- Cardiac Glycoside
- Heart failure
- Atrial flutter
- Atrial fibrillation
- How they work
- Block sodium and potassium channels in the heart
- Causing an increase in sodium and calcium ions in cardiac cells.
- Increases force of contractions
- Increases vagal activity in the heart
- Decreases heart rate
- Cardiac Glycosides have a narrow therapeutic window.
- Digoxin is the most commonly prescribed Cardiac Glycoside.
- Monitor for side effects
- Loss of appetite
- Monitor for signs of toxicity (digitalis toxicity)
- Blurred vision
- Yellow vision or Halo vision
- Always check APICAL PULSE for 1 full minute prior to administration
- HR < 60 bpm – HOLD MEDICATION, and contact provider
- Always check APICAL PULSE for 1 full minute prior to administration
- Monitor potassium levels closely
- Hypokalemia and hyperkalemia should be reported to provider immediately
- Low potassium levels = increased risk for toxicity
- High potassium levels = decrease effectiveness of medication
- AV block
- Wolff-Parkinson-White Syndrome
- Impaired renal function
- Monitor drug levels closely due to narrow therapeutic window
- Therapeutic Level – 0.8-2mg/ml
- Cardiac Glycosides may be prescribed to help with perfusion in patients who have heart failure and atrial arrhythmias.
- Patients should be educated on signs of toxicity and instructed to conact their provider immediately if toxicity is suspected.
So, in this video, we gonna talk about the cardiac glycoside. In this slide, I just want to put some interesting thing about this cardiac glycoside. These drugs, human being has been using these drugs for like, last 200 years or about, maybe 150 years, I guess. Because they were first used in 1875. They are derived from foxglove plant, this is name of the plant that they were extracted these drugs from in old days. Now, they were used in dropsy in 1875, started using in dropsy. What is dropsy? Dropsy is an edema. So, whenever the patient have edema, they were giving this extract of the plant and it was really helping in treating these edemas. Now, actually, it wasn’t treating the edema. These drugs treating heart failure. Now, one of the signs and symptoms of heart failure is edema. So, they were giving these drugs to treat this dropsy, means edema, actually it was treating the heart failure. And they started using these drugs in 1875. So, it’s kinda interesting stuff I just want to put in here.
So, let’s talk about the mechanism of action of these drugs. So, there are only 3 drugs in this categories, been used nowadays is Digoxin, Digitoxin, Quabain. The mostly, you may have hear the term is the Digoxin, often used for heart failure, and some other cardiac medication which will occur in the next slides. But, the first mechanism of action is increase the concentration of sodium and calcium ions in cardiac cells. And that will increase the force of contraction. And it also increase the vagal activity to the heart which is increase in parasympathetic nervous system flow to the heart which will decrease the rate of contraction, that means the heart rate. Now, this one is, the second one is easy to understand, so, like it increase the parasympathetic system, it’s gonna decrease the heart rate.
The first one we’ll talk about it in detail, and this mechanism of action is optional to understand ‘cause I’m just explaining, so, it makes more sense. So, this is a cardiac cell wall. Now, there are many, let’s draw it right here. Now, there are two phases of cardiac cycle. The first one is called Depolarization, that means contraction when the heart squeezes. The second one is Repolarization, when the ventricle relaxes. Now, in order to do a contraction and relaxation, ion movement across the cardiac cells plays a really really important part. So, let’s think this is a cardiac cell wall. And their sodium channels already in the cardiac cell. It’s called sodium leaking channels. What does that mean? There is a slight amount of sodium is always coming into the cardiac cell. So, during the depolarization, what happens, this sodium comes into the cell slowly, slowly and it builds up into this cardiac cell. Let’s make a cell like kinda square. Now, when there’s enough concentration of sodium in the cardiac cell, what happens is, there’s another channel, it’s called sodium calcium channel. Now, this channel does not require any kind of energy. When there’s enough concentration of sodium in the cardiac cell, it opens this channel and increase the flow of sodium and calcium into the cardiac cell. When there is a enough concentration, let’s say, enough concentration of sodium and calcium in the cardiac cell, it will contract, cause the depolarization and contraction. Now, in the repolarization, what happens, there’s another channel, not that too many channels, I know it’s kinda really like a little bit confusing but if you pay attention really close, it will make more sense. There’s a channel, it’s called the sodium potassium channel. Now, during the repolarization, this channel will close and this channel will open. And what it does, it actually throws out that sodium that came in to the cell during depolarization and brings in the potassium. So, it throws out this sodium out and it brings the potassium in and balances out the ion concentration across the cell wall. This medication, what they do, is blocks this pump. So, cardiac glycoside blocks this sodium channel, sodium potassium channel. That means, sodium won’t be going out easily and potassium won’t be coming in easily. That means the increased concentration of sodium will stay in the cells. That means, this channel will bring more calcium. More sodium, more calcium will cause increased force of contraction. This one is a little bit complicated but this is how the cardiac glycoside works. As a nurse, you don’t really have to know in detail this much but keep in mind that this sodium, calcium and potassium ions plays a really important role in this cardiac glycoside mechanism of action. ‘Cause whenever we’ll be talking about the side effects, we’ll be talking about the ion concentration as well. Like a high potassium concentration will do what to cardiac glycoside or how low potassium concentration will do what to this cardiac glycoside. So, that’s the mechanism of action.
Let’s talk about what disease condition we use this. Now, since we know this medication increases the force of contraction, it can be used in the heart failure. ‘Cause a heart failure is basically a pump failure and this medication will help heart to pump really effectively in order to get the blood out of the heart into the systemic circulation. This one also, since we know this medication also increases the parasympathetic nervous system or parasympathetic nervous outflow to the heart and decreases the heart rate, this medication can be used in atrial flutter, with RVR and atrial fibrillation with RVR in order to control the rate because they gonna decrease the heart rate. So, the main use is in heart failure and to control rate in atrial flutter and atrial fibrillation.
Side effect. Very important part of this medication and often tested in NCLEX. This medication can cause nausea, vomiting and diarrhea. Loss of appetite (Anorexia). Headache. It can cause anxiety. It will cause the blurred vision and/or yellowish vision also called as a ‘Halo vision.’ This is a really really important side effects to know for this cardiac glycoside like digoxin and often often tested in the NCLEX. Like, what is the first signs and symptoms of digitalis toxicity. And they’ll have several option. The first one is the blurred vision or yellowish vision and anorexia is the first signs and symptoms of the digitalis toxicity, that is really really important. And it can cause confusion and hallucinations as well. So yeah, this one is really important to remember for NCLEX.
Now, we know this whole mechanism of action of this cardiac glycosides is based on sodium, calcium and potassium. So, these medications are contraindicated with the hypokalemia. The normal concentration of potassium is 3.5 to 5.2. Now, if a patient has a low potassium concentration or low potassium level, there’s a high chance that they’ll get toxicity of these compounds. So, hypokalemia causes the digitalis toxicity and this is often tested question in NCLEX as well. They’ll have like, okay, so which patients, the patients on Digoxin, which level you should report to the physician? And there will be several values and options and one of them would be potassium 2.4 which is really really low because the normal is 3.5 to 5.2. And, it can cause the digitalis toxicity. Hyperkalemia, so, this is opposite to hypokalemia like it decreases the effectiveness of the medications. So, like if you have a high concentration of the potassium, this medication will not be able to work. If they have a AV block, Wolff-Parkinson-White syndrome or impaired renal functions. These medications are contraindicated.
And, the another thing to remember about these drugs, they have a narrow safety margin, that means, their therapeutic level range is really really narrow. You can refer over therapeutic level videos in order to know more about these range. And, you need to, they do the, like if the patient is on the hospital, they do the digoxin level pretty much every morning in order to make sure this patient receiving the right dose of these medications. And also, another thing I need to turn here is, as a nurse, before you give this medication, always always check heart rate. If patient’s heart rate is below 60, do not give this medication and notify physician. So, that’s the important thing to remember for NCLEX as well. Check pulse before giving this medication. It’s not like radial pulse, you want to check the apical pulse, the real real heart rate. So, make sure you do that one before giving this medication to any patient.
So, that was it about the cardiac glycoside. If you have any questions, you can e-mail us and ask us. Thanks for watching this video. Thank you.