Heart Failure Drugs Flashcards
What is the primary treatment goal of heart failure?
Alleviation of symptoms, so basic stuff like vasodilators, positive inotropes, etc
What is the secondary treatment goal of heart failure?
Prevent progression of cardiac remodeling
Explain what Class I to Class IV of the heart failure classification. Basically, which is worst/best?
Class I is the best
Class IV is basically dying in the hospital
What is the most common reason for development of HF?
Coronary artherosclerosis and MI’s
Why do diuretics help in HF?
Reduction of preload
What’s the only diuretic that’s actually shown to improve morbidity and mortality?
Spironolactone
What is the MOA of aldosterone antagonists?
Binds to MR receptors, blocking aldosterone from binding there. So reduction in aldosterones functions (Na/K exchange)
What are the two aldosterone antagonists to know?
Spironolactone and eplernone
What are the ADEs for aldosterone antagonists?
Hyperkalemia (MOST DANGEROUS SIDE EFFECT)
Endocrine Effects-more spironolactone than eplerenone
GI problems
CNS-HA, lethargy
What is the important difference between spironolactone and eplernone?
Spironolactone is more likely to act as an androgen receptor antagonist, causing more endocrine issues
Can you use CCB or BBs in HF? why?
No nondihydropyradines, cause they reduce contractility
BBs yes cuz they reduce renin secretion
What are the four positive inotropic classes?
Cardiac glycosides
Beta adrenergic and dopaminergic agents
Phosphodiasterase inhibitors
Calcium sensitizing agents
What is the cardiac glycoside to know?
Digoxin
What is cardiac glycosides MOA?
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
So to sum it up some, what does cardiac glycosides do
Increases contractility, but also increases parasympathetic outflow, decreases sympathetic outflow
Digoxin is a p glycoprotein substrate but not a ____
CYP substrate
What is digoxins ADEs?
Cardiac effects- Arrhythmias
Toxicity- CNS stuff like delerium, also GI and Visual problems
What is the treatment for digoxin toxicity?
Digibind
What is digoxin mainly used for?
HF with A fib (see anti arrythmics) IDK
What is dobutamines MOA?
B1 and B2 agonists
What are dobutamines ADEs?
Basically stuff you would expect. B1 excess problems like arrhythmias
What class is milrinone?
Phosphodiasterase 3 inhibitor
What is milrinones MOA?
Blocks PDE3, leading to increased concentrations of cAMP, leading to increased myocardial contractility and vasodilation in the venous and arterial system
What drug class is levosimendan?
Calcium sensitizing agent
What is levosimendans MOA?
Increased interactions between calcium and the contractile proteins, leading to positive inotropic effects
Is levosimendan available in the US?
NNOOO
What can levosimendan cause?
Arrhythmias
What is the HCN channel blocker?
Ivabradine
What does HCN channels do?
Activated by hyperpolarization and cyclic nucleotides. contributes to diastolic depolarization
What is Ivabradines MOA?
Blocks HCN channel, reduces pacemaker activity in SA node. So blocking HR is main effect
How is ivabradine beneficial in HF?
By reducing HR, it creates a more favorable balance between myocardial oxygen demand and it improves diastolic myocardial perfusion
How is ivabradine metabolized?
CYP3A4
What is ivabradines ADEs?
Arrhythmias, Phosphenes (floaty sparkles), teratogenix
What is the MOA of isosorbide dinitrate\hydralazine?
Decreases ventricular filling by increasing venous capacitance
What is Nesirtides MOA?
Activates BNP receptors which are the guanylyl cyclase type receptors. This leads to increased cGMP, leading to more relaxation. Same concept as sodium nitropresside
What does nesirtide do the cardiac system overall?
Decreases preload and afterload
What is the Neprilysin inhibitor?
Sacubitril
What is important to understand about sacubitrils delivery considerations?
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
