This is a classic ABG sequence:
| ABG | Admission (on 2 L O2) | Day 2 (Bipap 100%) |
|---|---|---|
| pH |
7.28 |
7.52 |
| pCO2 | 89 | 52 |
| pO2 | 60 | 373 |
| HCO3 | 42 | 42 |
Your tasks are to understand and explain the course of events for this woman having a COPD exacerbation.
1. What is the initial acid-base disorder?
The patient has a chronic respiratory acidosis with metabolic compensation. I cannot remember the calculations, so I found a calculator online.
2. What is the second day disorder?
This disorder goes by the name post-hypercapnic metabolic alkalosis. I sometimes use the phrase "revealed metabolic alkalosis". It occurred because the patient had an appropriate compensation for a chronic respiratory acidosis, and then we successfully improved ventilation – lowering the pCO2 faster than the kidneys can adjust.
3. What would you do now?
We gave the patient acetazolamide to lower the HCO3 . Here are the subsequent ABGs:
| ABG | Day 3 | 5 hrs later | Day 4 |
|---|---|---|---|
| pH | 7.63 |
7.41 |
7.36 |
| pCO2 | 40 | 59 | 62 |
| pO2 | 56 | 83 | 74 |
| HCO3 | 42 | 37 | 35 |
We give the acetazolamide to add stimulation to ventilation.
{ 1 comment… read it below or add one }
The disorder the second day techincally is a post hypercapneic metabolic alkalosis. This is common in patients with chronic CO2 retention that are ventilated to a normal level.
But in practice this is essentially a relative (not absolute) respiratory alkalosis in the sense these people have reset their CO2s usually around 60. When you provide more ventilation than that to them, you are essentially breathing them into an alkalosis that is not normal for them and that they won't tolerate because they will ultimately reset back to 60.
Attempting to stimulate their ventilation with Diamox is a reasonable approach, but it rarely allows them to reset to a normal pCO2 and a normal pH. The underlying compensatory metabolic alkalosis is a stimulus to hypoventilation that works at cross purposes to the Diamox.
I think the best approach in this patient is to stabilize from a cardiac standpoint, investigate any reversible pulmonary component (upper airway obstruction, bronchospasm) and titrate the oxygen appropriately.
These patients can be stable for many years with pCO2s between 50 and 60 and relatively normal pHs.
My general rule, one that I am happy to discuss because it is unsettled, is to avoid correcting respiratory acid/base problems with metabolic means and vice -versa. Stabilize the primary problem and let the body fix the ph problem.