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A Primer on Arterial Blood Gas Analysis
Andrew M. Luks, MD
Arterial blood gases play an important role in the work-up and management of critically ill patients and patients with a variety of pulmonary complaints and disorders. For example, they are used to guide the adjustment of ventilator parameters on mechanically ventilated patients and are also a standard part of the work-up of patients who present with unexplained hypoxemia or dyspnea. It is, therefore, important that students and physicians be able to interpret the results of arterial blood gas sampling, determine the patient’s acid-base status and assess the adequacy of oxygenation.
This primer describes a clinical approach to interpreting arterial blood gases. It will outline a step-wise approach to interpreting the acid-base status and generating differential diagnoses for the observed problems. It will then address the proper means for assessing the adequacy of oxygenation and determining the etiology of any observed abnormalities.
The physiologic principles underlying acid-base physiology are beyond the scope of this review and will not be considered here, but information about this topic can be obtained from the following additional resources:
- HuBio 541 Course Syllabus : http://courses.washington.edu/hubio541/secure/syllabus/06AcidBase.pdf
- Murray and Nadel’s Textbook of Respiratory Medicine : http://www.mdconsult.com/das/book/body/121296754- 2/0/1288/55.html?tocnode=51470230&fromURL=55.html#4-u1.0-B0-7216-0327- 0..50010-0_
Acid-Base Status
Terms and Normal Values Before reviewing the assessment of acid-base status, it is helpful to review the normal values for the main acid-base parameters and some basic terminology.
The normal values for acid-base parameters are as follows:
- pH: 7.38 - 7.
- Pa CO 2 : 36 - 44 mmHg
- Bicarbonate: 22 – 26 mmol/L
Be aware that the normal ranges for these parameters will vary slightly from laboratory to laboratory.
The following terminology is applied to acid-base interpretation:
- Acidemia : refers to a low blood pH (< 7.38). Patients with a low pH, are said to be “acidemic.”
- Alkalemia : refers to a high blood pH (> 7.42). Patients with a high pH are said to be “alkalemic.”
- Acidosis : refers to any process that, if left unchecked, will lead to acidemia. This can occur through one of two mechanisms. - A respiratory acidosis is present when the PCO 2 is high (> 44) - A metabolic acidosis is present when the HCO 3 -^ is low (< 22)
- Alkalosis : refers to any process that if left unchecked will lead to alkalemia. This can occur through one of two mechanisms. - A respiratory alkalosis is present when the PCO 2 is low (< 36) - A metabolic alkalosis is present when the HCO 3 -^ is high (> 26)
It is important to keep these terms straight in your mind and in your communications with others. It is common for people to refer to the patient with a low pH, for example, and say they are “acidotic.” Similarly, they often refer to the patient with a high pH as “alkalotic.” This is incorrect terminology. When you are referring to the patient and their pH, the correct terminology is as follows:
- The patient with a low pH has “acidemia” or is “acidemic.”
- The patient with a high pH has “alkalemia” or is “alkalemic”
How the Data Are Presented While the laboratory will always label each value in the arterial blood gas results, it is not uncommon for residents, fellows and attending physicians to either write or state the results without labeling each value. For example, rather than stating: “the pH is 7.40, the PCO 2 is 40, the PO 2 is 85 and the HCO 3 -^ is 24” they may simply state or write: “7.4/40/85/24.”
If ABG results are presented in this manner, by convention, they will be written or spoken in the following order: pH Æ PCO 2 Æ PO 2 Æ HCO 3 -
Before you get started…. Make Sure the Numbers Are Consistent
41 7. 40 7. 39 7. 38 7. 35 7. 32 7. 25 7.
- Compare the calculated pH to the measured pH. If they are similar, your sample is valid. If the values are far apart, there may be a measurement error.
A Step-Wise Approach to Acid-Base Status Interpretation As with reading an electrocardiogram or a chest x-ray, it is important to use a system when reading arterial blood gases. Adhering to a system will allow you to identify the primary and compensatory process and any additional disorders that may be present.
A suggested step-wise approach for reading an arterial blood gas is as follows:
- Examine the pH and comparing it to the normal range
- Identify the primary process that led to the change in pH
- Calculate the serum anion gap
- Identify the compensatory process (if one is present)
- Identify if any other disorders are present or there is a mixed acid-base process.
Each of these steps is described below in greater detail. After working through these steps, you should be able to give a one- or two-sentence synopsis of the patient’s acid- base status such as “This patient has a primary respiratory acidosis with a compensatory metabolic alkalosis.”
As you go through this process, try not to lose track of the clinical scenario that led to the blood gas being drawn in the first place. You will use the results and their interpretation to help you figure out what is going on with the patient. In addition, you should always ask if the results make sense in light of what you know about the patient’s case. If the results do not make sense, either your interpretation was wrong or there may be some additional processes at work that were not recognized on the initial analysis.
With that in mind, the main steps in interpreting an arterial blood gas in greater detail are presented below.
- Step 1 : Examine the pH and compare it to the normal range. As noted above, if the pH is low, the patient has an acidemia. If the pH is above this range, the patient has an alkalemia. Be aware that patients can have mixed metabolic disorders (eg. concurrent metabolic acidosis and alkalosis) that can give them a pH in the normal range. This will be discussed further below.
- Step 2 : Determine the primary process that led to the change in the pH :
For a patient with a low pH (acidemia)
- If the PCO 2 is elevated (> 44), the primary process is a respiratory acidosis
- If the HCO 3 -^ is low (< 22), the primary process is a metabolic acidosis
For a patient with a high pH (alkalemia)
- If the PCO 2 is low (< 36), the primary process is a respiratory alkalosis
- If the HCO 3 -^ is high (> 26), the primary process is a metabolic alkalosis
This framework is depicted in Figure 1.
Examples of how to work through this step are provided in Example Set 1 below.
- Step 3 : Calculate the serum anion gap (SAG) :
Serum Anion Gap (SAG) = Na +^ - (Cl-^ + HCO 3 - )
You should use the bicarbonate from the chemistry panel for this calculation. If this value is elevated (> 12), the person is deemed to have an “elevated anion gap.” This implies that the patient has a primary elevated serum anion gap metabolic acidosis
does not generate an anion gap in order to compensate for a primary respiratory disorder.
Be aware, however, that an elevated anion gap acidosis may not be the only primary process. For example, patients with salicylate intoxication may have a primary respiratory alkalosis and a concurrent primary elevated anion gap acidosis at the same time. An example of this situation is provided in Example Set 2.
Example Set 2
A 30 year-old woman is brought into the emergency room with altered mental status. Her friends found her at home with an empty bottle of aspirin by her bedside. Her S (^) p O 2 is 99% and she is obviously hyperventilating on exam. An arterial blood gas is obtained as part of her initial work-up and reveals: pH 7.56, PCO 2 22, PO2 110, HCO 3 Š17. On her chemistry panel, her sodium is 137, chloride 99, bicarbonate 18.
Step 1: The pH is high (alkalemia)
Step 2: The PCO 2 is low (respiratory alkalosis) and the bicarbonate is low (metabolic acidosis). A high pH with a low PCO 2 indicates that the primary process is a respiratory alkalosis.
Step 3: The serum anion gap is elevated at 20. As a result, she also has an elevated anion gap acidosis going on at the same time.
Summary: This combination of alkalemia due to a primary respiratory alkalosis with a concurrent elevated anion gap metabolic acidosis is classic for salicylate intoxication.
You should also note that the normal anion gap is affected by the patient’s serum albumin level. As a general rule of thumb, the normal anion gap is roughly three times the albumin value. By way of example, for a patient with an albumin of 4.0, the normal anion gap would be 12. For a patient with chronic liver disease and an albumin of 2.0, the upper limit of normal for the anion gap would be 6. Other people propose that the ceiling value for a normal anion gap is reduced by 2.5 for every 1g/dL reduction in the plasma albumin concentration.
- Step 4 : Identify the compensatory process (if one is present). In general, the primary process is followed by a compensatory process, as the body attempts to bring the pH back towards the normal range. - If the patient has a primary respiratory acidosis (high PCO 2 ) leading to acidemia: the compensatory process is a metabolic alkalosis (rise in the serum bicarbonate).
- If the patient has a primary respiratory alkalosis (low PCO 2 ) leading to alkalemia: the compensatory process is a metabolic acidosis (decrease in the serum bicarbonate)
- If the patient has a primary metabolic acidosis (low bicarbonate) leading acidemia, the compensatory process is a respiratory alkalosis (low PCO 2 ).
- If the patient has a primary metabolic alkalosis (high bicarbonate) leading to alkalemia, the compensatory process is a respiratory acidosis (high PCO 2 )
The compensatory processes are summarized in Figure 2.
Examples of how to work through these steps are provided in Example Set 3 on the following page.
Important Points Regarding Compensatory Processes There are several important points to be aware of regarding these compensatory processes:
- The body never overcompensates for the primary process. For example, if the patient develops acidemia due to a respiratory acidosis and then subsequently develops a compensatory metabolic alkalosis (a good example of this is the COPD patient with chronic carbon dioxide retention), the pH will move back towards the normal value of 7.4 but will not go to the alkalemic side of normal This might result in a pH of 7.36, for example but should not result in a pH such as 7.44 or another value on the alkalemic side of normal. If the pH appears to “over-compensate” then an additional process is at work and you will have to try and identify it. This can happen with mixed acid-base disorders, which are described further below.
- The pace of compensation varies depending on whether it is respiratory or metabolic compensation. Respiratory compensation for primary metabolic disturbance is almost immediate. For example, if someone infused hydrochloric acid through an IV and gave the patient a metabolic acidosis, the patient would rapidly begin hyperventilating and generate a respiratory alkalosis that would move the pH back towards normal. Metabolic compensation for primary respiratory abnormalities, however, is slow and may take several days. For example, if someone travels to high altitude and begins to hyperventilate due to the low oxygen levels in the atmosphere, initially there will be no metabolic compensation and they will have a high pH. Over several days, however, metabolic compensation will occur and the pH will return back towards normal.
- Despite the compensatory mechanisms, the pH may not return all the way to normal. For example, consider the following arterial blood gas in a patient with acute toluene toxicity: pH 6.95, PCO 2 9, HCO 3 -^ 2. This is a primary metabolic acidosis but despite a huge degree of hyperventilation and a marked compensatory respiratory alkalosis, the pH still remains very low. In other situations (eg. a compensated respiratory acidosis in a patient with obesity hypoventilation, or the compensated respiratory alkalosis in a pregnant woman), the pH will return closer to the normal range
- What may appear to be a compensatory process may not actually represent true compensation. For example, consider a patient who develops an acute respiratory acidosis (large rise in the PCO 2 ). Even though this is an acute process and renal compensation has not occurred, the bicarbonate value may read 27 on the ABG. This appears elevated and would suggest metabolic compensation is starting to occur but may, in fact, not represent true compensation. How does this occur? Remember that a key relationship that governs acid-base physiology is the following:
H 2 O + CO 2 ' H 2 CO 3 ' H+^ + HCO 3 -
If there is a large rise in the PCO 2 , this equation will shift towards the right and the levels of bicarbonate will transiently increase. Similarly, a large fall in the PCO 2 would shift the equation to the left and the bicarbonate would transiently decrease. How can you figure out whether the observed changes in bicarbonate represent true compensation or changes due to this relationship? The answer lies in another value you will see reported with the arterial blood gas – the base excess. In general, as you may recall from respiratory physiology, the base excess is defined as the difference between the patient’s HCO 3 -^ after correction to a pH of 7.4 by a change in the PCO 2 and the normal HCO 3 -^ at pH 7.4. It can be used in the following manner to interpret changes in the HCO 3 -^ levels.
- If the base excess is between – 2 and + 2 then the observed changes in bicarbonate are due to movement based on the equation above and there is no metabolic acidosis or alkalosis.
- If the base excess is less than – 2, then there is a metabolic acidosis, which may be the compensatory process. Another term for this is a base deficit.
- If the base excess is greater than + 2, then there is a metabolic alkalosis, which may be the compensatory process.
Be aware that if the base excess is less than -2 or greater than + 2, and therefore, a metabolic process is present, the base excess value itself does not tell you whether this is a primary process or a compensatory process. It only tells you a metabolic process is present. You still need to work through the steps described here to tell whether it is the primary process or the compensatory process.
- What appears as a lack of compensation may actually represent an acute process on top of a chronic process. In some cases, patients may live in a chronically compensated state of acid-base disturbance and then deviate from that state due to an acute problem. The best example is the patient with very severe COPD who might have chronic respiratory acidosis with metabolic compensation at baseline. The arterial blood gas for this patient might look like the following: pH 7.35, PCO 2 55, PO 2 70, HCO 3 -^ 32. Now, suppose the patient develops a severe exacerbation and comes into the ER. At that point in time, an arterial blood gas may show pH 7.25, PCO 2 65, PO 2 62, HCO 3 -^ 33. The PCO 2 is now 10 mm Hg higher than before and the pH is now much further away from 7.40. If you didn’t have the initial blood gas for comparison, you would say this patient has a respiratory acidosis with only partial compensation. However, knowing the prior acid-base status, it would be more
- If the Delta Delta > 26, the patient is holding onto bicarbonate and there is an additional metabolic alkalosis. If you found an alkalosis (either the compensatory or the primary process) in the initial step above, then the alkalosis you identify here represents the same process. If however, you identify an acidosis in the initial steps and then this last step reveals the presence of alkalosis, you have found an additional metabolic process.
Be aware that for these calculations to work, the chemistry panel and blood gas must have been drawn at roughly the same time. If, for example, you obtain a blood gas on a patient during a code on a patient at 6PM, you cannot use the morning chemistry panel from 6AM to do these calculations.
Examples of how to work through this last step of the process are provided in Example Set 4 below.
Example Set 4
Case A You are working in the emergency room when the paramedics bring in a 45 year-old man who was found down in Pioneer Square. He is somnolent but arouseable. He has emesis on his shirt. He is hypotensive and tachycardic. Labs are drawn and reveal the following: room air ABG: pH 7.22, PCO 2 29, PO 2 78, HCO 3 -^ 11. Chemistry panel: Na +^ 131, Cl -^ 90, HCO 3 -^ 12. Glucose 135.
Step 1: The pH is low (acidemia) Step 2: The PCO 2 is low (respiratory alkalosis) and the bicarbonate is low (metabolic acidosis). Therefore, the metabolic acidosis is the primary process. Step 3: The serum anion gap is elevated at 29. There is, therefore, an elevated anion gap acidosis. Step 4: The respiratory alkalosis is the compensatory process for the metabolic acidosis. Step 5:
The Delta Gap = Measured SAG Š Normal SAG = 29 Š 12 = 17 Calculate the Delta Delta: Delta Gap + measured bicarbonate = 17 + 12 = 29 Since the Delta Delta is above a normal bicarbonate level, there is a concurrent metabolic alkalosis at work.
Summary: The patient has a primary elevated anion gap acidosis with respiratory compensation (which is not complete) and a concurrent metabolic alkalosis. You would need to sort through the differential diagnosis for an elevated anion gap acidosis to identify the cause of that problem. The metabolic alkalosis is likely due to vomiting.
Example Set 4 (continued)
Case B A 60 year-old man was recently in the hospital for treatment of aspiration pneumonia for which he as treated with levofloxacin and clindamycin. One week later, he presents to the ER with severe diarrhea, abdominal pain and hypotension. He is admitted to the ICU where an arterial blood gas shows: pH 7.29, PCO 2 25, PO 2 89, HCO 3 -^ 10. On his chemistry panel, he has: Na+^ 129, Cl -^ 99, HCO 3 -^ 10. Glucose 135.
Step 1: The pH is low (acidemia) Step 2: The PCO 2 is low (respiratory alkalosis) and the bicarbonate is low (metabolic acidosis). Therefore, the metabolic acidosis is the primary process. Step 3: The serum anion gap is elevated at 20. There is, therefore, an elevated anion gap acidosis. Step 4: The respiratory alkalosis is the compensatory process for the metabolic acidosis. Step 5:
The Delta Gap = Measured SAG Š Normal SAG = 20 Š 12 = 8 Calculate the Delta Delta: Delta Gap + measured bicarbonate = 8 + 10 = 18 Since the Delta Delta is below the normal bicarbonate level, there is a concurrent non-gap metabolic acidosis at work.
Summary: The patient has a primary elevated anion gap acidosis with respiratory compensation and a concurrent non-gap metabolic acidosis. He likely has sepsis from C.Difficile Colitis as the cause of his elevated anion gap acidosis. The non-gap acidosis may be from his severe diarrhea (a source of bicarbonate loss).
Case C A 56 year-old woman with chronic kidney disease presents to the emergency room with increasing dyspnea. She is noted to be tachypneic, but is afebrile, has a normal lung exam and a normal appearing chest x-ray. An arterial blood gas is drawn and reveals: pH 7.28, PCO 2 29, PO 2 85, HCO 3 -^ 16. On her chemistry panel, the sodium is 131, chloride 105 and HCO 3 -^ 15.
Step 1: The pH is low (acidemia) Step 2: The PCO 2 is low (respiratory alkalosis) and the bicarbonate is low (metabolic acidosis). Therefore, the metabolic acidosis is the primary process. Step 3: The serum anion gap is normal at 11. The patient, therefore, does not have an elevated anion gap acidosis Step 4: The respiratory alkalosis is the compensatory process for the metabolic acidosis. Step 5:
The Delta Gap = Measured SAG Š Normal SAG = 11 Š 12 - Calculate the Delta Delta: Delta Gap + measured bicarbonate = -1 + 15 = 14 The Delta Delta is below the normal bicarbonate level. This tells us there is a non-gap acidosis, but in this case, this acidosis is actually the same acidosis that you identified in Steps 2 and 3 and there are no additional metabolic processes at work.
Summary: The patient has chronic kidney disease. Many such patients develop non-gap acidoses due to renal tubular acidosis.
As noted above, in several of these cases (eg. carbon monoxide poisoning, excess beta-agonists), the elevated anion gap derives from accumulation of lactate.
You should also be aware that there is a differential diagnosis for a low serum anion gap. It includes the following items:
- Fall in unmeasured anions (eg. Hypoalbuminemia)
- Increased unmeasured cations (hyperkalemia, hypercalcemia, hypermagnesemia)
- Lithium
- Multiple Myeloma
- Bromide (found in Pyridostigmine Bromide used in the treatment of myasthenia gravis and some herbal medications)
- Normal Anion Gap Metabolic Acidosis (non-gap acidosis) : The differential diagnosis includes:
- Gastrointestinal bicarbonate losses:
- Diarrhea
- Ureteral Diversion (ileal loop)
- Renal bicarbonate losses:
- Carbonic anhydrase inhibitors (eg. acetazolamide)
- Renal tubular acidosis
- Aldosterone inhibitors or hypoaldosteronism
If the cause of the non-gap acidosis is not clear based on the patient history, you can identify whether the problem is renal or gastrointestinal losses by calculating a urine anion gap:
Urine Anion Gap (UAG) = (Urine Na +^ + Urine K+^ ) – Urine Cl -
A positive value (UAG > 0) suggests the metabolic acidosis is due to a renal etiology, whereas a negative value (UAG < 0) points to a gastrointestinal source.
- Metabolic Alkalosis : The differential diagnosis includes:
Chloride Responsive Alkaloses:
- Vomiting
- Nasogastric suction
- Diuretics
Chloride Unresponsive Alkaloses:
- Hyperaldosteronism
- Cushing’s syndrome
- Licorice ingestion
- Bartter’s syndrome
- Excess alkali intake (eg. milk alkali syndrome)
If the cause of the metabolic alkalosis is not clear based on the patient history, you can obtain a urine chloride level to help determine the cause. If the urine chloride level is < 15 the patient has a “chloride responsive alkalosis” which can be corrected with saline (NaCl) administration. This typically happens with gastrointestinal losses or intravascular volume depletion (i.e. a contraction alkalosis with diuretic use). If the urine chloride is > 15, the patient has a “Chloride Unresponsive Alkalosis”
- Respiratory Acidosis : A primary respiratory acidosis implies that the patient is hypoventilating or not ventilating enough in the face of high CO 2 production. This can be seen in the following settings: - Acute intoxication with narcotics or other sedative medications - Severe metabolic encephalopathy - Obesity hypoventilation - Severe chronic obstructive pulmonary disease - Acute upper airway obstruction - Neuromuscular disorders (eg. Guillan Barre, Myasthenia Gravis, Botulism, Amyotrophic Lateral Sclerosis) - Later stages of a severe asthma exacerbation (eg. the patient is tiring out) - Thoracic cage trauma (flail chest) - Inappropriately low minute ventilation settings on mechanical ventilation
- Respiratory Alkalosis : A primary respiratory alkalosis implies that the patient is hyperventilating. This can be seen in the following settings:
- Early stages of an asthma exacerbation
- Anxiety attack
- Acute hypoxia (hypoxic ventilatory response)
- Pregnancy or other cases of elevated progesterone
- Cirrhosis and/or hepatic encephalopathy
- Salicylate intoxication
- Central nervous system disease
Use Old Arterial Blood Gas Results to Your Advantage There are certain clinical situations where a review of the patient’s prior arterial blood gas results can be of great value (if the patient did, in fact, have a sample drawn in the past). To see how prior ABG results may be of use, consider the following scenario.
term of the alveolar gas equation (PI O 2 = [PB – 47] FI O 2 ). For example, the PI O 2 while breathing ambient air at sea level is 150 mmHg whereas if you live in Boise, Idaho, where the average PB is 695 mmHg, the PI O 2 of room air is 135 mmHg.
Once you have calculated this value, the AaO 2 Difference is calculated as follows:
AaO 2 D = PA O 2 – Pa O (^2)
The normal value for the AaO 2 Difference is about 10-15 mm Hg. If you determine that the patient has a normal AaO 2 Difference, then the hypoxemia can be attributed to hypoventilation or a low inspired partial pressure of oxygen. If, however, you find that the patient has an elevated AaO 2 difference then they have some process going on that is causing shunt or low V/Q, such as pneumonia, that is contributing to the observed hypoxemia.
There are a few important points to be aware of regarding the use of the AaO 2 Difference.
- In order to use the alveolar gas equation you must have an accurate assessment of the F (^) I O 2. The FI O 2 will be accurate when your patient is on room air, non-invasive or invasive mechanical ventilation or is on a high-flow facemask system. When patients are on supplemental oxygen using nasal cannula, regular face masks, Venturi masks or non-rebreather masks, the FI O 2 is not reliable; these systems often deliver less gas flow than the patient is requiring for their minute ventilation and, as a result, they end up entraining in a lot of room air which dilutes out the intended inspired oxygen concentration.
- The “normal” AaO 2 Difference increases with age. Some sources state that the upper limit of normal for the AaO 2 Difference is equal to: 2.5 + (0.21 x age).
- The “normal” AaO 2 Difference varies based on the FI O 2. On an FI O 2 of 1.0, the normal AaO 2 difference is 100 mmHg. Also, if you go to high altitude, where the barometric pressure is decreased and the PI O 2 falls, the normal AaO 2 Difference is lower than 10.
- Make sure you are using the correct value for R. In general, we use a value of 0.8. However, if your patient is on an FI O 2 of 1.0, then R is taken to be 1.
Assessing the Adequacy of Gas Exchange Suppose your patient has Pa O 2 of 85 that results in an Sp O 2 around 97-98%. Even though these values are adequate for sustaining the patient, they do not mean that gas exchange is normal. In fact, a patient can have a Pa O 2 and Sp O 2 in this range and still have markedly abnormal gas exchange. As a result, whenever you interpret the Pa O 2 on an arterial blood gas, you must look at that number in light of the amount of oxygen that
is being delivered to the patient. There are several ways you can get a sense of this value:
- The P/F Ratio : This is the ratio of the Pa O 2 (in mmHg) to the F (^) I O 2 (expressed as a decimal). The smaller the value, the worse the patient’s gas exchange. For example, consider a patient with a Pa O 2 of 80. If they are on an FI O 2 of 0.3, the P/F ratio is
- If they are, instead, on FI O 2 of 0.8, the P/F ratio is only 100, a much worse value that signifies greater impairment in gas exchange. The P/F ratio is commonly used in patients on mechanical ventilation as part of the assessment of whether they have the Acute Respiratory Distress Syndrome (ARDS). A P/F ratio below 300 is consistent with Acute Lung Injury, while a P/F ratio below 200 is consistent with ARDS (provided the patient meets the other criteria including a CXR with diffuse bilateral opacities and evidence that cardiac function is normal).
- The AaO 2 Difference : The same number that is used to help determine the cause of hypoxemia can also be used to determine the adequacy of gas exchange. In patients with an elevated AaO 2 Difference, larger values imply a greater degree of either low V/Q areas and/or shunt. The size of the AaO 2 Difference does not help you distinguish between low V/Q and shunt, however. The way to make that determination is to measure the response to supplemental oxygen administration. The Pa O 2 will rise and the AaO 2 difference will shrink in patients with low V/Q as the primary cause of their hypoxemia (eg. the COPD patient during an exacerbation) whereas in shunt, supplemental oxygen does not lead to improvements in the Pa O 2.
Both methods for assessing the adequacy of gas exchange require an accurate FI O (^2) measurement, which, as noted above, can only be assured if the patient is on room air, a high flow face mask, non-invasive mechanical ventilation or invasive mechanical ventilation.
Special Situations To Be Aware of In Evaluating the Pa O 2 on an ABG There are a few special situations of which you should be aware when assessing the Pa O 2 on an arterial blood gas.
- The Hypothermic Patient : Hypothermia can affect the accuracy of the Pa O (^2) measurement by causing changes in the position of the Hb-O 2 dissociation curve. If you do not inform the laboratory of the patient’s body temperature at the time the sample was measured, you may measure an artificially high Pa O 2. To understand how this happens, consider the following scenario. Suppose you see a patient in the emergency room with a temperature of 32°C and draw an ABG while he is still at that temperature. At this point in time, his Hb-O 2 dissociation curve has shifted to the left and, as a result, for any given oxygen content of the arterial blood, the Pa O 2 is lower than it would be at a normal temperature. When the sample is sent to the lab and placed in the blood gas analyzer, however, the machine will warm the sample to 37°C before doing the measurement. This warming process shifts the Hb-O (^2) dissociation curve back to the right. Because the oxygen content of the blood has
