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ABG Analysis
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.
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 :
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.
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
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 .
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)
34.
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
42. RESPIRATORY ACIDOSIS
H2O + CO2 H2CO3 H+ + HCO3
-
Cause - hypoventilation
Retention of CO2
Drives equation rightward
Increases both [H+] and [HCO3
-]
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
-]
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
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
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
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)
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