Heart Failure

Question 1

Describe the 4 NYHA classifications of heart failure

Answer 1

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

Question 2

What drug is mainstay therapy for Class I HF and above?

Answer 2

ACEI

Question 3

What effect do ACEIs have on HR/contractility?

Answer 3

(trick question)- NONE

Question 4

What are 4 advantages of ACEIs given after an MI?

Answer 4

1. inhibit LV remodeling/hypertrophy
2. modify progression of chronic CHF
3. tolerance does not develop
4. no neurohormonal activation or reflex tachycardia

Question 5

What are the 2 generic ARBs? What ARB is used in combination with hydrochlorothiazide?

Answer 5

• Losartan and Irbesartan

- Valsartan is combined with hydrocholorothiazide

Question 6

What are 3 side effects of ARBs?

Answer 6

decrease GFR
increase K+
hypotension

Question 7

How does the use of diuretics improve symptoms of congestion in HF?

Answer 7

decreased volume and preload

Question 8

What effect do diuretics have on cardiac output?

Answer 8

(trick)- NONE

[unless excessive preload reduction]

Question 9

What 2 neurohormones become increased with use of diuretics?

Answer 9

Noradrenaline and Angiotensin II

Question 10

What is an important side effect of chronic diuresis?

Answer 10

hyponatremia

Question 11

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?

Answer 11

Spironolactone

Question 12

What are the only 3 Beta-blockers that may be used in the setting of HF?

Answer 12

Bisoprolol
Metoprolol (sustained release)
Carvedilol

Question 13

What is the mechanism of action of bisoprolol and others in its class to treat HF?

Answer 13

(beta-blockers)

Blocks high circulating levels of catecholamines to inhibit adverse effects of sympathetic nervous system

Question 14

What are 2 important points in starting treatment of metoprolol or others in its class?

Answer 14

(beta-blocker)

1. Patient must be stable
2. Should be started at very low dose and slowly titrated up; do not stop suddenly

Question 15

What class is digoxin and how does it work?

Answer 15

• 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

Question 16

What are 6 hemodynamic effects of Digoxin?

Answer 16

1. increase cardiac output
2. increase LVEF
3. increase exercise tolerance
4. increase natriuresis
5. decrease LVEDP
6. decrease neurohormonal activation (noradrenaline, RAAS)

Question 17

Where in the body is digoxin eliminated?

Answer 17

kidney

renal function needs to be taken into account when dosing

Question 18

Digoxin is hard to manage due to its narrow therapeutic-toxic window- what does digoxin toxicity cause?

Answer 18

cardiac arrhythmias-

most commonly atrial tachycardia and AV block

Question 19

What did a digoxin trial find about its effects on heart failure management?

Answer 19

no effect on mortality but increases quality of life and reduces hospitalizations

Question 20

In what patients might digoxin be indicated? and in what dosage?

Answer 20

LOW dose

Stage III, stabilized with adequate renal function

Question 21

What is the mechanism of action of Dobutamine?

Answer 21

β1 receptor agonist –> Positive inotrope (contractility) and chronotrope (heart rate)

• at low doses stimulates Beta-2 - peripheral vasodialtion
• at higher doses stimulates alpha - vasoconstriction

Question 22

In what patients might Dobutamine be indicated?

Answer 22

Acutely decompensated patients (about half will die after 6 months)

Question 23

What are the side effects of Dobutamine?

Answer 23

Quick acting, but can develop tachyphylaxis (tolerance) after 48 hours

Question 24

What is Milrinone and what is its mechanism of action?

Answer 24

Phosphodiesterase IIIa inhibitor
(PDE IIIa breaks down cAMP)
-increased cAMP –> increased: Inotropy (contractility), chronotropy (heart rate), lusitropy (relaxation), vasodilation

Question 25

What are the side effects of Milrinone?

Answer 25

Increased hypotensive and atrial arrhythmia events acutely. 2 month mortality nearly 50% higher than placebo

Question 26

Which 3 drugs may be given IV in acute HF only as a last resort?

Answer 26

Dobutamine
Milrinone
Nesiritide

Question 27

What is Nesiritide? Therapeutic use?

Answer 27

synthetic B-natriuretic peptide

-no difference in mortality or significant improvement of symptoms (last resort drug)