Heart Failure & Antiarrhythmics Flashcards
Which drugs block the RAAS compensatory mechanisms?
- ARNIs (Sacubitril/Valsartan)
- ACE Inhibitors (Captopril/Lisinopril)
- ARBs
An aldosterone antagonist should be added for most patients as long as:
- Kidney function can tolerate the medication
- They do not have hyperkalemia
Example: Spironolactone
When would Ivabradine be indicated for treatment?
When heart rates are high despite maximal beta-blocker doses.
Which drugs decrease the sympathetic stimulation of compensatory mechanisms?
Beta Blockers (Bisoprolol, Carvedilol, and Metoprolol)
What are the prototypes for ACE Inhibitors? Include the MOA and possible adverse effects.
Prototypes: Captopril and Lisinopril
MOA: slows progression of HF and reduces mortality
- Lowers peripheral resistance
- Lowers blood volume
- Dilates veins which will decrease preload, pulmonary congestion, and edema
What would be the prototype for beta blockers r/t HF? What are the most important adverse effects and contraindications of these drugs?
Prototypes: Bisoprolol, Carvedilol, and Metoprolol
A/E:
- Bronchospasms in nonselective
- Hypotension/Bradycardia
- Box Warning: Do not stop abruptly taking the medication, may cause rebound excitation.
Contraindications:
- Asthma/COPD
- Hypotension, Severe Bradycardia, and Shock.
What are the benefits of vasodilators? Name 2 of them.
Benefits: they decrease blood pressure and relax blood vessels.
- Hydralazine with Isosorbide
- Nesiritide
What are the 3 key points about Hydralazine with Isosorbide?
- They are only approved for black patients.
- They decrease the workload of the heart
- Hypotension and reflex tachycardia are common.
What are the 5 key points with Nesiritide?
- It is a B-type Natriuretic Peptide
- It lowers preload and afterload
- It is only available as an IV infusion
- It can cause severe hypotension
- Only available in the hospital
Which drug classes are cardiotonic inotropic drugs? What will they do and what do they affect?
Classes:
1. Cardiac Glycosides (Digoxin)
2. Phosphodiesterase Inhibitors (Milrinone)
3. HCN Blockers (Ivabradine)
4. ARNIs (Sacubitril/Valsartan)
They affect the intracellular calcium cells in the heart muscle leading to increased contractility.
What is digitalization?
A procedure done where a dose of digoxin is gradually increased until tissue becomes saturated with the medication and symptoms of HF disppear.
It can be done rapidly with IV digoxin or over 7 days as an outpatient with PO digoxin.
What is the MOA of Digoxin, the route, and onset of the medication?
MOA:
- Inhibits enzyme responsible for sodium and potassium ion exchange
- increases intracellular calcium and allows more calcium to enter myocardial cells
Results in:
- Increased force of contraction
- Increased renal perfusion and cardiac output
- Slowed HR
- Decreased conduction velocity through the AV node
Routes: PO and IV
- Onset of IV: 5-30 minutes
- Onset of PO: 30-120 minutes
When caring for a patient on Digoxin, which labs will need to be monitored and what are the therapeutic ranges?
Labs: Potassium and Digoxin levels
- Digoxin levels should be drawn 6-12 hours after a dose
Therapeutic Range: 0.5-2ng/mL
What are the adverse effects of digoxin? Include contraindications.
A/E:
- arrhythmias
- vision changes
- digoxin toxicity (anorexia, n/v, malaise, depression, life-threatening arrhythmias)
Contraindications:
- allergy
- heart block, MI, ventricular dysrhythmias
- pregnancy/lactation
- renal insufficiency
What are the drug interactions with Digoxin? How do those drugs interact with the medication?
- St. John’s Wort and Psyllium (decreases the effectiveness of digoxin)
- Ginseng, Hawthorn, and black Licorice (increase digoxin toxicity)
- Potassium Losing Diuretics (increase the risk of arrhythmias)