ABG3. PaCO 2 HCO 3 O - SaO. lactate. electrolytes. hemoglobin ABG. arterial blood gas analysis. Interpreting and using the. mm Hg. hemoglobin.

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1 ABG hemoglobin SaO arterial blood gas electrolytes hemoglobin O 2 tate CO 2 HCO 3 O ABG3 mm Hg blood Use this 5step approach to help manage patients on mechanical ventilation. By Jin Xiong Lian, BSN, RN, CNS A HCO 3 blood gas mm Hg hemoglobin SaO 2 electrolytes Interpreting and using the arterial blood gas analysis An arterial blood gas (ABG) analysis can tell you about a patient s oxygenation, acidbase 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 fivestep approach to ABG 26 l Nursing2010CriticalCare l Volume 5, Number 3

2 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. 15 Physiology of ABGs The components of an ABG analysis are, SaO 2, hydrogen ion concentration (),, HCO 3, base excess, and serum levels of hemoglobin,, glucose, and electrolytes (sodium, potassium, calcium, and chloride). Because HCO 3 and base excess both yield similar information on the status of base (alkali), I ll only discuss HCO 3. The parameters most frequently used, SaO 2,,, HCO 3, and 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. Normal ABG values Normal values for these parameters vary among labs, but in general are Pao 2, 80 to 100 mm Hg Sao 2, 95% to 100%, 7.35 to 7.45 Paco 2, 35 to 45 mm Hg HCO 3, 22 to 26 meq/l, less than 2 mmol/l in critically ill patients. 1,2,69 Oxygenation: and SaO 2 Ninetyseven percent of oxygen in the blood is bound to hemoglobin, and this oxyhemoglobin, measured as SaO 2, 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 represents the amount of oxygen dissolved in arterial blood. For critically ill patients or patients with chronic obstructive pulmonary disease (COPD), an SaO 2 of 90% or 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 Sshaped oxyhemoglobin dissociation curve (see Oxyhemoglobin dissociation curve), which illustrates the relationship between SaO 2 and is the fundamental factor that determines SaO 2, or hemoglobin s affinity for oxygen. An increase in raises SaO 2 and decreased lowers the SaO 2 level. The oxyhemoglobin dissociation curve shows that a of at least 60 mm Hg is required to maintain an SaO 2 greater than 90%. Tissue hypoxia occurs when the is less than 60 mm Hg. 12,14,15 Hemoglobin s affinity for oxygen is also affected by the patient s,, body temperature, and level of 2,3bisphosphoglycerate (BPG, also called diphosphoglycerate, a substance in red blood cells). 14 Decreased (acidosis), increased, 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 (alkalosis), decreased, 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. 6,1217 So a patient with alkalosis and a left shift can be hypoxic, even with SaO 2 levels greater than 90%. 16 As you know, oxygen saturation can also be measured by pulse oximetry. But SpO 2 readings are influenced by many factors, including bright ambient May l Nursing2010CriticalCare l 27

3 Interpreting and using the arterial blood gas analysis 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, SpO 2 doesn t provide information about other variables, including,,, and hemoglobin. 4,10,13 Therefore, ABGs are often indicated for critically ill patients to ensure they receive prompt and appropriate care. Acidbase balance: A patient s reflects the concentration of hydrogen ions (H + ) in arterial blood. These two values have an inverse relationship: a low means more acid in the blood as the result of increased H + concentration. Conversely, lowered H + concentration leads to a higher as the blood becomes more alkaline. 4,6,11,14 The elimination and production of H + (acid) and HCO 3 (bicarbonate, an alkali) are controlled by the respiratory and metabolic systems. Three mechanisms work together to keep the within the normal range. Chemical buffer systems. The carbonic acidbicarbonate buffer system is found in extracellular fluids. Carbonic acid (H 2 CO 3 ) is a weak acid, which can dissociate into either water (H 2 O) and carbon dioxide (CO 2 ) or H + and HCO 3. 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 in the blood and intracellular fluids, phosphate also influences the acidity of urine in response to acidbase derangement. The phosphate buffer system plays a lesssignificant role than the other buffer systems in maintaining acidbase 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 acidbase balance, adjusting the amount of excretion and reabsorption of H + and HCO 3 as well as producing new HCO 3. When the blood is acidic, the kidneys excrete more H + and retain HCO 3. (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 acidbase balance is profound and sustainable. Oxyhemoglobin dissociation curve normal Oxygen saturation (%) Left shift (alkalosis) temperature 2,3BPG Right shift (acidosis) temperature 2,3BPG (mm Hg) 28 l Nursing2010CriticalCare l Volume 5, Number 3

4 Interpreting and using the arterial blood gas analysis Types of acidbase imbalances 12,23 HCO 3 Respiratory acidosis Uncompensated <7.35 >45 mm Hg Normal Partially compensated <7.35 >45 mm Hg >26 meq/l Fully compensated 7.35 to 7.39 >45 mm Hg >26 meq/l Metabolic acidosis Uncompensated <7.35 Normal <22 meq/l Partially compensated <7.35 <35 mm Hg <22 meq/l Fully compensated 7.35 to 7.39 <35 mm Hg <22 meq/l Respiratory alkalosis Uncompensated >7.45 <35 mm Hg Normal Partially compensated >7.45 <35 mm Hg <22 meq/l Fully compensated 7.41 to 7.45 <35 mm Hg <22 meq/l Metabolic alkalosis Uncompensated >7.45 Normal >26 meq/l Partially compensated >7.45 >45 mm Hg >26 meq/l Fully compensated 7.41 to 7.45 >45 mm Hg >26 meq/l Mixed respiratory and metabolic acidosis <7.35 >45 mm Hg <22 meq/l Mixed respiratory and metabolic alkalosis >7.45 <35 mm Hg >26 meq/l Pulmonary regulation. The respiratory system plays a significant role in regulating H + concentrations. CO 2, a waste product of metabolism, is eliminated via exhalation. The patient s respiratory rate and depth of respirations determine how much CO 2 is exhaled. The respiratory center in the brainstem can respond rapidly to changes by adjusting the respiratory rate and depth of breathing. Respiration: External respiration is the pulmonary gas exchange that involves the physiological processes of pulmonary ventilation and perfusion and diffusion of oxygen and CO 2 between the pulmonary capillaries and alveoli. Any disturbance in these processes will lead to hypoxemia and/or hypercapnia (CO 2 retention). 14,18 Internal respiration is the exchange of oxygen and CO 2 between tissue cells and capillaries. This process requires adequate tissue perfusion and a normal. 14,18 Causes of increased 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 You can estimate your patient s respiratory function by reviewing and values. An increase in and a decrease in and SaO 2 (hypoxemia) are commonly caused by respiratory failure or cardiovascular collapse. Respiratory acidosis is defined as a above 45 mm Hg due to hypoventilation and a below 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 below 35 mm Hg and 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 30 l Nursing2010CriticalCare l Volume 5, Number 3

5 Metabolic status: HCO 3 As mentioned earlier, the kidneys play a vital role in maintaining acidbase balance. The liver also produces HCO 3, 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 less than 7.35 and HCO 3 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 Metabolic alkalosis is defined as a greater than 7.45 and an HCO 3 greater than 26 meq/l. Causes include diuretics, corticosteroids, excessive vomiting, dehydration, Cushing syndrome, liver failure, and hypokalemia. 1,2,6,7,11,2325 Compensation When a patient has an acidbase 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, the patient s respiratory center is stimulated and the patient hyperventilates to blow off more CO 2 and raise the. 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 CO 2 to lower the. Respiratory compensation occurs within minutes. 6,11,25 On the other hand, respiratory acidosis triggers the kidneys to excrete more H + and elevate HCO 3 in an effort to maintain a nearnormal, and respiratory alkalosis will activate the metabolic system to retain H + and to lower serum HCO 3. Metabolic regulation takes several hours to days to affect the. 6,11,23,25 When these compensatory mechanisms restore a normal, we say the patient s acidbase 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 between 7.35 and 7.40 is considered normal acidic; a between 7.41 and 7.45 is considered normal alkalotic. So if the is below 7.4, the primary imbalance is acidosis. When the 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 and HCO 3 parameters. If the compensation mechanism fails to return the to a normal range, it s known as partially compensated, which is shown by three abnormal parameters (,, and HCO 3 ). One abnormality, either respiratory or metabolic disturbance, that moves the in the same direction toward acidosis or alkalosis is the primary cause. The other derangement that moves the to the opposite direction is the compensatory change. 2,7,11,12,25,26 When the and either or HCO 3 are abnormal, but the counterpart is normal, compensation hasn t occurred. This is often associated with an acute problem. Abnormalities of both and HCO 3 may indicate mixed respiratory and metabolic disorders, which can move the in the same or opposite directions. A combined derangement can lead to acidosis or alkalosis, or produce a normal. When both respiratory ( ) and metabolic (HCO 3 ) components move the in the same direction to cause acidbase 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 levels Some modern blood gas analyzers also provide levels. Hypermia can be caused by increased production, reduced clearance, or medications such as epinephrine, nitroprusside, or metformin. A mildtomoderate increase is defined as 2 to 4 mmol/l. Lactic acidosis is characterized by persistently elevated, 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 moreintense medical and nursing care is needed for patients with severe hypermia. 24,27,28 The most common cause of an acute elevation is shock (including septic, cardiogenic, and hemorrhagic). 8,24,27 Anaerobic metabolism from tissue hypoperfusion increases the production of acids, including lactic May l Nursing2010CriticalCare l 31

6 Interpreting and using the arterial blood gas analysis 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 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 levels and. 1,9,17,24,2732 A normal level generally implies that the patient has adequate tissue perfusion, although abnormal levels aren t necessarily the result of tissue hypoxia. Patients with increased BG PaCO arterial blood gas 2 mm Hg 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 during treatment suggested significant improvement in tissue perfusion and oxygenation. Monitoring 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 clearance is often caused by tissue hypoxia or organ dysfunction. Persistent elevations are associated with poor outcomes. 8,27,3234 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 and SaO 2 parameters of the ABG. Increasing the FiO 2 and using positive endexpiratory pressure (PEEP) are the key means SaO blood emoglobin O 2 electrolytes A normal level generally implies that the patient has adequate tissue perfusion. to improving oxygenation. However, administering an FiO 2 greater than 0.50 for more than 72 hours may cause oxygen toxicity. High levels of PEEP may cause alveolar overdistention, ventilatorinduced lung injury (VILI), and hemodynamic compromise. Once the patient is adequately oxygenated, the FiO 2 and PEEP should be reduced to O g minimize harm. Reduce the FiO 2 first if the patient is hemodynamically stable. If the patient is hypotensive despite adequate intravascular volume, reduce the PEEP first A person s minute ventilation (respiratory rate multiplied by tidal volume [V T ]) controls the elimination of CO 2 and, consequently, affects the levels of and. With volume control ventilation, the preset respiratory rate and V T 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 V T and, therefore, is commonly prescribed for synchronized intermittent mandatory ventilation (SIMV), pressure support ventilation, and other modes, to lower for patients who have spontaneous breaths. 17,3537 During an acute episode of respiratory distress, patients often need mechanical ventilation to improve oxygenation and ventilation. Later, hypoxia may be eliminated but abnormal levels and respiratory acidosis may persist. The appropriate intervention at this stage is to increase ventilatory support for minute ventilation, but wean down FiO 2 and/or PEEP. Increasing minute ventilation often is achieved by increasing preset V T, respiratory rate, or pressure support. The above adjustment will lower the patient s and raise the. 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 tate CO 2 HCO 3 mm 32 l Nursing2010CriticalCare l Volume 5, Number 3

7 To manage hypoxic patients without hypercapnia, the FiO 2 and/or PEEP are often increased to improve oxygenation. But ventilatory support in terms of minute ventilation wouldn t need to be increased 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 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 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 Steps to interpreting ABGs Follow this fivestep approach to interpreting your patient s ABGs. 1. Is the patient hypoxic? Look at the Pao 2 and Sao What is acidbase balance? Check the. 3. How is pulmonary ventilation? Look at the Paco What is the metabolic status? Review the HCO Is there any compensation or other abnormalities? What is the primary cause of acidbase imbalance and which derangement is the result of secondary (compensatory) change? Examine serum and electrolyte results; match Paco 2 and HCO 3 parameters with the. Using the above fivestep approach we can interpret ABGs easily in a systemic and logical way without confusion. failed to demonstrate such risk. 39,40,4246 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 and HCO 3 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 in opposite directions, resulting in a normal. Assess and monitor your patient, and treat the underlying causes of acidbase 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 FiO 2 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 fivestep approach (see Steps to interpreting ABGs) can help you interpret ABGs and manage your patient s condition. Putting theory into practice A 55yearold man with communityacquired pneumonia was admitted to the ICU for respiratory distress. He was alert, but dyspneic, with an SaO 2 of 87% on supplemental oxygen at 15 L/min via nonrebreather mask. You use the fivestep approach to interpret his admission ABGs: SaO 2 of 87% and of 56 mm Hg reveal hypoxemia May l Nursing2010CriticalCare l 33

8 Interpreting and using the arterial blood gas analysis of 7.26 confirms acidosis of 60 mm Hg indicates that his minute ventilation was inadequate, which lowered the HCO 3 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 FiO 2 of 0.90, pressure support BG PaCO arterial blood gas 2 mm Hg of 6 cm H 2 O, and PEEP of 10 cm H 2 O. Three hours later, you review his ABGs: of 84 mm Hg indicates adequate oxygenation of 7.34 is still acidotic of 53 mm Hg reflects less profound hypercapnia, but ventilatory support in terms of minute ventilation is still inadequate to normalize his and eliminate respiratory acidosis. HCO 3 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 toward acidosis. This was the primary cause of his acidbase imbalance. However, the metabolic process attempted to normalize the. 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 H 2 O. Two days later, his ventilator settings were FiO 2 down to 0.60, pressure support decreased to 8 cm SaO blood emoglobin O 2 electrolytes If a mechanically ventilated patient s BP drops rapidly after PEEP is increased, suspect dehydration. H 2 O, and PEEP continued at 10 cm H 2 O. His ABGs were, 7.38;, 49 mm Hg;, 85 mm Hg; HCO 3, 30 meq/l, and, 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 FiO O g 2 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 FiO 2 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 SaO 2 was 87% with oxygen at 12 L/min via nonrebreather mask. A chest Xray showed bilateral pulmonary edema. His ABGs at this point were, 7.39;, 44 mm Hg;, 57 mm Hg; HCO 3, 25 meq/l, and, 1.3 mmol/l. The ABGs showed no acidbase imbalance. Both and HCO 3 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. tate CO 2 HCO 3 mm Using values Let s look at a case scenario that demonstrates the value of levels in the ABG. A 42yearold 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 SaO 2 of 90%. He was oliguric. He was receiving I.V. infusions of propofol and morphine. You use the fivestep approach to analyze his ABGs: 34 l Nursing2010CriticalCare l Volume 5, Number 3

9 of 63 mm Hg and SaO 2 of 90% suggest hypoxia based on his age of 7.20 is consistent with acidosis of 52 mm Hg indicates inadequate pulmonary ventilation to blow off CO 2 HCO 3 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 toward acidosis, so the patient is diagnosed with a mixed respiratory and metabolic acidosis with hypoxia. The patient was mechanically ventilated on volume controlsimv mode with a rate of 14 breaths/min, V T of 550 ml, FiO 2 of 0.50, PEEP of 10 cm H 2 O, and pressure support of 8 cm H 2 O. 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: of 96 mm Hg indicates no hypoxia of 7.31 remains acidotic of 32 mm Hg reflects hyperventilation HCO 3 of 20 meq/l indicates a less profound metabolic disturbance toward acidosis 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 and metabolic process (as shown by the HCO 3 and values) traveled in the same dir ection, his acidbase imbalance is primarily caused by the metabolic alteration. The low 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 thirdspace 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, 7.39;, 33 mm Hg;, 99 mm Hg; HCO 3, 21 meq/l; and, 1.9 mmol/l, indicating a fully compensated metabolic acidosis. The dramatic normalization of and 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: of 93 mm Hg indicated he was welloxygenated of 7.30 was acidotic Elevated of 52 mm Hg indicated that his CO 2 elimination was inadequate HCO 3 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 controlsimv mode with a preset rate of 12, V T of 550 ml, PEEP of 10 cm H 2 O, pressure support of 8 cm H 2 O, and FiO 2 of Three hours later, his temperature was F (39.5 C) and ABGs were, 7.32;, 55 mm Hg;, 91 mm Hg; HCO 3, 25 meq/l; and, 1.0 mmol/l. The normal HCO 3 level suggested his metabolic compensation hadn t started. The patient had respiratory acidosis with worsening CO 2 retention, and his fever increased his CO 2 production. His ventilatory support was adequate in terms of oxygenation; but it was inadequate for ventilation: Minute ventilation needed to be increased to enhance CO 2 removal. With SIMV volume control ventilation, the set respiratory rate or V T (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 CO 2 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. Act quickly In a critical care setting, a patient s condition can change rapidly and dramatically. Using a fivestep approach to ABG interpretation can identify an acidbase disorder quickly and accurately so you May l Nursing2010CriticalCare l 35

10 Interpreting and using the arterial blood gas analysis 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. REFERENCES 1. Lynch F. Arterial blood gas analysis: implications for nursing. Paediatr Nurs. 2009;21(1): Simpson H. Interpretation of arterial blood gases: a clinical guide for nurses. Br J Nurs. 2004;13(9): Coggon JM. Arterial blood gas analysis. 1: Understanding ABG reports. Nurs Times. 2008;104(18): Allibone L, Nation N. A guide to regulation of blood gases: part one. Nurs Times. 2006;102(36): Roman M, Thimothee S, Vidal JE. Arterial blood gases. Medsurg Nurs. 2008;17(4): Pruitt WC, Jacobs M. Interpreting arterial blood gases: easy as ABC. Nursing. 2004;34(8): Allibone L, Nation N. A guide to regulation of blood gases: part two. Nurs Times. 2006;102(46): Levy B. Lactate and shock state: the metabolic view. Curr Opin Crit Care. 2006;12(4): Wilder D. The clinical utility of lactic acid testing with ABGs in the neonatal setting a case study. Neonatal Intensive Care. 2008;21(2): Metelli G. Respiratory assessment and ICP: a case study. Australas J Neurosci. 2001;14(1): Allen K. Fourstep method of interpreting arterial blood gas analysis. Nurs Times. 2005;101(1): Brown B, Eilerman B. Understanding blood gas interpretation. Newborn Infant Nurs Rev. 2006;6(2): Woodrow P. Arterial blood gas analysis. Nurs Stand. 2004; 18(21): Tortora G, Derrickson B. Principles of Anatomy and Physiology. 11th ed. Hoboken, NJ: John Wiley & Sons; Hamilton C, Steinlechner B, Gruber E, Simon P, Wollenek G. The oxygen dissociation curve: quantifying the shift. Perfusion. 2004;19(3): Elliott M, Tate R, Page K. Do clinicians know how to use pulse oximetry? A literature review and clinical implications. Aust Crit Care. 2006;19(4): Dooley J, Fegley A. Laboratory monitoring of mechanical ventilation. Crit Care Clin. 2007;23(2): Johnson KL. Diagnostic measures to evaluate oxygenation in critically ill adults: implications and limitations. AACN Clin Issues. 2004;15(4): Zwerneman K. Endtidal carbon dioxide monitoring: a VITAL sign worth watching. Crit Care Nurs Clin North Am. 2006;18(2): Wheeler AP, Bernard GR. Acute lung injury and the acute respiratory distress syndrome: a clinical review. Lancet. 2007; 369(9572): Frye AD. Acute lung injury and acute respiratory distress syndrome in the pediatric patient. Crit Care Nurs Clin North Am. 2005;17(4): Suratt BT, Parsons PE. Mechanisms of acute lung injury/ acute respiratory distress syndrome. Clin Chest Med. 2006;27(4): Isenhour JL, Slovis CM. When should you suspect a mixed acidbase disturbance? Arterial blood gas analysis: a 3step approach to acidbase disorder. J Respir Dis. 2008; 29(2): Charles JC, Heilman RL. Metabolic acidosis. Hosp Physician. 2005;41(3): Woodruff DW. Take these 6 easy steps to ABG analysis. Nurs made Incredibly Easy. 2006;4(1): Ruholl L. Arterial blood gases: analysis and nursing responses. Medsurg Nurs. 2006;15(6): McKenzie MS, Howell MD. Using to detect occult hypoperfusion in sepsis. Int J Intensive Care. 2009;16(1): Smith I, Kumar P, Molloy S, et al. Base excess and as prognostic indicators for patients admitted to intensive care. Intensive Care Med. 2001;27(1): Gorman D, Calhoun K, Carassco M, et al. Take a rapid treatment approach to cardiogenic shock. Nurs Crit Care. 2008;3(4): Wilder D. The clinical utility of lactic acid trending with ABGs in the critical care setting: a case study. Respir Ther. 2008;3(3): Lighthall GK, Pearl RG. Volume resuscitation in the critically ill: choosing the best solution: how do crystalloid solutions compare with colloids? J Crit Illness. 2003;18(6): Sennoun N, Montemont C, Gibot S, Lacolley P, Levy B. Comparative effects of early versus delayed use of norepinephrine in resuscitated endotoxic shock. Crit Care Med. 2007;35(7): Gasparovic H, Plestina S, Sutlic Z, et al. Pulmonary release following cardiopulmonary bypass. Eur J Cardiothorac Surg. 2007;32(6): Venkatesh B, Meacher R, Muller MJ, Morgan TJ, Fraser J. Monitoring tissue oxygenation during resuscitation of major burns. J Trauma. 2001;50(3): Lian JX. Know the facts of mechanical ventilation. Nurs Crit Care. 2008;3(5): Santanilla JI, Daniel B, Yeow M. Mechanical ventilation. Emerg Med Clin North Am. 2008;26(3): Spritzer CJ. Unraveling the mysteries of mechanical ventilation: a helpful stepbystep guide. J Emerg Nurs. 2003;29(1): Lian JX. Managing a severe acute asthma exacerbation. Nurs Crit Care.2009;4(2): Barreiro TJ, Gemmel DJ. Noninvasive ventilation. Crit Care Clin. 2007;23(2): Kaminski J, Kaplan PD. The role of noninvasive positive pressure ventilation in the emergency department. Top Emerg Med. 1999;21(4): Yeow M, Santanilla JI. Noninvasive positive pressure ventilation in the emergency department. Emerg Med Clin North Am. 2008;26(3): Pierce LNB. Modes of mechanical ventilation. In: Pierce LNB, ed. Management of the Mechanically Ventilated Patient. 2nd ed. St. Louis, MO. Elsevier Saunders; Stoltzfus S. The role of noninvasive ventilation: CPAP and Bi PAP in the treatment of congestive heart failure. Dimens Crit Care Nurs. 2006;25(2): Vital FM, Saconato H, Ladeira MT, et al. Noninvasive positive pressure ventilation (CPAP or bilevel NPPV) for cardiogenic pulmonary edema. Cochrane Database Syst Rev. 2008;3:CD Ho KM, Wong K. A comparison of continuous and bilevel positive airway pressure noninvasive ventilation in patients with acute cardiogenic pulmonary oedema: a metaanalysis. Crit Care (London, England). 2006;10(2):R Levitt MA. A prospective, randomized trial of bipap in severe acute congestive heart failure. J Emerg Med. 2001;21(4): Jin Xiong Lian is a clinical nurse specialist in the intensive care unit at Concord Repatriation General Hospital, a teaching hospital for the University of Sydney in Australia. 36 l Nursing2010CriticalCare l Volume 5, Number 3