ABG_ANALYSIS
18 August 2024 23:15
When to order an ABG?
1. Any respiratory distress/respiratory failure
2. Poisoning – eg opiates, OPP, methanol, gaseous poisonings
3. Acute/chronic renal failure/ uremia
4. State of hypo perfusion eg. Septic shock
5. To manage ventilator settings
6. To determine type of respiratory failure
7. DKA
8. COPD, bronchial asthma, pneumonitis, ARDS, Pneumothorax
9. Anxiety
10. Diarrhoea, vomiting
11. MODS
12. Neuromuscular disorders – myasthenia, GBS
13. Head injury with poor GCS
14. Cyanosis
15. Sudden onset of dyspnea
16. Cardiac diseases – CCF, CHD
17. Cardiac arrest, post CPR
18. Burns
19. Chest x-ray showing infiltrates
20. Pulmonary embolism
Common questions
• What are other adjuncts to know about oxygenation and ventilation status of the
patient?
• What are the 3 components of ABG report?
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• Can a venous sample be taken for analysis?
• Can we rely on the chemistry and metabolic components of ABG reading?
• Does oxygen supplementation change value of PO2 in ABG?
Answers
1. Saturation probe and ETCO2
2. Gases – pH, pCO2, pO2, cHCO3-, BE, cSO2
Chemistry – Na, K, Cl, Ca, cTCO2, base excess, Hb , HCT, anion gap
Metabolic – glucose, lactate, creatinine
3. Differences in measured blood gas values between arterial and venous blood are most
pronounced for PO2, as PO2 is the only clinical reason for obtaining arterial collections.
PO2 is generally approximately 60 mm Hg lower in venous blood after O2 is released in
the capillaries, whereas PCO2 is 2 to 8 mm Hg higher in venous blood. pH is generally
only
0.02 to 0.05 pH units lower in a venous sample. 0.52 mmol/l for HCO3
4. Electrolytes results on ABG can be significantly affected by pre-analytical variables
such as hemolysis (especially K concentrations), fibrin clots within the specimen,
inadequate mixing of the specimen with anticoagulant and varying the ratio of blood
sample to anticoagulant. Other possible reasons could be use of conventional syringes
flushed with liquid heparin which could lead to dilution of sample volume and thus
underestimation of electrolytes on ABG. Results of electrolytes on ABG and electrolyte
analyzer cannot be used in inter-exchangeable manner and should be interpreted with
caution.
5. Yes, for sure
ARTERIAL BLOOD GAS PROS AND CONS
1. Advantages
• gold standard test for determining the arterial metabolic milieu (pH, PaCO2, HCO3)
• can determine PaO2
2. Disadvantages
• pH, PCO2 (if normocapnic), HCO3 and base excess from a VBG are usually adequate for
clinical decision making
• SpO2 is usually sufficient for clinical decision making unless pulse oximetry is unreliable
for other reasons (e.g. shock state, poor pick up)
• painful (should be performed with local anesthetic in conscious patients)
• increased risk of bleeding and hematoma
• risk of pseudo aneurysm and AV fistula
• infection
• nerve injury
• digital ischemia
• injury to staff
• delays in care
• serial exams may be needed
INTERPRETATION OF ARTERIAL BLOOD GASES
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Blood gas analysis is a commonly used diagnostic tool to evaluate the partial pressures of
gas in blood and acid-base content.
A "blood gas analysis" can be performed on blood obtained from anywhere in the
circulatory system (artery, vein, or capillary).
An arterial blood gas (ABG) explicitly tests blood taken from an artery.
ABG analysis assesses the patient's partial pressures of oxygen (PaO2) and carbon dioxide
(PaCO2). PaO2 provides information on the oxygenation status, and PaCO2 offers
information on the ventilation status (chronic or acute respiratory failure). PaCO 2 is
affected by hyperventilation (rapid or deep breathing), hypoventilation (slow or shallow
breathing), and acid-base status. Although oxygenation and ventilation can be assessed
non-invasively via pulse oximetry and end-tidal carbon dioxide monitoring, respectively,
ABG analysis is the standard.
COMPONENTS OF ABG - GASES
PH: measures hydrogen ion concentration in the blood, it shows blood’ acidity or alkalinity
Normal range – 7.35-7.45
PCO2 :It is the partial pressure of CO2 that is carried by the blood for excretion by
the lungs, known as respiratory parameter Normal range – 35-45 mmHg
PO2: It is the partial pressure of O2 that is dissolved in the blood , it reflects the body
ability to pick up oxygen from the lungs. Normal range – 80-100 mmHg
HCO3 : known as the metabolic parameter, it reflects the kidney’s ability to retain and
excrete bicarbonate
Normal range – 20-28 mmol/L
For calculation purposes – use 24 as ideal HCO3
Base excess – it is a marker of metabolic acidosis or alkalosis.
A high base excess (> +2mmol/L) indicates that there is a higher than normal amount of
HCO3– in the blood, which may be due to a primary metabolic alkalosis or a compensated
respiratory acidosis.
A low base excess (< -2mmol/L) indicates that there is a lower than normal amount of
HCO3– in the blood, suggesting either a primary metabolic acidosis or a compensated
respiratory alkalosis. Normal range - +2 to -2
OTHER COMPONENTS
Electrolytes
A venous or arterial blood gas is a good way to quickly check potassium and sodium
values. This is particularly important in the immediate management of cardiac arrhythmias
as it gives an immediate result.
Lactate
Lactate is produced as a by-product of anaerobic respiration. A raised lactate can be caused
by any process which causes tissue to use anaerobic respiration. It is a good indicator of
poor tissue perfusion
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Haemoglobin
Haemoglobin acts as a guide but is notoriously inaccurate in an ABG. Lab samples should
be used to verify results
Glucose
Don’t forget to check this. Glucose is especially pertinent in the management of the patient
who has decreased consciousness or seizures. It is also important in patients with known or
suspected diabetes.
Glucose may also be raised in patients with severe sepsis or other metabolic stress
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PRE-PROCEDURE
• Record patient inspired oxygen concentration
• Check patient temperature
• Explain the procedure to the patient
• Provide privacy for client
• If not using heparinized syringe , heparinize the needle
• Perform modified Allen's test if radial artery is chosen for sample.
• 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.
Modified Allen’s test
Have the patient flex the selected upper extremity at the elbow and clench a raised fist for 30
seconds. Apply pressure over the ulnar and radial arteries to occlude the blood flow. After 5
seconds, the patient may unclench the raised fist. The palm will now appear pale, white, or
blanched. Then, pressure over the ulnar artery is released while the radial artery compression
is maintained. In 10 to 15 seconds, the palm returns to its original color, indicating adequate
ulnar collateral blood flow. If the palm does not return to its actual color, it is an abnormal
test and unsafe to puncture the radial artery.
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• 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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Complications
Arterio-spasm
Hematoma
Hemorrhage
Distal ischemia
Infection
Numbness
Before you withdraw a sample for ABG
After any change in FiO2 wait for 20min
And wait for 30 min after any change in ventilatory parameters to ensure steady state.
CONTRAINDICATIONS
• Cellulitis or other infections over puncture site
• Absence of palpable arterial pulse
• Negative result of an Allen test/modified Allen test
• Coagulopathies / anticoagulant therapy
• History of arterial spasm following previous puncture
• Severe Peripheral Vascular Disease
• Arterial grafts
• Dialysis shunt – choose another site
TECHNICAL ERRORS IN SAMPLING EXCESSIVE HEPARIN
Ideally pre-heparinised syringes should be used
Syringes flushed with 1:1000 heparin and rinsed
Do not leave excessive heparin in the syringe
Heparin has dilutional effect:
• Low HCO3
• Low PCO2
• High Sr Na
TECHNICAL ERRORS IN SAMPLING
ALTERATION OF RESULTS WITH SIZE OF SYRINGE/NEEDLE AND VOL OF
SAMPLE
Syringes must have > 50% blood
Use only 3ml or smaller syringes
25% lower values if 1 ml sample taken in 10ml syringe (0.25ml heparin in needle)
TECHNICAL ERRORS IN SAMPLING AIR BUBBLES IN BLOOD SAMPLE
In air, PO2 is 150 mm of Hg & PCO2 is 0
Contact with air bubble will lead to higher PO2 and lower PCO2
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Seal syringe immediately after sampling
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• A left shift will increase oxygen's affinity for [Link] a left shift condition
(alkalosis, hypothermia, etc.) oxygen will have a higher affinity for hemoglobin.
• SaO2 will increase at a given PaO2, but more of it will stay on the hemoglobin and
ride back through the lungs without being used. This can result in tissue hypoxia even
when there is sufficient oxygen in the blood.
• A right shift decreases oxygen's affinity for hemoglobin. In a right shift (acidosis,
fever, etc.) oxygen has a lower affinity for hemoglobin. Blood will release oxygen
more readily.
• This means more O2 will be released to the cells, but it also means less oxygen will be
carried from the lungs in the first place
• Traditionally the curve starts with:
○ pH at 7.4,
○ temperature at 37 Centigrade, and ○
PaCO2 at 40.
Changes from these values are called "shifts".
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Oxygenation (PaO2)
Your first question when looking at the ABG should be “Is this patient hypoxic?” as
hypoxia is the most immediate threat to life.
PaO2 should be >10 kPa (75mmHg) when oxygenating on room air in a healthy patient.
If the patient is receiving oxygen therapy their PaO2 should be approximately 10kPa less
than the % inspired concentration FiO2 (so a patient on 40% oxygen would be expected
to have a PaO2 of approximately 30kPa /225mmHg).
Oxygen delivery devices and flow rates
A common question is “What percentage of oxygen does this device deliver at a given
flow rate?”. Below is a quick reference guide, providing some approximate values for
the various oxygen delivery devices and flow rates you’ll come across in practice.
Nasal cannulae
As with all oxygen delivery devices, there is a significant amount of variability depending on
the patient’s breathing rate, depth and how well the oxygen delivery device is fitted. Below are
some guides to various oxygen flow rates and the approximate percentage of oxygen
delivered:4
• 1L / min – 24%
• 2L/ min – 28%
• 3L/ min – 32%
• 4L / min – 36%
Simple face mask
The oxygen delivery of simple face masks is highly variable depending upon oxygen flow rate,
the quality of the mask fit, the patient’s respiratory rate and their tidal volume. Simple face
masks can deliver a maximum FiO2 of approximately 40%-60% at a flow rate of 15L/min.
These masks should not be used with flow rates less than 5L/min.³
Reservoir mask (also known as a non-rebreather mask)
Reservoir masks deliver oxygen at concentrations between 60% and 90% when used at a flow
rate of 10–15 l/min.³ The concentration is not accurate and will depend on the flow of oxygen
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as well as the patient’s breathing pattern. These masks are most suitable for trauma and
emergency use where carbon dioxide retention is unlikely.
Type 2 respiratory failure
Type 2 respiratory failure involves hypoxaemia (PaO2 is <8 kPa / 60mmHg) with
hypercapnia (PaCO2 >6.0 kPa / 45mmHg). It occurs as a result of alveolar hypoventilation,
which prevents the patient from being able to adequately oxygenate and eliminate CO2
from their blood.
Hypoventilation can occur for a number of reasons including:
• Increased resistance as a result of airway obstruction (e.g. COPD).
• Reduced compliance of the lung tissue/chest wall (e.g. pneumonia, rib fractures, obesity).
• Reduced strength of the respiratory muscles (e.g. Guillain-Barré, motor neurone disease).
• Drugs acting on the respiratory centre reducing overall ventilation (e.g. opiates).
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ARTERIAL BLOOD GAS ANALYSIS: ACID-BASE BALANCE
Disturbances of acid-base balance:
1. Metabolic
2. Respiratory
• Metabolic processes are those that primarily alter the HCO3 concentration in the blood. A
decrease in serum HCO3 (base) leads to a metabolic acidosis, while an increase in serum
HCO3 leads to a metabolic alkalosis.
• Respiratory processes alter the pH by changing the CO2 levels.
• CO2 is a respiratory acid. CO2 accumulation causes an acid state in the blood (through
carbonic acid), and as respirations (respiratory rate and/or tidal volume) increase, the body
eliminates more CO2 (acid) and is left with a respiratory alkalosis. A decrease in ventilation
leads to retention and increased levels of CO2, and thus a respiratory acidosis.
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3. CNS Depression -head injury, medications such as narcotics, sedatives or anesthesia
4. Neuromuscular Disease and Impairment
5. Ventilatory Restriction—due to pain, chest wall injury/ deformity, or abdominal
distension
INCREASED CO2 PRODUCTION
• Large caloric loads
• Malignant hyperthermia
• Intensive shivering
• Prolonged seizure activity
• Thyroid storm
• Extensive thermal injury (burns)
RESPIRATORY ALKALOSIS
pH, CO2, Ventilation
CO2 HCO3 ( Cl to balance charges )
hyperchloremia)
Causes CHAMPS
C – CNS Disease e.g. Intracerebral hemorrhage,CVA
Cirrhosis
H – Hypoxia – pneumonia, pulmonary oedema
A – Anxiety
M – more ventilation
P – Progesterone
S – Salicylate/Sepsis
T - Thyrotoxicosis
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The delta gap: The difference between the patient’s anion gap and the normal anion gap
is termed the delta gap. This amount is considered an HCO3 equivalent, because for
every unit rise in the anion gap, the HCO3 should lower by 1 (by buffering). Thus,
if the delta gap is added to the measured HCO3 , the result should be in the normal range
for HCO3 ; elevation indicates the additional presence of a metabolic alkalosis
• ∆ HCO3 = Normal HCO3 – Measured HCO3
24 – Measured HCO3
Ideally ∆Anion Gap = ∆HCO3
Non Gap Metabolic Acidosis
H - Hyper alimentation
A - Acetazolamide
R - RTA
D - Diarrhea
U - Uretero-pelvic shunt
P - Pancreatic Fistula
S – Spironolactone
Negative anion gap occurs rarely as a laboratory artifact in severe cases of
hypernatremia, hyperlipidemia, and bromide intoxication.
Winter's formula is an equation used to calculate the expected partial pressure of carbon
dioxide (PCO2) in a patient's arterial blood gas (ABG):
𝐸𝐸𝐸𝐸𝐸𝐸𝐸𝐸𝐸𝐸𝐸2=(1.5×𝐸𝐸𝐸𝐸𝐸𝐸𝐸𝐸3)+(8±2)
METABOLIC ALKALOSIS
^pH, ^HCO3
• PCO2 by 0.1 for every 1mEq/L in ^HCO3
Causes – CLEVER PD
C- Contraction
L - Liquorice
E - Endocrine: Conn’s / Cushing’s / Bartter’s
V - Vomiting / NG Suction
E - Excess Alkali
R - Refeeding Alkalosis
P - Post Hypercapnea
D - Diuretics and Chronic diarrhoea
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TREATMENT
Treatment of metabolic acidosis
The underlying condition behind the acidosis must be treated. In some cases, sodium
bicarbonate is prescribed to return the blood to a normal pH. Severe cases can lead to
shock and can be life threatening.
Full Correction Dose (mmol) = 0.3 x base deficit (mmol/L) x wt(kg)
This amount of sodabicarb must be given in 24 hours
50% in first 6 hours followed by remaining 50% over next 18 hours
Treatment of respiratory acidosis
○ A doctor should be seen immediately to treat acute respiratory acidosis, as this
can be a life threatening condition. Treatment is targeted to the cause.
○ Bronchodilator medications may be given to correct some forms of airway
obstruction. If your blood oxygen level is too low, you may require oxygen.
Noninvasive positive pressure ventilation or a breathing machine may be
necessary.
Alkalosis : treatment
• Carbon dioxide level needs to return to normal if respiratory alkalosis.
• If rapid breathing caused by anxiety, taking slow, deep breaths can often improve
symptoms and regulate oxygen level.
• If tests reveal that a low oxygen level, need to receive oxygen through a mask.
• If rapid breathing is caused by pain, then treating the pain will help to bring
respiratory rate back to normal and improve symptoms.
• If alkalosis is caused by a loss of chemicals such as chloride or potassium, then
prescribe medications or supplements to replace these chemicals.
• Some cases of alkalosis result from an electrolyte imbalance, which may be
corrected by drinking plenty of fluids or drinks that contain electrolytes.
• Most people recover from alkalosis once they receive treatment.
Example 1
Jane Doe is a 45-year-old female admitted to the nursing unit with a severe asthma
attack. She has been experiencing increasing shortness of breath since admission three
hours ago. Her arterial blood gas result is as
follows Clinical Laboratory:
pH 7.22
PaCO2 55
HCO3 25
Follow the steps:
1. Assess the pH. It is low therefore, we have acidosis.
2. Assess the PaCO2. It is high and in the opposite direction of the pH.
3. Assess the HCO3. It has remained within the normal range (22-26).
Acidosis is present (decreased pH) with the PaCO2being increased, reflecting a primary
respiratory problem. For this patient, we need to improve the ventilation status by
providing oxygen therapy, mechanical ventilation or by administering bronchodilators.
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Example 2
John Doe is a 55-year-old male admitted with a recurring bowel obstruction. He has
been experiencing intractable vomiting for the last several hours, Here is his arterial
blood gas result: Clinical Laboratory:
pH 7.50
PaCO2 42
HCO3 33
Follow the steps again:
1. Assess the pH. It is high (normal 7.35-7.45), therefore, indicating alkalosis.
2. Assess the PaCO2. It is within the normal range (normal 35-45).
3. Assess the HCO3. It is high (normal 22-26) and moving in the same direction as the
pH.
Alkalosis is present (increased pH) with the HCO3 increased, reflecting a primary
metabolic problem. Treatment of this patient might include administration of I.V. fluids
and measures to reduce the excess base.
Example3
A vomiting, ill-appearing patient with alcohol use disorder has laboratory results
showing
• Na: 137
• K: 3.8
• Cl: 90
• HCO3 : 22
• pH: 7.40
• Pco2: 41
• Po2: 85
At first glance, the results appear unremarkable. However, calculations show elevation
of the anion gap:
137 − (90 + 22) = 25 (normal, 10 to 12) indicating a metabolic acidosis.
Respiratory compensation is evaluated by Winters formula:
Predicted Pco2= 1.5 (22) + 8 ± 2 = 41 ± 2
Predicted = measured, so respiratory compensation is appropriate.
Because there is metabolic acidosis, the delta gap is calculated, and the result is added to
measured HCO3 :
25 − 10 = 15
15 + 22 = 37
The resulting corrected HCO3 is above the normal range for HCO3 , indicating a
primary metabolic alkalosis is also present. Thus, the patient has a mixed acid-
base disorder.
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