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Understanding Blood Gas Interpretation
Abstract Blood gases are the most common and one of the most important laboratory values performed in the neonatal intensive care unit. Because of technological advances including surfactant and high-frequency ventilation, the need for immediate responses to rapidly changing clinical conditions is of utmost importance. An arterial or capillary blood gas is a clinical tool for determining an infant’s pulmonary and metabolic status. An infant can easily be overventilated, underventilated, or metabolically unstable, which can affect their longterm outcome. Therefore, nurses need to have a basic understanding of acidbase physiology and accurate interpretation skills to be a competent and skilled neonatal intensive care unit nurse. This article presents a brief review of blood gas interpretation. n 2006 Elsevier Inc. All rights reserved. Keywords: Blood gasses, Infant, Metabolic status
Understanding Blood Gas Interpretation By Beth Brown, RNC, MSN, and Bonnie Eilerman, RN, MSN, CNP
A
n arterial or capillary blood gas is a clinical assessment tool for determining an infant’s pulmonary and metabolic status. The pulmonary component of the blood gas yields information on ventilation and oxygenation. The metabolic component reflects potential for changes in enzyme function and nerve and muscle activity. Blood gases are the basis for diagnosis and management of infants with cardiorespiratory disease, metabolic disorders, and overall management in premature infants. By integrating acidbase physiology, blood gas interpretation skills, and clinical history, the neonatal intensive care unit staff can accurately assess an infant’s current condition and help take the appropriate steps to correct the imbalance and, therefore, improve outcomes. Acid-base balance refers to the complex mechanisms through which the body strives to achieve and maintain a homogenous internal environment. This environment is reflected in a serum pH of 7.35 to 7.45. An acid is a substance that can donate hydrogen ions (H+) to alkaline solutions to neutralize the effect of bases. A base is an alkaline substance that can combine with acids to accept hydrogen ions neutralizing the effect of the base.1 The body has many ways to achieve this environment, mainly through the use of buffer systems. The goal of the buffer systems is to regulate the H+ concentration in the body and, therefore, regulate the pH. This concentration must be kept as steady as possible because only slight changes in H+ from the normal value can cause significant alterations in all physiological processes. Delivery of oxygen to the cell, the cellular use of oxygen, and the hormonal regulation of metabolism are all affected by the pH of the body. There are three main body systems that help to regulate pH: the chemical buffer systems, the respiratory center, and renal control.
Buffer Systems
T From the Good Samaritan Hospital, Neonatal Intensive Care Unit, Cincinnati, OH. Address correspondences to Beth Brown, RNC, MSN, 1174 Kylemore Court, Dayton, OH 45459. n 2006 Elsevier Inc. All rights reserved. 1527-3369/06/0602-0130$10.00/0 doi:10.1053/j.nainr.2006.03.005
he chemical buffer systems include the carbonic acid-bicarbonate system, protein buffer system, and the phosphate buffer system. The carbonic acidbicarbonate system is a weak, yet fast buffer that occurs in the extracellular fluid. Carbon dioxide (CO2) and water are made from the oxidization of carbohydrates, fats and proteins. These combine to form carbonic acid. Carbonic acid then splits into hydrogen, an acid, and bicarbonate, a base. Bicarbonate, which is regenerated and stored in the kidneys, can also bind to any excessive amount of hydrogen, thereby reversing the equation and forming carbonic acid.2 This buffer system explains neonatal acidosis because of the immature kidneys of a preterm infant. These premature kidneys cannot hold on to bicarbonate, losing it into the urine. Therefore, there is less bicarbonate to Newborn and Infant Nursing Reviews, Vol 6, No 2 (June), 2006: pp 57 - 62
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bind with the excess hydrogen, and the blood becomes acidic. By use of the carbonic anhydrase equation below, one can see how this process moves in both directions. H2 O þ
CO2
water carbon dioxide
X
H2 CO3
carbonic acid
X
Hþ
hydrogen ion
þ
HCO 3
bicarbonate
The protein buffer system is the most powerful and plentiful buffering system using proteins of cells and plasma. The cell membrane is composed almost entirely of proteins and lipids.2 As the extracellular pH changes, the body adapts by diffusing hydrogen and bicarbonate in and out of the cell membranes by way of these proteins. This is a slow process, up to several hours and intracellular electrolytes such as sodium and potassium may be displaced as the hydrogen or bicarbonate enter the cell. Clinically, this may account for a degree of hypernatremia or hyperkalemia. Hemoglobin is part of the protein buffering system. When the body is acidotic, hemoglobin will act as a buffer. Therefore, the oxygen carrying capacity may be reduced.2 In addition, one of the implications of this buffering system is the displacement of intracellular electrolytes such as sodium and potassium when H+ enters the cell. The main components in the phosphate buffer system are monohydrogen phosphate (HPO4) and dihydrogen phosphate (H2PO4). When a strong acid is added to these two phosphates, only a weak acid is formed, and when a strong base is added also, only a weak base is formed. Phosphate acts predominantly as an intracellular and urinary buffer. Because phosphate is eliminated in the urine, this system is particularly important in buffering fluids in the kidney tubules.3 Respiratory regulation is primarily responsible for the elimination of volatile acids (carbon dioxide). The respiratory center (lungs) controls the pH by varying the amount of CO2, which is excreted by exhalation.2 This is referred to in the blood gas as the Pco2. The chemoreceptors in the brain will sense within minutes that the Pco2 is increasing and then will send messages to the respiratory center to accelerate the rate and depth of breathing. This way, the lungs can respond to a change in H+ concentration within minutes. The metabolic reaction between bicarbonate (HCO3) and H+ produces carbonic acid, which will then dissociate into water and CO2 (as described earlier; see carbonic anhydrase equation above). To prevent CO2 from accumulating and carbonic acid from forming again, leading to acidosis, the lungs will excrete the CO2. The carbonic anhydrase equation is catalyzed by the enzyme carbonic anhydrase. This reaction moves to the right when Pco2 levels are high and moves to the left when Pco2 levels are low.4 The renal system (kidneys) controls the pH by varying the rate of excretion of HCO3, the base that neutralizes
carbonic acid. The kidneys are the slowest physiologic regulators. They take hours to commence their work and may take up to several days to take effect, but they do have the most sustained response. The kidneys provide the most important route for the excretion and buffering of metabolic acids and are also responsible for maintaining the plasma levels of HCO3, the most important buffer of H+. The kidneys control pH balance by excreting either acidic urine or basic urine. The overall mechanism by which the kidneys control the excretion of H+ and the retention of bicarbonate occurs by four main mechanisms: excretion of H+, reabsorption of bicarbonate, production of bicarbonate, and formation of ammonia.2
Permissive Hypercapnia
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lthough a normal level of Pco2 is 35–45 millimeters of mercury, in many situations, levels outside this are considered bacceptable.Q Mechanical ventilation and the resulting baro-/volutrauma on the lungs can highly contribute to the development of bronchopulmonary dysplasia. The major determinant of lung injury is tidal volume or the volume of air instilled into the lungs by a ventilator. This parameter is also the primary one that affects Pco2 levels. The higher the tidal volume is, the more the lungs are stretched and the more baro-/ volutrauma occurs. Permissive hypercapnia is a strategy that attempts to minimize this by allowing relatively high levels of Pco2, provided the pH does not fall below a minimal value (typically 7.20). This is accomplished by providing a low inspiratory volume and pressure and decreasing the extent of lung tissue stretch. The current trend is to wean the ventilator settings to achieve a Pco2 of 50–60 millimeters of mercury. Even higher Pco2 levels are tolerated in nonventilated, older infants with bronchopulmonary dysplasia (Pco2 65–70 millimeters of mercury). The concept that higher Pco2 levels are bsafeQ and bwell toleratedQ is based on limited data and needs to be studied further,5 although strong trends indicate the possibility of important benefits without increased adverse affects.6 The specific ideal, safe range for Pco2 levels in the neonatal population is still under debate.
Oxygenation
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cid base balance also effects tissue oxygenation. The Oxygen Hemoglobin Dissociation Curve is a measure of the affinity that hemoglobin has for oxygen. Oxygen is carried in the blood by being dissolved in the plasma and attached to hemoglobin in the red blood cells. The concentration of oxygen in the arterial plasma is expressed as Pao2, whereas the concentration of oxygen on hemo-
Understanding Blood Gas Interpretation
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With a left shift, there is an increased attraction between oxygen and hemoglobin. Therefore, hemoglobin picks up oxygen more easily and does not release it until a lower Pao2 level is reached. This can impede oxygen release to the tissues, but it facilitates the unloading of carbon dioxide and the uptake of oxygen in the lungs.4 Fetal hemoglobin has decreased 2.3 diphosphoglycerate (DPG) and has a high oxygen affinity causing a shift to the left. Fetal hemoglobin is the main hemoglobin that transports oxygen in the developing fetus during the last 7 months of pregnancy. This special hemoglobin has a higher affinity for oxygen, so it holds on to oxygen tighter. Once delivered, infants automatically turn off the production of hemoglobin F (fetal) and turn on the production of hemoglobin A (adult). It takes about 2 years for an infant to completely switch over to adult hemoglobin. Fig 1. Oxyhemoglobin disassociation curve can be shifted to the left by hypothermia, alkalosis, hypocarbia, or decreased 23 DPG. The curve can be shifted to the right by hyperthermia, acidosis, hypercarbia, or increased 2–3 DPG levels. This figure is reprinted from Comprehensive Neonatal Nursing, with permission from Elsevier Inc.
globin is expressed as percent saturation (SaO2) on the pulse oximetry monitor. When there is no oxygen on the hemoglobin, it is 0% saturated; when the hemoglobin is carrying as much oxygen as possible, it is 100% saturated. The desired level of oxyhemoglobin saturation in a normal healthy term infant is 90% –94% saturation.7 The oxyhemoglobin saturation (% sat or O2 sat) is the most valuable test for detecting hypoxemia. It is not a sensitive measure for high blood oxygen levels and provides no information regarding pH, carbon dioxide, or serum bicarbonate levels. When Pao2 reaches approximately 60 millimeters of mercury, the hemoglobin is almost completely saturated with oxygen, making the SaO2 nearly 100%.8 Therefore, if the SaO2 is more than approximately 94%, the Pao2 could be either acceptable (50 – 80 millimeters of mercury) or undesirably high (N80 millimeters of mercury). Cyanosis is generally noted only at a Pao2 of less than 40 millimeters of mercury in neonates.8 When an infant has received surfactant, for example, the oxygen saturation increases, and it is important to wean the Fio2 to maintain a saturation between 90% and 94% to prevent hyperoxygenation and the exposure to oxygen toxicity. When there is an increased affinity for oxygen, less oxygen is released at the tissue level. When there is a decreased affinity for oxygen, then more oxygen is released to the tissues. Factors that can shift the curve to the right include temperature, pH, and hemoglobin structure. The factors that shift the curve to the left include hypothermia, alkalemia, hypocapnia, and fetal hemoglobin. These factors increase the affinity of hemoglobin for oxygen (Fig 1).
Acid Base Imbalances
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espiratory acidosis occurs when carbon dioxide is not promptly vented by the lungs and the CO2 combines with water to form carbonic acid. This condition results in a buildup of CO2. A blood gas may exhibit a low pH, high Pco2 and a normal HCO3 (Table 1).9 Respiratory acidosis is due to a decrease in alveolar ventilation. The treatment consists of determining the cause and ensuring effective ventilation. Metabolic acidosis 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. This condition reflects a low pH, normal Pco2, and a low HCO3.9 The causes of metabolic acidosis consist of the overproduction of acids due to abnormal metabolism (inborn errors or anaerobic metabolism), the decreased excretion of acids due to impaired renal function, and the excessive loss of bicarbonate through the gastrointestinal tract (severe diarrhea). To determine treatment, determine the cause, consider a hypoxic event, and determine whether the condition is a metabolic vs mixed acidosis. Treatment will then include ensuring effective ventilation and the administration of volume and/or buffers such as sodium bicarbonate. Respiratory alkalosis occurs when CO2 is excreted by the lungs in excess of its production rate by the body. The level Table 1. Summary of Blood Gases
Respiratory acidosis Metabolic acidosis Respiratory alkalosis Metabolic alkalosis
pH
Pco2
HCO3
A7.35 A7.35 z7.45 z7.45
z Normal A Normal
Normal A Normal z
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of carbonic acid falls producing an excess amount of HCO3 in relation to the acid content. This condition reflects a high pH, low Pco2, and a normal HCO3.9 The cause of respiratory alkalosis is an increase in alveolar ventilation (may be associated with central nervous system disorders and birth asphyxia). The treatment consists of determining the cause and then decreasing minute ventilation. Metabolic alkalosis occurs whenever acid is excessively lost or alkali is excessively retained. The acid-base ratio of the body is altered. This condition reflects a high pH, normal Pco2, and a high HCO3.9 The cause of metabolic alkalosis may be excessive administration of sodium bicarbonate; loss of acid-containing gastric secretions through vomiting, gastric suction, or gastric fistula; diuretic therapy resulting in loss of H+ into the urine, hyperadrenoccorticism, or potassium loss; movement of H+ intracellularly with potassium deficiency, which may also result from diuretic therapy; and rarely, H+ loss into the stool. Metabolic alkalosis is often associated with chronic respiratory disease. The treatment of metabolic alkalosis consists of determining and treating the cause. Examples may include increasing the blood volume or replacing potassium or chloride losses. Table 2 summarizes the blood gas alterations seen in various states.
Table 2. Classification of Blood Gases
Disturbance Respiratory acidosis Uncompensated Compensated Respiratory alkalosis Uncompensated Compensated Metabolic acidosis Uncompensated Compensated Metabolic alkalosis Uncompensated Compensated
pH
Pco2
HCO3
Bass excess/deficit
b7.35 Normal
z z
Normal z
Normal Excess N +2
N7.35 Normal
A A
Normal A
Normal Deficit N 2
b7.35 Normal
Normal A
A A
Deficit N 2 Deficit N 2
N7.45 Normal
Normal z
z z
Excess N +2 Excess N +2
W
a base deficit below 2 reflects a metabolic acidosis. A bicarbonate level higher than 26 milliequivalents per liter and/or a base excess of more than 2 reflects a metabolic alkalosis. Significant changes in bicarbonate levels are due to a metabolic process. The base excess/deficit value represents the number of milliequivalents per liter above or below the normal value. This value calculates the quantity of acid or alkali required to return the plasma to a normal pH under standard conditions.
Step One: Evaluate pH
Step Four: Compensated, Uncompensated, or Partially Compensated
Interpretation of Blood Gases hen interpreting arterial blood gases, a systematic approach should be used. The following case study will help illustrate this six-step process to interpret blood gases.
The first step is to evaluate the pH and determine the direction of the acid-base imbalance. A normal pH falls between 7.35–7.45. A pH higher than 7.45 equals alkalosis and a pH less than 7.35 equals acidosis. A normal pH does not necessarily indicate the absence of an acid base disturbance. If there is more than one acid-base imbalance in process, the pH identifies the process in control. Step Two: Evaluate the Respiratory Component The second step is to evaluate the ventilation. A Pco2 greater than 45 millimeters of mercury is related to ventilatory failure and respiratory acidosis. A Pco2 less than 35 millimeters of mercury is related to alveolar hyperventilation and respiratory alkalosis. Step Three: Evaluate the Metabolic Component The third step is to evaluate the metabolic process. A bicarbonate level below 22 milliequivalents per liter and/or
The fourth step in evaluating blood gases is to determine the primary and compensating disorder. Many times, two acid-base imbalances occur together. One is the primary imbalance, and the other is the body attempting to return the pH to normal. The pH is what determines the process in control. The body will not compensate to a pH above or below 7.4. It is important to remember that three stages of compensation can exist. First, look at the pH and assess whether it is normal, high, or low. With complete compensation, the pH is normal, although the original cause of the acid-base problem may be present. Both the Pco2 and HCO3 are abnormal. When compensation is complete, to identify the primary disorder, consider a pH between 7.35 and 7.40 indicative of primary acidosis and a pH between 7.41 and 7.45 indicative of primary alkalosis. During partial compensation, the pH is trying to approach normal, but is still abnormal, and the Pco2 and HCO3 are both abnormal. Noncompensation reflects an abnormal pH and an alteration of only Pco2 or HCO3.
Understanding Blood Gas Interpretation
Table 3. Normal Blood Gas Values
Step Five: Oxygenation The fifth step is to evaluate the oxygenation. This can only be accurately determined through an arterial blood gas sample. Assess whether the patient is hypoxemic and whether the hypoxemia is mild, moderate, or severe. Mild hypoxemia may be considered with a Pao 2 40 - 50 millimeters of mercury; moderate hypoxemia, 30- 40 millimeters of mercury; and severe hypoxemia, below 30 millimeters of mercury.
61
Source pH Po2 Pco2 HCO3 HCO3 (preterm) Bass excess/deficit Anion gap
Arterial
Capillary
7.35 -7.45 50 - 80 mm Hg 35 - 45 mm Hg 22 - 26 mEq/L 20 - 24 mEq/L 2 + 2 8 - 12 mEq/L
7.35 - 7.45 40 - 50 mm Hg 35 - 45 mm Hg 22 - 26 mEq/L 20 - 24 mEq/L 2 + 2 8 - 12 mEq/L
Step Six: Interpret The final step is to interpret the blood gas. Analyze the primary disorder, the oxygenation status, and the degree of compensation. For example, when analyzing a blood gas with a pH of 7.25, Pco2 of 65, HCO3 of 30, and Po2 of 35, the pH would indicate acidosis. Next, the Pco2 of 65 would indicate the respiratory component is elevated, indicating respiratory acidosis. The HCO3 of 30 would indicate that the metabolic component has changed in the alkalotic direction, indicating compensation. However, the pH is still outside the reference range, indicating only partial compensation. Therefore, this blood gas would be bpartially compensated respiratory acidosis with moderate hypoxemia.Q Table 2 shows changes in blood gas components in various states.
Case Study
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aby Brown (Fig 2) is a 24-week-gestation male infant who is 4 days old. His birth weight was 600 grams, and he is on a conventional ventilator. The ventilator settings are the following: peak inspiratory pressure, 19; positive end-expiratory pressure, 5; pressure support, 6;
rate, 30; and Fio2, 40%. His current weight is 510 grams, serum glucose is 180, and serum sodium is 151. This blood gas was drawn from an umbilical artery catheter. pH 7.17 Pco2, 45 millimeters of mercury HCO3, 17 milliequivalents per liter base deficit, 10 Pao2, 55 millimeters of mercury
Evaluate the state of his acid-base balance by going through the six-step process. Refer to Table 3 for normal values.
Step One Evaluate pH: A pH of 7.17 is low, which equals acidosis.
Step Two Evaluate the respiratory component: A Pco2 of 45 millimeters of mercury is in the reference range.
Step Three Evaluate the metabolic component: The HCO3 is 17 milliequivalents per liter, and base deficit is 10, which reflects a metabolic acidosis.
Step Four
Fig 2. 24 week gestational age male whose blood gas is: pH 7.17 pCO2 45 mm Hg HCO3 17 mEq/L BD-10 paO2 55 mm Hg.
Compensated, uncompensated, or partially compensated? There is no compensation because the Pco2 is within reference range. In order for compensation to take place, the Pco2 would decrease in an attempt to correct for the severe lack of base.
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Step Five Oxygenation: The oxygenation is within the reference range for an arterial blood gas.
References
Step Six Interpret. This gas would be considered an uncompensated metabolic acidosis with no hypoxemia. In this case, this is likely to be related to hyperglycemia (blood glucose level of 180 mg/dL) and dehydration as evidenced by the elevated sodium level (151 mEq/L). Treatment would focus on correction of the hyperglycemia and either a fluid bolus of normal saline or an increase in intravenous maintenance fluid volume. No respiratory changes would be required because the Pco2 is within normal limits.
Summary
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with the long-term outcome. It is important to interpret the blood gas correctly so that the need for and effect of treatment can be fully appreciated.
ith an understanding the acid base balance of the neonate, tissue oxygenation can be optimized along
1. In: Lynam L, ed. Acid-base basics. Neonatal Network: the Journal of Neonatal Nursing. 1990;9(1):67 - 68. 2. Coleman NJ, Houston L. Demystifying acid-base regulation. Retrieved December 19, 2003 from NetNurse Notes, MaNaInk Education Website: http://www.manaink.com/nurse/acidbase.html; 2002. 3. Porth CM. Pathophysiology. concepts of altered health states (4th ed). Philadelphia (PA), J.B. Lippincott Company; 1994. 4. Askin DF. Interpretation of neonatal blood gases, Part I: Physiology and acid–base homeostasis. Neonatal Netw. 1997;16(5):17 - 21. 5. Varughese M, Patole S, Shama A, Whitehall J. Permissive hypercapnia in neonates: the case of the good, the bad, and the ugly. Pediatr Pulmonol. 2002;33(1):56 - 64. 6. Thome UH, Carlo WA. Permissive hypercapnia. Semin Neonatol. 2002;7(5):409 - 419. 7. Kornhauser MS. Blood gas interpretation, In: Spitzer AR, ed. Intensive care of the fetus and neonate. (2nd ed). Philadelphia (PA), Elsevier; 2005:523 - 539. 8. In: Fanaroff AA, Martin RJ, eds. Neonatal-perinatal medicine. (6th ed). St. Louis (MO): Mosby Year Book; 1997. 9. Askin DF. Interpretation of neonatal blood gases, Part II: disorders of acid base balance. Neonatal Netw. 1997;16(6):23 - 29.
Understanding Blood Gas Interpretation By Beth Brown, RNC, MSN, and Bonnie Eilerman, RN, MSN, CNP
A
n arterial or capillary blood gas is a clinical assessment tool for determining an infant’s pulmonary and metabolic status. The pulmonary component of the blood gas yields information on ventilation and oxygenation. The metabolic component reflects potential for changes in enzyme function and nerve and muscle activity. Blood gases are the basis for diagnosis and management of infants with cardiorespiratory disease, metabolic disorders, and overall management in premature infants. By integrating acidbase physiology, blood gas interpretation skills, and clinical history, the neonatal intensive care unit staff can accurately assess an infant’s current condition and help take the appropriate steps to correct the imbalance and, therefore, improve outcomes. Acid-base balance refers to the complex mechanisms through which the body strives to achieve and maintain a homogenous internal environment. This environment is reflected in a serum pH of 7.35 to 7.45. An acid is a substance that can donate hydrogen ions (H+) to alkaline solutions to neutralize the effect of bases. A base is an alkaline substance that can combine with acids to accept hydrogen ions neutralizing the effect of the base.1 The body has many ways to achieve this environment, mainly through the use of buffer systems. The goal of the buffer systems is to regulate the H+ concentration in the body and, therefore, regulate the pH. This concentration must be kept as steady as possible because only slight changes in H+ from the normal value can cause significant alterations in all physiological processes. Delivery of oxygen to the cell, the cellular use of oxygen, and the hormonal regulation of metabolism are all affected by the pH of the body. There are three main body systems that help to regulate pH: the chemical buffer systems, the respiratory center, and renal control.
Buffer Systems
T From the Good Samaritan Hospital, Neonatal Intensive Care Unit, Cincinnati, OH. Address correspondences to Beth Brown, RNC, MSN, 1174 Kylemore Court, Dayton, OH 45459. n 2006 Elsevier Inc. All rights reserved. 1527-3369/06/0602-0130$10.00/0 doi:10.1053/j.nainr.2006.03.005
he chemical buffer systems include the carbonic acid-bicarbonate system, protein buffer system, and the phosphate buffer system. The carbonic acidbicarbonate system is a weak, yet fast buffer that occurs in the extracellular fluid. Carbon dioxide (CO2) and water are made from the oxidization of carbohydrates, fats and proteins. These combine to form carbonic acid. Carbonic acid then splits into hydrogen, an acid, and bicarbonate, a base. Bicarbonate, which is regenerated and stored in the kidneys, can also bind to any excessive amount of hydrogen, thereby reversing the equation and forming carbonic acid.2 This buffer system explains neonatal acidosis because of the immature kidneys of a preterm infant. These premature kidneys cannot hold on to bicarbonate, losing it into the urine. Therefore, there is less bicarbonate to Newborn and Infant Nursing Reviews, Vol 6, No 2 (June), 2006: pp 57 - 62
57
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bind with the excess hydrogen, and the blood becomes acidic. By use of the carbonic anhydrase equation below, one can see how this process moves in both directions. H2 O þ
CO2
water carbon dioxide
X
H2 CO3
carbonic acid
X
Hþ
hydrogen ion
þ
HCO 3
bicarbonate
The protein buffer system is the most powerful and plentiful buffering system using proteins of cells and plasma. The cell membrane is composed almost entirely of proteins and lipids.2 As the extracellular pH changes, the body adapts by diffusing hydrogen and bicarbonate in and out of the cell membranes by way of these proteins. This is a slow process, up to several hours and intracellular electrolytes such as sodium and potassium may be displaced as the hydrogen or bicarbonate enter the cell. Clinically, this may account for a degree of hypernatremia or hyperkalemia. Hemoglobin is part of the protein buffering system. When the body is acidotic, hemoglobin will act as a buffer. Therefore, the oxygen carrying capacity may be reduced.2 In addition, one of the implications of this buffering system is the displacement of intracellular electrolytes such as sodium and potassium when H+ enters the cell. The main components in the phosphate buffer system are monohydrogen phosphate (HPO4) and dihydrogen phosphate (H2PO4). When a strong acid is added to these two phosphates, only a weak acid is formed, and when a strong base is added also, only a weak base is formed. Phosphate acts predominantly as an intracellular and urinary buffer. Because phosphate is eliminated in the urine, this system is particularly important in buffering fluids in the kidney tubules.3 Respiratory regulation is primarily responsible for the elimination of volatile acids (carbon dioxide). The respiratory center (lungs) controls the pH by varying the amount of CO2, which is excreted by exhalation.2 This is referred to in the blood gas as the Pco2. The chemoreceptors in the brain will sense within minutes that the Pco2 is increasing and then will send messages to the respiratory center to accelerate the rate and depth of breathing. This way, the lungs can respond to a change in H+ concentration within minutes. The metabolic reaction between bicarbonate (HCO3) and H+ produces carbonic acid, which will then dissociate into water and CO2 (as described earlier; see carbonic anhydrase equation above). To prevent CO2 from accumulating and carbonic acid from forming again, leading to acidosis, the lungs will excrete the CO2. The carbonic anhydrase equation is catalyzed by the enzyme carbonic anhydrase. This reaction moves to the right when Pco2 levels are high and moves to the left when Pco2 levels are low.4 The renal system (kidneys) controls the pH by varying the rate of excretion of HCO3, the base that neutralizes
carbonic acid. The kidneys are the slowest physiologic regulators. They take hours to commence their work and may take up to several days to take effect, but they do have the most sustained response. The kidneys provide the most important route for the excretion and buffering of metabolic acids and are also responsible for maintaining the plasma levels of HCO3, the most important buffer of H+. The kidneys control pH balance by excreting either acidic urine or basic urine. The overall mechanism by which the kidneys control the excretion of H+ and the retention of bicarbonate occurs by four main mechanisms: excretion of H+, reabsorption of bicarbonate, production of bicarbonate, and formation of ammonia.2
Permissive Hypercapnia
A
lthough a normal level of Pco2 is 35–45 millimeters of mercury, in many situations, levels outside this are considered bacceptable.Q Mechanical ventilation and the resulting baro-/volutrauma on the lungs can highly contribute to the development of bronchopulmonary dysplasia. The major determinant of lung injury is tidal volume or the volume of air instilled into the lungs by a ventilator. This parameter is also the primary one that affects Pco2 levels. The higher the tidal volume is, the more the lungs are stretched and the more baro-/ volutrauma occurs. Permissive hypercapnia is a strategy that attempts to minimize this by allowing relatively high levels of Pco2, provided the pH does not fall below a minimal value (typically 7.20). This is accomplished by providing a low inspiratory volume and pressure and decreasing the extent of lung tissue stretch. The current trend is to wean the ventilator settings to achieve a Pco2 of 50–60 millimeters of mercury. Even higher Pco2 levels are tolerated in nonventilated, older infants with bronchopulmonary dysplasia (Pco2 65–70 millimeters of mercury). The concept that higher Pco2 levels are bsafeQ and bwell toleratedQ is based on limited data and needs to be studied further,5 although strong trends indicate the possibility of important benefits without increased adverse affects.6 The specific ideal, safe range for Pco2 levels in the neonatal population is still under debate.
Oxygenation
A
cid base balance also effects tissue oxygenation. The Oxygen Hemoglobin Dissociation Curve is a measure of the affinity that hemoglobin has for oxygen. Oxygen is carried in the blood by being dissolved in the plasma and attached to hemoglobin in the red blood cells. The concentration of oxygen in the arterial plasma is expressed as Pao2, whereas the concentration of oxygen on hemo-
Understanding Blood Gas Interpretation
59
With a left shift, there is an increased attraction between oxygen and hemoglobin. Therefore, hemoglobin picks up oxygen more easily and does not release it until a lower Pao2 level is reached. This can impede oxygen release to the tissues, but it facilitates the unloading of carbon dioxide and the uptake of oxygen in the lungs.4 Fetal hemoglobin has decreased 2.3 diphosphoglycerate (DPG) and has a high oxygen affinity causing a shift to the left. Fetal hemoglobin is the main hemoglobin that transports oxygen in the developing fetus during the last 7 months of pregnancy. This special hemoglobin has a higher affinity for oxygen, so it holds on to oxygen tighter. Once delivered, infants automatically turn off the production of hemoglobin F (fetal) and turn on the production of hemoglobin A (adult). It takes about 2 years for an infant to completely switch over to adult hemoglobin. Fig 1. Oxyhemoglobin disassociation curve can be shifted to the left by hypothermia, alkalosis, hypocarbia, or decreased 23 DPG. The curve can be shifted to the right by hyperthermia, acidosis, hypercarbia, or increased 2–3 DPG levels. This figure is reprinted from Comprehensive Neonatal Nursing, with permission from Elsevier Inc.
globin is expressed as percent saturation (SaO2) on the pulse oximetry monitor. When there is no oxygen on the hemoglobin, it is 0% saturated; when the hemoglobin is carrying as much oxygen as possible, it is 100% saturated. The desired level of oxyhemoglobin saturation in a normal healthy term infant is 90% –94% saturation.7 The oxyhemoglobin saturation (% sat or O2 sat) is the most valuable test for detecting hypoxemia. It is not a sensitive measure for high blood oxygen levels and provides no information regarding pH, carbon dioxide, or serum bicarbonate levels. When Pao2 reaches approximately 60 millimeters of mercury, the hemoglobin is almost completely saturated with oxygen, making the SaO2 nearly 100%.8 Therefore, if the SaO2 is more than approximately 94%, the Pao2 could be either acceptable (50 – 80 millimeters of mercury) or undesirably high (N80 millimeters of mercury). Cyanosis is generally noted only at a Pao2 of less than 40 millimeters of mercury in neonates.8 When an infant has received surfactant, for example, the oxygen saturation increases, and it is important to wean the Fio2 to maintain a saturation between 90% and 94% to prevent hyperoxygenation and the exposure to oxygen toxicity. When there is an increased affinity for oxygen, less oxygen is released at the tissue level. When there is a decreased affinity for oxygen, then more oxygen is released to the tissues. Factors that can shift the curve to the right include temperature, pH, and hemoglobin structure. The factors that shift the curve to the left include hypothermia, alkalemia, hypocapnia, and fetal hemoglobin. These factors increase the affinity of hemoglobin for oxygen (Fig 1).
Acid Base Imbalances
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espiratory acidosis occurs when carbon dioxide is not promptly vented by the lungs and the CO2 combines with water to form carbonic acid. This condition results in a buildup of CO2. A blood gas may exhibit a low pH, high Pco2 and a normal HCO3 (Table 1).9 Respiratory acidosis is due to a decrease in alveolar ventilation. The treatment consists of determining the cause and ensuring effective ventilation. Metabolic acidosis 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. This condition reflects a low pH, normal Pco2, and a low HCO3.9 The causes of metabolic acidosis consist of the overproduction of acids due to abnormal metabolism (inborn errors or anaerobic metabolism), the decreased excretion of acids due to impaired renal function, and the excessive loss of bicarbonate through the gastrointestinal tract (severe diarrhea). To determine treatment, determine the cause, consider a hypoxic event, and determine whether the condition is a metabolic vs mixed acidosis. Treatment will then include ensuring effective ventilation and the administration of volume and/or buffers such as sodium bicarbonate. Respiratory alkalosis occurs when CO2 is excreted by the lungs in excess of its production rate by the body. The level Table 1. Summary of Blood Gases
Respiratory acidosis Metabolic acidosis Respiratory alkalosis Metabolic alkalosis
pH
Pco2
HCO3
A7.35 A7.35 z7.45 z7.45
z Normal A Normal
Normal A Normal z
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of carbonic acid falls producing an excess amount of HCO3 in relation to the acid content. This condition reflects a high pH, low Pco2, and a normal HCO3.9 The cause of respiratory alkalosis is an increase in alveolar ventilation (may be associated with central nervous system disorders and birth asphyxia). The treatment consists of determining the cause and then decreasing minute ventilation. Metabolic alkalosis occurs whenever acid is excessively lost or alkali is excessively retained. The acid-base ratio of the body is altered. This condition reflects a high pH, normal Pco2, and a high HCO3.9 The cause of metabolic alkalosis may be excessive administration of sodium bicarbonate; loss of acid-containing gastric secretions through vomiting, gastric suction, or gastric fistula; diuretic therapy resulting in loss of H+ into the urine, hyperadrenoccorticism, or potassium loss; movement of H+ intracellularly with potassium deficiency, which may also result from diuretic therapy; and rarely, H+ loss into the stool. Metabolic alkalosis is often associated with chronic respiratory disease. The treatment of metabolic alkalosis consists of determining and treating the cause. Examples may include increasing the blood volume or replacing potassium or chloride losses. Table 2 summarizes the blood gas alterations seen in various states.
Table 2. Classification of Blood Gases
Disturbance Respiratory acidosis Uncompensated Compensated Respiratory alkalosis Uncompensated Compensated Metabolic acidosis Uncompensated Compensated Metabolic alkalosis Uncompensated Compensated
pH
Pco2
HCO3
Bass excess/deficit
b7.35 Normal
z z
Normal z
Normal Excess N +2
N7.35 Normal
A A
Normal A
Normal Deficit N 2
b7.35 Normal
Normal A
A A
Deficit N 2 Deficit N 2
N7.45 Normal
Normal z
z z
Excess N +2 Excess N +2
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a base deficit below 2 reflects a metabolic acidosis. A bicarbonate level higher than 26 milliequivalents per liter and/or a base excess of more than 2 reflects a metabolic alkalosis. Significant changes in bicarbonate levels are due to a metabolic process. The base excess/deficit value represents the number of milliequivalents per liter above or below the normal value. This value calculates the quantity of acid or alkali required to return the plasma to a normal pH under standard conditions.
Step One: Evaluate pH
Step Four: Compensated, Uncompensated, or Partially Compensated
Interpretation of Blood Gases hen interpreting arterial blood gases, a systematic approach should be used. The following case study will help illustrate this six-step process to interpret blood gases.
The first step is to evaluate the pH and determine the direction of the acid-base imbalance. A normal pH falls between 7.35–7.45. A pH higher than 7.45 equals alkalosis and a pH less than 7.35 equals acidosis. A normal pH does not necessarily indicate the absence of an acid base disturbance. If there is more than one acid-base imbalance in process, the pH identifies the process in control. Step Two: Evaluate the Respiratory Component The second step is to evaluate the ventilation. A Pco2 greater than 45 millimeters of mercury is related to ventilatory failure and respiratory acidosis. A Pco2 less than 35 millimeters of mercury is related to alveolar hyperventilation and respiratory alkalosis. Step Three: Evaluate the Metabolic Component The third step is to evaluate the metabolic process. A bicarbonate level below 22 milliequivalents per liter and/or
The fourth step in evaluating blood gases is to determine the primary and compensating disorder. Many times, two acid-base imbalances occur together. One is the primary imbalance, and the other is the body attempting to return the pH to normal. The pH is what determines the process in control. The body will not compensate to a pH above or below 7.4. It is important to remember that three stages of compensation can exist. First, look at the pH and assess whether it is normal, high, or low. With complete compensation, the pH is normal, although the original cause of the acid-base problem may be present. Both the Pco2 and HCO3 are abnormal. When compensation is complete, to identify the primary disorder, consider a pH between 7.35 and 7.40 indicative of primary acidosis and a pH between 7.41 and 7.45 indicative of primary alkalosis. During partial compensation, the pH is trying to approach normal, but is still abnormal, and the Pco2 and HCO3 are both abnormal. Noncompensation reflects an abnormal pH and an alteration of only Pco2 or HCO3.
Understanding Blood Gas Interpretation
Table 3. Normal Blood Gas Values
Step Five: Oxygenation The fifth step is to evaluate the oxygenation. This can only be accurately determined through an arterial blood gas sample. Assess whether the patient is hypoxemic and whether the hypoxemia is mild, moderate, or severe. Mild hypoxemia may be considered with a Pao 2 40 - 50 millimeters of mercury; moderate hypoxemia, 30- 40 millimeters of mercury; and severe hypoxemia, below 30 millimeters of mercury.
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Source pH Po2 Pco2 HCO3 HCO3 (preterm) Bass excess/deficit Anion gap
Arterial
Capillary
7.35 -7.45 50 - 80 mm Hg 35 - 45 mm Hg 22 - 26 mEq/L 20 - 24 mEq/L 2 + 2 8 - 12 mEq/L
7.35 - 7.45 40 - 50 mm Hg 35 - 45 mm Hg 22 - 26 mEq/L 20 - 24 mEq/L 2 + 2 8 - 12 mEq/L
Step Six: Interpret The final step is to interpret the blood gas. Analyze the primary disorder, the oxygenation status, and the degree of compensation. For example, when analyzing a blood gas with a pH of 7.25, Pco2 of 65, HCO3 of 30, and Po2 of 35, the pH would indicate acidosis. Next, the Pco2 of 65 would indicate the respiratory component is elevated, indicating respiratory acidosis. The HCO3 of 30 would indicate that the metabolic component has changed in the alkalotic direction, indicating compensation. However, the pH is still outside the reference range, indicating only partial compensation. Therefore, this blood gas would be bpartially compensated respiratory acidosis with moderate hypoxemia.Q Table 2 shows changes in blood gas components in various states.
Case Study
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aby Brown (Fig 2) is a 24-week-gestation male infant who is 4 days old. His birth weight was 600 grams, and he is on a conventional ventilator. The ventilator settings are the following: peak inspiratory pressure, 19; positive end-expiratory pressure, 5; pressure support, 6;
rate, 30; and Fio2, 40%. His current weight is 510 grams, serum glucose is 180, and serum sodium is 151. This blood gas was drawn from an umbilical artery catheter. pH 7.17 Pco2, 45 millimeters of mercury HCO3, 17 milliequivalents per liter base deficit, 10 Pao2, 55 millimeters of mercury
Evaluate the state of his acid-base balance by going through the six-step process. Refer to Table 3 for normal values.
Step One Evaluate pH: A pH of 7.17 is low, which equals acidosis.
Step Two Evaluate the respiratory component: A Pco2 of 45 millimeters of mercury is in the reference range.
Step Three Evaluate the metabolic component: The HCO3 is 17 milliequivalents per liter, and base deficit is 10, which reflects a metabolic acidosis.
Step Four
Fig 2. 24 week gestational age male whose blood gas is: pH 7.17 pCO2 45 mm Hg HCO3 17 mEq/L BD-10 paO2 55 mm Hg.
Compensated, uncompensated, or partially compensated? There is no compensation because the Pco2 is within reference range. In order for compensation to take place, the Pco2 would decrease in an attempt to correct for the severe lack of base.
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Step Five Oxygenation: The oxygenation is within the reference range for an arterial blood gas.
References
Step Six Interpret. This gas would be considered an uncompensated metabolic acidosis with no hypoxemia. In this case, this is likely to be related to hyperglycemia (blood glucose level of 180 mg/dL) and dehydration as evidenced by the elevated sodium level (151 mEq/L). Treatment would focus on correction of the hyperglycemia and either a fluid bolus of normal saline or an increase in intravenous maintenance fluid volume. No respiratory changes would be required because the Pco2 is within normal limits.
Summary
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with the long-term outcome. It is important to interpret the blood gas correctly so that the need for and effect of treatment can be fully appreciated.
ith an understanding the acid base balance of the neonate, tissue oxygenation can be optimized along
1. In: Lynam L, ed. Acid-base basics. Neonatal Network: the Journal of Neonatal Nursing. 1990;9(1):67 - 68. 2. Coleman NJ, Houston L. Demystifying acid-base regulation. Retrieved December 19, 2003 from NetNurse Notes, MaNaInk Education Website: http://www.manaink.com/nurse/acidbase.html; 2002. 3. Porth CM. Pathophysiology. concepts of altered health states (4th ed). Philadelphia (PA), J.B. Lippincott Company; 1994. 4. Askin DF. Interpretation of neonatal blood gases, Part I: Physiology and acid–base homeostasis. Neonatal Netw. 1997;16(5):17 - 21. 5. Varughese M, Patole S, Shama A, Whitehall J. Permissive hypercapnia in neonates: the case of the good, the bad, and the ugly. Pediatr Pulmonol. 2002;33(1):56 - 64. 6. Thome UH, Carlo WA. Permissive hypercapnia. Semin Neonatol. 2002;7(5):409 - 419. 7. Kornhauser MS. Blood gas interpretation, In: Spitzer AR, ed. Intensive care of the fetus and neonate. (2nd ed). Philadelphia (PA), Elsevier; 2005:523 - 539. 8. In: Fanaroff AA, Martin RJ, eds. Neonatal-perinatal medicine. (6th ed). St. Louis (MO): Mosby Year Book; 1997. 9. Askin DF. Interpretation of neonatal blood gases, Part II: disorders of acid base balance. Neonatal Netw. 1997;16(6):23 - 29.