Neonatal Blood Gas Interpretation

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:

1. Identify probable causes of an acid-base disorder
2. List normal ABG parameters for pH, PaCO₂, and HCO₃
3. Identify individual ABG values as normal, acidotic, or alkalotic
4. Recognize and label arterial blood gases with acid-base disorders
5. Define compensated and uncompensated

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

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)

Where:

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:

Respiratory acidosis results from the formation of excess carbonic acid because of increased carbon dioxide.⁴

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:

Respiratory alkalosis results from alveolar hyperventilation leading to a deficiency of carbonic acid.⁴

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:

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

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:

Metabolic alkalosis is an excess concentration of bicarbonate in the extracellular fluid. It is caused by problems leading to increased loss of acid.⁶

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.

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:

• Infection control or universal precautions. All types of blood gas sampling carry the risk of transmission of infection to the infant through the introduction of organisms into the bloodstream. In addition, the risk of exposing the clinician to the infant’s blood makes it necessary to take appropriate precautions.
• Bleeding disorders. The potential for bruising and excessive bleeding should be evaluated, particularly if an arterial puncture is being considered.
• Steady-state. Ideally, blood gases should measure the infant’s condition in a state of equilibrium. After changing ventilator settings or disturbing the infant, a period of 20 to 30 minutes should be allowed for arterial blood chemistry to reach a steady state. This period will vary from infant to infant.

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:

The following steps can be used as a systematic way of evaluating parameters in neonatal blood gases¹:

1. Assess pH
2. Assess respiratory component
3. Assess metabolic component
4. Assess the compensation status
5. Complete the acid-base classification
6. Formulate a plan

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

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:

• Room Air
  • pH = 7.22 mmHg PaCO2 = 61 mmHg PaO2 = 70 mmHg HCO3- = 24 mEq/l
    • The pH is lower than normal; therefore, it would be labeled acidotic
    • PaCO2 is higher than normal; therefore, it would be labeled acidotic
    • PaO2 is within the normal range. Is the patient working to maintain the PaO2?
    • HCO3 - is within the normal range
    • It is obvious that the patient is suffering from acidosis, but is it respiratory or metabolic?
    • Is it compensated or uncompensated?
    • The HCO3 - is normal; therefore, it is not metabolic, but respiratory.
    • The ABG is uncompensated because the pH is not within the normal range
    • Uncompensated respiratory acidosis - consider CPAP
• Mechanical ventilation rate 25, PIP 18, PEEP +4, FiO2 30% (33-week gestational age)
  • pH = 7.49 mmHg PaCO2 = 26 mmHg PaO2 = 95 mmHg HCO3- = 22 mEq/l
    • The pH is high, indicating alkalemia.
    • The PaCO2 is low, indicating a respiratory alkalosis.
    • HCO3 - is normal.
    • There is no compensation (pH is not normal).
    • PaO2 is too high.
    • Uncompensated respiratory alkalosis - consider reducing the rate or PIP and weaning oxygen.
• Room Air infant with necrotizing enterocolitis on continuous gastric suction, TPN with sodium, and potassium acetate. Capillary blood gas
  • pH = 7.52 mmHg PCO2 = 41 mmHg PO2 = 55 mm Hg HCO3- = 35 mEq/l
    • The pH is high, indicating alkalemia.
    • The PCO2 is high normal.
    • The metabolic component is high, indicating a metabolic acidosis.
    • There is no compensation (pH is not normal).
    • The PO2 is adequate (capillary blood gas).
    • Uncompensated metabolic alkalosis – consider eliminating the acetate and use chloride salts.
• Premature infant receiving TPN (total parenteral nutrition) with adequate calories but the infant continues with weight loss. Capillary refill is sluggish and capillary gases:
  • pH = 7.27 mmHg PCO2 = 36 mmHg PO2 = 57 mmHg HCO3- = 15 mEq/l
    • The pH is low, indicating an acidosis.
    • The PCO2 is normal.
    • The metabolic component is low, indicating a metabolic problem.
    • There is no compensation (pH is not normal).
    • The PO2 is adequate (capillary blood gas).
    • Uncompensated metabolic acidosis - consider giving volume to help metabolize lactic acid and adding acetates to lower metabolic acid load.
• A premature infant on mechanical ventilation for respiratory distress (Rate 30, PIP 19, PEEP +5, and FiO2 40%). The infant has lost weight and has a serum sodium of 148 mEq/l.
  • pH = 7.28 PaCO2 49 mmHg PaO2 = 56 mmHg HCO3- = 18 mEq/l
    • The pH is low, indicating an acidemia.
    • The PaCO2 is high, indicating respiratory acidosis.
    • The metabolic component is low, indicating a metabolic problem.
    • There is no compensation (pH is not normal).
    • The PaO2 is adequate.
    • Uncompensated mixed respiratory and metabolic acidosis – increase ventilator rate. Consider giving volume to correct hypovolemia, which may be causing the metabolic acidosis.

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:

• pH 7.30
• PCO2 56 mmHg
• HCO3– 26 mEq/liter
• PO2 40 mmHg

The steps for analysis indicate the following:

1. The pH is low, indicating acidosis.
2. The PCO2 is high, indicating a respiratory problem.
3. The metabolic component (HCO3–) is normal.
4. No compensation is present (pH is not normal).
5. This is uncompensated respiratory acidosis.
6. Oxygenation is adequate.
7. Treatment should be aimed at improving alveolar ventilation. Depending on the infant’s clinical status and chest x-ray findings, treatment could consist of nasal CPAP or intermittent positive pressure ventilation.

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