Heart Failure Pharm Flashcards
Pharmacological Treatment of HF
- ACE inhibitors or ARBs, ARNI
- Beta Blocker
- Mineralocorticoid Receptor Antagonist
- SLGT2 Inhibitor
Diuretics
Digitalis
Nitrates
RAAS Inhibitors in HF:
ACEI, ARB, ARNI
RAAS Inhibitors in HF: ARNI
Angiotensin Receptor-Neprilysin Inhibitor
Sacubitril/Valsartan
RAAS Inhibitors in HF: ACEI, ARB, ARNI: MOA
Survival benefit
-Decrease in mortality with decreased EF
MOA:
- Decreases preload + afterload
- Suppresses aldosterone which helps in cardiac remodeling
Use highest dose possible
RAAS Inhibitors in HF: ACEI, ARB, ARNI:
Which one is favored and why?
ARNI is currently thought to be BEST: newer + more expensive
ARBs might be better tolerated
RAAS Inhibitors in HF: ACEI, ARB, ARNI: AE
Hypotension
Hyperkalemia
Cough (ACEI)
Beta Blockers in HF: Prototype
carvedilol (Coreg)
-Beta and alpha blockade
carvedilol (Coreg): MOA
-Protects against SNS activation and dysrhythmias, -Reverses cardiac remodeling
carvedilol (Coreg): AE
- *Hypotension
- Fluid retention or worsening HF
- Fatigue
- Bradycardia
Mineralocorticoid Receptor Antagonist: Spironolactone
- 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
SLGT2 Inhibitors in HF
dapagliflozin
dapagliflozin: MOA
*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
Diuretics in HF: First-line therapy
Loop Diuretics
-furosemide (Lasix)
Volume overload
Oral or IV
Furosemide: AE
Hypokalemia
Hypotension
Digoxin toxicity
Biggest Concern with HF and diuretics
Potassium Imbalances
Dysrhythmias
Is there a survival benefit of HF and diuretics?
NONE only symptom relief
Inotropic Drugs
Cardiac glycosides: Digitalis (digoxin)
-considered a second line drug because of increased risk for dysrhythmias
Sympathomimetics: Dopamine and Dobutamine
-makes heart squeeze harder
What does positive inotropic effect mean?
If we can increase the contractility of the heart muscle then we can increase the force of contraction: Increasing the CARDIAC OUTPUT
Inotropic Agent: Digitalis (Digoxin): Class
Cardiac Glycoside
-made from Foxglove plant
Digitalis (Digoxin): MOA
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)
Digitalis (Digoxin): AE
Cardiac dysrhythmias
Digitalis toxicity
Digitalis Toxicity
Who is at risk?
- Increased Age
- Women
- Digoxin + Diuretics
Preventing Toxicity
- reduced dose
- serum drug levels, periodic monitoring of levels
- supplemental potassium
Digitalis (Digoxin): Nursing Implications
Monitor serum potassium levels
-Low potassium can cause digitalis toxicity!
-Usually due to diuretics
DYSRHYTHMIAS + DYSFUNCTION
Digitalis Toxicity Symptoms
Bradycardia Headache Dizziness Confusion Nausea Visual disturbances: blurry/yellow vision
Preventing Bradycardia w/Digitalis
Take apical pulse for a FULL minute prior to administering
- hold if pulse <60 bpm
- monitor cardiac rhythm
Pt teaching: Take your own pulse
Digitalis Toxicity Antidote
Digoxin Immune Fab (Digibind)
-given IV