Dosing & Uses
Dosage Forms & Strengths
tablet
- 12.5mg
- 25mg
- 50mg
- 100mg
Acute Hypertension
12.5-25 mg PO; may repeat PRN
Hypertension (Alone or with Thiazide)
Initial: 25 mg PO q8-12hr, increase gradually based on response (may start lower in some patients)
Maintenance: 25-150 mg PO q8-12hr
450 mg/day maximum
Congestive Heart Failure (With Diuretics and Digitalis)
Initial: 6.25-12.5 mg PO q8hr in conjunction with cardiac glycoside and diuretic therapy
Target therapy: 50 mg q8hr
450 mg/day maximum
Left Ventricular Dysfunction After Myocardial Infarction
6.25 mg PO initially followed by 12.5 mg q8hr
Increase to 25 mg PO q8hr over next few days; THEN
Target dose: 50 mg PO q8hr
Diabetic Nephropathy
25 mg PO q8hr
Dosing Considerations
Beneficial for many patients at risk for heart disease; reduces risk of MI, stroke, diabetic nephropathy , microalbuminuria, new onset DM
Consider starting an ACE inhibitor in high-risk patients, even if no HTN or CHF
May prolong survival in CHF, may preserve renal function in DM
May help to prevent migraine HA
Good choice in hyperlipidemia patients
Requires weeks for full effect; to start, use low dose and titrate every 1-2wk
Administration
Take on an empty stomach
Dosage Forms & Strengths
tablet
- 12.5mg
- 25mg
- 50mg
- 100mg
Hypertension (Off-label)
Neonates: 0.05-0.1 mg/kg/dose q8-24hr, titrate dose up to 0.5 mg/kg/dose q6-24hr
Infants: 0.15-0.3 mg/kg/dose; titrate dose upward to maximum 6 mg/kg/day in 1-4 divided doses; 2.5-6 mg/kg/day usually required
Children: 0.3-0.5 mg/kg/dose; titrate to maximum 6 mg/kg/day divided q6-12hr
Older children: 6.25-12.5 mg/dose q12-24hr; titrate to no more than 6 mg/kg/day divided q6-12hr
Adolescents: 12.5-25 mg/dose q8-12hr; may increase by 25 mg/dose q1-2Weeks to maximum 450 mg/day
Other Information
Take on an empty stomach
Acute hypertension
12.5-25 mg PO; may repeat PRN
Hypertension (alone or with thiazide)
Initial: 25 mg PO q8-12hr, increase gradually based on response (may start lower in some patients)
Maintenance: 25-150 mg PO q8-12hr
450 mg/day maximum
Congestive heart failure (with diuretics and digitalis)
Initial: 6.25-12.5 mg PO q8hr in conjunction with cardiac glycoside and diuretic therapy
Target therapy: 50 mg q8hr
450 mg/day maximum
Left ventricular dysfunction after myocardial infarction
6.25 mg PO initially followed by 12.5 mg q8hr
Increase to 25 mg PO q8hr over next few days; THEN
Target dose: 50 mg PO q8hr
Diabetic nephropathy
25 mg PO q8hr
Interactions
Interaction Checker
No Results
Contraindicated
Serious - Use Alternative
Significant - Monitor Closely
Minor
Adverse Effects
>10%
Hyperkalemia (1-11%)
1-10%
Hypersensitivity rxns (4-7%)
Skin rash (4-7%)
Dysgeusia (2-4%)
Hypotension (1-2.5%)
Pruritus (2%)
Cough (0.5-2%)
Chest pain (1%)
Palpitations (1%)
Proteinuria (1%)
Tachycardia (1%)
Frequency Not Defined
Cardiac arrest
Orthostatic hypotension
Ataxia
Confusion
Depression
Somnolence
Angioedema
Photosensitivity
Neutropenia
ARF if renal artery stenosis
Renal impairment
Impotence
Warnings
Black Box Warnings
Discontinue as soon as possible when pregnancy detected; affects renin-angiotensin system causing oligohydramnios, which may result in fetal injury and/or death
Contraindications
Hypersensitivity to ACE inhibitors
Anuria
History of ACEI-induced angioedema
Hereditary or idiopathic angioedema
Coadministration of neprilysin inhibitors (eg, sacubitril) with ACE inhibitors may increase angioedema risk; do not administer ACE inhibitors within 36 hr of switching to or from sacubitril/valsartan
Bilateral renal artery stenosis
Do not coadminister with aliskiren in patients with diabetes mellitus or with renal impairment (ie, GFR <60 mL/min/1.73 m²)
Cautions
Aortic stenosis/hypertrophic cardiomyopathy, hypotension, biliary cirrhosis or biliary obstruction, myelosuppression, electrolyte imbalance, hyperuricemia or gout, SLE, hepatic or renal impairment
Avoid concomitant use with lithium
Less effective in African-Americans
Excessive hypotension if concomitant diuretics or volume-depleted; start with 6.25 mg q8hr
Risk of hyperkalemia, especially with K+ sparing diuretics
Dual blockade of the renin angiotensin system with ARBs, ACE inhibitors, or aliskiren associated with increased risk for hypotension, hyperkalemia, and renal function changes (including acute renal failure) compared to monotherapy
Blood levels don't correlate with BP response
Food decreases absorption
ACE inhibition also causes increased bradykinin levels which putatively mediates angioedema
Coadministration with mTOR inhibitors (eg, temsirolimus, everolimus, sirolimus) may increase risk for angioedema
Intestinal angioedema, that presented with abdominal pain, reported in patients treated with ACE inhibitors
Neutropenia (<1000/mm³ with myeloid hypoplasia reported with captopril; risk is dependent on clinical status of patient
Causes false positive urine acetone
Pregnancy & Lactation
Pregnancy Category: C; D in 2nd & 3rd trimesters
Discontinue as soon as pregnancy detected; during the second and third trimesters of pregnancy, drugs that act directly on the renin-angiotensin have been associated with fetal injury that includes hypotension, neonatal skull hypoplasia, anuria, reversible or irreversible renal failure, and death
Lactation: enters breast milk/not recommended (AAP states compatible with nursing)
Pregnancy Categories
A: Generally acceptable. Controlled studies in pregnant women show no evidence of fetal risk.
B: May be acceptable. Either animal studies show no risk but human studies not available or animal studies showed minor risks and human studies done and showed no risk. C: Use with caution if benefits outweigh risks. Animal studies show risk and human studies not available or neither animal nor human studies done. D: Use in LIFE-THREATENING emergencies when no safer drug available. Positive evidence of human fetal risk. X: Do not use in pregnancy. Risks involved outweigh potential benefits. Safer alternatives exist. NA: Information not available.Pharmacology
Mechanism of Action
Angiotensin converting enzyme (ACE) inhibitors dilate arteries and veins by competitively inhibiting the conversion of angiotensin I to angiotensin II (a potent endogenous vasoconstrictor) and by inhibiting bradykinin metabolism; these actions result in preload and afterload reductions on the heart
ACE inhibitors also promote sodium and water excretion by inhibiting angiotensin-II induced aldosterone secretion; elevation in potassium may also be observed
ACE inhibitors also elicit renoprotective effects through vasodilation of renal arterioles
ACE inhibitors reduce cardiac and vascular remodeling associated with chronic hypertension, heart failure, and myocardial infarction
Pharmacokinetics
Half-life: 1.9 hr (healthy); 2.06 (heart failure); 20-40 hr (anuria); significantly increase in CrCl <20 mL/min
Onset: PO: initial response: 15-30 min; peak response: 60-90 min
Duration: PO (multiple dose): 8-12 hr
Peak plasma time: PO: 0.5-1.5 hr
Therapeutic range: 0.05-0.5 mcg/mL
Bioavailability: 70-75%
Protein bound: 25-30%
Vd: 0.7 L/kg
Metabolism: liver (50%)
Metabolites: captopril-cysteine disulfide (inactive)
Total body clearance: 0.8 L/kg/hr
Renal clearance: 0.4 L/kg/hr
Excretion: mainly urine (95%)
Dialyzable: Yes (HD)
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Formulary
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