ATERIAL BLOOD GASES.....................

Thank you

1. Blood Gas Analysis and it’s
Clinical Interpretation
Dr. Ujjwal Sarkar
Registrar
Cardiology department
Kyamch

2. OUTLINE:
•Introduction
•Definition
•Indication
•ABG component
•Normal value
•Procedure:
preparatory –performance –follow up
phase
•Complication
•acid-base disorders
•Result interpretation
•compansation
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3. Introduction
The major function of the pulmonary system (lungs and
pulmonary circulation) is to deliver oxygen to cells and
remove carbon dioxide from the cells.
If the patient’s history and physical examination reveal
evidence of respiratory dysfunction, diagnostic test will
help identify and evaluate the dysfunction.
ABG analysis is one of the first tests ordered to
assess respiratory status because it helps evaluate gas
exchange in the lungs.
An ABG test can measure how well the person's lungs
and kidneys are working and how well the body is using
energy.
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4. DEFINITION
It is a diagnostic procedure in which a
blood is obtained from an artery directly
by an arterial puncture or accessed by a
way of indwelling arterial catheter
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5. indication
To obtain information about patient ventilation
(PCO2) , oxygenation (PO2) and acid base balance
Monitor gas exchange and acid base abnormalities
for patient on mechanical ventilator or not
To evaluate response to clinical intervention and
diagnostic evaluation ( oxygen therapy )
An ABG test may be most useful when a person's
breathing rate is increased or decreased or when
the person has very high blood sugar levels, a
severe infection, or heart failure
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6. A.Y.T 6

7. COMPONENTS OF THE
ABG
pH: Measurement of acidity or alkalinity, based on the hydrogen
(H+).
Pao
2 :The partial pressure oxygen that is dissolved in arterial
blood.
PCO
2
: The amount of carbon dioxide dissolved in arterial blood
HCO
3: The calculated value of the amount of bicarbonate in the
blood.
SaO
2:The arterial oxygen saturation.
Base Excess, Lactate and electrolytes are measured Variables
HCO
3(Measured or calculated)

8. Normal values:
Reference ranges
pH: 7.35 –7.45
PaCO2: 4.7 –6.0 kPa || 35.2 –45 mmHg
PaO2: 11 –13 kPa || 82.5 –97.5 mmHg
HCO3–: 22 –26 mEq/L
Base excess (BE): -2 to +2 mmol/L
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9. EQUIPMENT
Blood gas kit OR
1ml syringe
23-26 gauge needle
Stopper or cap
Alcohol swab
Disposable gloves
Plastic bag & crushed ice
Lidocaine (optional)
Vial of heparin (1:1000)
Par code or label
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10. Preparatory phase:
Record patient inspired oxygen concentration
Check patient temperature
Explain the procedure to the patient
Provide privacy for client
If not using hepranized syringe , hepranize
the needle
Perform Allen's test
Wait at least 20 minutes before drawing blood
for ABG after initiating, changing, or
discontinuing oxygen therapy, or settings of
mechanical ventilation, after suctioning the
patient or after extubation.
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11. ALLEN’STEST
It is a test done to determine that
collateral circulation is present from the
ulnar artery in case thrombosis occur in
the radial
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12. Sites for obtaining abg
Radial artery ( most common )
Brachial artery
Femoral artery
Radial is the most preferable
site used because:
It is easy to access
It is not a deep artery which
facilitate palpation,
stabilization and puncturing
The artery has a collateral
blood circulation
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13. Performance phase:
Wash hands
Put on gloves
Palpate the artery for maximum pulsation
If radial, perform Allen's test
Place a small towel roll under the patient wrist
Instruct the patient to breath normally during
the test and warn him that he may feel brief
cramping or throbbing pain at the puncture
site
Clean with alcohol swab in circular motion
Skin and subcutaneous tissue may be
infiltrated with local anesthetic agent if
needed
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14. Insert needle at 45
radial ,60brachial and 90
femoral
Withdraw the needle and
apply digital pressure
Check bubbles in syringe
Place the capped syringe
in the container of ice
immediately
Maintain firm pressure
on the puncture site for
5 minutes, if patient has
coagulation abnormalities
apply pressure for 10 –
15 minutes
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15. Follow up phase:
Send labeled, iced specimen to the lab
immediately
Palpate the pulse distal to the puncture site
Assess for cold hands, numbness, tingling or
discoloration
Documentation include: results of Allen's test,
time the sample was drawn, temperature,
puncture site, time pressure was applied and if
O2 therapy is there
Make sure it’s noted on the slip whether the
patient is breathing room air or oxygen. If
oxygen, document the number of liters . If the
patient is receiving mechanical ventilation, FIO2
should be documented
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16. complication
Arteriospasm
Hematoma
Hemorrhage
Distal ischemia
Infection
Numbness
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17. Type 1 vstype 2 respiratory failure
Type 1 respiratory
failureinvolveshypoxaemia(PaO2<8 kPa /
60mmHg) withnormocapnia(PaCO2<6.0 kPa /
45mmHg).
Type 2 respiratory
failureinvolveshypoxaemia(PaO2<8 kPa / 60mmHg)
withhypercapnia(PaCO2>6.0 kPa / 45mmHg)
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18. Type 1 respiratory failure causes
Pneumonia.
Pulmonary embolism & Pulmonary edema.
Acute respiratory distress syndrome (ARDS)
Pulmonary fibrosis.
Asthma.
Chronic obstructive pulmonary disease (COPD)
Pneumothorax.
Drug overdose.
Sepsis.
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19. Type 2 respiratory failure causes
Chronic obstructive pulmonary disease (COPD)
Asthma, Pulmonary edema, embolism & Pneumonia,
Severe anemia
Neuromuscular diseases (e.g., myasthenia gravis,
Chest wall deformities (e.g., kyphoscoliosis)
Obesity hypoventilation syndrome
Drug overdose (e.g., opioids, benzodiazepines)
Respiratory depression due to anesthesia or sedation,
Airway obstruction (e.g., foreign body aspiration,
laryngospasm)
Respiratory muscle fatigue due to prolonged
mechanical ventilation
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20. A look at acids and bases
The body constantly works to maintain a balance
(homeostasis) between acids and bases. Without
that balance, cells can’t function properly. As cells
use nutrient to produce the energy, two by-
products are formed H+ & CO2. acid-base balance
depends on the regulation of the free hydrogen ions
Even slight imbalance can affect metabolism and
essential body functions. Several conditions as
infection or trauma and medications can affect
acid-base balance
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21. Compensation
The respiratory and metabolic system works
together to keep the body’s acid-base balance
within normal limits.
The respiratory system responds to metabolic
based PH imbalances in the following manner:
* metabolic acidosis: ↑respiratory rate and depth
(↓PaCO2)
* metabolic alkalosis: ↓respiratory rate and depth
(↑PaCO2)
The metabolic system responds to respiratory
based PH imbalances in the following manner:
*respiratory acidosis: ↑HCO3 reabsorption
*respiratory alkalosis: ↓HCO3 reabsorption
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22. Step 3-4: Is there appropriate compensation?
Is it chronic or acute?
Respiratory Acidosis
Acute (Uncompensated): for every 10increase in pCO2 -> HCO3
increases by 1and there is a decrease of 0.08in pH
Chronic (Compensated): for every 10 increase in pCO2 -> HCO3
increases by 4 and there is a decrease of 0.03in pH
Respiratory Alkalosis
Acute (Uncompensated): for every 10 decrease in pCO2 -> HCO3
decreases by 2 and there is a increase of 0.08in PH
Chronic (Compensated): for every 10decrease in pCO2 -> HCO3
decreases by 5and there is a increase of 0.03in PH
Partial Compensated: Change
in pH will be between 0.03 to
0.08 for every 10 mmHg
change in PCO2

23. Respiratory acidosis
Respiratory acidosis is caused byinadequate
alveolar ventilationleading toCO2retention.
Arespiratoryacidosiswould have the
followingcharacteristicson anABG:
↓pH
↑CO2
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24. Respiratory acidosis
Phase PH PaCO2 HCO3
UNCOMPENSATED ↓ ↑ ------
Because there is no response from the kidneys yet to
acidosis the HCO3 will remain normal
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Phase PH PaCO2 HCO3
FULLCOMPENSATED N ↑ ↑
Phase PH PaCO2 HCO3
PARTIALCOMPENSATED ↓ ↑ ↑
PH return to normal PaCO2 & HCO3 levels are still high to
correct acidosis
The kidneys start to respond to the acidosis by increasing
the amount of circulating HCO3

25. Causesofrespiratoryacidosis:
Respiratory depression (e.g. opiates)
Guillain-Barre: paralysis leads to an inability to
adequately ventilate
Asthma
Chronic obstructive pulmonary disease (COPD)
Iatrogenic (incorrect mechanical ventilation settings
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26. Respiratory acidosis treatment
Treatment is aimed at the underlying disease, and may
include:
Bronchodilator medicines and corticosteroids to
reverse some types of airway obstruction.
Noninvasive positive-pressure ventilation (called CPAP
or BiPAP)
Oxygen if your blood oxygen level is low.
Treatment to stop smoking
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27. Respiratory alkalosis
Respiratory alkalosis is caused
byexcessivealveolarventilation(hyperventilation) resulting in more
CO2than normal being exhaled. As a result, PaCO2is reduced and pH
increases causingalkalosis.
Arespiratoryalkalosiswould have the followingcharacteristicson
anABG:
↑pH
↓CO2
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28. Respiratory alkalosis
Phase PH PaCO2 HCO3
UNCOMPENSATED ↑ ↓ ------
Because there is no response from the kidneys yet to
acidosis the HCO3 will remain normal
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Phase PH PaCO2 HCO3
FULLCOMPENSATED N ↓ ↓
Phase PH PaCO2 HCO3
PARTIALCOMPENSATED ↑ ↓ ↓
PH return to normal PaCO2 & HCO3 levels are still low to
correct alkalosis
The kidneys start to respond to the alkalosis by
decreasing the amount of circulating HCO3

29. Causesofrespiratoryalkalosis:
Anxiety (i.e. panic attack)
Pain: causing an increased respiratory rate.
Hypoxia: resulting in increased alveolar ventilation in
an attempt to compensate.
Pulmonary embolism
Pneumothorax
Iatrogenic (e.g. excessive mechanical ventilation)
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30. Treatment for respiratory alkalosis
Breathe into a paper bag. Fill the paper bag with
carbon dioxide by exhaling into it. ...
Get reassurance. The symptoms of respiratory alkalosis
can be frightening. ...
Restrict oxygen intake into the lungs. To do this, try
breathing while pursing the lips or breathing through
one nostril.
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31. Metabolic acidosis
Increased acid production or acid ingestion.
Decreased acid excretion or increased rate of
gastrointestinal and renal HCO3–loss.
A metabolic acidosis would have the following
characteristics on an ABG:
↓pH
↓HCO3-
↓BE
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32. Metabolic acidosis
Phase PH PaCO2 HCO3
UNCOMPENSATED ↓ ------- ↓
Because there is no response from the lungs yet to
acidosis the PaCO2 will remain normal
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Phase PH PaCO2 HCO3
FULL COMPENSATED N ↓ ↓
Phase PH PaCO2 HCO3
PARTIALCOMPENSATED ↓ ↓ ↓
PH return to normal PaCO2 & HCO3 levels are still low to
correct acidosis
The lungs start to respond to the acidosis by decreasing
the amount of circulating PaCO2

33. Calculate the anion gap
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. EXAMPLE
Calculate Anion gap
 ABG 7.23/17/235 on 50% VM
 BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5/ Albumin 2.
AG = Na –Cl –HCO3 (normal 12 ±2)
123 –97 –7 = 19
AG corrected = AG + 2.5[4 –albumin]
= 19 + 2.5 [4 –2]
= 19 + 5 = 24

35. Delta Gap
Delta gap = (actual AG –12) + HCO3
(19-12) +7 = 14
Delta gap < 18 -> additional non-gap metabolic
acidosis
So Metabolic acidosis anion and non anion gap

36. Delta Gap importance
A delta gap must be determined if an anion gap is
present. If the gap is less than -6, then a NAGMA is
present. If the gap is greater than 6, then an
underlying metabolic alkalosis is present.If the gap is
between -6 and 6 then only an anion gap acidosis
exists
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37. Causes of a high anion gap
metabolic acidosis
(typically relate to increased production/ingestion or
reduced excretion of H+ by the kidneys):
Diabetic ketoacidosis
Lactic acidosis
Aspirin overdose
Renal failure
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38. Causes of a normal anion gap
metabolic acidosis
(typically due to loss of bicarbonate which is
subsequently replaced by chloride in the plasma,
resulting in a stable overall anion concentration):
Gastrointestinal loss of HCO3–(e.g. diarrhoea,
ileostomy, proximal colostomy)
Renal tubular disease
Addison’s disease
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39. Metabolic Acidosis Treatment
If acid-base status is available, HCO3 (mEq) required
dosages should be calculated as follows: 0.2 x weight
(kg) x base deficit.
Alternatively:
HCO3 (mEq) required = 0.5 x weight (kg) x [24 -
serum HCO3 (mEq/L)].
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40. Metabolic alkalosis
Metabolic alkalosis occurs as aresult ofdecreased
hydrogen ion concentration, leading toincreased
bicarbonate, or alternatively a direct result of
increased bicarbonate concentrations.
Ametabolic alkalosiswould have the
followingcharacteristicson anABG:
↑pH
↑HCO3-
↑BE
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41. Causesofmetabolicalkalosis
Gastrointestinal loss of H+ions (e.g. vomiting,
diarrhoea)
Renal loss of H+ions (e.g. loop and thiazide diuretics,
heart failure, nephrotic syndrome, cirrhosis, Conn’s
syndrome)
Iatrogenic (e.g. addition of excess alkali such as milk-
alkali syndrome
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42. Metabolic alkalosis treatment
uses an intravenous (IV) line to deliver fluid and other
substances, such as:Saline infusion.Potassium
replacement.Magnesium replacement
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43. Mixed respiratory and metabolic
acidosis
Amixed respiratory and metabolic acidosiswould
have the followingcharacteristicson anABG:
↓pH
↑CO2
↓HCO3–
Causesofmixed respiratory and metabolic
acidosisinclude:
Cardiac arrest
Multi-organ failure
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44. mixed respiratory and metabolic
alkalosis
A mixed respiratory and metabolic alkalosiswould
have the followingcharacteristicson anABG:
↑pH
↓CO2
↑HCO3–
Causesofmixedrespiratoryandmetabolicalkalosis:
Liver cirrhosis in addition to diuretic use
Hyperemesis gravidarum
Excessive ventilation in COPD.
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45. Base Excess
Thebaseexcessis another surrogate marker of
metabolicacidosisoralkalosis:
Ahighbase excess (> +2mmol/L) indicates that there
is a higher than normal amount of HCO3–in the
blood, which may be due to a primarymetabolic
alkalosisor a compensatedrespiratory acidosis.
Alowbase excess (< -2mmol/L) indicates that there is
a lower than normal amount of HCO3–in the blood,
suggesting either a primarymetabolic acidosis or a
compensatedrespiratory alkalosis.
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46. Serum lactate
is an important marker of prognosis and resolution in
many critical illnesses.
Normal Range
0.5 -2.2 mmol/L
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47. Importance
Causes of Hyperlactataemia
Anaerobic muscular activity-heavy exertion, seizures,
severe asthma
Global hypoperfusion-shock, cardiac arrest, heart
failure
Regional ischaemia-mesenteric, limb, burns, trauma,
compartment syndrome, soft tissue necrosis
Reduced tissue oxygen delivery-severe hypoxia, severe
anaemia, carbon monoxide poisoning
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48. Thank you
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