An arterial blood gas (ABG) analysis can tell you about a patient's oxygenation, acid-base balance, pulmonary function, and metabolic status. This indispensable tool helps you assess and monitor critically ill patients in the ICU or other critical care settings.
As a critical care nurse, you're often the first healthcare provider who receives ABG results, and you'll monitor changes in the ABG results during the patient's stay in the ICU. In this article, I'll review the indications and physiology of ABGs, and introduce a five-step approach to ABG interpretation, focusing on how it can be used in managing mechanically ventilated patients.
When an ABG analysis is needed
The common indications for ABGs are:
- Respiratory compromise, which leads to hypoxia or diminished ventilation.
- Peri- or postcardiopulmonary arrest or collapse.
- Medical conditions that cause significant metabolic derangement, such as sepsis, diabetic ketoacidosis, renal failure, heart failure, toxic substance ingestion, drug overdose, trauma, or burns.
- Evaluating the effectiveness of therapies, monitoring the patient's clinical status, and determining treatment needs. For instance, clinicians often titrate oxygenation therapy, adjust the level of ventilator support, and make decisions about fluid and electrolyte therapy based on ABG results.
- During the perioperative phase of major surgeries, which includes the preoperative, intraoperative, and postoperative care of the patient.1-5
Physiology of ABGs
The components of an ABG analysis are PaO2, SaO2, hydrogen ion concentration (pH), PaCO2, HCO3-, base excess, and serum levels of hemoglobin, lactate, glucose, and electrolytes (sodium, potassium, calcium, and chloride). Because HCO3- and base excess both yield similar information on the status of base (alkali), I'll only discuss HCO3-. The parameters most frequently used—PaO2, SaO2, pH, PaCO2, HCO3-, and lactate—often are adequate in diagnosing and managing most clinical situations, so I'll focus on them.
See Normal ABG values for more details. Let's look more closely at each parameter.
Oxygenation: PaO2 and SaO2
Ninety-seven percent of oxygen in the blood is bound to hemoglobin, and this oxyhemoglobin, measured as SaO2, is a key means to transport oxygen to tissue cells.2,6,10 The remaining 3% of oxygen is dissolved in the blood, and exerts pressure on the plasma. The PaO2 represents the amount of oxygen dissolved in arterial blood. For critically ill patients or patients with chronic obstructive pulmonary disease (COPD), an SaO2 of 90% or PaO2 of 60 mm Hg may be acceptable.2,6,7,10,11
Each hemoglobin molecule can carry a maximum of four oxygen molecules. Hemoglobin's affinity for binding with oxygen is demonstrated by the S-shaped oxyhemoglobin dissociation curve (see Oxyhemoglobin dissociation curve), which illustrates the relationship between SaO2 and PaO2.12-15 PaO2 is the fundamental factor that determines SaO2, or hemoglobin's affinity for oxygen. An increase in PaO2 raises SaO2 and decreased PaO2 lowers the SaO2 level. The oxyhemoglobin dissociation curve shows that a PaO2 of at least 60 mm Hg is required to maintain an SaO2 greater than 90%. Tissue hypoxia occurs when the PaO2 is less than 60 mm Hg.12,14,15
Hemoglobin's affinity for oxygen is also affected by the patient's pH, PaCO2, body temperature, and level of 2,3-bisphosphoglycerate (BPG, also called diphosphoglycerate, a substance in red blood cells).14 Decreased pH (acidosis), increased PaCO2, elevated body temperature, or increased BPG will reduce hemoglobin's affinity for oxygen and cause the oxyhemoglobin dissociation curve to shift to the right. This loose bond means that hemoglobin has more difficulty binding with oxygen in pulmonary alveoli, but oxygen dissociates from hemoglobin more easily for tissue cells to use.
In contrast, increased pH (alkalosis), decreased PaCO2, decreased temperature, or reduced BPG will shift the oxyhemoglobin dissociation curve to the left, indicating an increase in hemoglobin's affinity for oxygen. As a result, oxygen is easily bound by hemoglobin in the lungs, but the tighter bond also means that tissue cells have more difficulty taking up oxygen from the blood.6,12-17 So a patient with alkalosis and a left shift can be hypoxic, even with SaO2 levels greater than 90%.16
As you know, oxygen saturation can also be measured by pulse oximetry. But SpO2 readings are influenced by many factors, including bright ambient light, decreased peripheral perfusion, vasoconstriction, hypothermia, shivering and motion artifact, hyperbilirubinemia, abnormal hemoglobins such as methemoglobinemia, cardiac dysrhythmias, and certain skin or nail conditions. In addition, SpO2 doesn't provide information about other variables, including pH, PaCO2, PaO2, and hemoglobin.4,10,13 Therefore, ABGs are often indicated for critically ill patients to ensure they receive prompt and appropriate care.
Acid-base balance: pH
A patient's pH reflects the concentration of hydrogen ions (H+) in arterial blood. These two values have an inverse relationship: a low pH means more acid in the blood as the result of increased H+ concentration. Conversely, lowered H+ concentration leads to a higher pH as the blood becomes more alkaline.4,6,11,14
The elimination and production of H+ (acid) and HCO3- (bicarbonate, an alkali) are controlled by the respiratory and metabolic systems. Three mechanisms work together to keep the pH within the normal range.
- Chemical buffer systems. The carbonic acid-bicarbonate buffer system is found in extracellular fluids. Carbonic acid (H2CO3) is a weak acid, which can dissociate into either water (H2O) and carbon dioxide (CO2) or H+ and HCO3-. Bicarbonate buffers can bind excess H+ or release them into plasma to prevent major changes in H+ concentration.
Proteins in plasma and cells, such as albumin and hemoglobin, can also absorb or release H+, and act as a protein buffer system. The phosphate buffer system predominantly stays in intracellular and renal tubular fluids. Apart from regulating the pH in the blood and intracellular fluids, phosphate also influences the acidity of urine in response to acid-base derangement. The phosphate buffer system plays a less-significant role than the other buffer systems in maintaining acid-base balance.1,4,12,14
All buffer systems respond to changes in H+ concentration rapidly, but their actions are temporary.
- Renal regulation. The kidneys are the principal organs in maintaining acid-base balance, adjusting the amount of excretion and reabsorption of H+ and HCO3- as well as producing new HCO3-. When the blood is acidic, the kidneys excrete more H+ and retain HCO3-. (The reverse is true if the blood is alkaline.) However, because it's a metabolic process, renal regulation occurs slowly, taking several hours to days. But if the patient's renal function is normal, renal regulation of acid-base balance is profound and sustainable.
- Pulmonary regulation. The respiratory system plays a significant role in regulating H+ concentrations. CO2, a waste product of metabolism, is eliminated via exhalation. The patient's respiratory rate and depth of respirations determine how much CO2 is exhaled. The respiratory center in the brainstem can respond rapidly to pH changes by adjusting the respiratory rate and depth of breathing.
External respiration is the pulmonary gas exchange that involves the physiological processes of pulmonary ventilation and perfusion and diffusion of oxygen and CO2 between the pulmonary capillaries and alveoli. Any disturbance in these processes will lead to hypoxemia and/or hypercapnia (CO2 retention).14,18
Internal respiration is the exchange of oxygen and CO2 between tissue cells and capillaries. This process requires adequate tissue perfusion and a normal pH.14,18
Causes of increased PaCO2 include increased metabolism (such as from fever), inadequate ventilation, diminished diffusion that often results from pulmonary consolidation or edema, and poor perfusion or an increased ventilation/perfusion (V/Q) mismatch.6,10,18,19 A V/Q mismatch is an imbalance between alveolar ventilation and perfusion. If ventilated alveoli don't receive adequate perfusion, blood gas exchange doesn't occur. On the other hand, semicollapsed or collapsed alveoli may be adequately perfused, but ventilation is inadequate or doesn't occur. V/Q mismatch and poor diffusion commonly occur in acute respiratory distress syndrome (ARDS), and are the major reasons for hypoxia and hypercapnia.20-22
You can estimate your patient's respiratory function by reviewing PaCO2 and PaO2 values. An increase in PaCO2 and a decrease in PaO2 and SaO2 (hypoxemia) are commonly caused by respiratory failure or cardiovascular collapse.
Respiratory acidosis is defined as a PaCO2 above 45 mm Hg due to hypoventilation and a pH below 7.35. Causes include respiratory infections, severe airflow obstruction (as in COPD or asthma), neuromuscular disorders such as multiple sclerosis, massive pulmonary edema, pneumothorax, central nervous system depression, spinal cord injury, and chest wall injury.
Respiratory alkalosis is defined as a PaCO2 below 35 mm Hg and pH more than 7.45 due to hyperventilation. Causes include pain, anxiety, early stages of pneumonia or pulmonary embolism, hypoxia, brainstem injury, severe anemia, and excessive mechanical ventilation.1,2,6,7,11,23
Metabolic status: HCO3-
As mentioned earlier, the kidneys play a vital role in maintaining acid-base balance. The liver also produces HCO3-, various proteins (buffers), and enzymes, so a patient's metabolic status is closely related to his kidney and liver function.2,6,11,13,14
Metabolic acidosis is defined as pH less than 7.35 and HCO3- less than 22 mEq/L. Causes include renal failure, diabetic ketoacidosis, lactic acidosis, sepsis, shock, diarrhea, drugs, and toxins such as ethylene glycol and methanol.20-22
Metabolic alkalosis is defined as a pH greater than 7.45 and an HCO3- greater than 26 mEq/L. Causes include diuretics, corticosteroids, excessive vomiting, dehydration, Cushing syndrome, liver failure, and hypokalemia.1,2,6,7,11,23-25
When a patient has an acid-base imbalance, the respiratory and metabolic systems try to correct the imbalances each has produced. For example, when increased metabolism or decreased renal excretion causes an increase in H+ ions that lowers pH, the patient's respiratory center is stimulated and the patient hyperventilates to blow off more CO2 and raise the pH. On the other hand, if the patient had metabolic alkalosis, the respiratory center would be suppressed and the decreased rate and depth of respiration would retain CO2 to lower the pH. Respiratory compensation occurs within minutes.6,11,25
On the other hand, respiratory acidosis triggers the kidneys to excrete more H+ and elevate HCO3- in an effort to maintain a near-normal pH, and respiratory alkalosis will activate the metabolic system to retain H+ and to lower serum HCO3-. Metabolic regulation takes several hours to days to affect the pH.6,11,23,25
When these compensatory mechanisms restore a normal pH, we say the patient's acid-base imbalance is fully compensated. This situation is often seen in patients with a chronic disorder—patients with COPD and respiratory acidosis are often compensated by a metabolic alkalosis.
Note that a pH between 7.35 and 7.40 is considered normal acidic; a pH between 7.41 and 7.45 is considered normal alkalotic. So if the pH is below 7.4, the primary imbalance is acidosis. When the pH is greater than 7.4, it indicates primary alkalosis. The compensation involves the opposite direction of respiratory and metabolic processes, and is demonstrated by abnormal PaCO2 and HCO3- parameters.
If the compensation mechanism fails to return the pH to a normal range, it's known as partially compensated, which is shown by three abnormal parameters (pH, PaCO2, and HCO3-). One abnormality, either respiratory or metabolic disturbance, that moves the pH in the same direction toward acidosis or alkalosis is the primary cause. The other derangement that moves the pH to the opposite direction is the compensatory change.2,7,11,12,25,26
When the pH and either PaCO2 or HCO3- are abnormal, but the counterpart is normal, compensation hasn't occurred. This is often associated with an acute problem. Abnormalities of both PaCO2 and HCO3- may indicate mixed respiratory and metabolic disorders, which can move the pH in the same or opposite directions. A combined derangement can lead to acidosis or alkalosis, or produce a normal pH.
When both respiratory (PaCO2) and metabolic (HCO3-) components move the pH in the same direction to cause acid-base disorders, we say mixed respiratory and metabolic acidosis or alkalosis. A mixed respiratory and metabolic acidosis is commonly seen in patients with cardiorespiratory arrest or collapse.7,11,12,23,25,26
Looking at lactate levels
Some modern blood gas analyzers also provide lactate levels. Hyperlactatemia can be caused by increased lactate production, reduced lactate clearance, or medications such as epinephrine, nitroprusside, or metformin. A mild-to-moderate increase is defined as 2 to 4 mmol/L. Lactic acidosis is characterized by persistently elevated lactate, typically greater than 5 mmol/L, and usually is accompanied by metabolic acidosis. Lactate levels greater than 4 mmol/L are associated with poor patient outcome and higher mortality, so more-intense medical and nursing care is needed for patients with severe hyperlactatemia.24,27,28
The most common cause of an acute lactate elevation is shock (including septic, cardiogenic, and hemorrhagic).8,24,27
Anaerobic metabolism from tissue hypoperfusion increases the production of acids, including lactic acid. Multiple trauma, burns, and septic or hemorrhagic shock lead to intravascular volume deficit or cardiovascular collapse. Consequently, patients often develop metabolic acidosis with acute lactate elevation (lactic acidosis). Early and aggressive fluid resuscitation is crucial to patient survival. Restoring tissue perfusion by fluid resuscitation, inotropic support, or other interventions often normalizes lactate levels and pH.1,9,17,24,27-32
A normal lactate level generally implies that the patient has adequate tissue perfusion, although abnormal levels aren't necessarily the result of tissue hypoxia. Patients with increased lactate levels need a thorough assessment and investigation.
Lactate has been used as one of the markers for systemic hypoperfusion or sepsis severity.27,33 For patients with septic shock or severe burn, the end point of fluid resuscitation isn't clearly established. Occult tissue hypoperfusion or covert shock may exist, despite normotension and adequate urine output.27,34
A rapid decrease in lactate during treatment suggested significant improvement in tissue perfusion and oxygenation. Monitoring lactate levels can evaluate the effectiveness and efficiency of resuscitative therapies. Lactate is also used as a marker of quality of care in sepsis management.27 However, a delay in lactate clearance is often caused by tissue hypoxia or organ dysfunction. Persistent lactate elevations are associated with poor outcomes.8,27,32-34
When your patient is on mechanical ventilation
Mechanical ventilation aims to improve oxygenation and ventilation. In a mechanically ventilated patient, ABGs can guide clinicians in titrating ventilatory support and weaning.17,35,36
The patient's oxygenation needs are reflected in the PaO2 and SaO2 parameters of the ABG. Increasing the FiO2 and using positive end-expiratory pressure (PEEP) are the key means to improving oxygenation. However, administering an FiO2 greater than 0.50 for more than 72 hours may cause oxygen toxicity. High levels of PEEP may cause alveolar overdistention, ventilator-induced lung injury (VILI), and hemodynamic compromise. Once the patient is adequately oxygenated, the FiO2 and PEEP should be reduced to minimize harm. Reduce the FiO2 first if the patient is hemodynamically stable. If the patient is hypotensive despite adequate intravascular volume, reduce the PEEP first.36-38
A person's minute ventilation (respiratory rate multiplied by tidal volume [VT]) controls the elimination of CO2 and, consequently, affects the levels of PaCO2 and pH. With volume control ventilation, the preset respiratory rate and VT determine minute ventilation. For pressure control ventilation, minute ventilation is influenced by the preset inspiratory pressure, respiratory rate, inspiratory time, respiratory resistance, and lung compliance. Pressure support ventilation increases spontaneous VT and, therefore, is commonly prescribed for synchronized intermittent mandatory ventilation (SIMV), pressure support ventilation, and other modes, to lower PaCO2 for patients who have spontaneous breaths.17,35-37
During an acute episode of respiratory distress, patients often need mechanical ventilation to improve oxygenation and ventilation. Later, hypoxia may be eliminated but abnormal PaCO2 levels and respiratory acidosis may persist. The appropriate intervention at this stage is to increase ventilatory support for minute ventilation, but wean down FiO2 and/or PEEP. Increasing minute ventilation often is achieved by increasing preset VT, respiratory rate, or pressure support. The above adjustment will lower the patient's PaCO2 and raise the pH. However, high levels of ventilatory support may increase the patient's risk of VILI. At times, some degree of hypercapnia and respiratory acidosis is allowed to manage severe ARDS or status asthmaticus in an effort to minimize VILI.21,38
To manage hypoxic patients without hypercapnia, the FiO2 and/or PEEP are often increased to improve oxygenation. But ventilatory support in terms of minute ventilation wouldn't need to be increased.35-37
Mechanical ventilation can be invasive or noninvasive. The two modes of noninvasive positive pressure ventilation (NPPV) are continuous positive airway pressure (CPAP) and bilevel positive airway pressure (BiPAP). With CPAP, continuous positive airway pressure is given to spontaneously breathing patients during inspiration and expiration via a tightly fitting nasal or facial mask. Like PEEP in invasive mechanical ventilation, CPAP increases alveolar recruitment and improves oxygenation. CPAP is indicated for hemodynamically stable patients with hypoxia and/or cardiogenic pulmonary edema, and can alleviate hypercapnia to some degree.39-42
In BiPAP, inspiratory and expiratory positive airway pressures are set separately. Expiratory pressure produces the same effect as PEEP, and the gap between inspiratory and expiratory pressure creates a pressure support for spontaneous breaths. BiPAP can improve a patient's oxygenation and ventilation quickly, and is indicated for hypercapnic patients with hypoxemia.39-43
NPPV can cause rhinorrhea, conjunctivitis, skin breakdown, and hypotension. Some clinicians also worry that BiPAP may increase the risk of acute myocardial infarction in patients with cardiogenic pulmonary edema, although other studies have failed to demonstrate such risk.39,40,42-46 Monitor your patient closely.
Prompt endotracheal intubation and invasive mechanical ventilation is indicated when a patient can't tolerate NPPV or has a contraindication to NPPV, such as decreased level of consciousness, excessive airway secretions, hemodynamic instability, life-threatening cardiac dysrhythmias, severe or worsening acidosis, or rapid clinical deterioration.39,40,42,43
ABG results should be interpreted in light of the patient's medical history, present health status, and medical therapies. When the patient's PaCO2 and HCO3- are both abnormal, this information will help you determine if another abnormality is the result of compensation or dual pathology. Remember that full compensation or mixed respiratory and metabolic disorders can move pH in opposite directions, resulting in a normal pH. Assess and monitor your patient, and treat the underlying causes of acid-base derangement as well as correcting abnormal parameters. Monitor your patient's response to changes in ventilator settings and inform the healthcare provider as necessary.
For instance, suppose your mechanically ventilated patient's ABGs show hypoxemia, although the patient's FiO2 is high. A higher level of PEEP is often prescribed for patients in this clinical scenario. But PEEP reduces venous return and cardiac output, so if the patient's BP drops rapidly after PEEP is increased, suspect dehydration—dehydrated patients are more sensitive to increased PEEP. After a fluid challenge or interventions to expand intravascular volume, dehydrated patients often tolerate increased PEEP.
Now let's look at two case scenarios to see how the five-step approach (see Steps to interpreting ABGs) can help you interpret ABGs and manage your patient's condition.
Putting theory into practice
A 55-year-old man with community-acquired pneumonia was admitted to the ICU for respiratory distress. He was alert, but dyspneic, with an SaO2 of 87% on supplemental oxygen at 15 L/min via nonrebreather mask. You use the five-step approach to interpret his admission ABGs:
- SaO2 of 87% and PaO2 of 56 mm Hg reveal hypoxemia
- pH of 7.26 confirms acidosis
- PaCO2 of 60 mm Hg indicates that his minute ventilation was inadequate, which lowered the pH
- HCO3- of 24 mEq/L indicates no change in metabolic status
- Lactate of 0.7 mmol/L implies that tissue perfusion is adequate.
The patient has an uncompensated respiratory acidosis with hypoxemia. Because the patient was alert and breathing spontaneously, BiPAP is ordered, and the patient's oxygen saturation immediately increases.
However, because of excessive airway secretions, the patient was endotracheally intubated 50 minutes later. Pressure support mode ventilation was used with an FiO2 of 0.90, pressure support of 6 cm H2O, and PEEP of 10 cm H2O. Three hours later, you review his ABGs:
- PaO2 of 84 mm Hg indicates adequate oxygenation
- pH of 7.34 is still acidotic
- PaCO2 of 53 mm Hg reflects less profound hypercapnia, but ventilatory support in terms of minute ventilation is still inadequate to normalize his PaCO2 and eliminate respiratory acidosis.
- HCO3- has risen to 28 mEq/L, suggesting the metabolic system is attempting to compensate for the respiratory acidosis.
The patient's respiratory compromise moved the pH toward acidosis. This was the primary cause of his acid-base imbalance. However, the metabolic process attempted to normalize the pH. The above abnormal HCO3 result was the compensatory change.
The patient was diagnosed with a partially compensated respiratory acidosis. Although his hypoxemia had been eliminated, the ventilatory support in terms of ventilation was still inadequate. Elevating pressure support is the key way to enhance minute ventilation for a spontaneously breathing patient, so pressure support was increased to 12 cm H2O.
Two days later, his ventilator settings were FiO2 down to 0.60, pressure support decreased to 8 cm H2O, and PEEP continued at 10 cm H2O. His ABGs were pH, 7.38; PaCO2, 49 mm Hg; PaO2, 85 mm Hg; HCO3-, 30 mEq/L, and lactate, 0.9 mmol/L, consistent with a fully compensated respiratory acidosis.
His heart rate was between 80 and 90 beats/min with BP of 130/70 mm Hg. The patient had been ventilated with an FiO2 greater than 0.60 for 2 days. Because he was hemodynamically stable, the priority in weaning him from mechanical ventilation at this stage would be to lower the FiO2 to minimize oxygen toxicity. On the other hand, if the patient's BP and urine output were low despite adequate fluid replacement, the healthcare provider might consider lowering the level of PEEP.
On the sixth day, the patient was extubated and placed on supplemental oxygen at 3 L/min via nasal cannula. Six hours later, his SaO2 was 87% with oxygen at 12 L/min via nonrebreather mask. A chest X-ray showed bilateral pulmonary edema. His ABGs at this point were pH, 7.39; PaCO2, 44 mm Hg; PaO2, 57 mm Hg; HCO3-, 25 mEq/L, and lactate, 1.3 mmol/L. The ABGs showed no acid-base imbalance. Both PaCO2 and HCO3- were within normal limits. But hypoxemia was the major problem again, so CPAP was indicated. CPAP can recruit the collapsed alveoli and small airways caused by pulmonary edema as well as improving oxygenation. The patient was discharged from the ICU after 2 more days.
Using lactate values
Let's look at a case scenario that demonstrates the value of lactate levels in the ABG.
A 42-year-old male patient had burns over 60% of his body surface area. On admission, his BP was 95/60 mm Hg with a heart rate of 132, respiratory rate of 8, temperature 96° F (35.5° C), and SaO2 of 90%. He was oliguric. He was receiving I.V. infusions of propofol and morphine. You use the five-step approach to analyze his ABGs:
- PaO2 of 63 mm Hg and SaO2 of 90% suggest hypoxia based on his age
- pH of 7.20 is consistent with acidosis
- PaCO2 of 52 mm Hg indicates inadequate pulmonary ventilation to blow off CO2
- HCO3- of 17 mEq/L suggests a metabolic alteration toward acidosis
- Lactate of 5.2 mmol/L indicates tissue hypoxia due to burn injury.
Both respiratory and metabolic disturbances moved the pH toward acidosis, so the patient is diagnosed with a mixed respiratory and metabolic acidosis with hypoxia. The patient was mechanically ventilated on volume control-SIMV mode with a rate of 14 breaths/min, VT of 550 mL, FiO2 of 0.50, PEEP of 10 cm H2O, and pressure support of 8 cm H2O.
Burn injury often causes significant loss of intravascular volume, as evidenced by the patient's low BP and reduced urine output. He was given intensive fluid resuscitation, and 4 hours later, his BP was 140/70 mm Hg and his urine output was greater than 0.8 mL/kg/hour. You again analyze his ABGs:
- PaO2 of 96 mm Hg indicates no hypoxia
- pH of 7.31 remains acidotic
- PaCO2 of 32 mm Hg reflects hyperventilation
- HCO3- of 20 mEq/L indicates a less profound metabolic disturbance toward acidosis
- lactate of 3.4 mmol/L implies that his tissue perfusion and oxygenation have improved significantly because of the aggressive fluid resuscitation and other interventions.
Because the pH and metabolic process (as shown by the HCO3- and lactate values) traveled in the same direction, his acid-base imbalance is primarily caused by the metabolic alteration. The low PaCO2 indicates that he hyperventilated to compensate for the metabolic derangement.
These ABGs show a partially compensated metabolic acidosis without hypoxemia. However, because of ongoing fluid loss and third-space fluid shift (a fluid shift common after burns), he'll still need intravascular volume expansion to maintain good tissue perfusion and adequate urine output. Twelve hours later, your patient's ABGs are pH, 7.39; PaCO2, 33 mm Hg; PaO2, 99 mm Hg; HCO3-, 21 mEq/L; and lactate, 1.9 mmol/L, indicating a fully compensated metabolic acidosis. The dramatic normalization of pH and lactate level suggests that the patient received prompt and appropriate treatment.
On the third day postadmission, the patient underwent debridement of necrotic tissue and a skin graft surgery. He was readmitted to ICU postoperatively, and you again analyze his ABGs:
- PaO2 of 93 mm Hg indicated he was well-oxygenated
- pH of 7.30 was acidotic
- Elevated PaCO2 of 52 mm Hg indicated that his CO2 elimination was inadequate
- HCO3- of 24 mEq/L implied no metabolic disturbance or compensation
- Lactate of 1.3 mmol/L was within the normal range, indicating he had adequate tissue perfusion during surgery.
He had an uncompensated respiratory acidosis. He was ventilated on volume control-SIMV mode with a preset rate of 12, VT of 550 mL, PEEP of 10 cm H2O, pressure support of 8 cm H2O, and FiO2 of 0.40.
Three hours later, his temperature was 103.2° F (39.5° C) and ABGs were pH, 7.32; PaCO2, 55 mm Hg; PaO2, 91 mm Hg; HCO3-, 25 mEq/L; and lactate, 1.0 mmol/L. The normal HCO3- level suggested his metabolic compensation hadn't started. The patient had respiratory acidosis with worsening CO2 retention, and his fever increased his CO2 production.
His ventilatory support was adequate in terms of oxygenation; but it was inadequate for ventilation: Minute ventilation needed to be increased to enhance CO2 removal. With SIMV volume control ventilation, the set respiratory rate or VT (or both) can be increased to enhance minute ventilation.
The patient's total respiratory rate was 12 breaths/min, which equaled the set SIMV rate. This rate suggested that due to sedation, the patient had not yet gained spontaneous breaths postoperatively. Increasing the level of pressure support wouldn't alter his minute ventilation or improve CO2 removal at this stage. Once the patient starts to trigger the ventilator, you may need to increase pressure support to help resolve his respiratory acidosis.
In a critical care setting, a patient's condition can change rapidly and dramatically. Using a five-step approach to ABG interpretation can identify an acid-base disorder quickly and accurately so you can intervene appropriately. If your patient is mechanically ventilated, good ABG interpretation skills can guide clinicians in adjusting the ventilator settings to meet the patient's needs.
Normal ABG values
Normal values for these parameters vary among labs, but in general are
- Pao2, 80 to 100 mm Hg
- Sao2, 95% to 100%
- pH, 7.35 to 7.45
- Paco2, 35 to 45 mm Hg
- HCO3-, 22 to 26 mEq/L
- lactate, less than 2 mmol/L in critically ill patients.1,2,6-9
Steps to interpreting ABGs
Follow this five-step approach to interpreting your patient's ABGs.
- Is the patient hypoxic? Look at the Pao2 and Sao2.
- What is acid-base balance? Check the pH.
- How is pulmonary ventilation? Look at the Paco2.
- What is the metabolic status? Review the HCO3-.
- Is there any compensation or other abnormalities? What is the primary cause of acid-base imbalance and which derangement is the result of secondary (compensatory) change?
Examine serum lactate and electrolyte results; match Paco2 and HCO3- parameters with the pH.
Using the above five-step approach we can interpret ABGs easily in a systemic and logical way without confusion.