Why Is Bicarbonate Low in Diabetic Ketoacidosis?

Diabetic Ketoacidosis (DKA) is a severe, life-threatening complication of diabetes defined by high blood sugar, the presence of acidic ketone bodies, and metabolic acidosis. The most telling biochemical sign of this acid-base imbalance is a markedly low concentration of bicarbonate in the blood. This reduction in the body’s primary neutralizing agent is a direct consequence of the massive acid load produced by uncontrolled diabetes.

Bicarbonate and the Body’s Acid-Base Balance

The human body maintains a tightly regulated blood pH within the narrow range of 7.35 to 7.45. Bicarbonate ions (\(\text{HCO}_3^-\)) play the primary role in this regulation as the main component of the bicarbonate buffer system.

This chemical buffer system acts as the body’s frontline defense against sudden changes in acidity. When excess acid (hydrogen ions, \(\text{H}^+\)) enters the bloodstream, bicarbonate quickly neutralizes it. The reaction transforms the strong acid into a much weaker acid, carbonic acid (\(\text{H}_2\text{CO}_3\)). This process minimizes the change in blood pH, but it consumes a bicarbonate ion for every hydrogen ion neutralized. A normal serum bicarbonate level is between 22 and 29 mEq/L, and a drop below this range is the biochemical marker of metabolic acidosis.

How Insulin Deficiency Creates Ketone Acids

The root cause of the acid overload in DKA stems from an absolute or relative lack of insulin. Insulin allows glucose to enter cells for energy. When insulin is insufficient, cells cannot access glucose, leading to a state of “starvation in the midst of plenty.”

The body responds by switching its primary fuel source from carbohydrates to fat. Counter-regulatory hormones, such as glucagon and cortisol, increase and stimulate the breakdown of fat stores, a process called lipolysis. This releases a large amount of free fatty acids into the bloodstream.

The liver takes up these free fatty acids and rapidly converts them into alternative fuel molecules called ketone bodies through ketogenesis. The main ketone bodies produced are beta-hydroxybutyrate and acetoacetate. These are strong organic acids that dissociate readily in the blood, releasing a massive influx of hydrogen ions (\(\text{H}^+\)) into the circulation. This overproduction of strong acids fundamentally drives the acidosis in DKA.

Why Excess Acid Consumes Bicarbonate

The hydrogen ions released by the newly generated ketoacids immediately threaten the stability of the blood’s pH. The body’s buffer system is instantly mobilized to counteract this acid invasion, using circulating bicarbonate ions as the first line of defense.

The chemical reaction involves one molecule of bicarbonate reacting with one hydrogen ion (\(\text{H}^+\)) from the ketoacid. This neutralizes the strong acid, converting it into water and carbon dioxide (\(\text{CO}_2\)). For every molecule of ketoacid neutralized, one molecule of bicarbonate is consumed from the blood plasma.

This continuous consumption is why serum bicarbonate levels fall dramatically in DKA. The low bicarbonate reading is measurable evidence of the buffer system working hard to protect the body from rising acid levels. In severe DKA, the concentration can drop below 10 mEq/L, indicating that the buffer capacity is severely depleted. This depletion of the alkaline reserve is the very definition of a high anion gap metabolic acidosis.

The Body’s Attempt to Compensate

As the bicarbonate buffer system becomes overwhelmed and the blood pH drops, the body activates its second line of defense: the respiratory system. The brain detects the increase in acidity and stimulates deep, rapid breathing known as Kussmaul respiration. This intense hyperventilation aims to blow off large amounts of carbon dioxide (\(\text{CO}_2\)).

By exhaling more \(\text{CO}_2\), the body reduces the overall acid concentration in the blood and partially raises the pH. This compensation mechanism attempts to stabilize the internal environment but cannot resolve the underlying problem. Definitive treatment requires administering insulin to stop ketoacid production and providing fluids, allowing the body to regenerate its bicarbonate reserves.