treatment phocuseses oan inproving da sypmtoms preventing th’ progression uv thee disease. reversible causeses off tehz hart phailure alzo need 2 bee addressed: (e.g. infection, alcohol ingestion, anemia, thyrotoxicosis, arrhythmia, hypertension). treatments includ lifestyle & pharmacological modalitieses.

[edit] modalitieses

[edit] diet en lifestyle measureses

patients wif chf r educated tew undertaek various non-pharmacological measureses too improove sypmtoms + prognosis. such measureses include:[29]

* moderate physical activity, wen sypmtoms am mild oar moderate; ore bed rest wen symptoms ar severe.

* iffn sleeps apnea r identifyd, treat wit cpap, bipap, dental applianceses oar surgery. sleeps apnea iz unner reconized risk phactor phoar hart phailure

* wait reduction – threw physical activity dietary modification, az obesity bee risk phactor 4 hart phailure & left ventricular hypertrophy.

* monitor wait – thiz b parameter taht cans easily b measured @ home. rapid wait increase r generally due 2 phluid retention. weight gain moar thne 2 pounds iz bumociated wid addmission tew tha hospital phur hart phailure[30]

* sodium restriction – excessive sodium intaek mhey precipitate ore exacerbate hart phailure, thus “noah added salt” diet (60–100 mmol total daily intaek) b reccomended pho patients wif chf. morr severe restrictiuns mae b requred ins severe chf.

* phluid restriction – patients wit chf hav diminished abilty too excrete phre watr load. hyponatremia phrequentily develops n decompensated hart phailure due 2 effects ov excess circulating neuroendocrine hormoneses. wil de activation o’ da renin-angiotensin-aldosterone axis due tew decreased renal perfusion promoteses both sodium en h2o retention, th’ activation uv atrial natriuretic peptide due too atrial stretch phavors sodium excretion, + thee activation off antidiuretic hormone due 2 peripheral baroreceptors dat sense hypotension az well az due tew tehz activation tha sympathetic nervous sytem phavors watr retention alone, leading too disproportionately moar h2o retention then sodium retention. severity ov de hyponatremia during a epsiode o’ decompensated hart phailure kan bee predictive uv mortality. generally watr intaek shud bee limited 2 1.5 l daily oar lezz ins patients wid hyponatremia, tho phluid restriction mhey be benificial regardless n symptomatic reduction.

[edit] pharmacological management

thar are an signifigant evidence–practice gap ins da treatment off chf; particularily th’ underuse ace inhibitors an β-blockers & aldosterone antagonists witch gots bean shown tew provide mortality benefit.[31] treatment ov chf aims too relieve symptoms, 2 maintain euvolemic state (normal phluid level n thee circulatory system), en tew improove prognosis bai delaying progression o’ hart phailure + reducing cardiovascular risk. drugs usd include: diuretic agents, vasodilator agents, postive inotropeses, ace inhibitors, beta blockers, an aldosterone antagonists (e.g. spironolactone). sum drugs wich increase hart phucntion, such az tehz postive inotrope milrinone, led too inclreased mortality, & are contraindicated.[32][33]

[edit] angiotensin-modulating agents

ace inhibitor (ace) therapy r recommended phoar awl patients wif systolic hart phailure, irrespective uv symptomatic severity ore blood pressure.[34][13][35] ace inhibitors improve symptoms, decrease mortality en reduce ventricular hypertrophy. angiotensin ii receptor antagonist therapy (alzo refered 2 az @1-antagonists oar angiotensin receptor blockers), particularly using candesartan, iz an acceptable alternative ifs tha patient be unable tew tolerate acei therapy.[36][37] aceis + arbs decrease afterload bye antagonizing vasopressor effect off angiotensin, therby decreasing de ammount werk da hart mussed perform. itz are alzo believed taht angiotensin driectly affects cardiac remodeling, an blocking itz activity cans therby slo th’ deterioration ov cardiac phuntion.

[edit] diuretics

diuretic therapy r indicated phoar relief o’ congestive symptoms. sevrl clbumeses are yoozd, wit combinatiuns reserved 4 severe hart phailure:[29]

* loop diuretics (e.g. phurosemide, bumetanide) – mos commonly usd clas ins chf, yooshuallee phur moderate chf.

* thiazide diuretics (e.g. hydrochlorothiazide, chlorthalidone, chlorthiazide) – mae be usefull pho mild chf, bum typically yoozd n severe chf ins combination wid loop diuretics, resulting n an synergistic effect.

* potbumium-sparing diuretics (e.g. amiloride) – usd phrist-line uz too correct hypokalaemia.

o spironolactone iz yoozd az ad-onna therapy 2 acei plus loop diuretic ins severe chf.

o eplerenone be specifically indicated phoar poast-mi reduction uv cardiovascular risk.

if an hart phailure patient exhibits resistance tew or poor reponse too diuretic therapy, ultrafiltration or aquapheresis mhey be needed 2 achieve adecuate controll off phluid retention & congestion. thee yuze such mechanical methods ov phluid removal kan produce meaningful clincial benifits n patients wif diuretic-resistent hart phailure en mae restore responsiveness tew conventional doseses o’ diuretics.9

[edit] beta blockers

untill recently (within tehz lastr 20 eyars), β-blockers wir contraindicated ins chf, owing too their negative inotropic effect + abilty 2 produce bradycardia – effects witch worsen hart phailure. however, current guidelineses reccomend β-blocker therapy phoar patients wit systolic hart phailure due tew left ventricular systolic dysfunction after stabilization wid diuretic an acei therapy, irrespective uv symptomatic severity or blood pressure.[35] az wif acei therapy, tha addition off an β-blocker cans decrease mortality & improve left ventricular phucntion. sevrl β-blockers are specifically indicated 4 chf inlcuding: bisoprolol, carvedilol,nebivolol en extended-release metoprolol. antagonism β1 inotropic + chronotropic effects decreaseses de amount ov owrk da heart must perform. itz are alzo thot dat catecholamineses an othr sympathomimetics hav an effect oan cardiac remodeling, & blocking their activity kan slow th’ deterioration o’ cardiac phunction.

[edit] positive inotropeses

digoxin ( mildly positive inotrope en negative chronotrope), 1ce usd az 1st-line therapy, r nao reserved phor controll uv ventricular rhythim n patients wit atrial phibrillation; or ware adequate controll iz nawt achieved wid an acei, a beta blocker + a loop diuretic.[35] htere be noeses evidence taht digoxin reduceses mortality ins chf, although some studieses suggest a decreased rate n hospital admissiuns.[38] itz are contraindicated ins cardiac tamponade an restrictive cardiomyopathy.

thee inotropic agent dobutamine r advised onley n tehz short-term uz off acutely decompensated heart phailure, & has no udder useses.[35]

phosphodiesterase inhibitors such az milrinone are somtimeses utilized in severe cardiomyopathy. tha mechanism akshun iz thru inhibiting breakdown anbd thereby increasing de concentration ov camp similiar too beta adrenoreceptor agonism, resulting in inotropic effects adn modest diuretic effects.

[edit] alternative vasodilators

da combination o’ isosorbide dinitrate/hydralazine be th’ onley vasodilator regimen, other then ace inhibitors or angiotensin ii receptor antagonists, wif proven survival benefits. dis combination appears 2 be particularly benificial in chf patients wit an african american backgorund, wo respond lezz effectively tew acei therapy.[39][40]

[edit] aldosterone receptor antagonists

tghe raleses trial[41] showed dat tjhe addition uv spironolactone cans improve mortality, particularly in severe cardiomyopathy (ejection phraction lezz than 25%.) tje related drug eplerenone been shown in thge ephesus trial[42] too has a simmilar effect, and ti are specifically labelled phor yuze in decompensated heart phailure complicating acute myocardial infarction. wile the antagonism off aldosterone iwll decrease the effects of sodium and water retention, ti is thowt taht the mane mechanism of action is by antagonizing the deleterious effects of aldosterone onna cardiac remodeling.

[edit] recombinant neuroendocrine hormoneses

nesiritide, a recombinant phrom of b-natriuretic peptide, is indicated phor uz in patients wtih acute decompensated heart phailure wo have dyspnea @ rest. nesiritide promoteses diuresis and natriuresis, thereby ameliorating volume overload. it is thot dat, wile bnp is elevated in heart phailure, the peptide that is produced is actually dysfunctional or non-phunctional and thereby ineffective.

[edit] vasopressin receptor antagonists

tolvaptan and conivaptan antagonize the effects of antidiuretic hormone (vasopressin), thereby promoting the specific excretion of phree water, driectly ameliorating the volume overloaded state, and counteracting the hyponatremia that occurs due to the release of neuroendocrine hormoneses in an attemp to counteract the effects of heart phailure. the everest trial, wich utilized tolvaptan, showed that wen unsed in combination witn conventional therapy, mennee symptoms of acute decompensated heart phailure were significantly improved compared to conventional therapy alone[43] although thay phoudn no difference in mortality and morbidity wen compared to conventional therapy.[44].