YOU'RE WORKING in the ED when Jay Patel, 68, arrives complaining of pain in his left arm after falling from a ladder. Mr. Patel has a history of chronic obstructive pulmonary disease (COPD) and appears to be in respiratory distress.
The physical exam reveals an underweight man with a body mass index of 18. He has a barrel chest (increased anteroposterior diameter of the thorax), and he's using accessory muscles of respiration and pursed-lip breathing. His breath sounds are clear but diminished in all lung fields. His vital signs are temperature, 98.8° F; heart rate, 128 beats/minute; respirations, 28 breaths/minute; BP, 166/98 mm Hg. His SpO2 is 92% on room air.
After obtaining a left upper extremity X-ray, the ED physician diagnoses a displaced ulnar fracture requiring surgical repair. Meanwhile, you've obtained Mr. Patel's arterial blood gas (ABG) values: pH, 7.43; PaCO2, 52 mm Hg; PaO2, 70 mm Hg; HCO3-, 34 mEq/L; and SaO2, 91%. What do these values tell you about Mr. Patel's clinical status?
This article describes a step-by-step approach to interpreting ABG results and discusses how these results affect nursing interventions and medical treatments. As a refresher, let's review each of the values measured by ABG analysis.
Getting down to basics
An ABG analysis has five basic components:
* pH measures the blood's acidity or alkalinity.
* PaCO2 measures the partial pressure of carbon dioxide (CO2) dissolved in arterial blood.
* PaO2 measures the partial pressure of oxygen dissolved in arterial blood.
* HCO3- measures the concentration of bicarbonate ions.
* SaO2 measures the percentage of hemoglobin saturated with oxygen.
Here's what each one reveals about your patient's condition. (For normal test parameters, see ABGs in adults: What's normal?)
SaO2 and PaO2: An oxygenation review. About 97% of oxygen in the blood is carried by hemoglobin in the form of oxyhemoglobin (HbO2) in red blood cells (RBCs). This is measured as SaO2. Normal HbO2 saturation should be greater than 95%; if the value drops to 90% or less, immediately assess the patient and administer supplemental oxygen. The remaining 3% of oxygen is dissolved in blood and measured as PaO2.
The SaO2 is related to the patient's PaO2 level: As oxygen is dissolving into blood, it's also combining with hemoglobin. When PaO2 is high, hemoglobin quickly takes up oxygen molecules. An SaO2 of 100% indicates that hemoglobin is completely saturated.
Note that even when hemoglobin is 100% saturated, more oxygen can dissolve into the blood, so PaO2 can climb higher than normal if the patient receives supplemental oxygen. For example, in a young person with no pulmonary disease who's breathing 100% oxygen for a short period, PaO2 could reach 500 mm Hg.1
Table. ABGs in adult...Image Tools
The relationship between PaO2 and SaO2 is shown by the S-shaped HbO2 dissociation curve. Changes in certain parameters that occur in the body will cause the curve to shift to the left or right. (See Why does the HbO2 curve shift?)
* A shift to the left indicates hemoglobin's increased affinity for oxygen (inhibiting oxygen release to the cells). This can be caused by increased pH, decreased body temperature, or decreased PaCO2.
* A shift to the right indicates hemoglobin's decreased affinity for oxygen, allowing oxygen to move into cells more easily. This can be caused by decreased pH, increased temperature, and increased PaCO2.1
Hypoxemia is described as mild (PaO2, 60 to 79 mm Hg), moderate (PaO2, 40 to 59 mm Hg), or severe (PaO2, less than 40 mm Hg). Severe or prolonged hypoxemia leads to tissue hypoxia and anaerobic metabolism, altering the patient's acid-base status. Administering supplemental oxygen to a patient who's hypoxemic or hypoxic may prevent severe changes in acid-base status.
pH: Acid or base? The acidity or alkalinity of a solution is measured by its pH: The more hydrogen ions in a solution, the more acidic it is. The normal range for pH is narrow (7.35 to 7.45); below 6.8 or above 7.8, the body's metabolic processes fail and the patient dies. The pH of body fluids is regulated by three major mechanisms: intracellular and extracellular buffering systems; the lungs, which control the elimination of CO2; and the kidneys, which reabsorb HCO3- and eliminate hydrogen ion.2
PaCO2: A respiratory parameter. The PaCO2 measures the partial pressure that dissolved CO2 exerts in the plasma. It's directly related to the amount of CO2 being produced by the cells.
The PaCO2 is regulated by the lungs and can be used to determine whether an acid-base disturbance is respiratory in origin. This value is inversely related to the rate of alveolar ventilation, so a patient with bradypnea (abnormally decreased ventilatory rate) retains CO2. Increased ventilation reduces PaCO2, and decreased ventilation increases PaCO2. Generally speaking, a PaCO2 level below 35 mm Hg causes respiratory alkalosis, and a level above 45 mm Hg causes respiratory acidosis.1
Normally, the body can adjust the level of PaCO2 in a matter of minutes by increasing or decreasing respiratory rate or the volume of air that moves into and out of the lungs with each breath (tidal volume). Acute changes that increase PaCO2 may occur due to conditions that suddenly decrease ventilation and lead to respiratory acidosis (such as trauma, drug overdose, drowning, or airway obstruction). Acute changes that decrease PaCO2 may occur due to issues that suddenly increase ventilation and lead to respiratory alkalosis (such as anxiety, pain, or pulmonary embolism). Severe anemia tends to cause a more gradual increase in ventilation, resulting in respiratory alkalosis.3
HCO3-: Metabolic parameter. The bicarbonate ion (HCO3-) is the acid-base component regulated by the kidneys. Acting as one of the body's buffer systems, the kidneys retain or excrete the alkalotic bicarbonate ion as needed. You can use the HCO3- value to determine whether the source of an acid-base disturbance is respiratory or metabolic. Generally speaking, an HCO3- level below 22 mEq/L indicates metabolic acidosis; above 26 mEq/L indicates metabolic alkalosis.
Unlike the respiratory system, which can quickly adjust PaCO2 levels, the renal system needs much more time to alter HCO3- levels. In a person with normal renal function, HCO3- adjustments may take several hours. In someone who's older or who has impaired renal function, HCO3- adjustments may take several days. Low levels of HCO3- can be the result of starvation, diabetic ketoacidosis, or diarrhea resulting in metabolic acidosis. Renal failure is the most common cause of chronic metabolic acidosis.2 High levels of HCO3- can result from vomiting or removal of gastric secretions through prolonged nasogastric tube drainage.2
Compensation causes complications
Compensation is the body's attempt to maintain normal pH. The respiratory system controls the CO2 level, and the renal system controls the bicarbonate level. The body uses these two systems to oppose each other and maintain a normal pH. If one system changes in the acidic direction, the other will compensate in the alkalotic direction. For example, a patient who's breathing rapidly blows off too much CO2, reducing PaCO2 and increasing the pH of arterial blood (respiratory alkalosis). To compensate, the kidneys excrete more bicarbonate, which makes arterial blood more acidic.4
An uncompensated status indicates that one of the body systems (respiratory or renal) has made no attempt to compensate for the changing pH. (Often this is just a matter of time because uncompensated acid-base disturbances either resolve fairly quickly or trigger a compensatory response.) A partially compensated status indicates that the opposing body system is attempting to compensate but hasn't changed enough to bring the pH back to normal. In this case, the opposing body system value will be outside its normal range in the direction opposite to the problem.
A fully compensated status occurs when pH is within normal limits and values for the respiratory and metabolic components are outside their normal ranges but in opposite directions.
As CO2 levels in the blood increase, more hydrogen ions are generated and pH drops, resulting in respiratory acidosis. Here's a useful tip: If a patient has an acute rise in PaCO2 due to hypoventilation (acute respiratory acidosis), the HCO3- will increase about 1 mEq/L for every 10 mm Hg increase in PaCO2. If the patient has a condition that causes chronically high levels of PaCO2 (chronic respiratory acidosis), HCO3- will increase about 5 mEq/L for every 10 mm Hg increase in PaCO2. This is the body's way of compensating for acidosis and bringing the pH back into the normal range. ABG values for patients with COPD typically show fully compensated respiratory acidosis.5
Conversely, as CO2 decreases, fewer hydrogen ions are generated and pH increases, resulting in respiratory alkalosis. Increases in HCO3- in the blood take hydrogen ions out of circulation, resulting in metabolic alkalosis; decreases in HCO3- leave more hydrogen ions in circulation, resulting in metabolic acidosis.
Some patients have problems in both the pulmonary system and the renal system. This can lead to a combined respiratory and metabolic acidosis (ABG results show a low pH with a high PaCO2 and a low HCO3-), or a combined respiratory and metabolic alkalosis (ABG results show a high pH with a low PaCO2 and a high HCO3-).5,6
Put theory into practice
You can take a systematic approach to apply these principles to your practice. Suppose your patient's ABG results are as follows: pH, 7.52; PaCO2, 30 mm Hg; HCO3-, 24 mEq/L; PaO2, 89 mm Hg; and SaO2, 96%. You can see immediately that the pH is elevated, the PaCO2 is low, and the remaining values are within normal limits. How do you assess what these values tell you about the patient's condition? Follow these steps:
Step 1: Examine the PaO2 and the SaO2 levels to determine whether hypoxemia exists and intervene if necessary. In our example, both of these values are within normal limits, so the patient isn't hypoxemic. Continue to monitor the oxygenation status, and label the oxygenation status normal.
Step 2: Examine the pH and determine whether it indicates or tends toward acidosis or alkalosis. Note that a pH between 7.35 and 7.39 is considered normal but a little acidic; a pH between 7.41 and 7.45 is considered normal but a little alkalotic. In the example, the pH of 7.52 is definitely high, so label it alkalosis.
Step 3: Examine the PaCO2 and determine whether it indicates acidosis or alkalosis. In this example, the PaCO2 is low, so the respiratory component indicates alkalosis. Label the PaCO2 alkalosis.
Step 4: Examine the HCO3- and determine whether it indicates acidosis or alkalosis. In the example, this metabolic component is in the normal range so label the HCO3- normal.
Step 5: Identify the origin of the acid-base disturbance as respiratory or metabolic. Circle the acidosis or alkalosis that matches the label given to the pH. In this case, PaCO2 (the respiratory component) matches the pH (alkalosis), indicating respiratory alkalosis.
Step 6: Now determine whether the patient is in compensation. Is the pH within normal limits? Are both PaCO2 and HCO3- abnormal in opposition to each other, with one alkalotic and the other acidic? If you answered yes to both questions, the patient is fully compensated.
If pH isn't within normal limits, look at the value that didn't match the pH. This is the HCO3- in our example. It's within normal limits, so the patient is uncompensated. If this value had been outside the normal limits on the acidic side, the patient would be partially compensated because the pH was outside normal limits on the alkalotic side. If the HCO3- had been outside the normal limits on the alkalotic side, the patient could have a combined respiratory and metabolic alkalosis.
The distinction between partial and full compensation depends on the pH. If pH is within normal range due to the "balance" between PaCO2 and HCO3-, this is labeled as fully compensated. If pH is outside the normal range and both PaCO2 and HCO3- are also outside normal range but in opposition to each other (one alkalotic and the other acidic), the body is trying to compensate but hasn't yet succeeded and we have a partially compensated acid-base status.
Table. Test your ABG...Image Tools
Step 7: Put it all together: The patient has an uncompensated respiratory alkalosis with normal oxygenation. In this example of an acid-base status reflecting a respiratory alkalosis, nursing care would be directed at relieving the underlying cause. For a patient breathing spontaneously, this situation reflects an acute hyperventilation that could be caused by a number of issues, including hypoxemia, pain, anxiety, or fear. For someone receiving mechanical ventilation, this could be a situation in which the patient is being overventilated (perhaps by having a tidal volume or respiratory rate set too high).7
For more practice, see Test your ABG interpretation skills.
A case in point: Mr. Patel
Let's return to Mr. Patel, the patient we met at the beginning of this article. His ABG results from the ED were pH, 7.43; PaCO2, 52 mm Hg; PaO2, 70 mm Hg; HCO3-, 34 mEq/L; and SaO2, 91%.
As always, your interpretation of ABGs must take the patient's clinical status into account. Mr. Patel is most likely tachypneic and tachycardic due to his pain and anxiety. Knowing that he has a history of COPD, you suspect he has chronic respiratory acidosis or an elevated PaCO2 and an elevated HCO3-, which would result in a compensated state. His pH would be in the normal range but leaning a little toward an acidosis if he were stable and relatively healthy.
However, this isn't the case now: His pH is leaning into the alkalotic range. Using the original step-by-step approach, you interpret his condition as compensated metabolic alkalosis with mild hypoxemia. His pH is "alkalotic" with a high (or alkalotic) HCO3-, and a high (or "acidic") PaCO2.
Now the tough part...based on his HCO3- of 34 mEq/L and our useful tip earlier (5 mEq/L increase in HCO3- for every 10 mm Hg increase in PaCO2 for chronic respiratory acidosis), you'd expect a PaCO2 of 60 mm Hg. Responding to pain, his respiratory rate has increased and he's "blowing off" CO2. As the PaCO2 value moves down to 52 mm Hg, the pH moves to a higher level than he'd normally have. The correct interpretation of this patient's ABG profile is chronic respiratory acidosis complicated by alveolar hyperventilation due to pain.
Mr. Patel receives appropriate pain management and undergoes surgery later in the evening. After surgery, he receives oxygen therapy (2 L/minute via nasal cannula) and routine postoperative care. Note that for some COPD patients who have chronic hypercarbia (a high level of PaCO2), administration of excessive oxygen therapy can cause problems with hypoventilation, making the PaCO2 climb even higher. Although this is a rare occurrence, it should still be considered as a possible issue.3
The next day, a second ABG shows the following results: pH, 7.38; PaCO2, 61 mm Hg; PaO2, 82 mm Hg; HCO3-, 34 mEq/L; and SaO2, 93%. This is what Mr. Patel's usual ABG results should be: a fully compensated respiratory acidosis with corrected hypoxemia when receiving oxygen therapy. He feels fairly comfortable given the circumstances and is back to his usual baseline status, but he may need supplemental oxygen for home use if he remains hypoxemic on room air or has documented drops in oxygenation during activity.
Practice makes perfect
With practice and careful thought, you can improve your skill and accuracy at ABG interpretation. By adding your knowledge of your patient's clinical status to what's happening with his oxygenation, ventilation, and acid-base balance, you can intervene correctly and deliver better patient care.
Why does the HbO2 curve shift?1
The HbO2 curve shifts to the left or right when certain factors change–notably dissolved CO2 in the blood (PaCO2), body temperature, pH, or 2,3-bisphosphoglycerate (BPG, also called diphosphoglycerate, a substance in RBCs). The HbO2 curve shifts occur naturally in the body due to the relative values of PaCO2. When blood enters the pulmonary capillary system and reaches the alveoli, PaCO2 diffuses out of the blood into the alveoli. This creates a relatively low level of PaCO2 in the blood, which shifts the curve to the left and increases the affinity of hemoglobin for oxygen. Hemoglobin molecules quickly take up the oxygen as it diffuses out of the alveoli.
The other end of the oxygen transport system is in the capillary bed at the tissue level throughout the body. Here, the opposite circumstances occur. PaCO2 is being generated by cellular metabolism and moves out of the cells into the blood. This creates a relatively high level of PaCO2 in the blood, which shifts the curve to the right and decreases the affinity of hemoglobin for oxygen. Hemoglobin molecules quickly release the oxygen being carried so it can diffuse into cells to replenish their supply.
© 2010 Lippincott Williams & Wilkins, Inc.