ADS – Acid-base disorders

During EBM week, we learned that one of the most common reasons why learners motivate themselves to learn something that they don’t otherwise want to learn is a fear of failure or humiliation. Not that I didn’t want to learn this, as acid-base disorders was an area that weren’t touched upon in the undergrad curriculum (except for one lecture in the renal elective), but Dr. Brown’s lecturing style certainly motivates one to do the pre-readings and do them well.

I won’t go over WHAT was taught as I feel that I have a good grasp on what was covered and I just need to practice it – any patient who has labs drawn, or arterial blood gases done, I will try to evaluate them and see if there is an acid-base disorder. I have a good idea of what causes each of the disorders, and how that will influence drug therapy – example is a metabolic acidosis where replenishment of bicarb is necessary… but bicarbonate is reconstituted in a bag of NS…which has 154 mEq/L. Not nice!

Normal pCO2 = 40 mm Hg
Normal HCO3 = 24 mm Hg (21-28)
Normal anion gap = 10 (8-12)… ADJUST NORMAL down by 2 for every 10 g/L drop in serum albumin (N = 42-46 g/L)

One pearl I must record though is that potassium usually follows blood pH changes due to shunting of potassium (a cation) into or out of the cell to maintain ion balance.
– As pH DECREASES in acidemia, potassium INCREASES
– As pH INCREASES in alkalemia, potassium DECREASES

I’m more a systems kind of person and I like a systematic way of evaluating anything. For that reason, I found acid-base disorders to be easy to wrap my head around. As long as I have the labs, the blood pH is the main anchor and will let me determine whether it is an acidemia or alkalemia. The corroborating signs, symptoms, and labwork will allow me to confirm that the drug therapy for the appropriate diagnosis is the best for the patient.


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