Heart Failure Agents

Question 1

Decreased CO activates production of

Answer 1

NE, AN-II, and endothelial (ET)

Question 2

Decreased cardiac output activates production of NE, AN-II, and ET, which causes

Answer 2

Vasoconstriction and increased afterload

Question 3

Result in greater cardiac work for a given level of ventricular filling pressure

Answer 3

Positive inotropic agents

Question 4

Improve symptoms of HF by moving patients to lower cardiac filling pressures along the same ventricular function curve

Answer 4

Diuretics

Question 5

Function to decrease ECF volume/preload and curtail remodeling/fibrosis

-Ex: spironolactone

Answer 5

Diuretics

Question 6

Function to decrease preload and/or afterload

Answer 6

Vasodilators

Question 7

Function to reduce arrhythmogenesis, curtail remodeling, and reduce undesired sympathetic effects

Answer 7

Beta-adrenergic antagonists

Question 8

Primarily used to relieve congestive symptoms in patients with CHF

Answer 8

Loop diuretics

Question 9

Reduce extracellular fluid volume and ventricular filling pressure (preload)

Answer 9

Loop diuretics

Question 10

Also reduce extracellular fluid volume by correcting Na imbalances

Answer 10

Thiazides

Question 11

Typically elevated in CHF

-Increases LV remodeling and fibrosis

Answer 11

Aldosterone

Question 12

When added w/ an ACE inhibitor, ntagonize cardiac remodeling and increase survival

Answer 12

Low doses of aldosterone antagonists

Question 13

Side effects include hypokalemic, metabolic alkalosis, ototoxicity, and hyperglycemia

Answer 13

Loop diuretics

Question 14

Can unveil ectopic pacemakers and cause arrhythmias

-Critical to monitor w/ diuretics

Answer 14

Low K+ levels

Question 15

Induce prostaglandin and NO generation from endothelial cells, which reduce venous return and pulmonary congestion

Answer 15

Loop Diuretics

Question 16

Indicated for patients allergic to sulfonamides but can cause more ototoxicity than furosemide

Answer 16

Ethacrynic acid

Question 17

Side effects include hypokalemic, metabolic alkalosis, hypomagnesemia, hyponatremia, and hypercalcemia

Answer 17

Thiazides

Question 18

Include blockers of ENaC Na+ channel and direct aldosterone antagonists

Answer 18

K+ sparing diuretics

Question 19

Aldosterone release from the adrenal gland is promoted by

Answer 19

Hyperkalemia and high AN-II

Question 20

Major side effects are hyperchloremic metabolic acidosis and gynecomastia

Answer 20

K+ sparing diuretics

Question 21

Prevent myocardial and vascular fibrosis

Answer 21

Aldosterone antagonists

Question 22

Decrease afterload by lowering peripheral resistance and reduce preload by reducing aldosterone secretion

Answer 22

ACE inhibitors (the -prils)

Question 23

Function by decreasing the conversion of AN-I to AN-II

Answer 23

ACE inhibitors

Question 24

ACE inhibitors cause a decrease in synthesis of aldosterone which can increase the risk of

Answer 24

Hyperkalemia

Question 25

A substance that stimulates prostaglandin formation and NO output

Answer 25

Bradykinin

Question 26

Cause a decrease in the degradation of bradykinin

Answer 26

ACE inhibitors

Question 27

Associated w// high bradykinin levels

Answer 27

Cough and angioneurotic edema

Question 28

Used for grades II-IV CHF and most frequently used in conjunction w/ diuretics and digitalis

Answer 28

ACE inhibitors

Question 29

In acute failure, decrease left ventricular diastolic volume and prevent further ventricular dilation, and improve exercise tolerance

Answer 29

ACE inhibitors

Question 30

A major concern when using ACE inhibitors w/ K+ sparing diuretics is

Answer 30

Hyperkalemia

Question 31

ACE inhibitors are contraindicated with

Answer 31

Bilateral renal artery stenosis

Question 32

Block the AT1 receptors and function similarly to ACE inhibitors

Answer 32

Angiotensin II Receptor Blockers (ARBs) -The -sartans

Question 33

Does not affect bradykinin duration or its production of prostaglandins or NO

Answer 33

ARBs

Question 34

More selective for inhibition of AN-II

Answer 34

ARBs

Question 35

May be particularly effective in a subset of black patients who have been reported to be less responsive to ACE inhibitors

Answer 35

Hydralazine + Isosorbide dinitrate

Question 36

A nonpeptidic drug that inhibits the protease renin

Answer 36

Aliskiren

Question 37

Functions via dual inhibition of neprylisin and angiotensin receptors which reduces mortality and hospitalization for HF

Answer 37

LCZ696

Question 38

Dilates both arterial and venous vessels to increase CO

Answer 38

Nitro dilators such as nitroprusside

Question 39

Recommended in patients w/ symptoms of HF and asymptomatic patients w/ decreased LVEF or a history of MI

Answer 39

Beta-blockers

Question 40

Have the adverse effects of symptomatic fatigue, hypotension, and bradycardia/heart block

Answer 40

Beta-blockers

Question 41

Attenuate the adverse effects of high concentrations of catecholamines -decrease HR and arrhythmogenesis

Answer 41

Beta blockers

Question 42

Long term, will prevent deterioration of myocardial function and reverse adrenergically mediated myocardial dysfunction

Answer 42

Beta blockers

Question 43

Cardiac glycosides, beta-1 agonists, Ca2+ sensitizers, and bypyridines are all

Answer 43

Positive inotropic agents

Question 44

Cardiac glycosides such as digitalis and digoxin block the

Answer 44

Na+/K+ ATPase

Question 45

The action of digitalis is antagonized by

Answer 45

K+

Question 46

Fewer deaths from HF are balanced w/ more death from sudden death because of narrow therapeutic index w/

Answer 46

Digoxin

Question 47

Does seem to support the ability of ACE inhibitors to retard progressive cardiac deterioration in CHF

Answer 47

Cardiac Glycosides

Question 48

Shortens the action potential of cardiac tissue

Answer 48

Ouabain

Question 49

What are the three main variants of cardiac glycosides?

Answer 49

Ouabain, Digoxin, and Digitoxin

Question 50

Has low lipid solubility and is almost never used

Answer 50

Ouabain

Question 51

Increase CO, decrease heart size, decrease venous pressure, and produce diuresis

Answer 51

Cardiac Glycosides

Question 52

Cause decreased sympathetic output and increased vagal activity -also increase renal perfusion

Answer 52

Cardiac Glycosides

Question 53

Therapeutically, digitalis enhances vagal tone and reduces sympathetic activity

Answer 53

Digitalis

Question 54

Slows conduction velocity and increases refractoriness in the AV node

Answer 54

Digitalis

Question 55

At toxic levels, digitalis causes

Answer 55

AV block

Question 56

Digitalis-induced tachyarrhythmias are treated w/

Answer 56

K+, lidocaine, or digitalis antibody

Question 57

Phosphodiesterase inhibitors selective for PDE3, which is found in cardiac smooth muscle

Answer 57

Milrinone and Enoximone

Question 58

In the heart, cause increase cAMP and phosphorylation/activation of L-type calcium channels

Answer 58

Milrinone and Enoximone

Question 59

Milrinone and Enoximone in vascular smooth muscle cause increased cAMP-mediated deactivation of myosin light chain kinase, causing

Answer 59

Vasodilation

Question 60

Causes fatal arrhythmias and bone marrow and liver toxicity

Answer 60

Milrinone toxicity

Question 61

Useful for treatment of HF not accompanied by hypotension

Answer 61

Dobutamine

Question 62

A synthetic analog of dopamine that stimulates Beta1-Beta2 and alpha receptors -Increases contractility through Beta-1 effect but does not increase peripheral resistance

Answer 62

Dobutamine

Question 63

Acts at beta-1 and peripheral alpha receptors to stimulate heart under conditions in which there is a drop in BP

Answer 63

Norepinephrine

Question 64

Used for “warm” septic shock

Answer 64

NE

Question 65

Acts at beta-1, beta-2, and peripheral alpha-receptors - used for increasing contraction an HR - Used for “cardiac arrest”

Answer 65

Epinephrine

Question 66

Occurs after MI or cardiogenic shock

Answer 66

Acute HF