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A. Request an order for an antiemetic: Although nausea is a symptom of digoxin toxicity, administering an antiemetic may mask a serious underlying problem. It should not be the first intervention without further assessment of the client’s condition.
B. Check the client's vital signs: Digoxin toxicity can cause bradycardia, hypotension, and arrhythmias. The client's symptoms (nausea, weakness, and visual disturbances) are classic signs of digoxin toxicity. Assessing vital signs is the priority to determine if there is immediate hemodynamic instability, which would guide further urgent interventions.
C. Suggest that the client rests before eating the meal: Fatigue may be related to digoxin toxicity or underlying heart failure, but suggesting rest delays necessary clinical assessment and does not address the potentially serious symptoms.
D. Request a dietitian consult: While nutrition is important for clients with CHF, the presence of nausea, weakness, and visual disturbances suggests possible digoxin toxicity, which requires immediate clinical evaluation not dietary consultation.

• Losartan: As an angiotensin II receptor blocker (ARB), losartan reduces aldosterone secretion, leading to decreased potassium excretion and potential hyperkalemia, especially in patients with renal impairment or those on potassium supplements.

• Furosemide: This loop diuretic promotes the excretion of sodium and potassium in the urine, commonly resulting in hypokalemia. Patients on furosemide often require potassium monitoring or supplementation.
• Spironolactone: A potassium-sparing diuretic and aldosterone antagonist, spironolactone reduces potassium excretion in the distal nephron. This can lead to hyperkalemia, particularly when used with other potassium-elevating drugs.
• Lisinopril: An ACE inhibitor that blocks the conversion of angiotensin I to II, reducing aldosterone levels and thereby decreasing potassium excretion. This places patients at risk for hyperkalemia.
• Digoxin: This cardiac glycoside may cause hypokalemia indirectly by increasing sensitivity to potassium shifts. Additionally, low potassium levels enhance digoxin toxicity, so maintaining normal potassium is critical during therapy.