When respiratory acidosis with a normal A-a gradient is identified, two questions arise:
psst.. If you don’t know what A-a gradient is, click here 😉
It’s important because the treatment differs. Acute respiratory acidosis and for that matter acute-on chronic respiratory acidosis needs non-invasive ventilation while chronic compensated respiratory acidosis does not really need NIV unless the clinical picture suggests a significant acute illness that doesn’t get corrected with medical management like bronchodilators etc. Allow me to explain.
The context gives you the biggest clue. If someone has an acute history of deterioration it is likely to be acute. For example, acute breathlessness of a couple of days on a background of COPD is different from someone being seen in the out-patient clinic with stable symptoms of breathlessness on exertion with a chronically elevated PaCo2 and mild acidosis. Moral of the story, always look at the entire clinical picture.
The answer lies in the level of compensation that has occurred. What does this mean?
Recall that the pH of the body is very tightly controlled to help tissues function optimally and perform their metabolic activities. Take the example of the myocardium, persistent acidemia irritates the myocardium enough to cause arrhythmias and even ischemia. See Figure 1 to understand what’s happening inside!
In order to keep the pH within the normal range the buffering systems always compensate in the same direction.
The equation below illustrates this well:
pH=6.1+log (HCO3– /0.03PCo2)
Don’t be afraid, you won’t have to click that back button in a hurry 😉
This equation basically says that pH ∝ HCO3– / PCo2
If PCo2 increases, HCO3– should rise to compensate, to keep the pH constant and vice versa.
In acute respiratory acidosis of a day or two, this rise in HCO3– is immediate but minimal as the compensatory mechanisms are in the blood which has a limited buffering capacity. Every 10mm of Hg or 1.3 kpa increase in PCo2 is matched by a 1 meq/L rise in HCO3– (1). Inevitably, the compensation is not enough to offset the PCo2, hence pushing the system into acidosis.
In the face of persistent hypercapnia, the kidneys get into gear. They start peeing out H+ while generating HCO3– that gets pumped into the blood stream. The HCO3– now rises manifold. For every 10 mm of Hg (or 1 kpa) rise in PCo2 the HCO3– increases by 3.5 meq/L (1). This process is slower and takes between 3 to 5 days. In this case, the pH is brought back to normal or near-normal despite the significantly elevated pCo2.
Say, a COPD patient presents with an acute exacerbation and a pCo2 of 80 mm of Hg. In an acute setting, using the above equation, this results in a calculated pH of 7.17 with a HCO3– rise of 4 meq/L (assuming a baseline mean HCO3– of 24 meq/L).
The same pCo2 of 80 mm of Hg, if chronically elevated, can result in a calculated pH of 7.29 with a HCO3– rise of 14 meq/L!
We can see how an acute deterioration results in a much bigger drop in pH with the same rise in pCo2!
A final word, if the calculated compensatory rise in HCO3– is not in keeping with the observed value, it points to a mixed acid-base disorder. This is a separate topic that we don’t need to address now, you will be pleased to hear!
To sum it all up:
References
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