A common problem faced by trainees in Internal Medicine is acid-base disorders. Here, we will discuss the causes of acid-base disorders rather than the diagnosis on the basis of arterial blood gases. Specifically, we will discuss metabolic disturbances.
1) How does potassium affect acid-base status?
Changes in potassium often affect the metabolic acid/base status and vice versa. This is explained by the movement of excess potassium into cells which is balanced in part by intracellular hydrogen ions moving out to the extracellular fluid, and vice versa. This is termed "Internal Potassium Balance:"
Metabolic acidosis tends to be associated with hyperkalemia (exceptions below).
Metabolic alkalosis tends to be associated with hypokalemia (exceptions below).
2) How does volume status affect acid-base status?
Hypovolemia can predispose patients to contraction alkalosis in some cases. There are a few reasons for this:
1. Loss of large volumes of low-bicarbonate, sodium-containing fluid leads to bicarbonate concentration rises because of contraction of the ECF volume with a constant quantity of bicarbonate. This often occurs with IV loop diuretics.
2. High aldosterone - In the cortical collecting duct, high aldosterone released due to volume contractions leads to potassium and hydrogen ion excretion to balance sodium reabsorption. Hydrogen ion loss causes alkalosis, as does hypokalemia itself for the reasons stated above.
3. Angiontensin II - Released as part of RAAS activation in hypovolemia, angiontensin II acts at the Na+/H+ exchanger in the proximal tubules to enhance sodium absorption and H+loss, leading to alkalosis.
Therefore, contraction alkalosis can be seen in some patients with volume depletion.
Metabolic Acidosis
A) Increased Anion Gap
In these cases, extra anions (paired with H+) are introduced to the blood. The H+ is consumed by HCO3- in the buffer system and the only component that remains is the anion, which creates the anion gap. One mnemonic that can be used to remember these causes is MUDPILES:
Methanol
Uremia (chronic kidney disease)
Diabetic Ketoacidosis
Propylene glycol/Paraldehyde
Iron overload/Isoniazid use
Lactic acidosis
Ethylene glycol
Salicylates
B) Non-Anion Gap
In these cases, no new anions are being introduced to the blood. Instead, either HCO3- is excessively lost or renal acid is not being excreted.
Note that "hyperchloremic metabolic acidosis" is interchangeable with "non-anion gap metabolic acidosis." This is because chloride is proportionately increased when HCO3- is lost or H+ accumulates (no extra anions are present).
Causes:
1. Diarrhea - Loss of bicarbonate rich fluid results in acidosis. It is important to note that although diarrhea typically causes a metabolic acidosis, it can also cause a metabolic alkalosis in the following cases:
- Laxative abuse
- Villous adenoma
- Congenital chloroidorrhea (rare)
2. Bowel conduits for urine - These conduits are created during ureteric or bladder operations. When urine is exposed to gut mucosa, it reabsorbs chloride in exchange for HCO3-, leading to acidosis.
3. Renal Tubular Acidosis
These diseases result from the kidney's inability to acidify the urine due to several reasons. Note that potassium and acid/base disturbance associations in these cases do not follow the usual pattern listed above.
Metabolic alkalosis results from additional creation of bicarbonate combined with a process which prevents renal excretion of the excess bicarbonate. Patients with metabolic alkalosis compensate by hypoventilating and should raise the PCO2 by about 0.7 mm Hg for every 1 meq/L elevation in the bicarbonate. This initially lowers the arterial pH toward normal and is most effective acutely, but then becomes less effective over time.
The differential diagnosis for metabolic alkalosis can be broken down into two groups, according to the urinary chloride levels:
Grrrrrrrrrrrrrreat.
Here's a more physiological approach to acid-base disturbances from NEJM.
