Every heart failure drug class side by side, sorted by the question that matters most: does it only relieve symptoms, or does it help the patient live longer? Then where it fits, what it causes and what to watch.
| Drug class and examples | How it helps | Symptoms only, or survival? | Place in therapy | Main adverse effects and cautions | Avoid / do not combine | Monitoring and patient education | Source |
|---|---|---|---|---|---|---|---|
| Diuretics loop diuretics (mainstay); thiazides | Less sodium and water retention, so lower preload and less congestion | Symptoms only: no evidence of slowed progression or lower mortality | Loops are the mainstay for fluid; thiazides are not potent enough for most patients; not mandatory therapy | Volume depletion, low potassium and magnesium; see the diuretic chart | Low potassium or magnesium together with digoxin | Daily weights: a rise over several days is fluid, not tissue. Restrict dietary sodium and fluid. | L9 slide 52 slide 53 slide 51 slide 19 |
| Angiotensin-converting enzyme (ACE) inhibitors | Lower preload, afterload and sympathetic activation; reduce left ventricular hypertrophy, dilation and remodeling | Survival: slow progression, decrease mortality, fewer hospital admissions, better exercise tolerance | Given with a beta blocker irrespective of symptoms (a survival drug is not optional) | Impaired renal function, hypotension, high potassium, cough, angioedema | Never with sacubitril-valsartan (36 hour washout when switching) | Check renal function and potassium; the potassium effect adds to potassium-sparing drugs and supplements. | L9 slide 54 slide 55 slide 56 slide 60 slide 81 |
| Beta blockers carvedilol, metoprolol succinate (extended release), bisoprolol only: these three have a mortality benefit | Improve exercise tolerance and hemodynamics (raise ejection fraction), slow progression | Survival: fewer hospitalizations, less need for transplant, decreased mortality | First line in class II to IV heart failure; with an ACE inhibitor irrespective of symptoms | Classically considered contraindicated in heart failure: they can worsen it if started wrongly | Unstable patients: start only when stable | Start with very low doses and titrate up slowly over weeks (in hospital preferred); watch for worsening heart failure signs, and weight. Do not stop abruptly (added background). | L9 slide 57 slide 58 slide 59 slide 60 |
| Aldosterone antagonists spironolactone, eplerenone | Neurohormonal inhibition and slowed remodeling of the left ventricle | Survival: mortality reduction in advanced (class III or IV) heart failure; slows progression | Added in advanced heart failure | Hyperkalemia; spironolactone gynecomastia (about 10 percent of men, may respond to a lower dose); eplerenone causes much less gynecomastia | Not eligible when potassium is above 5 or creatinine above 2.5 | Check potassium and renal function; if gynecomastia occurs, switch to eplerenone. | L9 slide 73 slide 37 slide 38 |
| Digoxin | Raises contractility (blocks the sodium-potassium pump, so calcium rises); also lowers sympathetic and raises parasympathetic activity and resets the baroreflex | Symptoms only: better symptoms, exercise tolerance and quality of life, fewer hospitalizations, no survival benefit | Add-on in symptomatic patients already on optimal ACE inhibitor, beta blocker and diuretic therapy; an option for rate control in atrial fibrillation with heart failure | Toxicity: nausea, yellow-green halos, confusion, bradycardia, any arrhythmia | Advanced atrioventricular block, severe bradycardia or sick sinus syndrome, ventricular ectopy, Wolff-Parkinson-White syndrome; low potassium or magnesium or high calcium raise the risk | Serum levels are monitored; digoxin immune Fab reverses toxicity. See the digoxin chart. | L9 slide 63 slide 66 slide 67 slide 68 slide 71 slide 65 slide 72 |
| Phosphodiesterase 3 inhibitors milrinone, inamrinone | Direct stimulation of contraction plus balanced arterial and venous dilation: lower afterload, higher cardiac output | Symptoms only: short-term support; long-term use is linked to higher mortality | Short-term intravenous use in acute decompensated heart failure. (Added background: it suits the hypertensive patient, because it also dilates vessels.) | Ventricular arrhythmias, thrombocytopenia (less with milrinone) | Long-term use | (Added background: started in hospital, then the patient is moved to usual oral therapy.) | L9 slide 74 slide 75 slide 76 |
| Intravenous inotropes dobutamine, dopamine | Dobutamine is a selective beta-1 agonist: force of contraction rises more than rate. Dopamine acts through dopamine and beta receptors | Symptoms only: intravenous support to stabilize | Short-term use in decompensation. (Added background: they suit the hypotensive patient, whereas the vasodilating phosphodiesterase 3 inhibitors suit the hypertensive patient.) | (Added background: tachycardia and arrhythmias from beta-1 stimulation; dopamine carries an FDA boxed warning for tissue injury if it leaks out of the vein.) | Not for long-term use | Intravenous infusion in hospital only. | L9 slide 77 |
| Ivabradine hyperpolarization-activated cyclic nucleotide-gated channel blocker | Inhibits the pacemaker current in the sinoatrial node: lowers heart rate, no effect on contractility | Decreases hospitalization and heart failure death | Add-on when the patient is maxed out on beta blockers, in normal sinus rhythm with a heart rate above 70 | Atrial fibrillation, symptomatic bradycardia, visual impairment (phosphenes: transient brightness, halos, multiple images; often resolves) | Contraindications similar to beta blockers: hypotension, heart block, pacemaker | Warn about visual brightness changes; check heart rate and rhythm. | L9 slide 79 slide 80 |
| Sacubitril-valsartan neprilysin inhibitor plus an angiotensin receptor blocker | Blocking neprilysin lets natriuretic peptide and bradykinin build up: vasodilation, natriuresis and diuresis, less myocardial growth and fibrosis | Survival: reduces cardiovascular death and hospitalization | Replaces an ACE inhibitor in chronic heart failure | Hypotension, hyperkalemia, cough, renal insufficiency | Never with an ACE inhibitor; allow a 36 hour washout | Switching plan: stop the ACE inhibitor, wait the washout, then start. Check blood pressure, potassium and renal function. | L9 slide 81 |
| Sodium-glucose cotransporter 2 inhibitors dapagliflozin, empagliflozin | Block glucose reabsorption in the kidney (originally a diabetes drug): glucose and fluid are lost in the urine | Survival: reduce mortality and hospitalizations in stable, chronic heart failure with reduced ejection fraction | A necessary add-on for stable chronic heart failure with reduced ejection fraction | Hypotension (volume loss), fungal urinary tract infections | Caution with low blood pressure | Warn about genital and urinary fungal infections; fluid status. | L9 slide 82 |