Participants will understand how to interpret and respond to ABG results in the neonate.
Participants will understand how to interpret and respond to ABG results in the neonate.
At the completion of this module, the learner will be able to:
An adjunct to clinical assessment of respiratory disease is chemical assessment via blood gases. The purpose of obtaining blood gases in a neonate is to determine if the baby is adequately ventilating and/or perfusing. Blood gases are the basis for analyzing if oxygenation is adequate and for deducing what the acid-base balance is in a particular neonate. The medical plan of care for the neonatal patient includes the frequency of blood gas determination, and it is every care provider’s responsibility to be cognizant of each blood gas sample drawn on the patient. The value of timely and accurate interpretation of blood gas results cannot be questioned.
Technological advances, including artificial surfactant and high-frequency ventilation, have increased the need for rapid response to changing clinical conditions. Equipment that will allow in-line blood gas monitoring with an indwelling probe is now available. It makes possible more frequent sampling without the concern of excessive blood loss, which is a major concern for the tiny neonates.
pH: The symbol used to measure the hydrogen ion (H+) concentration. As the H+ concentration increases, the pH decreases (acidosis); as the H+ decreases, the pH increases (alkalosis). A severely depressed pH indicates acute decompensation.
Acid-Base Balance: The pH is the result of the plasma bicarbonate/plasma carbonic acid relationship.
Acid: A substance that can donate H+; excess causes decreased pH (<7.25).
Base: A substance capable of accepting H+; a decrease of H+ causes increased pH (>7.45).
Lungs: Controls pH by varying the amount of CO2 that is excreted.
Kidneys: Controls pH by varying the rate of excretion of HCO3-.
Acidosis: A physiologic state where a significant base deficit is present.
Metabolic Acidosis: This occurs when a disorder adds acid to the body or causes alkali to be lost faster than the buffer system (lungs or kidneys) can regulate the load.
Respiratory Acidosis: This occurs when the lungs do not promptly vent carbon dioxide, and carbon dioxide combines with bicarbonate to form carbonic acid.
Alkalosis: A physiologic state in which there is more than a normal base present.
Metabolic Alkalosis: This occurs whenever acid is excessively lost, or alkali is excessively retained. The acid-base ratio of the body is altered.
Respiratory Alkalosis: This occurs when carbon dioxide is excreted by the lungs in excess of its production rate by the body; the level of carbonic acid falls, producing an excess amount of bicarbonate in relation to the acid content.
Compensation: The secondary physiologic process occurring in response to a primary disturbance in the acid-base balance by which the deviation of pH is lessened.
Correction: This is a change in the system originally affected by the primary disturbance by some intervention using available therapy.
The classification and interpretation of blood gases are based on a set of normal values. Values for the term and preterm infant differ slightly from values for the adult because of immaturity and the presence of fetal hemoglobin. In addition, the exact values accepted as normal may vary from institution to institution.1
|Arterial Blood Gas||Normal Values|
|pH||7.35 - 7.45|
|PaCO2||5 - 45 mm Hg|
|PaO2||50 - 70 mm Hg (term infant)|
45 - 65 mm Hg (preterm infant)
|HCO3||22 - 26 mEq/liter|
|Base Excess||-2 - + 2 mEq/liter|
|O2 saturation||92 - 94 %|
Acid-base balance is maintained within narrow limits by complex interactions between the respiratory system and the kidneys. There are four major components to the arterial blood gas: pH, PaCO2, bicarbonate (HCO3-) or base excess, and PaO2. Oxygen diffuses across the alveolar-capillary membrane, moved by the difference in oxygen pressure between the alveolus and the blood. In the blood, oxygen dissolves in the plasma and binds to hemoglobin. Arterial oxygen content (CaO2) is the sum of dissolved and hemoglobin bound oxygen as described by the following equation:
CaO2 = (1.37 x Hb x SaO2) + (0.003 x PaO2)
CaO2 = Arterial oxygen content (ml/100 ml of blood)
1.37 = Milliliters of oxygen bound to 1 g of hemoglobin at 100 percent saturation
Hb = Hemoglobin concentration (g/dl)
SaO2 = Percent of hemoglobin bound to oxygen (%)
0.03 = Solubility factor of oxygen in plasma (ml/mm Hg)
PaO2 = Oxygen partial pressure in arterial blood (mm Hg)
In the equation for arterial oxygen content, the first term (1.37 x Hb x SaO2) is the amount of oxygen bound to hemoglobin. The second term (0.003 x PaO2) is the amount of oxygen dissolved in plasma. Most of the oxygen in the blood is carried by hemoglobin.2
For example, if a premature infant has a PaO2 of 60 mm Hg, a SaO2 of 92 percent, and a hemoglobin concentration of 14 g/dl, CaO2 is the sum of oxygen bound to hemoglobin (1.37 x 14 x 92/100) = 17.6 ml, plus the oxygen dissolved in plasma (0.003 x 60) = 0.1 ml. In this example, only one percent of oxygen in the blood is dissolved in plasma; 99 percent is carried by hemoglobin.
If the infant has an intraventricular hemorrhage and hemoglobin concentrations drop to 10.5 g/dl, but PaO2 and SaO2 remain the same, CaO2 equals 13.4 ml/dl of blood. Thus, without any change in PaO2 or SaO2, a 25 percent drop in hemoglobin concentration reduces the amount of oxygen in arterial blood by 24 percent. This concept is important to remember when taking care of patients with respiratory disease. These patients need to be monitored and, if low, corrected to keep an adequate level of oxygenation.
The force that loads hemoglobin with oxygen in the lungs and unloads it in the tissues is the difference in partial pressure of oxygen. In the lungs, alveolar oxygen partial pressure is higher than capillary oxygen partial pressure so that oxygen moves to the capillaries and binds to the hemoglobin. Tissue partial pressure of oxygen is lower than that of the blood, so oxygen moves from hemoglobin to the tissue.2
Several factors can affect the affinity of hemoglobin for oxygen. The relationship between partial pressure of oxygen and hemoglobin is referred to as the oxyhemoglobin dissociation curve. Alkalosis, hypothermia, hypocapnia, and decreased levels of 2, 3-diphosphoglycerate (2, 3 DPG) increase the affinity of hemoglobin for oxygen. Acidosis, hyperthermia, hypercapnia, and increased 2, 3 DPG have the opposite effect, decreasing the affinity of hemoglobin for oxygen. This is referred to as hemoglobin dissociation curve shifting to the right.3
This characteristic of hemoglobin facilitates oxygen loading in the lung and unloading in the tissue where the pH is lower, and the PaCO2 is higher. Fetal hemoglobin, which has a higher affinity for oxygen than adult hemoglobin, is more fully oxygenated at lower PaO2 values. This high affinity is represented by a left shift on the curve of dissociation of hemoglobin.
Once loaded with oxygen, the blood should reach the tissues to transfer oxygen to the cells. Oxygen delivery to the tissue depends on cardiac output (CO) and arterial oxygen content (CaO2): Oxygen delivery = CO x CaO2.
The key concept is that when assessing a patient’s oxygenation, more information than just PaO2 and SaO2 should be considered. PaO2 and SaO2 may be normal, but if hemoglobin concentration is low or cardiac output is decreased, oxygen delivery to the tissue is decreased.1
The pH scale is a mathematical expression of the acid-base balance of a solution. The number of hydrogen ions in a solution determines the acidity of that solution. An acid solution can donate hydrogen ions; a base solution can accept hydrogen ions. Blood pH is determined by the balance between acids, which results from the byproducts of metabolism, and the body’s buffer systems. For example, if the carbon dioxide is not excreted effectively by the lungs, it combines with water to form carbonic acid, which leads to an excess of hydrogen ions and the development of acidemia.
There are three major blood buffers to neutralize the acid in order to maintain the acid-base balance. Of the three buffers (hemoglobin, serum protein, and bicarbonate), the bicarbonate system is predominant. Bicarbonate combines with hydrogen to form carbon dioxide and water, thereby buffering the acids and balancing the pH. If the carbon dioxide cannot be excreted by the lungs, the hydrogen ions can be returned to the solution and result in acidemia.
The lungs are primarily responsible for the carbon dioxide level (PaO2), and the kidneys control the plasma bicarbonate (HCO3-). Acting as an acid, carbon dioxide will add hydrogen ions, and bicarbonate acting as a base accepts ions. As the PaCO2 rises or HCO3- falls, the pH will become more acidotic. As the CO2 falls or HCO3- rises the pH will become more alkalotic.1
PaCO2 is directly related to the respiratory status, pH abnormalities resulting from abnormal PaCO2 are considered respiratory in origin. Any abnormalities in HCO3- are considered metabolic in origin. Base excess (BE) reflects the concentration of buffer. Normal range is 0 +/- 2 mEq/liter of base. Positive values express an excess of base or a deficit of acid; negative values express a deficit of base or an excess of acid. When the base excess is negative, it is sometimes referred to as the base deficit.
The body attempts to maintain a normal pH in two ways:
Critically ill neonates may be limited in their ability to compensate for problems. Respiratory disease limits the body’s ability to lower PaCO2 effectively, and the neonatal kidney may be ineffective in conserving bicarbonate.
The terms applied to acid-base disorders can be a source of confusion. Alkalemia and acidemia refer to measurements of blood pH; acidosis and alkalosis refer to the underlying pathologic process. A blood pH of less than 7.35 is said to be acidemic; a pH greater than 7.45 is alkalemic. The partial pressure of carbon dioxide and bicarbonate levels determine, respectively, the respiratory and metabolic contributions to the acid-base equation. For each disorder, compensatory mechanisms are indicated. Correction occurs where possible by addressing the underlying problem.
Respiratory acidosis results from the formation of excess carbonic acid because of increased carbon dioxide.4
|CNS depression – maternal narcotics during labor, asphyxia, severe intracranial bleeding, neuromuscular disorder, CNS dysmaturity (apnea or prematurity)||Decreased Ventilation-Perfusion ratio|
|Obstructed airways, meconium aspiration, choanal atresia, bloody mucus, blocked endotracheal tube, external compression of the airway||Decreased alveolar ventilation and decreased lung compliance|
|HMD, chronic pulmonary insufficiency||Injuries to thoracic cage|
|Diaphragmatic hernia, phrenic nerve paralysis, and pneumothorax||Iatrogenic (inadequate mechanical ventilation)|
Compensation: over three to four days, the kidneys increase the rate of hydrogen ion secretion and bicarbonate reabsorption. Compensated respiratory acidosis is characterized by a low normal pH, with increased carbon dioxide and increased bicarbonate, caused by the retention of bicarbonate in the kidney to compensate for elevated carbon dioxide levels.
Respiratory alkalosis results from alveolar hyperventilation leading to a deficiency of carbonic acid.4
|Iatrogenic (mechanical ventilation)|
CNS irritation (pain)
|Increase in alveolar ventilation|
Compensation: the kidneys decrease hydrogen secretion by retaining chloride and excreting fewer acid salts. Bicarbonate reabsorption is also decreased. The pH will be high normal with low carbon dioxide and low bicarbonate levels.
Metabolic acidosis is a deficiency in the concentration of bicarbonate in the extracellular fluid. It is caused by any systemic disease that increases acid production or retention, or problems leading to excessive base losses. Examples are hypoxia leading to lactic acid production, renal disease, and loss of base because of diarrhea.5
|Decreased tissue perfusion|
Renal tubular acidosis
|Increase in lactic acid production|
Increase in organic acids
Loss of base
Loss of base
Compensation: if healthy, the lungs will blow off additional carbon dioxide through hyperventilation. If renal disease is not a problem, the kidneys will respond by increasing the excretion of acid salts and the re-absorption of bicarbonate. The pH will be below normal with low levels of carbon dioxide and bicarbonate ions.
Metabolic alkalosis is an excess concentration of bicarbonate in the extracellular fluid. It is caused by problems leading to increased loss of acid.6
Iatrogenic (gave too much HCO3)
|Loss of acid|
Loss of acid
Loss of H+ ion via the kidney
Adding a base
Citrate in anticoagulant is metabolized
Compensation: the lungs compensate by retaining carbon dioxide through hypoventilation. The pH will be high normal with high levels of carbon dioxide and bicarbonate ions.
|Respiratory Acidosis||Metabolic Acidosis||Respiratory Alkalosis||Metabolic Alkalosis|
Analysis of blood gases provides the clinician the basis for determining the adequacy of alveolar ventilation and perfusion. It is crucial that this test is collected and evaluated with an understanding of appropriate techniques and potential sources of error.
Regardless of the type of sample obtained, attention should be given to the following factors:
Arterial blood can be obtained either from an indwelling line or through an intermittent sampling of a peripheral artery. The choice of sample site will depend on the clinical situation. An indwelling arterial catheter should be placed when it is anticipated that the neonate will require frequent arterial blood sampling. Several criteria are used to determine the need for an indwelling line. The criteria include gestational age, disease process, and the amount of oxygen required. Common sites for indwelling arterial lines are the umbilical, radial, posterior tibial, and dorsalis pedis arteries.1
Capillary blood can be “arterialized” by warming the skin to increase local blood flow. Samples can be obtained from the outer aspects of the heel or the side of a finger or toe. When perfusion is normal, it has been shown that capillary pH and PCO2 correlate well with arterial values. PO2 correlates if the partial pressure of oxygen in arterial blood is < 60, but not at higher levels.1
The interpretation of blood gas data should follow a logical pattern. Initially, evaluate the pH to determine if an acidemia or alkalemia is present. Then evaluate the respiratory parameter (PaCO2) and the metabolic parameter (HCO3-) to determine if the acidemia or alkalemia is respiratory or metabolic in origin. The clinical picture can become complex if abnormalities exist in both systems simultaneously. A review of the infant’s clinical status, previous blood gas values, and treatment measures will help determine whether this is an ongoing compensation mechanism or two independent abnormalities.
The arterial blood gas provides information about the pulmonary component of oxygenation, specifically the PaO2. Hypoxemia refers to a lower than normal arterial PO2, and hypoxia refers to inadequate oxygen supply to the body tissue. Preterm infants have a lower acceptable PaO2 value because HbgF results in increased oxygen delivery at lower PaO2.
Hypoxemia results from lung disease or cyanotic congenital heart disease. Hypoxia may result from a number of factors, including heart failure, anemia, abnormal hemoglobin affinity for oxygen, and a decreased PaO2. The most common cause of hypoxemia is mismatching of ventilation and perfusion. It occurs when the amount of blood perfusing an alveolus or the amount of fresh gas entering the alveolus is not adequate for gas exchange. Normally in the lungs, some alveoli are better ventilated than others. Clinically significant mismatching results when decreased ventilation or perfusion interferes with the ability of the lung to provide adequate gas exchange.1
PaO2 of less than 45 to 50 mmHg is associated with vasoconstriction of pulmonary vasculature and vasodilation of the ductus arteriosus. Low PaO2s are implicated in the etiology of persistent pulmonary hypertension of the newborn (PPHN).
Hyperoxemia (PaO2 > 100 mmHg) should also be avoided, especially in the preterm infant, where high levels of oxygen in the blood are associated with retinal injury. When interpreting neonatal PaO2s, it is important to identify whether the sample is pre- or post-ductal in its origin because of the potential impact of shunting across the ductus resulting in lower PaO2 in post ductal samples.1
Examples of Arterial Blood Gas Levels for Different Conditions:
|BE (base excess)||-2|
|BE (base excess)||-4|
|BE (base excess)||0|
|BE (base excess)||-10|
|BE (base excess)||+8|
The following steps can be used as a systematic way of evaluating parameters in neonatal blood gases1:
Acid-base imbalances are corrected where possible, through manipulation of the system that is causing the primary problem. This is done as follows:
Respiratory acidosis: assist in the removal of carbon dioxide through the application of nasal continuous positive airway pressure (CPAP) or mechanical ventilation. For infants already on mechanical ventilation, removal of carbon dioxide can be facilitated by increasing the rate, peak inspiratory pressure (PIP), or positive end-expiratory pressure (PEEP). Sodium bicarbonate is usually not recommended for treating respiratory acidosis because it reacts with acids to form carbon dioxide
Respiratory alkalosis: for mechanically ventilated infants, reduce the rate of pressure on the ventilator.
Metabolic acidosis: where possible, treat the cause of the acidosis. If the acidosis is severe, sodium bicarbonate can be administered at a dose of 2 mEq/kg or according to the following formula1:
Base deficit x (weight in kg) x (0.3)
The amount of bicarbonate calculated by this formula should theoretically correct half of the base deficit and should be administered slowly over 30 to 60 minutes. Fluid replacement may also be of benefit in treating metabolic acidosis because it helps the infant to metabolize lactic acid.
Metabolic alkalosis: treat the cause by removing acetate from IV fluids, by reducing diuretic doses, and by treating hyponatremia, hypokalemia, and hypochloremia.1
Compensation occurs in response to a primary disturbance in acid-base equilibrium whereby the change in the pH is relieved. Compensation is a change in the system not originally affected by the primary disturbance. Correction is a change in the system originally affected by the primary disturbance, using available therapy by the clinician.7
The retention of bicarbonate characterizes compensated respiratory acidosis as a result of the adjustment in renal function. The primary disturbance is the accumulation of carbon dioxide, thus increasing carbonic acid concentration. The kidneys respond to this disturbance by holding on to HCO3. This compensation by the kidneys can take several days if not corrected by ventilation therapy. When fully compensated the pH is near normal and PaCO2 values, and HCO3 are increased.7
Compensated metabolic acidosis is characterized by hyperventilation activated by the primary disturbance of an accumulation of acid that devours the available base. CO2 excreted through the lungs, lowers the carbonic acid concentration to match the lower available bicarbonate. When fully compensated, the pH is near normal, and the PaCO2 and serum HCO3 values are both low.7
Compensated respiratory alkalosis is characterized by the kidneys increasing their secretion of bicarbonate to restore the bicarbonate/carbonic acid ratio to normal. The primary disturbance is caused by hyperventilation and excessive elimination of CO2. When fully compensated, the pH is near normal, but PaCO2 and serum HCO3 are at the lower end of normal.7
Compensated metabolic alkalosis is characterized by hypoventilation to diminish the elimination of CO2. The primary disturbance is the accumulation of bicarbonate by retaining CO2 the appropriate reaction between sodium bicarbonate and carbonic acid is restored. When compensated, the pH is almost normal, but the PaCO2 and serum bicarbonate values are elevated.8
|Disorder||Primary Component Affected||Compensatory Effect||Correction|
pH < 7.35
|Decreased PCO2||Give bicarbonate and treat the cause|
pH < 7.35
|Increased PCO2||Increase HCO3||Increase or assist ventilation|
pH > 7.45
|Increased HCO3||Increased PCO2||Give KCl|
pH > 7.45
|Decreased PCO2||Decreased HCO3||Attempt to stop hyperventilation|
Correction of acidosis-alkalosis can be achieved sooner if one manipulates ventilator settings or gives bicarbonate to achieve the desired value. If the pressure or rate on the ventilator is increased, CO2 will be blown off. If the rate or pressure is decreased, CO2 will be retained. Severe metabolic acidosis should be treated with sodium bicarbonate 2 mEq/kg slow IV push. HCO3 should be diluted 1:1 with sterile H2O and ensure adequate ventilation.7
For acute correction of HCO3 base deficit: Base deficit X (wt in kg) X (0.3) Hypoxemia secondary to ventilator perfusion mismatching may be improved through the administration of supplemental oxygen. In addition, oxygenation can be improved by increasing the mean airway pressure in an infant receiving mechanical ventilation. See summary below:
|Blood Gas Imbalance||Ventilator Changes|
|Hypoxemia low PaO2||Increase FiO2|
|Hyperoxia high PaO2||Decrease FiO2|
|Hypercapnia high PaCO2||Increase respiratory rate|
Increase PIP (tidal volume)
Increase inspiratory time
Increase the flow rate
Decrease dead space
|Hypocapnia low PaCO2||Decrease respiratory rate|
Decrease inspiratory time
Decrease flow rate
Increase dead space
|High PaCO2, low PaO2||Increase inspiratory time|
|High PaCO2, high or normal PaO2||Decrease PEEP|
Disorders of acid-base balance are diagnosed almost as frequently as blood gas sampling is undertaken in the neonatal population. Sick neonates have respiratory and metabolic systems that are in constant change in response to disease processes and also to therapeutic interventions. Quick responses to these changes will minimize the time an infant spends outside the desired range of blood pH and potential complications of treatments such as airway pressure (barotraumas) and oxygen.
Arterial sampling allows for the assessment of oxygenation, the ability to remove carbon dioxide and acid-base status. Capillary blood samples are useful for evaluating CO2 removal and acid-base status but are not useful for evaluating oxygenation. It is important to approach blood gas interpretation systematically and to integrate physiology with the clinical history to provide optimal patient care and outcome. Monitoring a critically ill infant with a pulse oximeter will provide continuous information on his status by determining the pulse oxygen saturation. Intermittent assessment of the arterial blood gases will yield specific information on the acid-base balance.
An infant born at 31 weeks gestation is two hours old with the following physical findings: respiratory rate 94 breaths per minute, heart rate 162 beats per minute, temperature 36.5°C (97.7°F), and grunting with moderate retractions.
Capillary blood gas results are as follows:
The steps for analysis indicate the following: