Drugs used in heart failure

Question 1

Inotropic agents

Answer 1

1. Cardiac glycosides
2. Bipyridines
3. Beta-adrengergic receptor agonists

Question 2

Cardiac glycosides

Answer 2

Digoxin

Question 3

Bipyridines

Answer 3

Inamirone
Milrinone

Approved for the short-term support of the circulation in acute decompensated heart failure

Question 4

Beta adrenergic receptor agonsits

Answer 4

Dobutamine

Dopamine

Question 5

Agents without positive ionotropic effects

Answer 5

1. Diuretics
2. ACE inhibitors
3. ARBs
4. Vasodilators
5. Beta-adrenergic receptor blockers
6. Natriuretic peptide

Question 6

Drugs that reduce mortality

Answer 6

ACE inhibitors
ARBs
Beta blockers
Aldosterone receptor antagonists

Question 7

4 loop diuretics

Answer 7

Furosemide
bumetanide
torsemide
ethacrynic acid

Question 8

Diuretics

Answer 8

Reduces preload with no significant effect on afterload

Reduces extracellular fluid volume, venous pressure, and preload

Question 9

Inhibition of the affects of ANG II and how it affects preload and afterload

Answer 9

Preload- intravascular volume is reduced by blocking aldosterone secretion

Afterload- via vasodilation

Question 10

ANG II

Answer 10

• Vasoconstrictor
• Increases retention of Na and water
• Potentiates catecholamine release

Question 11

Adverse effects of ACE inhibits

Answer 11

Cough, angioedema, hypokalemia

Question 12

Aldosterone antagonists

Answer 12

K sparing diuretic

Spironolactone and eplerenone

Question 13

Conivaptan

Answer 13

Vasopressin/ADH/Antidiuretic hormone antagonist- K sparing diuretic
Prevents water retention due to excess ADH

Question 14

K sparing diuretics

Answer 14

Aldosterone antagonists

Vasopressin antagonists

Question 15

Drugs that reduce preload

Answer 15

• Venodilators
• ACE inhibitors
• ARBs
• Diuretics

Question 16

Drugs the reduce afterload

Answer 16

• Arteriodilators
• ACE inhibitors
• ARBs

Question 17

Digoxin

Answer 17

Cardiac glycoside
Used to treat heart failure and atrial fibrillation

MOA: inhibits membrane bound Na/K ATPase, causing an increase in the contraction of the cardiac sarcomere

• Rise in intracellular Na- reduces the removal of Ca
• Ca accumulates in the myocyte
• Narrow therapeutic index!

Question 18

Digoxin toxicity

Answer 18

Depolarization of the resting potential, shortening of the AP, and the appearance of oscillatory depolarizing afterpotentials following normal evoked APs –> premature depolarizations, ectopic beats

Arrhythmias!

If allowed to progress can result in fatal fibrillation

At toxic levels, sympathetic outflow is increased

Question 19

Interactions of digoxin with K, Ca, and Mg

Answer 19

Hyperkalemia- reduces the effects of digoxin- binds to competing sites on the Na/K ATPase. Inhibits abnormal cardiac automaticity
Hypokalemia- potentiates the toxic effects

Hypercalcemia: increases toxic effects- accelerates overloading of intracellular stores

Hypomagnesmia: increases toxic effects

Question 20

Bipyridines MOA

Answer 20

Increases contractility and vasodilation

MOA: selective inhibition of phosphodiesterase isozyme 3- increases cAMP –>

• Directly stimulates myocardial contractility and acceleration of myocardial relaxation
• Causes balanced arterial and venous dilation with a consequent fall in systemic and pulmonary vascular resistances and left and right heart filling pressure
• inactivation of myosin light chain kinase causes smooth muscle relaxation