Treatment Of Congestive Heart Failure

Question 1

Which classes of drugs are proven to improve survival and reduce hospitalization in chronic CHF? Which are used only for symptomatic relief?

Answer 1

Improved survival (ACE inhibitors, ARBs, Aldosterone antagonists, Certain B-Blockers, Nitrates and Hydralazine).
Symptomatic relief (Diuretics, Digoxin and Vasodilators).

Question 2

What drugs can we give to counteract the activation of the RAAS?

Answer 2

1) ACE inhibitors and ARBs (Block the action of angiotensin).
2) Aldosterone antagonists (Block the effects of increased aldosterone secretion).

Question 3

What drugs can we give to counteract the sodium and water retention?

Answer 3

1) Loop diuretics.

2) Thiazides diuretic.

Question 4

What drugs can we give to counteract the increased sympathetic activity?

Answer 4

Certain B-Blockers: Metoprolol, Carvedilol and Bisoprolol.
Vasodilators.
*Never want to started B-Blockers in someone with a Decompensated CHF.

Question 5

In a CHF, What drug improve survival and reduce mortality?

Answer 5

B-Blockers.

Question 6

How can you increase contractility (cardiac output)?

Answer 6

Digoxin (positive inotrope, increase contractility and CO but there is not survival benefit.

Question 7

What is the mechanism of the Digoxin?

Answer 7

Direct inhibition of Na/K ATPase -> indirect inhibition of Na/Ca exchanger -> Increase intracellular calcium -> positive inotropy. Stimulates vagus nerve that decrease heart rate.

Question 8

What are the clinical use for digoxin?

Answer 8

Chronic heart failure (increase contractility).
Atrial fibrillation (Decrease conduction at AV node and depression of SA node).

Question 9

What are the symptoms of digoxin toxicity?

Answer 9

1) Cholinergic effects (Nauseas, vomiting, diarrhea).
2) Blurry yellow vision.
3) EKG abnormalities (Bradycardia).

Question 10

What patients are more predispose to digoxin’s toxicity?

Answer 10

Renal failure (decrease excretion).
Hypokalemia (permissive for digoxin binding at K-binding site on Na/K ATPase).
Quinidine (decrease digoxin clearance; displaces digoxin from tissue-binding sis).

Question 11

What is the treatment of Digoxin toxicity?

Answer 11

Correct any hypokalemia.
Magnesium.
Anti-digoxin antibody fragments.
Atropine for the bradycardia.
Temporary pacemaker.

Question 12

a 76-year-old Caucasian man who is competitive bodybuilder comes to the physician complaining that he has started “getting anaerobic” very quickly when exercising. Upon further questioning, you determine that he is experiencing shortness of breath after only 2-3 minutes of exercise. Physical examination shows mild pedal edema. His lungs are clear. An echocardiogram shows an estimated left ventricular ejection fraction of 25% without valvular dysfunction. What are the mechanisms of action of the drug classes proven reduce mortality in this patient?

Answer 12

ACE inhibitors, ARBs, Aldosterone antagonists and B-Blockers.

Question 13

What are the drugs used in a chronic CHF patient?

Answer 13

ACE inhibitors, ARBs, Aldosterone antagonists, B-Blockers, Diuretics, Vasodilators and Digoxin.

Question 14

What is the treatment of Acute CHF with pulmonary edema?

Answer 14

Nitrates.
Oxygen.
Loop diuretics.
Inotropic drugs.
Positioning.

Question 15

What medication are used to treat chronic heart failure?

Answer 15

2) Survival
ACE inhibitors.
ARBs.
Aldosterone Antagonists.
B-Blockers.
1) Symptomatic improvement:
Digoxin.
Diuretics. 
Vasodilators.

Question 16

What medication are used to treat acute heart failure?

Answer 16

Nitrates, oxygen, loop diuretics, inotropes and positioning.

Question 17

What are the mechanism of action of the cardiac glycoside (e.g., digoxin)?

Answer 17

Inhibit the Na-K ATPase which increased intracellular calcium.

Question 18

Which adverse effects are associated with digitalis toxicity?

Answer 18

Cardiac arrhythmia, vomiting, visual disturbances and confusion.

Question 19

Name the only oral inotropic agent:

Answer 19

Digoxin

Question 20

Describe the three-step mechanism by wich digitalis Potentiates myocardial contractility:

Answer 20

1) Inhibition of Na/K ATPase.
2) Buildup of intracellular Na.
3) High intracellular Na impairs Na-Ca antiport, causing increased intracellular Ca.

Question 21

What is the unique side effect of digoxin on the heart?

Answer 21

Dysrrhytmia.

Question 22

Which agent can be used to counteract the cardiac toxicity of digoxin? By what mechanism?

Answer 22

K supplementation. Digoxin binds near K site on Na/K ATPase. When K is low, digoxin has better access and vice versa.

Question 23

What are the unique neurotoxicities of digoxin?

Answer 23

Headache, Nauseas, altered color perception, blurred vision, tinnitus.

Question 24

For which Arrhytmia is digoxin commonly used?

Answer 24

Atrial Fibrillation.

Question 25

What is the B-agonist of choice for inotropic support in heart failure?

Answer 25

Dobutamine.

Question 26

Which antiarrhythmic is useful for abolishing Torsades de pointes and digoxin toxicity?

Answer 26

Magnesium.

Question 27

By which mechanism do B-antagonists and phosphodiesterase inhibitors potentiate myocardial contractility?

Answer 27

These agents increase cAMP which promotes increased intracellular calcium.

Question 28

what Antihypertensive agents are used to treat CHF?

Answer 28

Diuretics, ACEi, B-Blockers.

Question 29

What Antihypertensive agent should be avoided in CHF?

Answer 29

Verapamil.