What each drug is FOR, and what you tell the patient. 60 entries across the Exam 3 lectures, each citing its slide. Indications and patient education are the two things students under-study most.
| Drug or class | Tier | Indications | Patient education & practical notes | Source |
|---|---|---|---|---|
| Diuretics: how the nephron works | ||||
| Diuretics definition and fluid balance | Indication | Diuretics increase urine flow and/or sodium and chloride excretion. A sustained imbalance between sodium and chloride intake and loss is fatal: too much means volume overload and pulmonary edema; too little means volume depletion and cardiovascular collapse. | The goal is balance, never maximum fluid removal: the same drug that clears a congested lung can empty the circulation if over-used. | L9 slide 4 |
| Diuretic braking how the kidney fights back | Indication | The kidneys receive about a fifth of the cardiac output, so they defend their blood flow. Counter-regulation ("diuretic braking") includes activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system, a lower blood pressure (less pressure natriuresis), a lower atrial natriuretic peptide with a higher antidiuretic hormone, and renal cell hypertrophy. | This counter-regulation is why a diuretic's effect fades over time. | L9 slide 5 |
| Filtration glomerulus | Indication | Glucose, sodium, potassium, chloride, bicarbonate and amino acids are all filtered. About 150 to 180 liters are filtered a day but only 1 to 2 liters are excreted, so most of what is filtered is reabsorbed further down the nephron. | A diuretic only needs to block a small fraction of reabsorption to change urine output a great deal. | L9 slide 7 |
| Proximal tubule site of reabsorption | Indication | Reabsorbs glucose, amino acids and organic solutes; weak acids and bases are excreted into the lumen. 60 to 70 percent of the filtrate is reabsorbed here (carbonic anhydrase inhibitors act in this segment). | Where a drug acts predicts what it does to potassium, calcium and acid-base balance: learn the segment first. | L9 slide 8 |
| Loop of Henle concentrates the urine | Indication | Concentrates urine and reabsorbs sodium. Descending limb: water leaves the lumen. Ascending limb: about 25 percent of sodium is reabsorbed and the limb is impermeable to water. Loop diuretics work at this site. | Blocking this limb removes about a quarter of the filtered sodium, and the segments downstream cannot reabsorb enough to make up for it, so it gives the largest diuresis. | L9 slide 9 |
| Distal tubule site of thiazides | Indication | About 5 percent of sodium is reabsorbed here. Thiazide diuretics act at this site. Added background: aldosterone mainly drives sodium and potassium handling in the late distal tubule and collecting duct; antidiuretic hormone controls the water channels of the collecting duct. | Thiazides act after the loop, which is why they are weaker than loop diuretics. | L9 slide 10 |
| Collecting duct site of potassium-sparing drugs | Indication | 2 to 3 percent of sodium is reabsorbed; antidiuretic hormone controls the water channels, while aldosterone controls sodium and potassium handling. Potassium-sparing diuretics act at this site. | Aldosterone pulls sodium in and pushes potassium out here; blocking it (or the sodium channels it controls) is what spares potassium. | L9 slide 11 |
| Loop diuretics | ||||
| Loop diuretics furosemide, bumetanide, torsemide, ethacrynic acid | Indication | Inhibit the sodium-potassium-2 chloride carrier on the luminal membrane of the thick ascending limb of the loop of Henle. Four agents: furosemide, bumetanide, torsemide and ethacrynic acid. | Class before agent: if a stem describes this carrier or the thick ascending limb, the class is loop diuretic. Ethacrynic acid does not follow the naming pattern of the others, so learn it by name. | L9 slide 12 |
| Loop diuretics furosemide, bumetanide, torsemide, ethacrynic acid | Indication | Major actions: inhibit sodium chloride reabsorption by 20 to 25 percent; raise urine output by up to 4 liters a day; increase potassium excretion; increase calcium and magnesium excretion. | Know the effect on each electrolyte: loops lower potassium, calcium and magnesium. A stem asking which diuretic lowers calcium is asking for a loop diuretic. | L9 slide 13 |
| Loop diuretics furosemide, bumetanide, torsemide, ethacrynic acid | Indication | Pulmonary edema, nephrotic syndrome (protein loss disrupts fluid regulation), cirrhosis of the liver (ascites), hypercalcemia (used with saline), heart failure, renal failure or insufficiency and hypertension. | Reach for a loop diuretic whenever a lot of fluid must come off. Hypercalcemia is treated with a loop diuretic plus saline because loops increase calcium excretion. | L9 slide 17 |
| Loop diuretics furosemide, bumetanide, torsemide, ethacrynic acid | Indication | Loop diuretics are effective in patients with a creatinine clearance below 30 milliliters per minute. Thiazides classically lose effect at low clearance (metolazone is the exception). | Added background: a patient who is still making urine on a loop diuretic does not necessarily have good kidney function, because the drug can force urine out of poorly working kidneys. | L9 slide 16 |
| Loop diuretics furosemide, bumetanide, torsemide, ethacrynic acid | Education-heavy | Systemic vasodilator actions: loop diuretics stimulate prostaglandins (prostaglandin E2), an effect blocked by nonsteroidal anti-inflammatory drugs, and have a direct relaxant effect on muscle (mechanism not understood). | This is the reason nonsteroidal anti-inflammatory drugs blunt a loop diuretic's effect. | L9 slide 14 |
| Loop diuretics furosemide, bumetanide, torsemide, ethacrynic acid | Education-heavy | Interaction: nonsteroidal anti-inflammatory drugs blunt the natriuretic and blood pressure response. Interaction: aminoglycosides potentiate ototoxicity. | Ask about over-the-counter pain relievers; a patient whose "water pill" stopped working may be taking one. Avoid stacking ear-toxic drugs. | L9 slide 19 |
| Loop diuretics furosemide, bumetanide, torsemide, ethacrynic acid | Education-heavy | Interaction: lithium (clearance falls, toxicity rises). Interaction: warfarin (the two compete for plasma protein binding). Interaction: digitalis (potassium and magnesium loss raise the risk of arrhythmias). | Loop diuretics lower potassium and magnesium, which is the setup for digoxin toxicity; check electrolytes in anyone taking both. | L9 slide 19 |
| Thiazide diuretics | ||||
| Thiazide diuretics chlorothiazide, hydrochlorothiazide, chlorthalidone, metolazone, indapamide | Indication | Inhibit the sodium-chloride transporter in the luminal membrane of the distal convoluted tubule (the major action). Agents: chlorothiazide, hydrochlorothiazide, chlorthalidone, metolazone and indapamide. | Class before agent: a distal-tubule sodium-chloride transporter blocker is a thiazide. | L9 slide 21 |
| Thiazide diuretics chlorothiazide, hydrochlorothiazide, chlorthalidone, metolazone, indapamide | Indication | Increase sodium chloride excretion (up to 5 percent of the filtered load) and urine output (1 to 2 liters a day); increase potassium and magnesium excretion; decrease renal calcium excretion (the opposite of loop diuretics). | Calcium is the contrast to memorize: loops waste calcium, thiazides keep it. | L9 slide 22 |
| Thiazide diuretics chlorothiazide, hydrochlorothiazide, chlorthalidone, metolazone, indapamide | Education-heavy | Calcium-containing kidney stones (calcium oxalate): by holding calcium back from the urine, thiazides leave less to crystallize. Added background: thiazides raise serum calcium, so they cause hypercalcemia rather than treat it (loop diuretics with saline treat it). | Counter-intuitive but true: serum calcium may rise slightly while urine calcium, and so stone formation, falls. | L9 slide 24 |
| Thiazide diuretics chlorothiazide, hydrochlorothiazide, chlorthalidone, metolazone, indapamide | Indication | Hypertension, renal failure, cirrhosis of the liver and congestive heart failure. In heart failure, thiazides are generally not potent enough, and loop diuretics are used instead. | Thiazides are standard drugs for blood pressure but are not the drugs for large fluid overload. | L9 slide 24 |
| Thiazide diuretics chlorothiazide, hydrochlorothiazide, chlorthalidone, metolazone, indapamide | Drug of choice | Low-dose thiazides are preferred for hypertension, with few adverse effects. They work best in elderly patients, African American patients and sodium-retentive states. Short term they lower blood volume and cardiac output; chronically they lower total peripheral resistance (direct vasorelaxant effects, less sodium in arteriolar walls, less "waterlogging"). | Patients with hypertension who retain sodium respond best. Added background: thiazides are the diuretic usually chosen for long-term blood pressure control; loop diuretics are kept for fluid overload and advanced kidney disease. | L9 slide 25 |
| Thiazide diuretics chlorothiazide, hydrochlorothiazide, chlorthalidone, metolazone, indapamide | Education-heavy | Thiazides classically lose effect when creatinine clearance is low (below about 30 to 40 milliliters per minute); metolazone remains effective at lower clearance. Added background: newer trial data show that chlorthalidone can still lower blood pressure in advanced chronic kidney disease. | Added background: metolazone is the thiazide added to a loop diuretic when a patient with poor kidney function still needs more diuresis. | L9 slide 28 |
| Thiazide diuretics chlorothiazide, hydrochlorothiazide, chlorthalidone, metolazone, indapamide | Monitoring | Interaction: nonsteroidal anti-inflammatory drugs block prostaglandins and weaken the natriuretic action. Interaction: digitalis: thiazides increase digitalis toxicity, so potassium should be kept above 4.0 mEq per liter. | Check the potassium of anyone taking a thiazide and digoxin together. | L9 slide 29 |
| Potassium-sparing diuretics | ||||
| Potassium-sparing diuretics amiloride, triamterene | Indication | Block luminal sodium channels in the collecting duct. They inhibit 2 to 3 percent of sodium chloride reabsorption, decrease the gradient for potassium secretion (so potassium is spared) and give a modest increase in urine flow. | These are weak diuretics used for what they do to potassium, not for volume. | L9 slide 30 |
| Potassium-sparing diuretics amiloride, triamterene | Indication | Amiloride and triamterene are the two agents; both are sold as fixed combinations with hydrochlorothiazide. | A combination product contains a thiazide as well, so it lowers sodium and keeps potassium at once. | L9 slide 31 |
| Potassium-sparing diuretics amiloride, triamterene | Education-heavy | Same uses as the other diuretics but much less natriuretic and diuretic effect. Most often used in combination with other diuretics or antihypertensive drugs. | Their main job is to offset the potassium lost with loop diuretics and thiazides. Added background: salt substitutes are usually potassium chloride, so a patient on a potassium-sparing diuretic should check with the prescriber before using one. | L9 slide 32 |
| Aldosterone antagonists | ||||
| Aldosterone normal actions | Indication | Aldosterone binds its receptor, which translocates to the nucleus and activates protein synthesis: more sodium channels in the membrane and more activity of the sodium-potassium adenosine triphosphatase (ATPase) pump, with more energy production in the distal convoluted tubule. | More sodium channels means more sodium and water retained and more potassium lost; excess aldosterone therefore causes low potassium. | L9 slide 34 |
| Aldosterone antagonists spironolactone, eplerenone | Indication | Spironolactone and eplerenone bind the steroid (aldosterone) receptor but the complex does not translocate to the nucleus, so aldosterone's actions are blocked. Most effective when aldosterone is high; they block 2 to 3 percent of sodium chloride reabsorption and reduce potassium loss; modest effect on lipids, glucose and uric acid. | The drug is a receptor antagonist, so it needs aldosterone to be present to matter: it works best in states of high aldosterone. | L9 slide 36 |
| Aldosterone antagonists spironolactone, eplerenone | Indication | Primary aldosteronism, hypertension, heart failure (advanced; see the heart failure section), edematous conditions, cirrhosis (secondary hyperaldosteronism) and nephrotic syndrome. | Both a diuretic and a survival drug in advanced heart failure. In the heart failure section the same drug class is described for class III or IV failure; learn it as advanced failure. | L9 slide 37 |
| Carbonic anhydrase inhibitors | ||||
| Carbonic anhydrase inhibitors acetazolamide, dichlorphenamide, methazolamide | Indication | Inhibit carbonic anhydrase: bicarbonate absorption in the proximal tubule falls by 80 to 90 percent, so less hydrogen ion is produced and less sodium-hydrogen exchange occurs. Short-term effect: sodium and potassium excretion rises about 5 percent; after 3 to 5 days the effect falls to 1 to 3 percent. | These are the weakest diuretics because the rest of the nephron makes up for the loss. Bicarbonate is trapped in the tubule and lost in the urine. | L9 slide 39 |
| Carbonic anhydrase inhibitors acetazolamide, dichlorphenamide, methazolamide | Indication | Acetazolamide, dichlorphenamide and methazolamide. | Class before agent: three agents, all ending in -zolamide or -phenamide. | L9 slide 40 |
| Carbonic anhydrase inhibitors acetazolamide, dichlorphenamide, methazolamide | Indication | Other uses: glaucoma (lowers bicarbonate in the ciliary body; dorzolamide and brinzolamide), epilepsy (metabolic acidosis, central nervous system effects) and mountain (altitude) sickness. | Used as diuretics rarely; their value is in these other uses. Added background: for altitude sickness the metabolic acidosis makes the patient breathe faster, which helps at low oxygen pressure. | L9 slide 42 |
| Heart failure: the disease | ||||
| Heart failure etiology | Indication | Ischemic heart disease and myocardial infarction cause 50 to 60 percent of cases. Other causes: hypertension, idiopathic dilated cardiomyopathy, other cardiomyopathies (alcoholic, viral, hypertrophic) and drug-induced failure. | Treating blood pressure and coronary disease helps prevent heart failure. | L9 slide 45 |
| Heart failure systolic dysfunction | Indication | Systolic dysfunction is decreased contractility from loss of myocardial muscle mass, left ventricular hypertrophy or dilated cardiomyopathy. It is assessed as a reduced ejection fraction. | Systolic failure is the type the survival drugs (ACE inhibitors, three beta blockers, aldosterone antagonists) were proved in. | L9 slide 46 |
| Heart failure diastolic dysfunction | Indication | Diastolic dysfunction is impaired relaxation: thicker, stiffer ventricles relax less well, and ischemia impairs removal of calcium from the cytosol back into the sarcoplasmic reticulum. Ventricular filling falls, so cardiac output falls, with symptoms despite a preserved ejection fraction. | A normal ejection fraction does not rule out heart failure. | L9 slide 47 |
| Heart failure compensatory response | Indication | Compensation: increased preload (sodium and water retention), vasoconstriction, tachycardia and increased contractility from sympathetic activation, and left ventricular hypertrophy. These begin as help and become a vicious cycle: lower cardiac output drives neuroendocrine activation, sodium and water retention and a higher afterload. | Each drug class breaks one link of the cycle: diuretics lower preload, angiotensin-converting enzyme inhibitors lower afterload, beta blockers blunt sympathetic drive. | L9 slide 48 |
| Heart failure decompensation | Education-heavy | Common precipitants of decompensation: lack of compliance, uncontrolled hypertension, cardiac arrhythmias, inadequate therapy, inappropriate medications or fluid overload, acute anginal chest pain, pulmonary infection and emotional stress. | Counsel on diet and medication adherence: missed medicines and salty or fluid-heavy meals are the commonest avoidable triggers. | L9 slide 50 |
| Heart failure nonpharmacologic therapy | Education-heavy | Restrict dietary sodium and fluid; physical activity may improve functional status. | Tell the patient to limit salt and fluid and to stay active as tolerated. | L9 slide 51 |
| Heart failure: diuretics, ACE inhibitors and beta blockers | ||||
| Diuretics in heart failure loop diuretics | Drug of choice | Loop diuretics are the mainstay of heart failure therapy: they decrease sodium and water retention and so lower preload, for symptomatic benefit. Thiazide diuretics are not potent enough for most patients with heart failure. | Loops relieve congestion and swelling; they are not what extends life. | L9 slide 52 |
| Diuretics in heart failure what they do not do | Education-heavy | Diuretics are for symptomatic relief only. There is no evidence they decrease progression or mortality, and they are not mandatory therapy. | A drug that improves mortality stays on whatever the symptoms; a drug for symptoms only is not mandatory. Added background: some patients adjust the loop diuretic dose by their daily weight. | L9 slide 53 |
| Daily weight monitoring fluid status | Monitoring | Monitoring the patient's weight is a good way to detect worsening fluid overload. A gain over several days is fluid, not tissue. | Teach daily weights at the same time each morning and a clear rule for when to call; a rising weight means fluid is building up. | L9 slide 52 |
| ACE (angiotensin-converting enzyme) inhibitors in heart failure | Drug of choice | Angiotensin-converting enzyme inhibitors decrease preload, afterload and sympathetic activation and decrease left ventricular hypertrophy, dilation and remodeling, so they slow progression and decrease mortality. Patients should be on an angiotensin-converting enzyme inhibitor and a beta blocker irrespective of symptoms. | These are survival drugs: they stay on even when symptoms are controlled. Added background: angiotensin receptor blockers are the alternative when cough develops, and can be used with caution after angioedema. | L9 slide 54 |
| ACE (angiotensin-converting enzyme) inhibitors in heart failure | Indication | Benefits: hemodynamic improvement, improved exercise tolerance, decreased heart failure symptoms, fewer hospital admissions, slowed progression of disease and prolonged survival. | The benefit list is the reason to keep titrating the drug up to the target tolerated amount. | L9 slide 55 |
| Beta blockers in heart failure carvedilol, metoprolol succinate, bisoprolol | Indication | Beta blockers were classically considered contraindicated in heart failure. The three with a mortality benefit are carvedilol, metoprolol succinate (extended release) and bisoprolol. | Only these three: other beta blockers have not been shown to lower mortality in heart failure. The succinate (extended-release) metoprolol is the one that lasts all day. | L9 slide 57 |
| Beta blockers in heart failure carvedilol, metoprolol succinate, bisoprolol | Education-heavy | Keys to successful use: the patient should be stable before initiation (hospital initiation was traditionally preferred); start with very low doses and titrate up slowly (over several weeks); monitor for worsening heart failure signs and symptoms. | "Low and slow": starting too fast or in an unstable patient can worsen heart failure. Tell the patient that benefit builds over months and that symptoms may briefly worsen. | L9 slide 58 |
| Beta blockers in heart failure carvedilol, metoprolol succinate, bisoprolol | Indication | Benefits: improved exercise tolerance, hemodynamic improvement (increased ejection fraction), slowed disease progression, fewer hospitalizations, less need for transplant and decreased mortality. | Like angiotensin-converting enzyme inhibitors, these are survival drugs rather than symptom drugs. | L9 slide 59 |
| Beta blockers in heart failure carvedilol, metoprolol succinate, bisoprolol | Drug of choice | First-line therapy in class II to IV heart failure. Patients should be on an angiotensin-converting enzyme inhibitor and a beta blocker irrespective of symptoms. | Anyone with systolic heart failure should be on both unless contraindicated or not tolerated. | L9 slide 60 |
| Digoxin | ||||
| Digoxin cardiac glycoside | Indication | A lactone ring and a steroid nucleus are essential for activity; the sugar molecules influence absorption, half-life and metabolism. | Digoxin is a cardiac glycoside: steroid core, lactone ring and sugars. | L9 slide 61 |
| Digoxin cardiac glycoside | Indication | Inotropic action (the older mechanism): digoxin inhibits the sodium-potassium adenosine triphosphatase (ATPase); intracellular sodium rises, so intracellular calcium rises through the sodium-calcium exchanger and the fiber shortening (force of contraction) increases. | Block the sodium pump, retain sodium, bring in calcium, contract harder: this is a positive inotrope. | L9 slide 62 |
| Digoxin cardiac glycoside | Indication | Neurohormonal actions (the newer mechanism): decreased sympathetic and increased parasympathetic activity, resensitized baroreflex, lower heart rate, more parasympathetic activity at the atrioventricular node, and decreased renin-angiotensin-aldosterone system activity, so less remodeling, better perfusion and higher cardiac output. | Part of the benefit is a slower heart rate that lets the ventricles fill for longer. | L9 slide 63 |
| Digoxin cardiac glycoside | Indication | Clinical benefits: improved symptoms, exercise tolerance and quality of life, and fewer hospitalizations. No survival benefit. | Digoxin is a symptom drug: it is never mandatory, unlike angiotensin-converting enzyme inhibitors and the three beta blockers. | L9 slide 66 |
| Digoxin cardiac glycoside | Indication | Place in therapy: no evidence of slowed disease progression; primary use is in symptomatic patients already on optimal angiotensin-converting enzyme inhibitor, beta blocker and diuretic therapy; considered in symptomatic heart failure with systolic dysfunction; can be used for rate control in atrial fibrillation with heart failure. Added background: it is generally an add-on, not the first drug for rate control. | Add it when a patient is still symptomatic on the survival drugs. Added background: because it is cleared by the kidneys, kidney disease makes it accumulate. | L9 slide 67 |
| Digoxin cardiac glycoside | Monitoring | Target blood level 0.5 to 1 ng/mL; higher concentrations may be associated with worse outcomes in heart failure. | A narrow target range is why digoxin is one of the few heart failure drugs monitored with a drug level. | L9 slide 65 |
| Digoxin immune Fab antidote | Indication | Digoxin immune Fab is an antibody fragment that binds digoxin (affinity for digoxin is higher than digoxin's affinity for the sodium-potassium adenosine triphosphatase (ATPase)); it is produced by immunizing healthy sheep with digoxin coupled to human serum albumin, and it rapidly reverses toxicity. | This is the antidote for life-threatening toxicity. Added background: removing the digoxin can unmask the atrial fibrillation or heart failure it was treating. | L9 slide 72 |
| Other heart failure drugs | ||||
| Aldosterone antagonists in heart failure spironolactone, eplerenone | Indication | Spironolactone gives a mortality reduction in advanced (class III or IV) heart failure. Patients are not eligible if potassium is above 5 or serum creatinine is above 2.5. Gynecomastia occurs in about 10 percent of men. Eplerenone has less effect on androgen receptors and does not usually cause gynecomastia. Mechanism: neurohormonal inhibition, slowed remodeling of the left ventricle and slowed progression of heart failure. | Check potassium and kidney function before and during treatment. If a man on spironolactone develops breast enlargement, switching to eplerenone avoids it. | L9 slide 73 |
| Phosphodiesterase (type III) inhibitors milrinone, inamrinone | Indication | Cyclic adenosine monophosphate (cyclic AMP) phosphodiesterase (type III) inhibitors. Inotropic and vasodilator actions: direct stimulation of myocardial contraction, balanced arterial and venous dilation, decreased afterload and increased cardiac output. | Both a stronger squeeze and a lower afterload. Added background: because they also dilate vessels, they suit acute failure with an adequate blood pressure rather than a low one. | L9 slide 75 |
| Phosphodiesterase (type III) inhibitors milrinone, inamrinone | Indication | Approved for short-term intravenous use in acute decompensated heart failure. Long-term use is associated with higher mortality and morbidity than placebo. | These are in-hospital stabilizing drugs, transitioned off once the patient is stable and on usual oral therapy; they are never for long-term use. | L9 slide 76 |
| Dobutamine and dopamine intravenous inotropes | Indication | Dobutamine is a selective beta-1 agonist: intravenous infusion stimulates the force of contraction more than the rate; short-term use to stabilize patients. Dopamine is given by intravenous infusion and acts through dopamine and beta receptors. | Added background: when decompensation comes with low blood pressure, an agent that does not rely on vasodilation, such as dobutamine, is generally favored over milrinone; low-dose dopamine has not been shown to protect kidney function. | L9 slide 77 |
| Ivabradine hyperpolarization-activated channel blocker | Indication | Blocks the hyperpolarization-activated cyclic nucleotide-gated (HCN) channel, inhibiting the pacemaker current in the sinoatrial node: reduces heart rate without affecting contractility. Used in heart failure patients maxed out on beta blockers, in normal sinus rhythm with a heart rate above 70 beats per minute; decreases hospitalization and heart failure related death. | Add-on only: it replaces neither the beta blocker nor the angiotensin-converting enzyme inhibitor; it needs a regular sinus rhythm. | L9 slide 79 |
| Sacubitril-valsartan neprilysin inhibitor with an angiotensin receptor blocker | Indication | Sacubitril is a neprilysin inhibitor, formulated with valsartan. Neprilysin normally degrades vasoactive peptides (natriuretic peptide, bradykinin); inhibition causes vasodilation, natriuresis and diuresis and inhibits growth and fibrosis of myocardial tissue. Used to reduce the risk of cardiovascular death and hospitalization in heart failure. | It carries an angiotensin receptor blocker, so it takes the place of an angiotensin-converting enzyme inhibitor or receptor blocker. | L9 slide 81 |
| Sacubitril-valsartan neprilysin inhibitor with an angiotensin receptor blocker | Education-heavy | Do not use along with an angiotensin-converting enzyme inhibitor, and give a 36-hour washout period to avoid adverse effects. | When switching from an angiotensin-converting enzyme inhibitor, stop it and wait 36 hours before the first sacubitril-valsartan. | L9 slide 81 |
| Sodium-glucose cotransporter 2 (SGLT2) inhibitors dapagliflozin, empagliflozin | Indication | Dapagliflozin and empagliflozin are indicated for stable, chronic heart failure with reduced ejection fraction, where they reduce mortality and hospitalizations. Originally developed for diabetes: they make the kidneys not reabsorb glucose. | The patient will pass glucose in the urine; counsel on hydration and on genital and urinary hygiene. Added background: these drugs are also used in heart failure with preserved ejection fraction. | L9 slide 82 |