = 24 - (5 ×(PaCO2-40) / 10)

61. 5)Metabolic Acidosis
For complete compensation,
expected PaCO2 = (1.5 × HCO3
-) + 8
6)Metabolic Alkalosis
For complete compensation,
expected PaCO2 = (0.7 × HCO3
-) + 20

62. Thank You…