Cardiac glycosides, also called digitalis glycosides, are medications derived from the foxglove plant, Digitalis purpurea. They are commonly used for the treatment of atrial arrhythmias, such as atrial flutter and atrial fibrillation, which are caused by rapid, uncoordinated contractions of the atria. In addition, cardiac glycosides can be prescribed for congestive heart failure when other medications fail.
Now, the most commonly used cardiac glycoside is digoxin, which can be given orally, intravenously, and intramuscularly. Once administered, digoxin works by reversibly inhibiting the sodium-potassium ATPase located in the cell membrane of cardiomyocytes. Normally the sodium-potassium ATPase pumps three sodium ions out of the cell for every two potassium ions that it pumps in, and to do this, it consumes one ATP molecule for energy.
When the sodium-potassium ATPase is inhibited by digoxin, sodium builds up inside the cell. This interrupts the sodium-calcium exchanger on the cell membrane, which normally pumps one calcium ion out in exchange for three sodium ions. As a result, digoxin causes calcium to build up within cardiomyocytes, allowing the cardiac muscle fibers to contract more efficiently, which leads to an increase in the force of the heart’s contractions and cardiac output. In turn, the increase in cardiac output increases the renal blood flow and urine output, which also helps reduce peripheral edema.
Digoxin also stimulates the vagus nerve, which provides the parasympathetic supply to the heart, and reduces the conduction velocity through the AV node. These two effects combined result in a decreased heart rate. But because parasympathetic innervation is much richer in the atria, these effects mainly involve the atria.
Now, a major drawback is that digoxin has a very narrow therapeutic window, which means that small variations in its blood concentration can easily cause toxicity. Some common side effects of digoxin that can indicate toxicity include gastrointestinal disturbances, such as anorexia, nausea, vomiting, and rarely diarrhea. In addition, due to vagus nerve stimulation, digoxin can result in conduction defects like bradycardia and even heart block. Additionally, the increased intracellular calcium may predispose clients to arrhythmias.
Other side effects include neurologic symptoms, such as confusion, disorientation, and visual disturbances like diplopia, blurred vision, or xanthopsia, which is when things appear yellow. Some clients may also develop a bullous, erythematous maculopapular rash. Finally, in acute digoxin toxicity, too many sodium-potassium ATPases are inhibited at the same time, which can result dangerously in hyperkalemia; treatment involves slowly going back to normal potassium levels, as well as administration of digoxin-specific antibody fragments or digoxin immune Fab, which binds to and inactivates digoxin.
Now, digoxin should be used with caution in certain conditions that may predispose to digoxin toxicity. These include electrolyte abnormalities like hypokalemia, hypomagnesemia, and hypercalcemia, all of which increase the binding of digoxin to the cell; as well as renal dysfunction, since digoxin is excreted through the kidneys. The risk of toxicity is also increased by medications that compete with digoxin for the binding site or inhibit its renal clearance, such as amiodarone, verapamil, diltiazem, and quinidine.
Finally, digoxin is contraindicated in clients with heart blocks, which could be worsened; ventricular arrhythmia, which can be treated with medications that are more effective and safer than digoxin; and myocardial infarction, where the increase in contractility could damage the infarcted myocardium.
Alright, when a client with heart failure is prescribed digoxin, perform a baseline assessment, including weight, vital signs, and heart and lung sounds. Then, assess the location and extent of any edema that’s present. Be sure to review your client’s laboratory test results, noting their brain natriuretic peptide and atrial natriuretic peptide, as well as electrolytes, especially potassium, and renal function tests. Finally, review diagnostic tests such as ECG and ejection fraction.
Next, be sure to explain to your client how the medication will help their heart to beat more effectively. And be sure to stress the importance of taking the medication as prescribed, at the same time every day, and to never stop taking it abruptly. Then, teach your client how to take their own pulse, and instruct them to count their heart beat for a full minute before taking their medication. Advise them that they should not take the medication if their heart rate is less than 60 beats per minute; instead they should wait one hour and recheck their pulse; if their heart rate is still less than 60 beats per minute, they should contact their healthcare provider right away.
Next, remind your client to closely follow their healthcare regimen, including moderate physical activity, and a low sodium and low fat diet. If a potassium-wasting diuretic is also prescribed as part of their medication regimen, teach them to help maintain a normal potassium level by including some potassium rich foods in their daily diet, such as bananas, oranges, broccoli, and potatoes.
Then, teach your client how to recognize symptoms of hypokalemia, such as muscle twitches, weakness, or fatigue, and stress the importance of contacting their healthcare provider immediately if these occur. Finally, teach them to recognize symptoms of digoxin toxicity, such as anorexia, nausea, vomiting, and visual disturbances like blurred or yellow vision; if they experience any of these symptoms, advise them to contact their healthcare provider immediately.
Now, when administering digoxin intravenously, be sure to assess your client's apical pulse for a full minute, and ensure they are on continuous ECG monitoring and have a patent IV in place. Next, confirm that both emergency equipment and the antidote, digoxin immune Fab, are readily available. Keep a close eye on their cardiac rhythm, assessing for bradycardia or arrhythmias, and continue to monitor their blood pressure, potassium level, and serum digoxin levels for the therapeutic range of 0.5 to 2 nanograms/mL. Lastly, continue to monitor your client for signs and symptoms of digoxin toxicity.
Finally, be sure to evaluate for the therapeutic response of digoxin therapy, such as a decrease in the signs and symptoms of heart failure, absence of medication side effects, as well as an improved quality of life for your client.
Alright, as a quick recap... Digoxin is a cardiac glycoside that is given for atrial arrhythmias and heart failure. Digoxin slows the heart rate, increases the force of cardiac contractions, and increases cardiac output. It has a narrow therapeutic window, 0.5 to 2 nanograms/mL, which means that small changes in blood levels can cause toxicity. Signs of toxicity include anorexia, nausea, and visual disturbances. When caring for a client receiving digoxin therapy, nursing considerations include performing a baseline assessment, closely monitoring the client’s response to the medication and for possible side effects, as well as instructing the client how to safely take the medication and recognize the signs of toxicity