Congestive Heart Failure (CHF) Therapy PDF

Part 4 4: The erapy of conges stive hea art failurre (CHF)) █ Bas sic inform mation Definittion: Hearrt failure (HF) ( is a progresssive clinical synd drome in...

Part 4 4: The erapy of conges stive hea art failurre (CHF)) █ Bas sic inform mation Definittion: Hearrt failure (HF) ( is a progresssive clinical synd drome in which e either stru uctural or functional f abnorm malities im mpair the ability of the heeart to meet the metabolic m demands of the body. b. Classiffication, clinical c pic cture, and theerapeutic aim: Ana atomical classificat c ion Leftt-sided he eart failure e (LSHF): – Usually du ue to syste emic hyperttension. – T The cardin nal manifes stations arre those off pulmona ary congesstion e.g. tachyp- t nea, dysppnea (diffic culty in brreathing), orthopnea a (dyspneaa on lyingg back), paroxysma al nocturnnal dyspne ea, cough with expectorationns, bilatera al basal lung crepittation, etc.. Right-sided heart h failu ure (RSHF)): – Usually duue to pulmo onary hype o lung disease. ertension or – TThe cardinal manifestationss are tho ose of sy ystemic congestio on e.g. congestedd neck veins, conge ested liver, bilateral leg edemaa, right ven ntricular hypertroph hy, etc. Tottal or cong gestive he e (CHF): co eart failure ombination n between the two. Patthological classifica ation Sys stolic dysffunction (decreased ( d contracctility) is caused c byy reduced muscle pow wer e.g, MII, cardiomyyopathies, and ventrricular hypertrophy (sstrain). Ven ntricular hyppertrophy can c be caaused by p pressure overload o (e e.g, system mic or pulmonary hyppertension and aortic or pulm monic valvee stenosis s) or volum me overloa ad (e.g, valvvular regurrgitation, high-outpu h ut states e.g. e thyrotoxicosis aand arterio ovenous fistu ula). Diastolic dyssfunction (restrictio ( on in ventrricular filling) is cauused by inc creased ventricular stiffness e.g. ventricul ar hypertrrophy, infilttrative myo ocardial diseases 173  (e.g g. amyloido osis), myoocardial isschemia an nd MI, an nd pericard dial diseas se (e.g, periicarditis an nd fibrosis)). Thee decrease ed COP le eads to the e follo owing com mpensato ory mec chanisms:  Sympa athetic overactivitty leadingg to tachyc cardia.  Renal ischemia → ++ o of RAAS → VC (A Ang-II) an nd fluid re etention (a aldosterone e) → ↑ afterload a and a preloa ad → morem HF and a edemma (viciouss circle). Clin nical class sification HF is classifie ed by the New Yorrk Heart Association A n (NYHA) iinto the fo ollowing classses: NYHA Class S Symptom I (mild) No symptoms while performing ordinary N y physical activity (w walking, climbing sta airs, etc.). II (mild)) Mild symptoms (mil d shortne M ess of bre eath, palppitations, fatigue, and/or angina) and sliight limitation during ordinary p physical ac ctivity. III (mod derate) Marked limitation in a M activity due e to sympttoms, evenn during le ess than ordinary acttivity. Com mfortable only at rest. IV (seve ere) Severe limittations with S h symptom ms even while at restt. Mostly bedbound patients. p 174 █ Therrapy of heart h failu ure Non n-drug the erapy = life e style mo odification n: – Rest. – Dietary sodium (salt)) and fat re estriction. – AAvoid stre ess, smokinng and alc ohol. – WWeight redduction. – Control of risk factors e.g. surgical correction c of valvullar diseas ses and ttreatment of hyperthhyroidism, hypertension, etc. – A gs that ↑ BP Avoid drug P: e.g. symmpathomimetics, sodiu um containning drugs, etc. Dru ug therapy y: – Positive in notropic drugs:  Carrdiac glyco osides (Diggitalis).  Dop pamine & dobutamin d ne (used for short terrm only).  Pho osphodiestterase inhi bitors: inammrinone & milrinone.. – Diuretics. – A ACEIs. – V Vasodilatoors: nitrates s and hydrralazine – Other drug gs: e.g. betta-blockerrs and spironolactonee. ▌Carddiac glycoosides: Digoxin, Digitox xin, Ouaba ain Source e and chemistry – Nattural plant derivatives s (Foxglovve plant). – Carrdiac glycoosides conntain a lacttone ring and a a stteroid (aglycone) mo oiety attachhed to sug gar molecules. – Dig goxin is thee most widely used. Pharm macokinetics of digo oxin – Dig goxin distriibutes to most m bodyy tissues and a accum mulates in n cardiac tissue. Thee concentrration of th he drug in the heart is i twice that in skeleetal muscle e and at leasst 15 timess that in plasma. – Elim mination iss renal. Do ose adjusttment should be done accord ding to creeatinine clearance. anism of action Mecha a Pos sitive inotrropic effec ct: 175