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# ACE Inhibitors
## Overview
Angiotensin-Converting Enzyme (ACE) inhibitors block the conversion of angiotensin I to the potent vasoconstrictor angiotensin II, leading to decreased systemic vascular resistance and reduced aldosterone secretion. They also inhibit the breakdown of bradykinin.
## Primary Indications
* Hypertension
* Heart failure (HFrEF)
* Post-myocardial infarction
* Chronic kidney disease (diabetic nephropathy/proteinuria)
## Adult Dosing (Common Representative Agents)
* **Lisinopril:** Hypertension: Start 10 mg QD; max 40 mg/day. Heart Failure: Start 2.5–5 mg QD; target 20–40 mg/day.
* **Enalapril:** Hypertension: Start 5 mg BID; max 40 mg/day. Heart Failure: Start 2.5 mg BID; target 10–20 mg BID.
* **Ramipril:** Hypertension: Start 2.5 mg QD; max 20 mg/day. Heart Failure/Post-MI: Start 1.25–2.5 mg BID; target 5 mg BID.
* *Note: Specific initial doses and titration intervals vary by institutional protocol and patient comorbid conditions.*
## Pediatric Dosing
* **Lisinopril:** (Age ≥6 years): Hypertension: 0.07 mg/kg QD (max 5 mg); titrate up to 0.6 mg/kg/day (max 40 mg).
* **Enalapril:** Hypertension: 0.08 mg/kg QD (max 5 mg); titrate based on response; max 0.6 mg/kg/day.
* *Consult neonatal/pediatric dosing references (e.g., Harriet Lane) as dosing is highly weight-based and indication-dependent.*
## Dose Adjustments
* **Renal Impairment:** Reduce starting doses and monitor creatinine closely. Usually contraindicated or require significant reduction in severe renal artery stenosis (bilateral) or stage 4/5 CKD.
* **Hepatic Impairment:** Use caution; may require dose reduction (especially for prodrugs like enalapril converted to enalaprilat).
## Contraindications
* History of angioedema (idiopathic, hereditary, or ACE-inhibitor induced).
* Pregnancy (Category D/X: fetotoxicity/teratogenicity).
* Concomitant use with aliskiren in patients with diabetes.
* Use within 36 hours of sacubitril/valsartan (due to angioedema risk).
## Adverse Effects
* **Common:** Dry, hacking cough (due to bradykinin accumulation).
* **Serious:** Angioedema (life-threatening airway obstruction), hyperkalemia, acute kidney injury (AKI), symptomatic hypotension.
* **Rare:** Neutropenia, agranulocytosis.
## Key Drug Interactions
* **Potassium-sparing diuretics/Potassium supplements:** High risk of severe hyperkalemia.
* **NSAIDs:** Increased risk of AKI and reduced antihypertensive efficacy.
* **Lithium:** May increase lithium levels/toxicity.
* **Aliskiren or ARBs:** Avoid dual RAAS blockade; increases mortality/renal risk.
## Monitoring
* **Baseline/Titration:** Serum creatinine, BUN, and serum electrolytes (potassium) should be checked 1–2 weeks after initiation or dose change.
* **Blood Pressure:** Monitor for orthostatic hypotension.
* **Clinical:** Assess for signs of angioedema; if dry cough becomes intolerable, consider switching to an ARB.
## Clinical Pearls
* **Cough:** The ACE-inhibitor induced cough is dose-independent and resolves within 1–4 weeks of discontinuation.
* **First-dose hypotension:** Particularly common in HF patients or those on high-dose diuretics; consider holding diuretics 2–3 days before starting ACE inhibitor.
* **Renal protection:** Expect a transient rise in serum creatinine (up to 30%) upon initiation; this is often an acceptable hemodynamic response, not necessarily a sign of permanent injury.
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*Disclaimer: This information is for educational purposes and does not replace professional clinical judgment. Always verify current prescribing information, institutional protocols, and patient-specific factors via reliable pharmacological databases (e.g., Lexicomp, UpToDate) before prescribing or administering medication.*
