45 Arterial Blood Gas Interpretation
Arterial blood gas (ABG) analysis plays a pivotal role in the management of critically ill patients. Although no randomized controlled study has ever been performed evaluating the benefit of ABG analysis in the intensive care unit (ICU), it is likely this technology stands alone as the diagnostic test which has had the greatest impact on the management of critically ill patients; this has likely been translated into improved outcomes. Prior to the 1960s, clinicians were unable to detect hypoxemia until clinical cyanosis developed. ABG analysis became available in the late 1950s when techniques developed by Clark, Stow and coworkers, and Severinghaus and Bradley permitted measurement of the partial pressures of oxygen (PaO2) and carbon dioxide (PaCO2) in arterial blood.1–3 The ABG remains the definitive method to diagnose, categorize, and quantitate respiratory failure. In addition, ABG analysis is the only clinically applicable method of assessing a patient’s acid-base status. ABGs are the most frequently ordered test in the ICU and have become essential to the management of critically ill patients.4 Indeed, a defining requirement of an ICU is that a clinical laboratory should be available on a 24-hour basis to provide blood gas analysis.5
ABGs are reported to be the most frequently performed test in the ICU.4 There are, however, no published guidelines and few clinical studies that provide guidance as to the indications for ABG sampling.6 It is likely that many ABGs are performed unnecessarily. Muakkassa and coworkers studied the relationship between the presence of an arterial line and ABG sampling.7 These authors demonstrated that patients with an arterial line had more ABGs drawn than those who did not, regardless of the value of the PaO2, PaCO2, the Acute Physiology and Chronic Health Evaluation (APACHE) II score, or the use of a ventilator. In that study, multivariate analysis demonstrated that the presence of an arterial line was the most powerful predictor of the number of ABGs drawn per patient independent of all other measures of the patient’s clinical status. Roberts and Ostryznuik demonstrated that with use of a protocol they were able to reduce the number of ABGs by 44%, with no negative effects on patient outcomes.4
The ubiquitous use of pulse oximetry in the ICU has made the need for frequent ABG sampling to monitor arterial oxygenation unnecessary. Furthermore (as discussed later), venous blood gas analysis can be used to estimate arterial pH and bicarbonate (HCO3−) but not arterial carbon dioxide tension (PaCO2). Previously, ABGs were drawn after every ventilator change and with each step of the weaning process; such an approach is no longer recommended.
The indications for ABG analysis should be guided by clinical circumstances. However, as a “general rule” all patients should have an ABG performed on admission to the ICU and/or following (10-15 minutes) endotracheal intubation. Patients with respiratory failure should have an ABG performed at least every 24 to 48 hours. Patients with type II respiratory failure (see definitions later in this chapter) will require more frequent ABG sampling than those with type I respiratory failure. Furthermore, patients with complex acid-base disorders and patients undergoing permissive hypoventilation will require more frequent ABG sampling.
ABG specimens may be obtained from an indwelling arterial catheter or by direct arterial puncture using a heparinized 1- to 5-mL syringe. Indwelling arterial catheters should generally not be placed for the sole purpose of ABG sampling, as they are associated with rare but serious complications. Arterial puncture is usually performed at the radial site. When a radial pulse is not palpable, the brachial or femoral arteries are suitable alternatives. Serious complications from arterial puncture are uncommon; the most common include pain and hematoma formation at the puncture site. Laceration of the artery (with bleeding), thrombosis, and aneurismal formation are rare but serious complications.8,9
ABG analysis is typically performed on whole blood. The partial pressure of oxygen (PaO2,), partial pressure of carbon dioxide (PaCO2), and pH are directly measured with standard electrodes and digital analyzers; oxygen saturation is calculated from standard O2 dissociation curves and may be directly measured with a co-oximeter. The bicarbonate (HCO3−) concentration is calculated using the Henderson-Hasselbalch equation:
where pKA is the negative logarithm of the dissociation constant of carbonic acid. The base excess is defined as the quantity of strong acid required to titrate blood to pH 7.40 with a PaCO2 of 40 mm Hg at 37°C. In practice, acid is not titrated as suggested but calculated using a variety of established formulae or normograms. The base excess thus “removes” the respiratory element of acid-base disturbance and identifies the metabolic contribution to interpret with pH and [H+]. The standard bicarbonate is broadly similar and is the calculated [HCO3−] at a PaCO2 of 40 mm Hg. Although the base excess and standard bicarbonate allow for a metabolic acidosis to be diagnosed, they provide few clues as to the pathophysiology or underlying diagnosis.
As with any diagnostic test, it is important that the specimen for an ABG measurement be collected and processed correctly and that quality assurance methods exist to ensure the accuracy of the measurements. Aside from interlaboratory variation, errors in calibration and electrode contamination with protein or other fluids may alter results. Heparin is usually added to the blood to prevent coagulation, and dilution with older liquid solutions previously caused spuriously low PaCO2. Sample preparation is important because air bubbles falsely elevate PaO2.
An ABG provides a rapid and accurate assessment of oxygenation, ventilation, and acid-base status. These three processes are closely interrelated with each other, and an alteration in one process will affect the other two. However, for the sake of simplicity and ease of understanding, each will be discussed separately.
The arterial CO2 content as reflected by arterial CO2 tension (PaCO2) at any given moment depends on the quantity of CO2 produced and its excretion through alveolar ventilation (VA) and can be expressed by the equation, PaCO2 ∼ CO2/VA. The alveolar ventilation is that portion of total ventilation that participates in gas exchange with pulmonary blood. If it is assumed that CO2 production is constant, then CO2 homeostasis can be simplified to 1/VA ∼ PaCO2. Thus PaCO2 becomes very useful for the assessment of alveolar ventilation. High PaCO2 (>45 mm Hg) indicates alveolar hypoventilation, and low PaCO2 (<35 mm Hg) implies alveolar hyperventilation.
The ultimate aim of the cardiorespiratory system is to provide adequate delivery of oxygen to the tissues. This is largely dependent upon cardiac output, hemoglobin (Hb) concentration, and Hb saturation. The PaO2 is a measure of the oxygen tension in plasma; while the dissolved fraction makes a negligible contribution to oxygen delivery (<2%), it is a major factor affecting Hb saturation. In turn, the PaO2 is dependent on the concentration of oxygen in the inspired air (FIO2), oxygen exchange in the lung (V/Q mismatching), and the venous oxygen saturation (SmvO2). The PaO2 must always be interpreted in conjunction with the FIO2 and age.
The PaO2 alone provides little information regarding the efficiency of oxygen loading into the pulmonary capillary blood. The PaO2 is determined largely by the FIO2 and the degree of intrapulmonary shunting (Figure 45-1). The PaO2 must therefore always be interpreted in conjunction with the FIO2. The PaO2 alone does not quantitate the degree of intrapulmonary shunt, which is required for assessing the severity of the underlying lung disease and in guiding the approach to oxygen therapy and respiratory support. There are various formulas for calculating the intrapulmonary shunt, including the classic “shunt equation,” which is the gold standard but requires mixed venous sampling through a pulmonary artery catheter, and the alveolar-arterial oxygen gradient equation (Table 45-1). Clinically the PaO2-to-FIO2 ratio (PaO2/FIO2) is most commonly used to quantitate the degree of ventilation/perfusion mismatching (V/Q). Since the normal PaO2 in an adult breathing room air with an FIO2 of 0.21 is 80 to 100 mm Hg, the normal value for PaO2/FIO2 is between 400 and 500 mm Hg. A PaO2/FIO2 ratio of less than 200 most often indicates a shunt of greater than 20%. A notable limitation of the PaO2/FIO2 is that it does not take into account changes in PaCO2 at a low FIO2, which tends to have a considerable effect on the ratio.
The normal arterial oxygen tension decreases with age (see Table 45-1). The normal PaO2 at sea level and breathing room air is approximately 85 to 90 mm Hg at the age of 60 and 80 to 85 mm Hg at the age of 80 years.
The PaO2 is primarily used for assessment of oxygenation status, since PaO2 accurately assesses arterial oxygenation from 30 to 200 mm Hg, whereas SaO2 is normally a reliable predictor of PaO2 only in the range of 30 to 60 mm Hg. However, oxygen saturation as measured by pulse oximetry (SpO2) or by ABG analysis (SaO2) is a better indicator of arterial oxygen content than PaO2, since approximately 98% of oxygen is carried in blood combined with Hb. Hypoxemia is defined as a PaO2 of less than 80 mm Hg at sea level in an adult patient breathing room air; the concomitant decrease in cell/tissue oxygen tension is known as hypoxia (or tissue hypoxia). The degree of hypoxia in patients with hypoxemia depends on the severity of the hypoxemia and the ability of the cardiovascular system to compensate. Hypoxia is unlikely in mild hypoxemia (PaO2 = 60-79 mm Hg). Moderate hypoxemia (PaO2 = 45-59 mm Hg) may be associated with hypoxia in patients with anemia or cardiovascular dysfunction. Hypoxia is almost always (but with a few exceptions) associated with severe hypoxemia (PaO2 <45 mm Hg). However, it must be recognized that the human body has an extraordinary capacity to adapt to hypoxemia. Indeed, patients with cyanotic heart disease do not have evidence of tissue hypoxia at rest. Most remarkably, at the top of Mount Everest (29,028 ft; 253 torr) and without supplemental oxygen, experienced mountain climbers have been reported to have a mean PaO2 of between 24 and 28 mm Hg in the absence of tissue hypoxia.12,13
The normal diet generates volatile acid (CO2), primarily from carbohydrate metabolism, and nonvolatile acid (hydrogen ion, H+) from protein metabolism. The aim of the body’s homeostatic system is to maintain pH within a narrow range, and pH homeostasis is accomplished through the interaction of the lungs, kidneys, and blood buffers. Alveolar ventilation allows for excretion of CO2. The kidneys must reclaim filtered bicarbonate (HCO3−), because any urinary loss leads to gain of H+. In addition, the kidney must excrete the daily acid load generated from dietary protein intake. Less than half of this acid load is excreted as titratable acids (i.e., phosphoric and sulfuric acids); the remaining acid load is excreted as ammonium. The blood pH is determined by the occurrence of these physiologic processes and by the buffer systems present in the body.
The history of assessing the acid-base equilibrium and associated disorders is intertwined with the evolution of the definition of an acid. In the 1950s, clinical chemists combined the Henderson-Hasselbalch equation and the Brønsted-Lowry definition of an acid to produce the current bicarbonate ion–centered approach to metabolic acid-base disorders.14 Stewart repackaged pre-1950 ideas of acid-base in the late 1970s, including the Van Slyke definition of an acid.15 Stewart also used laws of physical chemistry to produce a new acid-base approach.14 This approach, using the strong ion difference (SID) and the concentration of weak acids (particularly albumin), pushes bicarbonate into a minor role as an acid-base indicator rather than as an important mechanism:
The SID is not identical to anion gap (AG) and contains [lactate], although it does share a number of parameters, and the trends will often be close. The normal SID has not been well established, but the quoted range is 40 to 42 mEq/L.
As the SID approaches zero, anions “accumulate” and acidity increases. This approach provides a physicochemical model for “hyperchloremic acidosis” following 0.9% saline administration,21 and the systemic alkalosis of hypoalbuminemia (regarded as a weak acid).
Most clinicians use the bicarbonate ion–centered approach for the diagnosis and management of acid-base disorders; this approach is easier to understand and more practical. Furthermore, there are no clinical data to suggest that the Steward approach has any advantages over the classic (bicarbonate) approach.16 The Henderson-Hasselbalch equation describes the fixed interrelationship between PaCO2, pH, and HCO3− being described as pH = pKc log HCO3−/dissCO2. If all the constants are removed, the equation can be simplified to pH = HCO3−/PaCO2 (∼Kidney/Lung). The HCO3− is controlled mainly by the kidney and blood buffers. The lungs control the level of PaCO2 by regulating the level of volatile acid, carbonic acid, in the blood. Buffer systems can act within a fraction of a second to prevent excessive change in pH. The respiratory system takes about 1 to 15 minutes and kidneys many minutes to days to readjust H+ ion concentration.