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ABG use in the emergency department.

Arterial blood gases provide a means to evaluate several critical aspects of a patient's condition. Specifically, arterial blood gases have long been considered the gold standard for initial evaluation of a patient's acid-base, ventilation and oxygenation status.

In addition, current blood gas machines also measure electrolytes, hemoglobin concentration and abnormal hemoglobin species, lactate, glucose, Blood Urea Nitrogen (BUN) or creatinine. ABGs, in conjunction with these additional analytes, provide a comprehensive view of the patient at a single point in time. Thus, the clinician can make a comprehensive assessment of the patient and often a differential diagnosis of acid-base and oxygenation disturbances.

A Systematic Approach

Effective blood gas interpretation and application requires the clinician to have an organized and systematic approach. The method I suggest can be referred to as the "ABCs of Blood Gas Application." These so-called ABCs are acid-base balance, blood oxygenation and cellular oxygenation. A clinician should think through each of these areas discretely and completely.

Acid-base assessment also includes ventilation assessment as the PaCO2 is the primary indicator of respiratory acid-base disturbances and ventilation. Blood oxygenation looks at the effectiveness of the lungs in getting inspired oxygen into the pulmonary capillary blood. The simplest index of blood oxygenation is the P/F (PaO2/FIO2) ratio. Finally, cellular oxygenation assessment looks beyond the PaO2 or SpO2 (oxygen saturation as measured by pulse goniometry) in order to ensure that the tissues and cells are receiving adequate oxygenation.

Case Application

Our patient in this case is a 64-year-old male with shortness of breath in the emergency department, history and physical demonstrated a male with a barrel-shaped chest, forced expiration, a 50 pack per year history of smoking, mild disorientation, lethargy and a productive cough with yellow secretions.

Breath sounds revealed bilateral rhonchi suggesting moderate bilateral secretions. A chest X-ray showed lung hyper-aeration and flattened diaphragms.

Acid-Base Balance

Let us approach this blood gas using the ABCs described above. Classify the patient's acid-base status. Determine the most logical definitive diagnosis and suggest appropriate treatment.

The blood gas acid-base status can be classified as a partially compensated respiratory acidosis. Because metabolic compensation (bicarbonate retention) is nearly complete (ipH back to normal range), and the patient's history and physical strongly suggests COPD, this is likely a chronic hypercapneic condition.

Indeed, if one were to plot this data on an acid-base map, it would fall into the band for a simple chronic respiratory acidosis. In other words, the data are consistent with a simple chronic pulmonary problem and appropriate renal compensation. It is interesting to note that chronic pH is often not fully compensated back to the normal range despite maximal renal response.

Actually, most acid-base disturbances are compensated only approximately 50 percent of the way back to normal following a maximal compensatory response.

Patients with relatively severe COPD will manifest chronic CO2 retention. Classic thinking was that this was due to long term depression of the hypoxic drive. Others have demonstrated that the CO2 retention is due primarily to severe ventilation-per-fusion mismatch. Regardless of the exact mechanism that is responsible, the primary clinical concern remains the same. That is, administration of excessive oxygen therapy may further exacerbate the hypercapnia with concomitant worsening acidosis and potential deleterious effects.

It is also interesting to note that two conclusions could be reached by simply evaluating the electrolytes. First, as described above, the bicarbonate is elevated. If electrolytes were not drawn with the blood gases, bicarbonate is often reported as total CO2 from central laboratories. If this were the case, total CO2 would likewise be high because it is primarily comprised of bicarbonate.

Secondly, it can be noted that the chloride is low (normal CI is about 103 mEq/L). When bicarbonate is elevated, as in compensation for chronic CO2 retention, chloride must decrease in order to maintain electro-neutrality in the plasma. Thus, bicarbonate elevation, regardless of cause, is typically associated with low Chloride (hypochloremia).

Blood Oxygenation

Remember that blood oxygenation looks at the efficiency of oxygen uptake in the lungs via the PaO2/FIO2 (P/F) ratio. A normal P/F ratio is 0.4 to 0.5. An even easier way to look at this is to simply take the PaO2 and divide it by the percentage oxygen the patient is receiving.

For example, on room air, a normal PaO2 is near 100 mmHG and the percentage of oxygen inspired is roughly 20 percent. Dividing this percentage into the PaO2 gives us a score of 5. This would be equivalent to a P/F ratio of 500 but simplifies matters even further. Because PaO2 decreases with aging, and we allow some room for clinical decision making, a normal adult clinical PaO2 can be as low as 80 mmHg. In this case breathing room air would lead to an O2 score of 4. Thus a normal O2 score is 4 to 5.

The O2 score is the simplest and most expedient measure of intrapulmonary shunting. The O2 score is inversely related to pulmonary shunting. In other words, the higher the shunt and the more severe the problem with oxygen uptake into the pulmonary capillary blood, the lower the O2 score will be. The O2 score and P/F ratio may be somewhat misleading when PaCO2 is outside the normal range.

A high PaCO2 (hypoventilation) will lower the PaO2 without pathological increase in pulmonary shunting. This may lead to an overestimation of shunting when this simple index is used. Conversely, a low PaCO2 (hyperventilation) may slightly underestimate pulmonary shunting. Changes in cardiac output may likewise change PaO2 and the O2 score, particularly in the patient with a concurrent substantial pulmonary shunt.

In our patient, the PaO2 is measured as 42 mmHg. Because the patient is breathing room air, the P/F ratio is .21 or roughly an O2 score of 2. This O2 score is highly suggestive of increased pulmonary shunting. However, it is important to realize that the P/F ratio can be particularly misleading in hypercapnia. Therefore, in this case, a (PAO2-PaO2) difference would be a more useful method for evaluating pulmonary shunting. The normal PAO2-PaO2 on room air is less than 20 mm Hg.

The PAO2 can be calculated by the formula PAO2 = (PB -PH20) x FIO2 - 1.2 (PaCO2). In other words, the barometric pressure (assumed 760 mmHg at sea level) minus water vapor pressure (47 mmHg at BTPS) times the room air FIO2 (0.21) minus 1.2 x PaCO2 (65 mm Hg in this patient) results in a PAO2 of 72 mm Hg.

The PAO2-PaO2 difference is (72 mmHg - 42 mmHg), or 30 mmHg. Because the PAO2-PaO2 exceeds the normal 20 mmHg, increased physiological shunting is also present. Therefore, this patient's hypoxemia is due to a combination of hypoventilation and increased pulmonary shunting. Increased pulmonary shunting would likely be due to COPD possibly worsened by the acute exacerbation.

The mild fever and adventitious breath sounds suggest a potential pneumonia superimposed on the COPD. The patient should also be evaluated for leukocytosis and possibly a sputum culture. Certainly the clinical picture presented suggests an aggressive approach to secretion clearance and bronchial hygiene. Antibiotics may be beneficial over the short run.

A PaO2 of 42 mmHg and a SaO2 of 72 percent suggests severe hypoxemia, which is potentially life threatening. Therefore oxygen therapy is certainly indicated. Despite the relatively severe degree of hypoxemia, the patient should be treated with low-flow oxygen therapy.

One study suggested that PaO2 typically increases about 3 mmHg for each 1-percent increase in FIO2. The American College of Chest Physicians also suggests a target PaO2 of 60 mmHg in COPD.

This PaO2 should provide an SaO2 near 90 percent without the potential adverse effects of worsening hypercapnia. Based on the assumption that a normal breathing individual will receive an FIO2 of near 0.28 on a 2 L/min nasal cannula, this would be a logical starting point. Of course the flow rate could be titrated to a satisfactory pulse oximetry reading as well.

Despite the substantial hypercapnia (PaCO2 of 65 mmHg), mechanical ventilation is not indicated due to the relatively normal pH. Low doses of oxygen have been shown to be effective in relieving hypoxemia in many of these patients while avoiding potential adverse consequences of mechanical ventilation in this population.

Mechanical ventilation in COPD has been associated with further compromise of the airway, ventilatory dependence and difficulty weaning. These patients can also be challenging to ventilate with their breathing patterns, potential over distention and pneumothorax, and perplexing PCO2 targets. Therefore, mechanical ventilation should be used only as a last resort when further deterioration occurs in PaCO2, pH or level of consciousness. Indeed, if some form of ventilatory assistance is required, it is probably best to proceed with noninvasive ventilation first.

In severe hypoxemia (PaO2 < 45 mmHg), it is likely that the ability of the cardiopulmonary system to compensate for the severity of the hypoxemia will be exceeded. So it is common to generally consider severe hypoxemia to be associated with life-threatening cellular hypoxia.

Because our patient has only moderate hypoxemia and an intact cardiopulmonary system, it is unlike that he is hypoxic. Furthermore, individuals with chronic hypoxemia are less likely to be hypoxic than those with acute hypoxemia.

Overall Assessment and Intervention

This patient appears to be suffering from an acute exacerbation of COPD due to the accumulation of secretions and possibly pneumonia. The elevated alveolar-arterial oxygen difference demonstrates increased physiological shunting superimposed on chronic hypoventilation.

Aggressive bronchial hygiene and oxygen therapy are indicated. The target PaO2 should be approximately 60 mmHg to avoid cellular hypoxia,

excessive work of breathing and worsening hypercapnia. Narcotics and depressants should also be avoided even if this patient appears anxious because they may be associated with worsening hypercapnia in this population.

SaO2 72%
pH 7.33
PaCO2 65 mm Hg
PaO2 42 mm Hg
[HCO3] 33 mEq/L

B/P 1 38/92 mm Hg
RR 32/min
HR 115/min
Temp 380C

Na 140 mEq/L
CI 91 mEq/L
K 4.8 mEq/L

William Malley, MS, RRT, CPFT, FAARC


William Malley, MS, RRT, CPFT, is Administrative Director of Respiratory/Pulmonary Services at The Western Pennsylvania Hospital in Pittsburgh, PA. Feel free to direct questions, comments, correspondence or additional cases to
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Author:Malley, William
Publication:FOCUS: Journal for Respiratory Care & Sleep Medicine
Date:Mar 1, 2010
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