The document provides a comprehensive overview of arterial blood gas (ABG) analysis, detailing its significance in clinical settings for assessing acid-base balance, oxygenation, and ventilation. It outlines the procedure for obtaining ABG samples, indications for use, contraindications, and common errors in sampling, while emphasizing the importance of maintaining a narrow pH range for proper cellular function. Additionally, the document discusses the analysis of ABG results, including calculating anion gaps and differentiating various acid-base disorders.

1. Blood Gas Analysis and it’s Clinical
Interpretation
By Dr. Paritosh

2. What is an ABG?
 It is a diagnostic procedure in which blood is
obtained from an artery directly by an arterial
puncture or accessed by a way of indwelling arterial
catheter and evaluated for blood pH.
• USES:
1. To assess ACID BASE BALANCE in critical
illness.
2. To assess adequacy of oxygenation and
ventilation

3.  Site - (Ideally) Radial Artery
Brachial Artery
Femoral Artery
 It is most commonly retrieved from the Radial
artery for the following reasons:
1. It is Superficial and easy to locate.
2. It possesses collateral circulation.

4. • Ask the patient to make a tight fist.
• Using the middle and index fingers of both hands, apply pressure to the wrist. Compress the radial and ulnar arteries at the same time (never use the thumb to detect
the artery).
• While maintaining pressure, ask the patient to open the hand slowly. Lower the hand and release pressure on the ulnar artery only.
• Positive test: The hand flushes pink or returns to normal color within 15 seconds
• Negative test: The hand does not flush pink or return to normal color within 15 seconds, indicating a disruption of blood flow from the ulnar artery to the hand
• If the Allen's test is negative, the radial artery should not be used.

5. Indications
 Respiratory failure - in acute and chronic
states.
 Any severe illness which may lead to a
metabolic acidosis - for example: Cardiac
failure, Liver failure, Renal failure.
 Hyperglycaemic states associated with Diabetes
mellitus.
 Multiorgan failure.

6. Indications
 Sepsis
 Burns
 Poisoning
 Toxins
 Ventilated Patients
 Sleep Studies

7. Contraindications
 An abnormal Allen test (Assessment of collateral
circulation).
 Local infection or distorted anatomy at the potential
puncture site (eg, from previous surgical
interventions, congenital or acquired
malformations, or burns).
 The presence of arteriovenous fistulas or vascular
grafts.
 Known or suspected severe peripheral vascular
disease of the limb involved.

8.  Severe Coagulopathy.
 Anticoagulation therapy with warfarin, heparin and
derivatives, aspirin is not a contraindication for
arterial vascular sampling in most cases.
 Use of thrombolytic agents, such as streptokinase
or tissue plasminogen activator.

9. WHY IS IT IMPORTANT FOR OUR
BODY TO MAINTAIN A NARROW PH?
1. An appropriate pH regulates the
availability of oxygen to our cells.
2. LOWER pH: REDUCE AFFINITY:
prevent adequate uptake of O2 by
hemoglobin.
3. HIGHER pH: INCREASE AFFINITY:
prevent release of O2 to our cells.
4. Outside the narrow PH range,
proteins get denatured, enzymes
stop functioning thus ceasing
cellular respiration and causing
eventual death.

10. Outline
1. Components of ABG
2. How to obtain an ABG sample
3. Common Errors During ABG Sampling
4. Simple steps in analyzing ABGs
5. Calculate the anion gap and delta gaps
6. Differentials for specific acid-base disorders

11. COMPONENTS OF THE ABG
 pH: Measurement of acidity or alkalinity, based on the hydrogen
(H+). 7.35 – 7.45
 Pao2 :The partial pressure oxygen that is dissolved in arterial
blood. 80-100 mm Hg.
 PCO2: The amount of carbon dioxide dissolved in arterial blood.
35– 45 mmHg
 HCO3 : The calculated value of the amount of bicarbonate in the
blood. 22 – 26 mmol/L
 SaO2:The arterial oxygen saturation.
>95%
 pH,PaO2 ,PaCO2 , Lactate and electrolytes are measured Variables
 HCO3 (Measured or calculated)

12. Obtaining the ABG sample

14. Common Errors during ABG Sampling
Delayed Analysis
 Consumption of O2 & Production of CO2
continues after blood drawn
Iced Sample maintains values for 1-2 hours
Uniced sample quickly becomes invalid within 15-
20 minutes
PaCO2  3-10 mmHg/hour
PaO2 
pH  due to lactic acidosis generated by
glycolysis in R.B.C.

15. Parameter 37 °C (Change
every 10 min)
4 °C (Change
every 10 min)
 pH 0.01 0.001
 PCO2 1 mm Hg 0.1 mm Hg
 PO2 0.1 vol % 0.01 vol %
Temperature Effect on Change of ABG
Values
Common Errors during ABG Sampling

16. FEVER OR HYPOTHERMIA
1. Most ABG analyzers report data at N body temp
2. If there is severe hyper/hypo-thermia, values of
pH & PCO2 at 37 ° C can be significantly different
from pt’s actual values
3. Changes in PO2 values with temperature are also
predictable
Hansen JE, Clinics in Chest Med 10(2), 1989 227-237
 If Patients temperature is < 37°C
Subtract 5 mmHg pO2, 2 mmHg pCO2 and Add
0.012 pH per 1C decrease of temperature
Common Errors during ABG Sampling

17. AIR BUBBLES
1. pO2 150 mmHg & pCO2 0 mmHg in air bubble on (Room Air)
2. Mixing with sample leads to  PaO2 &  PaCO2
To avoid air bubbles, sample should be drawn very slowly
and preferably in a glass syringe
Steady State:
 Sampling should done during steady state after change in
oxygen therapy or ventilator parameter
 Steady state is achieved usually within 3-10 minutes
Common Errors during ABG Sampling

18. Leucocytosis :
  pH and Po2; and  Pco2
 0.1 ml of O2 is consumed/dL of blood in 10
min in patients with N number of TLCs
 Marked increase in patients with very high
TLC/platelets counts – hence immediate
chilling/analysis is essential
EXCESSIVE HEPARIN
Dilutional effect results in  HCO3
- & PaCO2
Only .05 ml heparin required for 1 ml blood.
So the syringe should be emptied of heparin after flushing
Common Errors during ABG Sampling

19.  TYPE OF SYRINGE
1. pH & PCO2 values remain unaffected
2. PO2 values drop more rapidly in plastic syringes (ONLY
if PO2 > 400 mm Hg)
 Differences usually not of clinical significance and so
plastic syringes are used
 Risk of alteration of results  with:
1. size of syringe/needle
2. volume of sample
 HYPERVENTILATION OR BREATH HOLDING
May lead to erroneous lab results
Common Errors during ABG Sampling

20. Contd…
 Buffer Base:
 It is the total quantity of buffers in blood including
both volatile(Hco3) and nonvolatile (as
Hgb,albumin,Po4)
 Base Excess/Base Deficit:
 Amount of strong acid or base needed to restore
plasma pH to 7.40 at a PaCO2 of 40 mm Hg,at
37*C.
 Calculated from pH, PaCO2 and HCT
 Negative BE also referred to as Base Deficit
 True reflection of non respiratory (metabolic) acid
base status
 Normal value: -2 to +2mEq/L

21. Arterial vs Venous Sample
 The venous oxygen is lower than the arterial
oxygen.
 The PCO2 will be higher in venous than arterial
blood.
 Arterial blood is bright red colour, but venous
blood is dark maroon in colour

22. CENTRAL EQUATION OF ACID-BASE
PHYSIOLOGY
 Henderson Hasselbach Equation:
 where [ H+] is related to pH by
 To maintain a constant pH, PCO2/HCO3- ratio should be
constant
 When one component of the PCO2/[HCO3- ]ratio is altered,
the compensatory response alters the other component in the
same direction to keep the PCO2/[HCO3- ] ratio constant
 [H+] in nEq/L = 24 x (PCO2 / [HCO3 -] )
 [ H+] in nEq/L = 10 (9-pH)

23. Compensatory response or Regulation
of pH
By 3 mechanisms:
 Chemical buffers:
 React instantly to compensate for the addition or
subtraction of H+ ions
 CO2 elimination:
 Controlled by the respiratory system
 Change in pH result in change in PCO2 within minutes
 HCO3- elimination:
 Controlled by the kidneys
 Change in pH result in change in HCO3-
 It takes hours to days and full compensation occurs in 2-
5 days

24. Steps for ABG analysis
1. What is the pH? Acidemia or Alkalemia?
2. What is the primary disorder present?
3. Is there appropriate compensation?
4. Is the compensation acute or chronic?
5. Is there an anion gap?
6. If there is a AG, check the delta gap?
7. What is the differential for the clinical processes?

25. Step 1:
 Look at the pH: is the blood acidemic or alkalemic?
 EXAMPLE :
 65yrs Male with CKD presenting with nausea, diarrhea
and acute respiratory distress
 ABG pH- 7.23/pO2-17/ pCO2- 23. 5
 Na-123/Cl-97/ HCO3 - 37/ BUN -119 /
Creatinine -5.1
 ACIDMEIA OR ALKALEMIA ????

26. EXAMPLE
 ABG: pH - 7.23/pO2 -17/ pCO2 - 23.5
 Labs: Na+123/ Cl 97/ HCO -37/ BUN 119/
Creatinine 5.1
 PH = 7.23 , HCO: 37
 Acidemia

27. Step 2: What is the primary disorder?
What disorder is
present?
pH pCO2 HCO3
Respiratory
Acidosis
pH low high high
Metabolic Acidosis pH low low low
Respiratory
Alkalosis
pH high low low
Metabolic Alkalosis pH high high high

28. Contd….
Metabolic Conditions are suggested if
pH changes in the same direction as pCO2 or pH is
abnormal but pCO2 remains unchanged
Respiratory Conditions are suggested if:
pH changes in the opposite direction as pCO2 or pH is
abnormal but HCO3- remains unchanged

29. EXPECTED CHANGES IN ACID-BASE DISORDERS
Primary Disorder Expected Changes
Metabolic acidosis PCO2 = 1.5 × HCO3 + (8 ± 2)
Metabolic alkalosis PCO2 = 0.7 × HCO3 + (21 ± 2)
Acute respiratory acidosis delta pH = 0.008 × (PCO2 - 40)
Chronic respiratory acidosis delta pH = 0.003 × (PCO2 - 40)
Acute respiratory alkalosis delta pH = 0.008 × (40 - PCO2)
Chronic respiratory alkalosis delta pH = 0.003 × (40 - PCO2)
From: THE ICU BOOK - 2nd Ed. (1998) [Corrected]

30. Step 3-4: Is there appropriate
compensation? Is it chronic or acute?
 Respiratory Acidosis
 Acute (Uncompensated): for every 10 increase in pCO2 -> HCO3
increases by 1 and there is a decrease of 0.08 in pH
 Chronic (Compensated): for every 10 increase in pCO2 -> HCO3
increases by 4 and there is a decrease of 0.03 in pH
 Respiratory Alkalosis
 Acute (Uncompensated): for every 10 decrease in pCO2 -> HCO3
decreases by 2 and there is a increase of 0.08 in PH
 Chronic (Compensated): for every 10 decrease in pCO2 -> HCO3
decreases by 5 and there is a increase of 0.03 in PH
1 4
2 5
10
 Partial Compensated: Change
in pH will be between 0.03 to
0.08 for every 10 mmHg
change in PCO2

31. Step 3-4: Is there appropriate
compensation?
 Metabolic Acidosis
 Winter’s formula: Expected pCO2 = 1.5[HCO3] + 8 ± 2
OR
 pCO2 = 1.2 ( HCO3)
 If serum pCO2 > expected pCO2 -> additional respiratory
acidosis and vice versa
 Metabolic Alkalosis
 Expected PCO2 = 0.7 × HCO3 + (21 ± 2)
OR
 pCO2 = 0.7 ( HCO3)
 If serum pCO2 < expected pCO2 - additional respiratory
alkalosis and vice versa

32. EXAMPLE
 ABG 7.23/17/235 on 50% VM
 BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5.
 Winter’s formula : 17= 1.5 (7) +8 ±2 = 18.5(16.5 –
20.5)
 So correct compensation so there is only one
disorder Primary metabolic

33. Step 5: Calculate the anion gap
 AG used to assess acid-base status esp in D/D of
met acidosis
  AG &  HCO3
- used to assess mixed acid-base
disorders
 AG based on principle of electroneutrality:
 Total Serum Cations = Total Serum Anions
 Na + (K + Ca + Mg) = HCO3 + Cl + (PO4 + SO4
+ Protein + Organic Acids)
 Na + UC = HCO3 + Cl + UA
 Na – (HCO3 + Cl) = UA – UC
 Na – (HCO3 + Cl) = AG
 Normal =12 ± 2

34. Contd…
 AG corrected = AG + 2.5[4 – albumin]
 If there is an anion Gap then calculate the
Delta/delta gap (step 6) to determine
additional hidden nongap metabolic acidosis
or metabolic alkalosis
 If there is no anion gap then start analyzing
for non-anion gap acidosis

35. Step 6: Calculate Delta Gap
 Delta gap = (actual AG – 12) + HCO3
 Adjusted HCO3 should be 24 (+_ 6) {18-30}
 If delta gap > 30 -> additional metabolic alkalosis
 If delta gap < 18 -> additional non-gap metabolic
acidosis
 If delta gap 18 – 30 -> no additional metabolic
disorders

36. Primary Acid Base Disturbances
 Metabolic Acidosis
 Metabolic Alkalosis
 Respiratory Acidosis
 Respiratory Alkalosis

37. Metabolic Acidosis
Metabolic acidosis is a condition that occurs when the body produces
excessive quantities of acid or when the kidneys are not removing enough acid
from the body. Blood pH is low (less than 7.35) due to increased production of
hydrogen ions by the body or the inability of the body to form bicarbonate
(HCO3-) in the kidney.

38. Metabolic Acidosis: Anion Gap
Acidosis

39. Non-Gap Metabolic Acidosis
 For non-gap metabolic acidosis, calculate the urine anion
gap
 URINARY AG
Total Urine Cations = Total Urine Anions
Na + K + (NH4 and other UC) = Cl + UA
(Na + K) + UC = Cl + UA
(Na + K) – Cl = UA – UC
(Na + K) – Cl = AG
 Distinguish GI from renal causes of loss of HCO3 by estimating
Urinary NH4+ .
 Hence a negative UAG (average-20 meq/L) seen in GI, while
positive value (av +23 meq/L) seen in renal disease.
UAG = UNA + UK – UCL
Kaehny WD. Manual of Nephrology 2000; 48-62

40. Causes of Non Anion Gap Metabolic Acidosis - DURHAM
Diarrhea, ileostomy, colostomy, enteric fistulas
Ureteral diversions or pancreatic fistulas
Renal Tubular Acidosis, Acute Kidney Injury
Hydrochloric acid administration
Acetazolamide, Addison’s
Miscellaneous – hypocapnia, toulene, sevelamer, cholestyramine ingestion

41. Sign and Symptoms

42. Management
 Put the patient in the resuscitation area, or transfer to a high-
dependency area as soon as feasible.
 Put the patient on an ECG monitor, SaO2 monitor and
BP/HR monitor.
 In patients who are clinically unwell and have deteriorating
SaO2levels or conscious levels, consider intubation and
assisted ventilation
 Get large-bore IV access (a central venous line may be needed)
and rehydrate aggressively. Use colloids if necessary.

43.  Consider catheterization to monitor urine output and obtain
urine for analysis.
 If there is any possibility of drug or toxin ingestion, give initial
therapies such as activated charcoal/chelating
agents/emetics, dependent on the specific compound ingested
and guidelines for poisoning.
 Obtain specialist input as soon as possible.

44.  The major problem is suppression of myocardial
contractility and unresponsiveness to
catecholamines caused by the acidemic state.
 This may lead to a vicious cycle of hypo-perfusion,
worsening lactic acidosis and further cardiac
suppression, causing multi-organ failure.
 If pH is <7.1-7.2 then cardiac arrhythmias are
likely.

45. Role of Sodium Bicarbonate

46. Contd..

47. General Principles of NAHCO3
administration
 The amount of hypertonic bicarbonate which can
be given is limited by the sodium concentration.
 Each 50-ml ampule of bicarbonate will increase the
sodium concentration by roughly ~1-1.5 mEq/L
 Occasionally, it’s the patients who are hypoxemic
and who are extremely difficult to ventilate
(typically due to status asthmaticus or severe
ARDS) that require exogenous bicarbonate
administration

48.  The safest approach to these patients may be to administer
exogenous bicarbonate, with a goal of increasing the
bicarbonate level to ~30-35 mEq/L
 This will generally amount to shifting patients from a state of
mild metabolic acidosis (most patients start off with a
bicarbonate of ~20 mEq/L) to mild metabolic alkalosis
 The optimal rate of alkalinization is unknown, and likely
varies depending on the individual patient scenario.
 In most cases, gradual alkalization (e.g. 25-100 mEq
bicarbonate per hour) is sufficient.

49.  Bicarbonate administration will cause a transient
increase in pCO2 during its administration, which
will cause a transient reduction in pH.
 However, once completed, pCO2 will decrease to
baseline and the added bicarbonate will increase
the pH.
 If bicarbonate is administered more slowly, then
transient pCO2 elevations are smaller.

50. Anesthetic Considerations
Acidemia can potentiate the depressant effects of
most sedatives and anesthetic agents on the central
nervous and circulatory systems.
Because most opioids are weak bases, acidosis can
increase the fraction of the drug in the nonionized
form and facilitate penetration of the opioid into the
brain.

51.  Circulatory depressant effects of both volatile and
intravenous anesthetics can also be exaggerated.
 Halothane is more arrhythmogenic in the presence
of acidosis.
 Succinylcholine should generally be avoided in
acidotic patients with hyperkalemia to prevent
further increases in plasma [K+].

52. Metabolic Alkalosis
 Metabolic alkalosis is primary increase in HCO3-
with or without compensatory increase in Pco2
 pH may be high or nearly normal
 It is a relatively frequent clinical problem that is
most commonly due to the loss of hydrogen ions
from the gastrointestinal tract or in the urine.

53. Metabolic Alkalosis
 Calculate the urinary chloride to differentiate saline
responsive vs saline resistant
 The patients must be off diuretics in order to interpret urine
chloride
Saline responsive UCL<25 Saline-resistant UCL >25
Vomiting If hypertensive: Cushings, Conn’s, RAS,
renal failure with alkali administartion
Diuretics
Thiazide
If not hypertensive: severe hypokalemia,
hypomagnesemia, Bartter’s, Gittelman’s,
licorice ingestion
Cystic Fibrosis Exogenous corticosteroid administration

54. Management
Saline responsive alkalosis
 Adequate correction of volume - IV Isotonic Saline
 H1 inhibitor or PPI to decrease gastric secretion
 Avoid exogenous sources of alkali such as NaHCO3
infusion
 If alkalosis is due to diuretics, dose reduction may
be required, KCL supplementation, spironolactone
or carbonic anhydrase inhibitor can also be added.

55. Saline Resistant Metabolic Alkalosis
 Needs specific treatment of underlying causes
(surgical treatment of pituitary tumor or adrenal
adenoma in Cushing syndrome)
 Supportive treatment such as spironolactone

56. Sign and Symptoms

57. Respiratory Alkalosis
Respiratory alkalosis is defined as a primary decrease in Paco2.
Mechanism is usually an inappropriate increase in alveolar
ventilation relative to CO2 production.

58. Respiratory Alkalosis
Causes of Respiratory Alkalosis
Anxiety, pain, fever
Hypoxia, CHF
Lung disease with or without hypoxia – pulmonary embolus, reactive
airway, pneumonia
CNS diseases
Drug use – salicylates, catecholamines, progesterone
Pregnancy
Sepsis, hypotension
Hepatic encephalopathy, liver failure
Mechanical ventilation
Hypothyroidism
High altitude

59. Sign and Symptoms

60. Treatment
 Treatment is aimed at the condition that causes
respiratory alkalosis.
 Breathing into a paper bag -- or using a mask
that causes you to re-breathe carbon dioxide –
sometimes helps reduce symptoms.

61. Respiratory Acidosis
 Respiratory acidosis is defined as a primary
increase in PaCO2.
This increase drives the reaction:
 H2O+CO2  H2CO3  H+ +HCO3−
 Leads to an increase in [H+] and a decrease in
arterial pH.
[HCO3−] is increased

62. Causes of Respiratory Acidosis
Differentials of Respiratory Acidosis
Myopathies
Neuropathies
Flail Chest
Pneumothorax
Pleural Effusion
COPD
Malignancy
Pulmonary Edema
Malignant Hyperthermia
Drug Induced
Thyroid Storm

63. Symptoms of Respiratory Acidosis

64. Treatment
 Treatment is aimed at the underlying disease, and
may include:
 Bronchodilators to reverse pathological airway
obstruction
 Oxygen Supplementation, if the blood oxygen level
is low
 Noninvasive positive-pressure ventilation (CPAP or
BiPAP) or a breathing machine

65. Thank You!!