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]

Overview

An arterial blood gas (also called "ABG'S") 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

Hydrogen Ion Regulation

• The body maintains a narrow pH range by 3 mechanisms:
• Chemical buffers (extracellular and intracellular) react instantly to compensate for the addition or subtraction of H+ ions.
• CO2 elimination is controlled by the lungs (respiratory system). Decreases (increases) in pH result in decreases (increases) in PCO2 within minutes.
• HCO3- elimination is controlled by the kidneys. Decreases (increases) in pH result in increases (decreases) in HCO3-. It takes hours to days for the renal system to compensate for changes in pH.

• Renal excretion of acid from tissues is achieved by combining hydrogen ions with either urinary buffers to form titratable acid, such as phosphate (HPO4-  +  H+  →  H2PO4-), urate, and creatinine, or with ammonia to form ammonium (NH3  +  H+  →  NH4+) [1].
• When increased quantities of acid must be excreted by the kidney, the major adaptive response is an increase in ammonia production (derived from the metabolism of glutamine) with a resultant increase in ammonium excretion into the urine.
• Acid-base status is usually assessed by measuring the components of the bicarbonate-carbon dioxide buffer system in blood:

 Dissolved CO2  +  H2O  ↔  H2CO3  ↔  HCO3-  +  H+

• When blood gas analysis is carried out, the partial pressure of CO2 (PCO2) and the pH are each measured using analytical electrodes. The serum bicarbonate (HCO3-) concentration is then calculated with the Henderson-Hasselbalch equation.

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. Each of the simple acid-base disorders is associated with a compensatory respiratory or renal response that limits the change in ratio and therefore in pH (figure 1) [9].
• When a metabolic acid-base disorder reduces the serum HCO3 (metabolic acidosis) or increases the HCO3 (metabolic alkalosis), there should be an appropriate degree of respiratory compensation moving the PCO2 in the same direction as the serum HCO3 (falling in metabolic acidosis and rising in metabolic alkalosis). The respiratory compensation mitigates the change in the ratio of the serum HCO3 to PCO2 and therefore in the pH. Respiratory compensation in metabolic acidosis or alkalosis is a rapid response. With metabolic acidosis, for example, the response begins within 30 minutes [10] and is complete within 12 to 24 hours [11].
• When a respiratory acid-base disorder causes the PCO2 to increase (respiratory acidosis) or decrease (respiratory alkalosis), compensation occurs in two phases. There is an immediate, small change in serum HCO3 (in the same direction as the PCO2 change), which is due to whole body buffering mechanisms. If the respiratory disorder persists for more than minutes to hours, the kidneys respond by producing larger changes in serum HCO3 (again, in the same directionas the PCO2). These HCO3 changes mitigate the change in pH. Renal compensations are mediated by increased hydrogen ion secretion (which raises the serum HCO3 concentration) in respiratory acidosis and decreased hydrogen ion secretion and urinary HCO3 loss in respiratory alkalosis. The renal compensation takes three to five days for completion. As a result, the expected findings are very different in acute (whole body buffering without significant renal compensation) and chronic (full renal compensation) respiratory acid-base disorders. (See 'Respiratory acid-base disorders' below.)
• The compensatory renal and respiratory responses are thought to be mediated, at least in part, by parallel pH changes within sensory and regulatory cells including renal tubule cells and cells in the respiratory center [12]. The magnitude of the compensatory response is proportional to the severity of the primary acid-base disturbance.
• It follows from the above discussion that a high HCO3 concentration may be due to metabolic alkalosis or compensation for chronic respiratory acidosis. Conversely, a low HCO3 may be due to metabolic acidosis or compensation for chronic respiratory alkalosis. Analogous issues apply to a high or low PCO2. At least two of the three variables in the Henderson-Hasselbalch equation (pH, HCO3, PCO2) must be measured to assess an acid-base disorder (and if two are measured, the third can be deduced).
• The expected degree of compensation for each acid-base disorder has been determined empirically by observations in humans with either spontaneous or experimentally induced simple acid-base disorders (figure 1). The degree of compensation is usually defined by the decrease or increase in arterial PCO2 from its normal range (in metabolic acid-base disorders) or the decrease or increase in serum HCO3 from its normal range (in respiratory acid-base disorders). This approach presumes that the patient had normal values prior to the onset of the acid-base disorder. Thus, in the absence of known baseline values, there is the potential for error if the patient's acid-base status was not normal at the onset of the disorder.

Respiratory Compensation

• 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.

Indications

• 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

• 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 interpretion 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.

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Reference Ranges and Interpretation

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

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.

Acid-base balance

• Acute and chronic metabolic acidosis
• Acute and chronic respiratory acidosis
• Acute and chronic metabolic alkalosis
• Acute and chronic respiratory alkalosis

Respiratory acidosis

Respiratory acidosis is a disturbance in acid-base balance usually due to alveolar hypoventilation that can be acute or chronic. It is characterized by an increased PaCO2 >45 mmHg (hypercapnia) and a reduction in pH (pH <7.35). The mechanisms, etiologies, and clinical manifestations, as well as the distinction between acute and chronic hypercapnia and the approach to patients with hypercapnic respiratory failure are discussed separately (table 2). (See "Mechanisms, causes, and effects of hypercapnia" and "The evaluation, diagnosis, and treatment of the adult patient with acute hypercapnic respiratory failure".)

Respiratory alkalosis

Respiratory alkalosis is usually due to alveolar hyperventilation which leads to a decrease in PaCO2 (hypocapnia) and an increase in the pH. It can also be acute or chronic. In acute respiratory alkalosis, the PaCO2 level is below the lower limit of normal (<35 mmHg or 4.7 kPa) and the serum pH is appropriately alkalemic (>7.45) (figure 11). In states of chronic respiratory alkalosis, the PaCO2 level is also below the lower limit of normal (<35 mmHg or 4.7 kPa), but the pH level is at or close to normal. Calculating the appropriate compensatory response to acute respiratory alkalosis is described separately. (See "Simple and mixed acid-base disorders", section on 'Respiratory alkalosis'.)

A respiratory alkalosis develops when the lungs are stimulated to remove more carbon dioxide than is produced metabolically in the tissues. The stimulus to increase respiratory drive is controlled by central and peripheral factors (algorithm 1). Thus, respiratory alkalosis is commonly encountered in anxiety, panic, pain, fever, psychosis, and hyperventilation syndrome. Respiratory alkalosis can also be found in any medical condition that increases alveolar ventilation including pulmonary embolism, heart failure, or mechanical ventilation, as well as in stroke, meningitis, high altitude, right-to-left shunts, pregnancy, hyperthyroidism, and aspirin overdose (table 3 and algorithm 2). Decreased carbon dioxide production from excessive sedation, skeletal muscle paralysis, hypothermia, or hypothyroidism is a rare mechanism that may contribute to respiratory alkalosis but is rarely a primary etiology for hypocapnia.

Acute hypocapnia can induce cerebral vasoconstriction resulting in dizziness and lightheadedness. Paresthesias of the hands, feet or mouth may also be present due to peripheral hypocalcemia (from increased binding of calcium to serum albumin). Patients may also complain of chest pain or dyspnea and severe cases can be associated with carpopedal spasm, tetany, mental confusion, syncope, and seizures. Acute hypocapnia causes a reduction of serum levels of potassium and phosphate secondary to increased intracellular shifts of these ions. Hyponatremia and hypochloremia are rare. Consequently, severe alkalosis (>7.6) is worrisome for the development of seizures and cardiac instability. (See "Hyperventilation syndrome", section on 'Clinical presentation'.)

Respiratory alkalosis is typically managed by treating the underlying cause (eg, reassurance, anxiolytic, pain control) and using maneuvers to reduce alveolar ventilation (eg, sedation, reduce respiratory rate and/or tidal volume when on mechanical ventilation).

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. [16-19]
• On the other side, air bubbles exist in the sample can cause a falsely high PaO2 and a falsely low PaCO2. Remove the bubbles after the sample has been withdrawn can minimize this effect. [17,21]. [10]
• If acidic heparin is used, heparin can decrease the pH. Heparin amount should be minimized.
• If compared to pulmnoary artery catheter, arterial pH is higher and PaCO2 was lower in peripheral ABG.

Mixed disorders

• Some patients have two, three, or more relatively independent acid-base disorders.
• These mixed disorders include
• combinations of metabolic disorders (eg, vomiting-induced metabolic alkalosis plus hypovolemia-induced lactic acidosis)
• mixed metabolic and respiratory disorders (eg, metabolic acidosis and respiratory alkalosis in salicylate intoxication)
• As discussed in the preceding section, the evaluation of patients with acid-base disorders initially requires identification of the major disorder, and then determination of whether or not the degree of compensation is appropriate. If the compensation is not appropriate, then this is indicative of a second acid-base disorder (ie, a mixed acid-base disorder is present). The following examples are illustrative:
• 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 (which could be produced by acute hyperventilation due to the discomfort of obtaining the blood sample).
• If respiratory acidosis is the 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.
• By contrast, if the serum HCO3 is higher than expected, then metabolic alkalosis complicates the respiratory acidosis and the arterial pH may be inappropriately "normal."

Anion gap

• Determination of the serum anion gap (AG) is an important step in the differential diagnosis of acid-base disorders and especially metabolic acidosis [1-5].
• The serum AG represents the difference between the primary measured cation (Na) and the primary measured anions (Cl and HCO3):

   Serum AG  =  Na  -  (Cl  +  HCO3)

• normal range of 3 to 9 mEq/L[6,7].

• Albumin, which is negatively charged, is the single largest contributor to the AG. the AG must be adjusted downward in patients with hypoalbuminemia. [2,8].
• Conversely, the expected baseline value for the AG must be adjusted upward using the same correction factor in patients with hyperalbuminemia [8].

• The serum AG is elevated in those metabolic acidoses 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.
• The degree to which the AG rises in relation to the fall in HCO3 varies with the cause of the metabolic acidosis.
• This represents the delta AG/delta HCO3 ratio.

Related Chapters

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

References

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