A 24-year-old woman with a medical history of bronchial asthma comes to the office due to shortness of breath and wheezing for the past 2-3 days. She developed a cold 4 days ago and is not feeling well. The patient has a nebulizer at home and used multiple doses of albuterol with little response prior to arriving. She takes no other medications. The patient is diaphoretic and in moderate respiratory distress. Respiratory examination shows bilateral wheezing, diffusely decreased breath sounds, and increased use of accessory muscles of respiration. Laboratory results reveal a serum potassium of 3 mEq/L. Which of the following mechanisms is the most likely cause of this patient's hypokalemia?

Question

A 24-year-old woman with a medical history of bronchial asthma comes to the office due to shortness of breath and wheezing for the past 2-3 days.  She developed a cold 4 days ago and is not feeling well.  The patient has a nebulizer at home and used multiple doses of albuterol with little response prior to arriving.  She takes no other medications.  The patient is diaphoretic and in moderate respiratory distress.  Respiratory examination shows bilateral wheezing, diffusely decreased breath sounds, and increased use of accessory muscles of respiration.  Laboratory results reveal a serum potassium of 3 mEq/L.  Which of the following mechanisms is the most likely cause of this patient's hypokalemia?

Quizplus · Accepted Answer

11ec160b_3c68_6a52_9249_731ceeba86cf_MD0001_00 Hypokalemia is a common medical condition that can result from several mechanisms, including decreased oral intake, renal or gastrointestinal loss, and increased entry into cells. In a patient receiving multiple doses of albuterol, the most likely etiology is intracellular shift of potassium. Potassium is primarily stored intracellularly (~98% of total body stores) through the action of the Na-K-ATPase pump, which exchanges sodium for potassium against their concentration gradient. The large concentration difference of intracellular (~150 mEq/L) to extracellular potassium (~4 mEq/L) is a major driver of the resting membrane potential. Alterations in this ratio can impair action potential generation, explaining why patients with marked hyper- or hypokalemia can develop muscular weakness and cardiac arrhythmias. Beta-adrenergic activity increases the activity of the Na-K-ATPase pump; therefore, both endogenous catecholamines and therapeutic beta-2 agonists (eg, albuterol, dobutamine) can cause transient hypokalemia due to increased transport of potassium intracellularly. Similar effects can also occur with sympathomimetics (eg, pseudoephedrine) and insulin, which also increase Na-K-ATPase activity. (Choice A) Decreased oral intake of potassium is a rare cause of hypokalemia. Because the kidneys can lower potassium excretion in the setting of reduced potassium intake, most patients do not develop hypokalemia unless fasting is prolonged (eg, starvation). (Choice B) Respiratory acidosis may occur as a complication of asthma or chronic obstructive pulmonary disease due to CO₂ retention; however, acidosis causes potassium to shift to the extracellular space, leading to hyperkalemia (not hypokalemia). In contrast, alkalosis causes intracellular shift of potassium, resulting in transient hypokalemia. (Choice C) Significant diaphoresis (eg, marathon running in a hot climate) can result in potassium depletion. However, normal sweating (as could occur in patients with increased work of breathing) would not result in significant potassium loss. (Choice D) Increased urinary potassium loss can occur due to diuretic use or elevated aldosterone levels (eg, renovascular disease, primary hyperaldosteronism). While beta-1 agonists can result in increased renin release (leading to elevated aldosterone levels and increased renal potassium loss), beta-2 agonists (eg, albuterol) do not have a significant effect on urinary potassium excretion. Educational objective: Potassium is primarily stored intracellularly (~98% of total body stores) through the action of the Na-K-ATPase pump. Beta-adrenergic activity increases the activity of the Na-K-ATPase pump; therefore, both endogenous catecholamines and therapeutic beta-2 agonists (eg, albuterol, dobutamine) can cause transient hypokalemia due to increased transport of potassium intracellularly.

A 24-Year-Old Woman with a Medical History of Bronchial Asthma