Index
An arterial blood gas (ABG) test measures the amount of blood gases, such as oxygen and carbon dioxide.
An arterial blood gas test requires a small volume of blood to be drawn from the radial artery with a syringe and a thin needle, but the femoral artery in the groin or other site is sometimes used.
Blood can also be drawn from an arterial catheter . An arterial blood gas test measures the arterial blood pressure oxygen tension values, the arterial partial pressure of carbon dioxide, and the pH of the blood.
In addition, arterial oxygen saturation can be determined. Such information is vital when dealing with critically ill patients or respiratory illnesses .
Therefore, the arterial blood gas test is one of the most common tests performed on patients in intensive care units.
At other levels of care, pulse oximetry plus transcutaneous carbon dioxide measurement is a less invasive alternative method of obtaining similar information.
An arterial blood gas test can also measure the level of bicarbonate in the blood. Many blood gas analyzers also report concentrations of lactate, hemoglobin, various electrolytes, oxyhemoglobin, carboxyhemoglobin, and methemoglobin.
Arterial-blood gas tests are used primarily in pulmonology and intensive care medicine to determine gas exchange across the alveolocapillary membrane.
Blood gas tests also have a variety of applications in other areas of medicine. Disorder combinations can be complex and difficult to interpret, which is why calculators, nomograms, and rules of thumb are commonly used.
The arterial and blood gas samples were originally sent from the clinic to the medical laboratory for analysis. Today, the analysis can be done in the laboratory or as a point-of-care test, depending on the equipment available in each clinic.
Why is it necessary to order a blood gas test?
The use of an arterial blood gas analysis is necessary in view of the following advantages:
- Helps establish the diagnosis.
- Guide treatment plan.
- Helps in managing the fan.
- Improved acid / base handling; allows optimal function of medications.
- Acid / base status can alter electrolyte levels critical to a patient’s condition.
Accurate results for an arterial blood gas depend on the correct way to collect, handle, and analyze the sample.
Clinically important errors can occur in any of the above steps, but arterial blood gas measurements are particularly vulnerable to preanalytical errors.
The most common problems encountered include non-arterial samples, air bubbles in the sample, inadequate or excessive anticoagulant in the sample, and delayed analysis of an uncooled sample.
What happens during the test?
You will likely have an arterial blood gas test in a hospital, but your doctor may be able to do it in his or her office.
Your doctor or other healthcare professional will use a small needle to draw some of your blood, usually from your wrist. Instead, they could take it from an artery in your groin or on the inside of your arm above your elbow.
Before the arterial blood gas test, your doctor or other healthcare professional may apply pressure to the arteries in your wrist for several seconds. The procedure, called a modified Allen test, checks that blood flow to your hand is normal.
Also, if you are on oxygen treatment but can breathe without it, your doctor may perform the arterial gas test after the oxygen has been turned off for 20 minutes.
Collecting blood from an artery is likely to hurt more than drawing blood from a vein, because arteries are deeper than veins and there are sensitive nerves nearby. You may have a few minutes of discomfort during or after the test.
You may also feel lightheaded, dizzy, or nauseous while your blood is being drawn. To reduce the chance of bruising, you can gently press on the area for a few minutes after the needle comes out.
Possible preanalytical errors
Preanalytical errors occur in the following stages:
During preparation before sampling
Missing / incorrect identification of patient / sample.
Using the wrong type or amount of anticoagulant.
- Dilution due to the use of liquid heparin.
- Insufficient amount of heparin.
- Binding of electrolytes to heparin.
Inadequate stabilization of the patient’s respiratory condition; and improper withdrawal of the wash solution in arterial lines prior to blood collection.
During sampling / handling
Venous and arterial blood mixture during puncture. Air bubbles in the sample.
Any air bubbles in the sample should be expelled as soon as possible after removing the sample and before mixing it with heparin or before any cooling of the sample has taken place.
An air bubble whose relative volume is up to 1% of the blood in the syringe is a potential source of significant error and can seriously affect the partial pressure of the oxygen value (pO2). Insufficient mixing with heparin.
During storage / transportation
Improper storage and hemolysis of blood cells.
General storage recommendation
Do not cool the sample. Analyze within 30 min. For samples with high partial pressure of oxygen (PaO2), for example, shunt or with high white blood cell or platelet count are also analyzed within 5 minutes.
When the analysis is expected to take more than 30 minutes, the use of glass syringes and ice suspension is recommended.
During preparation before sample transfer
Visually inspect the sample for clots. Inadequate mixing of the sample before analysis.
Insufficient mixing can cause the sample to clot. It is recommended to thoroughly mix the blood sample by inverting the syringe 10 times and rolling it between the palms. This prevents stacking (like coins or plates) of red blood cells.
During anticoagulation
Modern blood gas syringes and capillaries are coated with various types of heparin to prevent clotting in the sample and within the blood gas analyzer:
- Unbalanced liquid heparin.
- Unbalanced dry heparin.
- Electrolytically balanced dry heparin (Na +, K +, Ca2 +).
- Ca2 + dry – balanced heparin.
Other anticoagulants, for example, citrate and ethylenediaminetetraacetic acid (EDTA) are both slightly acidic, increasing the risk of the pH falsely lowering.
Liquid heparin
The use of liquid heparin as an anticoagulant causes a dilution of the sample, that is, it dilutes the plasma, but not the content of the blood cells. As a consequence, parameters such as the partial pressure of carbon dioxide (pCO2) and electrolytes are affected.
Only 0.05 mL of heparin is required to anticoagulate 1 mL of blood.
The dead space volume of a standard 5 ml syringe with a 1 inch 22 gauge needle is 0.2 ml; filling the dead space of the syringe with heparin provides enough volume to anticoagulate a 4 ml blood sample.
If smaller sample volumes are obtained or more liquid heparin is left in the syringe, the dilution effect will be even greater.
The dilution effect also depends on the hematocrit value. Plasma electrolytes decrease linearly with plasma dilution together with the values of pCO2, cGlucose and hemoglobin concentration (ctHb).
The pH and pO2 values are not affected by dilution. The paO2 is only as small as 2% of the physically dissolved O2 in the plasma, so the oximetry parameters given in fractions (or%) will not be affected.
Syringes for blood gas analysis can have a wide range of heparin amounts. Units are typically administered as IU / mL (International Units of Heparin per milliliter) drawn with blood into the syringe.
To obtain a sufficient final concentration of heparin in the sample, the recommended volume of blood should be drawn into the syringe.
Example: a syringe containing 50 IU / ml when filled with 1.5 ml of blood means that the syringe contains a total of 75 IU of dry heparin.
If the user draws 2 ml of blood, the resulting heparin concentration will be too low and the sample may clot.
If the user draws just 1 ml, the resulting heparin concentration will be higher than desired, which can produce falsely low electrolyte results.
Heparin binds positive ions such as Ca2 +, K +, and Na +. Electrolytes bound to heparin cannot be measured with ion selective electrodes, and the end effect will be the measurement of unfortunate low values.
The binding effect and the resulting imprecision of the results are especially significant for corrected Ca2 +. The use of electrolyte balanced heparin significantly reduces the binding effect and the resulting imprecision.
The following steps are recommended for rapid interpretation of arterial blood gas:
- Check the consistency of the gas in the arterial blood.
When performing an arterial blood gas interpretation, always check the consistency of the report using the modified Henderson equation.
[H + -] [HCO3]
———————— = 24
PaCO2
The hydrogen ion is calculated by subtracting the two digits after the pH decimal point from 80, for example, if the pH is 7.23, then:
[H +] = 80 – 23 = 57
O
[H +] = 10 (9-pH)
Hydrogen can be calculated from: the pH value and corresponding H + ion concentration:
pH | H+ | pH | H+ |
6,70 | 200 | 7,40 | 40 |
6,75 | 178 | 7,45 | 35 |
6,80 | 158 | 7,50 | 32 |
6,85 | 141 | 7,55 | 28 |
6,90 | 126 | 7,60 | 25 |
6,95 | 112 | 7,65 | 22 |
7.00 | 100 | 7.70 | 20 |
7,05 | 89 | 7,75 | 18 |
7,10 | 79 | 7,80 | 16 |
7.15 | 71 | 7,85 | 14 |
7,20 | 63 | 7,90 | 13 |
7,25 | 56 | 7,95 | 11 |
7,30 | 50 | 8,00 | 10 |
7,35 | 45 |
Obtain a relevant medical history
When making an interpretation of an arterial blood gas, never comment on the arterial blood gas without obtaining a relevant medical history from the patient, which gives a clue to the etiology of the acid-base disorder.
For example, a patient with a history of hypotension, kidney failure, uncontrolled diabetic status, from treatment with drugs such as metformin is likely to have metabolic acidosis.
A patient with a history of diuretic use, bicarbonate administration, high nasogastric aspirate, and vomiting is likely to have metabolic alkalosis.
Respiratory acidosis could occur in chronic obstructive pulmonary disease (COPD), muscle weakness, postoperative cases, and opioid overdose, and respiratory alkalosis is likely to occur in sepsis, hepatic coma, and pregnancy.
Look at the oxygenation status of the patient
The oxygenation status of the patient is judged by the paO2 , however, a comment on the oxygenation status should never be made without knowing the corresponding fraction of inspired oxygen (FIO2). Calculate the expected paO2 (usually five times the FiO2).
Based on the expected paO2, it is classified as mild, moderate, and severe hypoxia.
Ventilation status : observe the paCO2.
Acid-base status : Identify the primary disorder by observing the pH.
pH> 7.40-Alkalemia: – 7.40-Acidemia.
Then look at paCO2 which is a respiratory acid, whether it is increased i.e.> 40 (acidosis) or decreased <40 (alkalosis) and if this explains the pH change then it is a respiratory disorder.
Otherwise, look at the trend of the HCO3- change (whether it increases alkalosis or decreases in acidosis): if it explains the pH change, then it is a metabolic disorder.
In a normal arterial gas
- pH and paCO2 move in opposite directions.
- Bicarbonate (HCO3-) and paCO2 move in the same direction.
When pH and paCO2 change in the same direction (which normally they shouldn’t), the main problem is metabolic; when pH and paCO2 move in opposite directions and paCO2 is normal, then the primary problem is respiratory.
Mixed Disorder : If HCO3 and paCO2 change in the opposite direction (which they normally should not), then it is a mixed disorder: pH can be normal with abnormal paCO2 or abnormal pH and normal paCO2).
If the trend of change in paCO2 and HCO3- is the same, check the percentage difference. The one with a greater% difference between the two is the one that is the dominant disorder.
For example : pH = 7.25 HCO3- = 16 paCO2 = 60.
Here the pH is acidotic and both paCO2 and HCO3- explain your acidosis: so look at the percentage difference.
Difference of HCO3-% = (24 – 16) / 24 = 0.33
Difference of paCO2% = (60 – 40) / 40 = 0.5
Therefore, respiratory acidosis is the dominant disorder.
Respiratory disorders
After the primary disorder is established as respiratory, the following points will help us get closer to the respiratory disorder:
- Ratio of the rate of change in H + to change in paCO2.
- Alveolar arterial oxygen gradient.
- Compensation.
Ratio of the rate of change in H + to change in paCO2
The above ratio of the rate of change in H + to change in paCO2 helps guide us to conclude whether the respiratory disorder is acute, chronic, or acute-chronic.
As we have seen, hydrogen can be calculated from Table 1 and the change in H + is calculated by subtracting the normal H + from the calculated H + ion.
ΔH +
——————- <0.3-Chronic
ΔPaCO2
> 0.8 agudo.
0.3-0.8 acute in chronic.
Alveolar arterial oxygen gradient
It is calculated as follows:
PaCO2
PAO2 = PiO2 – ————–
R
PiO2 = FiO2 (PB – PH2O)
PaCO2
PAO2 = FiO2 (PB-PH2O) – ————
R
Where PAO2, alveolar partial pressure of oxygen; PiO2, partial pressure of inspired oxygen; FiO2, fraction of inspired oxygen; PB, barometric pressure (760 mmHg at sea level); PH2O, water vapor pressure (47 mm Hg), PaCO2, partial pressure of carbon dioxide in the blood; A: The respiratory quotient is assumed to be 0.8.
PaCO2
= FiO2 (760 – 47) – ———–
0.8
Hypoxemic respiratory failure may be associated with a normal (10-15 mmHg) or increased arterial oxygen gradient. Differentials of extrapulmonary causes of respiratory failure:
- Central nervous system : depression of the respiratory center, due to causes such as drug overdose, primary alveolar hypoventilation and myxedema.
- Peripheral nervous system : spinal cord diseases, Guillain-Barré syndrome, amyotrophic lateral sclerosis.
- Respiratory muscles : hypophosphatemia, muscle fatigue, myasthenia gravis, and polymyositis.
- Chest wall diseases : ankylosing spondylitis, unstable chest, thoracoplasty.
- Pleural diseases : restrictive pleurisy.
- Upper airway obstruction : tracheal stenosis, vocal cord tumor
Compensation
Compensation rules
The compensatory response depends on the proper functioning of the organ system involved in the response (lungs or kidneys) and on the severity of the acid-base alteration.
For example, the probability of complete compensation in chronic respiratory acidosis is <15% when the paCO2 exceeds 60 mmHg.
Acute compensation occurs within 6 to 24 hours and chronic within 1 to 4 days. Respiratory compensation occurs faster than metabolic compensation.
In clinical practice, it is rare to see complete compensation. The maximum compensatory response in most cases is associated with only 50-75% return of the pH to normal.
However, in chronic respiratory alkalosis, the pH can return to normal in some cases.
Acute respiratory acidosis : [HCO3-] increases by 1 mEq / L for every 10 mmHg increase in paCO2 above 40.
Chronic : [HCO3-] increases by 3.5 mEq / L for every 10 mmHg increase in paCO2 above 40.
Acute respiratory alkalosis : [HCO3-] decreases by 2 mEq / L for every 10 mmHg decrease in paCO2 below 40.
Chronic : [HCO3-] decreases by 5 mEq / L for every 10 mmHg decrease in paCO2 below 40.
Metabolic disorders
In patients with metabolic acidosis, there is an excess of acid or a loss of base. This causes the HCO3-: H2CO3 ratio and pH to drop, while no change occurs in metabolic acidosis not compensated by pCO2.
As a result of compensatory mechanisms, the lungs in the form of CO2 excrete H2CO3 and the kidneys retain HCO3-.
Falls in pCO2 and the HCO3-: H2CO3 ratio and an increase in pH towards normality despite the fact that the concentrations of HCO3 and H2CO3 are lower than normal.
This is called compensated metabolic acidosis, and the expected paCO2 is calculated as paCO2 = [1.5 × HCO3 + 8] ± 2.
Anion gap
For more than 40 years, the anion gap theory has been used by clinicians to exploit the concept of electroneutrality and has been developed as an important tool for assessing acid-base disorder.
The anion gap is the difference between the charges of plasma anions and cations, calculated from the difference between the routinely measured concentration of serum cations (Na + and K +) and anions (Cl- and HCO3-).
Because electroneutrality must be maintained, the difference reflects the unmeasured ions. Normally, this gap or gap is filled with the weak acids (A-) mainly albumin and, to a lesser extent, phosphates, sulfates and lactates.
When the anion space is greater than that produced by albumin and phosphate, other anions (eg, lactates and ketones) must be present in a higher than normal concentration.
Anion gap = (Na + + K +) – [Cl- + HCO3-]
Due to its low and narrow extracellular concentration, K + is often omitted in the calculation. The normal value ranges from 12 ± 4 when K + is considered to 8 ± 4 when K + is omitted.
The main problem with the anion gap is its dependence on the use of the normal range produced by albumin and, to a lesser extent, phosphate, the level of which can be extremely abnormal in critically ill patients.
Because these anions are not strong anions, their charges will be altered by changes in pH.
Serum protein and phosphate, normal anion gap = 2 {albumin (gm / L)} + 0.5 {phosphate (mg / dL)}
Acid-base state
- In the acidic state, the anion gap decreases by 1-3.
- In the Alkalemic state, the anion gap increases by 2-5.
Main clinical uses of the anion gap
For signaling, the presence of metabolic acidosis and confirm other findings.
Helps to differentiate between the causes of metabolic acidosis: high anion gap vs normal anion gap metabolic acidosis.
In an inorganic metabolic acidosis (eg, due to infusion of hydrochloric acid (HCl)), the infused chloride (Cl-) replaces HCO3-, and the anion space remains normal.
In organic acidosis, the lost bicarbonate is replaced by the acid anion that is not normally measured. This means that the anion space increases.
Provide assistance in assessing the biochemical severity of acidosis and monitoring response to treatment.
In patients with metabolic alkalosis, there is an excess of base or a loss of acid that causes the HCO3-: H2CO3 ratio and pH to rise, but without causing any change in pCO2, which is called uncompensated metabolic alkalosis.
However, the kidney has a great capacity to excrete excess bicarbonate and, to maintain metabolic alkalosis, the elevated HCO3 concentration must be maintained through abnormal renal retention of HCO3-.
Compensatory respiratory acidosis can be so marked that pCO2 can rise to more than 55 mmHg. The expected paCO2 is calculated as paCO2 = [0.7 × HCO3- + 21] ± 2 or 40 + [0.7 ΔHCO3]. This is called compensated metabolic alkalosis.
Most patients with metabolic alkalosis can be treated with chloride ions in the form of sodium chloride (NaCl) (sensitive saline) instead of potassium chloride (KCl) (which is preferable).
When sodium chloride is administered, Cl ions are delivered, so blood volume increases and excess aldosterone secretion decreases.
Thus, excessive urinary K + loss and excessive HCO3 reabsorption are stopped. When metabolic alkalosis is due to the effects of excessive aldosterone or other mineralocorticoids, the patient does not respond to sodium chloride (resistant to saline) and requires potassium chloride.
Based on urinary chloride, metabolic alkalosis is divided into:
Sensitive or extracellular chloride volume depletion (urinary chloride <20).
Vomiting, diuretic, post-hypercapnia, chronic diarrhea, resistant to chlorides (urinary chloride> 20), severe potassium depletion.
Mineralocorticoid excess : primary hyperaldosteronism, Cushing’s syndrome, ectopic adrenocorticotropic hormone (ACTH).
Secondary hypereldosteronism : renovascular disease, malignant hypertension, congestive heart failure (CHF), cirrhosis .
Mixed disorders
Mixed metabolic abnormalities (such as the high anion gap of diabetic ketoacidosis plus the normal anion gap of diarrhea) can be identified using the relationship between the anion gap and HCO3-, which is called the gap-gap relationship.
It is the ratio of change in the anion gap (ΔAG) to change in HCO3- (ΔHCO3-).
When hydrogen ions accumulate in the blood, the decrease in serum HCO3 is equivalent to the increase in the anion space and the increase in excess anion gaps / HCO3 deficit ratio is unity, that is, a pure increase in the anion gap metabolic acidosis.
When there is an acidosis of the normal anion gap, the ratio approaches zero. When there is mixed acidosis (high anion gap + normal anion gap), the gap-gap relationship indicates the relative contribution of each type to acidosis.
If it is <1, it suggests that there is an associated normal anion gap metabolic acidosis and if it is> 2 it suggests that there is an associated metabolic acidosis.
What do the results mean?
Arterial blood gas test results are generally available in less than 15 minutes. But your doctor cannot diagnose a problem from the results of an arterial blood gas test alone. Then they’ll probably do other tests too.
Arterial blood gas test results can show if:
- Your lungs are getting enough oxygen.
- Your lungs are removing enough carbon dioxide.
- Your kidneys are working properly.
Values for normal results vary. If your results are not normal, there could be many reasons why, including certain illnesses or injuries that affect your breathing.
Your doctor will consider your results in light of your general health and conditions, as well as other test results, and then recommend next steps to improve your health.