Treatment of Congestive Heart Failure Flashcards
heart contracts less forcefully and blood is pumped out (reduced ejection fraction)
systolic dysfunction
heart is stiff and does not relax normally (reduced filling)
diastolic dysfunction
- cardiac output high as the heart works hard to keep up with greatly increased body demands
- healthy heart exhausted by working too hard
- causes: hyperthyroidism, anemia, AV shunts, thiamine deficiency (beriberi)
- inotropic drug response is poor
high output heart failure
- CO low b/c heart unable to keep up with tissue metabolic demands
- heart unable to pump enough blood to meet tissue needs
- causes: CAD, HTN, MI, arrhythymias, rheumatic heart disease
- inotropic drug response good
low output heart failure
myocardial muscle mass and muscle wall thickness are increased to maintain cardiac performance, but can lead to ischemic changes
myocardial hypertrophy
dilation and other slow structural changes in the heart, can include proliferation of connective tissue, of abnormal myocardial cells. mycocytes die at accelerated rate with remaining cells under even greater stress
remodeling
in CHF _______ is elevated by increase in blood volume and venous tone
preload
venodilators reduce _______ by dilating peripheral veins to retain more blood and keep blood away from the heart
preload
diuretics and salt reduction reduce _______ by decreasing blood volume
preload
in CHF ________ rises because of increases in sympathetic and renin-angiotensin activity which elevate peripheral resistance via arterial constriction
afterload
arteriodilators reduce ________ by decreasing peripheral resistance
afterload
inotropic drugs increase myocardial?
contractility
B-blcokers reduce cardiac work by slowing?
heart rate
reduce preload with which drugs?
diuretics, venodilators
reduce afterload with which drugs?
arteriodilators
reduce energy expenditure and reflex tachycardia with?
B-antagonists
increase contractility with which drugs?
inotropics
step 1 of CHF treatment: use ________ to reduce cardiac workload, if stable, patient with systolic dysfunction add _________
ACE inhibitor
B-blocker
step 2 of CHF treatment: if persistent symptoms add ________ antagonist
aldosterone
step 3 of CHF treatment: if persistent add ________, _______
-for AA patients add _________ instead b/c drugs that inhibit RAAS system are less effective
digoxin, ARB
hydralazine/isosorbide dinitrate
ACEIs, ARBs, beta blockers, aldosterone receptor antagonists, and combined hydralazine-nitrate prolong?
life
infuse IV in acute decompensated CHF as long as cerebral and renal perfusion can be maintained despite reduction in systemic BP
- balanced vasodilator, working on veins and arteries, reduced preload and afterload
- excessive hypotension side effect
sodium nitroprusside
-relax arteriolar smooth muscles, produce vasodilation
calcium channel blockers (amlodipine, felodipine)
- negative inotropic effect (worsen ventricular function, potentially harmful in CHF)
- long term treatment improves symptoms of CHF by slowing HR and contraction velocity to improve CO, exercise tolerance, and ventricular function
B-antagonists
- reduce mortality in HF
- side effects: hyperkalemia, gynecomastia, renal insufficiency
aldosterone antagonists (spironolactone, eplerenone)
- inotropic glycoside, treatment of CHF and atrial fibrillation
- increase cardiac contractility
- quinidine, amiodarone, captropril, verapemil, diltiazem and cyclosporine enhance toxicity
digoxin
- inotropic and smooth muscle relaxing properties
- inactivate cAMP and cGMO
- increase contractility by increasing cAMP and inward calcium flux in the heart
- only for treatment in acute heart failure
PDE inhibitors
