Exam 2 - Heart Failure

Question 1

What drug classes are used to reduce preload?

Answer 1

Diuretics or venodilators

Question 2

What drug classes are used to reduce afterload?

Answer 2

Arteriodilator

Question 3

What drug classes are used to increase contractility?

Answer 3

Inotropic drug

Question 4

What drug classes are used to reduce energy expenditure?

Answer 4

B-adrendergic antagonist

Question 5

What is the MOA of diuretics in regards to HF?

Answer 5

• Reduce salt and H2O retention

- Reduce venous pressure leading to reduced edema and cardiac size

Question 6

What diuretics are used in HF and can reduce mortality rate?

Answer 6

Spironolactone and eplerenone (aldosterone antagonists)

Question 7

What is the MOA for an ACE inhibitor?

Answer 7

Inhibits ACE, preventing the conversion of Angiotensin I to Angiotensin II

Question 8

What is the MOA for an ARB?

Answer 8

Block Angiotensin II from binding to AT1 receptor

Question 9

What is the current DOC of HF treatment today?

Answer 9

ACE inhibitors

Question 10

What is the primary therapeutic effect of ACE inhibitors and ARBs in HF?

Answer 10

Diminish cardiac workload by:

• Decreasing afterload: Decrease in angiotensin II-induced vasoconstriction
• Decreasing preload: Decreased aldosterone release

Question 11

What are adverse effects associated with ACE inhibitors and ARBs?

Answer 11

Dry cough with ACE, but not with ARB

Question 12

What is the MOA for Sacubitril/Valsartan (Entresto)?

Answer 12

2 drugs: (ARNI: ARB + Neprilysin Inhibitor)

• ARB will block Angiotensin II from binding to AT1 receptor
• Neprilysin inhibitor will reduce the degradation of natriuretic peptides, bradykinin and others

Question 13

What is the key to decreasing mortality associated with using an ARNI (Sacubitril/Valsartan)?

Answer 13

The neprilysin inhibitor portion will reduce cardiac remodeling as it prevents the degradation of natriuretic peptides, bradykinin and others

Question 14

What are some adverse effects of Sacubitril/Valsartan (Entresto)?

Answer 14

• Hypotension
• Hyperkalemia (ARB portion is inhibiting aldosterone which will cause an increased K+ concentration) (will occur especially if using a K+ sparing diuretic)
• Cough and angioedema (due to increased bradykinin)

Question 15

What are contraindications/precautions for Sacubitril/Valsartan (Entresto)?

Answer 15

• Pregnancy

- Concurrent use with ACE inhibitor due to risk of angioedema

Question 16

Carvedilol and Metoprolol belong to which class of HF medications?

Answer 16

B-blockers - “alol”

Question 17

What are the therapeutic effects of B-blockers?

Answer 17

• Decrease mortality
• Decrease renin secretion
• Decrease effects of high concentration of catecholamines
• Decrease HR
• Decrease remodeling

Question 18

When are B-blockers effective in HF?

Answer 18

Only effective in early stages of HF and can be dangerous in severe or end-stage due to its negative inotropic effect

Question 19

Sodium nitroprusside (Nitropress), Isosorbide dinitrate, and Hydralazine belong to what class of HF drugs?

Answer 19

Vasodilators

Question 20

How are sodium nitroprusside (Nitropress), Isosorbide dinitrate, and Hydralazine effective in HF?

Answer 20

• Reduce preload
• Reduce afterload
• Reduce damaging remodeling of the heart

Question 21

What is the MOA of Dobutamine and what is it used for?

Answer 21

• Selective B1-agonist

- Short-term treatment of severe refractory HF

Question 22

What is the MOA of Dopamine and what is it used for?

Answer 22

• Low dose –> D1 in kidney –> vasodilation
• Mod. dose –> B1 in heart –> inotropic effect
• High dose –> a in vessels –> vasoconstriction/increase BP

Short-term treatment of severe refractory HF, especially if increase in BP is needed

Question 23

What is the MOA for Digoxin (Lanoxin)?

Answer 23

Inhibition of membrane sodium pump Na+, K+-ATPase (digitalis receptor), ultimately leading to an increase in intracellular calcium and increased contractility. Digitalis will also directly increase vagal stimulation (baroreflex-like effect) and decrease sympathetic tone, leading to a slowed HR.

Question 24

What are indications/therapeutic effects of Digoxin?

Answer 24

• HF (CO is increased; last agent used)
• Improves exercise intolerance in HF
• Anti-arrhythmic in non-HF

Question 25

What are some adverse effects of Digoxin?

Answer 25

• GI disturbances are earliest signs of toxicity
• Narrow margin of safety
• CNS
• Arrhythmias (ventricular fibrillation is most common cause of death)

Question 26

What is the differing affect of Digoxin in a failing heart versus a non-failing heart?

Answer 26

CO is increased in the failing but not in the normal heart due to increased peripheral vasoconstriction in normal individuals. As HR decreases, SV increases.

Question 27

What is the most common cause of death in patients taking Digoxin?

Answer 27

Ventricular fibrillation

Question 28

What should be done regularly in a patient taking Digoxin?

Answer 28

• EKGs

- Measure K+ and digitalis

Question 29

How do you treat the following Digoxin intoxications:

1) Minor (GI)
2) Moderate (arrhythmias)
3) Severe (overdose/life-threatening arrhythmias)

Answer 29

1) discontinue or reduce dose digitlis
2) Oral or IV potassium and discontinue/reduce digitalis
3) Immunotherapy with Digitalis Immune Fab, oral or IV potassium, and discontinue/reduce digitalis

Question 30

Should you perform a cardioversion in a patient suffering from digitalis-induced arrhythimas?

Answer 30

No cardioversion except for ventricular fibrillation

Question 31

What are some pharmacodynamic interactions associated with Digoxin?

Answer 31

• Interaction with thiazide or loop diuretics can lead to hypokalemia
• B-blockers can further decrease activity of SA node activity
• CCBs will decrease contractility and are contraindicated in HF (decreases Digoxin effectiveness)