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Arterial blood gases

Arterial blood gases
Literature review current through: Jan 2024.
This topic last updated: Jul 10, 2023.

INTRODUCTION — An arterial blood gas (ABG) is a test that measures the oxygen tension (PaO2), carbon dioxide tension (PaCO2), acidity (pH), oxyhemoglobin saturation (SaO2), and bicarbonate (HCO3) concentration in arterial blood. Some blood gas analyzers also measure the methemoglobin, carboxyhemoglobin, and hemoglobin levels. Such information is vital when caring for patients with critical illness, respiratory, or metabolic diseases.

The sites, techniques, and complications of arterial sampling and the interpretation of ABGs are reviewed here. Interpretation of venous blood gases and detailed discussion of acid-base disturbances are discussed separately. (See "Simple and mixed acid-base disorders" and "Venous blood gases and other alternatives to arterial blood gases".)

INDICATIONS AND CONTRAINDICATIONS — ABGs are frequently used for the following:

Identification and monitoring of acid-base disturbances

Measurement of the partial pressures of oxygen (PaO2) and carbon dioxide (PaCO2)

Assessment of the response to therapeutic interventions (eg, insulin in patients with diabetic ketoacidosis)

Detection and quantification of the levels of abnormal hemoglobins (eg, carboxyhemoglobin and methemoglobin)

Procurement of a blood sample in an acute emergency setting when venous sampling is not feasible (most tests can be performed from an arterial sample)

Absolute contraindications for ABG sampling include the following [1]:

An abnormal modified Allen's test (see 'Ensure collateral circulation' below)

Local infection, thrombus, or distorted anatomy at the puncture site (eg, previous surgical interventions, congenital or acquired malformations, burns, aneurysm, stent, arteriovenous fistula, vascular graft)

Severe peripheral vascular disease of the artery selected for sampling

Active Raynaud syndrome (particularly sampling at the radial site)

If a contraindication is present, in many cases an alternative site or consideration for using venous blood should be sought for sampling.

Supra therapeutic coagulopathy and infusion of thrombolytic agents (eg, during streptokinase or tissue plasminogen activator infusion) are relative contraindications to arterial needle stick and absolute contraindications to indwelling catheter insertion. Although no cutoff has been suggested by any international societies, we suggest avoiding repeated arterial needle sticks when the international normalized ratio is ≥3 and/or the activated partial thromboplastin time is ≥100 seconds.

Similarly, arterial needle stick and catheterization can be performed in patients with thrombocytopenia a platelet count >50 x 109/L, but is generally avoided in those whose count is ≤30 x 109/L. For those with counts between 30 and 50 x 109/L limited needle stick sampling is sometimes performed, when necessary, with increased compression time. A platelet count <50 x 109/L is generally a contraindication to arterial catheter insertion.

A history of Raynaud disease or Raynaud disease without active spasm, as well as evidence of poor peripheral perfusion (eg, cyanotic digits), are also considered by most experts as relative contraindications to radial arterial sampling.

Therapeutic anticoagulation is not a contraindication for arterial needle puncture, although the risk of bleeding is higher, but it is a relative contraindication for the insertion of an indwelling catheter. Increased vessel compression is appropriate in such patients. Aspirin or other antiplatelet agents (eg, clopidogrel) are not a contraindication for arterial vascular sampling in most cases.

TECHNICAL CHALLENGES — ABG sampling may be difficult to perform in patients who are uncooperative or in whom pulses cannot be easily identified (eg, shock, vasopressor infusion, arteriosclerosis from end-stage kidney disease, calcification of the vessel wall). Difficulties can also arise when the patient cannot be positioned appropriately (eg, cannot fully extend the wrists for radial artery access due to tremor or joint contractures) or in patients with obesity or who are edematous in whom large amounts of subcutaneous tissue may obscure the usual anatomic landmarks. In some of these scenarios, ultrasound may be useful to locate the artery and reduce potential complications of repeated puncture and consequent injury to the target vessel and surrounding tissue.

ARTERIAL SAMPLING — Arterial blood is required for an ABG. It can be obtained by percutaneous needle puncture or from an indwelling arterial catheter. Written consent is not usually required for arterial needle stick puncture but is required for the insertion of an indwelling catheter. Regardless, the risks and benefits of each procedure should be explained to the patient.

Ultrasound is not routinely used but can be used to direct access when sampling by the standard approach has been unsuccessful or is not feasible (eg, weak pulses, patient on multiple vasopressors, patients with obesity). When used, ultrasound-guided access may increase the operator's ability to enter the vessel and helps minimize injury to the artery and adjacent nerves and veins.

Needle puncture — Percutaneous needle puncture refers to the withdrawal of arterial blood via a needle stick. It needs to be repeated every time an ABG is performed, since an indwelling catheter is not inserted. Thus, it is suitable for patients who require a limited number of arterial draws (eg, daily or less than once daily during an admission to hospital). If recurrent sampling (eg, more than four draws in 24 hours) is required, clinicians should, at minimum, rotate puncture sites (eg, right and left radial) or consider placing an indwelling catheter. (See 'Indwelling catheters' below and "Intra-arterial catheterization for invasive monitoring: Indications, insertion techniques, and interpretation".)

Site selection — The initial step in percutaneous needle puncture is locating a palpable artery. Common sites include the radial, femoral, brachial, dorsalis pedis, or axillary artery. There is no evidence that any site is superior to the others. However, the radial artery is used most often because it is accessible and more comfortable for the patient than the alternative sites. The radial artery is also typically used for outpatients, while all sites can be used for inpatients who require an ABG.

Radial artery – The radial artery is best palpated between the distal radius and the tendon of the flexor carpi radialis when the wrist is extended (figure 1 and figure 2). Although infrequently performed, the arm can be taped (at the level of the forearm and palm) to an armboard with the palm facing upward; a large roll of gauze also can be placed between the wrist and the armboard in a position that extends the wrist. Over extension should be avoided as extension of the overlying flexor tendons may make the pulse difficult to detect.

Brachial artery – The brachial artery is best palpated medial to the biceps tendon in the antecubital fossa, when the arm is extended and the palm is facing up (figure 3). The arm is placed on a firm surface (an armboard can be used similar to that described for the radial artery above) with the shoulder slightly abducted, the elbow extended, and the forearm in full supination. The needle should be inserted just above the elbow crease at a 30-degree angle (figure 4). It is usually harder to access because it runs deeper in the arm than the radial artery.

Femoral artery – The femoral artery is best palpated just below the midpoint of the inguinal ligament, when the lower extremity is extended and the patient is lying supine (figure 5). The needle should be inserted at a 90-degree angle just below the inguinal ligament (figure 6).

Axillary artery – The axillary artery is best palpated in the axilla, when the arm is abducted and externally rotated (figure 7). The needle should be inserted as high into the apex of the axilla as possible (figure 8).

Dorsalis pedis – The dorsalis pedis artery can be occluded by the forefinger followed by compression of the nail bed of the great toe and assessment of the rapidity with which color returns to the nail bed after pressure is released from the great toe (figure 9). The needle can be inserted at a 30-degree angle lateral to the extensor tendon at the level of the midfoot.

Ensure collateral circulation — One of the risks associated with arterial puncture is ischemia distal to the puncture site (see 'Complications' below). Although rarely performed in practice, identifying collateral flow to the region supplied by the artery can be used by clinicians prior to puncture. While limited studies have found variable accuracy associated with such evaluations, we believe that patients, and in particular high risk patients, undergoing radial or dorsalis pedis artery puncture should have the collateral flow to those vessels evaluated [2,3]. Our belief is based upon the concept that it avoids potential harm by identifying patients who have impaired collateral circulation and who are therefore at increased risk of an ischemic complication, and in whom an alternative site should be sought. In addition, the evaluation can be performed quickly at the bedside and at no cost.

Radial and dorsalis pedis artery puncture are at highest risk of this complication (because they are small in diameter). They receive collateral supply from the ulnar and lateral plantar artery, respectively. It is this collateral supply that is identified by the following tests:

Radial artery – The Allen's test or modified Allen's test are bedside tests that can be performed in patients undergoing radial artery puncture to demonstrate collateral flow from the ulnar artery through the superficial palmar arch (figure 1) [4].

Modified Allen's test – The patient's hand is initially held high with the fist clenched. Both the radial and ulnar arteries are compressed firmly by the two thumbs of the investigator (figure 10). This allows the blood to drain from the hand. The hand is then lowered and the fist is opened (the palm will appear white). Overextension of the hand or wide spreading of the fingers should be avoided because it may cause false-normal results. The pressure is released from the ulnar artery while occlusion is maintained on the radial artery. A pink color should return to the palm, usually within six seconds, indicating that the ulnar artery is patent and the superficial palmar arch is intact. Although the timing of return of circulation to the palm varies considerably, the test is generally considered abnormal if ten seconds or more elapses before color returns to the hand (picture 1).

The Allen's test – The Allen's test (from which the modified Allen's test evolved) is performed identically, except these steps are executed twice: once with release of pressure from the ulnar artery while occlusion is maintained on the radial artery, and once with release of pressure from the radial artery while occlusion is maintained on the ulnar artery.

Other – Finger pulse plethysmography, Doppler flow measurements, and measurement of the arterial systolic pressure of the thumb have been described but are not routinely used [5].

Dorsalis pedis artery – An Allen's test to assess the collateral circulation of the posterior tibialis is performed by elevating the leg until the plantar skin blanches followed by compression of dorsalis pedis pulse by the clinician's thumb and lowering of leg to dependency. The foot rapidly resumes its normal color if the posterior tibial artery flow is adequate.

The risk of ischemic complications is low for the axillary artery because the arm receives good collateral flow through the thyrocervical trunk and subscapular artery. Thus, no collateral supply testing is typically performed prior to arterial puncture. However, assessing distal brachial and radial artery pulses is appropriate in patients who have had anatomic, pathologic abnormalities of the thoracic outlet; if distal pulses are weak, an alternative site should be sought.

The femoral artery is large such that ischemia is rare. However, the distal pedal pulses of the lower limb should be assessed first. If pedal pulses are severely diminished or absent, peripheral arterial disease may be present and an alternative arterial puncture site should be sought.

Similarly, pulses distal to the brachial artery must be assessed prior to the procedure. In patients with absent pulses at the wrist (ie, in the radial and ulnar arteries), an alternative site for arterial sampling should be sought.

Equipment — As for all procedures, the equipment necessary should be brought to the bedside prior to the procedure. This includes:

Nonsterile gloves

Antiseptic skin solution (eg, chlorhexidine and povidone-iodine are solutions)

ABG kit OR a pre-heparinized 3 mL ABG syringe with a 22 to 25-gauge needle and syringe cap

2 × 2-inch sterile gauze

Adhesive bandage

Plastic hazard bag with ice (if not provided in the kit)

Sharp object container

Lidocaine (eg, 1 or 2 percent) without epinephrine may be required should the clinician feel that anesthesia is necessary or the patient requests it.

ABG kits (picture 2) are used by clinicians in most institutions to draw arterial blood. Kits contain a heparinized plastic syringe with the plunger already pulled back to allow for the collection of 2 mL of blood, a protective needle sleeve, a needle, syringe cap, and ice bag. The sleeve, while attached to the syringe, locks the needle within itself to prevent direct contact between operator and needle. It is removed to expose the needle. The prefilled heparin is expelled (incomplete dismissal of heparin falsely lowers the partial pressure of carbon dioxide), and the plunger is then repositioned at the 2 mL mark.

Alternatively a heparinized ABG syringe can be used. Approximately 2 mL of lithium heparin (1000 units/mL) can be aspirated into a syringe through a 22 to 25-gauge needle and then pushed out; the plunger should be left leaving a small empty volume (eg, usually 2 mL) in the syringe.

Technique — Once a palpable artery has been located, blood is withdrawn using the following steps.

The planned puncture site should be sterilely prepared.

Local analgesia with injectable 1 to 2 percent lidocaine can be administered but is not usually performed [6,7]. If local anesthesia is employed (eg, requested by the patient, difficult or prolonged needle stick is preempted), 0.5 to 1 mL of the anesthetic is injected to create a small dermal papule at the site of puncture; using larger amounts or injecting the anesthetic into deeper planes may distort the anatomy and hinder identification of the vessel [7]. Traditionally, it was believed that the injection of lidocaine is as painful as the procedure itself so many clinicians avoid using it for this reason. However, in our experience, when performed by personnel experienced in arterial draws, no anesthesia is typically needed.

Although no anesthesia is typically performed, one study that compared levels of pain associated with the procedure reported that patients who received mepivacaine and cryoanalgesia had less pain than those who received no anesthetic [8]. Topical anesthetic cream did not appear to have a significant effect on pain. Another study reported analgesic effect with ethyl chloride spray [9].

ABG kits are used by clinicians in most institutions to draw arterial blood. Alternatively, a heparinized syringe can be used. The kit or syringe is prepared as described above. (See 'Equipment' above.)

One or two fingers should be used to gently palpate the artery while holding the needle in the other hand. Both fingers should be proximal to the desired puncture site; placing the nondominant middle finger distally and the nondominant index finger proximally, with the needle insertion site in between, is not recommended, because of the increased risk of needle stick injury. The artery should be punctured with the needle at a 30 to 45-degree angle (radial, brachial, axillary, dorsalis pedis) or at a 90-degree angle (femoral artery) relative to the skin. The syringe fills on its own (ie, pulling the plunger is usually unnecessary). Approximately 2 to 3 mL of blood should be removed.

For patients with poor distal perfusion (eg, hypovolemia, shock, vasopressor therapy) who may exhibit a weak arterial pulse, the operator may need to pull back the syringe plunger, although this increases the risk of venous blood sampling.

If arterial flow is lost during the arterial draw, the needle may have moved outside the vessel lumen. The needle may be pulled back slightly and repositioned to a point just below the skin; subsequent redirection using the maneuver described above should be attempted to reaccess the artery. Multiple blind or stabbing movements of the needle while it is inserted deeply in the patient's limb should be avoided since this increases the risk of local injury and pain.

After withdrawing a sufficient volume of blood, the needle should be removed while simultaneously applying pressure to the puncture site with sterile gauze until hemostasis is achieved. This usually takes five minutes in a non-anticoagulated patient; avoid checking the puncture site until local pressure has been maintained for at least this period as this increases the risk of hemorrhage or a hematoma. In patients who have a coagulopathy or are on anticoagulation therapy, it may be necessary to apply local pressure for a longer time. Once hemostasis is achieved, apply an adhesive bandage over the puncture site.

When ABG kits are used, apply the needle protective sleeve then untwist the sleeve and place it in the sharp object container. When an ABG syringe is used, recap, remove, and discard the needle, being careful to avoid a needle stick injury. After discarding the needle, remove the excess air in the syringe by holding it upright and gently tapping it, allowing any air bubbles present to reach the top of the syringe, from where they can then be expelled. Cap the syringe, roll it between the hands for a few seconds to allow blood to mix with the heparin (prevents clotting), then place on ice in the hazard bag and send it for analysis.

Postprocedural care — Patients should be monitored for new symptoms such as skin color changes, persistent or worsening pain, active bleeding, and impaired movement or sensation of the limb. Monitoring is particularly important in patients who are subsequently supra therapeutic on anticoagulants or are given thrombolytics, as bleeding may be observed in such patients even though the needle stick occurred a few hours prior.

Complications — In general, serious complications due to arterial percutaneous needle puncture are rare.

Common complications of ABG sampling include the following:

Local pain and paresthesia

Bruising

Local minor bleeding

Less common complications include:

Vasovagal response

Local hematoma from moderate or major bleeding

Artery vasospasm

Rare complications include:

Infection at the puncture site

Arterial occlusion from a local hematoma

Air or thrombus embolism

Local anesthetic anaphylactic reaction

Local nerve injury

Needle stick injury to health care personnel (limited due to use of ABG kits)

Pseudoaneurysm formation

Vessel laceration

Should local bleeding, hematoma, vasospasm, and/or arterial thrombus be severe, compartment syndrome and limb ischemia can occur. Compartment syndrome may manifest as pain, paresthesias, pallor, and absence of pulses. Limb skin color changes, absent pulses, and distal coldness may be seen in ischemic injury. Although unproven, rotating puncture sites and placing firm pressure on the puncture site for at least five minutes after each arterial draw is thought to decrease the risk of these complications. (See "Acute compartment syndrome of the extremities" and "Clinical features and diagnosis of acute lower extremity ischemia" and "Embolism to the upper extremities".)

While vasopressor use may increase the risk of vasospasm, when indicated (eg, for shock), these agents should not be adjusted to avoid or treat this complication. (See "Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock", section on 'Vasopressors' and "Use of vasopressors and inotropes".)

Persistent pain, paresis, or paresthesia of the limb may indicate nerve injury which generally resolves spontaneously.

Infection at the puncture site should be considered in the presence of regional erythema and fever and treated with antibiotics accordingly.

Indwelling catheters — Arterial blood can also be obtained via an indwelling arterial catheter. Indwelling catheters provide continuous access to arterial blood, which is helpful when frequent blood gases are needed (eg, patients in respiratory failure on mechanical ventilation, patients requiring serial ABGs for monitoring acid-base disorders). The sample preparation and care are the same as for ABGs drawn using a needle, which is described above. (See 'Needle puncture' above.)

Insertion, complications, and use of an arterial catheter are described separately. (See "Intra-arterial catheterization for invasive monitoring: Indications, insertion techniques, and interpretation".)

TRANSPORT AND ANALYSIS — The arterial blood sample should be placed on ice during transport to the lab and then analyzed as quickly as possible. This reduces oxygen consumption by leukocytes or platelets (ie, leukocyte or platelet larceny), which can cause a factitiously low partial pressure of arterial oxygen (PaO2) [10,11]. This effect is most pronounced in patients whose leukocytosis or thrombocytosis is profound. In addition, it reduces the likelihood of error due to gas diffusion through the plastic syringe or the presence of air bubbles. (See 'Sources of error' below.)

Results are usually available within 5 to 15 minutes. Analysis of arterial blood is usually performed by automated blood gas analyzers, which automatically transport the specimen to electrochemical sensors to measure acidity (pH), partial pressure of carbon dioxide (PaCO2), and PaO2:

The PaCO2 is measured using a chemical reaction that consumes CO2 and produces a hydrogen ion, which is sensed as a change in pH [12].

The PaO2 is measured using oxidation-reduction reactions that generate measurable electric currents [12].

The pH is measured indirectly with an electrode tip which determines the voltage using a reference potential, calibrated in pH units, where the voltage is proportional to the concentration of hydrogen ions.

Bicarbonate is not measured directly but calculated from measured pH and PaCO2 using the Henderson-Hasselbalch equation.

Arterial oxygen saturation (SaO2) is based upon the equation developed by Severinghaus [13]: SO2 = (23,400 * (PaO23 + 150 * PaO2)-1 + 1)-1 or the Oxygen hemoglobin disassociation curve, which is affected by temperature, pH and levels of 2,3 diphosphoglycerate (DPG).

Automated blood gas analyzers rinse the system, calibrate the sensors, and report the results. Rigorous quality control by the laboratory is essential for accurate results.

Arterial blood gas measurements by the analyzer are affected by temperature. Specifically, pH increases and both PaO2 and PaCO2 decrease as temperature declines (table 1) [14,15]. Modern automated blood gas analyzers can report the pH, PaO2, and PaCO2 at either 37ºC (the temperature at which the values are measured by the blood gas analyzer) or at the patient's body temperature. Most centers report the values of pH, PaCO2, and PaO2 at 37ºC, even if the patient's body temperature is different. However, this practice is controversial [14-17].

Co-oximetry is used to measure carboxyhemoglobin and methemoglobin levels in arterial blood, the details of which are described separately. (See "Pulse oximetry", section on 'Carboxyhemoglobin'.)

INTERPRETATION

Normal values — The range of normal values varies among laboratories. In general, normal values for acidity (pH), the partial pressure of carbon dioxide (PaCO2) and bicarbonate concentration (HCO3) are as follows:

pH – 7.35 to 7.45

PaCO2 – 35 to 45 mmHg (4.7 to 6 kPa)

HCO3 – 21 to 27 mEq/L

Normal values for the partial pressure of arterial oxygen (PaO2) and arterial oxygen saturation (SaO2) have not been defined because a threshold below which tissue hypoxia occurs has not been identified. In our opinion, it is reasonable to consider a resting PaO2 >80 mmHg (10.7 kPa) and SaO2 >95 percent normal, unless the new values are substantially different than prior values. As an example, an SaO2 of 96 percent may be abnormal if the patient's previous SaO2 was 100 percent. (See "Measures of oxygenation and mechanisms of hypoxemia", section on 'Measures of oxygenation'.)

Nonsmokers may have up to 3 percent carboxyhemoglobin at baseline (ie, 3 percent of total hemoglobin); smokers may have levels of 10 to 15 percent. Levels above these respective values are considered abnormal. Normal individuals have approximately 1 percent methemoglobin in arterial blood. (See "Pulse oximetry", section on 'Carboxyhemoglobin' and "Carbon monoxide poisoning", section on 'Diagnosis' and "Methemoglobinemia", section on 'How are the levels regulated?'.)

Oxygenation — Measurement of PaO2 and SaO2 provide data on oxygenation that can also be used to calculate indices of oxygenation including the alveolar-arterial gradient (A-a gradient), partial pressure of arterial oxygen/fraction of inspired oxygenation ratio (PaO2/FiO2), and oxygen delivery (DO2).

Hypoxemia — Oxygen is necessary for aerobic metabolism such that low levels of oxygen (hypoxemia) are deleterious, the mechanisms of which are discussed separately. (See "Oxygen delivery and consumption" and "Measures of oxygenation and mechanisms of hypoxemia".)

Hyperoxia — Too much supplemental oxygen (hyperoxia) also has deleterious effects, the details of which are discussed separately. (See "Adverse effects of supplemental oxygen".)

Ventilation — Measurement of pH, PaCO2, and base excess provide sufficient data to accurately assess patients for the presence of acute and chronic forms of respiratory acidosis and alkalosis (ie, indices of ventilation).

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 'Response to respiratory alkalosis'.)

A respiratory alkalosis develops when the lungs are stimulated to remove more carbon dioxide that 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 in adults", 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).

Acid-base balance — Measurement of pH, PaCO2, and base excess provide sufficient data to accurately assess simple and mixed acid-base disturbances which are discussed separately in the following topics:

Acute and chronic metabolic acidosis (table 4) (see "Approach to the adult with metabolic acidosis" and "Pathogenesis, consequences, and treatment of metabolic acidosis in chronic kidney disease")

Acute and chronic respiratory acidosis (table 2) (see "The evaluation, diagnosis, and treatment of the adult patient with acute hypercapnic respiratory failure" and "Mechanisms, causes, and effects of hypercapnia")

Acute and chronic metabolic alkalosis (table 5) (see "Causes of metabolic alkalosis" and "Clinical manifestations and evaluation of metabolic alkalosis" and "Pathogenesis of metabolic alkalosis" and "Treatment of metabolic alkalosis")

Acute and chronic respiratory alkalosis (table 3) (see 'Ventilation' above)

Abnormal hemoglobins — Measurement of abnormal hemoglobins is rarely indicated. While some laboratories routinely measure levels of carboxyhemoglobin and methemoglobin, others require a specific request for testing when abnormally high levels are suspected.

Carboxyhemoglobinemia — Elevated levels of carboxyhemoglobin are most commonly seen in carbon monoxide poisoning. Carbon monoxide poisoning should be suspected in patients with neurologic symptoms and a history of exposure (smoke inhalation from a fire, exposure to vehicle exhaust). Further details regarding the diagnosis and treatment of carbon monoxide poisoning are discussed separately. (See "Carbon monoxide poisoning" and "Inhalation injury from heat, smoke, or chemical irritants".)

Methemoglobinemia — Methemoglobinemia can be congenital (eg, cytochrome b5 reductase or cytochrome b5 deficiency, hemoglobin M disease) or acquired (usually drugs or toxins (table 6)). Methemoglobinemia should be suspected in the appropriate clinical context (eg, following lidocaine administration) when patients demonstrate a reduction in peripheral saturation and become cyanotic. It is supported when the oxygen saturation as measured by pulse oximetry (SpO2) is more than 5 percent lower than the oxygen saturation calculated from arterial blood gas analysis (SaO2) ("saturation gap") and when pulse oximetry shows an oxygen saturation ≤90 percent and the arterial oxygen partial pressure is ≥70 mmHg. A detailed discussion of the etiology, diagnosis, and treatment of methemoglobinemia is provided separately. (See "Methemoglobinemia".)

Sources of error — Regardless of the method used to withdraw arterial blood, several sources of error exist that can typically be easily avoided by good sample care.

Gas diffusion through the plastic syringe and consumption of oxygen by leukocytes is a potential source of error that results in a falsely low PaO2 when the sample is left for prolonged periods at room temperature. However, the clinical significance of this error is minimal if the sample is placed on ice and analyzed within 15 minutes [18-21]. While using a glass syringe will prevent gas diffusion, this solution is impractical.

The heparin that is added to the syringe as an anticoagulant can decrease the pH if acidic heparin is used and the dismissal of heparin from the syringe is incomplete. It can also dilute the PaCO2, resulting in a falsely low value [18,22]. When an ABG syringe is used, the amount of heparin solution used should be minimized and at least 2 mL of blood should be obtained. Detailed discussion of ABG equipment is discussed above. (See 'Equipment' above.)

Air bubbles that exceed 1 to 2 percent of the blood volume can cause a falsely high PaO2 and a falsely low PaCO2 [12]. The magnitude of this error depends upon the difference in gas tensions between blood and air, the exposure surface area (which is increased by agitation), and the time from specimen collection to analysis. The clinical significance of this error can be decreased by gently tapping on the syringe to remove the bubbles after the sample has been withdrawn and analyzing the sample as soon as possible [19,23]. (See 'Technique' above.)

Some studies suggest that ABGs estimate the systemic acid-base balance and oxygenation but do not accurately reflect tissue levels in states of shock [24-26]. As an example, one study of patients who underwent cardiopulmonary resuscitation compared blood gas values in blood simultaneously drawn from an arterial catheter and a pulmonary artery catheter (PAC) [24]. Compared with PAC samples, arterial pH was higher (7.42 versus 7.14) and PaCO2 was lower (32 mmHg versus 74 mmHg). If PAC results more closely reflect the acid-base status at the tissue level, then the arterial measurements can lead to the mistaken assumption that acid-base balance in tissues is being maintained. However, measurement of ABGs from PACs to assess gas exchange is impractical (PACs are rarely placed) and not adequately validated such that it cannot be routinely recommended.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Assessment of oxygenation and gas exchange".)

SUMMARY AND RECOMMENDATIONS

Definition – An arterial blood gas (ABG) is a test that measures the oxygen tension (PaO2), carbon dioxide tension (PaCO2), acidity (pH), oxyhemoglobin saturation (SaO2), and bicarbonate (HCO3) concentration in arterial blood. Some blood gas analyzers also measure the methemoglobin, carboxyhemoglobin, and hemoglobin levels. (See 'Introduction' above.)

Indications and contraindications – The following are considered reasonable indications and contraindications (see 'Indications and contraindications' above):

ABGs are frequently used to detect and monitor indices of oxygenation, ventilation, and acid-base balance, as well as quantify levels of carboxyhemoglobin and methemoglobin.

Absolute contraindications include an abnormal modified Allen's test, distorted anatomy, infection, or severe peripheral vascular disease at the puncture site. Arterial blood draws, and in particular, catheter insertion, should be avoided in patients with severe coagulopathy or in whom thrombolytic therapy is being administered as well as in patients with active Raynaud disease. Therapeutic anticoagulation and antiplatelet agents including aspirin are not generally considered as contraindications to ABG needle stick sampling.

Technical challenges – Technical challenges arise in patients who are uncooperative or in whom pulses cannot be easily identified (eg, shock, vasopressor use), as well as in patients who cannot be positioned appropriately (eg, joint contractures) or in patients with obesity or who are edematous when the usual anatomic landmarks are hard to identify. In such cases, ultrasound may be useful to locate the artery and reduce potential complications of repeated puncture and consequent injury to the target vessel. (See 'Technical challenges' above.)

Arterial sampling – Percutaneous needle puncture refers to the withdrawal of arterial blood via a needle stick. It needs to be repeated every time an ABG is performed. Thus, it is suitable for patients who require a limited number of arterial draws (eg, daily or less than once daily during an admission to hospital). If recurrent sampling is required, clinicians should at minimum rotate puncture sites (eg, right and left radial) or consider placing an indwelling catheter (see 'Arterial sampling' above):

Site selection – Common sites include the radial, femoral, brachial, axillary, or dorsalis pedis artery. There is no evidence that any site is superior to the others. However, the radial artery is used most often because it is accessible and more comfortable for the patient than the alternative sites. (See 'Site selection' above.)

Collateral circulation – For patients undergoing radial or dorsalis pedis artery puncture, we suggest evaluating the collateral flow to those vessels prior to puncture (eg, modified Allen's test for radial artery puncture) (Grade 2C). For other sites, distal pulses can be assessed prior to arterial puncture. Poor collateral flow or weak distal pulses should prompt arterial puncture at an alternate site. (See 'Ensure collateral circulation' above.)

Technique – Once the target artery has been identified, the planned puncture site should be sterilely prepared. Injectable lidocaine is typically not used. The artery should be punctured with a small needle and syringe, 2 to 3 mL of blood should be withdrawn, and then the needle should be removed. Finally, pressure should be applied to the puncture site for five minutes or longer. (See 'Technique' above.)

Complications – Complications due to percutaneous needle puncture are rare but include pain, bleeding, bruising, hematoma, nerve injury, and vasospasm. Infection, limb ischemia, and compartment syndrome are rare but serious complications. (See 'Complications' above.)

Indwelling catheters – Indwelling catheters provide continuous access to arterial blood, which is helpful when frequent blood gases are needed (eg, patients in respiratory failure on mechanical ventilation, patients requiring serial ABGs for monitoring acid-base disorders). The sample preparation and care are the same as for ABGs drawn using a needle. (See 'Indwelling catheters' above and "Intra-arterial catheterization for invasive monitoring: Indications, insertion techniques, and interpretation".)

Avoiding error – Regardless of the method used to withdraw the arterial blood, the amount of heparin solution should be minimized, at least 2 mL of blood should be obtained, air bubbles should be removed, and the specimen should immediately be placed on ice and analyzed as quickly as possible. Results are usually available within 5 to 15 minutes. (See 'Sources of error' above and 'Transport and analysis' above.)

Interpretation – When interpreting ABGs, we consider the following:

Normal ranges – The range of normal values varies among laboratories. In general, the normal pH is 7.35 to 7.45, the normal PaCO2 is 35 to 45 mmHg (4.7 to 6 kPa), and the normal HCO3 concentration is 21 to 27 mEq/L. Normal PaO2 and SaO2 have not been defined; however, it seems reasonable to consider a resting PaO2 >80 mmHg (10.7 kPa) and SaO2 >95 percent normal, unless the new values are substantially different than prior values. (See 'Normal values' above.)

Assessing abnormal values – Measurement of the PaO2 and SaO2 provide data on oxygenation (hypoxemia or hyperoxia). Measurement of the pH, PaCO2, and base excess provide sufficient data to accurately assess ventilation (respiratory acidosis and alkalosis) as well as assess complex and simple acid-base disturbances (metabolic and respiratory acidosis and alkalosis). Measurement of carboxyhemoglobin and methemoglobin is rarely indicated but should be assessed when abnormally high levels are suspected (eg, carbon monoxide poisoning, lidocaine-induced methemoglobinemia, respectively). (See 'Oxygenation' above and 'Ventilation' above and 'Acid-base balance' above and 'Abnormal hemoglobins' above.)

Sources of error – Sources of error include gas diffusion (falsely low PaO2), incomplete dismissal of heparin (falsely low pH and PaCO2), and air bubbles (falsely high PaO2 and a falsely low PaCO2). ABGs estimate the systemic acid-base balance but may not reflect the acid-base status at the tissue level in states of shock. (See 'Sources of error' above.)

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Topic 1648 Version 36.0

References

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