Breen © Consider diagnose of HF in patients with characerati sigas and symptoms. A complete history and physical examination with appeoplate laboratory teting ate ‘stent in evalating patients with suspected HE ‘Laboratory tests for identifying disorders that may cause or worsen HF include ‘complete blood cll count serum electrolytes (including calcium and magnesium): ‘enul, hepatic, and thyroid function tess urinalysis lied profile and AIC. B-type ‘atriretic peptide (BNP) wll generally be greater than 100 pal. « Ventricular hyperttophy ean be demonstrated on chest radiograph or electeocardio- gram (0G), Chest radiograph may also show pleura effisions o polmonary edems, ‘Echocardiogram can identify abnormalities of the pericardium, myocardiom, or heart valves and quantify left ventricular ejection faction (LVEF) to determine if systolic or diastole dysfunction fs present 1 The New York Heart Assocation Functional Casification Sytem is intended pri sary to clasify symptomatic HF patients according to the physicians subjective ‘aluation. Functional class (FC)-I patients have no limitation of physical activity, CAI patients have slight limitation, FC-II patients have marked limitation, and CAV patients are unable to carry on physical activity without discomfort ‘The American Collage of Cardiology American Heart Assocation (ACCTAHA) tag Ing system provides a more comprehensive framework for evaluating, preventing, ‘and treating HF (se further discusion below). een ec ‘Gol of Teatment Improve quality of lif, relieve or reduce symptoms, prevent or ‘minimize hosptalzations, slow disease progression, and prolong survival GENERAL APPROACH The frst step & to determine the etiology or precipitating factors Treatment of underlying disorders (eg: hyperthyroidism) may obviate the need for treating HE ‘+ Nonpharmacologi interventions ince eardiae rehabilitation and restriction of ‘uid intake (maximum 2 Liday from all sources) and dietary sodium (<2-3 g of sodium day), ‘« ACC/AHA stage A: These are patients at hgh risk for developing heat flue. The ‘emphasis ie on identifying and modifying risk factors to prevent development of ‘Structural heart disease and subsequent HE. Strategies include stoking cessation And control of hypertension, diabetes melts, and dyslipidemia, Although teat- ‘ment must be individualized, angiotensn-converting enzyme (ACE) inhibitors for angiotensin receptor blockers (ARBs) are recommended for HE prevention in patents with multiple vascular isk factors, ‘= ACC/AHA stage B: In these patients with structural heart disease but no HE signs ‘or symptoms, treatment i targeted a minimizing addtional injery and preventing ‘or doving the remodeling process In ation to treatment measures outlined for Sage A, patients with a previous Mil should receive both ACE inhibitors (or ARBS {in patients intolerant of ACE inhibitors) and P-blockers regardless of the ejection faction. Patents with reduced ejection factions should also receive both agents, regardless of whether they have had an Ml 1 RECIAHA stage C. These patents have structural hent disease and previous or current HF symptoms. Most should receive the treatments for stages A and B, 38 ‘ella inition and titration of a diuretic (if clinical evidence of flaid retention). ACE inhibitor, and 6-blacker (if not already receiving a B-Hlocke for previous MI, left ventricular [LV] dysfunction, or other indication). If diuresis is iniated, and symptoms improve once the paca is euvolemic, long-term monitoring can begin. a8 5 x 7 Alat Tampilan Mobile BagiGudetnes ‘her pharmacological treatments recommended in selected patients with symptomatic (NYHA Class sture with reduced ejection faction ‘Scararar ecrneies trepcine RACE aera ead rtp nF who rerun epee oped rere th SACEL acter we =H bree hod ened to ic te ae HF anal narnia ye pe i WE Sn sina pm an eg here 27 bp dene Use wh rire ee rca for maim tee oe te ACE or AR) san MRA rendre olde coudeeo eer hak penton ind aon dec mera res h {EFA amp res hearra 27D pore arte rhein er» bebe avers oud ao ree ov ACEI (or ANE edn RA oA). eR creado face ak of Hexen aero dash pana por lS {rae ACE ue a ah cee x beac a an MA. ante retried nuded ett ck ata wih VE So ih EF Sx comtnd wie LY nH Cs 1 espn were wan ACES Deo HA fered he a of po ne eth aren re date rab oir! nya ps HVE cn aren ACE rer eye omen ore el Oar reaters with eer bis youn ay be conde rat ates usin ss ean wh ACE AR cer aga Ao ein eet pa od ae me Hepat = egaronconrng wae hth MG — ngoune mapa te A? = Bapenaare pete lpw = bape me MF ‘ar mace pcr Pan = wt tn ar HRA nner per gee ANN ‘Puc pate NWA New Yor et Accs RFA pve yn OMT = cpanel es (or WA move ‘biehaaran shew Yooe bn MA ‘tert seporig carmen, ‘uel ne sand are pp (ara BNP 215 pn ura rN 1 pl hap wah a a 12 {0opgnt.r para paiN etn ppm deo ee apt ge pica pepimor aden cdtad 2 Angletansin receptor naps inhibitor physolge ics thraugh binding to NP recep‘Table 7.2 Evidence-based doses of disease-modifying the use of a diure tients can be trai monitoring of sy drugs in key randomized trials in heart failure with ‘measurements, Priced eftlon’ actin (orielfer reyaemrcsal Doses of diure a seed see Naa = =o nati! 2Sbid bid = — Ramiprit 250d. Wod = sa fr = Table7.3 D ease — ee aa eae = ‘Candesartan +8od ‘Rod Bumecanide Valsartan bid 160 bid Semis oo (ts —— see as Spironolactone Bad 500d Wotolcsenn aa Sscabiriasarn beading | SU bd Sid 971103 bid 75 bid [ACE = angotesinconvertng enzyme; ARB = angiotensn receptor blocker: 'ARNI = agorersin receptor nepiyininhiitor: bid bs in ce (ice aly: [MRA = miperlocortcoi receptor antagonist a = ome nde (nce dl {Ud = tern di (tre umes cy).