ACE inhibitors and ARBs are “bread-and-butter” cardiovascular drugs on Step 1 and Step 2—especially when a question stem screams HTN + diabetes, HFrEF, or post-MI remodeling. The trick is remembering (1) what they do, (2) what they raise, and (3) the side effects that show up again and again.
The Quick Mnemonic: ACEi = “C(A)PTOPril makes you COUGH + SWELL + K↑”
Think: ACE inhibitors trap bradykinin.
ACE inhibitor name clue: most end in -pril
Examples: lisinopril, enalapril, captopril
One-liner
ACE inhibitors block angiotensin II production and block bradykinin breakdown → vasodilation + ↓aldosterone (but ↑bradykinin side effects).
Visual/Mnemonic Device (shareable)
ACEi: “ACE = Aches in the face”
Picture a patient taking an ACE inhibitor who suddenly gets:
- Angioedema (face/lip swelling)
- Cough (dry)
- Elevated potassium ()
Why? Bradykinin goes up when ACE is inhibited.
ARBs: “ARBs avoid Airway irritation (no bradykinin)”
ARB name clue: most end in -sartan
Examples: losartan, valsartan, candesartan
One-liner
ARBs block the angiotensin II receptor (AT) → same BP/aldosterone benefits as ACEi but no bradykinin buildup → less cough/angioedema.
Boards logic: ACEi = cough/angioedema more likely, ARB = used when ACEi not tolerated.
Mechanism in 10 seconds (high-yield)
Where they act in RAAS
- ACE inhibitors: block conversion Ang I → Ang II and decrease bradykinin breakdown
- ARBs: block Ang II binding AT receptor
Net physiologic effects (both classes)
- ↓ Ang II → ↓ vasoconstriction
- ↓ aldosterone → ↓ Na/HO retention
- ↑ (less aldosterone = less potassium excretion)
- Efferent arteriole dilation in the kidney → ↓ intraglomerular pressure
“What do they treat?” (USMLE short list)
High-yield indications
- Hypertension (especially with compelling indications)
- HFrEF (mortality benefit)
- Post-MI (limits remodeling; improves survival)
- Diabetic nephropathy / CKD with albuminuria
- ↓ intraglomerular pressure → ↓ proteinuria
Adverse effects: the Step favorites
ACE inhibitors (classic)
- Cough (dry, persistent)
- Angioedema (can be life-threatening)
- Hyperkalemia
- Hypotension (especially first dose if volume depleted)
- ↑ Creatinine (expected mild rise, but watch for big jumps)
ARBs
- Hyperkalemia
- Hypotension
- ↑ Creatinine
- Much less cough/angioedema than ACEi (but not zero risk for angioedema)
Contraindications & testable warnings
Absolute “don’t do it”
- Pregnancy: ACEi/ARBs are teratogenic
- Associated with fetal renal malformations, oligohydramnios
- Bilateral renal artery stenosis
- Efferent dilation can tank GFR → acute kidney injury
- History of ACEi-induced angioedema
- Avoid ACE inhibitors; ARBs may be considered with caution depending on context/institution
Step-style kidney clue
If a patient has renal artery stenosis, angiotensin II is helping maintain GFR by constricting the efferent arteriole.
Blocking RAAS → efferent dilation → GFR drops → creatinine rises.
Rapid comparison table (memorize this)
| Feature | ACE inhibitors (-pril) | ARBs (-sartan) |
|---|---|---|
| Blocks | ACE enzyme | AT receptor |
| Bradykinin level | ↑ | No increase |
| Cough | Yes | No (rare) |
| Angioedema | Yes | Much less |
| Hyperkalemia | Yes | Yes |
| Pregnancy | Contraindicated | Contraindicated |
| Renal artery stenosis | Can precipitate AKI | Can precipitate AKI |
Classic USMLE vignettes (pattern recognition)
- Dry cough after starting lisinopril → bradykinin effect → switch to an ARB
- Diabetic patient with microalbuminuria → start ACEi/ARB to reduce proteinuria
- Creatinine rises significantly after ACEi + abdominal bruit/vascular disease → think renal artery stenosis
- Pregnant patient with HTN → avoid ACEi/ARB (think alternatives like labetalol, nifedipine, methyldopa)
Final “sticky” summary (shareable)
- ACE inhibitors (-pril): “Cough + Angioedema + ↑” because bradykinin ↑
- ARBs (-sartan): “Same benefits, fewer bradykinin problems”
- Both: great for HFrEF, diabetic nephropathy, post-MI, but avoid in pregnancy and bilateral renal artery stenosis