A 45-year-old attorney travels to the Caribbean islands for vacation. While away she develops profuse vomiting and diarrhea due to an unknown gastrointestinal (GI) pathogen. She is able to fly home but becomes profoundly dehydrated, unable to keep up with her GI fluid losses. On her second day back from the trip, her husband returns home from work to find her somnolent and minimally responsive with decreased respiratory effort. He immediately calls 911 and an ambulance arrives to transport her to her local emergency department (ED).

In the ED she is clearly dehydrated with dry mucous membranes and loss of her normal skin turgor. Her heart rate is 124 and her blood pressure is measured at 100/70 mm Hg. In addition, she appears somnolent and has a severely diminished respiratory drive, requiring endotracheal intubation for her severe hypoventilation. Her initial arterial blood gas shows a pH of 7.55 (normal 7.40 to 7.44), with a partial pressure of carbon dioxide (PCO₂) of 66 mm Hg (normal 40). Her arterial partial pressure of oxygen is normal at 95 mm Hg.

With concern for dehydration, the covering ED physician places a central venous catheter and begins intravenously administering fluids to replace volume loss. After a half hour of volume administration, the patient returns to stable vital signs and again begins to produce urine. However, the nurse is concerned because despite this improvement, the patient remains weak and lethargic, unable to follow commands. In addition, the cardiac monitor shows what the nurse believes to be an abnormal rhythm. The resident orders an electrocardiogram (ECG), which shows prominent U waves. A serumelectrolyte panel is ordered, which reveals a potassium level of 1.7 mg/dL (nl 3.5 to 5.0 mg/dL). After aggressive potassium repletion, the patient once again begins following commands and regains her strength, able to tolerate eventual extubation. She is discharged home on hospital day number two.

Metabolic alkalosis is the most common acid-base abnormality seen in hospital inpatients. Severe alkalosis is an extremely serious problem as
mortality rates can exceed 50%. Alkalosis can lead to diffuse arterial constriction with perfusion reduction. Thus, common signs of alkalosis include decreased mental status and seizures. In addition, severe alkalosis can cause hypoventilation, leading to hypoxemia. Finally, alkalosis can lead to life-threatening hypokalemia due to cellular shifts of potassium for hydrogen ions in an attempt to correct serum pH.

Metabolic alkalosis is defined as a pathologic increase in the serum bicarbonate (HCO_3-) concentration. This occurs either as a gain in bicarbonate or a loss of acid. Compensation occurs through action of the respiratory system, with hypoventilation to lead to retained CO₂ and increased acid. Typical blood gas values show a pH value around 7.50 with PCO₂ values around 60 mm Hg.

There are many causes of metabolic alkalosis. First is loss of hydrogen ions, leading to bicarbonate excess. Hydrogen losses occur commonly in the gastrointestinal tract. GI losses include vomiting and nasogastric suction. A second source of alkalosis occurs as a response to hypokalemia. In this setting, potassium will shift out of cells as compensation. Hydrogen ions shift intracellularly, leading to alkalosis. Finally, a third etiology of metabolic alkalosis is due to loss of bicarbonate-poor, chloride-rich extracellular fluid as can occur with dehydration in the setting of diuretic therapy. The lower fluid levels contain a relative excess in serumbicarbonate, leading to a “contraction alkalosis.�

This patient developed a metabolic alkalosis due to a combination of GI losses from vomiting and diarrhea and also had contraction due to extracellular fluid losses. Her presentation was typical in the sense that she was somnolent and hypoventilated to compensate for her alkalosis. In the case described previously, there was failure to replete a low potassium level in the setting of metabolic alkalosis. Patients with metabolic alkalosis have intracellular shifting of potassium, which allows hydrogen ions to shift extracellularly to help correct pH. For this reason, patients with metabolic alkalosis can manifest severe hypokalemia. No potassium was checked until the patient developed ECG changes. The principal clinical manifestations of hypokalemia include lethargy and muscle weakness. In addition, U waves are often seen on ECG tracings. Hypokalemia by itself is unlikely to cause life-threatening arrhythmias. However, one must always be cognizant of other electrolyte abnormalities associated with hypokalemia, such as hypomagnesemia, which is known to cause serious arrhythmias. It is, however, important to be cautious with potassium repletion, as overaggressive repletion in the setting of alkalosis can lead to life-threatening hyperkalemia. This occurs when the alkalosis is corrected and intracellularly
stored potassium returns to the extracellular compartment. This can be especially problematic in the setting of acute renal failure, which can occur in dehydrated patients. Thus, vigilance with cautious potassium repletion of potassium to normal to high normal levels is of paramount importance for patients with metabolic alkalosis.