Arterial Blood Gases

1/10/2018 Arterial blood gases - 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: Aug 2018. | This topic last updated: Mar 16, 2017.
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 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's 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.
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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's disease or Raynaud's 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
obese or edematous patients with large amounts of subcutaneous tissue which 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, obese patients). 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 "Arterial catheterization techniques for invasive monitoring".)
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:
● Non sterile 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 pre-
empted), 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.
● 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 re-access 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".)
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 is 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 "Arterial catheterization
techniques for invasive monitoring".)
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) [8,9].
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 [10]
● The PaO2 is measured using oxidation-reduction reactions that generate measurable electric currents [10]
● 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 [11]: 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) [12,13]. 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 [12-15].
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 "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 "Clinical features,
diagnosis, and treatment of methemoglobinemia", section on 'Inaccuracy of routine pulse oximetry and blood gas
analysis'.)
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
"Oxygenation and mechanisms of hypoxemia".)
Hyperoxia — Too much supplemental oxygen (hyperoxia) also has deleterious effects, the details of which
are discussed separately. (See "Oxygen toxicity".)
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 'Respiratory alkalosis'.)
A respiratory alkalosis develops when the lungs are stimulated to remove more carbon dioxide than is
produced metabolically in the tissues. The stimulus to increase respiratory drive is controlled by central and
peripheral factors (algorithm 1). Thus, respiratory alkalosis is commonly encountered in anxiety, panic, pain,
fever, psychosis, and hyperventilation syndrome. Respiratory alkalosis can also be found in any medical
condition that increases alveolar ventilation including pulmonary embolism, heart failure, or mechanical
ventilation, as well as in stroke, meningitis, high altitude, right-to-left shunts, pregnancy, hyperthyroidism,
and aspirin overdose (table 3 and algorithm 2). Decreased carbon dioxide production from excessive
sedation, skeletal muscle paralysis, hypothermia, or hypothyroidism is a rare mechanism that may contribute
to respiratory alkalosis but is rarely a primary etiology for hypocapnia.
Acute hypocapnia can induce cerebral vasoconstriction resulting in dizziness and lightheadedness. Paresthesias
of the hands, feet or mouth may also be present due to peripheral hypocalcemia (from increased binding of
calcium to serum albumin). Patients may also complain of chest pain or dyspnea and severe cases can be
associated with carpopedal spasm, tetany, mental confusion, syncope, and seizures. Acute hypocapnia causes a
reduction of serum levels of potassium and phosphate secondary to increased intracellular shifts of these ions.
Hyponatremia and hypochloremia are rare. Consequently, severe alkalosis (>7.6) is worrisome for the
development of seizures and cardiac instability. (See "Hyperventilation syndrome", section on 'Clinical
presentation'.)
Respiratory alkalosis is typically managed by treating the underlying cause (eg, reassurance, anxiolytic, pain
control) and using maneuvers to reduce alveolar ventilation (eg, sedation, reduce respiratory rate and/or tidal
volume when on mechanical ventilation).
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 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
"Genetics and pathogenesis of congenital and acute toxic methemoglobinemia" and "Clinical features, diagnosis,
and treatment of 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 [16-19]. 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 [16,20]. 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 [10]. 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 [17,21].
(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 [22-24]. 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) [22]. 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.
SUMMARY AND RECOMMENDATIONS
● 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.)
● 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
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severe coagulopathy or in whom thrombolytic therapy is being administered as well as in patients with active
Raynaud's disease. Therapeutic anticoagulation and antiplatelet agents including aspirin are not generally
considered as contraindications to ABG needle stick sampling. (See 'Indications and contraindications'
above.)
● 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 obese or edematous patients 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.)
● 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):
• 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.)
• 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.)
• 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 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 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 is the same as for ABGs drawn using a
needle. (See 'Indwelling catheters' above and "Arterial catheterization techniques for invasive monitoring".)
● 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.)
● 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.)
● 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 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 Subscription and License Agreement.
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, American Heart A
ssociation, 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. Hess CE, Nichols AB, Hunt WB, Suratt PM. Pseudohypoxemia secondary to leukemia and thrombocytosis.
N Engl J Med 1979; 301:361.
9. Mehta A, Lichtin AE, Vigg A, Parambil JG. Platelet larceny: spurious hypoxaemia due to extreme
thrombocytosis. Eur Respir J 2008; 31:469.
10. Williams AJ. ABC of oxygen: assessing and interpreting arterial blood gases and acid-base balance. BMJ
1998; 317:1213.
11. Severinghaus JW. Simple, accurate equations for human blood O2 dissociation computations. J Appl
Physiol Respir Environ Exerc Physiol 1979; 46:599.
12. Shapiro BA. Temperature correction of blood gas values. Respir Care Clin N Am 1995; 1:69.
13. Hansen JE. Arterial blood gases. Clin Chest Med 1989; 10:227.
14. Bacher A. Effects of body temperature on blood gases. Intensive Care Med 2005; 31:24.
15. 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.
16. Bageant, RA. Variations in arterial blood gas measurements due to sampling techniques. Respir Care
1975; 20:565.
17. 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.
18. Evers W, Racz GB, Levy AA. A comparative study of plastic (polypropylene) and glass syringes in blood-
gas analysis. Anesth Analg 1972; 51:92.
19. 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.
20. Hansen JE, Simmons DH. A systematic error in the determination of blood PCO2. Am Rev Respir Dis
1977; 115:1061.
21. 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.
22. 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.
23. 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.
24. 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 21.0
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
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.
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.
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.
Femoral artery anatomy
Schematic representation of the relationship of the common femoral artery to

the femoral vein and femoral nerve.
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.
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.
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.
Anatomy of dorsalis pedis artery
The dorsalis pedis artery is located lateral to the extensor hallucis longus
tendon.

Support, 1994.
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.
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 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.
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.
The effect of temperature on blood gas measurements
Temperature
pH PCO 2 PO 2
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.
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 central Sedative overdose (eg, narcotic or benzodiazepine, some anesthetics, tricyclic
respiratory drive antidepressants)
Encephalitis
Stroke
Central and obstructive sleep apnea
Obesity hypoventilation
Congenital central alveolar hypoventilation
Brainstem disease
Metabolic alkalosis
Hypothyroidism*
Hypothermia
Starvation
Decreased respiratory Primary spinal Thoracic cage disorders Metabolic disorders Δ

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

Muscular dystrophy Succinylcholine and
Polymyositis neuromuscular
Tetanus blockade
Transverse myelitis Procainamide

(eg, multiple
sclerosis)
Tick paralysis
Acute intermittent
porphyria
Eaton Lambert
syndrome
Neuralgic amyotrophy
Periodic paralysis
Glycogen storage and
mitochondrial diseases
Increased dead space (gas exchange abnormalities; pulmonary parenchymal causes or airway disorders)
Anatomic Short shallow breathing
Physiologic Pulmonary embolism (usually severe)

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.
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.
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.
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
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.
Major causes of metabolic acidosis according to mechanism and anion gap
Mechanism of
Increased AG Normal AG
acidosis
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 renal function is preserved; due
function is impaired) 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 HCO 3 )
Pyroglutamic acid (5-

oxoproline)
Loss of bicarbonate or Diarrhea or other intestinal losses (eg, tube drainage)

bicarbonate precursors
Type 2 (proximal) RTA
Posttreatment of ketoacidosis
Carbonic anhydrase inhibitors
Ureteral diversion (eg, ileal loop)
Decreased renal acid Chronic kidney disease Chronic kidney disease and tubular dysfunction (but
excretion relatively preserved glomerular filtration rate)
Type 1 (distal) RTA
Type 4 RTA (hypoaldosteronism)
AG: anion gap; RTA: renal tubular acidosis.
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 acidosis, metabolic acidosis, or both)
Laxative abuse (may manifest metabolic acidosis, metabolic acidosis, or both)
Alkali administration with reduced renal function

Calcium-alkali syndrome*
Bicarbonate ingestion/infusion with impaired renal 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" (NaHCO 3 and alkaline calcium and bismuth salts).
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
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)
Naphthoquinone (used in chemical synthesis)
Nitrates and nitrites (eg, amyl nitrite, farryl nitrite, sodium nitrite, nitrate- and nitrite-containing foods, nitric oxide,
well water)
Nitrobenzene (used as a solvent)
Paraquat (used in herbicides)
Resorcinol (used in resin melting and wood extraction)
Inherited disorders (extremely rare)

Cytochrome b5-reductase deficiency
Hemoglobin M disease
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 and information on congenital
methemoglobinemia syndromes.
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.
Contributor Disclosures
Arthur C Theodore, MD Grant/Research/Clinical Trial Support: Genentech [Mycophenolate (Scleroderma,
Interstitial lung disease)]. Scott Manaker, MD, PhD Consultant/Advisory boards: Expert witness in workers'
compensation and in medical negligence matters [General pulmonary and critical care medicine]. Equity
Ownership/Stock Options (Spouse): Johnson & Johnson; Pfizer (Numerous medications and devices). Other
Financial Interest: Director of ACCP Enterprises, a wholly owned for-profit subsidiary of ACCP [General
pulmonary and critical care medicine (Providing pulmonary and critical care medicine education to non-members
of ACCP)]. Geraldine Finlay, MD Nothing 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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Author: Arthur C Theodore, MD

● Identification and monitoring of acid-base disturbances

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's syndrome (particularly sampling at the radial site)

● Non sterile gloves

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

● 2 × 2 inch sterile gauze

● Sharp object container

● The planned puncture site should be sterilely prepared.

Common complications of ABG sampling include the following:

● Local pain and paresthesia

● Local minor bleeding

Less common complications include:

● Local hematoma from moderate or major bleeding

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

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

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

Carboxyhemoglobinemia — Elevated levels of carboxyhemoglobin are most commonly seen in carbon

Methemoglobinemia — Methemoglobinemia can be congenital (eg, cytochrome b5 reductase or cytochrome

SUMMARY AND RECOMMENDATIONS

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Topic 1648 Version 21.0

Anatomy of the radial artery

Schematic representation of the arterial supply to the ventral surface of the

Graphic 55221 Version 5.0

Radial artery cannulation

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 the

Graphic 57543 Version 1.0

Brachial artery puncture

Technique of brachial artery puncture. The brachial artery is palpable in the

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 femoral artery to

Graphic 75120 Version 1.0

Femoral artery puncture

Graphic 50204 Version 2.0

Axillary artery anatomy

Graphic 55334 Version 4.0

Axillary artery puncture

Technique of axillary artery puncture. The arm should be hyperabducted and

Adapted from American Heart Association. Textbook of Advanced Cardiac Life

Graphic 67106 Version 1.0

Anatomy of dorsalis pedis artery

Redrawn from American Heart Association. Textbook of Advanced Cardiac Life

Graphic 54240 Version 4.0

Modified Allen test

Redrawn from American Heart Association. Textbook of Advanced Cardiac Life

Graphic 70306 Version 1.0

The Allen test

Graphic 79685 Version 4.0