Nursing care
Angiotensin Receptor Blockers: what to check before you give it
Written and reviewed by Dana Whitfield, RN, MSN · 4 min read · Updated September 2026
Short answer
Angiotensin receptor blockers lower blood pressure by blocking the AT1 receptor rather than the enzyme, so they are prescribed most often when an ACE inhibitor caused a persistent dry cough. They carry the same core risks, hyperkalemia, renal effects, and hypotension, and although angioedema is far less common than with ACE inhibitors, the risk does not disappear entirely.
Why this drug and not another
ARBs and ACE inhibitors both interrupt the renin-angiotensin-aldosterone system, but at different points. ACE inhibitors block the enzyme that converts angiotensin I to angiotensin II, and in doing so they also block the breakdown of bradykinin, which is what causes the dry, persistent cough and, in some patients, angioedema. ARBs act downstream, blocking angiotensin II at the AT1 receptor directly, so bradykinin accumulation is far less of an issue.
That mechanism difference is the reason ARBs such as losartan and valsartan are the standard substitute when a patient develops an ACE inhibitor cough that will not resolve. The blood pressure and renal protective benefits carry over because the end result, less angiotensin II activity, is the same; only the route there has changed, and with it the cough all but disappears in most patients.
Administration and timing
Most ARBs are given once daily and can be taken with or without food, which supports adherence in patients managing several medications. Losartan and valsartan follow this pattern; check the specific product for any exceptions, since bioavailability can vary slightly between agents in the class.
Establish a baseline blood pressure and heart rate before the first dose and reassess after any dose change, since the antihypertensive effect builds over the first one to two weeks rather than appearing immediately. Encourage the patient to take the dose at the same time each day, and advise against stopping abruptly, particularly if the drug is also being used for renal protection in diabetic nephropathy.
Monitoring parameters
Check serum potassium and renal function, BUN and creatinine, before starting and periodically during therapy. ARBs reduce aldosterone secretion, which reduces potassium excretion, so hyperkalemia is an expected risk, especially alongside potassium-sparing diuretics, potassium supplements, or NSAIDs.
Monitor blood pressure regularly, watching for symptomatic hypotension, dizziness, or lightheadedness, particularly after the first dose or a dose increase and in patients who are also volume depleted. In patients with renal artery stenosis, a rise in creatinine after starting the drug can signal a critical drop in renal perfusion and needs prompt reporting rather than being dismissed as an expected lab shift.
Adverse effects to report
Report hyperkalemia symptoms, muscle weakness, irregular heartbeat, or paresthesias, along with any significant rise in serum potassium on labs. Report a sustained drop in blood pressure with dizziness or syncope, and any marked rise in creatinine that suggests reduced renal perfusion.
Report facial, lip, or tongue swelling and any difficulty breathing or swallowing immediately, this is angioedema, and although it occurs far less often with ARBs than with ACE inhibitors, it can still happen and is a medical emergency. A patient who developed angioedema on an ACE inhibitor is not automatically safe on an ARB; the risk is reduced, not eliminated, and the switch is made with that caveat in mind.
Contraindications and cautions
ARBs are contraindicated in pregnancy, particularly the second and third trimesters, because of fetal renal toxicity and other harms; any patient of childbearing age should be counselled on effective contraception and the drug stopped as soon as pregnancy is confirmed or planned.
Use caution in bilateral renal artery stenosis, where blocking angiotensin II can critically reduce glomerular filtration, and in significant hyperkalemia or renal impairment, where the drug's effect on potassium and creatinine needs closer monitoring. Combining an ARB with an ACE inhibitor or a direct renin inhibitor is generally avoided, since dual RAAS blockade raises the risk of hyperkalemia and renal injury without a clear added benefit.
Teaching points the exam tests
The exam wants the nurse to know that ARBs are the go-to substitute when an ACE inhibitor causes a cough, and to know why: the mechanism spares bradykinin, which is what drove the cough in the first place. Expect questions that test whether the student recognises this switch as pharmacologically sound rather than arbitrary.
The exam also tests angioedema recognition, swelling of the face, lips, tongue, or throat with respiratory compromise, as an emergency requiring the drug to be held and the prescriber notified immediately, and tests the nurse's ability to catch hyperkalemia and hypotension on routine labs and vitals before they become symptomatic. Expect a question pairing ARB use with pregnancy as an absolute contraindication.
The next step on this is the same as on everything else here: answer questions and read the rationales. Our pharmacology practice questions are the closest set to what this page covers.
One question from the pharmacology set
A client with heart failure is started on furosemide 40 mg PO daily. Which findings should the nurse report to the provider before administering the next dose? Select all that apply.
Rationale
Furosemide is a loop diuretic, so the two things you are watching are potassium and kidney function. A potassium of 2.9 mEq/L is below the 3.5–5.0 reference range and puts the client at risk for dysrhythmia — hold and report. Muscle cramps with palpitations are the clinical face of that same hypokalemia, so they are reported together, not separately. A creatinine that doubles signals the diuresis has outrun renal perfusion. A blood pressure of 132/78 and a 1 kg loss are the expected response to the drug working, not reasons to hold it.
Answer: A, D, E
Common questions
Why does an ARB not cause the cough that ACE inhibitors cause?
ACE inhibitors block the enzyme that also breaks down bradykinin, so bradykinin builds up and irritates the airway, causing a dry cough. ARBs act at the angiotensin II receptor instead, leaving bradykinin metabolism largely untouched, which is why the cough resolves in most patients switched to an ARB.
Can a patient who had angioedema on an ACE inhibitor safely take an ARB?
The risk is meaningfully lower but not zero, so the switch is made cautiously and with clear teaching on the signs of facial or airway swelling. Any prior history of angioedema on either drug class should be documented and flagged before the ARB is started.
What electrolyte should the nurse watch most closely with ARBs?
Potassium. ARBs reduce aldosterone activity, which reduces potassium excretion, so hyperkalemia is the electrolyte disturbance to monitor, especially in patients also taking potassium-sparing diuretics or supplements.
Are ARBs safe in pregnancy?
No. They are contraindicated, particularly in the second and third trimesters, due to fetal renal toxicity and other adverse outcomes. Any patient who becomes pregnant while on an ARB should have the drug stopped and the prescriber notified promptly.
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