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Today we are discussing DIGOXIN
Digoxin is a cardiac glycoside - which are drugs derived from digitalis, a substance naturally occurring in foxglove plants.
How it works…
Cardiac glycosides inhibit the sodium-potassium pump, thereby increasing intracellular calcium, which causes the heart muscle to contract more efficiently. They produce a positive inotropic effect, meaning they increase the force of the contraction of the heart. At the same time they also produce a negative chronotropic effect, wherein they decrease the heart rate, while also slowing electrical conduction through the AV node (negative dromotropic effect).
So when we give DIGOXIN, we are effectively increasing our cardiac contractility, while decreasing the heart rate and prolonging the cardiac refractory period.
- let’s do a quick review here to better understand what’s happening when we give this medication -
If we think about how the heart works for a second and really visualize it, we will better understand exactly how the cardiac glycosides like digoxin work and therefore how they can help in certain instances.
…so, blood flows into the right atrium through the tricuspid valve to the right ventricle through the pulmonic valve into our pulmonary circulation (pulmonary arteries —> gas exchange —> pulmonary veins) into the left atrium through the mitral valve into the left ventricle through the aortic valve up into the aortic arch and out into systemic circulation.
In order to keep the blood moving throughout, the heart is relaxing (i.e. chambers are filling with blood) and then contracting (i.e. squeezing blood into the next section of the heart or into systemic circulation).
The fill time (time when the heart is relaxed and chambers are filling with blood) is dependent upon how quickly the heart is beating - the faster the heart rate (HR), the less fill time between contractions and conversely, the slower the heart rate, the longer the fill time between contractions.
DIGOXIN allows the heart to slow down (decreases the heart rate) meaning that it will have a longer fill time between contractions. Increased fill time means more blood fills the left ventricle, before the medication then causes increased contractility (a more efficient squeeze) when it contracts causing more blood to pump into circulation with each beat. This leads to increased cardiac output (CO).
decreased HR + increased contractility = increased CO
and increased CO leads to less blood backing up into the lungs and venous circulation causing issues like edema & pulmonary congestion.
so…If that’s how it works and what it does, in what instances would this be useful?
instances like Heart Failure (HF), cardiogenic shock, atrial fibrillation; atrial flutter; SVT
Other useful info about :
· therapeutic index: 0.5 to 2 ng/mL
· antidote: digoxin immune fab (Digibind)
· contraindications: ventricular dysrhythmias; 2nd & 3rd degree heart block
· use caution: patients with renal disease, hypothyroidism, hypokalemia
· side effects: headache, hypotension, fatigue, bradycardia, dizziness
· adverse effects: digoxin toxicity (presents with GI manifestations - anorexia, N/V/D; blurred vision or yellow-green halos; diplopia, weakness, drowsiness, bradycardia)
· nursing considerations/patient teaching:
monitor digoxin levels and for digoxin toxicity
monitor electrolytes, especially potassium (toxicity is more likely to happen with hypokalemia, hypomagnesemia, hypothyroidism, and hypercalcemia)
monitor apical pulse for 60 sec prior to administering med - if < 60 bpm hold med and notify HCP
teach patient how to take their own pulse and to do it prior to taking med every time
how & when to take: don’t miss dose; do NOT take a double dose if you missed previous dose; do NOT open, chew or crush capsules
talk to HCP before taking any OTC meds
teach patient signs/symptoms of digoxin toxicity and to report immediately
diet: sodium restricted; potassium rich to keep potassium levels normal
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