Chapter 8 Acid-Base Balance
|Cations (mEq/L)||Anions (mEq/L)|
|Na+ 140||Cl– 103|
|Ca2+ 5 (2.5 mmol/l)||Proteins 16|
|Mg2+ 2 (1 mmol/L)||Organic 4|
|H+ 0.000040 (40 nmol/L)||Other inorganics 3|
From Halperin M, Goldstein M: Fluid, Electrolyte, and Acid-Base Physiology, 2nd ed. Philadelphia, Saunders, 1994, Table 1-2.
which can be rewritten as:
Pharmacology note: Because sodium reabsorption in the proximal tubule is indirectly coupled to bicarbonate reabsorption, carbonic anhydrase inhibitors such as acetazolamide exert a diuretic effect by blunting sodium reabsorption. However, this diuretic action is weak because of the capacity of more distal sites, particularly the Na+-K+-2Cl− cotransporter in the loop of Henle, to increase sodium reabsorption. They also interfere with reclamation of bicarbonate in the proximal tubule, the site at which 80% of filtered bicarbonate is reclaimed (the distal sites do not have a capacity to greatly increase their bicarbonate absorption). The loss of bicarbonate can cause acidosis (normal anion gap type) when carbonic anhydrase inhibitors are used as diuretics. In fact, clinically, carbonic anhydrase inhibitors are used much more often for their ability to increase bicarbonate excretion and thus treat a metabolic alkalosis (e.g., contraction alkalosis in an overly diuresed patient) than they are used as a diuretic.
Note: The model of nondiffusible being trapped in the tubular lumen is an oversimplification of renal handling. In fact, is produced, partially reabsorbed, and then dissociated to NH3, which is recycled in the renal medulla, where its high concentration prompts diffusion back into the tubular lumen; there, it combines again with secreted H+ to form . The net result is that ends up back in the tubular lumen.
Clinical note: In renal failure, in which the GFR is substantially reduced, less H+ ions may be secreted into the tubular fluid because of a reduced number of functioning nephrons. The result is an accumulation of acid in the plasma, leading to the metabolic acidosis that is characteristic of advanced renal failure.
Clinical note: Acidosis can develop because of bicarbonate depletion (metabolic acidosis) or carbon dioxide accumulation (respiratory acidosis), or both. In either situation, the kidneys attempt to compensate by increasing H+ excretion. Similarly, alkalosis can occur because of an increase in bicarbonate or a decrease in CO2. In this situation, the kidneys decrease H+ excretion in an effort to bring the pH back toward the normal range (rarely does it bring the pH into the normal range, which implies complete compensation).
A 67-year-old woman is admitted to the hospital for evaluation of several days of profuse watery diarrhea. She is extremely fatigued. She has tachycardia (HR 125) and tachypnea (RR 20) and appears dehydrated on exam. Blood work reveals the following:
This patient’s diarrhea has resulted in the loss of -rich intestinal fluid, causing a hyperchloremic metabolic acidosis. Note that this is a normal anion gap metabolic acidosis because there is no production of an unmeasured anion. Based on Winter’s formula, appropriate respiratory compensation (through hyperventilation) should result in a drop in Pco2 from 40 to approximately 32 (expected Pco2 = 1.5 ×  + 8 ± 2). Therefore, this patient is experiencing a normal anion gap metabolic acidosis (from diarrhea) with appropriate respiratory compensation. She needs aggressive hydration.