About

➀ Read and Learn

The following course content

Introduction   

Digoxin is one of the oldest cardiac medicines still in use today. It was first derived from the foxglove plant in 1930 – a plant that is famously poisonous (1). Digoxin is a unique medication because it helps control dysrhythmias and is also a positive inotrope. This combination of effects has not been found in any other medicine to date and explains why digoxin continues to be used.  

Unfortunately, digoxin also has a higher likelihood of producing toxicity than most medications. Digoxin toxicity (also called digitalis toxicity) can be life-threatening, so it is important to understand how to identify and treat this condition.  

Digoxin Pharmacology 

It is meaningful to discuss what digoxin does and how it is used. Digoxin is classified as a cardiac glycoside. It works by binding to sodium-potassium pumps in the heart (1). This results in stronger contractions of heart muscle, slower heart rate, and a reduction in AV node conduction.  

For patients, this leads to improved cardiac output from stronger contractions and therefore larger stroke volumes. Slowing the heart rate and conduction through the heart also helps control arrhythmias, such as atrial fibrillation. This means that it helps prevent abnormal heart rhythms while increasing the pumping function of the heart. Other antiarrhythmic medications typically decrease cardiac output, making digoxin preferable in patients who cannot tolerate a decrease in cardiac output (2).  

Unfortunately, these beneficial effects come with a risk. Digoxin has a narrow therapeutic index, meaning there is only a small margin between a therapeutic dose and a toxic dose. The therapeutic range for digoxin is just 0.8-2.0 nanograms/milliliter of blood (4). This narrow therapeutic index and the fact that digoxin has been shown to improve symptoms but not mortality has led to digoxin losing favor (1, 2).  

Digoxin Monitoring 

The potential for digoxin to create toxicity requires careful monitoring of drug levels during digoxin therapy. Current guidelines recommend patients starting digoxin therapy have serum digoxin levels checked 7-10 days after starting therapy (4). While the therapeutic range of digoxin is 0.8-2.0ng/mL, newer research suggests targeting a therapeutic level of <1.2ng/mL (4).  

Once a therapeutic level is established, patients should have their digoxin levels checked every 6-12 months (4). Levels should also be checked if the patient is experiencing symptoms of toxicity, or if they have a change in their renal function (4).  

Digoxin undergoes little metabolism and is excreted unchanged in the urine (1). This means a decrease in renal function can easily lead to higher serum levels of digoxin at the same dose. Serial ECGs should be checked annually and when adjusting dosages or new symptoms arise (4).  

Risk Factors for Digoxin Toxicity 

Several factors can put a person at a higher risk of digoxin toxicity. The two most important risk factors are older age and renal dysfunction. The majority of digoxin toxicity occurs in older patients, especially those with declining renal function (2). Other risk factors include hypokalemia, hypomagnesemia, hypercalcemia, dehydration, hypoxemia, and myocardial ischemia (2). A classic digoxin toxicity patient would be an older, malnourished patient who has had a decline in urine output.  

Medications that can increase serum digoxin levels include amiodarone, captopril, gentamicin, erythromycin, itraconzaole, quinidine, ranolazine, telaprevir, tetracycline, and verapamil (5). Rather than trying to remember all those names, just remember that digoxin can be increased by several antibiotics, and some antiarrhythmics and blood pressure medications. 

Diagnosis of Digoxin Toxicity 

A diagnosis of digoxin toxicity is based on clinical suspicion, ECG findings, and serum digoxin levels. Many of the symptoms of digoxin toxicity are vague, so they must be coupled with a thorough history.  

Signs of digoxin toxicity can include gastrointestinal, cardiac, or neurological symptoms. The gastrointestinal symptoms include loss of appetite, nausea, vomiting, and diarrhea. Neurological symptoms include headache, confusion, lethargy, and vision changes such as blurred vision or seeing halos. The cardiac symptoms are related to abnormal heart rhythms, commonly bradycardia-dysrhythmias that may progress to ventricular tachycardia. These dysrhythmias affect cardiac output and lead to hypotension and/or cardiogenic shock.  

ECG findings suggestive of digoxin toxicity include ST segment depression (especially those with a scooped-out appearance), T wave flattening, U waves, and arrhythmias.  

Below you can see examples of what these ECG findings look like (6): 

Treatment of Digoxin Toxicity 

Treatment of digoxin toxicity includes reducing or holding the dose of digoxin, administering digoxin immune antibody fragments, and supportive care.  

Reducing or holding the dose of digoxin is appropriate for patients with mild symptoms (2). Digoxin immune antibody fragments, otherwise known as DigiFab or DigiBind, are used in serious or life-threatening digoxin toxicity. DigiFab works by binding to and inactivating the circulating digoxin (3). The recommended dosing for digoxin immune fab is 1 vial (40mg) for every 0.5mg digoxin ingested in acute overdose (3). For chronic overdose, the dose is calculated with the following formula: serum digoxin concentration (ng/mL) * weight (kg)/100 = dose in vials (3). Hypokalemia is common after DigiFab administration. This typically resolves on its own, but potassium levels should be monitored closely (2).  

Supportive care depends on the patient’s presentation and their heart rhythm. Unstable patients with a slow heart rate (bradycardia), should be treated with medications to increase their heart rate, such as dopamine, dobutamine, or epinephrine (2).  

For patients who devolve into ventricular tachycardia, treat according to ACLS guidelines. Hyperkalemia is common with digoxin toxicity; it can be treated with diuresis, IV insulin with dextrose, and IV calcium administration (2).  

While dialysis may seem tempting to treat digoxin toxicity, especially with hyperkalemia, digoxin is not cleared well by dialysis (2). Patients should have continuous ECG monitoring until their toxicity has fully resolved (2).  

Conclusion

Digoxin is a unique medication that can offer benefits to patients suffering from arrhythmias. However, because of its narrow therapeutic index, it requires careful monitoring.  Nurses caring for patients on digoxin therapy should be aware of the signs and symptoms of digoxin toxicity. It is also important to understand the risk factors for toxicity, and the appropriate treatment should toxicity occur. Hopefully, this course has provided you with this knowledge and a new level of confidence in how to identify and manage digoxin toxicity.  

➁ Complete Survey

Give us your thoughts and feedback

➂ Click Complete

To receive your certificate