Heart Failure Drugs

Question 1

What is the primary treatment goal of heart failure?

Answer 1

Alleviation of symptoms, so basic stuff like vasodilators, positive inotropes, etc

Question 2

What is the secondary treatment goal of heart failure?

Answer 2

Prevent progression of cardiac remodeling

Question 3

Explain what Class I to Class IV of the heart failure classification. Basically, which is worst/best?

Answer 3

Class I is the best

Class IV is basically dying in the hospital

Question 4

What is the most common reason for development of HF?

Answer 4

Coronary artherosclerosis and MI’s

Question 5

Why do diuretics help in HF?

Answer 5

Reduction of preload

Question 6

What’s the only diuretic that’s actually shown to improve morbidity and mortality?

Answer 6

Spironolactone

Question 7

What is the MOA of aldosterone antagonists?

Answer 7

Binds to MR receptors, blocking aldosterone from binding there. So reduction in aldosterones functions (Na/K exchange)

Question 8

What are the two aldosterone antagonists to know?

Answer 8

Spironolactone and eplernone

Question 9

What are the ADEs for aldosterone antagonists?

Answer 9

Hyperkalemia (MOST DANGEROUS SIDE EFFECT)
Endocrine Effects-more spironolactone than eplerenone
GI problems
CNS-HA, lethargy

Question 10

What is the important difference between spironolactone and eplernone?

Answer 10

Spironolactone is more likely to act as an androgen receptor antagonist, causing more endocrine issues

Question 11

Can you use CCB or BBs in HF? why?

Answer 11

No nondihydropyradines, cause they reduce contractility

BBs yes cuz they reduce renin secretion

Question 12

What are the four positive inotropic classes?

Answer 12

Cardiac glycosides
Beta adrenergic and dopaminergic agents
Phosphodiasterase inhibitors
Calcium sensitizing agents

Question 13

What is the cardiac glycoside to know?

Answer 13

Digoxin

Question 14

What is cardiac glycosides MOA?

Answer 14

It binds to and inhibits Na/K ATPase, keeping intracellular Na elevated. This activates the Na/Ca pump, pumping Na out in exchange for Ca. More Ca means more contraction
Also, effects baroreceptors responsiveness to change in bp

Question 15

So to sum it up some, what does cardiac glycosides do

Answer 15

Increases contractility, but also increases parasympathetic outflow, decreases sympathetic outflow

Question 16

Digoxin is a p glycoprotein substrate but not a ____

Answer 16

CYP substrate

Question 17

What is digoxins ADEs?

Answer 17

Cardiac effects- Arrhythmias

Toxicity- CNS stuff like delerium, also GI and Visual problems

Question 18

What is the treatment for digoxin toxicity?

Answer 18

Digibind

Question 19

What is digoxin mainly used for?

Answer 19

HF with A fib (see anti arrythmics) IDK

Question 20

What is dobutamines MOA?

Answer 20

B1 and B2 agonists

Question 21

What are dobutamines ADEs?

Answer 21

Basically stuff you would expect. B1 excess problems like arrhythmias

Question 22

What class is milrinone?

Answer 22

Phosphodiasterase 3 inhibitor

Question 23

What is milrinones MOA?

Answer 23

Blocks PDE3, leading to increased concentrations of cAMP, leading to increased myocardial contractility and vasodilation in the venous and arterial system

Question 24

What drug class is levosimendan?

Answer 24

Calcium sensitizing agent

Question 25

What is levosimendans MOA?

Answer 25

Increased interactions between calcium and the contractile proteins, leading to positive inotropic effects

Question 26

Is levosimendan available in the US?

Answer 26

NNOOO

Question 27

What can levosimendan cause?

Answer 27

Arrhythmias

Question 28

What is the HCN channel blocker?

Answer 28

Ivabradine

Question 29

What does HCN channels do?

Answer 29

Activated by hyperpolarization and cyclic nucleotides. contributes to diastolic depolarization

Question 30

What is Ivabradines MOA?

Answer 30

Blocks HCN channel, reduces pacemaker activity in SA node. So blocking HR is main effect

Question 31

How is ivabradine beneficial in HF?

Answer 31

By reducing HR, it creates a more favorable balance between myocardial oxygen demand and it improves diastolic myocardial perfusion

Question 32

How is ivabradine metabolized?

Answer 32

CYP3A4

Question 33

What is ivabradines ADEs?

Answer 33

Arrhythmias, Phosphenes (floaty sparkles), teratogenix

Question 34

What is the MOA of isosorbide dinitrate\hydralazine?

Answer 34

Decreases ventricular filling by increasing venous capacitance

Question 35

What is Nesirtides MOA?

Answer 35

Activates BNP receptors which are the guanylyl cyclase type receptors. This leads to increased cGMP, leading to more relaxation. Same concept as sodium nitropresside

Question 36

What does nesirtide do the cardiac system overall?

Answer 36

Decreases preload and afterload

Question 37

What is the Neprilysin inhibitor?

Answer 37

Sacubitril

Question 38

What is important to understand about sacubitrils delivery considerations?

Answer 38

HAS TO BE given with an arb at the minimum. Sacubitril inhibits neprilysin, which is an enzyme that degrades BNP (BNP is a vasodilator and diuretic). But neprilysin also breaks down ANG II. So if you inhibit neprilysin, you have a lot of ANG II floating around