Medical Management of Heart Failure Flashcards
Discuss the NY Heart Association Functional Classifications of heart failure.
Class I: W/o limitations in physical activity. II: Slight limitations in physical activity, but comfortable at rest. III: Marked limitation of physical activity, but comfortable at rest. IV: Inability to carry on physical activity w/o discomfort, & symptoms may be present at rest.
What are the JACC stages in the development of HF, and how is each managed?
A: At high risk for HF (HTN, CAD, diabetes, obesity, metabolic syndrome, FH, cardiotoxin use, etc.) –> Treat RFs (HTN, HLD, diabetes, encourage exercise, discourage drug use, etc.); Drugs: ACEi or ARB. B: Sturctural heart disease without signs or symptoms of HF (previous MI, LV remodeling incl. LVH/low EF, asymptomatic valvular disease) –> Treat: ACEi or ARB, BB in select patients (in those with compensated heart disease). C: Structural heart disease with prior or current symptoms of HF –> Treat: Salt restriction + Diuretics (for symptoms), ACEi/ARBs, BB; in selected pts: aldosterone antagonist, digitalis, hydralazine/nitrates; consider device: biventricular pacing, implantable defibrillaor. D: Refractory HF (prognosis < 6 months) – Consider end-of-life care or extraordinary measures: heart transplant, chronic inotropes, permanent mechanical support, experiments.
1st line treatment for CHF &/or LV dysfunction? Does tolerance develop? What are the effects on PCWP, LVEDP, SVR, BP, CO, exercise tolerance, HR, contractility, flow, diuresis, reflex tachycardia? What drugs are probably as good as these but are not used as often? What side effects do these drugs? Can the two be used together?
ACE Inhibitors – Increase survival, quality of life & decrease hospitalizations in those with chronic CHF; also inhibit LV remodeling post-MI. Decrease PCWP, LVEDP, SVR, BP, increase CO & exercise tolerance, no change in HR or contractility, inrease flow, increase diuresis, no reflex tachycardia. Probably as effective but not used as often are angiotensin II receptor blockers (ARBs) – dilate arteries and veins, diuresis, inhibit cardiac remodeling AND do not cause a cough (though may cause angioedema along with hyperkalemia and decreaed GFR). Can be used in tandem, but must monitor kidneys.
Are diuretics used to treat CHF? Why? Do they effect CO? What are the effects of neurohormonal activation? What are contraindications and side effects? Which diuretic has been shown to significantly reduce mortality in class III/IV CHF? Why is compliance poor with this drug? What similar drug circumvents this compliance?
Yes – For symptomatic improvement of congestion. Despite decreases in volume and prealod, CO is not directly affected (though still may decrease with large preload reduction). Neurohormonal activation: increases NE & AngII. Contraindications: Hypovolemia. Side effects: Volume contraction + Electrolyte disturbances – This is dangerous because of the risk of arrythmias. Spironolactone (aldosterone antagonist) significantly reduces risk of death (30%). Compliance is poor in men because of gynecomastia, althoug the new drug Eplerenone does not cause this.
Why are beta-blockers used in CHF? What are they considered in terms of treating CHF? Which are the only 3 that have support to be used in CHF? What is the recommendation for these drugs? What is an important “no-no” about use of these drugs?
BB are used despite negative chronotropic and inotropic effects because blocking sympathetics will help the heart in the long-run. Considered 2nd line in treatment of CHF only behind ACEi/ARBs. ONLY: Bisoprolol, Metoprolol, Carvedilol. Must be initiated at a low dose (because initially, CO will decrease, and it must be known whether the patient can withstand this) and then gradually increased. CANNOT be withdrawn rapidly.
Digoxin/Digitalis class & MOA? Hemodynamic effects? Neurohormonal effects? What limits the use of this drug? How is it eliminated?
Cardiac glycoside; Inhibits Na/K/ATPase (increases
contractility by increasing intracellular Na, leading to increased Na/Ca countertransport, bringing more Ca inside the cell); increases vagal activity to heart (reduces SA firing [HR], conduction through AV node). Hemodynamic effects: Improves LV function (increase CO, increase EF, decrease EDP, increase exercise tolerance, natriuresis). Decreases neurohormonal activation (NE, PNS, RAAS, increases vagal tone, normalizes arterial baroreceptors). Use is limited by a VERY narrow therapeutic-toxic window (mostly arrhythmias). Eliminated in kidneys, so dose according to renal func.
Dobutamine MOA? Use? What is the timing? Will this cause an increase in NE release? How is this given?
β1 receptor agonist – positive inotrope and chronotrope. Use is in acutely decompensated patients, nut about half will die after 6 months! Quick acting )1-2 min onset, 2 min half-life), but can develop tachyphylaxis after 48 hours — No NE release. Given IV.
Milrinone MOA? Use? Will tolerance develop? Is this similar to dobutamine in the sense of increased mortality in the long-run? How is this given? How is it cleared?
Phosphodiesterase IIIa inhibitor – Inhibits cAMP breakdown – Facilitating inotropy, chronotropy, lusitropy (relaxation), vasodilation. Use is limited to short-term infusions (48-72 hrs). Increased hypotensive and atrial arrhythmia events acutely. No tolerance. 2 month mortality nearly 50% higher than placebo. Given IV. Depends on renal clearance.
What drug is a synthetic BNP? Is this drug effective?
Nesiritide. Not effective.
To summarize it all, say whether the drug improves symptoms, decreases mortality, prevents CHF, and affects neurohormonal control: Diuretics, Digoxin, Inotropes, Nitrates, ACEi/ARBs, BB, Aldosterone antagonist.
Diuretics: Y, ?, ?, No. Digoxin: Y, =, minimal, Y. Inotropes: Y, No, ?, No. Nitrates: Y, Y (if due to ischemia), ?, No. ACEi/ARBs: Y, YES!, Y, Y. BB: Y, Y, Y, Y. Aldosterone antagonist (in those with III/IV): Y, Y, ?, Y.
What drugs are 1st line for diastolic heart failure? Why?
Nitrates and Diuretics – Reduce filling pressure without compromising CO.
What are the three most important determinants of myocardial oxygen use? What does internal element work equal? Does this play a role in oxygen consumption as well?
Systolic wall tension, heart rate, contractility. Internal element’s work = heart rate times systolic wall
tension (Wie = HR x T), Wie is a major determinant of myocardial oxygen consumption as well.
The chief mechanism by which alterations in oxygen consumption in the heart are achieved is _____.
Changes in coronary blood flow.
