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Nursing Field Notes / Cardio · Antihypertensive Drug Classes

ARBs 🫀

Angiotensin Receptor Blockers — the "-SARTAN" drugs

NG-137 CARDIO ADHD-friendly visual edition

Block angiotensin II from binding the AT1 receptor — downstream in the RAAS pathway. Same end result as an ACE inhibitor (less vasoconstriction, less aldosterone, lower BP), but angiotensin II is still made — it just can't act. Because bradykinin is untouched, ARBs are the go-to substitute when a client can't tolerate the ACE-inhibitor cough.

📄 Simple Nursing original — opens in Drive →

🔗 Paired with NG-091 ACE Inhibitors — same pathway, same job, constantly confused on exams. Open the ACE Inhibitor page → to see the side-by-side comparison and the shared RAAS diagram.
🫀 -SARTAN = ARBLosartan, valsartan, irbesartan — blocks the AT1 receptor, downstream.
🚫 No cough, no angiedemaBradykinin pathway is untouched — the #1 reason to pick an ARB over an ACE inhibitor.
🧎 First-dose hypotensionSame teaching as ACE inhibitors — rise slowly, first dose at bedtime.
🍌 Watch potassiumSame hyperkalemia risk as ACE inhibitors — avoid salt substitutes.
💊

WHAT IT DOES

STEP 1 · THE MECHANISM

Same cascade as ACE inhibitors — the block just happens one step later.

🧬 The RAAS pathway — where ARBs block it

EXAM TIP ARBs block angiotensin II at the AT1 receptor — angiotensin II is still made, it just can't bind and do its job. This is the SAME shared diagram used on the ACE Inhibitor page — compare where each class blocks the cascade.

Angiotensinogen made by the liver RENIN (kidney, ↓perfusion) Angiotensin I inactive ✕ ACE (lungs) (ACE inhibitors block HERE — see NG-091) ✅ Bradykinin untouched ARBs don't act on ACE, so bradykinin breakdown is normal. No buildup — no dry cough, minimal angiedema risk This is why ARBs replace an ACE inhibitor the cough won't quit. Angiotensin II still made — normally ✕ binds AT1 receptor ARBs block HERE (-SARTAN) AT1 receptors vascular smooth muscle + adrenal cortex Vasoconstriction → blocked at receptor Aldosterone (adrenal cortex) → Na⁺/H₂O retention → blocked here too — ⬇K⁺ excretion ⬇ BLOOD PRESSURE
🧠 "TAN blocks the target, not the tap." Angiotensin II still flows (the "tap" isn't shut, unlike with -pril), but it can't dock at the receptor — so it can't do its job.

🔤 Say the suffix — it tells you the class

  • -SARTAN = ARB 🫀
  • Losartan (Cozaar) — 50 mg once daily PO
  • Valsartan (Diovan) — 80–160 mg once daily PO
  • Irbesartan (Avapro) — 150 mg once daily PO
🧠 "SAR-TAN, easy to ID-tify." Every ARB generic name ends in -sartan — no exceptions, unlike some other drug families.

⭐ Why we give it — indications

  • Hypertension
  • Heart failure — alternative when ACE inhibitor not tolerated
  • Diabetic nephropathy — same renal protection as ACE inhibitors
  • Often first-choice in Black patients on monotherapy in some guideline pathways, and when an ACE-inhibitor cough has already occurred
🧠 "Same job, no cough." Wherever you'd reach for an ACE inhibitor, an ARB is the backup plan when the cough won't quit.

💊 Common generics, trade names & typical adult dosing

GenericTradeTypical doseRoute
LosartanCozaar50 mg once dailyPO
ValsartanDiovan80 mg or 160 mg once dailyPO
IrbesartanAvapro150 mg once dailyPO

Doses shown are typical starting/maintenance figures — titrate to the prescriber's order and the client's response.

🧠 All once-daily. Unlike captopril's multiple-times-a-day dosing, the ARB family is built for once-a-day adherence.
⚠️

WATCH FOR

STEP 2 · THE DANGER LIST

No cough — but the same hypotension, potassium, and pregnancy risks carry straight over from the ACE inhibitors.

🧎 First-dose orthostatic hypotension

🛏️ Lying / seated BP stable ? 🧍 Stands fast BP drops → dizzy / falls

Biggest drop after the very first dose, same as ACE inhibitors. Give the first dose at bedtime, teach rise slowly, and use fall precautions especially in older adults.

🧠 "Both PRIL and TAN drop you fast." This is a RAAS-wide effect — identical teaching for both drug classes.

🍌 Hyperkalemia risk — identical mechanism

low normal 3.5–5.0 high ARBs push K⁺ this way ➜

Blocking the AT1 receptor blocks aldosterone release just as effectively as blocking ACE — kidney keeps K⁺ instead of excreting it. Same monitoring: avoid salt substitutes, watch peaked T waves, check labs.

🧠 "Downstream doesn't mean different destination." ARBs block a later step, but the K⁺-sparing effect on the adrenal gland is the same as an ACE inhibitor's.

❌ Contraindications — absolute no

🤰Pregnancy2nd/3rd trimester — same fetal renal risk as ACE inhibitors
🩸Bilateral renalartery stenosis
🍌Hyperkalemiapre-existing
💧Volume depletionsevere dehydration
🚫Don't combineARB + ACE inhibitor together — no added benefit, added risk
🧠 "Never PRIL + TAN at the same time." Dual RAAS blockade raises hyperkalemia and acute kidney injury risk without improving outcomes — pick one class, not both.
🗣️

TEACH

STEP 3 · WHAT THE CLIENT NEEDS TO HEAR

Same rise-slowly and potassium teaching as ACE inhibitors — but no cough conversation needed.

✅ Teaching checklist

1
🧎 Rise slowly — sit, then stand, especially the first few doses
2
🧂 Avoid salt substitutes — many contain potassium chloride
3
🧪 Routine labs — potassium & renal function
4
🚻 Confirm no pregnancy before starting; stop immediately if pregnant
5
✅ Reassure: unlike an ACE inhibitor, this class is not expected to cause a dry cough
🧠 "Same slow rise, no dry surprise." Everything you teach for an ACE inhibitor applies here — minus the cough conversation.

💊 Drug interactions to flag

  • NSAIDs — reduced antihypertensive effect
  • Potassium-sparing diuretics — elevated K⁺ (hyperkalemia)
  • Lithium — possible lithium toxicity
  • Loop diuretics — decreased diuretic effect
  • Hypoglycemics (insulin) — increased hypoglycemia risk
🧠 Interactions mirror the ACE inhibitor list almost line for line — because the downstream physiology they're both shutting off is the same.

🆚 ACE inhibitor vs ARB — tell them apart

FeatureACE Inhibitor (-PRIL)ARB (-SARTAN)
BlocksThe enzyme (Angiotensin I → II) — upstreamThe AT1 receptor — downstream
BradykininBuilds up (ACE breaks it down normally)Unaffected
Dry coughYes — classic side effectNO — this is why it's the substitute
AngiedemaYes (bradykinin-driven)Rare, lower risk
HyperkalemiaYesYes — same mechanism
First-dose hypotensionYesYes
PregnancyContraindicated 2nd/3rd trimesterContraindicated 2nd/3rd trimester
When to chooseFirst-line unless contraindicatedClient can't tolerate the ACE-inhibitor cough
🧠 "If they cough on the PRIL, switch to the TAN." The single most heavily tested fact in this whole pair of drugs — memorize it as a pair, not two separate cards.
⚡

QUICK RECALL

SAY IT OUT LOUD
🫀 -SARTANblocks the AT1 receptor, downstream — angiotensin II still forms
🚫 No bradykinin buildupno cough, minimal angiedema — the substitute for ACE intolerance
🧎 First dosegive at bedtime, rise slowly — same as ACE inhibitors
🍌 Hyperkalemiasame K⁺ risk, same salt-substitute teaching
🎯 Cover & check — 4 rapid-fire questions
Q1: Where do ARBs act in the RAAS pathway, compared to ACE inhibitors?
ARBs act downstream, at the AT1 receptor, blocking angiotensin II from binding. ACE inhibitors act upstream, at the enzyme, preventing angiotensin II from being made at all.
Q2: A client switches from lisinopril to losartan because of a cough. Why does this fix it?
ARBs don't affect ACE, so bradykinin is broken down normally and doesn't build up — no bradykinin buildup means no cough.
Q3: Should a client ever be on an ACE inhibitor AND an ARB together?
No — dual RAAS blockade increases hyperkalemia and acute kidney injury risk without added benefit.
Q4: What teaching is identical between ACE inhibitors and ARBs?
Rise slowly (first-dose orthostatic hypotension), avoid salt substitutes and potassium supplements, get routine potassium/renal labs, and avoid in pregnancy.