Pharmexam2pt2.txt

• Decrease signs and symptoms of congestion.
• Maintain normal lifestyle.
• Prolong life.

• Systolic dysfunction (most commom); results in reduced contractility
• Diastolic dysfunction; results in reduced ventricular filling

• reduced contractility
• decreased ejection fraction
• increased left vent end diastolic volume
• ventricular hypertrophy r/t pressure or volume overload

• reduced vent filling
• normal ejection fraction
• decreased left vent end diastolic volume

• heart failure leads to decreased cardiac output
• decreased CO leads to release of renin, angiotensin II, and aldosterone and stimulation of symp NS
• release of aldosterone increases reabsoption of water and sodium
• increased reabsoprtion increases plasma volume, preload, and edema
• stim of symp NS increases HR, contractility and vasoconstriction resulting in increased afterload and decreased CO

• compensatory mechanism activating the renin/angiotensin/aldosterone system, increasing stroke volume
• may result in volume overload, increased myocardial oxygen demand

• Frank-Starling mechanism
• increased heart rate: r/t SNS activation; increases oxygen demand, ischemia, arrhythmias, and decreases filling time
• vasoconstriction: decreases stroke volume
• ventricular hypertrophy and remodeling: increases myocardial cell death, ischemia, arrhythmias

reducing preload decreases the amount of blood returning to heart, therefore helping to alleviate symptoms of pumonary congestion

reducing afterload reduces the force that the heart must contract against, therefore allowing an increase in CO

diuretics, NSAIDS, nitrates, ACEI, nitroprusside, nesiritide

nitrates, ACEI, nitroprusside, nesiritide, hydralazine

beta blockers (metoprolol, carvedilol, bosoprolol), ACEI, ARBs, aldosterone antagonists (spironolactone)

• Left-sided heart failure
• Right-sided heart failure
• Excessive fluid loss
• Drug toxicities

Do nothing, this is normal.

Give fluids, patient is experiencing hypoperfusion.

Administer loop diuretics and vasodilators, pt is experiencing pumonary congestion.

Administer diuretics, vasodilators, pt is experiencing pulmonary congestion and hypoperfusion.

decrease preload, do no effect CO (decreases symptoms)

nitroglycerin, nitroprusside, nesiritide

• a vasodilator
• induces smooth muscle relaxation in veins and arteries (mainly venodilator)
• AE: HA, hypotension, tachycardia
• tolerance can develope w/i 12hrs (tachyphylaxis)

• vasodilaor
• potent, dilates veins and arteries
• decreases preload and afterload
• can become toxic quickly, usually short term med

• a vasodilator
• antagonizes renin/agiotensin/aldosterone system and SNS
• toxicity: excessive hypotension

milrinone, dobutamine, dopamine

• positive inotropic effect and vasodilation
• decreases preload and afterload
• used short term (long term increases mortality rate)

• inotropic effects
• beta 1 agonist leading to increased HR and contractility
• beta 2 agonist results in vasodilation

• inotropic effects
• increases MAP by stimulating alpha 1 receptors

• goal: relax heart so that it fills better, increase diastole
• low sodium diet (2g/day)
• diuretics
• ACEI
• beta blockers or nondihydropyridine CCBs (not nifedipine)

• lifestyle modifications
• diuretic plus ACEI and beta blocker
• hydralazine plus nitrates and/or digoxin in AA

• control symptoms of pumonary congestion and fluid overload
• do not increase survival (exceptions: spironolactone and inspra)

• mild to severe HF
• reduce mortality rate, esp in pts with CHF
• ACEI cough generall improves after several weeks
• correct dose is important

• often used for AA or pts who cannot tolerate ACEI or ARBs
• when used with diuretics and digoxin, reduces mortality (not as much asn ACEI)

• used in all stable HF pts
• protects heart from chronic toxicity of high norepinephrine levels (ischemia, remodeling)
• used in combo with ACEI
• contraindicated in symptomatic bradycardia, hypotension, 2/3 degree heart block

• ex: spironolactone
• major risk is hyperkalemia
• monitor serum creatinin and potassium before and after therapy initiation

• cardiac glycoside
• positive inotropic effect (direct) - inhibits Na-K pump increasing intracellular Na and Ca resulting in increased force of contraction
• vagotonic effect (take apical pulse and EKG before admin)
• high renal elimination
• dose based on IBW
• toxicities: bradycardia, arrhythmias, AV block, fatigue, vision probs, weakness, anorexia, nausea, hallucinations/confusion/insomnia
• not been shown to increase survival
• reduces risk of hospitalization when used with diuretic and ACEI

• increase effect w/o increasing levels: hypokalemia, hypomagnesemia (prob w/alcoholics), vagal stim, hyperstimulation
• increase levels: renal failure, amiodarone, verapamil, basing dose on actual wt instead of IBW, erythromycin (in some pts)
• decrease levels: antacids (binds w/dig in stomach) and rifampin (stims metabolism)

• NSAIDS (increases Na and H2O retention)
• drugs that cause adrenergic stimulation (decongestants, some beta blockers)
• TZDs (used to treat DM, can cause fluid retention)
• antiarrhythmics with negative inotropic activity (quinidine, procainamid) - good for diastolic HF, bad for systolic HF
• antiarrhythmics that prolong QTc interval (increases r/o arrhythmias)
• CCBs (may increase r/o death in systolic HF; nondihydropyridines like verapamil and diltiazam may be helpful in treating diastolic HF however)