Heart Failure Drugs Flashcards
Quinapril (or ANY -pril)
1) Use
2) Mechanism of Action
3) Benefits
1) First line therapy for Heart Failure w/Reduced LVEF
2) Angiotensin Converting Enzyme Inhibitor (ACEIs)-inhibits the conversion of Angiotensin I to Angiotensin II and inhibits the breakdown of Ang-(1-7) and Bradykinin
3) Improves survival and prevents progression of heart failure
Losartan (or ANY -sartan)
1) Use
2) Mechanism of Action
3) Benefits
1) Reasonable alternative to ACEIs for Heart Failure w/Reduced LVEF
2) Angiotensin Receptor Blocker(ARB)-competitive antagonists of AT1 receptors while activating AT2 Receptors and increased production of Ang-(1-7)
3) Comparable mortality benefits to ACEIs
Loop Diuretics
1) Use
2) Mechanism of Action
1) Management of “congestive” symptoms in Heart Failure
2) Inhibitor of Na+/K+/2Cl- Symporter in the THICK ASCENDING LIMB of the Loop of Henle which inhibits the reabsorption of Na+ and Cl- (interfering w/Na+ retention)
* Should NOT be used alone in Heart Failure patients*
Bisoprolol/Metoprolol
1) Use
2) Mechanism of Action
3) Benefits
4) Contraindications
1) Heart Failure w/Reduced LVEF, Arrhythmias
2) Selective Beta 1 Adrenergic Receptor Blocker-blocks SNS effects and prevents remodeling of the heart
3) Reduces death even when used alone
4) Bradycardia, Reactive Airway Disease
Carvedilol
1) Use
2) Mechanism of Action
3) Benefits
4) Contraindications
1) Heart Failure w/Reduced LVEF, Arrhythmias
2) Non-selective Beta 1, 2 and Alpha 1 Adrenergic Receptor Blocker-blocks SNS effects and prevents remodeling of the heart
3) Reduces death MORE than Bisoprolol/Metoprolol 4)Bradycardia, Reactive Airway Disease
Digoxin
1) Use
2) Mechanism of Action
1)Heart failure w/Atrial Fibrillation, Persistent Heart Failure with other drugs
2)Inhibition of Na+/K+ ATPase causing increased intracellular Ca2+ in cardiac muscle which increases cardiac contraction
Also increases Parasympathetic heart activity and increases renal Na+ excretion
Watch for TOXICITY
Isosorbide dinitrate
1) Use
2) Mechanism of Action
1) Decrease pre-load (Filling Pressure) in Heart Failure
2) Nitrovenodilator- converts to NO which increases cGMP, preventing interaction of myosin and actin causing relaxation of vascular smooth muscle
* Generally used in combo w/hydralazine*
Hydralazine
1) Use
2) Mechanism of Action
1) Decrease after-load (Systemic Vascular Resistance) in Heart Failure
2) Direct Arterial vasodilator- acts through the release of NO (NO required)
* Generally used w/Isosorbide dinitrate*
Nitroglycerin
1) Use
2) Mechanism of Action
1) L)Heart Failure d/t MI, Prompt reduction of ventricular filling pressures
2) Nitrovasodilator- converts to NO which increases cGMP, preventing interaction of myosin and actin causing relaxation of vascular smooth muscle
Dopamine
1) Use
2) Mechanism of Action
3) Adverse Effect
1) Support critically reduced arterial pressures during circulatory failure
* Does NOT help Heart Failure*
2) Beta and Alpha adrenergic agonists causing increased cardiac contractility and vasoconstriction
3) Tachycardia
Dobutamine
1) Use
2) Mechanism of Action
3) Adverse Effects
1) Systolic dysfunction and Congestion associated w/Heart Failure
2) Beta 1 and 2 Adrenergic receptor agonist
3) Tachycardia and arrhythmias
Inamrinone
1) Use
2) Mechanism of Action
1) Short term circulation support in Advanced Heart Failure
2) cAMP Phosphodiesterase Inhibitor-increased cAMP activates Protein Kinase A(PKA) leading to increased Ca2+ stimulating myocardial contraction
Milrinone
1) Use
2) Mechanism of Action
1) Short term circulation support in Advanced Heart Failure
2) cAMP Phosphodiesterase Inhibitor-increased cAMP activates Protein Kinase A(PKA) leading to increased Ca2+ stimulating myocardial contraction
* Less side effects, shorter half-life, and more PDE3 selective
