Heart Failure Medications Reference

Mechanism: Block angiotensin-converting enzyme, reducing angiotensin II production. Results in vasodilation (decreased afterload), reduced aldosterone secretion (decreased sodium/water retention), and anti-remodeling effects on the myocardium.

Examples: Lisinopril, enalapril, captopril, ramipril

Key nursing considerations:

• Monitor BP before each dose — hold for SBP < 90 mmHg or per protocol
• Monitor potassium — ACE inhibitors cause potassium retention (hyperkalemia risk, especially with K⁺-sparing diuretics)
• Monitor BUN and creatinine — renal function decline can occur, especially with bilateral renal artery stenosis
• ACE-inhibitor cough: Dry, persistent cough in 10–20% of patients (from bradykinin accumulation) — switch to ARB if intolerable
• Angioedema: Rare but potentially life-threatening — swelling of lips, tongue, throat. Contraindicated in history of angioedema.
• Contraindicated in pregnancy (teratogenic)
• Do not combine with ARNIs (sacubitril/valsartan) — 36-hour washout required

Mechanism: Block the angiotensin II receptor (AT1), producing similar hemodynamic effects as ACE inhibitors without the bradykinin accumulation. Result: vasodilation, reduced aldosterone, anti-remodeling.

Examples: Losartan, valsartan, candesartan, irbesartan

Key nursing considerations:

• First-line alternative when patient cannot tolerate ACE inhibitors (particularly for cough)
• Same BP, potassium, and renal function monitoring as ACE inhibitors
• Angioedema risk is lower than ACE-I but not zero — do not use in patients with ACE-I-induced angioedema
• Contraindicated in pregnancy

Mechanism: Sacubitril/valsartan (Entresto) combines ARB activity (valsartan) with neprilysin inhibition (sacubitril). Neprilysin inhibition prevents breakdown of natriuretic peptides (BNP, ANP), enhancing vasodilation and natriuresis on top of RAAS blockade.

Example: Sacubitril/valsartan (Entresto)

Key nursing considerations:

• Superior to enalapril in reducing HF mortality/hospitalization (PARADIGM-HF trial) — current guideline-preferred over ACE inhibitors for eligible HFrEF patients
• Critical: Must have a 36-hour washout period after stopping ACE inhibitor before starting — concurrent use causes high risk of angioedema
• BNP levels will be falsely elevated on Entresto (neprilysin inhibition prevents BNP breakdown) — use NT-proBNP for monitoring instead
• Monitor BP closely — significant hypotension risk; start low and titrate
• Monitor potassium and renal function (ARB component)
• Contraindicated in pregnancy, bilateral renal artery stenosis, history of angioedema

Mechanism: Block sympathetic (catecholamine) stimulation of the heart. Reduce heart rate, reduce myocardial oxygen demand, prevent dysrhythmias, and reverse ventricular remodeling. Three beta-blockers are specifically proven to reduce mortality in HFrEF: carvedilol, metoprolol succinate, and bisoprolol.

Examples: Carvedilol (Coreg), metoprolol succinate (Toprol-XL), bisoprolol

Key nursing considerations:

• Hold for HR < 60 bpm or SBP < 90 mmHg (verify hold parameters with provider)
• Never abruptly discontinue — rebound tachycardia and worsening HF can occur; taper if stopping
• Initiated only when patient is euvolemic (not in acute decompensation) — starting during active congestion worsens HF
• Carvedilol: non-selective, also blocks alpha-1 (additional vasodilation); must be taken with food to reduce orthostatic hypotension
• May mask hypoglycemia symptoms (tachycardia) in diabetic patients — monitor glucose closely
• Contraindicated in acute decompensated HF, cardiogenic shock, severe bradycardia, high-degree AV block

Mechanism: Block the Na⁺/K⁺/2Cl⁻ cotransporter in the thick ascending limb of Henle — the site responsible for reabsorbing ~25% of filtered sodium. Produce potent sodium and water excretion, rapidly reducing preload and fluid overload. Do not reduce mortality but dramatically reduce symptoms and hospitalizations.

Examples: Furosemide (Lasix), bumetanide (Bumex), torsemide

Key nursing considerations:

• Monitor urine output — response expected within 30–60 min of IV dose. Document hourly UO.
• Hypokalemia risk: Major side effect — monitor potassium before each dose. Replace potassium as ordered. Low K⁺ + digoxin = dangerous dysrhythmias.
• Monitor BUN and creatinine — over-diuresis causes pre-renal azotemia
• Monitor for hypotension — preload reduction can cause dizziness and falls
• Hold for SBP < 90 or per protocol; notify provider for inadequate urine response
• Ototoxicity risk with high doses or rapid IV infusion — administer IV furosemide no faster than 20 mg/min (or 4 mg/min for doses > 120 mg)
• Torsemide has superior oral bioavailability (80–100% vs 40–60% for furosemide) — better option when oral diuresis is inconsistent
• Assess for daily weight changes — best objective marker of fluid response

Mechanism: Block aldosterone receptors (mineralocorticoid receptors) in the distal tubule. Reduce sodium retention and potassium excretion. Also reduce cardiac fibrosis and reverse remodeling independently of their diuretic effect.

Examples: Spironolactone (Aldactone), eplerenone (Inspra)

Key nursing considerations:

• Hyperkalemia risk: Potassium-sparing — monitor K⁺ closely, especially when combined with ACE inhibitors or ARBs
• Contraindicated with K⁺ > 5.0 mEq/L or GFR < 30 mL/min
• Spironolactone can cause gynecomastia and breast tenderness in men (anti-androgenic effect) — eplerenone is more selective and avoids this
• Monitor BUN and creatinine — renal function decline can cause potassium accumulation
• Encourage low-potassium diet and avoid K⁺ supplements unless prescribed
• RALES trial (spironolactone) and EMPHASIS-HF trial (eplerenone) demonstrated significant mortality reduction in HFrEF