Arterial blood gas

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Priyamvada Singh, M.B.B.S. [2], Mohammed Abdelwahed M.D[3]

Overview

An arterial blood gas is a blood test that is performed specifically on arterial blood, to determine the concentrations of carbon dioxide, oxygen and bicarbonate, as well as the pH of the blood. Its main use is in pulmonology, to determine gas exchange levels in the blood related to lung function, but it is also used in nephrology, and used to evaluate metabolic disorders such as acidosis and alkalosis. As its name implies, the sample is taken from an artery, which is more uncomfortable and difficult than venipuncture.

Physiological bases

• PH (potential of hydrogen) is a numeric scale used to specify the acidity or basicity of a solution.
• It is the base 10 logarithm of the activity of the hydrogen ion.
• Solutions with a pH less than 7 are acidic and solutions with a pH greater than 7 are basic.
• The pH of the blood plasma is normally tightly regulated between 7.32 and 7.42.

Hydrogen ion regulation

• The body maintains a narrow PH range by 3 mechanisms:

Rapid lung compensation:

• CO2 elimination is controlled by the lungs. The decrease in pH results in decreases in PCO2. Increase in pH results in increases in PCO2.
• A metabolic acidosis excites the chemoreceptors and initiates a prompt increase in ventilation and a decrease in arterial PCO2.
• A metabolic alkalosis silences the chemoreceptors and produces a prompt decrease in ventilation and increase in arterial PCO2.

Slow kidney compensation:

• The renal compensation takes three to five days for completion.
• Renal compensations are mediated by increased hydrogen ion secretion in respiratory acidosis and decreased hydrogen ion secretion and urinary HCO3 loss in respiratory alkalosis.
• Chemical buffers react instantly to compensate for the addition or subtraction of H+ ions.
• Renal excretion of acid from tissues is achieved by combining hydrogen ions with urinary buffers to form titratable acid such as:
• Phosphate (HPO4-  +  H+  →  H2PO4-)
• Ammonia to form ammonium (NH3  +  H+  →  NH4+)
• HCO3 elimination is controlled by the kidneys. Decreases in pH result in increases in HCO3-. Increases in pH result in decreases in HCO3-.
• Acid-base status is usually assessed by measuring the components of the bicarbonate and carbon dioxide in blood:

CO2  +  H2O  ↔  H2CO3  ↔  HCO3-  +  H+

• The partial pressure of CO2 and the pH are each measured using electrodes. The serum bicarbonate (HCO3-) concentration is then calculated with the Henderson-Hasselbalch equation.

pH   =   6.10   +   log  ([HCO3-]  ÷  [0.03  x  PCO2])

• The Henderson-Hasselbalch equation shows that the pH is determined by the ratio of the serum bicarbonate (HCO3-) concentration and the PCO2, not by the value of either one alone.
• The degree of compensation is usually defined by the decrease or increase in arterial PCO2 from its normal range or the decrease or increase in serum HCO3 from its normal range.

Video shows physiology of acid-base balance

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Indications of ABG

• Identification of acid-base disturbances.
• Measurement of the partial pressures of oxygen and carbon dioxide.
• Assessment of the response to therapeutic interventions.
• Collection of a blood sample when venous sampling is not feasible.

Contraindications of ABG

• Radial samples are contraindicated in abnormal modified Allen's test.
• Abnormal anatomy at the puncture site such as:
• Congenital malformations
• Burns
• Aneurysm
• Arteriovenous fistula
• Active Raynaud's syndrome

Extraction and Analysis

• Arterial blood for blood gas analysis is usually extracted by a phlebotomist, nurse, or respiratory therapist.
• Blood may be taken from an easily accessible artery (typically the radial artery, but during unusual or emergency situations the brachial or femoral artery may be used), or out of an arterial line.
• The syringe is pre-packaged and contains a small amount of heparin, to prevent coagulation or needs to be heparinised, by drawing up a small amount of heparin and squirting it out again.
• Once the sample is obtained, care is taken to eliminate visible gas bubbles, as these bubbles can dissolve into the sample and cause inaccurate results.
• The sealed syringe is taken to a blood gas analyzer.
• If the sample cannot be immediately analyzed, it is chilled in an ice bath in a glass syringe to slow metabolic processes which can cause inaccuracy.
• Samples drawn in plastic syringes should not be iced and should always be analyzed within 30 minutes.
• The machine used for analysis aspirates this blood from the syringe and measures the pH and the partial pressures of oxygen and carbon dioxide. The bicarbonate concentration is also calculated. These results are usually available for interpretation within five minutes.
• Standard blood tests can also be performed on arterial blood, such as measuring glucose, lactate, hemoglobins, dys-haemoglobins, bilirubin and electrolytes.
• Contamination with room air will result in abnormally low carbon dioxide and (generally) normal oxygen levels. Delays in analysis (without chilling) may result in inaccurately low oxygen and high carbon dioxide levels as a result of ongoing cellular respiration.
• Lactate level analysis is often featured on blood gas machines in neonatal wards, as infants often have elevated lactic acid.
• Allen test is a medical sign used in the physical examination of arterial blood flow to the hands.

By Rhcastilhos - Gray1237.png, Public Domain, https://commons.wikimedia.org/w/index.php?curid=1618923

Radial ABG sampling

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Allen test for radial artery vasculatures

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Sources of error

• When the sample is left for prolonged periods at room temperature, consumption of oxygen may result in a falsely low PaO2. The sample should be analyzed within 15 minutes.
• On the other side, air bubbles exist in the sample can cause a falsely high PaO2 and a falsely low PaCO2. Removal of the bubbles after the sample has been withdrawn can minimize this effect.
• If acidic heparin is used, heparin can decrease the pH. Heparin amount should be minimized.
• If compared to pulmonary artery catheter, arterial pH is higher and PaCO2 was lower in peripheral ABG.

Complications of arterial blood gas

Complications of ABG include:

• Local pain and paresthesia
• Bruising
• Minor bleeding
• Vasovagal response
• Local hematoma
• Artery vasospasm
• Infection at the puncture site
• Arterial occlusion from a local hematoma
• Air embolism
• Anaphylactic reaction
• Local nerve injury
• Pseudoaneurysm formation
• Vessel laceration

Reference Ranges and Interpretation

Blood Gas Analysis

Blood gas analysis	Vessel	Range	Interpretation
Oxygen Partial Pressure (pO2)	Arterial	80 to 100 mmHg	Normal
		<80  mmHg	Hypoxia
	Venous	35 to 40 mmHg	Normal
Oxygen Saturation (SO2)	Arterial	>95%	Normal
		<95%	Hypoxia
	Venous	70 to 75%	Normal
pH	Arterial	<7.35	Acidemia
		7.35 to 7.45	Normal
		>7.45	Alkalemia
	Venous	7.26 to 7.46	Normal
Carbon Dioxide Partial Pressure (pCO2)	Arterial	<35 mmHg	Low
		35 to 45 mmHg	Normal
		>45 mmHg	High
	Venous	40 to 45 mmHg	Normal
Bicarbonate (HCO3−)	Arterial	<22 mmol/L	Low
		22 to 26 mmol/L	Normal
		>26 mmol/L	High
	Venous	19 to 28 mmol/L	Normal
Base Excess (BE)	Arterial	<−3.4	Acidemia
		−3.4 to +2.3 mmol/L	Normal
		>2.3	Alkalemia
	Venous	−2 to −5 mmol/L	Normal
Osmolar gap = Osmolality – Osmolarity		>10	Abnormal
Anion gap = [Na+] – {[Cl−]+[HCO3−]} Corrected AG = (measured serum AG) + (2.5 x [4.5 − Alb])		<8	Low
		8 to 16	Normal
		>16	High

Interpretation

• Arterial blood gas is interpreted in the following sequence for alkalosis and acidosis:

Step 1

• Normal pH is 7.35 - 7.45.
• pH < 7.35 is acidosis and > 7.45 alkalosis

Step 2

• Normal CO2 is 4.7 to 6.0 kPa or 35 - 45 mm Hg.
• Check for CO2 whether acidosis (> 45) or alkalosis (< 35)

Step 3

• Normal HCO3 (bicarbonates) 22 - 28 mmoL/liter.
• HCO3 < 22 acidosis, Hco3 > 28 alkalosis

Step 4

• Match whether pH is matching with carbondioxide or bicarbonate to determine the primary defect.
• If pH matches CO2 the primary defect is respiratory, whereas if pH matches HCO3 the primary defect is metabolic

Step 5

• After determining the primary defect check the opposite factor to see whether the defect is uncompensated, partially or fully compensated. For instance, the primary defect is respiratory acidosis then check the opposite factor i.e. HCO3 for compensation.

Step 6

• Check for oxygen saturation to see if hypoxemia is present or not.

Acid-base disturbances

• Metabolic acidosis
• Respiratory acidosis
• Metabolic alkalosis
• Respiratory alkalosis

Mixed disorders

• Some patients have two or three acid-base disorders such as metabolic acidosis and respiratory acidosis.
• The evaluation of patients with acid-base disorders initially requires identification of the major disorder.
• If metabolic acidosis is the primary disorder, an arterial PCO2 substantially higher than the expected compensatory response defines the mixed disorder of metabolic acidosis and respiratory acidosis, while an arterial PCO2 substantially lower than expected defines the mixed disorder of metabolic acidosis and respiratory alkalosis.
• If respiratory acidosis is a major disorder, then the serum HCO3 should be appropriately increased. If the serum HCO3 is not as high as expected, then metabolic acidosis also exists and the arterial pH may be substantially reduced.

Video shows mixed disorders

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Anion gap

• The anion gap (AG) is the difference between the measured positive cations and the measured negative anions in serum, plasma, or urine.

• Determination of the serum anion gap is an important step in the differential diagnosis of acid-base disorders and especially metabolic acidosis. If the gap is greater than normal, then high anion gap metabolic acidosis is diagnosed.

Serum AG  =  Na  -  (Cl  +  HCO3)

• The normal range of AG is 3 to 9 mEq/L.

• The AG must be adjusted downward in patients with hypoalbuminemia as albumin is the largest contributor to the AG. The expected baseline value for the AG must be adjusted upward using the same correction factor in patients with hyperalbuminemia.

• The serum AG is elevated in those metabolic acidosis that are due to the accumulation of any strong acid other than hydrochloric acid.
• The most common causes of acute high AG acidosis are lactic acidosis and ketoacidosis.

Video shows anion gap

{{#ev:youtube|qzU5UBxz4JA}}

Examples

Example 1

• pH = 7.01, CO2 = 28 mm Hg, HCO3 = 10 mmol/L, Oxygen saturation = 95%, pO2 = 95
• Step 1 - pH = 7.01, acidosis
• Step 2 - CO2 = 28 mm Hg, alkalosis
• Step 3 - HCO3 = 10 mmoL/L, acidosis
• Step 4 - Match the pH - pH is acidosis and HCO3 is acidosis so the primary defect is metabolic acidosis
• Step 5 - Since the primary defect is metabolic, check CO2 for compensation. Since CO2 is opposite to the pH it is trying to compensate. However, the pH is still acidosis and not normal so the compensation is only partial.
• Step 6 - Oxygen saturation is normal so no hypoxemia.
• Conclusion - Partially compensated metabolic acidosis without hypoxemia

Example 2

• pH = 7.50, CO2 = 40 mm Hg, HCO3 = 32 mmol/L, Oxygen saturation = 95%, pO2 = 90
• Step 1 - pH = 7.50, alkalosis
• Step 2 - CO2 = 40 mm Hg, normal
• Step 3 - HCO3 = 32 mmoL/L, alkalosis
• Step 4 - Match the pH - pH is alkalosis and HCO3 is alkalosis so the primary defect is metabolic alkalosis
• Step 5 - Since the primary defect is metabolic, check CO2 for compensation. Since CO2 is normal so it is uncompensated as CO2 is not trying to compensate.
• Step 6 - Oxygen saturation is normal but pO2 is low so hypoxemia.
• Conclusion - Uncompensated metabolic alkalosis with hypoxemia

Example 3

• pH = 7.44, CO2 = 20 mm Hg, HCO3 = 10 mmol/L, Oxygen saturation = 95%, pO2 = 95%
• Step 1 - pH = 7.44, normal
• Step 2 - CO2 = 20 mm Hg, alkalosis
• Step 3 - HCO3 = 10 mmoL/L, acidosis
• Step 4 - Match the pH - pH is normal but a pH of 7.44 is more inclined towards CO2 (alkalosis) so the primary defect is respiratory alkalosis
• Step 5 - Since the primary defect is respiratory, check HCO3 for compensation. Since pH is normal so it is fully compensated.
• Step 6 - Oxygen saturation is normal but pO2 is low so hypoxemia.
• Conclusion - Fully compensated respiratory alkalosis without hypoxemia.

Reference Ranges

Oxygen Partial Pressure (pO2)
Arterial pO2	70-100 mm Hg
Venous pO2	35-40 mmHg
Oxygen Saturation (SO2)
Arterial SO2	< 95%
Venous SO2	70-75%
Carbon Dioxide Partial Pressure (pCO2)
Arterial pCO2	35-45 mmHg
Venous pCO2	40-50 mmHg
Serum Bicarbonate (HCO3)
Arterial HCO3	20-27 mmol/l
Venous HCO3	19-28 mmol/l
pH
Arterial pH	7.35-7.45
Venous pH	7.26-7.46
Base Excess (BE)
Arterial BE	-3.4 - +2.3 mmol/l
Venous BE	-2 - -5 mmol/l

These are typical reference ranges, although various analysers and laboratories may employ different ranges.

Analyte	Range	Interpretation
pH	7.35 - 7.45	The pH or H+ indicates if a patient is acidemic (pH < 7.35; H+ >45) or alkalemic (pH > 7.45; H+ < 35).
H+	35 - 45 nmol/l (nM)	See above.
pO2	9.3-13.3 kPa or 80-100 mmHg	Normal pO2 is 80-100 mmHg (age-dependent).
pCO2	4.7-6.0 kPa or 35-45 mmHg	The carbon dioxide and partial pressure (PCO2) indicates a respiratory problem: for a constant metabolic rate, the PCO2 is determined entirely by ventilation. A high PCO2 (respiratory acidosis) indicates underventilation, a low PCO2 (respiratory alkalosis) hyper- or overventilation.
HCO3-	22 - 26 mmol/l	The HCO3- ion indicates whether a metabolic problem is present (such as ketoacidosis). A low HCO3- indicates metabolic acidosis, a high HCO3- indicates metabolic alkalosis.
SBCe	21 to 27 mM	the bicarbonate concentration in the blood at a CO2 of 5.33kPa, full oxygen saturation and 37 degrees Celcius.
Base excess	-2 to +2 mmol/l	The base excess indicates whether the patient is acidotic or alkalotic. A negative base excess indicates that the patient is acidotic. A high positive base excess indicates that the patient is alkalotic.
HPO42−	0.8 to 1.5 mM
total CO2 (tCO2 (P)c)	25 to 30 mM	This is the total amount of CO2, and is the sum of HCO3- and pCO2 by the formula: tCO2 = [HCO3-] + α*pCO2, where α=0.226 mM/kPa, HCO3- is expressed in molars (M) and pCO2 is expressed in kPa
total O2 (tO2e)		This is the sum of oxygen solved in plasma and chemically bound to hemoglobin.

References

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