Atrial Fibrillation
Atrial Fibrillation
Atrial Fibrillation (also called a-fib) is an irregular heartbeat that originates in the atria. It is the most common arrhythmia. This one is very important for you to know. While this module is long, it is crucial for you as a cardiac nurse to understand atrial fibrillation well.
Important Pathophysiology
Normally the electrical pathway for a cardiac contraction starts at the sinoatrial (SA) node at the top of the right atrial chamber. The current then runs down the lining in the atria to the atrioventricular (AV) node. In a-fib, the current is disrupted while traveling to the AV node. This can be due to an intrinsic pathway disturbance creating a circular loop of electrical activity, rogue cardiac myocytes that are not following the rules, electrolyte imbalances, toxic levels of substances like alcohol, or other reasons. The confusion of the electrical impulses causes the atrial myocytes to quiver (or fibrillate) and never contract completely. It’s very chaotic, as you will note in the below photo.
The waves of an ECG start with the P wave. The P wave occurs when the atria contract. Since the atria are not contracting in a-fib, there will not be a P wave. However, there are electrical signals that will make it through to the atrioventricular (AV) node and cause a contraction of the ventricles (the QRS complex).
This is because the heart is smart! It’s basically saying, “Whoa whoa whoa, now, atria! I don’t need all that jazz. I just need about 40–60 beats per minute. I’ll let a few of these crazy beats come through, but not all of that!”
Now, look back up at that photo. See how even though the atria in the heart on the right have erratic impulses, the ventricles still have a smooth conduction?
So, without any regular signal making it to the AV node, the AV node will create its own signal to ensure a contraction of the ventricles. The heart won’t just quit simply because the atria are acting crazier than a nurse without their pre-shift coffee!
The AV node intrinsically runs at forty to sixty beats per minute. However, some of the signals from the chaos upstairs (the atria) will make it to the AV node and send off a ventricular contraction. These signals are not at a regular interval, making the QRS complex occur irregularly on top of the AV node signals. Therefore, your a-fib heart rate is irregular.
The signals traveling down the atrial myocytes can be rapid fire as well. If the signal is caught in a loop, it could potentially be making contact with the AV node every time and causing the ventricles to contract at a rapid pace. If this is occurring, it is called rapid ventricular response (RVR). A patient is considered to have RVR if the heart rate is above 100 bpm. Patients with RVR can have their a-fib referred to as uncontrolled and if the rate is under 100 bpm (without RVR) it is considered controlled.
When you’re on the unit, most telemetry alarms are pre-set to go off if the heart rate gets above 130 bpm. However, if you’ve got someone who’s in a-fib and their heart rate is 120, that’s concerning. Just because the alarm isn’t going off doesn’t mean a problem isn’t occurring. A sudden flip into a-fib with RVR typically encompasses a pretty high heart rate—like 150 or above. This is definitely a drop everything and call the physician kind of thing. This isn’t a code, but it is an urgent situation. More on this shortly.
Treatment
It is important to know that about half of the cases of a-fib will resolve on their own (also called paroxysmal a-fib). But for the other half that do not resolve, treatment is vital to restore the heart to normal sinus rhythm and prevent any adverse outcomes such as a stroke or MI. Patients are at risk of forming a blood clot because the quivering in the atria creates a pooling of the blood where it is unable to flow normally and sometimes forms a clot. Also, any patient who has had cardiac surgery is at an increased risk for a-fib. This is because we’ve gone in there and messed with their heart (or as Dr. Julius Hibbert from The Simpsons says: “We tinkered with your ticker!”). Any time you do that, you’re increasing the risk for a-fib. The more you do to the heart, the higher the risk. Remember that a patient with a one-vessel CABG has a much lower risk for this occurring than someone who had a multiple vessel CABG and AVR/MVR at the same time.
There are two major concerns with a-fib. The first is a blood clot that gets sent through the vasculature and lodged into an artery—possibly in the brain, heart, or lungs. The second is that the electrical chaos turns into a more serious arrhythmia like v-tach, v-fib, or asystole. Both outcomes are concerning and reinforces why treatment is vital for our patients.
Classifications
Acute a-fib
- When the onset of a-fib has occurred less than forty-eight hours prior
Paroxysmal a-fib
- When the a-fib resolves on its own without any intervention
Persistent a-fib
- When the a-fib lasts longer than forty-eight hours
Permanent a-fib
- When all treatments have failed, and the patient still has a-fib[AK1]
New Onset (without rapid ventricular response)
Patients who have never experienced a-fib may not know they’re having an arrhythmia, especially if they are not having an RVR. They may feel totally fine, and we only know that it’s happened because we’ve got a cardiac monitor on them or obtained an ECG. However, most patients will have symptoms and not feel like they normally do. Not surprising, right? Their heart isn’t contracting effectively.
If a patient is in a new a-fib, this needs to be brought to the attention of the physician or advanced practice provider. Even if it is a-fib without RVR.
Okay, here’s where it can get a little confusing. If we physically see the patient flip into a-fib, we can look to convert them back to normal sinus rhythm with medications or a cardioversion. This is because we know exactly how long they’ve been in it. However, if we get an ECG or look at the cardiac monitor and note a-fib but are not sure when it started, we’ll look to thin their blood first, then convert. This is because if they’ve been in a-fib (even without RVR) for days, weeks, or months, they may have blood already pooling in their atria and a clot may be there already. If we suddenly put them into sinus rhythm and they now have these good, smooth, full atrial contractions, we’ll immediately send that clot flying into their lungs.
Medication options used for treating a-fib without RVR include:
Amiodarone
For hemodynamically stable a-fib, this is the first line medication. Studies have shown that it has the highest conversion rate from a-fib to sinus rhythm. It most likely would not be a permanent medication for the patient.
Flecainide
Although this medication is successful in restoring normal sinus rhythm, it is absolutely contraindicated in patients who have hearts with ischemia. Ischemia in the heart with this medication can cause lethal arrhythmias.
Propafenone
Just like with flecainide, propafenone is absolutely contraindicated in patients who have hearts with ischemia. Ischemia in the heart with this medication can cause lethal arrhythmias. If the patient isn’t having any ischemia, this medication is successful at restoring sinus rhythm.
Quinidine
This medication is currently controversial. It was used as a first-line medication, but a study showed increased adverse effects, such as a prolonged QTC, Torsades de Pointes, and increased mortality. But recently, newer studies have been questioning this older study and finding a higher conversion rate with Quinidine without the adverse side effects. As of right now, this is still considered a third line medication for conversion of a-fib to normal sinus rhythm.
Sotalol
Effective in converting a-fib to sinus rhythm, however, studies have shown that amiodarone maintains sinus rhythm for a much longer time than sotalol. Because of this, amiodarone is more commonly used.
Digoxin
This medication is thought to convert the patient to normal sinus rhythm, control the heart rate, and prevent recurrence of a-fib. It is still the #1 prescribed medication for this, however, recent studies are questioning that and have not found that digoxin is helpful in the conversion of a-fib.
New Onset With Rapid Ventricular Response
Patients with a-fib with rapid ventricular response (RVR) are more likely to be symptomatic.
Symptoms of a-fib with RVR include:
- palpitations
- racing heartbeat
- feeling like their heart is beating out of their chest
- fluttering of their heart
- dizziness
- chest pain
- fatigue
- altered mental status (confusion)
- syncope, or feeling like they’re going to pass out
- shortness of breath
When a patient is in RVR, it’s important that they are converted to normal sinus rhythm more quickly than those without RVR. This is because the heart can only sustain beating that fast for so long before it gives out. Plus, with that rapid beating, the ventricles are not filling enough, decreasing the CO. Unlike with patients who have a controlled rate, oral medications will not work fast enough, so IV medications will be given.
Please read the following treatment pathways with a grain of salt. You’re probably working with various cardiologists, cardiovascular surgeons, cardiothoracic surgeons, intensivists, etc. Their treatment course for this situation may differ from what we mention below. Medication and intervention selection is based upon many things, and if you’re working in the cardiac surgery world, the surgeon may want to approach it differently.
The most common medication given in unstable a-fib RVR is adenosine.
Adenosine works in a few ways. First, it binds to purinergic receptors in the vascular smooth muscle cells, relaxing the cells, allowing them to slow down the heart rate. Second, it binds to the Alpha-1 receptors in the sinoatrial node, inhibiting electrical current, which slows the heart rate down. Third, it binds to the nerve terminals in the atrioventricular node, decreasing the release of norepinephrine and reducing electrical activity. It should be noted that sometimes the binding to nerve terminals in the AV node can cause AV block.
The half-life of adenosine is less than ten seconds. If administered correctly, it will slow the heart’s electrical chaos down enough to reset it back to normal sinus rhythm. It’s pretty crazy to see it administered. You literally see the heart stop—flatline—then pick back up.
Having such a short half-life means administering adenosine correctly is super important. The IV needs to be as close to the heart as possible (so preferably not a small gauge hand IV—think large bore in the AC). Also, the medication needs to be given rapidly. The best way to do this is with a stopcock linking the adenosine in one syringe with a 10 mL flush. If possible, also try to give this medication right at the hub of the IV rather than through a J-loop connector.
You will start with a dose of 6 mg. If 6 mg of adenosine doesn’t work, an equal second dose is indicated. If it still doesn’t work, 12 mg of adenosine is then given. Make sure the patient is hooked up to the cardiac monitor, twelve-lead ECG, and defibrillator (it’s a messy number of stickers and wires). The physician or advanced practice provider will be at the bedside directing you on when to administer the medications so wait for their verbal order to give the medication.
Hit the rhythm printout button on the ECG to capture the conversion and make sure to have an actual twelve-lead ECG of the patient in normal sinus rhythm. You shouldn’t be doing this alone your first time. Again, this isn’t a code, per se, but an urgent situation. Your facility may require the code nurse/rapid response nurse/RRT nurse to be present for this procedure.
Another commonly used medication is IV amiodarone. This medication will be covered in detail in the medication module. When giving amiodarone for a-fib with RVR, you will give a bolus of the medication (a larger dose) along with a drip rate that you will titrate to the heart rate target. The amount of medication and the target heart rate will be decided by a physician or advanced practice provider and the pharmacist.
If the patient is not responding to the medications, the next step is to cardiovert them. This is done with the defibrillator and will have the same set up as adenosine with the cardiac monitor, twelve-lead ECG and defibrillator pads. This will be covered in more depth in the ACLS module.
Also, depending on timing, location, and situation, your patient may be brought down to a procedural area to have a cardioversion completed by a cardiologist, and not have it done at the bedside. This completely depends on the situation, but some of us have seen it work out that way where they were able to facilitate this quickly.
Chronic Controlled A-fib
Many patients live with a controlled-rate a-fib for the rest of their lives. These patients are at a higher risk for blood clots, so it’s important they are anticoagulated. The type of anticoagulation depends on quite a few things; however, many patients are placed on Coumadin. Education and follow-up is crucial with these patients; we need to ensure they’re being compliant with their medication and getting their INR checked regularly.
In addition to anticoagulation, they may need to be on medication to keep their heart rate below 100 and ensure their heart is contracting as effectively as possible. Depending on the entire clinical picture, they may be started on an ACE, ARB, calcium channel blocker, or beta blocker. These meds are extremely important as well.
One thing to watch out for in these patients is the development of CHF. Because the heart isn’t contracting effectively, fluid often accumulates, and the heart simply can’t keep up. They may need to be started on a regular diuretic.
It’s not uncommon for a patient admitted to the hospital with a history of a-fib to be on the following home meds: Coumadin, Lasix, Metoprolol, and potassium.
Chronic Uncontrolled A-fib
When medications and cardioversion do not work, we’ve got to look at a more invasive intervention. The next options include an implantable pacemaker, an ablation, or a Maze procedure.
Pacemakers will be covered more thoroughly in the pacemaker module.
An ablation is a procedure that involves destroying the cells in the atria that are causing irregular electrical impulses. The surgeon inserts a catheter that uses extreme cold (freezing) or extreme heat (burning), targeting specific cells, causing them to die. This is done in the hospital, and the patient may stay a day or so afterward to monitor their response and rhythm. However, an ablation could be unsuccessful also. Naturally, patients can only have so many ablations as well, as you can’t freeze or burn off all your myocytes.
The Maze procedure is performed during an open-heart surgery. The surgeon creates a “maze” pattern in the atria, disrupting the abnormal electrical current.