Gas Exchange

Arterial Blood Gas Testing

While there are many advantages of pulse oximetry in the non-invasive assessment of oxygenation, there are a number of clinical situations where a more definitive assessment of gas exchange is required. In addition to the direct measurement of arterial oxygenation, arterial blood gas testing also provides information on alveolar ventilation and acid-base status. Interpretation of arterial blood gas testing like most complex diagnostic studies involves an algorithmic approach to ensure that all aspects of the study are adequately assessed.

Algorithm for arterial blood gas interpretation

• Define overall acid-base disturbance
• Determine if disturbance is respiratory, metabolic or mixed
• For respiratory disturbances establish if these are acute, subacute or chronic
• For metabolic acidosis establish if associated with anion gap
• For metabolic acidosis is the respiratory response appropriate

Define overall acid-base disturbance

Arterial pH exist within a very narrow continuum between 7.35 and 7.45. Whenever physiologic forces attempt to deranged this narrow equilibrium the body will attempt to compensate usually initially from a respiratory standpoint and then over a period of several days from a renal perspective.

By definition if arterial pH is less than 7.35 we have an arterial acidosis, if pH is greater than 7.45 we have an arterial alkalosis.

Define primary process

Over the years I have seen numerous tables or algorithms that attempt to simplify the process of interpreting arterial blood gas testing. While I understand to intent to deconstruct a complex process into a more manageable format I feel that many of these approaches actually complicate the process and make it more difficult to implement.

I feel the most straightforward approach to to compare your data points from the ABG in the context of how the body should be responding to the overall disturbance identified in step one above.

In the presence of 'acidosis' we should increase our alveolar ventilation and reduce PaCO2 below 35. Conversely 'alkalosis' should leave to a reduction of alveolar ventilation and a rise in PCO2 above 45.

When the respiratory response is consistent with the overall acid-base disturbance then the primary process is respiratory in nature. If the respiratory response is opposite to the overall acid-base disturbance then the primary process is metabolic in nature.

What limits the respiratory compensation to a metabolic alkalosis?

Acute, subacute and chronic respiratory disturbances

Only in cases of an acute respiratory disturbance is there any clinical value of determining whether or not the process is acute or subacute/chronic. The clinical utility of this determination is quite limited but in situations where you are able to make this determination it can have a significant impact on your differential diagnosis.

Under acute circumstances for every 10 change in the PCO2 level there is a corresponding 0.8 change in arterial pH. By way of example if the patient is experiencing an acute respiratory alkalosis and the measured PCO2 is 30 you would expect the following change in pH:

Expected pH = 7.40 - ( ( (40 - PCO2)/10) *0.08)
Expected pH = 7.40 - ( ( (40-30)/10) * 0.08)
Expected pH = 7.40 - 0.8
Expect pH = 7.32

If in this particular example the pH is higher than 7.32 we can conclude that the patient has been hyperventilating long enough to induce metabolic compensation (18-24 hours) and the condition is either subacute or chronic.

Very rarely does one encounter chronic respiratory alkalosis but it will occasionally be seen in individuals with cirrhotic liver disease for what is felt to be an adequate metabolism of sex hormones resulting in low-grade hyperventilation.

On the converse side, chronic respiratory acidosis is far more common and in situations where it is seen generally indicate significant pulmonary dysfunction. Again as I implied above really only the identification of acute processes has any significant impact and you are able to conclude that the process is chronic if the individuals pH is normal or near normal. This is important to recognize in cases of a chronic respiratory acidosis for these individuals do not require the same intensity of acute interventions than those who are experiencing acute or subacute increases.

What is the diagnostic significance of an acute respiratory acidosis?

Anion Gap

The next 2 parameters for arterial blood gas interpretation only applied to situations where there is a metabolic acidosis.The first related to the determination of the anion gap is primarily responsible for assisting in the differential for that metabolic acidosis.

Anion gap = Na - (Cl + HCO3) normal 8-16

What substance contributes most significantly to a normal anion gap?

For the most part a low anion gap is extremely limited and application and the vast majority of the interest is in individuals with acidosis who have a a normal (nonanion gap acidosis) or an elevated value (anion gap acidosis).

Differential Anion Gap Acidosis

The differential for Anion Gap and Non-Anion Gap acidoses is a fertile breeding ground for acromyms. Back in the day when I needed to regurgitate this differential for rounds or a test, I found them helpful. Not that the internet is at the touch of our fingers they are all define the same way..... Google

What do you this is the most common cause of the follow acid-base disturbances:
Metabolic Acidosis in the Emergency Department
Metabolic Acidosis on a Hospitalized Patient
Metabolic Alkalosis in the Emergency Department
Metabolic Alkalosis in Medical Hospitalized Patient
Metabolic Alkalosis in a Surgical Hospitalized Patient
Respiratory Alkalosis in the Intensive Care Unit

Respiratory Compensation for Metabolic Acidosis

This last parameter is often not addressed in interpretation of arterial blood gas testing but I do feel it provides significant clinical utility. As we have already mentioned the appropriate compensatory response to a metabolic acidosis is hyperventilation but in certain situations the patient may either under or overcompensate.

Winter Formula

Expected PCO2 = (HCO3 x 1.5) + 8 +/- 2

Having a secondary respiratory alkalosis on the substrate of a metabolic acidosis is a very specific finding and only associated with salicylate poisoning.

What is the clinical significance of a patient presenting with a metabolic acidosis and a measured PCO2 of 38 but an expected PCO2 of 25?