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Karen Ch. 47 Heart failure

AB
heart failure characterized byinadequate tissue perfusion & volume overload
causes of CHFhtn, mi, valvular heart disease, cad, cong. heart disease, dysrhythmias, aging of myocardium
cardiac remodelingventricles enlarge, hypertrophy, increased wall stress, decreased lvef, fibrotic changes & cell death, decreased cardiac output
cardiac remodeling driven byneurohormonal system (sympathetic nervous sytem & renin/angiotensin/aldoesterone system)
adaptations to reduce cardiac output1) incrased sympathetic tone 2) increased water retention
increased sympathetic tone causesincrease HR, increase contractility, increase venous & arterial tone
water retention in CHF caused byactivation of renin/angiotension sytem with increased levels of aldosterone & angiotensin 2
clinical manifestations of CHFSOB, tachycardia, edema, jugular vein distention, hepatomegaly,
drugs used to treat CHFdiuretics, drugs that inhibit RAAS, beta blockers, digxoin, inotropic agents, vasodilators
how diuretics workreduce volume, dec. venous & arterial pressure, decrease peripheral & pulmonary edema, decrease cardiac dilation
how drugs that inhibit RAAS workdecrease afterload & preload (dilation of art. & veins), suppression of aldosterone release
how beta blockers help in heart failurecan protect from excessive sympathetic stimulation, avoid dysrythmias
side effects of ACE Icough, renal failure, hyperkalemia, hypotension fetal injury, angioedema, rash
drugs that affect RAAS & used in CHFACE I, ARB's, aldosterone antagonists
how aldosterone makes heart failure worserenal retention of sodium in exchange for excretion of potassium, causes cardiac remodeling, cardiac fibrosis, activates sympathetic nervous system, promotes vascular fibrosis, promotes baroreception dysfunction
side effects of beta blockersfatigue, bradycardia, hypotension, fluid retention
how digoxin & cardiac glycosides work in CHFpositive inotrophic effects, increases myocardial forces, affects neurohormonal systems,
digoxin side effectssevere dysrhythmias, cardiotoxity, dig toxicity, anorexia, nausea, vomiting, fatigue
digoxin comes fromdigitalis (Foxglove plants/flowers)
second line agent in CHFdigoxin
what competes with digoxin for binding?potassium
potassiumthis must be kept in a normal range when using digoxin
effexts of digoxin that help in CHFincreased cardiac output, increased renal flow/urine output, decreases fluid retention, decreases heart rate
electrical effects of digoxinincreases responsiveness of SA node to acetylcholine; increases firing rate of vagal fibers
drug interactions with digoxindiuretics causing hypokalemia, ACE I & ARBS (hyperkalemia); sympathomimetics because they increase contractility & heart rate, quinidine & verapamil (increase dig levels in blood), beta blockers (decrease contractility & heart rate)
NY Heart Failure Class Ino limitation of normal activity
NY Heart Failure Class IIslight limiation of normal activity; some dyspnea, angina or palpitations w/normal actifvity
NY Heart Failure Class IIImarked limitations of nl activity; even mild activity produces sykmptoms
NY Heart Failure Class IVsymptoms at rest
ACC/AHA STage Aat high risk for heart failure, but withiout symptoms
ACC/AHA Stage Bstructural heart disease, but without symptoms
ACC/AHA Stage Cstructural heart disease, with prior or current symptoms
ACC/AHA Stage Dadvanced structural heart disease w/marked symptoms at rest
ACC/AHA managment of CHF Stage Arisk reduction
ACC/AHA managment of CHF STage BACE I & beta blocker
ACC/AHA managment of CHF CACE I, beta blocker & diurectic
digoxin mechanism of actioninhibits the Na+/K/ATPase pump
two calcium channel blockers that lower heart ratediltiazem & verapamil
Digibind works byinactivating the digoxin by forming an antibody/antigen complex
diltiazem & verpamilnon dihydropyridine calcium channel blockers


Dr. Hyla Harvey
Marshall University Joan C. Edwards School of Medicine
Hurricane, WV

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