In my previous article (May 2010), I described a five-step method to interpret arterial blood gas (ABG) results (see Steps to interpreting ABGs). This article presents three case studies that illustrate how ABG analysis can help you better manage a patient who's on mechanical ventilation, by focusing on improving oxygenation, pulmonary ventilation, and acid-base balance.
The ABG analysis gives you information on oxygenation, acid-base balance, pulmonary function, and metabolic status. A patient's oxygenation needs are reflected in the PaO2 and SaO2 parameters of the ABG. The pH indicates acid-base status, and PaCO2 reveals the adequacy of pulmonary ventilation based on the patient's condition.
Normal values for ABGs 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
- serum lactate, less than 2 mmol/L in critically ill patients.1–6
Let's look at three patient scenarios to see how ABG analysis can help the healthcare team titrate ventilatory support and assist in weaning. A case study on metabolic acidosis was presented in the previous article.
A 36-year-old male with acute promyelocytic leukemia (APL) associated with bleeding from disseminated intravascular coagulation is receiving multiple units of platelets, fresh frozen plasma, packed red blood cells, and cryoprecipitate, in addition to fluid replacement, I.V. furosemide, and hydrocortisone. Later in the day, he develops acute respiratory distress and noncardiogenic pulmonary edema. You analyze his ABGs on admission to the ICU:
- PaO2 of 67 mm Hg indicates mild hypoxemia
- pH of 7.50 indicates alkalosis
- PaCO2 of 48 mm Hg indicates hypoventilation, which caused CO2 retention and respiratory acidosis
- HCO3- of 35 mEq/L implies a metabolic disturbance toward alkalosis
- lactate of 1.0 mmol/L is normal.
His lab work results also demonstrate hypokalemia, which often is associated with metabolic alkalosis, but in this case hypokalemia may be the result of diuretic therapy (furosemide isn't a potassium-sparing diuretic) or hydrocortisone administration. Because his pH and HCO3- have moved in the same direction toward alkalosis, you suspect that his acid-base disorder originates from a metabolic derangement. The compensatory change involves the respiratory parameter (PaCO2), which attempts to move the pH in the opposite direction, toward acidosis.
The patient is diagnosed with a partially compensated metabolic alkalosis with mild hypoxemia.
However, the above ABGs also could be interpreted this way: Acute respiratory distress from pulmonary edema elevated the patient's PaCO2 and caused respiratory acidosis. Furosemide and hydrocortisone caused metabolic alkalosis. The final product of this dual pathology, or mixed respiratory and metabolic processes, is an alkalosis. Considering the patient's medical history and treatments, this interpretation is most likely.
Remember, mixed metabolic and respiratory disorders can move the pH in the same or opposite directions. The final result can be acidotic, alkalotic, or a normal pH. Because critically ill patients often have comorbities and are receiving multiple treatments, the interactions between respiratory and metabolic systems can be complicated. Remember to interpret ABGs in light of the patient's history, current medical conditions, and interventions.
The patient is endotracheally intubated and mechanically ventilated with spontaneous mode ventilation with positive end-expiratory pressure (PEEP) of 10 cm H2O and an FiO2 of 0.40. His spontaneous tidal volume varies from 450 to 550 mL. Because of adequate spontaneous tidal volume, he doesn't need pressure support, and minor hypercapnia is allowed to compensate for his metabolic alkalosis. He's also given I.V. maintenance fluids and cautious potassium replacement. His electrolytes are monitored regularly.
On the next day, his ABGs are PaO2, 77 mm Hg; pH, 7.44; PaCO2, 51 mm Hg; HCO3-, 32 mEq/L, and lactate, 1.6 mmol/L. His potassium level is 4.5 mEq/L. These results reflect a fully compensated metabolic alkalosis. (Permissive hypercapnia is allowed if the patient's pH and oxygenation can be kept within normal ranges.) After 5 days in the ICU, the patient is transferred to the oncology unit for further management of APL.
A 73-year-old male is admitted to the ICU because of an infective exacerbation of chronic obstructive pulmonary disease (COPD). He's alert and obeys commands, but he's hypotensive and oliguric. Before admission, his oral intake was poor for a few days. You analyze his admission ABGs:
- PaO2 of 64 mm Hg suggests mild hypoxemia
- pH of 7.29 is acidotic
- PaCO2 of 77 mm Hg reflects poor pulmonary ventilation that caused respiratory acidosis
- HCO3- of 34 mEq/L suggests a metabolic compensation for his COPD and respiratory acidosis
- lactate of 2.9 mmol/L may indicate compromised tissue perfusion.
The elevated PaCO2 moved the pH toward acidosis. Therefore, respiratory acidosis is the primarily cause of his acid-base disorder. In contrast, increased HCO3- moved the pH in the opposite direction (alkalosis) for compensation. His ABGs reflect a partially compensated respiratory acidosis with mild hypoxia. The patient is put on bilevel positive airway pressure (BiPAP) ventilation to reduce his CO2 retention and to correct the pH. He's also administered antibiotics for his respiratory infection. Because he has COPD, administering a high FiO2 may blunt his respiratory drive, and an SaO2 of 90% is acceptable.7,8 Considering his medical history and PaO2 of 64 mm Hg, the FiO2 is set at 0.30 despite suboptimal oxygenation.
The patient's hypotension and oliguria are most likely the result of dehydration secondary to illness and poor oral intake, so I.V. fluids are administered.
Five hours later, the patient's ABGs are PaO2, 74 mm Hg; pH, 7.36; PaCO2, 52 mm Hg; HCO3-, 33 mEq/L; and lactate, 1.7 mmol/L, indicating a fully compensated respiratory acidosis. Effective lactate clearance indicated his fluid replacement was appropriate. He was discharged from the ICU on the third day.
A 59-year-old female with a history of hepatic cirrhosis and liver failure due to alcohol abuse is complaining of right-sided chest pain and has a productive cough for blood-tinged sputum. She's short of breath, restless, and agitated. On ICU admission, her temperature is 103° F (39.4° C) and ascites is noted. She's diagnosed with right lower lobe pneumonia. Because of respiratory failure, she's endotracheally intubated and placed on a mechanical ventilator, spontaneous mode ventilation with an FiO2 of 0.30, PEEP of 10 cm H2O, and pressure support of 5 cm H2O. One hour later, you check her ABGs:
- PaO2 of 83 mm Hg indicates that with ventilatory support her oxygenation is adequate
- pH of 7.53 reflects alkalosis
- PaCO2 of 24 mm Hg is caused by hyperventilation
- HCO3- of 20 mEq/L suggests a metabolic derangement toward acidosis
- lactate of 2.4 mmol/L is most likely the result of liver failure, not tissue hypoxia.
These results are consistent with a partially compensated respiratory alkalosis. Pain is causing her to hyperventilate, lowering her PaCO2 and increasing pH. Her fever may be caused by pneumonia, alcohol withdrawal, or both. Hypertension, restlessness, and agitation can be signs of alcohol withdrawal syndrome.9 She has respiratory alkalosis due to hyperventilation and a metabolic process toward acidosis, which compensates her respiratory alkalosis.
Liver failure, the probable cause of her increased lactate level, reduces the production of proteins (buffers) and HCO3-(alkali). Lactate is catabolized in the liver, so hepatic dysfunction increases the lactate level, and can cause a metabolic acidosis.5,10–13
Based on her ABGs and medical history, the patient is diagnosed with a mixed respiratory alkalosis and metabolic acidosis. Her dual pathology leads to an alkalosis. In view of her hepatic dysfunction, abnormal lactate levels might be an ongoing issue.
Her respiratory rate was higher than 50 breaths/minute and tidal volume varied from 300 to 370 mL. Ascites limited diaphragmatic movement, which compromised her tidal volume. Consequently, the respiratory center increased her respiratory rate to compensate. Increasing pressure support will increase tidal volume and may reduce her tachypnea, but can also lead to worsening respiratory alkalosis and increase the risk of ventilator-induced lung injury (VILI). Therefore, only 5 cm H2O of pressure support is applied to overcome the resistance created by the ventilator circuit. Maintaining PaO2 between 55 and 80 mm Hg, and SaO2 between 88% and 95%, can help minimize VILI in patients with acute respiratory distress syndrome.14 Permissive hypercapnia and mild permissive hypoxemia may be acceptable for some critically ill patients, after a careful risk-benefit analysis.15
Avoid giving acetaminophen for fever control because of the patient's liver failure. After carefully considering the potential risks and benefits, the healthcare providers decide not to change the patient's ventilator settings and to continue I.V. antibiotics for the pneumonia and analgesics for her pain. The alcohol withdrawal syndrome was treated with benzodiazepines. Her fever was managed with noninvasive external cooling measures.
On the following morning, her temperature was 101° F (38.3° C) and her ABGs are PaO2, 81 mm Hg; pH, 7.44; PaCO2, 28 mm Hg; HCO3-, 19 mEq/L; and lactate, 2.3 mmol/L, indicating a fully compensated respiratory alkalosis, or that an acid-base balance has been established by her mixed respiratory alkalosis and metabolic acidosis.
By following the five-step method, and considering your patients' medical history, current conditions, and treatments, you can quickly and accurately interpret ABG results and provide appropriate care for mechanically ventilated patients.
Steps to interpreting ABGs
Follow this five-step approach to interpreting your patient's ABGs.
- Is the patient hypoxemic? Look at the PaO2 and SaO2.
- What is the acid-base balance? Check the pH.
- How is the patient's pulmonary ventilation? Look at the PaCO2.
- What is the patient's metabolic status? Review the HCO3-.
- Is there any compensation or other abnormalities? What is the primary cause of the acid-base imbalance and which derangement is the result of secondary (compensatory) change?
Examine the serum lactate and electrolyte results: match PaCO2 and HCO3- parameters with the pH.
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