A 44-year-old man comes to the hospital due to acute onset of central chest pain radiating to the left arm. He used cocaine a few hours ago. Blood pressure is 160/100 mm Hg, pulse is 98/min, and respirations are 18/min. On examination, the patient appears anxious and diaphoretic. Electrocardiogram shows ST-segment elevation in the anterior leads. Laboratory studies reveal an elevated cardiac troponin level and a serum potassium concentration of 3.1 mEq/L. Which of the following is the most likely cause of this patient's hypokalemia?

Question

A 44-year-old man comes to the hospital due to acute onset of central chest pain radiating to the left arm.  He used cocaine a few hours ago.  Blood pressure is 160/100 mm Hg, pulse is 98/min, and respirations are 18/min.  On examination, the patient appears anxious and diaphoretic.  Electrocardiogram shows ST-segment elevation in the anterior leads.  Laboratory studies reveal an elevated cardiac troponin level and a serum potassium concentration of 3.1 mEq/L.  Which of the following is the most likely cause of this patient's hypokalemia?

Quizplus · Accepted Answer

11ec160b_3cf8_c3ef_9249_6ff8c600ea4a_MD0001_00 Low serum potassium is a common medical condition that can result from several mechanisms, including decreased oral intake, renal or gastrointestinal loss, or increased entry into cells. This patient with a cocaine-induced myocardial infarction most likely developed acute hypokalemia due to stress-related beta-adrenergic hyperactivity, which causes potassium to shift intracellularly. Severe physiologic stress (eg, myocardial infarction, head injury) results in significant endogenous catecholamine (eg, norepinephrine, epinephrine) release. Epinephrine activates the beta-2 receptor, leading to increased activity of the sodium-potassium ATPase pump and the sodium-potassium-2-chloride cotransporter, both of which transport potassium intracellularly. Adrenergic activity also stimulates the release of insulin, which further promotes intracellular potassium shifting. Although cocaine does not directly stimulate beta-2 receptors, it does increase catecholamine release, likely worsening hypokalemia. Similar intracellular shifts can be seen with beta-agonist medications (eg, albuterol, dobutamine) and sympathomimetics (eg, pseudoephedrine). Patients with other sources of potassium loss (eg, diuretics, diarrhea) are at increased risk. (Choice A) Hypokalemia due to decreased dietary intake of potassium typically occurs in patients with very poor oral intake (eg, anorexia, starvation, malignancy). (Choice B) Significant gastrointestinal potassium loss can occur with prolonged diarrhea or use of gastrointestinal cation exchangers that bind potassium in exchange for other cations (eg, sodium, calcium). (Choice D) Increased urinary potassium loss can occur with diuretic use and in the setting of elevated aldosterone levels (eg, renovascular disease, primary aldosteronism). Although hyperaldosteronism is associated with hypertension, this patient's elevated blood pressure is likely from cocaine use. (Choice E) Increased potassium uptake by cells during accelerated hematopoiesis (eg, administration of granulocyte-macrophage colony-stimulating factor, acute leukemia) may cause hypokalemia. However, this patient does not have these risk factors. Educational objective: Hypokalemia can result from the intracellular shift of potassium, which can occur due to beta-adrenergic hyperactivity (eg, beta-2 agonists, endogenous epinephrine release), increased insulin levels, elevated extracellular pH, or increased cell production (eg, acute leukemia).

A 44-Year-Old Man Comes to the Hospital Due to Acute