I love acid base physiology. As an internist hospitalist, being great at figuring out acid base physiology can sometimes mean the difference between life and death for patients. In some regards, being great at these disorders is what defines a great internist. Unlike this someecard explanation below, understanding how to interpret acid base physiology is a basic requirement for evaluating hospitalized patients. I feel so strongly about knowing how to evaluate acid base disorders, that I have included it as number six on my list of 20 golden rules for fleas. If you are an internist or planning on becoming a hospitalist, I highly recommend studying this stuff until you can figure it out in your sleep. Certifying boards love testing on this stuff, especially mixed acid base disorders, that will often be missed without knowing what you're doing. And your patients are counting on you to know it as well. They will likely give you a clinical scenario and then give you an answer option such as "primary respiratory acidosis, primary nongap metabolic acidosis, compensatory metabolic alkalosis". If you don't know how to systematically work up acid base disorders, they'll get you every time.
Here is a classic clinical acid base disorder scenario: A 47 year old woman presents as a direct admission to the hospital from clinic after 5 days of persistent nausea and vomiting. Her last bowel movement was 5 days ago. Initial laboratory was as follows:
Arterial Blood Gas
What is her acid base status? Before I do anything, I assume the data is correct. There are formulas that can verify if the data makes sense. I haven't looked at those formulas in ten years. I can usually tell by looking at an ABG if it makes sense clinically. Assuming the data is correct, I want to always know if the patient has an anion gap. As a general rule I take the Na - (Cl + HCO3). In this case 132- (84 + 20)=28. Her anion gap is 28. A normal anion gap is about 12. Therefore, she has a delta anion gap of 16. By definition, has an anion gap metabolic acidosis and the gap is 16.
The question is why? What is causing her anion gap? Remember your MUDPILES.
D: Diabetic ketoacidosis
L: Lactic Acidosis
E: Ethylene glycol (antifreeze) or Ethanol
S: Salicylate poisoning.
In the hospital setting, lactic acidosis is often the most common cause (Sepsis, hypotension, ACS, shock, trauma, ischemic bowel, gi bleeding are among the most common causes). Anything that reduces tissue perfusion can potentially cause lactic acidosis. With that in mind a lactate level was drawn. It returned at 10. There may be a component of uremia as well as starvation ketosis as well causing the other anion gap of 6. Regardless of the cause, she has a large anion gap which means she should be profoundly acidotic.
With an established anion gap present, let's take a look at the ABG. 7.35 represents an acidosis, although a wimpy acidosis. Therefore the patient has a primary acidosis and since she has an anion gap, this is a primary anion gap metabolic acidosis. Since the patient's ABG CO2 is not high (above 40) we can assume this is not a primary respiratory acidosis. In fact, patients often compensate a metabolic acidosis with a respiratory alkalosis (breathing faster to "blow off the anions") and getting their ABG CO2 below 40. Whenever you see a patient hyperventilating, make sure to consider their tachypnea as a physiological response to a metabolic acidosis and not necessarily due to shortness of breath. I see this multiple times a year and have saved a few lives by understanding the physiology of the patient in front of me.
The patient has a primary metabolic acidosis. And since they have an anion gap, they most likely have a primary anion gap metabolic acidosis. And they are compensating by increasing their respiratory rate to blow off CO2 to get their pH as close to normal (7.40) as possible. However, if you answered primary anion gap metabolic acidosis with compensating respiratory alkalosis, you would get the question wrong.
Why? You need to understand the numbers in front of you. If the patient's delta anion gap is 16 and the patient had no other metabolic issues to consider, then the patient's measured bicarb should decrease from the normal 24 down to 8 (or 24-16) and the patient's pH should be much less than 7.35 or the patients CO2 on ABG should be much less to compensate for the severe anion gap metabolic acidosis. Neither is true. How much less should they be? I don't know. Nor do I care. That's for the academic doctors to figure out in their morning reports with their residents, that is assuming their interns haven't already gone home because of the new intern work hour restrictions. As I said earlier, I haven't calculated the acid base calculations for a decade. It doesn't matter because after seeing thousands of blood gases the clinician effect kicks in and gestalt rules the day.
In this case the anion gap of 16 should force the measured bicarb down to 8 from 24. But it didn't. The measure bicarb is 20. Therefore something is forcing the bicarb up to 20 when it should be 8. It's not the increased respiratory drive. What causes a measure bicarb level to rise on a BMP? Five days of vomiting can do that. In fact, because the patient has been vomiting for five days, she also has a primary metabolic alkalosis, a contraction alkalosis that happens with volume depletion. Therefore, despite a severe and impressive anion gap metabolic acidosis, the patient's pH is barely acidotic because they have the combined benefit of a mild compensatory respiratory alkalosis and a primary metabolic alkalosis.
On the test, the answer to this question is primary metabolic alkalosis, primary anion gap metabolic acidosis and compensatory respiratory alkalosis. While I cannot entirely exclude a component of primary nongap metabolic acidosis (such as a chronic renal tubular acidosis or diarrhea) I would not expect the patient to have one, nor would I expect that to be an answer on a test.
If you are going to be an internist or a hospitalist, learn acid base disorders and learn them well. They will save your patients time and time again. That's our job. This is the type of work internists and hospitalists do every day in the hospital. We save lives because we are experts in this process. What is medical school like? This is what medical school is like. It's like drinking from a firehouse. This is what we learn in residency. This is internal medicine. This is the primary care we are taught. This is physician level primary care. The capabilities of primary care trained physicians are under appreciated and under marketed in a world where most lay people think primary care is about giving vaccines and refilling metformin scripts for diabetes. Few people appreciate the skills of the internists and hospitalists because few people will ever need them. If you do, however, thank your lucky stars we are here to help and that we have been trained to provide a type of intensive and thoughtful care few others can say for the critically ill.