Arterial Blood Gas Sampling

April 23, 2008
Ramaz Mitaishvili, MD

 Ramaz Mitaishvili, MD





Ramaz Mitaishvili, MD

RM Global Health



Alternative names

Arterial Blood Gas Analysis; ABG Sampling.

Outcome Goal

Proper collection of arterial blood samples.

Arterial Blood Gas Test Definition

Blood is drawn anaerobically from a peripheral artery (Radial, Brachial, Ulnar, Femoral, Axillary, Posterior Tibial or Dorsalis Pedis) via a single percutaneous needle puncture, or from an indwelling arterial cannula or catheter for multiple samples.

Either method provides a blood specimen for direct measurement of:

  • partial pressures of carbon dioxide (PaCO2);
  • oxygen (PaO2);
  • hydrogen ion activity (pH);
  • total hemoglobin (Hbtotal);
  • oxyhemoglobin saturation (HbO2);
  • dyshemoglobins carboxyhemoglobin (COHb);
  • methemoglobin (MetHb).

Purpose and indications

The purpose of arterial blood gas sampling is to assess patients respiratory status as well as acid base balance or for laboratory testing when venous blood is unavailable, and is frequently requested for seriously ill patients.
So, an arterial blood gas (ABG) will help in the assessment of oxygenation, ventilation, and acid-base homeostasis. It can also aid in the determination of poisonings (carboxyhemaglobinemia or methemaoglobinemia) and in the measurement of lactate concentration.

Arterial puncture is a relatively straight forward technique that is easily performed at the bedside.

Pulse oximetry will give a reasonable estimate of the adequacy of oxygenation in many circumstances but does not assess acid-base status or ventilation and should not be used alone in cases where these measurements are important.

Basic Conditions Diagnosed by ABG’s

  • Respiratory Acidosis
  • Anything which prevents the body from getting rid of excess CO2, increases acid which decreases pH
  • Respiratory Alkalosis
  • Anything which makes to body lose CO2, decreases acid, which increases pH
  • Metabolic Alkalosis
  • Anything which increases HCO3 increases base which increases pH
  • Metabolic Acidosis
  • Anything which decreases HCO3 decreases base which decreases pH

Apart from helping to establish a diagnosis, blood gases may also help to as certain the severity of a particular condition (e.g. metabolic acidosis in sepsis). This information can help to establish diagnosis, monitor severity, progression, and prognosis as well as guide therapy of:

  • respiratory failure,
  • cardiac failure,
  • renal failure,
  • hepatic failure,
  • diabetic ketoacidosis,
  • poisoning
  • sepsis

Normal Values in an ABG report at sea level:

 (Table 1)

   PaO2 in kPa (mm Hg) PaCO2 in kPa (mm Hg)   pH
HCO3 mmols/L 
  BD/BE    Sa O2 (%)
 Arterial Blood  11-13 (80-100)    4.7-5.9 (35-45)     7.36-7.44  21-28        +/-2   94-100
 Venous Blood
   5-5.6 (37-42)  5.6-6.7 (42-50)  7.34- 7.42      



(Table 2)


  Normal Range
 Anion Gap  8-16 mmols/L
 Osmolar Gap  10 mmols/L
 PaO2 (mmHg)/FiO2 (%)  More than 3


mm Hg = millimeters of mercury. At altitudes of 3,000 feet and above, the values for oxygen are lower. The arterial pO2 reduces with age. A rough guideline is that above the age of 40 years, paO2 = 105-age in years/2.

The pH of the blood is maintained within a normal range by a number of compensatory mechanisms, the most important being the body buffer mechanisms and the renal and respiratory systems. The degree of compensation varies between individuals and depends on the severity and duration of the primary problem and associated medical comorbidities. Respiratory compensation for metabolic problems is usually rapid and almost complete. The lungs respond quickly by increasing ventilation to blow off excessive carbon-dioxide (in metabolic acidosis) or decreasing ventilation to retain carbon-dioxide (in metabolic alkalosis). The latter compensation is less complete than the former for obvious reasons. The renal compensation for respiratory imbalances is slow and incomplete. The kidneys regulate extracellular fluid H+ ion concentration by secretion of H+ ions, reabsorption of filtered HCO3- ions, and the production of new HCO3- ions. Excess HCO3- is filtered into the renal tubules and eliminated in the urine. Depending on the need to excrete either an acid or a base load, the kidneys can excrete urine with a pH ranging from 4.5 to 8.0. A rough guide to the degree of compensation to primary changes in CO2 and HCO3 as a result of respiratory and metabolic imbalances respectively is shown in table 3.

Respiratory and renal compensation in acid-base imbalance

(Table 3)

Acid-base imbalance
Carbon-dioxide (mm Hg) 
Plasma bicarbonate (mmol/L)
 Metabolic acidosis
 Compensates (decreases) by 1.25 x X  Decreases by X
 Metabolic alkalosis
  Compensates (increases) by 0.75 x X     Increases by X
 Acute respiratory acidosis
    Increases by X   Compensates (increases) by 0.1 x X
 Chronic respiratory acidosis
 Increases by X  Compensates (increases) by 0.4 x X
 Acute respiratory alkalosis
   Decreases by X  Compensates (decreases) by 0.2 x X
 Chronic respiratory alkalosis  
  Decreases by X  Compensates (decreases) by 0.4 x X




Abnormalities of gas exchange


The first step is to detect the presence of hypoxia (i.e., less than 60 mm Hg on room air). Patients with clinically evident respiratory problems who have been given oxygen supplementation before blood gas analysis must be assumed to be hypoxic at this stage. If a patient is being given oxygen supplementation, then the ratio of the paO2 (in mm Hg) to FiO2 (in %) is used to detect hypoxia. Usually, the oxygen saturation of the blood is also noted which correlates with the paO2 of the arterial blood and helps in establishing the diagnosis of hypoxia. The saturation as obtained by a blood gas analysis is more accurate than that obtained by a pulse oximetry, as it is not influenced by shock states and skin pigmentation.


The paCO2 level must then be noted, which will help in differentiating between type I and type II respiratory failure. In type I respiratory failure, the paCO2 will be normal or low (</=45) and in type II respiratory failure, the paCO2 will be high (>45).

Causes of respiratory failure

(Table 4)

 Type I  Type II
 Atelectasis   CNS depression (drugs, sleep, head injury)
 Pulmonary edema (cardiogenic and non cardiogenic)   High spinal cord lesions
 Pneumonia  Phrenic nerve lesions
 Pleural effusion  Neuromuscular disorders
 Haemo/pneumothorax   Severe kyphoscoliosis
    Type I causes in an advanced state



Causes of type I respiratory failure include conditions with an impaired gas exchange and causes of type II respiratory failure include the causes of type I in an advanced state and conditions with impaired ventilation as shown in table 4. Differentiation between types I and II failure is essential to determine the etiology and institute further treatment. It may also rarely be used to restrict O2 supplementation in patients with type II disease because such patients are dependent on hypoxia for the respiratory drive and abolishing hypoxia might further suppress the CNS stimulation for respiration. Patients with persistent hypoxia, rising CO2 levels and respiratory acidosis require mechanical ventilation and are usually seen by the anesthetist at this stage.

In patients on a ventilator, hypoxia might indicate one of several things, including:

  • Accidental disconnection of the breathing circuit ( which should be evident by the alarms, fall in O2, fall in saturation on pulse oximetry, clinical evidence of respiratory distress, etc.).
  • Development of pneumothorax which could be detected clinically and might need confirmation by X-ray before intercostal tube drainage.
  • Development or worsening of pre-existing chest problems (bronchopneumonia, ARDS, pulmonary contusion) might require changes in settings of the ventilator like increasing FiO2 levels, ventilatory rate or tidal volume, adding or increasing PEEP, or changing to other modes of ventilation.

A high CO2 level is always associated with hypoxia unless the patient is on oxygen supplementation. However, hypercarbia associated with a normal oxygen level should also be approached with the same urgency as the patient might deteriorate rapidly. The possibility of a venous sample as a cause of unexpected hypercarbia and hypoxia should be kept in mind. In patients on a ventilator, moderate rise in CO2 levels are currently considered acceptable and interventions to correct these might be associated with significant side effects including barotraumas and hypotension (permissive hypercarbia). Similarly, patients with COPD have adapted to higher levels of carbon-dioxide and might not require correction to normal levels.
Acute changes in paCO2 result in predictable changes in pH. For every increase in paCO2 of 20 mm Hg (2.6 kPa) above normal, the pH falls approximately by 0.1. For every decrease of paCO2 of 10 mm Hg (1.3 kPa) below normal, the pH rises by 0.1. Any change in pH outside these parameters is therefore metabolic in origin. The kidneys take time to compensate for the change in pH the amount of renal compensation indicates the chronicity of the problem and the need for urgent correction. Correction will usually involve a combination of treatment of the cause, initiation of mechanical ventilation or modification of the settings and reduction of CO2 production.
Alveolar-arterial oxygen gradient (A-a) PO2: This is the difference in the oxygen partial pressures between the alveolar and arterial sides. In patients with type II respiratory failure, it may help to determine whether the patient has associated lung disease or just reduced respiratory effort.
The A-a gradient increases a little with age, but should be less than 2.6kPa (20mmHg). A normal gradient would imply conditions like CNS depression and neuromuscular disorders as the cause and a high gradient would imply some lung disease.

Abnormalities of acid base balance

pH of the blood:

The pH is usually maintained within a narrow range by a number of buffer systems in the body. A normal pH value may still be due to a well-compensated imbalance or a mixed acid base disorder and an abnormal value is definitely due to a poorly compensated acid base problem or due to both metabolic and respiratory derangements causing an imbalance in the same direction.

Serum bicarbonate:

The actual bicarbonate is the value calculated from the blood gas sample. The standard/corrected bicarbonate is the value obtained after correction of CO2 levels to 40mm Hg and at room temperature. It gives a better estimate of the metabolic problem causing acid base imbalance. The base deficit/excess is the amount of deviation of the standard bicarbonate from the normal. The metabolic problem could either be a low (base deficit or metabolic acidosis) or high (base excess or metabolic alkalosis) standard bicarbonate.


A primary metabolic derangement will be accompanied by some degree of respiratory compensation. The ability to detect the primary abnormality and the amount of compensation is hindered by other co-existing conditions causing respiratory acidosis and/or alkalosis. Coexisting medical problems can cause both metabolic acidosis and alkalosis.
Metabolic acidosis: Metabolic acidosis can be due to a variety of conditions. Treatment of metabolic acidosis is treatment of the cause. Direct administration of alkali (sodium bicarbonate) is reserved for severe cases. A number of conditions can result in metabolic acidosis, the most important among them being the under perfusion of tissues resulting in accumulation of lactic acid. Differentiation of the causes of metabolic acidosis requires the estimate of an entity called the ‘anion gap’.

Anion gap:

Body fluids including blood may contain a variable number of ions, but the total number of anions (negative ions) and cations (positive ions) are roughly the same. The ions that are usually measured in blood are cations like sodium and potassium and anions including chloride and bicarbonate. There are unmeasured ions in both groups (cations and anions), which also contribute to the ionic constitution of blood. The measured cations are usually greater than the measured anions by about 8-16mmol/L. This is because the unmeasured anions constitute a significant proportion of the total number of anions in blood. Proteins make this up predominantly, but also included are sulphates, phosphates, lactate and ketones.
Causes of a decreased anion gap include hypoalbuminaemia and severe haemodilution. Rarer causes include increase in minor cation concentrations like calcium and magnesium. Causes of a raised anion gap include dehydration and any cause of raised unmeasurable anions, like lactate, ketones and renal acids, along with treatment with drugs given as organic acids such as penicillin, salicylates and poisoning with methanol, ethanol and paraldehyde. Rarely it may be due to decreased minor cation concentrations such as calcium or magnesium.

Raised anion gap metabolic acidosis:

Accumulation of a number of acids can result in raised anion gap metabolic acidosis. In such cases, the reduction in serum HCO3- matches the anion gap. If not, a second acid base disorder should be kept in mind. When metabolic acidosis and alkalosis coexist, as in vomiting and ketoacidosis, the plasma HCO3- may be normal, and a raised anion gap may be the initial evidence of an underlying acid-base disturbance.
To differentiate between the many causes of ‘increased anion gap metabolic acidosis, we measure the osmolar gap that is the difference between the measured osmolarity and the calculated osmolarity.

Normal anion gap (hyperchloraemic) metabolic acidosis:

This usually results from conditions wherein there is a loss of alkali (i.e.HCO3-) or metabolic equivalent (eg, excretion of salts of organic anions in proportionate excess of chloride) or an accumulation of HCl or metabolic equivalent (eg, NH4Cl and chloride salts of amino acids).
Loss of HCO3- can occur either due to GI causes or due to renal causes (renal excretion or insufficient generation). In many surgical conditions, the cause is usually obvious.

Examples of extrarenal causes are excessive diarrhoea or drainage of gastrointestinal secretions, NH4Cl administration, parenteral nutrition, rapid saline infusion and congestive cardiac failure. Generation of large amounts of organic anions can sometimes produce this type of metabolic acidosis (and not one with a raised anion gap), if the kidneys can prevent their accumulation by rapid excretion.

Examples of renal causes include the various types of renal tubular acidosis (type I, type II and type IV).

Examples of different types of renal tubular acidosis (RTA)

(Table 5)

Type I (distal)  
Type II (proximal)   
  Type IV (def. NH4+ production)
 Urinary tract obstruction  Fanconi’s syndrome  Cortisol deficiency
 Interstitial nephritis  Myeloma light chain nephropathy  Urinary tract obstruction
 K+ sparing diuretics  Nephrotoxins  
   Genetic diseases     



Metabolic Alkalosis:

Metabolic alkalosis can result from the loss of acid, addition of alkali or both in the kidneys or elsewhere. Extrarenal sites include stomach (loss of acid), redistribution of alkali from the intracellular stores to the ECF (as in potassium or chloride depletion), oral administration (antacids, ion-exchange resins, milk alkali syndrome, oral HCO3-) and parenteral administration of alkali (citrate in blood transfusions, bicarbonate in severe metabolic acidosis). Renal causes of alkali excess include mineralocorticoid excess, response to long-standing hypercapnia (persists even after correction of respiratory acidosis), hypokalemia (promotes H+ secretion in the distal nephron) and ECF volume depletion (impaired HCO3- excretion). Certain conditions can cause metabolic alkalosis by a number of mechanisms (e.g. diuretic use causes both ECF depletion and hypokalemia).

Respiratory Alkalosis:

The principal cause of respiratory alkalosis (hypocapnia) is hypoxia and its causes (type I respiratory failure), further treatment of which has been detailed before. Other causes of acute respiratory alkalosis include anxiety, fever, pain, sepsis, hepatic failure, CNS disorders (stroke, infections), pulmonary disorders without hypoxia (infections and interstitial lung disease), delirium tremens and drugs (salicylate intoxication). Chronic causes include high altitude hypoxia, chronic hepatic failure, chronic pulmonary disease, CNS trauma, anaemia, hyperthyroidism, beriberi and pregnancy. Treatment should be directed towards the cause.

Contraindications/Concerns for Arterial Puncture

Contraindications may be absolute unless specified otherwise. Contraindications considered as a relative in terms of the risks to the patient under the importance of obtaining the sample!

  • Cellulites or other infections over the radial artery.
  • Absence of palpable radial artery pulse.
  • Negative results of an Allen test (collateral circulation test), indicating that only one artery supplies the hand and suggest to select another extremity as the site for arterial puncture.
  • Coagulopathies or medium-to-high-dose anticoagulation therapy (eg, heparin or coumadin, streptokinase, and tissue plasminogen activator but not necessarily aspirin) may be a relative contraindication for arterial puncture.
  • History of arterial spasms following previous punctures.
  • Severe peripheral vascular disease.
  • Abnormal or infectious skin processes at or near the puncture sites.
  • Arterial grafts.
  • Arterial puncture should not be pertormed through a lesion or through or distal to a surgical shunt (eg, as in a dialysis patient). If there is evidence of infection or peripheral vascular disease involving the selected limb, an alternate site should be selected.


Sampling may be performed by trained health care personnel in a variety of settings including (but not limited to) hospitals, clinics, physician offices, extended care facilities, and the home. However, because of the need for monitoring the femoral puncture site for an extended period, femoral punctures should not be performed outside the hospital.


Arterial blood sampling should be performed under the direction of a physician specifically trained in laboratory medicine, pulmonary medicine, anesthesia, or critical care. A recognized credential MD, DO, CRTT, RRT, RN, RPFT, CPFT, MT, MLT, RCVT, CPT I, CPT II, or equivalent is strongly recommended.

Femoral, axillary, and brachial arterial punctures are performed by MD ONLY!


The frequency with which sampling is repeated should depend on the clinical status of the patient and the indication for performing the procedure.

Repeated puncture of a single site increases the likelihood of hematoma, scarring, or laceration of the artery. Care should be exercised to use alternate sites for patients requiring multiple punctures. An indwelling catheter may be indicated when multiple sampling is anticipated.

Puncture sites

The Ulnar Artery may be used in the pediatric population. The ulnar artery in the adult is less accessible but may be used as a secondary site. Allen’s Test is checked prior to a Radial or Ulnar puncture

Approved puncture sites include radial, dorsalis pedis, and brachial arteries. The brachial artery will not be used on patients in Children’s Hospital. In the Emergency Department, femoral artery is an approved puncture site.
Brachial and femoral arteries should be reserved as a last option.

The radial artery on non dominant hand is the ideal site for an arterial puncture for the following reasons:

  • It is small, but superficial and easily accessible, and stabilized.
  • It is easily compressible with better control of bleeding
  • There is no nerve near by to worry about.
  • The collateral arch with ulnar artery minimizes the risk of occlusion.


Anatomical Review

The radial artery runs along the lateral aspect of the volar forearm deep to the superficial fascia. The artery runs between the styloid
process of the radius and the flexor carpi radialis tendon. The point of maximum pulsation of the radial artery can usually be palpated just proximal to the wrist.


Local Anesthesia

The use of local anesthetic for arterial puncture is not universal. The proposed reason for the use of local anesthetic is: To avoid pain

Heparinized Syringe
The syringe has to be heparinized to prevent clotting. It is important to have the right amount of heparin in the syringe. “Too much” or “too little heparin can alter the results.”


  •      The concern that the pain induced hyperventilation or apnea could alter the results of blood gases. This issue was specifically studied and the results indicate that an unanesthetized arterial puncture does provide an accurate measurement of resting pH and Pco2. Hence, the only reason to use local anesthetic is to avoid pain to the patient. If you are proficient, the first stick can be tried without the anesthetic. I strongly recommend the use of local anesthetic for beginners.
  •      Heparin will prevent the blood from clotting and allow the plunger to move with less resistance. Excessive amounts of heparin will alter ABG values

Necessary equipment

  • Protective eye wear.
  • Gloves.
  • Transilluminator (Optional)
  • Povidone-iodine swab.
  • Alcohol swabs.
  • “Two by two” gauze sponge.
  • Adhesive bandage & adhesive tape.
  • ABG sampling kit (recommended to preserve the integrity of the sample).
  • Bad protector.
  • Bag with ice (in which sample will be send to lab).
  • Collection tubes.
  • Appropriate identification labels.
  • Appropriate lab requisitions.



  1. Identify the patient.
  2. Explain the procedure and its purpose. Instruct the patient to report excessive pain during the procedure. A specific surgical consent is not generally obtained.
  3. Assess the patient by checking vital signs.

The patient’s medical record must be assessed carefully for any of the above and the physician notified. Check for physician’s order. Check the patient’s medical record for latex allergy. Pick up requisition and patient label

Before beginning of a procedure be sure to wash your hands using proper washing technique and follow universal precautions in this procedure.

Universal precautions must be applied in all circumstances involving blood or blood contaminated collection devices in the immediate area:
As with starting an IV the potential for contact with a patient’s blood while performing an arterial puncture is high and increases with the inexperience of the operator.  Gloves must be worn while doing an arterial puncture and if the risk of blood splatter is high, such as an agitated patient, the operator should consider face and eye protection as well as a gown.  In trauma patients the protocol calls for all team members to wear gloves, face and eye protection and gowns.  As well, there should no attempt to recap the arterial blood gas syringe once the cap is removed.  There is a rubber cube in each of the arterial blood gas kits that should be used to cover the needle tip prior to removing it from the syringe.
Needle sticks are the most frequent source of transmission of blood-borne diseases in health care workers


We begin the procedure with performing Allen test, to be sure that collateral circulation is an appropriate. Before beginning the actual procedure it is a good idea to make sure the patient is seated comfortably. He should rest his arm on a pillow in front of him, palm facing up. This position is necessary to perform the procedure and is the most comfortable for the patient. Try to hyperextend patient’s hand.

Allen Test

  1. Palpate by three fingers radial artery , than, on opposite site, the ulnar artery, which can’t be palpated, but we have to palpate area closest to ulnar artery.
  2. Ask patient to make a fist the tighter he or she can
  3. Stand at the patient’s side and compress both the radial and ulnar arteries with the index and middle fingers of both your hands for several second to occlude both arteries
  4. Ask patient to release fist
  5. Realize your grasp from ulnar artery. Normally, within 5 second pale palm turns pink, showing good collateral circulation and signifies a negative Allen’s test

Clean from center to periphery by circular motion (from inward to outward). Allow area to dry, than you should wipe away iodine with alcohol swab, again allowing skin to dry (approximately 20-30 sec)

If ulnar filling is poor do not proceed but try the other arm.  Documentation of inadequate circulation in the affected extremity must be done.

Actual Procedure


  1. Place a bed protection sheet under the site, ensure towel is in place.
  2. Clean the skin over the proposed site of puncture with alcohol first.
  3. Clean area with povidone- iodine (betadine) swab.
  4. Open ABG kit, which consist, from 3 parts. First peace is sponge cube to expel excessive air from syringe. Second, is black cap, to go over syringe to transport to lab, and last, heparinized syringe with needle attach. Slightly pull plunger back to be sure, that plunger is not stocked and blood can flow inside of syringe from pulsating artery.
  5. Remove cap, making sure that you’re seeing bevel. Don’t forget that bevel must be up when inserting facing flow of blood.
  6. Palpate area carefully. This is only your landmark to penetrate the skin in going no where.
  7. You should hold syringe little bit differently for ABG. Pretty much like a dart with angle 45 degrees.
  8. Syringe is ready to be inserted and put your finger on right place, and roll back on half way this finger and now you can insert needle into the skin. Do not touch prepped insertion site with fingers.
  9. When you puncture the artery there will be a sudden gush of arterial blood into the hub of the needle. You should watch pulsating backflow of blood into the syringe. Note: Suspect venous puncture if pulsation is minimal and blood dark in color.
  10. When blood return observed, hold needle very steadily, and either allow the syringe barrel to fill or aspirate to pre-determined amount. Remove needle quickly and apply firm pressure with gauze pad for five full minutes (or longer if the patient is on anticoagulant therapy or is thrombocytopenic double this time).
  11. Insert needle straight into the cube, than push down on the plunger to expel excessive air.
  12. Remove cube and needle as one and attach black cap to the tip of syringe. Gently mix the specimen by rolling it between your palms back and forth for 20 sec. to mix heparin and blood.
  13. Label specimen with a sticker from patient’s ID band. Record on the label the initials of the one who obtained the sample, the date, and the time. Place specimen on ice and transport to lab immediately.
  14. Discard needle with cube appropriately in sharp container.
  15. Place patient in a comfortable position.
  16. Inspect the puncture site to ensure that the bleeding has stopped.
  17. It is very important to return about 20 minutes later to check for adequate perfusion of the hand and for possible hematoma formation. Observe every hour within 2-3 hours, and than next day. Monitor patient, assess pulse and respiratory rate.  Note any abnormalities in the patient’s appearance or behavior.

The artery generally tends to be slippery, especially when it is elongated by arteriosclerosis. Stretching stabilizes the vessel. Let the patient rest his arm on a table, with his hand projecting beyond the edge. Dorsiflex the wrist be gently pressing down on the hand. This maneuver stretches and stabilizes the vessel.


  • If needle comes out of the artery during specimen aspiration, withdraw needle, hold pressure, and start over.
  • If no blood is returned, slowly and carefully withdraw needle to re-enter artery.
  • If no blood return after first attempt, withdraw needle to point just below skin surface, change direction and descend needle again.
  • And finally, if unsuccessful after two attempts, withdraw needle completely and carry out post-puncture care.


  • If you wish to use local anesthesia- draw 2% xylocaine into a syringe. Infiltrate the skin and the area around the radial artery with this local anesthetic. Insert needle at a 5 – 15 degree angle with the bevel directed upward such that it only extends into the epidermis. The entire bevel should be covered and lay just under the skin
  • You can use EMLA ® topical anesthetic cream (1 hour prior), or 1-2% lidocaine (3-5ml) instead of xylocaine (don’t forget double check patients history of allergy to latex or lidocaine)

Complications and How to Avoid

In general, an arterial puncture is an innocuous procedure, but occasionally complications may occur. Awareness of the types of complications and their contributory factors will help us to minimize their occurrence.

  • Pain.
  • Bruising.
  • Compression Neuropathy.
  • Aneurysm.
  • Spasms.
  • A.V. Fistula.
  • Infection.
  • Vasovagal response.
  • Air or thromb emboli.
  • Anaphylaxis from local anesthestic.
  • Mercury Embolism.

Most series who have prospectively evaluated complications of arterial puncture have come to the same conclusion. The procedure is safe, the occurrence of severe complications are rare and most of the complications are minor and temporary.


Generally, arterial punctures are painful and the patient will feel some discomfort or pain sometime after the procedure even if a local anesthetic was used. Pain during and following the procedure is a frequent complaint and is reported to occur in 10% of the patient population. When systemically looked for, tenderness at the puncture site was observed in 15% of patients. You can minimize the pain by using thin needles and by the use of local anesthetic. However, the local anesthetic is ineffective in preventing late symptoms. Sometimes the pain is felt proximal or distal to the puncture site and this type of pain could be secondary to arterial spasm. In most cases the discomfort following an arterial puncture is temporary and minor.
Hematoma (Bruising)
Leakage of blood into tissue due to lack of sufficient elastic tissue to seal puncture site, especially in elderly. Because the blood is under considerable pressure in the arteries, blood is initially more apt to leak from an arterial puncture than from a venipuncture site.  However, arterial puncture sites tend be close more rapidly due to the elastic nature of the arterial wall.  This elasticity tends to decrease with age; therefore, the probability of a hematoma formation is greater in older patient or in patients receiving anticoagulants. Bruising is the most frequently observed complication occurring at 30% of puncture sites. In most, it is mild but in some you could encounter large bruises. The bruising is more common at the radial site. The brachial and femoral arteries lie deep, and this may account for less frequently observed bruising at these sites. A hematoma can occur at the puncture site in patients on anticoagulation. Serious retro peritoneal hemorrhage has been reported. The hematoma formation in anticubital fossa is tolerated poorly and can result in median nerve compression and ischemic changes secondary to compression of the artery. Ensure using small diameter needle. Ensure proper technique in holding site X5 minutes post-puncture.
Occurs when patient receiving anticoagulant therapy or patients with known blood coagulation disorders. Two minutes after pressure is released inspect site for bleeding oozing or seepage of blood; continue pressure until bleeding ceases. Sometimes a longer compression time is necessary.

Compression Neuropathy

Compression neuropathy secondary to hematoma occurs at the cubitalfossa and the inguinal region. The fascia that holds the neurovascular bundle is tight and any extravasation of blood is tolerated poorly. In the anticubital fossa the brachial artery and the median nerve pass underneath the bicepital aponeurosis. This fascia is unyielding and any hematoma formation results in compression of the median nerve and brachial artery. If the fasciotomy is not performed, it could eventuate into Volkmann’s contracture. On radial artery puncture it is very rare, but some cases with temporary numbness of the hand were noticed.


Aneurysm of the punctured vessel has been reported. This occurs with repeated punctures. Fortunately this complication is rare.


May occur secondary to pain or anxiety. Spasms can temporarily decrease the pulse and cause pain. Occasionally the vessel can occlude secondary to thrombosis. Rarely has perivascular fibrosis and occlusion of the vessel been noted. The collateral arch with ulnar artery fortunately prevents any serious ischemic changes.

A.V. Fistula

Iatrogenic arteriovenous fistula has been reported rarely in patients who have hand multiple arterial punctures. This complication is rare.

Mercury Embolism

Mercury embolism has been reported in the days when mercury was used as an aerobic seal and mixing agent. This complication does not occur any more.

Infection of Health Care Provider

Occurs when health care provider contacts with infections contained in blood of infected patients. Universal blood & body fluid precautions should be implemented. All blood samples from all patients must be treated with full precautions.

Infection/inflammation adjacent to puncture site

Can caused when inadequate cleansing prior to puncture. Ensure appropriate cleansing technique. Avoid sites indicating presence of infection or inflammation.

Thrombus formation

Injury to the intima of the artery can lead to clot (thrombus) formation.  A large thrombus can obstruct the flow of blood and impair circulation.

Problems with the integrity of the ABG

The following are problems that can cause erroneous result in ABG analysis.

Air bubbles

If not removed immediately, oxygen from the bubbles can diffuse into the sample and CO2 can escape, changing the results.

Delay in cooling

Blood cells continue to consume oxygen and nutrients and produce acids and carbon dioxide at room temperature.  If the specimen remains at room temperature for more then 5 to 10 minutes, the pH, blood gases, and glucose values will change. Cooling to between 1ºC to 5ºC slows the metabolism and helps stabilize the specimen.  Processing the specimen as soon as possible after collection will ensure the most accurate results.

Venous blood mixed in ABG sample

Normal arterial blood is brighter, whereas venous blood is slightly darker in color.  Sometimes it is difficult to distinguish between arterial and venous blood in patients with poor oxygen content.  This will make their arterial blood appear as dark as venous blood.  The best way to be certain that a specimen is arterial is if the blood pulses into the syringe.  In some cases, such as with low cardiac output, a specimen may need to be aspirated.  In such instances, it is hard to be certain that the specimen is really arterial.

Improper anticoagulant

Heparin is the accepted anticoagulant for ABGs.  Oxalates, EDTA and citrates may alter results, especially pH. Too much heparin can cause erroneous results due to acidosis and too little can result in clotting.

Specimen Rejection

  • Inadequate volume of specimen for the test
  • Clotted
  • Incorrect or no identification
  • Wrong syringe used
  • Delay in delivering the sample for analysis
  • Not placed in ice
  • Air bubbles


Difficulties in obtaining a sample may occur if:

  • The patient is alkalotic or acidotic; an irritable or constricted vessel is more difficult to puncture.
  • Hypotension exists with a weak or absent pulse on palpation.
  • The patient is younger. The absence of atherosclerosis implies a healthy, muscular, ‘bouncy’ artery which may not be particularly easy to penetrate.
  • The patient suffers from diseases such as Parkinsons’, etc.
  • The patient is afraid and tense. This can be dealt with by reassuring the patient and reexplaining the procedure and its purpose.


Dorsalis Pedis

Arteries are small, but close to the surface of the anterior foot. This artery should not be used in patients with impaired circulation. Adequate collateral flow to the distal foot is checked with a Modified Allen’s Test.
One must have an order from MD/NNP before sticking feet. A Modified Allen’s Test is performed on the dorsalis pedis prior to puncture. The Posterior Tibial artery may be used in the pediatric population. Reverse the artery released if using the ulnar as puncture site.
Perform Allen’s or Modified Allen’s test to determine collateral circulation. If collateral circulation is not adequate do not perform Arterial Puncture.

Modified Allen’s Test

Elevate patient’s feet. Occlude dorsalis pedis artery; then blanch the great toe by compressing the toenail for several seconds. Release pressure on the nail and observe for flushing (rapid return of color indicates adequate collateral flow).
Compress the posterior tibial artery if it is being used as the puncture site (pediatric population).

Adults: 1 ml for ABG, and 2 ml for ABG with electrolytes
Infants: 0.3 ml for ABG, and 0.6 ml for ABG with electrolytes
Neonates: Volume of blood should not exceed 3-5% of the infant’s total blood volume (80ml/kg).

 PaO2  Partial pressure of oxygen in arterial blood
 FiO2   Fraction of oxygen in inspired air (0.21 for atmospheric air)
 PaCO2      Partial pressure of carbon dioxide in arterial blood
 H +   Hydrogen ion concentration expressed in nmol/L
 pH      Negative logarithm of (H+) expressed in nmol/L
 SaO2  Percentage of haemoglobin which oxygenated (oxyhaemoglobin), i.e. oxygen saturation
 HCO3   serum concentration of bicarbonate in mmol/L
 Base excess     Quantity of acid or base necessary to titrate 1 litre of blood to pH 7.4 at 370C with a PaCO2 of 5.3kPa
 Base deficit   Negative base excess
 Acid-base balance     The state in which the pH of the blood is maintained at approximately between 7.35 and 7.45
 Compensated acidosis/alkalosis    Underlying acidosis/alkalosis, but the pH of the blood has been returned to normal by compensatory mechanisms.







  • All attempts to perform Arterial Blood Gas Sampling whether successful or not must be documented in the patient’s medical record, i.e., Pulmonary Services Charge Sheets.  Information to be charted includes:
  • Site of puncture
  • Performance and success of Allen’s Test
  • Success (or lack of success) in obtaining the blood specimen
  • Number of attempts.  
  • Down stream pulse confirmed before and after the sample is obtained.  Cessation of bleeding, hematoma, bruising or oozing from puncture site.
  • Patient’s FiO2 and temperature.


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