Type of test Blood
Normal findings
pH
Adult/child: 7.35-7.45, Newborn: 7.32-7.49, 2 months-2 years: 7.34-7.46 ,pH (venous): 7.31-7.41
Pco2
Adult/child: 35-45 mm Hg, Child < 2 years: 26-41 mm Hg ,Pco2 (venous): 40-50 mm Hg
HCO3
Adult/child: 21-28 mEq/L, Newborn/infant: 16-24 mEq/L
Po2
Adult/child: 80-100 mm Hg, Newborn: 60-70 mm Hg, Po2 (venous): 40-50 mm Hg
O2 saturation
Adult/child: 95%-100% ,Elderly: 95% ,Newborn: 40%-90%
O2 content
Arterial: 15-22 vol %, Venous: 11-16 vol %
Base excess
0 ± 2 mEq/L
Alveolar to arterial O2 difference
< 10 mm Hg
Possible critical values
pH: 7.55
PCO2 : < 20, > 60
HCO3 : < 15, > 40
PO2 : < 40
O2 saturation: 75% or lower
Base excess: ± 3 mEq/L
Test explanation and related physiology
Measurement of ABGs provides valuable information in assessing and managing a patient’s respiratory (ventilation) and metabolic (renal) acid-base and electrolyte homeostasis. It is also used to assess adequacy of oxygenation. ABGs are used to monitor patients on ventilators, to monitor critically ill nonventilator patients, to establish preoperative baseline parameters, and to enlighten electrolyte therapy.
pH
The pH is inversely proportional to the actual hydrogen ion concentration. Therefore as the hydrogen ion concentration decreases, the pH increases and vice versa. The pH is a measure of alkalinity (pH > 7.4) and acidity (pH < 7.35). In respiratory or metabolic alkalosis, the pH is elevated; in respiratory or metabolic acidosis, the pH is decreased (Table 1).
Table1. Normal values for arterial blood gases and abnormal values in uncompensated acid-base disturbances
Pco2
The Pco2 is a measure of the partial pressure of CO2 in the blood. Pco2 is a measurement of ventilation capability. The faster and more deeply one breathes, the more CO2 is blown off and Pco2 levels drop. Therefore Pco2 is referred to as the respiratory component in acid-base determination because this value is controlled primarily by the lungs. As the CO2 level increases, the pH decreases. The CO2 level and the pH are inversely proportional. The Pco2 in the blood and cerebrospinal fluid is a major stimulant to the breathing center in the brain. As Pco2 levels rise, breathing is stimulated. If Pco2 levels rise too high, breathing cannot keep up with the demand to blow off or ventilate. As Pco2 levels rise further, the brain is depressed, and ventilation decreases further, causing coma.
The Pco2 level is elevated in primary respiratory acidosis and is decreased in primary respiratory alkalosis (see Table 2). Because the lungs compensate for primary metabolic acid-base derangements, Pco2 levels are affected by metabolic disturbances as well. In metabolic acidosis, the lungs attempt to compensate by blowing off CO2 to raise pH. In metabolic alkalosis, the lungs attempt to compensate by retaining CO2 to lower pH (Table 3).
Table3. Acid-base disturbances and compensatory mechanisms
Bicarbonate (HCO3 ) or CO2 content
Most of the CO2 content in the blood is HCO3 . The bicarbonate ion is a measure of the metabolic (renal/kidney) component of the acid-base equilibrium. It is regulated by the kidneys. This ion can be measured directly by the bicarbonate value or indirectly by the CO2 content. As the HCO3 level increases, the pH also increases; therefore the relationship of bicarbonate to pH is directly proportional. HCO3 is elevated in metabolic alkalosis and decreased in metabolic acidosis. The kidneys also are used to compensate for primary respiratory acid-base derangements. For example, in respiratory acidosis, the kidneys attempt to compensate by resorbing increased amounts of HCO3 . In respiratory alkalosis, the kidneys excrete HCO3 in increased amounts to lower pH.
Po2
This is an indirect measure of the oxygen content of arterial blood. Po2 is a measure of the tension (pressure) of oxygen dis solved in the plasma. This pressure determines the force of O2 to diffuse across the pulmonary alveoli membrane. The Po2 level is decreased in patients who:
• Are unable to oxygenate the arterial blood because of O2 diffusion difficulties (e.g., pneumonia)
• Have premature mixing of venous blood with arterial blood (e.g., in congenital heart disease)
• Have underventilated and overperfused pulmonary alveoli (Pickwickian syndrome or patients with significant atelectasis)
O2 saturation
Oxygen saturation is an indication of the percentage of hemoglobin saturated with O2 . When 92% to 100% of the hemoglobin carries O2 , the tissues are adequately provided with O2 , assuming normal O2 dissociation. As the Po2 level decreases, the percentage of hemoglobin saturation also decreases. When the Po2 level drops to lower than 60 mm Hg, small decreases in the Po2 level cause large decreases in the percentage of hemoglobin saturated with O2 . At O2 saturation levels of 70% or lower, the tissues are unable to extract enough O2 to carry out their vital functions.
O2 saturation is calculated by the blood gas machine using the following formula:
Pulse oximetry is a noninvasive method of determining O2 saturation.
O2 content
This is a calculated number that represents the amount of O2 in the blood. The formula for calculation is:
Nearly all O2 in the blood is bound to hemoglobin. O2 con tent decreases with the same diseases that diminish Po2 .
Base excess or deficit
This number is calculated by the blood gas machine by using the pH, Pco2 , and hematocrit. It represents the amount of buffering anions in the blood. HCO3 is the largest of these. Others include hemoglobin, proteins, and phosphates. Base excess is a way to take all these anions into account when determining acid base treatment based on the metabolic component. Negative base excess (deficit) indicates a metabolic acidosis (e.g., lactic acidosis). A positive base excess indicates metabolic alkalosis or compensation to prolonged respiratory acidosis.
Alveolar (A) to arterial (a) O2 difference (A-a gradient)
This is a calculated number that indicates the difference between alveolar (A) O2 and arterial (a) O2 . The normal value is less than 10 mm Hg (torr). If the A-a gradient is abnormally high, there is either a problem in diffusing O2 across the alveolar membrane (thickened edematous alveoli) or unoxygenated blood is mixing with the oxygenated blood.
Contraindications
• Patients with a negative Allen test result
• Patients with arteriovenous fistula proximal to the access site
• Patients with severe coagulopathy
Potential complications
• Occlusion of the artery used for access
• Penetration of other important structures anatomically juxta posed to the artery (e.g., nerve)
Interfering factors
• O2 saturation can be falsely increased with the inhalation of carbon monoxide.
* Respiration can be inhibited by sedatives or narcotics.
Procedure and patient care
Before
* Explain the procedure to the patient.
* Tell the patient that an arterial puncture is associated with more discomfort than a venous puncture.
• Notify the laboratory before drawing ABGs so that the equipment can be calibrated before the blood sample arrives.
• Perform the Allen test to assess collateral circulation.
• To perform the Allen test, make the patient’s hand blanch by obliterating both the radial and the ulnar pulses, and then release the pressure over the ulnar artery only. If flow through the ulnar artery is good, flushing will be seen immediately. The Allen test is then positive, and the radial artery can be used for puncture.
• If the Allen test is negative (no flushing), repeat it on the other arm.
• If both arms give a negative result, choose another artery for puncture.
During
• Note that arterial blood can be obtained from any area of the body in which strong pulses are palpable, usually from the radial, brachial, or femoral artery.
• Cleanse the arterial site.
• Use a small gauge needle to collect the arterial blood in an air-free heparinized syringe.
• After drawing blood, remove the needle and apply pressure to the arterial site for 3 to 5 minutes.
• Expel any air bubbles in the syringe.
• Cap the syringe and gently rotate to mix the blood and heparin.
• Note that an arterial puncture is performed by laboratory technicians, respiratory-inhalation therapists, nurses, or physicians in approximately 10 minutes.
After
• Place the arterial blood on ice and immediately take it to the chemistry laboratory for analysis.
• Apply pressure or a pressure dressing to the arterial puncture site for 3 to 5 minutes to avoid hematoma formation.
• Assess the puncture site for bleeding. Remember that an artery rather than a vein has been stuck.
Abnormal findings
Increased pH (alkalosis)
Metabolic alkalosis
- Hypokalemia
- Hypochloremia
- Chronic and high-volume gastric suction
- Chronic vomiting
- Aldosteronism
- Mercurial diuretics
Respiratory alkalosis
- Chronic heart failure
- Cystic fibrosis
- Carbon monoxide poisoning
- Pulmonary emboli
- Shock
- Acute and severe pulmonary diseases
- Anxiety neuroses
- Pain
- Pregnancy
Decreased pH (acidosis)
Metabolic acidosis
- Ketoacidosis
- Lactic acidosis
- Severe diarrhea
- Renal failure
Respiratory acidosis
- Respiratory failure
Increased Pco2
- Chronic obstructive pulmonary disease (COPD) (bronchitis, emphysema)
- Oversedation
- Head trauma
- Overoxygenation in a patient with COPD
- Pickwickian syndrome
Decreased Pco2
- Hypoxemia
- Pulmonary emboli
- Anxiety
- Pain
- Pregnancy
Increased HCO3
- Chronic vomiting
- Chronic and high-volume gastric suction
- Aldosteronism
- Use of mercurial diuretics
- Chronic obstructive pulmonary disease
Decreased HCO3
- Chronic and severe diarrhea
- Chronic use of loop diuretics
- Starvation
- Diabetic ketoacidosis
- Acute renal failure
Increased Po2 , increased O2 content
- Polycythemia
- Increased inspired O2
- Hyperventilation
Decreased Po2 , decreased O2 content
- Anemias
- Mucus plug
- Bronchospasm
- Atelectasis
- Pneumothorax
- Pulmonary edema
- Adult respiratory distress syndrome
- Restrictive lung disease
- Atrial or ventricular cardiac septal defects
- Emboli
- Inadequate O2 in inspired air (suffocation)
- Severe hypoventilation (e.g., oversedation, neurologic somnolence)
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