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ARTERIAL BLOOD GAS

ANALYSIS

BY-
SHIVAM SACHAN(JR II)
MODERATOR-
Dr. R.K YADAV(M.D)
What is an ABG
•Arterial Blood Gas

•Drawn from artery- radial, brachial, femoral

•It is an invasive procedure.

•Caution must be taken with patient on anticoagulants.

•Arterial blood gas analysis is an essential part of


diagnosing and managing the patient’s oxygenation
status, ventilation failure and acid base balance.
ABG analysis
 Why do we care ?
 Critical care requires a good understanding ,as acid
base disorders are one of the most common clinical
problems encountered in ICU.
 Helps in the differential and final diagnosis.
 Helps in determining treatment plan.
 Treating acid/base disorders helps medications work
better (i.e. antibiotics, vasopressors, etc.)
 Helps in ventilator management.
 Severe acid/base disorders may need dialysis.

Practical guidelines on fluid therapy ed.2 p.204


ABG Specimen Collection/Handling
Site Selection
ABG Specimen Collection/Handling
Hazards

 Hematoma

 Arterial laceration

 Hemorrhage

 Vasovagal reaction
 Sympathetic nervous system response to pain
 Loss of limb
Practical guidelines on fluid therapy ed.2 p.205
 Blood gas specimen should collected anaerobically
 Expel air bubbles immediately

In Vivo Values Air Contamination


pH 7.40 7.45
PCO2 40 30
PO2 95 110
 Blood gas specimen must be adequately anticoagulated
 Sodium heparin

 Lithium heparin (electrolytes)

 Sample volume should be 1 – 2 ml


 Each laboratory has its own protocol
 Sample should be analyzed as soon as possible
 If iced,sample can be stored

 Glass syringe – 1 hour

 Plastic syringe – 15 minutes

Remember: Blood is living tissue that continues to consume O2 and


produce CO2
Precautions
 Excessive Heparin Decreases bicarbonate and PaCO2
 Large Air bubbles not expelled from sample PaO2 rises,
PaCO2 may fall slightly.
 Fever or Hypothermia, Hyperventilation or breath holding
(Due to anxiety) may lead to erroneous lab results
 Care must be taken to prevent bleeding
Practical guidelines on fluid therapy ed.2 p.205
Normal Arterial Blood
Gas Values*
pH 7.35 - 7.45
PaCO2 35 - 45 mm Hg
PaO2 70 - 100 mm Hg **
SaO2 93 - 98%
HCO3¯ 22 - 26 mEq/L
%MetHb < 2.0%
%COHb < 3.0%
Base excess -2.0 to 2.0 mEq/L
* At sea level, breathing ambient air
** Age-dependent
The icu book ed.3 p.372t
Acid/Base Balance
The pH is a measurement of the acidity or alkalinity of the blood.

• It is inversely proportional to the no. of (H+) in the blood.



•The normal pH range is 7.35-7.45.

•Significant changes in the blood pH above 7.8 or below 6.8 will


interfere with cellular functioning, and if uncorrected, will lead to death.
SOME BASIC CONCEPTS
 Hydrogen ion concentration in ECF is determined by
the following equation -
[H+]nEq/L = 24 X PaCO2 / [ HCO3-]
 Hydrogen ion concentration is inversely proportional
to pH.
 From above statements it can be stated that-
HCO3-
pH ~ ---------
PaCO2
The icu book ed.3 p.531
ACID BASE CONTROL
 The determinants of extracellular pH indicate that
tight control of pH requires a fairly constant pco2/hco3
ratio.
 Thus, a proportional change in one of the
determinants must be accompanied by a proportional
change in other to keep the ratio constant.
 This is how the control system of acid-base balance
operates.
 Several different buffer systems exist to help maintain
a serum pH close to 7.4.
The icu book ed.3 p.531
14
Acid-base Terminology
Acidosis: Blood pH is less than 7.35.
Two types 1)Metabolic 2)Respiratory
Alkalosis: Blood pH is more than 7.45.
Two types 1)Metabolic 2)Respiratory
Acid-base Terminology (cont.)
Primary acid-base disorder: One of the four acid-base
disturbances that is manifested by an initial change in
HCO3- or PaCO2.
They are: metabolic acidosis (MAc), metabolic alkalosis
(MAlk), respiratory acidosis (RAc), and respiratory
alkalosis (RAlk).
If HCO3- changes first, the disorder is either MAc or
Malk.
If PaCO2 changes first, the problem is either RAlk or
RAc.
Compensation: The change in HCO3- or PaCO2 that
results from the primary event.
A Stepwise Approach
to Acid-Base
Interpretation

The icu book ed.3 p.537


Stage I: Identify the Primary Acid-
Base Disorder
 Measured PaCO2 and pH are used to determine if an
acid-base disturbance is present and, if so, to identify
the primary acid-base disorder.
 Rule 1: An acid-base abnormality is present if either the
PaCO2 or the pH is outside the normal range.
 Rule 2: If the pH and PaCO2 are both abnormal, compare
the directional change. If both change in the same
direction (both increase or decrease), the primary
acid-base disorder is metabolic, and if both change in
opposite directions, the primary acid-base disorder is
respiratory.
pH paco2 Hco3(compensation)

Res.Acidosis

Res.Alkalosis

Met. Acidosis

Met.Alkalosis
 Rule 3: If either the pH or PaCO2 is normal, there is a
mixed metabolic and respiratory acid-base disorder (one
is an acidosis and the other is an alkalosis).
 If the pH is normal, the direction of change in PaCO2
identifies the respiratory disorder, and if the PaCO2 is
normal, the direction of change in the pH identifies
the metabolic disorder.
 Remember that the compensatory responses to a
primary acid-base disturbance are never strong
enough to correct the pH, but act to reduce the
severity of the change in pH. Therefore, a normal pH
in the presence of an acid-base disorder always
signifies a mixed respiratory and metabolic acid-base
disorder.
EXPECTED CHANGES IN ACID-BASE DISORDERS

Primary Disorder Expected Changes


1. Metabolic acidosis PCO2 = 1.5 × HCO3 + (8 ± 2)
2. Metabolic alkalosis PCO2 = 0.7 × HCO3 + (21 ± 2)
3. Acute respiratory acidosis delta pH = 0.008 × (PCO2 - 40)
4. Chronic respiratory acidosis delta pH = 0.003 × (PCO2 - 40)
5. Acute respiratory alkalosis delta pH = 0.008 × (40 - PCO2)
6. Chronic respiratory alkalosis delta pH = 0.003 × (40 - PCO2)
Respiratory acidosis
7. Acute: HCO3- = 24 + 0.1 X Δ PCO2
8. Chronic: HCO3- = 24 + 0.3 X Δ PCO2
Respiratory alkalosis
9.Acute:HCO3- = 24 – 0.2X Δ PCO2
10.Chronic:HCO3- =24 – 0.4X Δ PCO2

From: THE ICU BOOK – Ed3.p.535


Stage II: Evaluate Compensatory
Responses
 The second stage of the approach is for cases
where a primary acid-base disorder has been
identified in Stage I. (If a mixed acid-base disorder
was identified in Stage I, go directly to Stage III.)
The goal in Stage II is to determine if the
compensatory responses are adequate and if there
are additional acid-base derangements.
 Rule 4: If there is a primary metabolic acidosis or
alkalosis, use the measured serum bicarbonate
concentration in Equation 1 or 2 to identify the expected
PaCO2.
 If the measured and expected PaCO2 are equivalent, the
condition is fully compensated.
 If the measured PaCO2 is higher than the expected PaCO2
- superimposed respiratory acidosis.
 If the measured PCO2 is less than the expected PaCO2 -
superimposed respiratory alkalosis.
 Rule 5: If there is a respiratory acidosis or alkalosis, use
the PaCO2 to calculate the expected pH using Equations
3,4 (for respiratory acidosis) or Equations 5,6 (for
respiratory alkalosis).
 Compare the measured pH to the expected pH to
determine if the condition is acute, partially compensated,
or fully compensated.
 For respiratory acidosis, if the measured pH is lower than the
expected pH for the acute, uncompensated condition-
superimposed metabolic acidosis.
 If the measured pH is higher than the expected pH for the
chronic, compensated condition-
superimposed metabolic alkalosis.
 For respiratory alkalosis, if the measured pH is higher than the
expected pH for the acute, uncompensated condition-
superimposed metabolic alkalosis.
 If the measured pH is below the expected pH for the chronic,
compensated condition-
superimposed metabolic acidosis.
Stage III: Use The “Gaps” to Evaluate
Metabolic Acidosis
 The final stage of this approach is for patients with a
metabolic acidosis, and it involves two determinations
known as gaps.
 The first is the anion gap, which is an estimate of
unmeasured anions that helps to identify the cause of a
metabolic acidosis.
 The second gap is a comparison of the change in the anion
gap and the change in the serum HCO3 concentration: the
gap between the two (known as the gap-gap) can uncover
mixed metabolic disorders (e.g., a metabolic acidosis and
alkalosis) that would otherwise go undetected.
The Anion Gap
 The anion gap is an estimate of the relative abundance of
unmeasured anions, and is used to determine if a metabolic
acidosis is due to an accumulation of non-volatile acids (e.g.,
lactic acid) or a net loss of bicarbonate (e.g., diarrhea).
 AG = Na+ – (Cl– + HCO3–)
 The normal value of the AG is 12 ± 4 mEq/L (range = 8 to 16
mEq/L).
 Metabolic acidoses are characterized as having an elevated AG
or a normal AG.
Influence of Albumin
 albumin is major source of unmeasured anions, and a 50%
reduction in the albumin concentration will result in a
75% reduction in the anion gap.
 Since hypoalbuminemia is common in ICU patients, the
influence of albumin on the AG must be considered in all
ICU patients.
 Reduction in serum albumin 1 gm% reduces anion gap by 2.5
mmol/l
The “Gap-Gap” or Delta gap

 Compare the change in AG with the change in serum


bicarbonate.

 Useful to identify additional or hidden metabolic


disorders.

 In a simple metabolic acidosis, the change in AG=the


decrease in bicarbonate i.e
ΔAG= ΔHCO3 or
measured AG-12 = 24- measured HCO3
 If the decrease in bicarbonate is more than the rise
in the AG, concurrent with the AG metabolic
acidosis there is also a second type of metabolic
acidosis present, a non-AG metabolic acidosis.

 If the decrease in bicarbonate is less than the rise


in AG, a metabolic alkalosis is concurrently
present with the AG metabolic acidosis.
Normal AG metabolic acidosis: GI or
Renal loss of bicarbonate?
 Calculate the urine anion gap (UAG)

 It provides information on whether the kidney is able to


produce ammonium (NH4+)
UAG =UK+ + UNa+ - UCl-
 A negative UAG suggest that bicarbonate losses are from
the GI tract.
 Positive UAG suggest that bicarbonate losses are from
kidney.
BASE EXCESS
 Is a calculated value which estimates the metabolic
component of an acid base abnormality.
 Normally between +2 to -2.
 It is an estimate of the amount of strong acid or base
needed to correct the met. component of an acid base
disorder (restore plasma pH to 7.40at a Paco2 40 mmHg).
 Amount of Hco3 in mM required to correct base exess
=0.3 X body weight X BE
TYPES OF ACID-BASE
DISORDERS
Metabolic Acidosis
 NORMAL ANION GAP
Diarrhea
Renal tubular acidosis (RTA)
Urinary tract diversions
Ammonium chloride intake
 INCREASED ANION GAP
Lactic acidosis
Ketoacidosis
Kidney failure
Poisoning
37
Metabolic Alkalosis
 CHLORIDE RESPONSIVE (urinary chloride <15 mEq/L)
Gastric losses,Diuretics
Chloride losing diarrhea
Cystic fibrosis
Post hypercapnia
CHLORIDE RESISTANT (urinary chloride >20 mEq/L)

 High BP -

Adrenal adenoma or hyperplasia,Renovascular disease,Renin-


secreting tumor
Cushing syndrome
Liddle syndrome
Normal BP -
 Gitelman syndrome ,Bartter syndrome
Base administration
Nelsons textbook of pediatrics ed.17 chapter 45
39
Respiratory Acidosis
 Mechanism
 Hypoventilation or Excess CO2 Production
 Etiology
 COPD
 Neuromuscular Disease
 Respiratory Center Depression
 Late ARDS
 Inadequate mechanical ventilation
 Sepsis or Burns
 Excess carbohydrate intake
41
Respiratory Alkalosis
 Risk Factors and etiology
 Hyperventilation due to
 extreme anxiety, stress, or pain
 elevated body temperature
 overventilation with ventilator
 hypoxia
 salicylate overdose
 hypoxemia (emphysema or pneumonia)
 CNS trauma or tumor
43
EXAMPLES
CASE1
 A pt. came with following reports - Na+, 135; K+, 3.0;
Cl–, 110; HCO3–, 10; AG, 15; Paco2, 25; pH, 7.20
what is your diagnosis ?
 Answer-
 Primary disorder metabolic acidosis.
 Expected pco2 = 1.5 × 10 + 8 ± 2 = 23 ± 2
Normal AG metabolic acidosis with adequate
compensation.
 CASE 2 -A patient’s arterial blood gas shows pH of
7.14, PaCO2 of 70 mm Hg, and HCO3- of 23 mEq/L.
How would you describe the likely acid-base
disorder(s)?
EXPECTED CHANGES IN ACID-BASE DISORDERS

Primary Disorder Expected Changes


1. Metabolic acidosis PCO2 = 1.5 × HCO3 + (8 ± 2)
2. Metabolic alkalosis PCO2 = 0.7 × HCO3 + (21 ± 2)
3. Acute respiratory acidosis delta pH = 0.008 × (PCO2 - 40)
4. Chronic respiratory acidosis delta pH = 0.003 × (PCO2 - 40)
5. Acute respiratory alkalosis delta pH = 0.008 × (40 - PCO2)
6. Chronic respiratory alkalosis delta pH = 0.003 × (40 - PCO2)
Respiratory acidosis
7. Acute: HCO3- = 24 + 0.1 X Δ PCO2
8. Chronic: HCO3- = 24 + 0.3 X Δ PCO2
Respiratory alkalosis
9.Acute:HCO3- = 24 – 0.2X Δ PCO2
10.Chronic:HCO3- =24 – 0.4X Δ PCO2

From: THE ICU BOOK – Ed3.p.535


 1. Acute elevation of PaCO2 leads to reduced pH, i.e., an
acute respiratory acidosis. However, is the problem only acute
respiratory acidosis or is there some additional process? For
every 10-mm Hg rise in PaCO2 (before any renal
compensation), pH falls about 0.08 units. Because this
patient's pH is down 0.26, or 0.02 more than expected for a 30-
mm Hg increase in PaCO2, there must be an additional
metabolic problem. Also note that with acute CO2 retention of
this degree, the HCO3- should be elevated 3 mEq/L. Thus a
low-normal HCO3- with increased PaCO2 is another way to
uncover an additional metabolic disorder. Decreased perfusion
leading to mild lactic acidosis would explain the metabolic
component.
Case 3. A 23-year-old man is being evaluated in the emergency room
for severe pneumonia. His respiratory rate is 38/min and he is
using accessory breathing muscles.
Na 154 mEq/L
pH 7.29 K+ 4.1 mEq/L
PaCO2 55 mm Hg Cl- 100 mEq/L
PaO2 47 mm Hg HCO3 24 mEq/L
SaO2 86%
HCO3- 23 mEq/L
Hb 13 gm%

How would you characterize his state of acid-base balance?


Case 3 - Discussion
The low pH, high PaCO2, and slightly low calculated HCO3- all point to
combined acute respiratory acidosis and metabolic acidosis. Anion gap is
elevated to 30 mEq/L indicating a clinically significant anion gap (AG)
acidosis, possibly from lactic acidosis.
DELTA AG =18
DELTA HCO3- =1 ,normally both should be equal.
Sugesstive of associated metabolic alkalosis,
and since pco2 is raised there is associated respiratory
acidosis.
THANK YOU…..

NEXT SEMINAR –
Dr. ESHA JAFA(JR II)

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