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:
- By correcting or altering the component responsible for the abnormality. For example, if an increased level of carbon dioxide in the blood is causing respiratory acidosis, the body will attempt to increase the excretion of carbon dioxide by the lungs and bring the causative factor, increased CO2, back to normal levels.
- By compensating through alterations in the component that is not primarily responsible for the abnormality, carbon dioxide and/or bicarbonate will be excreted or retained in order to balance the abnormal value. For example, if a high PaCO2 is causing respiratory acidosis, the body will attempt to excrete more acid and conserve HCO3- to compensate, although compensation by renal function is a slow mechanism and may take several days. If the PaCO2 is low, the body will rid itself of bicarbonate. The inverse is also seen. High HCO3- will be compensated by a high PaCO2; a low HCO3- will be compensated by a low PaCO2. Thus, subsequent abnormal values of carbon dioxide or bicarbonate may result from the compensation mechanism of the body attempting to bring the ratio of HCO3- to CO2 back to 20:1.
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
Blood gas findings: low pH, high PCO2, normal bicarbonate.
|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
Blood gas findings: high pH, low PCO2, and normal bicarbonate.
|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
Blood gas findings: low pH, low bicarbonate, normal PCO2.
|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
Blood gas findings: high pH, high bicarbonate, normal PCO2.
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.
Summary of Blood Gas Changes:
| ||Respiratory Acidosis||Metabolic Acidosis||Respiratory Alkalosis||Metabolic Alkalosis|