Exam 2 - Heart Failure Flashcards

1
Q

What drug classes are used to reduce preload?

A

Diuretics or venodilators

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2
Q

What drug classes are used to reduce afterload?

A

Arteriodilator

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3
Q

What drug classes are used to increase contractility?

A

Inotropic drug

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4
Q

What drug classes are used to reduce energy expenditure?

A

B-adrendergic antagonist

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5
Q

What is the MOA of diuretics in regards to HF?

A
  • Reduce salt and H2O retention

- Reduce venous pressure leading to reduced edema and cardiac size

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6
Q

What diuretics are used in HF and can reduce mortality rate?

A

Spironolactone and eplerenone (aldosterone antagonists)

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7
Q

What is the MOA for an ACE inhibitor?

A

Inhibits ACE, preventing the conversion of Angiotensin I to Angiotensin II

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8
Q

What is the MOA for an ARB?

A

Block Angiotensin II from binding to AT1 receptor

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9
Q

What is the current DOC of HF treatment today?

A

ACE inhibitors

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10
Q

What is the primary therapeutic effect of ACE inhibitors and ARBs in HF?

A

Diminish cardiac workload by:

  • Decreasing afterload: Decrease in angiotensin II-induced vasoconstriction
  • Decreasing preload: Decreased aldosterone release
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11
Q

What are adverse effects associated with ACE inhibitors and ARBs?

A

Dry cough with ACE, but not with ARB

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12
Q

What is the MOA for Sacubitril/Valsartan (Entresto)?

A

2 drugs: (ARNI: ARB + Neprilysin Inhibitor)

  • ARB will block Angiotensin II from binding to AT1 receptor
  • Neprilysin inhibitor will reduce the degradation of natriuretic peptides, bradykinin and others
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13
Q

What is the key to decreasing mortality associated with using an ARNI (Sacubitril/Valsartan)?

A

The neprilysin inhibitor portion will reduce cardiac remodeling as it prevents the degradation of natriuretic peptides, bradykinin and others

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14
Q

What are some adverse effects of Sacubitril/Valsartan (Entresto)?

A
  • Hypotension
  • Hyperkalemia (ARB portion is inhibiting aldosterone which will cause an increased K+ concentration) (will occur especially if using a K+ sparing diuretic)
  • Cough and angioedema (due to increased bradykinin)
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15
Q

What are contraindications/precautions for Sacubitril/Valsartan (Entresto)?

A
  • Pregnancy

- Concurrent use with ACE inhibitor due to risk of angioedema

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16
Q

Carvedilol and Metoprolol belong to which class of HF medications?

A

B-blockers - “alol”

17
Q

What are the therapeutic effects of B-blockers?

A
  • Decrease mortality
  • Decrease renin secretion
  • Decrease effects of high concentration of catecholamines
  • Decrease HR
  • Decrease remodeling
18
Q

When are B-blockers effective in HF?

A

Only effective in early stages of HF and can be dangerous in severe or end-stage due to its negative inotropic effect

19
Q

Sodium nitroprusside (Nitropress), Isosorbide dinitrate, and Hydralazine belong to what class of HF drugs?

A

Vasodilators

20
Q

How are sodium nitroprusside (Nitropress), Isosorbide dinitrate, and Hydralazine effective in HF?

A
  • Reduce preload
  • Reduce afterload
  • Reduce damaging remodeling of the heart
21
Q

What is the MOA of Dobutamine and what is it used for?

A
  • Selective B1-agonist

- Short-term treatment of severe refractory HF

22
Q

What is the MOA of Dopamine and what is it used for?

A
  • Low dose –> D1 in kidney –> vasodilation
  • Mod. dose –> B1 in heart –> inotropic effect
  • High dose –> a in vessels –> vasoconstriction/increase BP

Short-term treatment of severe refractory HF, especially if increase in BP is needed

23
Q

What is the MOA for Digoxin (Lanoxin)?

A

Inhibition of membrane sodium pump Na+, K+-ATPase (digitalis receptor), ultimately leading to an increase in intracellular calcium and increased contractility. Digitalis will also directly increase vagal stimulation (baroreflex-like effect) and decrease sympathetic tone, leading to a slowed HR.

24
Q

What are indications/therapeutic effects of Digoxin?

A
  • HF (CO is increased; last agent used)
  • Improves exercise intolerance in HF
  • Anti-arrhythmic in non-HF
25
What are some adverse effects of Digoxin?
- GI disturbances are earliest signs of toxicity - Narrow margin of safety - CNS - Arrhythmias (ventricular fibrillation is most common cause of death)
26
What is the differing affect of Digoxin in a failing heart versus a non-failing heart?
CO is increased in the failing but not in the normal heart due to increased peripheral vasoconstriction in normal individuals. As HR decreases, SV increases.
27
What is the most common cause of death in patients taking Digoxin?
Ventricular fibrillation
28
What should be done regularly in a patient taking Digoxin?
- EKGs | - Measure K+ and digitalis
29
How do you treat the following Digoxin intoxications: 1) Minor (GI) 2) Moderate (arrhythmias) 3) Severe (overdose/life-threatening arrhythmias)
1) discontinue or reduce dose digitlis 2) Oral or IV potassium and discontinue/reduce digitalis 3) Immunotherapy with Digitalis Immune Fab, oral or IV potassium, and discontinue/reduce digitalis
30
Should you perform a cardioversion in a patient suffering from digitalis-induced arrhythimas?
No cardioversion except for ventricular fibrillation
31
What are some pharmacodynamic interactions associated with Digoxin?
- Interaction with thiazide or loop diuretics can lead to hypokalemia - B-blockers can further decrease activity of SA node activity - CCBs will decrease contractility and are contraindicated in HF (decreases Digoxin effectiveness)