Heart Failure Flashcards
Describe the 4 NYHA classifications of heart failure
Class I: cardiac disease but NO limitations of physical activity
Class II: slight limitation in activity, comfortable at rest
Class III: marked limitation, comfortable at rest
Class IV: symptoms at rest
What drug is mainstay therapy for Class I HF and above?
ACEI
What effect do ACEIs have on HR/contractility?
(trick question)- NONE
What are 4 advantages of ACEIs given after an MI?
- inhibit LV remodeling/hypertrophy
- modify progression of chronic CHF
- tolerance does not develop
- no neurohormonal activation or reflex tachycardia
What are the 2 generic ARBs? What ARB is used in combination with hydrochlorothiazide?
- Losartan and Irbesartan
- Valsartan is combined with hydrocholorothiazide
What are 3 side effects of ARBs?
decrease GFR
increase K+
hypotension
How does the use of diuretics improve symptoms of congestion in HF?
decreased volume and preload
What effect do diuretics have on cardiac output?
(trick)- NONE
[unless excessive preload reduction]
What 2 neurohormones become increased with use of diuretics?
Noradrenaline and Angiotensin II
What is an important side effect of chronic diuresis?
hyponatremia
What drug has been proven effective in low dose combined with ACEIs to reduce death and hospitalization in patients with Class III or IV HF?
Spironolactone
What are the only 3 Beta-blockers that may be used in the setting of HF?
Bisoprolol
Metoprolol (sustained release)
Carvedilol
What is the mechanism of action of bisoprolol and others in its class to treat HF?
(beta-blockers)
Blocks high circulating levels of catecholamines to inhibit adverse effects of sympathetic nervous system
What are 2 important points in starting treatment of metoprolol or others in its class?
(beta-blocker)
- Patient must be stable
- Should be started at very low dose and slowly titrated up; do not stop suddenly
What class is digoxin and how does it work?
- Cardiac Glysoside
- potent inhibitor of Na+/K+ pump –> intracellular Na+ build-up –> ineffective Na+/Ca++ exchanger –> Ca++ remains in cell –> increased contractility
- also increases vagal activity to heart
What are 6 hemodynamic effects of Digoxin?
- increase cardiac output
- increase LVEF
- increase exercise tolerance
- increase natriuresis
- decrease LVEDP
- decrease neurohormonal activation (noradrenaline, RAAS)
Where in the body is digoxin eliminated?
kidney
renal function needs to be taken into account when dosing
Digoxin is hard to manage due to its narrow therapeutic-toxic window- what does digoxin toxicity cause?
cardiac arrhythmias-
most commonly atrial tachycardia and AV block
What did a digoxin trial find about its effects on heart failure management?
no effect on mortality but increases quality of life and reduces hospitalizations
In what patients might digoxin be indicated? and in what dosage?
LOW dose
Stage III, stabilized with adequate renal function
What is the mechanism of action of Dobutamine?
β1 receptor agonist –> Positive inotrope (contractility) and chronotrope (heart rate)
- at low doses stimulates Beta-2 - peripheral vasodialtion
- at higher doses stimulates alpha - vasoconstriction
In what patients might Dobutamine be indicated?
Acutely decompensated patients (about half will die after 6 months)
What are the side effects of Dobutamine?
Quick acting, but can develop tachyphylaxis (tolerance) after 48 hours
What is Milrinone and what is its mechanism of action?
Phosphodiesterase IIIa inhibitor
(PDE IIIa breaks down cAMP)
-increased cAMP –> increased: Inotropy (contractility), chronotropy (heart rate), lusitropy (relaxation), vasodilation
What are the side effects of Milrinone?
Increased hypotensive and atrial arrhythmia events acutely. 2 month mortality nearly 50% higher than placebo
Which 3 drugs may be given IV in acute HF only as a last resort?
Dobutamine
Milrinone
Nesiritide
What is Nesiritide? Therapeutic use?
synthetic B-natriuretic peptide
-no difference in mortality or significant improvement of symptoms (last resort drug)
