Nursing Field Notes / Cardio · Antihypertensive Drug Classes
ACE Inhibitors 🫀
Angiotensin-Converting Enzyme Inhibitors — the "-PRIL" drugs
NG-091CARDIOADHD-friendly visual edition
Block ACE, the enzyme that converts Angiotensin I → Angiotensin II — upstream in the RAAS pathway. Less angiotensin II means less vasoconstriction and less aldosterone, so blood pressure drops. Because ACE also breaks down bradykinin, blocking it lets bradykinin build up — that's the signature dry cough & angiedema that ARBs do NOT cause.
🔗 Paired with NG-137 ARBs — same pathway, same job, constantly confused on exams. Open the ARB page → to see the side-by-side comparison and the shared RAAS diagram.
🫀 -PRIL = ACE inhibitorLisinopril, enalapril, captopril, ramipril — blocks ACE, upstream of angiotensin II.
🤧 Dry cough / angiedemaBradykinin builds up because ACE can't break it down anymore. ARBs don't do this.
🧎 First-dose hypotensionGive the first dose at bedtime; teach the client to rise slowly.
🍌 Watch potassiumACE inhibitors keep K⁺ IN → hyperkalemia risk, especially with K⁺-sparing diuretics or salt substitutes.
💊
WHAT IT DOES
STEP 1 · THE MECHANISM
One pathway explains the whole drug class — block the enzyme, and everything downstream of it shrinks.
🧬 The RAAS pathway — where ACE inhibitors block it
EXAM TIP ACE inhibitors block Angiotensin I → Angiotensin II, the conversion step. This is the SAME shared diagram used on the ARB page — compare where each class blocks the cascade.
🧠 "PRIL blocks the Pril-conversion, not the reception." ACE inhibitors act upstream, at the enzyme — angiotensin II is never made. ARBs act downstream, at the receptor — angiotensin II is made but can't bind. Same ending pathway, different blockade point.
🔤 Say the suffix — it tells you the class
-PRIL = ACE inhibitor 🫀
Lisinopril (Prinivil, Zestril)
Enalapril (Vasotec) — also comes IV as enalaprilat
🧠 "PRIL" sounds like "drill" — it drills into the ACE enzyme upstream, before angiotensin II ever exists.
⭐ Why we give it — indications
Hypertension — first-line in many guidelines
Heart failure — reduces afterload & remodeling
Post-MI — cardioprotective
Diabetic nephropathy — protects the kidney by lowering intraglomerular pressure
🧠 "Pril protects the kidney AND the heart." One drug, two organs it's guarding — that's why it's a diabetic/CKD favorite even at normal BP.
💊 Common generics, trade names & typical adult dosing
Generic
Trade
Typical range
Route
Lisinopril
Prinivil, Zestril
10–40 mg once daily
PO
Enalapril
Vasotec
5–40 mg/day (1–2 doses)
PO / IV (enalaprilat)
Captopril
Capoten
dosed 2–3×/day, empty stomach
PO
Ramipril
Altace
2.5–20 mg/day
PO
Ranges are typical adult maintenance doses — always titrate to the prescriber's order and the client's response; practice varies by indication.
🧠 Captopril = "Capture it on an empty stomach." It's the odd one out — shortest acting, dosed multiple times a day, food cuts its absorption.
⚠️
WATCH FOR
STEP 2 · THE DANGER LIST
The cough is annoying, the angiedema is an airway emergency, and the potassium creeps up quietly.
🚨 Angiedema — airway emergency
Angiedema can happen with the first dose or years into therapy. It is bradykinin-driven, not allergic in the usual IgE sense — antihistamines and epinephrine may not fully reverse it. Higher risk in Black patients and those with a prior history of angiedema on any ACE inhibitor.
🧠 "No PRIL, ever again." A client with ACE-inhibitor angiedema does not get re-challenged with any -pril — switch classes (often to an ARB, though ARBs carry a small residual risk too).
🧎 First-dose orthostatic hypotension
Biggest drop after the very first dose. Give it at bedtime the first time, and teach the client to rise slowly — sit on the edge of the bed before standing.
🧠 "First pril, first fall risk." Same first-dose orthostatic teaching applies to ARBs — it's a RAAS-wide effect.
🍌 Hyperkalemia risk
Aldosterone normally makes the kidney excrete K⁺. Block aldosterone → K⁺ stays in → hyperkalemia. Watch peaked T waves on ECG. Avoid stacking with K⁺-sparing diuretics, K⁺ supplements, and salt substitutes (often potassium chloride).
🧠 "Pril keeps potassium." Teach clients to check the ingredient label on salt substitutes before assuming "salt-free" is safe.
Lithium — decreased clearance → possible lithium toxicity
Diuretics (loop/thiazide) — additive hypotension, especially the first dose
🧠 "Pril + NSAID = pressure won't fall, kidneys might." NSAIDs fight the BP-lowering effect and stress the kidney at the same time.
🆚 ACE inhibitor vs ARB — tell them apart
Feature
ACE Inhibitor (-PRIL)
ARB (-SARTAN)
Blocks
The enzyme (Angiotensin I → II) — upstream
The AT1 receptor — downstream
Bradykinin
Builds up (ACE breaks it down normally)
Unaffected
Dry cough
YES — classic side effect
No
Angiedema
Yes (bradykinin-driven)
Rare, lower risk
Hyperkalemia
Yes
Yes — same mechanism
First-dose hypotension
Yes
Yes
Pregnancy
Contraindicated 2nd/3rd trimester
Contraindicated 2nd/3rd trimester
When to choose
First-line unless contraindicated
Client can't tolerate the ACE-inhibitor cough
🧠 "If they cough on the PRIL, switch to the TAN." That single sentence is the most heavily tested fact in this whole pair of drugs.
⚡
QUICK RECALL
SAY IT OUT LOUD
🫀 -PRILblocks ACE, upstream — angiotensin II never forms
🤧 Cough & angiedemabradykinin buildup — unique to ACE inhibitors, not ARBs
🧎 First dosegive at bedtime, rise slowly
🍌 Hyperkalemiaskip salt substitutes, monitor K⁺
🎯 Cover & check — 4 rapid-fire questions
Q1: Where in the RAAS pathway do ACE inhibitors act?
Upstream, at the ACE enzyme — they block the conversion of Angiotensin I to Angiotensin II.
Q2: Why do ACE inhibitors cause a dry cough but ARBs don't?
ACE also breaks down bradykinin. Blocking ACE lets bradykinin build up, causing cough and angiedema. ARBs act at the receptor and never touch bradykinin.
Q3: A client on lisinopril reports lip and tongue swelling. What's the priority?
Angiedema — an airway emergency. Stop the drug, protect the airway, notify the provider immediately, and never re-challenge with another ACE inhibitor.
Q4: What should the client avoid to prevent hyperkalemia?
Salt substitutes (often potassium chloride), potassium supplements, and potassium-sparing diuretics without provider guidance — and get routine K⁺/renal labs.