Crit Care Nurse 2002 Jun; 22(3): 22-40
Cover Article
CE
Assessing Tissue Oxygenation
Barbara E. Berry, RN, PhD
Agnes Eugine Pinard, RN, BSN, MS/HSA
Barbara E. Berry is director of nursing at the Mailman Center for Child Development, Department of Pediatrics, School of Medicine, University of Miami, Miami, Fla.
Agnes Eugine Pinard is nursing project manager at the Mailman Center for Child Development, Department of Pediatrics, School of Medicine, University of Miami.
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This article has been designated for CE credit. A closed-book, multiple-choice examination follows this article, which tests your knowledge of the following objectives:
- Describe the correlation of hemoglobin concentration to tissue oxygenation
- Understand the role of laboratory assessment in evaluation of tissue oxygenation
- Recognize the relationship of acid-base balance to tissue oxygenation
To provide the comprehensive nursing care that is necessary and is expected by informed consumers, nurses need an expanded knowledge base. This need is especially apparent in hospitals, where the acuity of patients is high. Accurate assessment, prompt recognition, and proper management of adverse changes are vital components in the nursing care of patients with compromised functioning. Although physical examination is important, the need for understanding the principles of gas diffusion and laboratory assessment of tissue oxygenation, including interpretation of hemoglobin concentration, oxygen saturation, cardiac output, and acid-base balance (Table 1
), must not be overlooked.
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DIFFUSION OF GASES
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At sea level, atmospheric pressure is 760 mm Hg. The air we breathe is a mixture of gases containing 79% nitrogen, 21% oxygen, traces of carbon dioxide (approximately 0.04%), and other elements. The partial pressure of oxygen (PO2) can therefore be calculated by multiplying the percentage of oxygen by the atmospheric pressure4:
0.21 (oxygen) x 760 mm Hg = 159.6 mm Hg.
The partial pressure of carbon dioxide (PCO2) can be calculated in the same manner:
0.0004 (carbon dioxide) x 760 mm Hg = 0.3 mm Hg.
The concentrations of gases in alveolar air are not the same as the concentrations in atmospheric air, however, because alveolar air is only partially replaced by atmospheric air with each breath. As soon as atmospheric air enters the respiratory passages, it is exposed to dead space air and fluids that cover respiratory surfaces. Thus, oxygen reaches the alveoli at approximately 103 mm Hg (PAO2). Likewise, the carbon dioxide level in the alveoli is approximately 40 mm Hg (PACO2).4
According to the principles of diffusion, gas exposed to a liquid will dissolve in the liquid until equilibrium of the gaseous phase of the mixture is reached and will exert the same partial pressure in the gaseous phase of the liquid as it did in the gaseous mixture. Diffusion of gases in the lung illustrates this point. Alveolar oxygen and capillary blood are separated by a very thin alveolar membrane. Oxygen diffuses across this membrane until the partial pressure of the oxygen in capillary blood is the same as that in the alveoli (103 mm Hg). A small amount of blood from the right side of the heart that fails to pass through alveolar capillaries because of shunting mixes with the oxygenated blood going to the left side of the heart and slightly reduces the partial pressure of oxygen in the arterial blood (PaO2) to approximately 95 mm Hg.4
Because each gas is independent of the others in its ability to dissolve in a liquid, the principles of diffusion hold true for diffusion of carbon dioxide from the blood to the alveoli. That is, net diffusion occurs from areas of higher pressure to areas of lower pressure until equilibrium is reached. Blood from the right side of the heart contains carbon dioxide at a higher pressure (P
CO2, ~46 mm Hg) than that of alveoli (~40 mm Hg), so some carbon dioxide diffuses out of capillary blood into the alveoli, from which it is expired into the atmosphere, and the blood that is returned to the left side of the heart and into systemic circulation has a partial pressure (PaCO2) of approximately 40 mm Hg.4
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OXYGENATION
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Pulmonary ventilation is defined as the inspiration and expiration of air (gases).4 Ventilatory failure is defined as having a PaO2 of 50 mm Hg or less or a PaCO2 of 50 mm Hg or greater.1 Although ventilation is the only method of eliminating carbon dioxide, factors other than ventilation influence oxygenation. Oxygen deficiency or tissue hypoxia has many causes4 (Table 2).
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OXYGEN TRANSPORT IN THE BLOOD
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Hemoglobin transports almost all oxygen from the lungs to the tissues. Oxygen is transported in the blood in 2 forms: a negligible amount is dissolved in the plasma (~3% of total transported oxygen), and a considerably greater amount (97%) is bound to hemoglobin in red blood cells. The PaO2 determines how much oxygen is transported in each form.4
Oxygen Transport in the Plasma
Under normal conditions, 0.003 mL of oxygen can be dissolved in 100 mL of blood plasma for each 1 mm Hg of PaO2. 3,4 For example, 100 mL of blood plasma contains 0.3 mL of dissolved oxygen at a PaO2 of 100 mm Hg:
If PaO2 x 0.003 = milliliters of dissolved oxygen in 100 mL of plasma, then 100 x 0.003 = 0.3 mL of dissolved oxygen in 100 mL of plasma.
Oxygen Transport in Red Blood Cells
The amount of oxygen that can be delivered to the tissues also depends on the hemoglobin content of the blood. The normal range of hemoglobin in adults is 12 to 16 g per 100 mL (120–160 g/L) of blood, and each gram of hemoglobin can bind with approximately 1.34 mL of oxygen at full saturation.3 For example, approximately 20 mL of oxygen is transported in every 100 mL of blood when the hemoglobin content is 15 g, PaO2 is 100 mm Hg, and the hemoglobin is 100% saturated with oxygen:
If hemoglobin content (in grams per milliliter of blood) x 1.34 x oxygen saturation = milliliters of oxygen bound to hemoglobin per 100 mL of blood, then 15 x 1.34 x 1.00 = 20.1 mL of oxygen per 100 mL of blood.
However, oxygen transport can be reduced when either hemoglobin level or oxygen saturation is abnormal. For example, only 13.4 mL of oxygen is transported at a hemoglobin content of 10 g at the same PaO2 and oxygen saturation (PaO2 is 100 mm Hg, and the hemoglobin is 100% saturated with oxygen):
If hemoglobin content (grams per milliliter of blood) x 1.34 x oxygen saturation = milliliters of oxygen attached to hemoglobin per 100 mL of blood, then 10 x 1.34 x 1.00 = 13.4 mL of oxygen per 100 mL of blood.
Total Oxygen Content in the Blood
Total oxygen content in the blood can be dramatically reduced when hemoglobin content, PaO2, or oxygen saturation is abnormal. For example, consider the situation when oxygen saturation is 70%, PaO2 is 40 mm Hg, and hemoglobin is 12 g/100 mL of blood:
If 40 x 0.003 = 0.12 mL of oxygen in plasma, and 12 x 1.34 x 0.70 = 11.26 mL of oxygen in red blood cells, then total oxygen content = 11.38 mL of oxygen in 100 mL of blood.
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CARDIAC OUTPUT
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When tissue oxygenation is assessed, another important consideration is cardiac output, which ultimately determines the amount of oxygen delivered. At a hemoglobin level of 15 g/mL, a PaO2 of 100 mm Hg, and an oxygen saturation of 100%, 20 mL of oxygen is transported in 100 mL of blood, which is equivalent to 200 mL of oxygen per liter of blood. Normal (adult) cardiac output is 5 L/min,4 so approximately 1 L of oxygen can be delivered to the body tissues per minute (5 L/min x 200 mL of oxygen per liter of blood = 1000 mL or 1 L of oxygen delivered per minute). If the heart cannot pump enough blood (eg, ventricular failure, arrhythmias, reduced heart rate), the cardiac output and the amount of oxygen delivered to tissues are reduced. For example, if cardiac output is reduced by half, to 2.5 L/min, only 500 mL of oxygen will be delivered to the tissues per minute.
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ASSESSMENT OF TISSUE OXYGENATION
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Oxyhemoglobin Dissociation Curve
Exposing hemoglobin to oxygen tensions of 0 to 150 mm Hg results in an S-shaped curve known as the oxyhemoglobin dissociation curve (Figure 1). The equation that reproduces the oxyhemoglobin dissociation curve is calculated by most blood gas analyzers in clinical use.6 Normally, at a PaO2 of 27 mm Hg, hemoglobin is 50% saturated; at a PaO2 of 40 mm Hg, 75% saturated; at a PaO2 of 60 mm Hg, 90% saturated; at a PaO2 of 80 mm Hg, 95% saturated; and at a PaO2 of 97 mm Hg, 97% saturated1,3,7 (Figure 1).
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Figure 1 Oxyhemoglobin dissociation curve. With a normal hemoglobin level (~15 g/100 mL), a normal blood pH (~7.4), and a normal body temperature (~98.6°F/37°C), a PaO2 of 70 to 100 mm Hg is normal, a PaO2 of 45 to 70 mm Hg is relatively safe, and a PaO2 less than 45 mm Hg is dangerous.
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Tissue oxygenation and pulmonary oxygen uptake depend critically on the relationship demonstrated by the oxyhemoglobin dissociation curve. Although hemoglobin has a certain affinity for oxygen that allows blood to oxygenate tissue appropriately, various factors can alter this affinity and change the position of the oxyhemoglobin dissociation curve1,3,6 (Figure 2).
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Figure 2 Oxyhemoglobin dissociation curve with shifts. Shift to the left: higher oxygen saturation at any given PaO2, increased affinity of hemoglobin for oxygen, decreased release of oxygen to the tissues. Shift to the right: lower oxygen saturation at any given PaO2, decreased affinity of hemoglobin for oxygen, increased release of oxygen to the tissues.
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For instance, a shift of the curve to the right results in a decreased affinity of hemoglobin for oxygen. Although this decreased affinity increases the release of oxygen and is beneficial for tissue oxygenation when PaO2 is in a safe or normal range, a deficiency in oxygenation of arterial blood limits the amount of oxygen available to the tissues despite easier release of oxygen to the tissues when the PaO2 is less than 38 mm Hg.3,6 On the other hand, a shift to the left increases the capacity of hemoglobin to carry oxygen, but decreases unloading of oxygen to the tissues.1
A shift of the curve to the right or left depends on the acidity of the blood, carbon dioxide tension, body temperature, and concentration of 2,3-diphosphoglycerate (an organic phosphate in red blood cells that increases in level when anemia or chronic hypoxemia occurs). An increase in any of these factors will cause a shift of the curve to the right, and a decrease in any of these factors will result in a shift of the curve to the left.4
A shift to the right due to increased body temperature reflects increased cell metabolism, and a greater need for oxygen and is therefore adaptive. A shift to the right may also be compensatory in conditions of anemia and chronic hypoxemia.1 However, decreased levels of the enzymes that produce 2,3-diphosphoglycerate, a circumstance that may occur in blood that has been stored for transfusion, will shift the curve to the left and threaten the release of oxygen to the tissues.3 On the other hand, a shift of the curve to the left is adaptive in fetal blood, because the hemoglobin in fetal blood has a greater affinity for oxygen than does adult hemoglobin and therefore requires a lower tissue PO2 to release comparable amounts of oxygen molecules from hemoglobin.6
Oxygen Saturation
Oximetry is a method of measuring oxygen saturation. Pulse oximetry is based on measurement of the proportion of light transmitted by oxygenated forms of hemoglobin; a sensor is placed over a finger, toe, earlobe, or the bridge of the nose, and a numerical output is produced.3 The measured saturation is accurate only if the probe adequately detects and measures pulsatile blood flow. Factors that may influence accuracy include nail polish, low perfusion states (which may be the result of hypovolemia or hypothermia), and administration of peripheral vasoconstriction agents, which make it difficult to identify a pulse signal.8 Pulse oximetry is generally accurate only for oxygen saturations greater than 80%; therefore, arterial blood gas analysis is recommended for oxygen saturations less than 80%.8 Moreover, most clinicians consider an oxygen saturation of less than 90% significant and will not rely exclusively on pulse oximetry for measurement in such situations.3
Acid-Base Balance
Body fluids must maintain a normal acid-base balance in order for normal cellular function to sustain health and life. Acid-base balance can be described by measuring the pH (or acidity) of a substance on a scale that ranges from 1 to 14 (Figure 3).1,4 Normally, blood has a pH of 7.35 to 7.45. A pH value outside this range indicates a serious acid-base imbalance. The body has numerous compensatory mechanisms to correct an abnormal pH; however, if these mechanisms fail (Figure 4), cellular functions are impaired, and death will eventually result.1,2
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Figure 3 Acid-base balance. The hydrogen ion concentration of a solution is expressed as pH and indicates the acidity of the solution. The pH scale ranges from 1 to 14. As the concentration of hydrogen ions increases, the solution becomes more acidic, and the pH decreases. As the concentration of hydrogen ions decreases, the solution becomes more alkaline, and the pH increases. A neutral solution has a pH of 7.
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Figure 4 Plasma pH. Normal plasma is slightly alkaline, with a pH of approximately 7.35 to 7.45. When the pH deviates outside this range in either direction, signs and symptoms of acid-base imbalance will occur. Without compensatory mechanisms or intervention, cellular dysfunction and death may occur.
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Respiratory acid-base imbalances (acidosis or alkalosis) are triggered by respiratory disorders that result from inspiratory and/or expiratory dysfunction. Metabolic acid-base imbalances (acidosis or alkalosis) are triggered by metabolic disorders such as disorders of the gastrointestinal or renal system.2,9
Acidosis
Acidosis is the result of greater than normal amounts of acid or less than normal amounts of base (alkaline) in the blood (pH <7.35). Respiratory acidosis occurs with retention of excess carbonic acid (due to decreased expiration of carbon dioxide) and can be diagnosed on the basis of the increased PaCO2 in arterial blood gas sampling (Table 3). Metabolic acidosis occurs when body fluids contain an excessive amount of metabolic acids or a deficit of bases and can be diagnosed on the basis of the decreased bicarbonate level or base excess in arterial blood samples (Table 3).
Alkalosis
Alkalosis is the result of less than normal amounts of acid or greater than normal amounts of base (alkaline) in the blood (pH >7.45). Respiratory alkalosis occurs when excess carbonic acid is excreted (via increased rate and depth of expiration of carbon dioxide) and can be diagnosed on the basis of the decreased PaCO2 in arterial blood gas sampling (Table 3
). Metabolic alkalosis occurs when body fluids contain an excessive amount of bases or a deficit of acids and can be diagnosed on the basis of the increased bicarbonate level or base excess in arterial blood gas sampling (Table 3).
Compensatory Mechanisms
The ratio of bicarbonate to carbon dioxide is 20:1, and this ratio is normally maintained through compensatory mechanisms or chemical buffers present in the extracellular fluid, body cells, blood cells, and plasma. Buffer systems maintain acid-base balance in 2 ways: by correcting or altering the component responsible for the imbalance and by compensating through alterations in the component that is not primarily responsible for the imbalance. These buffer systems can act within a fraction of a second to prevent excessive changes in pH.2,9
Bicarbonate–Carbonic Acid Buffer System
The body’s major buffer system is the bicarbonatecarbonic acid compensatory mechanism. Normal blood pH is the result of a bicarbonate to carbon dioxide ratio of 20 to 1. The 20 in this ratio represents base or 24 mmol/L of bicarbonate. The 1 in this ratio represents acid or 1.2 mmol/L of carbonic acid. The 1 in this ratio may also represent a PaCO2 of 40 mm Hg, because carbon dioxide is a potential acid. That is, when carbon dioxide is dissolved in water, it becomes carbonic acid. Thus, when the level of carbon dioxide increases, the level of carbonic acid also increases, and when the level of carbon dioxide decreases, the level of carbonic acid also decreases. If the level of either bicarbonate or carbon dioxide is increased or decreased so that the 20:1 ratio is not maintained, acid-base imbalances occur.2
A ratio of less than 20:1 (20/1) indicates acidosis. A ratio of more than 20:1 indicates alkalosis. The diagnosis of acidosis or alkalosis can be verified by using the 20:1 formula. For example, for a patient with a pH of 7.22, a bicarbonate level of 21 mmol/L, and a PaCO2 of 55 mm Hg:
(Base) Given that the 20 in the 20:1 ratio represents 24 mmol/L bicarbonate, 21 mmol/L bicarbonate would be equivalent to a 17.5 mmol/L. First set up the simple proportion
and then cross-multiply to solve, (20 x 21)/24 = 420/24 = 17.5.
(Acid) If the 1 in the 20:1 ratio represents a PCO2 of 40 mm Hg, then a PCO2 of 55 mm Hg would be equivalent to 1.37 mm Hg. Again, set up the simple proportion
and cross-multiply to solve, (1 x 55)/40 = 55/40 = 1.37.
(Diagnosis) The ratio is less than 20:1 (17.5/1.37 = 12.8/1); therefore, the diagnosis is acidosis.
Respiratory Compensatory Mechanism
The respiratory center in the medulla is sensitive to concentrations of carbon dioxide and hydrogen ion in body fluids. Compensation by the respiratory center can occur rapidly (in minutes or seconds). When acidemia (decreased blood pH) occurs, the respiratory center in the medulla is stimulated. This stimulation results in increases in the rate and depth of respirations, thereby reducing the carbon dioxide (carbonic acid) level and increasing the pH of the blood. When alkalemia (increased blood pH) occurs, the respiratory center in the brain is inhibited. This inhibition results in decreases in the rate and depth of respirations, retention of carbon dioxide (carbonic acid), and decrease in the blood pH. The lungs compensate for both respiratory and metabolic imbalances. However, the lungs cannot compensate for acid-base disturbances when pulmonary dysfunction is severe. In these instances, the kidneys must provide compensation.2
Renal Compensatory Mechanism
Cells in the distal part of the renal tubules are sensitive to changes in the pH of the filtrate. When the pH is less than normal, hydrogen ions are excreted and bicarbonate is formed and retained. When the pH is greater than normal, hydrogen ions are conserved and base-forming ions are excreted. Renal compensation for imbalances is slow (hours to days). The kidneys cannot compensate for acid-base imbalances related to renal failure.2
Because total electrolyte levels must always be in electrochemical balance, electrolyte concentrations may change when acid-base imbalances occur. The primary electrolytes that are exchangeable and may be stimulated by acid-base imbalances to move in and out of intracellular and extra-cellular compartments are sodium, chloride, potassium, and bicarbonate (Table 4). Metabolic pH disturbances have a greater effect on electrolyte mechanisms than do respiratory pH disturbances.2,10
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CLINICAL STATES OF ACID-BASE IMBALANCE
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Clinical states of acid-base imbalance may be described as acidosis or alkalosis. Acidosis is the result of greater than normal concentrations of acid or less than normal concentrations of base in blood. Respiratory acidosis is caused by any condition that interferes with excretion of carbon dioxide by the lungs, and metabolic acidosis is caused by abnormal losses of bicarbonate or by accumulation of excess metabolic acids2,5,10 (Tables 5 and 6).
Alkalosis is the result of less than normal concentrations of acid or greater than normal concentrations of base in the blood. Respiratory alkalosis is caused by any condition that causes an increase in rate and depth of breathing, resulting in excessive elimination of carbon dioxide. Metabolic alkalosis is caused by any condition that causes loss of metabolic acids from the body or retention of bicarbonate2,5,10 (Tables 7 and 8).
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ANALYSIS OF ARTERIAL BLOOD GASES
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Analysis of arterial blood gas sampling (Figure 5 ) can be performed by following the 4 steps described in Table 9. Examples of arterial blood gas sampling with corresponding acid-base imbalances are given in Table 10. A practice test for interpreting results of arterial blood gas sampling is given in Table 11.
Assessing trends of arterial blood gas findings often provides more information relating to progress of the condition than does a single isolated arterial blood gas analysis. If compensation occurs, intervention is often unnecessary. Remember, treatment is considered for an imbalance only when the pH is abnormal. Be alert for abnormal PaO2, indicating hypoxia, and provide adequate supplemental oxygen.2,10 A case study is provided in Table 12 (page 40).
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Table 12 Case study: serial assessments, laboratory findings, results of arterial blood gas analysis, and interventions
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SUMMARY
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Although physical examination remains an important part of the nursing assessment, assessment of tissue oxygenation provides additional vital information. Nurses who are caring for patients with compromised functioning must have a basic understanding of the physiological relationships between oxygen saturation, cardiac output, and acid-base balance and must be able to plan nursing care based on this knowledge.
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Acknowledgments
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The authors thank Debbie Newland, RN, BSN, associate nurse manager of the pediatric intensive care unit, and Barry Gelman, MD, associate professor of clinical pediatrics at the University of Miami School of Medicine and attending physician in the pediatric intensive care unit, Jackson Memorial Hospital, Miami, Fla, for their consultation and assistance with this article.
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References
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- Shapiro BA, Peruzzi WT. Clinical Application of Blood Gases. 5th ed. St Louis, Mo: CV Mosby; 1994.
- Guyton A, Hall J. Textbook of Medical Physiology. 9th ed. Philadelphia, Pa: WB Saunders Co; 1996.
- Fischbach FT. Manual of Laboratory and Diagnostic Tests. 6th ed. Philadelphia, Pa: Lippincott; 1999.
- Lamb AB. Nunn’s Applied Respiratory Physiology. 5th ed. Oxford, England: Butterworth-Heinemann; 2000.
- Smeltzer SC, Bare BG, eds. Brunner and Suddarth’s Textbook of Medical-Surgical Nursing. Philadelphia, Pa: Lippincott; 2000.
- Pilbeam SP. Mechanical Ventilation: Physiology and Clinical Applications. 3rd ed. St Louis, Mo: CV Mosby; 1998.
- Halperin M, Goldstein M. Fluid, Electrolyte, and Acid-Base Physiology. 3rd ed. Philadelphia, Pa: WB Saunders Co; 1999.
- Murray J, Nadel J. Textbook of Respiratory Medicine. Vol 1. 2nd ed. Philadelphia, Pa: WB Saunders Co; 1994.
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DIFFUSION OF GASES
OXYGENATION
