NCLEX Question of the Day – Saturday, February 21, 2026

Today’s question targets safe cardiac medication management. You’ll practice spotting signs of toxicity, understanding drug–electrolyte interactions, and choosing the safest first action. This matters on real shifts because early recognition and a clear response prevent rhythm complications and avoidable deterioration.

Clinical Scenario

A 76-year-old man on a telemetry unit is being treated for chronic heart failure with preserved ejection fraction. He was discharged last month and readmitted yesterday for volume overload. Home medications include furosemide 40 mg PO twice daily and lisinopril 10 mg PO daily. The provider restarted digoxin 0.125 mg PO daily two days ago.

At 0800, the client reports new nausea and “halos” around lights. Telemetry shows sinus bradycardia at 48/min with occasional premature ventricular contractions. Blood pressure is 98/60, oxygen saturation 96% on room air, and he is alert and oriented. Labs: potassium 2.9 mEq/L, magnesium 1.6 mg/dL, creatinine 1.6 mg/dL.

The Question

Which action should the nurse take first?

Answer Choices

1. A. Administer the scheduled digoxin dose and recheck the heart rate in 1 hour.
2. B. Hold the digoxin, place the client on continuous cardiac monitoring, and notify the provider of the findings.
3. C. Give PRN ondansetron for nausea and encourage small, frequent meals.
4. D. Administer potassium chloride 40 mEq PO now and continue routine monitoring.

Correct Answer

B. Hold the digoxin, place the client on continuous cardiac monitoring, and notify the provider of the findings.

Detailed Rationale

This client has classic signs of potential digoxin toxicity: gastrointestinal symptoms (nausea, poor appetite), visual changes (yellow halos), and bradycardia with ectopy (PVCs). Three risk factors amplify this: hypokalemia (K 2.9), hypomagnesemia (Mg 1.6), and reduced renal clearance (creatinine 1.6) because digoxin is renally excreted. Low potassium increases digoxin’s effect at the sodium-potassium ATPase, making the myocardium more sensitive and prone to dysrhythmias.

The safest first action is to stop exposure to the suspected culprit and stabilize monitoring. Holding digoxin prevents further accumulation. Continuous monitoring is needed because the client already has bradycardia and PVCs, which can progress. Promptly notifying the provider enables rapid orders for serum digoxin level, electrolyte replacement (potassium and magnesium), and, if indicated, antidote therapy with digoxin immune Fab. The nurse should also assess an apical pulse for a full minute (hold if less than 60), review all meds for interactions (e.g., diuretics causing electrolyte loss), and obtain a 12-lead ECG if status changes.

What to assess, do, and monitor:

• Assess: apical pulse for 1 full minute, mental status, new visual changes, GI symptoms, perfusion signs (dizziness, syncope), and telemetry strips for worsening ectopy or heart block.
• Do: hold digoxin, keep on continuous cardiac monitoring, maintain IV access, verify recent labs, anticipate and implement electrolyte replacement per orders, and prepare to draw a digoxin level (ideally at steady state or at least 6–8 hours after dose).
• Monitor: heart rate/rhythm response to electrolyte correction, potassium and magnesium trends, renal function, and symptom resolution. Watch for indications for atropine (symptomatic bradycardia) or advanced interventions if instability occurs.

Why the Other Options Are Wrong

• A. Administering digoxin despite bradycardia and toxicity symptoms is unsafe. Standard practice is to hold if apical pulse less than 60 in adults or if toxicity is suspected. Waiting an hour risks worsening dysrhythmias.
• C. Treating nausea alone misses the root cause. Antiemetics may mask symptoms without addressing the cardiac risk. The priority is to stop digoxin exposure and correct electrolytes while monitoring rhythm.
• D. Potassium replacement is needed, but administering 40 mEq PO “now” without an order is outside scope and may be unsafe in a client with renal impairment. The sequence matters: hold the drug, ensure monitoring, notify the provider for targeted replacement (often IV if symptomatic or markedly low) and for a comprehensive plan that includes magnesium repletion and digoxin levels.

Key Takeaways

• Suspect digoxin toxicity with nausea, visual changes, and bradyarrhythmias—especially with low K/Mg or impaired renal function.
• First move: hold digoxin, monitor continuously, and notify the provider. Do not “wait and see.”
• Hypokalemia and hypomagnesemia make dysrhythmias more likely; correct both, not just potassium.
• Assess apical pulse for 1 minute before digoxin; hold if less than 60 in adults.
• Plan for labs: serum digoxin level, electrolytes, and renal function; anticipate possible digoxin immune Fab if severe.

On-shift mini-checklist

• Apical pulse 1 minute before digoxin; hold if less than 60 and call.
• Review K, Mg, Cr before dosing; request replacement/orders if low.
• Watch for GI/visual complaints and new brady or ectopy on telemetry.
• Maintain IV access; prepare for electrolyte repletion and ECG.
• Document findings, actions taken, and patient response clearly.

Quick Practice Extension

• Which additional lab abnormality, if present, would further increase the risk of digoxin toxicity, and why?
• A client on digoxin develops symptomatic bradycardia with hypotension. List the immediate steps you would take in order.

G S Sachin

I am a Registered Pharmacist under the Pharmacy Act, 1948, and the founder of PharmacyFreak.com. I hold a Bachelor of Pharmacy degree from Rungta College of Pharmaceutical Science and Research. With a strong academic foundation and practical knowledge, I am committed to providing accurate, easy-to-understand content to support pharmacy students and professionals. My aim is to make complex pharmaceutical concepts accessible and useful for real-world application.

Mail- Sachin@pharmacyfreak.com