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326 Exam 3 (Cardiology,GI,Endocrine) > Heart Failure Pharm > Flashcards

Heart Failure Pharm Flashcards

1
Q

Pharmacological Treatment of HF

A
  1. ACE inhibitors or ARBs, ARNI
  2. Beta Blocker
  3. Mineralocorticoid Receptor Antagonist
  4. SLGT2 Inhibitor

Diuretics
Digitalis
Nitrates

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2
Q

RAAS Inhibitors in HF:

A

ACEI, ARB, ARNI

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3
Q

RAAS Inhibitors in HF: ARNI

A

Angiotensin Receptor-Neprilysin Inhibitor

Sacubitril/Valsartan

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4
Q

RAAS Inhibitors in HF: ACEI, ARB, ARNI: MOA

A

Survival benefit
-Decrease in mortality with decreased EF

MOA:

  • Decreases preload + afterload
  • Suppresses aldosterone which helps in cardiac remodeling

Use highest dose possible

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5
Q

RAAS Inhibitors in HF: ACEI, ARB, ARNI:

Which one is favored and why?

A

ARNI is currently thought to be BEST: newer + more expensive

ARBs might be better tolerated

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6
Q

RAAS Inhibitors in HF: ACEI, ARB, ARNI: AE

A

Hypotension
Hyperkalemia
Cough (ACEI)

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7
Q

Beta Blockers in HF: Prototype

A

carvedilol (Coreg)

-Beta and alpha blockade

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8
Q

carvedilol (Coreg): MOA

A

-Protects against SNS activation and dysrhythmias, -Reverses cardiac remodeling

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9
Q

carvedilol (Coreg): AE

A
  • *Hypotension
  • Fluid retention or worsening HF
  • Fatigue
  • Bradycardia
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10
Q

Mineralocorticoid Receptor Antagonist: Spironolactone

A
  • We teach this is a Potassium sparing diuretic
  • NOT using for diuretic effect, instead for sodium/water retention to help with offloading the LV
  • Decreased hospitalizations and cardiac death
  • Must watch carefully for HYPERKALEMIA and worsening RENAL FAILURE
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11
Q

SLGT2 Inhibitors in HF

A

dapagliflozin

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12
Q

dapagliflozin: MOA

A

*MOA not on EXAM!

MOA in HF is not well understood

  • Thought to help with ventricular unloading through natriuresis/osmotic diuresis without actually depleting volume like traditional diuretics
  • May affect cardiac metabolism/bioenergetics
  • Either way decreases READMISSIONS, MORTALITY, + MORBIDITY
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13
Q

Diuretics in HF: First-line therapy

A

Loop Diuretics
-furosemide (Lasix)

Volume overload

Oral or IV

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14
Q

Furosemide: AE

A

Hypokalemia
Hypotension
Digoxin toxicity

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15
Q

Biggest Concern with HF and diuretics

A

Potassium Imbalances

Dysrhythmias

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16
Q

Is there a survival benefit of HF and diuretics?

A

NONE only symptom relief

17
Q

Inotropic Drugs

A

Cardiac glycosides: Digitalis (digoxin)
-considered a second line drug because of increased risk for dysrhythmias

Sympathomimetics: Dopamine and Dobutamine
-makes heart squeeze harder

18
Q

What does positive inotropic effect mean?

A

If we can increase the contractility of the heart muscle then we can increase the force of contraction: Increasing the CARDIAC OUTPUT

19
Q

Inotropic Agent: Digitalis (Digoxin): Class

A

Cardiac Glycoside

-made from Foxglove plant

20
Q

Digitalis (Digoxin): MOA

A

Inhibits sodium potassium ATP pump causing calcium to collect within the cells of the heart helping to increase MYOCARDIAL CONTRACTILITY

  • Increases blood flow to kidney helping to excrete sodium and water
  • Decreases sympathetic activation action and increases parasympathetic action (Decreased HR)
21
Q

Digitalis (Digoxin): AE

A

Cardiac dysrhythmias

Digitalis toxicity

22
Q

Digitalis Toxicity

A

Who is at risk?

  • Increased Age
  • Women
  • Digoxin + Diuretics

Preventing Toxicity

  • reduced dose
  • serum drug levels, periodic monitoring of levels
  • supplemental potassium
23
Q

Digitalis (Digoxin): Nursing Implications

A

Monitor serum potassium levels
-Low potassium can cause digitalis toxicity!
-Usually due to diuretics
DYSRHYTHMIAS + DYSFUNCTION

24
Q

Digitalis Toxicity Symptoms

A 
Bradycardia
Headache
Dizziness
Confusion
Nausea
Visual disturbances: blurry/yellow vision
25
Q

Preventing Bradycardia w/Digitalis

A

Take apical pulse for a FULL minute prior to administering

  • hold if pulse <60 bpm
  • monitor cardiac rhythm

Pt teaching: Take your own pulse

26
Q

Digitalis Toxicity Antidote

A

Digoxin Immune Fab (Digibind)

-given IV

326 Exam 3 (Cardiology,GI,Endocrine) (19 decks)

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