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Official reprint from UpToDate www.uptodate.com ©2016 UpToDate

Author Arthur C Theodore, MD

Section Editor Scott Manaker, MD, PhD

Deputy Editor Geraldine Finlay, MD

Arterial blood gases

All topics are updated as new evidence becomes available and our peer review process is complete.Literature review current through: May 2016. | This topic last updated: Sep 22, 2015.

INTRODUCTION — An arterial blood gas (ABG) is a test that measures the oxygen tension (PaO ), carbon dioxidetension (PaCO ), acidity (pH), oxyhemoglobin saturation (SaO ), and bicarbonate (HCO ) concentration in arterialblood. 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 acid­base disturbances are discussed separately.(See "Simple and mixed acid­base disorders" and "Venous blood gases and other alternatives to arterial bloodgases".)

INDICATIONS AND CONTRAINDICATIONS — Arterial blood gases (ABGs) are frequently used for the following:

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

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

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

Similarly, arterial needle stick and catheterization can be performed in patients with thrombocytopenia a plateletcount >50 x 10 /L, but is generally avoided in those whose count is ≤30 x 10 /L. For those with counts between 30and 50 x 10 /L limited needle stick sampling is sometimes performed, when necessary, with increased compressiontime. A platelet count <50 x 10 /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 peripheralperfusion (eg, cyanotic digits), are also considered by most experts as relative contraindications to radial arterialsampling.

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

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Identification and monitoring of acid­base disturbancesMeasurement of the partial pressures of oxygen (PaO ) and carbon dioxide (PaCO ) 2 2Assessment of the response to therapeutic interventions (eg, insulin in patients with diabetic ketoacidosis)Detection and quantification of the levels of abnormal hemoglobins (eg, carboxyhemoglobin andmethemoglobin)

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

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

Local infection or distorted anatomy at the puncture site (eg, previous surgical interventions, congenital oracquired 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)

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TECHNICAL CHALLENGES — Arterial blood gas sampling may be difficult to perform in patients who areuncooperative or in whom pulses cannot be easily identified (eg, shock, vasopressor infusion, arteriosclerosis fromend­stage kidney disease, calcification of the vessel wall). Difficulties can also arise when the patient cannot bepositioned appropriately (eg, cannot fully extend the wrists for radial artery access due to tremor or jointcontractures) or in obese or edematous patients with large amounts of subcutaneous tissue which may obscure theusual anatomic landmarks. In some of these scenarios, ultrasound may be useful to locate the artery and reducepotential complications of repeated puncture and consequent injury to the target vessel and surrounding tissue.

ARTERIAL SAMPLING — Arterial blood is required for an arterial blood gas (ABG). It can be obtained bypercutaneous needle puncture or from an indwelling arterial catheter. Written consent is not usually required forarterial needle stick puncture but is required for the insertion of an indwelling catheter. Regardless, the risks andbenefits 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 hasbeen unsuccessful or is not feasible (eg, weak pulses, patient on multiple vasopressors, obese patients). Whenused, ultrasound­guided access may increase the operator’s ability to enter the vessel and helps minimize injury tothe artery and adjacent nerves and veins.

Needle puncture — Percutaneous needle puncture refers to the withdrawal of arterial blood via a needle stick. Itneeds to be repeated every time an ABG is performed, since an indwelling catheter is not inserted. Thus, it issuitable for patients who require a limited number of arterial draws (eg, daily or less than once daily during anadmission to hospital). If recurrent sampling (eg, more than four draws in 24 hours) is required, clinicians should, atminimum, rotate puncture sites (eg, right and left radial) or consider placing an indwelling catheter. (See 'Indwellingcatheters' below and "Arterial catheterization techniques for invasive monitoring".)

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

Ensure collateral circulation — One of the risks associated with arterial puncture is ischemia distal to thepuncture site (see 'Complications' below). Although rarely performed in practice, identifying collateral flow to theregion supplied by the artery can be used by clinicians prior to puncture. While limited studies have found variableaccuracy associated with such evaluations, we believe that patients, and in particular high risk patients, undergoingradial or dorsalis pedis artery puncture should have the collateral flow to those vessels evaluated [2,3]. Our belief isbased upon the concept that it avoids potential harm by identifying patients who have impaired collateral circulationand who are therefore at increased risk of an ischemic complication, and in whom an alternative site should be

Radial artery – The radial artery is best palpated between the distal radius and the tendon of the flexor carpiradialis when the wrist is extended (figure 1 and figure 2). Although infrequently performed, the arm can betaped (at the level of the forearm and palm) to an armboard with the palm facing upward; a large roll of gauzealso can be placed between the wrist and the armboard in a position that extends the wrist. Over extensionshould 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 (anarmboard 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 elbowcrease at a 30 degree angle (figure 4). It is usually harder to access because it runs deeper in the arm than theradial artery.

Femoral artery – The femoral artery is best palpated just below the midpoint of the inguinal ligament, whenthe lower extremity is extended and the patient is lying supine (figure 5). The needle should be inserted at a 90degree 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 externallyrotated (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 is rarely accessed for arterial blood. It is best palpated lateral to theextensor hallucis longus tendon on the dorsum of the foot (figure 9). The needle can be inserted at a 30degree angle lateral to the extensor tendon at the level of the midfoot.

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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 indiameter). They receive collateral supply from the ulnar and lateral plantar artery, respectively. It is this collateralsupply that is identified by the following tests:

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

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

Similarly, pulses distal to the brachial artery must be assessed prior to the procedure. In patients with absent pulsesat 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 theprocedure. This includes:

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

ABG kits (picture 2) are used by clinicians in most institutions to draw arterial blood. Kits contain a heparinizedplastic syringe with the plunger already pulled back to allow for the collection of 2 mL of blood, a protective needlesleeve, a needle, syringe cap, and ice bag. The sleeve, while attached to the syringe, locks the needle within itself toprevent direct contact between operator and needle. It is removed to expose the needle. The prefilled heparin is

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

Modified Allen’s test – The patient's hand is initially held high with the fist clenched. Both the radial andulnar arteries are compressed firmly by the two thumbs of the investigator (figure 10). This allows theblood to drain from the hand. The hand is then lowered and the fist is opened (the palm will appearwhite). Overextension of the hand or wide spreading of the fingers should be avoided because it maycause false­normal results. The pressure is released from the ulnar artery while occlusion is maintainedon the radial artery. A pink color should return to the palm, usually within six seconds, indicating that theulnar artery is patent and the superficial palmar arch is intact. Although the timing of return of circulationto the palm varies considerably, the test is generally considered abnormal if ten seconds or more elapsesbefore color returns to the hand (picture 1).

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

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

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Dorsalis pedis artery – The dorsalis pedis artery can be occluded by the forefinger followed by compressionof the nail bed of the great toe and assessment of the rapidity with which color returns to the nail bed afterpressure is released from the great toe (figure 11).

Non sterile glovesAntiseptic skin solution (eg, chlorhexidine and povidone­iodine are solutions)ABG kit OR a pre­heparinized 3 mL ABG syringe with a 22 to 25­gauge needle and syringe cap2 × 2 inch sterile gauzeAdhesive bandagePlastic hazard bag with ice (if not provided in the kit)Sharp object container

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expelled (incomplete dismissal of heparin falsely lowers the partial pressure of carbon dioxide), and the plunger isthen repositioned at the 2 mL mark.

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

Postprocedural care — Patients should be monitored for new symptoms such as skin color changes, persistentor worsening pain, active bleeding, and impaired movement or sensation of the limb. Monitoring is particularlyimportant in patients who are subsequently supra therapeutic on anticoagulants or are given thrombolytics, asbleeding 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:

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 guage needle and then pushed out; the plunger should beleft leaving a small empty volume (eg, usually 2 mL) in the syringe.

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 largeramounts or injecting the anesthetic into deeper planes may distort the anatomy and hinder identification of thevessel [7]. Traditionally, it was believed that the injection of lidocaine is as painful as the procedure itself somany clinicians avoid using it for this reason. However, in our experience, when performed by personnelexperienced in arterial draws, no anesthesia is typically needed.

ABG kits are used by clinicians in most institutions to draw arterial blood. Alternatively, a heparinized syringecan 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. Bothfingers should be proximal to the desired puncture site; placing the nondominant middle finger distally and thenondominant index finger proximally, with the needle insertion site in between, is not recommended, becauseof the increased risk of needle stick injury. The artery should be punctured with the needle at a 30 to 45 degreeangle (radial, brachial, axillary, dorsalis pedis) or at a 90 degree angle (femoral artery) relative to the skin. Thesyringe fills on its own (ie, pulling the plunger is usually unnecessary). Approximately 2 to 3 mL of blood shouldbe removed.

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

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

After withdrawing a sufficient volume of blood, the needle should be removed while simultaneously applyingpressure to the puncture site with sterile gauze until hemostasis is achieved. This usually takes five minutes ina non anticoagulated patient; avoid checking the puncture site until local pressure has been maintained for atleast this period as this increases the risk of hemorrhage or a hematoma. In patients who have a coagulopathyor are on anticoagulation therapy, it may be necessary to apply local pressure for a longer time. Oncehemostasis 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 sharpobject container. When an ABG syringe is used, recap, remove, and discard the needle, being careful to avoida needle stick injury. After discarding the needle, remove the excess air in the syringe by holding it upright andgently tapping it, allowing any air bubbles present to reach the top of the syringe, from where they can then beexpelled. 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.

Local pain and paresthesia

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Less common complications include:

Should local bleeding, hematoma, vasospasm, and/or arterial thrombus be severe, compartment syndrome and limbischemia 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 arterialdraw is thought to decrease the risk of these complications. (See "Acute compartment syndrome of the extremities"and "Overview of acute arterial occlusion of the extremities (acute limb ischemia)".)

While vasopressor use may increase the risk of vasospasm, when indicated (eg, for shock), these agents should notbe adjusted to avoid or treat this complication. (See "Evaluation of and initial approach to the adult patient withundifferentiated 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 resolvesspontaneously.

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

Indwelling catheters — Arterial blood can also be obtained via an indwelling arterial catheter. Indwelling cathetersprovide continuous access to arterial blood, which is helpful when frequent blood gases are needed (eg, patients inrespiratory failure on mechanical ventilation, patients requiring serial ABGs for monitoring acid­base disorders). Thesample 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 catheterizationtechniques for invasive monitoring".)

TRANSPORT AND ANALYSIS — The arterial blood sample should be placed on ice during transport to the lab andthen analyzed as quickly as possible. This reduces oxygen consumption by leukocytes (ie, leukocyte larceny), whichcan cause a factitiously low partial pressure of arterial oxygen (PaO ) [8]. This effect is most pronounced in patientswhose leukocytosis is profound. In addition, it reduces the likelihood of error due to gas diffusion through the plasticsyringe 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 automatedblood gas analyzers, which automatically transport the specimen to electrochemical sensors to measure acidity(pH), partial pressure of carbon dioxide (PaCO ), and PaO :

BruisingLocal minor bleeding

Vasovagal responseLocal hematoma from moderate or major bleedingArtery vasospasm

Rare complications include:

Infection at the puncture siteArterial occlusion from a local hematomaAir or thrombus embolismLocal anesthetic anaphylactic reactionLocal nerve injuryNeedle stick injury to health care personnel (limited due to use of ABG kits)Vessel laceration

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The PaCO is measured using a chemical reaction that consumes CO and produces a hydrogen ion, which issensed as a change in pH [9]

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The PaO is measured using oxidation­reduction reactions that generate measurable electric currents [9] 2

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 PaCO using the Henderson­ 2

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

Arterial blood gas measurements by the analyzer are affected by temperature. Specifically, pH increases and bothPaO and PaCO decrease as temperature declines (table 1) [11,12]. Modern automated blood gas analyzers canreport the pH, PaO , and PaCO at either 37ºC (the temperature at which the values are measured by the bloodgas analyzer) or at the patient's body temperature. Most centers report the values of pH, PaCO , and PaO at 37ºC,even if the patient's body temperature is different. However, this practice is controversial [11­14].

Co­oximetry is used to measure carboxyhemoglobin and methemoglobin levels in arterial blood, the details of whichare described separately. (See "Pulse oximetry in adults", 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 (PaCO ) and bicarbonate concentration (HCO ) are as follows:

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

Nonsmokers may have up to 3 percent carboxyhemoglobin at baseline (ie, 3 percent of total hemoglobin); smokersmay have levels of 10 to 15 percent. Levels above these respective values are considered abnormal. Normalindividuals have approximately 1 percent methemoglobin in arterial blood. (See "Pulse oximetry in adults", sectionon 'Carboxyhemoglobin' and "Carbon monoxide poisoning", section on 'Diagnosis' and "Clinical features, diagnosis,and treatment of methemoglobinemia".)

Oxygenation — Measurement of PaO and SaO provide data on oxygenation that can also be used to calculateindices of oxygenation including the alveolar­arterial gradient (A­a gradient), partial pressure of arterialoxygen/fraction of inspired oxygenation ratio (PaO /FiO ), and oxygen delivery (DO ).

Hypoxemia — Oxygen is necessary for aerobic metabolism such that low levels of oxygen (hypoxemia) aredeleterious, 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 arediscussed separately. (See "Oxygen toxicity".)

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

Respiratory acidosis — Respiratory acidosis is a disturbance in acid­base balance usually due to alveolarhypoventilation that can be acute or chronic. It is characterized by an increased PaCO >45 mmHg (hypercapnia)and a reduction in pH (pH <7.35). The mechanisms, etiologies, and clinical manifestations, as well as the distinctionbetween acute and chronic hypercapnia and the approach to patients with hypercapnic respiratory failure arediscussed 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 adecrease in PaCO (hypocapnia) and an increase in the pH. It can also be acute or chronic. In acute respiratory

Hasselbalch equation

Arterial oxygen saturation (SaO ) is based upon the equation developed by Severinghaus [10]: SO = (23,400* (PaO + 150 * PaO ) + 1) or the Oxygen hemoglobin disassociation curve, which is affected bytemperature, pH and levels of 2,3 diphosphoglycerate (DPG).

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2­1 ­1

2 22 2

2 2

2 3

pH – 7.35 to 7.45

PaCO – 35 to 45 mmHg (4.7 to 6 kPa) 2

HCO – 21 to 27 mEq/L 3

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2

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2 2 2

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alkalosis, the PaCO level is below the lower limit of normal (<35 mmHg or 4.7 kPa) and the serum pH isappropriately alkalemic (>7.45) (figure 12). In states of chronic respiratory alkalosis, the PaCO level is also belowthe lower limit of normal (<35 mmHg or 4.7 kPa), but the pH level is at or close to normal. Calculating theappropriate compensatory response to acute respiratory alkalosis is described separately. (See "Simple and mixedacid­base disorders", section on 'Respiratory alkalosis'.)

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

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

Acid­base balance — Measurement of pH, PaCO , and base excess provide sufficient data to accurately assesssimple and mixed acid­base disturbances which are discussed separately in the following topics:

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

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

Methemoglobinemia — Methemoglobinemia can be congenital (eg, cytochrome b5 reductase or cytochrome b5deficiency, hemoglobin M disease) or acquired (usually drugs or toxins (table 6)). Methemoglobinemia should besuspected when the oxygen saturation as measured by pulse oximetry (SpO ) is more than 5 percent lower than theoxygen saturation calculated from arterial blood gas analysis (SaO ) ("saturation gap") and when pulse oximetryshows an oxygen saturation ≤90 percent and the arterial oxygen partial pressure is ≥70 mmHg. A detaileddiscussion of the etiology, diagnosis, and treatment of methemoglobinemia is provided separately. (See "Geneticsand pathogenesis of 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 thatcan typically be easily avoided by good sample care.

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A respiratory alkalosis develops when the lungs are stimulated to remove more carbon dioxide than isproduced metabolically in the tissues. The stimulus to increase respiratory drive is controlled by central andperipheral 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 medicalcondition that increases alveolar ventilation including pulmonary embolism, heart failure, or mechanicalventilation, as well as in stroke, meningitis, high altitude, right­to­left shunts, pregnancy, hyperthyroidism, andaspirin 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 torespiratory alkalosis but is rarely a primary etiology for hypocapnia.

2

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 adultpatient 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 "Clinicalmanifestations 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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SUMMARY AND RECOMMENDATIONS

Gas diffusion through the plastic syringe and consumption of oxygen by leukocytes is a potential source oferror that results in a falsely low oxygen tension (PaO ) when the sample is left for prolonged periods at roomtemperature. However, the clinical significance of this error is minimal if the sample is placed on ice andanalyzed within 15 minutes [15­18]. While using a glass syringe will prevent gas diffusion, this solution isimpractical.

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The heparin that is added to the syringe as an anticoagulant can decrease the pH if acidic heparin is used andthe dismissal of heparin from the syringe is incomplete. It can also dilute the PaCO , resulting in a falsely lowvalue [15,19]. When an ABG syringe is used, the amount of heparin solution used should be minimized and atleast 2 mL of blood should be obtained. Detailed discussion of ABG equipment is discussed above. (See'Equipment' above.)

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Air bubbles that exceed 1 to 2 percent of the blood volume can cause a falsely high PaO and a falsely lowPaCO [9]. The magnitude of this error depends upon the difference in gas tensions between blood and air, theexposure 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 bubblesafter the sample has been withdrawn and analyzing the sample as soon as possible [16,20]. (See 'Technique'above.)

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Some studies suggest that ABGs estimate the systemic acid­base balance and oxygenation but do notaccurately reflect tissue levels in states of shock [21­23]. As an example, one study of patients who underwentcardiopulmonary resuscitation compared blood gas values in blood simultaneously drawn from an arterialcatheter and a pulmonary artery catheter (PAC) [21]. Compared with PAC samples, arterial pH was higher(7.42 versus 7.14) and PaCO was lower (32 mmHg versus 74 mmHg). If PAC results more closely reflect theacid­base status at the tissue level, then the arterial measurements can lead to the mistaken assumption thatacid­base balance in tissues is being maintained. However, measurement of ABGs from PACs to assess gasexchange is impractical (PACs are rarely placed) and not adequately validated such that it cannot be routinelyrecommended.

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An arterial blood gas (ABG) is a test that measures the oxygen tension (PaO ), carbon dioxide tension(PaCO ), acidity (pH), oxyhemoglobin saturation (SaO ), and bicarbonate (HCO ) concentration in arterialblood. Some blood gas analyzers also measure the methemoglobin, carboxyhemoglobin, and hemoglobinlevels. (See 'Introduction' above.)

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ABGs are frequently used to detect and monitor indices of oxygenation, ventilation, and acid­base balance, aswell as quantify levels of carboxyhemoglobin and methemoglobin. Absolute contraindications include anabnormal modified Allen’s test, distorted anatomy, infection, or severe peripheral vascular disease at thepuncture site. Arterial blood draws and in particular catheter insertion should be avoided in patients with severecoagulopathy or in whom thrombolytic therapy is being administered as well as in patients with activeRaynaud’s disease. Therapeutic anticoagulation and antiplatelet agents including aspirin are not generallyconsidered 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 andconsequent 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 berepeated every time an ABG is performed. Thus, it is suitable for patients who require a limited number ofarterial draws (eg, daily or less than once daily during an admission to hospital). If recurrent sampling isrequired, clinicians should at minimum rotate puncture sites (eg, right and left radial) or consider placing anindwelling catheter (see 'Arterial sampling' above):

Common sites include the radial, femoral, brachial, axillary, or dorsalis pedis artery. There is no evidencethat any site is superior to the others. However, the radial artery is used most often because it isaccessible 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 flowto those vessels prior to puncture (eg, modified Allen’s test for radial artery puncture) (Grade 2C). For

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REFERENCES

1. AARC clinical practice guideline. Sampling for arterial blood gas analysis. American Association forRespiratory 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 arteryharvest. Ann Thorac Surg 2000; 70:1362.

4. Kaye W. Invasive monitoring techniques. In: Textbook of Advanced Cardiac Life Support, American HeartAssociation, Dallas.

5. Asif M, Sarkar PK. Three­digit Allen's test. Ann Thorac Surg 2007; 84:686.6. Guidelines for the measurement of respiratory function. Recommendations of the British Thoracic Society andthe 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: asurvey of current practice and a randomised double blind placebo controlled trial. J R Coll Physicians Lond1997; 31:645.

8. Hess CE, Nichols AB, Hunt WB, Suratt PM. Pseudohypoxemia secondary to leukemia and thrombocytosis. N

other sites, distal pulses can be assessed prior to arterial puncture. Poor collateral flow or weak distalpulses 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 shouldbe 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 rarebut serious complications. (See 'Complications' above.)

•

Indwelling catheters provide continuous access to arterial blood, which is helpful when frequent blood gasesare needed (eg, patients in respiratory failure on mechanical ventilation, patients requiring serial ABGs formonitoring acid­base disorders). The sample preparation and care is the same as for ABGs drawn using aneedle. (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 beminimized, at least 2 mL of blood should be obtained, air bubbles should be removed, and the specimenshould immediately be placed on ice and analyzed as quickly as possible. Results are usually available within5 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 normalPaCO is 35 to 45 mmHg (4.7 to 6 kPa), and the normal HCO concentration is 21 to 27 mEq/L. Normal PaOand SaO have not been defined; however, it seems reasonable to consider a resting PaO >80 mmHg (10.7kPa) and SaO >95 percent normal, unless the new values are substantially different than prior values. (See'Normal values' above.)

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Measurement of the PaO and SaO provide data on oxygenation (hypoxemia or hyperoxia). Measurement ofthe pH, PaCO , and base excess provide sufficient data to accurately assess ventilation (respiratory acidosisand alkalosis) as well as assess complex and simple acid­base disturbances (metabolic and respiratoryacidosis and alkalosis). Measurement of carboxyhemoglobin and methemoglobin is rarely indicated but shouldbe assessed when abnormally high levels are suspected (eg, carbon monoxide poisoning, lidocaine­inducedmethemoglobinemia, respectively). (See 'Oxygenation' above and 'Ventilation' above and 'Acid­base balance'above and 'Abnormal hemoglobins' above.)

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Sources of error include gas diffusion (falsely low PaO ), incomplete dismissal of heparin (falsely low pH andPaCO ), and air bubbles (falsely high PaO and a falsely low PaCO ). ABGs estimate the systemic acid­basebalance but may not reflect the acid­base status at the tissue level in states of shock. (See 'Sources of error'above.)

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Engl J Med 1979; 301:361.9. Williams AJ. ABC of oxygen: assessing and interpreting arterial blood gases and acid­base balance. BMJ1998; 317:1213.

10. Severinghaus JW. Simple, accurate equations for human blood O2 dissociation computations. J Appl PhysiolRespir Environ Exerc Physiol 1979; 46:599.

11. Shapiro BA. Temperature correction of blood gas values. Respir Care Clin N Am 1995; 1:69.12. Hansen JE. Arterial blood gases. Clin Chest Med 1989; 10:227.13. Bacher A. Effects of body temperature on blood gases. Intensive Care Med 2005; 31:24.14. Ream AK, Reitz BA, Silverberg G. Temperature correction of PCO2 and pH in estimating acid­base status: an

example of the emperor's new clothes? Anesthesiology 1982; 56:41.15. Bageant, RA. Variations in arterial blood gas measurements due to sampling techniques. Respir Care 1975;

20:565.16. 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; 32:365.17. Evers W, Racz GB, Levy AA. A comparative study of plastic (polypropylene) and glass syringes in blood­gas

analysis. Anesth Analg 1972; 51:92.18. 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; 10:910.19. Hansen JE, Simmons DH. A systematic error in the determination of blood PCO2. Am Rev Respir Dis 1977;

115:1061.20. Mueller RG, Lang GE, Beam JM. Bubbles in samples for blood gas determinations. A potential source of error.

Am J Clin Pathol 1976; 65:242.21. Weil MH, Rackow EC, Trevino R, et al. Difference in acid­base state between venous and arterial blood during

cardiopulmonary resuscitation. N Engl J Med 1986; 315:153.22. Adrogué HJ, Rashad MN, Gorin AB, et al. Assessing acid­base status in circulatory failure. Differences

between arterial and central venous blood. N Engl J Med 1989; 320:1312.23. Mathias DW, Clifford PS, Klopfenstein HS. Mixed venous blood gases are superior to arterial blood gases in

assessing acid­base status and oxygenation during acute cardiac tamponade in dogs. J Clin Invest 1988;82:833.

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GRAPHICS

Anatomy of the radial artery

Schematic representation of the arterial supply to the ventral surface ofthe hand. Collateral circulation to the radial artery is provided by theulnar artery through the deep and superficial volar arterial arches.

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Radial artery cannulation

Technique of radial artery cannulation. The radial artery is palpatedbetween the distal radius and the tendon of the flexor carpi radialis.

Redrawn from American Heart Association. Textbook of Advanced CardiacLife Support, 1994.

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Brachial artery anatomy

Schematic representation of the relationship of the brachial artery to theantecubital crease and the median nerve. The artery should be enteredjust above the antecubital crease.

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Brachial artery puncture

Technique of brachial artery puncture. The brachial artery is palpable inthe antecubital fossa just medial to the biceps tendon. The needleshould enter the brachial artery just above the antecubital crease.

Redrawn from American Heart Association. Textbook of Advanced CardiacLife Support, 1994.

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Femoral artery anatomy

Schematic representation of the relationship of the common femoralartery to the femoral vein and femoral nerve.

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Femoral artery puncture

Technique of femoral artery puncture. The femoral artery can be palpatedjust below the midpoint of the inguinal ligament. The needle should beinserted at a 90 degree angle toward the pulsation for a single sampling ofarterial blood. For catheter placement, the needle should be inserted at a45 degree angle in a cephalad direction (as shown).

Adapted from the American Heart Association. Textbook of Advanced CardiacLife Support 1994.

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Axillary artery anatomy

The axillary artery is palpated within the axilla when the arm is abducted andexternally rotated.

Adapted from American Heart Association. Textbook of Advanced Cardiac Life Support,1994.

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Axillary artery puncture

Technique of axillary artery puncture. The arm should be hyperabductedand externally rotated. The needle should be inserted into the artery ashigh as possible within the axilla.

Adapted from American Heart Association. Textbook of Advanced Cardiac LifeSupport, 1994.

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Anatomy of dorsalis pedis artery

The dorsalis pedis artery is located lateral to the extensor hallucislongus tendon.

Redrawn from American Heart Association. Textbook of Advanced CardiacLife Support, 1994.

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Modified Allen test

The patient's hand is initially held high while the fist is clenched andboth radial and ulnar arteries are compressed (A); this allows the bloodto drain from the hand. The hand is then lowered (B) and the fist isopened (C). After pressure is released over the ulnar artery (D), colorshould return to the hand within six seconds, indicating a patent ulnarartery and an intact superficial palmar arch.

Redrawn from American Heart Association. Textbook of Advanced CardiacLife Support, 1994.

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The Allen test

In the Allen test, the patient is instructed to make a fist, which will emptythe blood from the hand and fingers (A). The examiner's thumbs are thenpressed down across the thenar and hypothenar eminences to the wrist toocclude the radial and ulnar arteries. The patient then opens the hand,making sure not to overextend the fingers. The pressure on the ulnar arteryis then released while the radial artery is still compressed (B). The handdoes not fill with blood. Note the paleness of the hand on the right comparedwith the hand on left, indicating occlusion of the ulnar artery distal to thewrist (abnormal test result). If there is prompt return of color to the hand(indicating a normal test result), the test is repeated except this timepressure on the radial artery is released while the ulnar artery remainscompressed.

Reproduced with permission from: Olin JW, Lie JT, Thromboagiitis (Buerger'sdisease). In: Current management of hypertensive and vascular disease, CookieJP, Frohlich ED, (Eds), Mosby­Year Book, St Louis 1992. p.265. Copyright ©Elsevier Science.

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Cannulation of dorsalis pedis artery

Technique of cannulation of the dorsalis pedis artery. Before placement of acatheter in this artery, adequacy of collateral flow should be demonstrated.The artery should be occluded by pressure, and the great toe should beblanched by compression of the toenail for several seconds. While thedorsalis pedis artery is still being compressed, color should return rapidly tothe toe after pressure on the nail is released.

Redrawn from American Heart Association. Textbook of Advanced Cardiac LifeSupport, 1994.

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Components of 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 A­1 Medical Integration.

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The effect of temperature on blood gas measurements

TemperaturepH PCO PO

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, Kozelowski­Templin: Clinical Application of Blood Gases, ed 5. St. Louis,Mosby­Year Book, 1994, p. 128.

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Etiologies and mechanism of hypercapnia

Respiratory pathway affecting carbon dioxide elimination

Central nervous system

↓"Won't breathe"

Peripheral nervous system

↓

"Can't breathe"

Respiratory muscles

↓

Chest wall and pleura

↓

Upper airway

↓

Lungs Abnormal gas exchange: "Can't breatheenough"

Schematic figure representing the respiratory pathway, along which a variety of diseases can affectcarbon dioxide elimination and result in hypercapnia. Note that gas exchange abnormalities alone arerelatively uncommon causes of hypercapnia, but gas exchange problems in the setting of reducedmechanical capability of the ventilatory pump are very common explanations for acute and chronichypercapnia.

Mechanism and etiologies of hypercapnia

Mechanism Etiologies

Decreased minute ventilation (global hypoventilation; extra pulmonary causes)

Decreasedcentralrespiratorydrive

Sedative overdose (eg, narcotic or benzodiazepine, some anesthetics,tricyclic antidepressants)Encephalitis

StrokeCentral and obstructive sleep apneaObesity hypoventilation

Congenital central alveolar hypoventilationBrainstem disease

Metabolic alkalosisHypothyroidism*Hypothermia

Starvation

Decreasedrespiratoryneuromuscularor thoracic cagefunction

Primary spinalcord/lower motorneuron/muscledisorders

Cervical spineinjury or disease(eg, traumasyringomyelia)Amyotrophic lateralsclerosis

Thoracic cagedisorders

KyphoscoliosisThoracoplasty

Flail ChestAnkylosingspondylitisPectusexcavatum

Fibrothorax

Metabolic disorders

HypophosphatemiaHypomagnesemia

HypothyroidismHyperthyroidism

¶

Δ

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PoliomyelitisGuillain­Barrésyndrome

Phrenic nerveinjuryCritical illnesspolymyoneuropathy

Myasthenia gravisMuscular dystrophyPolymyositis

TetanusTransverse myelitis(eg, multiplesclerosis)

Tick paralysisAcute intermittentporphyriaEaton Lambertsyndrome

NeuralgicamyotrophyPeriodic paralysisGlycogen storageand mitochondrialdiseases

Toxins, poisoning,drugs

Tetanus

DinoflagellatepoisoningShellfish poisoning(red tide)

CiguaterapoisoningBotulismOrganophosphates

Succinylcholineand neuromuscularblockadeProcainamide

Increased dead space (gas exchange abnormalities; pulmonary parenchymal causes or airwaydisorders)

Anatomic Short shallow breathing

Physiologic Pulmonary embolism (usually severe)Pulmonary vascular disease (usually severe)

Dynamic hyperinflation (eg, upper and lower airway disorders includingchronic obstructive pulmonary disease, severe asthma)Endstage interstitial lung disease

Increased carbon dioxide production

FeverThyrotoxicosis

Increased catabolism (sepsis, steroids)OverfeedingMetabolic acidosis

Exercise

Multifactorial

Upper airway disorders

Severe laryngeal or tracheal disorders(stenosis/tumors/angioedema/tracheomalacia)Vocal cord paralysis

EpiglottitisForeign body aspirationRetropharyngeal disorders

Obstructive goiter

◊

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Decreased mechanical ventilation can also cause hypercapnic respiratory acidosis (eg, permissivehypercapnia). 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 themechanisms 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 clinicallysignificant diaphragmatic paresis/paralysis to occur. Δ Hypermagnesemia, hypokalemia, and hypercalcemia can also cause respiratory muscle weakness andcontribute to hypercapnia. ◊ Upper airway disorders are rare causes of hypercapnia. They either diminish total ventilation or lead todynamic hyperinflation and reduced tidal volume, while simultaneously causing increased work of breathingand carbon dioxide production.

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Compensations to acute respiratory acidosis andalkalosis

Combined significance bands for plasma pH and concentrations of H+and HCO3­ in acute respiratory acidosis and alkalosis in humans. Inuncomplicated acute respiratory acid­base 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 presenceof a complicating metabolic acid­base disturbance.

Arbus GS, Herbert LA, Levesque PR, et al. N Engl J Med 1969; 280:117. Bypermission from the New England Journal of Medicine.

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Respiratory pathway affecting carbon dioxideelimination

Schematic figure representing the respiratory pathway, along which avariety of diseases can affect carbon dioxide elimination and result inhypercapnia. Note that gas exchange abnormalities alone are relativelyuncommon causes of hypercapnia, but gas exchange problems in thesetting of reduced mechanical capability of the ventilatory pump arevery common explanations for acute and chronic hypercapnia.

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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

Right­to­left shunts

Pregnancy

Hyperthyroidism

Severe anemia

Hyperventilation on mechanical ventilation

Recovery phase metabolic acidosis

Chronic liver disease

Prolonged paralysis

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Respiratory system anatomy: Ventilation control

Schematic figure representing the respiratory pathway, along which avariety of diseases can affect carbon dioxide elimination and result inhypocapnia.

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Major causes of metabolic acidosis according to mechanism and aniongap

Mechanism ofacidosis

Increased AG Normal AG

Increased acidproduction

Lactic acidosis

Ketoacidosis

Diabetes mellitus

Starvation

Alcohol­associated

Ingestions

Methanol

Ethylene glycol

Aspirin

Toluene (if early or ifkidney function isimpaired)

Toluene ingestion (if late and if renal function ispreserved ­ due to excretion of sodium and potassiumhippurate in the urine)

Diethylene glycol

Propylene glycol

D­lactic acidosis

Pyroglutamic acid (5­oxoproline)

Loss of bicarbonate orbicarbonate precursors

Diarrhea or other intestinal losses (eg, tubedrainage)

Type 2 (proximal) RTA

Posttreatment of ketoacidosis

Carbonic anhydrase inhibitors

Ureteral diversion (eg, ileal loop)

Decreased renal acidexcretion

Chronic kidney disease Chronic kidney disease and tubular dysfunction(but relatively preserved glomerular filtrationrate)

Type 1 (distal) RTA

Type 4 RTA (hypoaldosteronism)

AG: anion gap; RTA: renal tubular acidosis.

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Major causes of metabolic alkalosis

Gastrointestinal hydrogen loss

Vomiting or nasogastric suction

Antacids in advanced renal failure

Congenital chloride diarrhea

Renal hydrogen loss

Primary mineralocorticoid excess

Loop or thiazide diuretics

Bartter or Gitelman syndrome

Posthypercapnic alkalosis

Hypercalcemia and the milk­alkali syndrome

Intracellular shift of hydrogen

Hypokalemia

Alkali administration

Contraction alkalosis

Massive diuresis

Vomiting or nasogastric suction in achlorhydria

Sweat losses in cystic fibrosis

Villous adenoma or factitious diarrhea (including laxative abuse)

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Agents known to cause methemoglobinemia

Acetanilide

p­Amino salicylic acid

Aniline, aniline dyes

Benzene derivatives

Clofazimine

Chlorates

Chloroquine

Dapsone

Local anesthetic agents

Benzocaine

Lidocaine

Prilocaine

Menadione

Metoclopramide

Methylene blue*

Naphthoquinone

Naphthalene

Nitrites

Amyl nitrite

Farryl nitrite

Sodium nitrite

Nitroglycerin

Nitric oxide

Nitrobenzene

Paraquat

Phenacetin

Phenazopyridine

Primaquine

Rasburicase

Resorcinol

Sulfonamides

* While methylene blue is a recognized treatment for methemoglobinemia, it is an agent with oxidantpotential, and may worsen the clinical situation, since in individuals with glucose­6­phosphatedehydrogenase deficiency it induces acute hemolysis that can further decrease oxygen delivery to thetissues. Paradoxically, in high doses methylene blue can also increase methemoglobinemia.

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Contributor DisclosuresArthur C Theodore, MD Nothing to disclose. Scott Manaker, MD, PhD Consultant/Advisory boards: Expert witnessin workers' compensation and in medical negligence matters [General pulmonary and critical care medicine]. EquityOwnership/Stock Options (Spouse): Johnson & Johnson; Pfizer (Numerous medications and devices). OtherFinancial Interest: Director of ACCP Enterprises, a wholly owned for­profit subsidiary of ACCP [General pulmonaryand critical care medicine (Providing pulmonary and critical care medicine education to non­members of ACCP)].Geraldine Finlay, MD Nothing to disclose.

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these areaddressed by vetting through a multi­level review process, and through requirements for references to be providedto support the content. Appropriately referenced content is required of all authors and must conform to UpToDatestandards of evidence.

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