Acid-Base Disorders in the Critically Ill Patient

Abstract

Acid-base disorders are common in the intensive care unit. By utilizing a systematic approach to their diagnosis, it is easy to identify both simple and mixed disturbances. These disorders are divided into four major categories: metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis. Metabolic acidosis is subdivided into anion gap and non-gap acidosis. Distinguishing between these is helpful in establishing the cause of the acidosis. Anion gap acidosis, caused by the accumulation of organic anions from sepsis, diabetes, alcohol use, and numerous drugs and toxins, is usually present on admission to the intensive care unit. Lactic acidosis from decreased delivery or utilization of oxygen is associated with increased mortality. This is likely secondary to the disease process, as opposed to the degree of acidemia. Treatment of an anion gap acidosis is aimed at the underlying disease or removal of the toxin. The use of therapy to normalize the pH is controversial. Non-gap acidoses result from disorders of renal tubular H + transport, decreased renal ammonia secretion, gastrointestinal and kidney losses of bicarbonate, dilution of serum bicarbonate from excessive intravenous fluid administration, or addition of hydrochloric acid. Metabolic alkalosis is the most common acid-base disorder found in patients who are critically ill, and most often occurs after admission to the intensive care unit. Its etiology is most often secondary to the aggressive therapeutic interventions used to treat shock, acidemia, volume overload, severe coagulopathy, respiratory failure, and AKI. Treatment consists of volume resuscitation and repletion of potassium deficits. Aggressive lowering of the pH is usually not necessary. Respiratory disorders are caused by either decreased or increased minute ventilation. The use of permissive hypercapnia to prevent barotrauma has become the standard of care. The use of bicarbonate to correct the acidemia is not recommended. In patients at the extreme, the use of extracorporeal therapies to remove CO 2 can be considered.

Figure 1

A systematic approach to acid-base disorders.

Figure 2

Because the concentration of unmeasured anions, predominantly albumin, is greater than that of unmeasured cations, there is an anion gap (AG) (Na⁺ − [Cl⁻ + HCO3⁻]) between 8 and 10 meq/L. The addition of an organic anion (i.e., lactate, β-hydroxybutyrate) increases the AG. However, when Cl⁻ is the anion that accompanies H⁺, there is no change in the AG.

Figure 3

Etiology of metabolic acidosis. HCMA, hyperchloremic metabolic acidosis; RTA, renal tubular acidosis.

Figure 4

Pyruvate, which is a byproduct of glycolysis, can enter the tricarboxcylic acid cycle where it is further metabolized to CO₂ and water, enter the Cori cycle to regenerate glucose, or, under anaerobic conditions, be hydrolyzed to lactate.

Figure 5

Relationship between AG acidosis and osmolality after ingestion of a toxic alcohol. Initially, the alcohol produces an increase in osmolality without an increase in the AG. Metabolism of the alcohol reduces the osmolality and increases the AG.

Figure 6

Etiology of a non–gap metabolic acidosis.

Figure 7

Etiology of a metabolic alkalosis.

Figure 8

Etiology of a metabolic alkalosis associated with nasogastric suction. Loss of gastric contents containing H⁺ and Na⁺ increases the serum HCO₃ and causes hypovolemia. Initially, the kidney excretes the excess HCO₃ along with K⁺ causing hypokalemia. Potassium comes out of cells in exchange for the shift of H⁺ into cells, worsening the alkalemia. Finally, hypovolemia activates neurohormonal mechanism that increases tubular reabsorption of HCO₃.