- Cardiac glycosides are used in patients with heart failure, atrial fibrillation, and atrial flutter
- HF: The heart is incapable of pumping adequately to supply oxygen to the body
- A-Fib: Cardiac dysrhythmias with rapid, uncoordinated contractions of the atrial myocardium
- Atrial flutter: Cardiac dysrhythmias with rapid contractions of 200-300 BPM
- Glycosides have 3 functions to increase contractility and stroke volume while decreasing HR
- Positive inotropic response:
- Increases myocardial contractions
- Inhibition of the sodium-potassium pump allows more sodium and calcium to be stored within cells
- The sodium-calcium pump brings in sodium and releases calcium from the cell but inhibition of the sodium-potassium pump prevents sodium from being released which inhibits the amount of sodium that is taken in/calcium released
- Increased intracellular calcium lowers membrane excitability
- Results in greater contractions
- Negative chronotropic response:
- Decreases HR
- Negative dromotropic response:
- Slows the speed of electrical conduction through the AV node
- Increased contractility increases CO, decreases preload and edema, and promotes fluid excretion
- Fluid retention in the lungs and extremities is decreased
Digoxin
- Digoxin is a secondary drug used for HF
- First-line medications include [[phosphodiesterase inhibitors]] (PDE) inhibitors and IV inotropic agents (dopamine and dobutamine)
- Digoxin is 20-30% protein-bound
- Digoxin can be given intravenously or orally
- The half-life of digoxin is 30-40 hours
- High risk for drug accumulation and digitalis toxicity
- Patients with kidney dysfunction can affect the excretion of digoxin
- Thyroid dysfunction can influence the metabolism of digoxin
- Hyperthyroidism: Increased dose
- Hypothyroidism: Decreased dose
Digitalis (Digoxin) Toxicity
- Cardiotoxicity is an adverse reaction to digoxin and can result in ventricular dysrhythmias
- Older adults are more prone to digitalis toxicity
- Digitalis toxicity may result in 1st, 2nd, or 3rd degree heart block
- Digoxin-immune Fab can be used to treat severe toxicity
- Symptoms of toxicity:
- Rhythm changes
- PVC
- Bradycardia
- GI issues
- Nausea/Vomiting
- Anorexia
- Diarrhea
- Neurological changes
- Blurred vision/Visual illusion
- Confusion/Delirium
- Headaches
Drug Interactions
- Potassium-wasting diuretics increase the effects of digoxin
- Increased risk for toxicity
- Hypokalemia increases the effects of digoxin in myocardial cells
- Cortisone drugs increase the effects of digoxin
- Cortisone preparations promote the reabsorption of sodium and the excretion of potassium, which can lead to hypokalemia
- Patients taking cortisone drugs or potassium-wasting diuretics should have a potassium-rich diet or take supplements
- Antacids decrease the effects of digoxin
- Antacids increase gastric pH and decrease the absorption of digoxin
- Antacid medications and digoxin meds should be staggered to prevent interactions
Phosphodiesterase Inhibitors
- Phosphodiesterase inhibitors (PDE) inhibitors are vasodilators and produce an inotropic response, similarly to cardiac glycosides
- Positive inotropic responses increase the contractility of the heart (increased CO)
- PDE inhibitors are a first-line medication for heart failure
- Using IV PDE inhibitors for more than 48-72 hours can cause severe cardiac dysrhythmias