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Cardiology > Heart Failure Agents > Flashcards

Heart Failure Agents Flashcards

1
Q

Decreased CO activates production of

A

NE, AN-II, and endothelial (ET)

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2
Q

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

A

Vasoconstriction and increased afterload

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3
Q

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

A

Positive inotropic agents

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4
Q

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

A

Diuretics

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5
Q

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

-Ex: spironolactone

A

Diuretics

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6
Q

Function to decrease preload and/or afterload

A

Vasodilators

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7
Q

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

A

Beta-adrenergic antagonists

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8
Q

Primarily used to relieve congestive symptoms in patients with CHF

A

Loop diuretics

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9
Q

Reduce extracellular fluid volume and ventricular filling pressure (preload)

A

Loop diuretics

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10
Q

Also reduce extracellular fluid volume by correcting Na imbalances

A

Thiazides

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11
Q

Typically elevated in CHF

-Increases LV remodeling and fibrosis

A

Aldosterone

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12
Q

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

A

Low doses of aldosterone antagonists

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13
Q

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

A

Loop diuretics

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14
Q

Can unveil ectopic pacemakers and cause arrhythmias

-Critical to monitor w/ diuretics

A

Low K+ levels

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15
Q

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

A

Loop Diuretics

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16
Q

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

A

Ethacrynic acid

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17
Q

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

A

Thiazides

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18
Q

Include blockers of ENaC Na+ channel and direct aldosterone antagonists

A

K+ sparing diuretics

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19
Q

Aldosterone release from the adrenal gland is promoted by

A

Hyperkalemia and high AN-II

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20
Q

Major side effects are hyperchloremic metabolic acidosis and gynecomastia

A

K+ sparing diuretics

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21
Q

Prevent myocardial and vascular fibrosis

A

Aldosterone antagonists

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22
Q

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

A

ACE inhibitors (the -prils)

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23
Q

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

A

ACE inhibitors

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24
Q

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

A

Hyperkalemia

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25
Q

A substance that stimulates prostaglandin formation and NO output

A

Bradykinin

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26
Q

Cause a decrease in the degradation of bradykinin

A

ACE inhibitors

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27
Q

Associated w// high bradykinin levels

A

Cough and angioneurotic edema

28
Q

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

A

ACE inhibitors

29
Q

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

A

ACE inhibitors

30
Q

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

A

Hyperkalemia

31
Q

ACE inhibitors are contraindicated with

A

Bilateral renal artery stenosis

32
Q

Block the AT1 receptors and function similarly to ACE inhibitors

A

Angiotensin II Receptor Blockers (ARBs)

-The -sartans

33
Q

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

A

ARBs

34
Q

More selective for inhibition of AN-II

A

ARBs

35
Q

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

A

Hydralazine + Isosorbide dinitrate

36
Q

A nonpeptidic drug that inhibits the protease renin

A

Aliskiren

37
Q

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

A

LCZ696

38
Q

Dilates both arterial and venous vessels to increase CO

A

Nitro dilators such as nitroprusside

39
Q

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

A

Beta-blockers

40
Q

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

A

Beta-blockers

41
Q

Attenuate the adverse effects of high concentrations of catecholamines

-decrease HR and arrhythmogenesis

A

Beta blockers

42
Q

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

A

Beta blockers

43
Q

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

A

Positive inotropic agents

44
Q

Cardiac glycosides such as digitalis and digoxin block the

A

Na+/K+ ATPase

45
Q

The action of digitalis is antagonized by

A

K+

46
Q

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

A

Digoxin

47
Q

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

A

Cardiac Glycosides

48
Q

Shortens the action potential of cardiac tissue

A

Ouabain

49
Q

What are the three main variants of cardiac glycosides?

A

Ouabain, Digoxin, and Digitoxin

50
Q

Has low lipid solubility and is almost never used

A

Ouabain

51
Q

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

A

Cardiac Glycosides

52
Q

Cause decreased sympathetic output and increased vagal activity

-also increase renal perfusion

A

Cardiac Glycosides

53
Q

Therapeutically, digitalis enhances vagal tone and reduces sympathetic activity

A

Digitalis

54
Q

Slows conduction velocity and increases refractoriness in the AV node

A

Digitalis

55
Q

At toxic levels, digitalis causes

A

AV block

56
Q

Digitalis-induced tachyarrhythmias are treated w/

A

K+, lidocaine, or digitalis antibody

57
Q

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

A

Milrinone and Enoximone

58
Q

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

A

Milrinone and Enoximone

59
Q

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

A

Vasodilation

60
Q

Causes fatal arrhythmias and bone marrow and liver toxicity

A

Milrinone toxicity

61
Q

Useful for treatment of HF not accompanied by hypotension

A

Dobutamine

62
Q

A synthetic analog of dopamine that stimulates Beta1-Beta2 and alpha receptors

-Increases contractility through Beta-1 effect but does not increase peripheral resistance

A

Dobutamine

63
Q

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

A

Norepinephrine

64
Q

Used for “warm” septic shock

A

NE

65
Q

Acts at beta-1, beta-2, and peripheral alpha-receptors

  • used for increasing contraction an HR
  • Used for “cardiac arrest”
A

Epinephrine

66
Q

Occurs after MI or cardiogenic shock

A

Acute HF

Cardiology (27 decks)

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