ACE Inhibitor Bradykinin Cough and Angioedema
ACE inhibitors block the conversion of angiotensin I to angiotensin II, but also prevent bradykinin degradation — causing the characteristic dry cough and, rarely, life-threatening angioedema. This mechanism is a high-yield topic on USMLE Step 1 and Step 2 CK. Mastering the bradykinin pathway distinguishes ACEi from ARBs and explains why switching drug classes resolves these side effects.
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5 CardsWhat drug class replaces ACE inhibitors when cough is intolerable?
What is the mechanism behind ACEi-induced angioedema vs. cough?
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What is the difference between ACE inhibitor cough and ACE inhibitor angioedema?
Cough occurs in ~10–15% of patients and is caused by bradykinin irritating airway epithelium — benign but bothersome. Angioedema is rarer (~0.1–0.7%) but life-threatening: bradykinin causes vascular leakage in the lips, tongue, and larynx, which cannot be reversed with antihistamines.
How do I know if my patient's cough is from an ACE inhibitor?
The ACEi cough is dry, persistent, and non-productive, beginning weeks to months after starting the drug. It resolves within 1–4 weeks of stopping. If cough precedes ACEi initiation or is productive, investigate other causes.
Why don't ARBs cause the same cough as ACE inhibitors?
ARBs block the AT1 receptor directly and do not inhibit ACE. This means bradykinin is still degraded normally by kininase II, preventing the bradykinin accumulation that drives the cough and angioedema seen with ACEi.
