The medication order for a client who receives nutrition via a feeding tube reads: “Give digoxin 0.125 mg per feeding tube once every morning.” The medication is available in a liquid form 50 mcg/mL. How many milliliters will the nurse give for each dose?

Hydrochlorothiazide is a thiazide diuretic that targets the distal convoluted tubule by inhibiting sodium-chloride symporters, thereby promoting potassium excretion and diuresis. It is indicated for hypertension and congestive heart failure management but frequently precipitates metabolic complications. This drug-induced electrolyte imbalance increases myocardial sensitivity to cardiac glycosides, potentially leading to lethal arrhythmias.

Rationale for correct answer

B. Thiazides increase sodium delivery to the late distal tubule, which accelerates the secretion of potassium into the urine. This process leads to hypokalemia, defined as serum potassium levels < 3.5 mEq/L. Low potassium is extremely dangerous for clients taking digoxin because it enhances drug binding to the sodium-potassium ATPase pump. This interaction significantly increases the risk of life-threatening digitalis toxicity.

Rationale for incorrect answers

A. Thiazide diuretics are known to decrease the renal excretion of calcium, which typically results in hypercalcemia rather than low levels. They enhance calcium reabsorption in the distal tubule, making them useful for patients with osteoporosis or kidney stones. Therefore, hypocalcemia is not a characteristic metabolic finding associated with the administration of hydrochlorothiazide therapy.

C. Thiazide and loop diuretics are definitively potassium-wasting agents that facilitate the loss of this cation. Hyperkalemia is only associated with potassium-sparing diuretics, such as spironolactone, or the use of ACE inhibitors. This result would be the physiological opposite of the expected effect of a 50 mg daily dose of hydrochlorothiazide.

D. Thiazide diuretics generally increase the renal excretion of magnesium, which leads to a state of hypomagnesemia. An elevated level, or hypermagnesemia, is rare and usually only occurs in the setting of advanced renal failure or excessive intake of antacids. Like potassium, low magnesium levels actually potentiate the toxic effects of digoxin on the cardiac conduction system.

Test-taking strategy

• Identify the drug interaction: The question pairs a thiazide diuretic (HCTZ) with digoxin. This is a classic "must-know" pharmacological combination in nursing.
• Recall the mechanism of HCTZ: Thiazides are non-potassium-sparing. Their primary metabolic side effect is the depletion of potassium, sodium, and magnesium.
• Prioritize the most dangerous imbalance: While several electrolytes change, hypokalemia is the most clinically significant because of its direct relationship with digoxin toxicity.
  • Digoxin competes with potassium for binding sites on the Na+/K+ ATPase pump.
  • Low potassium means more available binding sites for digoxin, leading to toxic levels even with standard doses.
• Eliminate based on "Hyper" vs "Hypo":
  • Thiazides waste potassium, so any "hyper" potassium option (option 3) is incorrect.
  • Thiazides "save" calcium, so a "hypo" calcium option (option 1) is incorrect.
  • Thiazides waste magnesium, making a "hyper" magnesium option (option 4) incorrect.

Take home points

• Hydrochlorothiazide frequently causes hypokalemia, which is a major risk factor for the development of digoxin toxicity.
• Clients on this combination must be taught to recognize signs of digitalis toxicity, such as yellow-green halos, nausea, and bradycardia.
• Serum potassium levels should be strictly monitored and maintained within the range of 3.5 to 5.0 mEq/L to ensure cardiac safety.
• High-potassium foods or oral potassium supplements are often required when taking thiazide diuretics to offset mandatory renal losses.

Furosemide is a sulfonamide-derived loop diuretic that inhibits the sodium-potassium-chloride symporter in the thick ascending limb. It induces potent natriuresis and volume depletion to manage congestive heart failure and acute edema. Adverse effects include ototoxicity, hyperuricemia, and severe hypokalemia. It is contraindicated in patients with anuria or hepatic coma.

Rationale for correct answer

B. Furosemide causes a significant reduction in intravascular volume by promoting the excretion of sodium and water. This rapid fluid shift directly lowers systemic blood pressure and cardiac preload. The nurse must perform a pre-administration assessment to prevent the exacerbation of hypotension or circulatory collapse. Ensuring hemodynamic stability is a priority nursing intervention during diuretic therapy.

Rationale for incorrect answers

A. Patients receiving loop diuretics are at high risk for developing orthostatic hypotension due to decreased blood volume. Rapidly changing positions can lead to syncope, falls, and subsequent physical injury. Patients should be instructed to dangle their legs at the bedside before standing. This allows the baroreceptor reflex to adjust to the change in gravity and pressure.

C. Diuretics should be administered in the morning to prevent nocturia, which significantly disrupts the sleep-wake cycle. Administering a potent loop diuretic at bedtime increases the frequency of nighttime urination and elevates the risk for falls in older adults. Morning dosing ensures that the peak diuresis occurs during the patient's active waking hours.

D. Furosemide is a non-potassium-sparing agent that promotes significant renal excretion of potassium ions. Patients are at high risk for hypokalemia, not hyperkalemia, and must often increase their intake of potassium-rich fruits. Avoiding fruits would aggravate potassium depletion, potentially leading to lethal cardiac arrhythmias. Maintaining serum potassium between 3.5 and 5.0 mEq/L is essential for cardiac conduction.