Up To Date. Gasometry

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Official reprint from UpToDate®

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Arterial blood gases

Author: Arthur C Theodore, MD
Section Editor: Scott Manaker, MD, PhD
Deputy Editor: Geraldine Finlay, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Feb 2023. | This topic last updated: Aug 10, 2022.
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)
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● 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.
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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
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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
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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.
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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.
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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.
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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

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● 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.
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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
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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
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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
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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)
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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
3/29/23, 2:09 PM 1648
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.
3/29/23, 2:09 PM 1648
• 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
3/29/23, 2:09 PM 1648
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.)
3/29/23, 2:09 PM 1648
• 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.)
Use of UpToDate is subject to the Terms of Use.
REFERENCES
1. AARC clinical practice guideline. Sampling for arterial blood gas analysis. American
Association for Respiratory Care. Respir Care 1992; 37:913.
2. Kohonen M, Teerenhovi O, Terho T, et al. Is the Allen test reliable enough? Eur J
Cardiothorac Surg 2007; 32:902.
3. Jarvis MA, Jarvis CL, Jones PR, Spyt TJ. Reliability of Allen's test in selection of patients for
radial artery harvest. Ann Thorac Surg 2000; 70:1362.
4. Kaye W. Invasive monitoring techniques. In: Textbook of Advanced Cardiac Life Support, A
merican Heart Association, Dallas.
5. Asif M, Sarkar PK. Three-digit Allen's test. Ann Thorac Surg 2007; 84:686.
6. Guidelines for the measurement of respiratory function. Recommendations of the British
Thoracic Society and the Association of Respiratory Technicians and Physiologists. Respir
Med 1994; 88:165.
7. Lightowler JV, Elliott MW. Local anaesthetic infiltration prior to arterial puncture for blood
gas analysis: a survey of current practice and a randomised double blind placebo
controlled trial. J R Coll Physicians Lond 1997; 31:645.
8. Pagnucci N, Pagliaro S, Maccheroni C, et al. Reducing Pain During Emergency Arterial
Sampling Using Three Anesthetic Methods: A Randomized Controlled Clinical Trial. J Emerg
Med 2020; 58:857.
9. Cakmak F, Gur A. Ethyl chloride spray, a local anesthetic in arterial blood gas sampling: A
randomized, controlled, double-blinded study. Am J Emerg Med 2022; 59:63.
10. Hess CE, Nichols AB, Hunt WB, Suratt PM. Pseudohypoxemia secondary to leukemia and
thrombocytosis. N Engl J Med 1979; 301:361.
11. Mehta A, Lichtin AE, Vigg A, Parambil JG. Platelet larceny: spurious hypoxaemia due to
extreme thrombocytosis. Eur Respir J 2008; 31:469.
12. Williams AJ. ABC of oxygen: assessing and interpreting arterial blood gases and acid-base
balance. BMJ 1998; 317:1213.
3/29/23, 2:09 PM 1648
13. Severinghaus JW. Simple, accurate equations for human blood O2 dissociation
computations. J Appl Physiol Respir Environ Exerc Physiol 1979; 46:599.
14. Shapiro BA. Temperature correction of blood gas values. Respir Care Clin N Am 1995; 1:69.
15. Hansen JE. Arterial blood gases. Clin Chest Med 1989; 10:227.
16. Bacher A. Effects of body temperature on blood gases. Intensive Care Med 2005; 31:24.
17. Ream AK, Reitz BA, Silverberg G. Temperature correction of PCO2 and pH in estimating
acid-base status: an example of the emperor's new clothes? Anesthesiology 1982; 56:41.
18. Bageant, RA. Variations in arterial blood gas measurements due to sampling techniques.
Respir Care 1975; 20:565.
19. Harsten A, Berg B, Inerot S, Muth L. Importance of correct handling of samples for the
results of blood gas analysis. Acta Anaesthesiol Scand 1988; 32:365.
20. Evers W, Racz GB, Levy AA. A comparative study of plastic (polypropylene) and glass
syringes in blood-gas analysis. Anesth Analg 1972; 51:92.
21. Smeenk FW, Janssen JD, Arends BJ, et al. Effects of four different methods of sampling
arterial blood and storage time on gas tensions and shunt calculation in the 100% oxygen
test. Eur Respir J 1997; 10:910.
22. Hansen JE, Simmons DH. A systematic error in the determination of blood PCO2. Am Rev
Respir Dis 1977; 115:1061.
23. Mueller RG, Lang GE, Beam JM. Bubbles in samples for blood gas determinations. A
potential source of error. Am J Clin Pathol 1976; 65:242.
24. Weil MH, Rackow EC, Trevino R, et al. Difference in acid-base state between venous and
arterial blood during cardiopulmonary resuscitation. N Engl J Med 1986; 315:153.
25. Adrogué HJ, Rashad MN, Gorin AB, et al. Assessing acid-base status in circulatory failure.
Differences between arterial and central venous blood. N Engl J Med 1989; 320:1312.
26. Mathias DW, Clifford PS, Klopfenstein HS. Mixed venous blood gases are superior to arterial
blood gases in assessing acid-base status and oxygenation during acute cardiac
tamponade in dogs. J Clin Invest 1988; 82:833.
Topic 1648 Version 35.0
3/29/23, 2:09 PM 1648
GRAPHICS
Anatomy of the radial artery
Schematic representation of the arterial supply to the ventral

surface of the hand. Collateral circulation to the radial artery is
provided by the ulnar artery through the deep and superficial volar
arterial arches.
Graphic 55221 Version 5.0
3/29/23, 2:09 PM 1648
Radial artery cannulation
Technique of radial artery cannulation. The radial artery is palpated

between the distal radius and the tendon of the flexor carpi radialis.
Redrawn from American Heart Association. Textbook of Advanced Cardiac Life

Support, 1994.
3/29/23, 2:09 PM 1648
Brachial artery anatomy
Schematic representation of the relationship of the brachial artery to

the antecubital crease and the median nerve. The artery should be
entered just above the antecubital crease.
3/29/23, 2:09 PM 1648
Brachial artery puncture
Technique of brachial artery puncture. The brachial artery is

palpable in the antecubital fossa just medial to the biceps tendon.
The needle should enter the brachial artery just above the
antecubital crease.

Support, 1994.
3/29/23, 2:09 PM 1648
Femoral artery anatomy
Schematic representation of the relationship of the common

femoral artery to the femoral vein and femoral nerve.
3/29/23, 2:09 PM 1648
Femoral artery puncture
Technique of femoral artery puncture. The femoral artery can be

palpated just below the midpoint of the inguinal ligament. The needle
should be inserted at a 90 degree angle toward the pulsation for a
single sampling of arterial blood. For catheter placement, the needle
should be inserted at a 45 degree angle in a cephalad direction (as
shown).
Adapted from the American Heart Association. Textbook of Advanced Cardiac Life
Support 1994.
3/29/23, 2:09 PM 1648
Axillary artery anatomy
The axillary artery is palpated within the axilla when the arm is abducted and
externally rotated.
Adapted from American Heart Association. Textbook of Advanced Cardiac Life Support, 1994.
3/29/23, 2:09 PM 1648
Axillary artery puncture
Technique of axillary artery puncture. The arm should be

hyperabducted and externally rotated. The needle should be
inserted into the artery as high as possible within the axilla.
Adapted from American Heart Association. Textbook of Advanced Cardiac Life

Support, 1994.
3/29/23, 2:09 PM 1648
Anatomy of dorsalis pedis artery
The dorsalis pedis artery is located lateral to the extensor hallucis

longus tendon.

Support, 1994.
3/29/23, 2:09 PM 1648
Modified Allen test
The patient's hand is initially held high while the fist is clenched and
both radial and ulnar arteries are compressed (A); this allows the
blood to drain from the hand. The hand is then lowered (B) and the
fist is opened (C). After pressure is released over the ulnar artery (D),
color should return to the hand within six seconds, indicating a
patent ulnar artery and an intact superficial palmar arch.

Support, 1994.
3/29/23, 2:09 PM 1648
The Allen test
In the Allen test, the patient is instructed to make a fist, which will
empty the blood from the hand and fingers (A). The examiner's
thumbs are then pressed down across the thenar and hypothenar
eminences to the wrist to occlude the radial and ulnar arteries. The
patient then opens the hand, making sure not to overextend the
fingers. The pressure on the ulnar artery is then released while the
3/29/23, 2:09 PM 1648
radial artery is still compressed (B). The hand does not fill with
blood. Note the paleness of the hand on the right compared with
the hand on left, indicating occlusion of the ulnar artery distal to the
wrist (abnormal test result). If there is prompt return of color to the
hand (indicating a normal test result), the test is repeated except
this time pressure on the radial artery is released while the ulnar
artery remains compressed.
Reproduced with permission from: Olin JW, Lie JT, Thromboagiitis (Buerger's disease).
In: Current management of hypertensive and vascular disease, Cookie JP, Frohlich
ED, (Eds), Mosby-Year Book, St Louis 1992. p.265. Copyright © Elsevier Science.
3/29/23, 2:09 PM 1648
Components of a typical arterial blood gas kit
Image displays a typical arterial blood gas kit: arterial blood gas syringe,
protective needle, syringe cap, iodine and alcohol preparation swabs, gauze,
patient label, biohazard ice bag, and adhesive bandage.
Reproduced with permission. Copyright © 2016 A-1 Medical Integration.
3/29/23, 2:09 PM 1648
The effect of temperature on blood gas measurements
Temperature
pH PCO2 PO2
ºC ºF
20 68 7.65 19 27
30 86 7.50 30 51
35 95 7.43 37 70
36 97 7.41 38 75
37 98 7.40 40 80
38 100 7.39 42 85
40 104 7.36 45 97
Adapted from: Shapiro, Peruzzi, Kozelowski-Templin: Clinical Application of Blood Gases, ed 5. St. Louis, Mosby-Year Book,
1994, p. 128.
3/29/23, 2:09 PM 1648
Etiologies and mechanism of hypercapnia
Respiratory pathway affecting carbon dioxide elimination

Central nervous system
"Won't breathe"
↓
Peripheral nervous system
Respiratory muscles
↓
"Can't breathe"
Chest wall and pleura
Upper airway
Lungs Abnormal gas exchange: "Can't breathe

enough"
Schematic figure representing the respiratory pathway, along which a variety of diseases can affect
carbon dioxide elimination and result in hypercapnia. Note that gas exchange abnormalities alone are
relatively uncommon causes of hypercapnia, but gas exchange problems in the setting of reduced
mechanical capability of the ventilatory pump are very common explanations for acute and chronic
hypercapnia.
Mechanism and etiologies of hypercapnia
Mechanism Etiologies
Decreased minute ventilation (global hypoventilation; extra pulmonary causes)
Decreased Sedative overdose (eg, narcotic or benzodiazepine, some anesthetics,

central tricyclic antidepressants)
respiratory Encephalitis
drive
Stroke
Central and obstructive sleep apnea
Obesity hypoventilation
Congenital central alveolar hypoventilation
Brainstem disease
Metabolic alkalosis
Hypothyroidism*
3/29/23, 2:09 PM 1648
Hypothermia
Starvation
Decreased Primary spinal Thoracic cage Metabolic disorders Δ

respiratory cord/lower motor disorders Hypophosphatemia
neuromuscular neuron/muscle Kyphoscoliosis Hypomagnesemia
or thoracic disorders Thoracoplasty Hypothyroidism
cage function Cervical spine injury Flail Chest Hyperthyroidism
or disease (eg,
Ankylosing
trauma
spondylitis
syringomyelia) ¶
Pectus
Amyotrophic lateral
excavatum
sclerosis
Fibrothorax
Poliomyelitis Toxins, poisoning,
Guillain-Barré drugs
syndrome Tetanus
Phrenic nerve injury Dinoflagellate
Critical illness poisoning
polymyoneuropathy Shellfish poisoning
Myasthenia gravis (red tide)
Muscular dystrophy Ciguatera
Polymyositis poisoning
Tetanus Botulism
Transverse myelitis Organophosphates

(eg, multiple Succinylcholine and
sclerosis) neuromuscular
Tick paralysis blockade
Acute intermittent Procainamide

porphyria
Eaton Lambert
syndrome
Neuralgic
amyotrophy
Periodic paralysis
Glycogen storage
and mitochondrial
diseases
Respiratory muscle
fatigue
Increased dead space (gas exchange abnormalities; pulmonary parenchymal causes or

airway disorders)
Anatomic Short shallow breathing
Physiologic Pulmonary embolism (usually severe)

3/29/23, 2:09 PM 1648
Pulmonary vascular disease (usually severe)

Dynamic hyperinflation (eg, upper and lower airway disorders including
chronic obstructive pulmonary disease, severe asthma)
Endstage interstitial lung disease
Increased carbon dioxide production
Fever
Thyrotoxicosis
Increased catabolism (sepsis, steroids)
Overfeeding
Metabolic acidosis
Exercise
Multifactorial
Upper airway disorders ◊

Severe laryngeal or tracheal disorders
(stenosis/tumors/angioedema/tracheomalacia)
Vocal cord paralysis
Epiglottitis
Foreign body aspiration
Retropharyngeal disorders
Obstructive goiter
Decreased mechanical ventilation can also cause hypercapnic respiratory acidosis (eg, permissive
hypercapnia). Importantly, any factor that limits the mechanical function of the ventilatory pump
(such as airway obstruction or weak muscles), when combined with a gas exchange abnormality
(increased physiological dead space), may lead to hypercapnia. For further details regarding the
mechanisms that underlie these pathologies, please refer to the UpToDate topic on mechanisms,
causes, and effects of hypercapnia.
* Hyperthyroidism is also a rare cause of respiratory muscle weakness.
¶ Injury or disease process needs to be between cervical spine level 3 and 5 (C3 to 5) for clinically
significant diaphragmatic paresis/paralysis to occur.
Δ Hypermagnesemia, hypokalemia, and hypercalcemia can also cause respiratory muscle weakness
and contribute to hypercapnia.
◊ Upper airway disorders are rare causes of hypercapnia. They either diminish total ventilation or
lead to dynamic hyperinflation and reduced tidal volume, while simultaneously causing increased
work of breathing and carbon dioxide production.
3/29/23, 2:09 PM 1648
Compensations to acute respiratory acidosis and

alkalosis
Combined significance bands for plasma pH and concentrations of

H+ and HCO3- in acute respiratory acidosis and alkalosis in humans.
In uncomplicated acute respiratory acid-base disorders, values for
the H+ and HCO3- concentrations will, with an estimated 95 percent
probability, fall within the band. Values lying outside the band
indicate the presence of a complicating metabolic acid-base
disturbance.
Arbus GS, Herbert LA, Levesque PR, et al. N Engl J Med 1969; 280:117. By permission
from the New England Journal of Medicine.
3/29/23, 2:09 PM 1648
Respiratory pathway affecting carbon dioxide

elimination
Schematic figure representing the respiratory pathway, along which

a variety of diseases can affect carbon dioxide elimination and result
in hypercapnia. Note that gas exchange abnormalities alone are
relatively uncommon causes of hypercapnia, but gas exchange
problems in the setting of reduced mechanical capability of the
ventilatory pump are very common explanations for acute and
chronic hypercapnia.
3/29/23, 2:09 PM 1648
Causes of respiratory alkalosis
Central nervous system Pain
Hyperventilation syndrome
Anxiety and panic disorders
Psychosis
Fever
Intracranial pathology (eg, stroke, meningitis encephalitis, tumors,

traumatic injury)
Drug withdrawal
Drugs and toxins Overdoses of salicylate, methylxanthine, catecholamines, nicotine
Progesterone and medroxyprogesterone
Doxapram
Toxic shock
Pulmonary Hypoxemia
Pneumothorax
Pneumonia
Pulmonary edema
Pulmonary embolism
Aspiration
Interstitial lung disease
Miscellaneous High altitude
Right-to-left shunts
Pregnancy
Hyperthyroidism
Severe anemia
Hyperventilation on mechanical ventilation
Recovery phase metabolic acidosis
Chronic liver disease
Prolonged paralysis
3/29/23, 2:09 PM 1648
Respiratory system anatomy: Ventilation control
Schematic figure representing the respiratory pathway, along which

a variety of diseases can affect carbon dioxide elimination and result
in hypocapnia.
3/29/23, 2:09 PM 1648
Major causes of metabolic acidosis
Mechanism of acidosis Increased AG Normal AG
Increased acid production Lactic acidosis
Ketoacidosis
Diabetes mellitus
Starvation
Alcohol associated
Ingestions
Methanol
Ethylene glycol
Aspirin
Toluene (if early or if kidney Toluene ingestion (if late and if

function is impaired) kidney function is preserved;
due to excretion of sodium and
potassium hippurate in the
urine)
Diethylene glycol
Propylene glycol
D-lactic acidosis A component of non-AG

metabolic acidosis may coexist
due to urinary excretion of D-
lactate as Na and K salts (which
represents potential HCO3)
Pyroglutamic acid (5-

oxoproline)
Loss of bicarbonate or Diarrhea or other intestinal

bicarbonate precursors losses (eg, tube drainage)
Type 2 (proximal) RTA
Posttreatment of ketoacidosis
Carbonic anhydrase inhibitors
Ureteral diversion (eg, ileal

loop)
Decreased renal acid excretion Severe kidney dysfunction Moderate kidney dysfunction
(eGFR <15 to 20 mL/min/1.73 (eGFR >15 to 20 mL/min/1.73
m2 ) m2 )
3/29/23, 2:09 PM 1648
Type 1 (distal) RTA

(hypokalemic)
Hyperkalemic RTA
Type 4 RTA (hypoaldosteronism)
Voltage defect
Large volume infusion of Diffusion acidosis

normal saline
AG: anion gap; RTA: renal tubular acidosis.
3/29/23, 2:09 PM 1648
Major causes of metabolic alkalosis
Gastrointestinal hydrogen loss

Vomiting or nasogastric suction
Congenital chloride diarrhea (congenital chloridorrhea)
Renal hydrogen loss

Primary mineralocorticoid excess (primary hyperaldosteronism, Cushing syndrome [usually
associated with ectopic ACTH] exogenous mineralocorticoids)
Mineralocorticoid excess-like states
Licorice ingestion
Liddle syndrome
Apparent mineralocorticoid excess
Loop or thiazide diuretics
Bartter or Gitelman syndrome
Status post chronic hypercarbia
Severe hypokalemia causing both intracellular hydrogen shift and renal hydrogen
excretion
Villous adenoma (may manifest metabolic alkalosis, metabolic acidosis, or both)
Laxative abuse (may manifest metabolic alkalosis, metabolic acidosis, or both)
Alkali administration with reduced renal function
Calcium-alkali syndrome*
Bicarbonate ingestion/infusion with impaired kidney function
Contraction alkalosis
* Formerly called the milk-alkali syndrome. Now more commonly generated by ingestion of calcium
carbonate rather than the historic combination of milk, cream, and "sippy powders" (sodium
bicarbonate and alkaline calcium and bismuth salts).
3/29/23, 2:09 PM 1648
Medications and chemicals that may cause acquired methemoglobinemia
Medications
Amino salicylic acid (also called p-aminosalicylic acid or 4-aminosalicylic acid)
Clofazimine
Chloroquine
Dapsone
Local anesthetics, topical sprays and creams including benzocaine (in teething rings and
ointments), lidocaine, and prilocaine
Menadione
Metoclopramide
Methylene blue*
Nitroglycerin
Phenacetin
Phenazopyridine
Primaquine
Rasburicase ¶
Quinones
Sulfonamides
Foods and beverages

Frozen or dried foods that use nitrites or sodium nitrate as a preservative
Mushrooms
Root vegetables, leafy-green vegetables, other vegetables
Well water (contains nitrates)
Chemicals and environmental substances
Acetanilide (used in varnishes, rubber, and dyes)
Anilines and aniline dyes (eg, diaper and laundry marking inks, leather dyes, red wax crayons)
Antifreeze
Benzene derivatives (used as solvents)
Chlorates and chromates (used in chemical and industrial synthesis)
Hydrogen peroxide (used as a disinfectant and cleaner)
Naphthalene (used in mothballs)
3/29/23, 2:09 PM 1648
Naphthoquinone (used in chemical synthesis)
Nitrates and nitrites (eg, amyl nitrite, farryl nitrite, sodium nitrite, nitric oxide). Sodium nitrate is
used as a food curing salt and has been ingested during suicide attempts.
Nitrogen-based fertilizers (runoff)
Nitrobenzene (used as a solvent)
Paraquat (used in herbicides)
Resorcinol (used in resin melting and wood extraction)
Refer to UpToDate topics on methemoglobinemia for additional details regarding these medications
and chemicals, as well as citations with supporting evidence for their role in causing
methemoglobinemia. Genetic/heritable causes of methemoglobinemia include M hemoglobins and
cytochrome b5-reductase deficiency (the latter is extremely rare).
G6PD: glucose-6-phosphate dehydrogenase.
* While methylene blue is a recognized treatment for methemoglobinemia, it also has oxidant
potential and may worsen the clinical status of individuals with G6PD deficiency because it induces
acute hemolysis that can further decrease oxygen delivery to the tissues. In high doses, methylene
blue can paradoxically increase methemoglobinemia.
¶ Risk of methemoglobinemia with rasburicase is especially high in individuals with G6PD deficiency;
rasburicase should be avoided in these individuals.
3/29/23, 2:09 PM 1648
Contributor Disclosures
Arthur C Theodore, MD No relevant financial relationship(s) with ineligible companies to disclose. Scott
Manaker, MD, PhD Other Financial Interest: Expert witness in workers' compensation and in medical
negligence matters [General pulmonary and critical care medicine]; National Board for Respiratory Care
[Director]. All of the relevant financial relationships listed have been mitigated. Geraldine Finlay, MD No
relevant financial relationship(s) with ineligible companies to disclose.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must
conform to UpToDate standards of evidence.
Conflict of interest policy

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Arterial blood gases

INDICATIONS AND CONTRAINDICATIONS

ABGs are frequently used for the following:

● Identification and monitoring of acid-base disturbances

● Procurement of a blood sample in an acute emergency setting when venous sampling is

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

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

● 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

• Other – Finger pulse plethysmography, Doppler flow measurements, and

Alternatively a heparinized ABG syringe can be used. Approximately 2 mL of lithium

● The planned puncture site should be sterilely prepared.

Complications — In general, serious complications due to arterial percutaneous needle

Common complications of ABG sampling include the following:

● Local pain and paresthesia

Less common complications include:

Rare complications include:

● Infection at the puncture site

Should local bleeding, hematoma, vasospasm, and/or arterial thrombus be severe,

TRANSPORT AND ANALYSIS

● The PaO2 is measured using oxidation-reduction reactions that generate measurable

curve, which is affected by temperature, pH and levels of 2,3 diphosphoglycerate (DPG).

Co-oximetry is used to measure carboxyhemoglobin and methemoglobin levels in arterial

● PaCO2 – 35 to 45 mmHg (4.7 to 6 kPa)

Nonsmokers may have up to 3 percent carboxyhemoglobin at baseline (ie, 3 percent of total

Respiratory acidosis — Respiratory acidosis is a disturbance in acid-base balance usually due

Respiratory alkalosis — Respiratory alkalosis is usually due to alveolar hyperventilation which

hyperventilation syndrome. Respiratory alkalosis can also be found in any medical

Acute hypocapnia can induce cerebral vasoconstriction resulting in dizziness and

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

Abnormal hemoglobins — Measurement of abnormal hemoglobins is rarely indicated. While

Carboxyhemoglobinemia — Elevated levels of carboxyhemoglobin are most commonly seen

Methemoglobinemia — Methemoglobinemia can be congenital (eg, cytochrome b5

SOCIETY GUIDELINE LINKS

SUMMARY AND RECOMMENDATIONS

● Indications and contraindications – The following are considered reasonable indications

• Absolute contraindications include an abnormal modified Allen's test, distorted

● Technical challenges – Technical challenges arise in patients who are uncooperative or in

● Arterial sampling – Percutaneous needle puncture refers to the withdrawal of arterial

• Collateral circulation – For patients undergoing radial or dorsalis pedis artery

• Complications – Complications due to percutaneous needle puncture are rare but

• Indwelling catheters – Indwelling catheters provide continuous access to arterial

● Interpretation – When interpreting ABGs, we consider the following:

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Anatomy of the radial artery

Schematic representation of the arterial supply to the ventral

Graphic 55221 Version 5.0

Radial artery cannulation

Technique of radial artery cannulation. The radial artery is palpated

Redrawn from American Heart Association. Textbook of Advanced Cardiac Life

Graphic 82119 Version 1.0

Brachial artery anatomy

Schematic representation of the relationship of the brachial artery to

Graphic 57543 Version 1.0

Brachial artery puncture

Technique of brachial artery puncture. The brachial artery is

Redrawn from American Heart Association. Textbook of Advanced Cardiac Life

Graphic 69312 Version 1.0

Femoral artery anatomy

Schematic representation of the relationship of the common