Hi, welcome back to cardiovascular nursing essentials. In this module we're going to go over atrial fibrillation and valvular heart disease. These are my disclosures and our learning objectives are similar to our previous modules where we are going to talk about pathophysiology and diagnostic findings and treatment strategies in alignment with guidelines for both of these diseases. You have your required and optional readings, of course some additional resources for your reference. So let's jump in and talk about atrial fibrillation first and I'm sure many of you are aware how common this is. It is the most common cardiac arrhythmia so we're seeing an increase in prevalence every year and that's really anticipated to continue to climb in numbers and we estimate that 12.1 million people will have AFib by 2030. So it's very important that we are recognizing it and treating it and we'll talk more about that but I think it's interesting too to note that people with European descent are more likely to get AFib than African Americans so kind of opposite of hypertension and then we do see it more common in women and that's typically related to their longer lifespan. So just a couple of tidbits to look to keep in mind. Our map so again you're going to see rates are higher in the east coast so it's not as focused in the southeast but mostly on the east to mid-US. So what is atrial fibrillation? We know it's very common, the most common arrhythmia and basically what happens is as you can see instead of the SA node firing, those electrical impulses are firing from multiple places so it kind of confuses the heart so the atria are not really coordinating with the ventricles. They're very irregular and typically we see a faster response so the heart rate can be increased so it's almost like an irritable heart. It's not kind of calm and everything's flowing normal. This one's got electrical impulses firing from multiple locations causing it to be irritable and irregular. It is a supraventricular tachycardia and the most important thing is it's really an ineffective atrial contraction. So what you're going to see on EKG is a lack of P waves so you will not find P waves and the atrial activity is going to be irregular and so as you can see on the strip, sometimes it will look like normal sinus rhythm at first glance but you've really got to take a minute look at your QRS complexes. Do you see those clear P waves? Remember how we read our EKGs and go back to that if you need to review but it's very distinct and once you get good at recognizing it, you'll be able to spot it pretty quickly. There are a couple different types. So paroxysmal atrial fibrillation is one that kind of resolves on its own or it is we revert to sinus rhythm within seven days of onset with some sort of intervention and so it can kind of come and go the frequency. So it's just kind of I think of it as it kind of comes and goes. Persistent AFib is any kind of AFib that remains for more than seven days and then we we call long-standing or persistent AFib anything that is occurring more than 12 months in duration and then permanent is really kind of that decision where a patient and a clinician use shared decision making to kind of stop making those attempts to restore normal sinus rhythm. Of course that's after a long discussion weighing of risk and benefits but sometimes patients get to that point where they just don't want to continue pursuing that and then non-valvular AFib comes from the absence of rheumatic MS or any sort of artificial heart valve or repair. So what are our risk factors? Pretty common when we think about you know cardiology or cardiovascular disease so things like our high blood pressure, obesity, diabetes, heart failure, ischemic heart disease but look at these other factors that are a little bit different including our age so the longer we live the higher risk we have which is you know not too shocking. That European ancestry, things like alcohol use and smoking are also pretty good indicators or risk factors. So how do our patients present? Again sometimes it can be pretty vague and similar to other cardiovascular diseases so they may express fatigue, shortness of breath, a little bit of hypotension, symptoms that are very similar to heart failure. They may even have some chest pain and they may feel if they're in a rapid ventricular response meaning it's going over 100 beats per minute. They may even feel that as palpitations are fluttering in their chest. It is also important to note though they may not feel any symptoms so many patients with AFib don't even know they have it because they've never had any symptoms or EKG or reason to suspect otherwise. So just keep that in mind they do not always have clear signs and symptoms. So when we evaluate it we want to look at their history kind of what you know we know the the value of a strong history. If we know they have AFib what triggered it? When did it first start? What classification is it? Is it paroxysmal? Does it come and go or is it persistent meaning it's been there? How long has it lasted? If it comes and goes you know does something trigger it and how long does that last? Does something make it better? Lab work we're really looking for kind of things that are reversible so generally it can be triggered by electrolyte imbalance so we want to check a CMP. Is it something with the thyroid? Maybe they're hyper or hypothyroid and we need to get their thyroid hormones in balance. Could they be anemic? So there's several underlying reasons that a patient may go into AFib and if we can reverse that and get them back into sinus rhythm that's what we want to do. Diagnostic testing so we've talked about ambulatory monitors, echoes, stress tests, things of those nature can be expected and then risk stratification. So we know that these patients are at high risk for stroke so we want to make sure that they're appropriately anticoagulated based on their risk score. So we have talked previously about the CHADS-2 and the CHADS-VASc score so you should see documentation of those. The CHADS-VASc score is actually the better tool to risk stratify patients because it's based on the CHADS-2 score just added some extra criteria including female and vascular disease and so it does give us a little bit more information. So basically anybody that scores a one or higher should be on an anticoagulation. So I just showed this and you can reference this. I know it's a little bit hard to read but you can see over the course of five years the advances that were made through research in the guidelines. So 2019 the focus guidelines for AFib actually recommend NOACs over Coumadin or Warfarin for anticoagulation. So we're moving away from that Coumadin with the INR checks and things of that nature more to those NOACs or the newer Novell oral anticoagulants. So I just got this on here for reference for you. You can print this slide off if you want to. The other thing that I like to highlight on here that's a class one indication is weight loss. So we're you know as nurses we're heavily embedded into lifestyle modification and lifestyle modification and education and weight loss is a significant risk reducer and is strongly recommended for these patients. So how do we manage? Obviously the first thing we want to do is control that rhythm and rate and ensure that we're protecting them from stroke as much as possible. So we talk about ventricular response and that means how fast the the ventricles are beating because it's not going to be in conjunction with the atria. So atria can be going slower than the ventricles and what we really want to do is maintain a controlled rate which is a normal heart rate with that 60 to 100 rate. So if we think about a rapid ventricular response that's something that's over 100 beats per minute or there can actually be a fib with a slow ventricular response which is under 60. So really we're trying to get that target range and keep that rate in control and try to get their rhythm and to get them into sinus rhythm. Acutely what we can do is if a patient is hypotensive, symptomatic like dizziness, maybe losing consciousness, we can do a dual chamber cardioversion. So we can do that emergently or it can be scheduled or we can use anti-arrhythmics for rhythm control. Long-term strategies are a little bit more challenging because you really have to look at is it a rate control or a rhythm control and that depends on each patient and what causes their afib. So it has to consider that patient's clinical situation. Again we're looking for long-term stroke prevention, maintaining that controlled rate and making sure that their hemodynamics are stable so that we want to make sure they're maintaining a good solid blood pressure. And again just harping on this because it's so important is that anti-coagulation for stroke risk reduction. Number one in long-term management is risk factor modification. So I can't stress it enough when we do things right and we get our body kind of in a in a happy state where blood pressure is good, blood glucose is good, weight is is where it's supposed to be, your sleep patterns are good and apnea is controlled, we can see a 50 percent reduction in arrhythmia. So that should be number one step is those lifestyle modifications. For rate control, we can use medication. So beta blockers can be your first line of defense. Specific calcium channel blockers, specifically diltiazem and verapamil are indicated and digoxin can be used if those others are not working. Looking at rhythm control, there are different things that we consider. So is the patient not responding to medications? Are they having symptoms? Are they on an anti-arrhythmic medication? You know those really aren't necessarily good for long term due to adverse effects and side effects and we may want to consider ablation. So when we're looking at anti-arrhythmics, these are not to be given lightly. So these do work kind of on a cellular level and they really impact those intracellular ions that are responsible for depolarization and repolarization. So they're really altering those sodium and potassium channels in the atrial cells. So there's a really fine line between these medications being therapeutic and detrimental. So these patients do require close monitoring. We say every six months, but it's usually much closer when a patient is initiated. We want to make sure we're checking EKGs, blood work, especially renal and liver functions to make sure that those are not being impacted by these medications. They can also cause EKG changes, specifically prolonged QTs, PR intervals, things of that nature. So we want to make sure that those are not lengthening because those can all have detrimental effects as well. So again, these are some considerations based on patient specific. So we want to be very cautious and just know all the side effects that these medications carry, because again, they can be detrimental in some cases. So you can see some of them can cause renal failure, liver failure, left ventricular hypertrophy. So they do require great care to make sure they're not at risk of developing further side effects or issues when they're on these medications. If the medications aren't working, we do have the option for ablation, which basically it takes heat and kind of cuts those pathways, those electric pathways. So it creates these little lesions that disrupt the pathway. So the electricity has to go back and follow the right pathway. So indications you can see, obviously symptomatic SVTs, other issues like atrial flutter, atrial fib, things like that. And we want to make sure that it's not just about the treatment and the ablation, but we're making sure that they are improving in their symptomatology post-procedure. Absolute contraindications, we do not want to do this in anybody that has a known atrial thrombus or a mobile LV thrombus. Mechanical heart valves, we generally do not want to go in and cross those with the catheters. And then we don't typically do these in pregnancy either. So success rates are actually as high as 80% for patients with paroxysmal a-fib without structural heart. And then sometimes for other forms of SVT, they can be 90% successful. So the lesions are very, very small. Again, it just helps redirect that electrical pathway. And this is just a picture here. I like this because we know the SA node is where our our internal conduction system starts. And so as you can see within a person that has a-fib, it's very chaotic in there. So we're trying to get rid of all these additional pathways and keep it confined to one. So it's that electrical isolation of the pulmonary veins and really targeting with radiofrequency ablation, those specific different focal impulses. It can be paired with a medication over a period of time, but obviously the whole goal is to reverse the a-fib and get people off of those medications. So as we mentioned, we do see that paroxysmal ablation is more successful in those that then persist in a-fib. And it's best to partner this not just with the ablation and thinking everything can go back to normal, but we want to make sure that they have those risk factor modifications in place to maintain that sinus rhythm. So often patients will think, oh, it's fixed. We see this in other areas like a PCI after a heart attack, and it's, no, you still have to do the work and the modifications to your lifestyle to make sure that you maintain a healthy heart. So let's talk about that anticoagulation because as you can see, overall risk of stroke in patients with a-fib is about five percent a year. So that's, you know, that may seem small, but that's a large enough number that, you know, obviously we want to prevent as many as possible. There are certain risk factors that we do have to adjust for, including age, any sort of prior stroke, LV dysfunction, or other comorbidities. So we just need to evaluate that stroke risk and evaluate the bleeding risk. So we have tools that can help us do that. We've talked about the CHADS-VASC, the CHADS-2 score, which evaluates stroke risk for anticoagulation. And then for bleeding risk, that's the HASBLED score. So become familiar with those so you know what to expect. And then your providers will decide on anticoagulation plan and set up a monitoring plan for their therapy. There are certain strategies that some may take based on patient conditions. So someone with a high risk of GI bleed may be better on Eliquis. So these are just some considerations and I just urge you to get familiar with it as they're very helpful just to know what to expect for the different anticoagulation medications. For those that cannot be on the anticoagulants there is the option to do aspirin but it is far less effective in reducing the risk of stroke when compared to Coumadin. So it's a consideration but it does not perform anywhere as close to Coumadin or the NOACs. So dual antiplatelet therapy and oral anticoagulation have similar bleeding risks so some may prescribe aspirin and Plavix but again it may be a little bit more effective than aspirin alone but it's still not very effective in preventing stroke and it has almost twice the bleeding rate. So this is not something that we want to offer routinely. Obviously patients with GI bleed and other issues we would consider this but it should not be a standard of care. If somebody cannot be on an anticoagulation medication at all there is the option to do a left atrial appendage or LAA occlusion procedure and that's for those people who are not able to take anticoagulation with contraindications because as we know those who cannot take those medications are at an increased risk of stroke at 40 percent. So what we found through research in trials is that 90 percent of cardiac emboli originate in the left atrial appendage and I'll show you where that is because it's not something that we typically see on a normal heart image but that's where most of them develop so we're really targeting to kind of limit or keep any clots in that appendage. Patients are on an anticoagulant after the procedure with the goal of getting them off of that. So it is an alternative to that long-term anticoagulation and so here is you can see this is the actual device or watchman device. It looks almost like a little parachute or maybe an octopus. You can see the left atria off of over here off of the left atria is this extra appendage so you could imagine that's where it's kind of really a nice atmosphere for clots to develop and then they can move out into the left atria and then to the rest of the body. So what we do is insert this device that kind of stops blood flow keeps those clots if there are any in there in the appendage and prevents them from moving out of there and eventually that appendage will actually kind of shrink in size. So the goal is to try to minimize any risk of clot formation without the patient being able to be on a anticoagulant. All right and with that we're gonna head over and talk about valvular heart disease. It is another common cardiovascular disease that we see in about two and a half percent of Americans. Rheumatic heart disease is the most common disease that affects the mitral or aortic valve so that is pretty common maybe not so much in the United States but worldwide it can cause a lot of issue with those two valves. So the most common aortic valve disease is associated with the highest percentage of death by a valvular heart disease so you can see it's this 61 percent so valvular heart disease in the aorta is most prevalent. So this is just a refresher of our heart valves and how that blood flows. So remember on the right side we've got that tricuspid valve which is three leafs. We have the mitral valve on the left side which is a bicuspid or two leaf valve and then we also have the pulmonary valve going from the right ventricle into the pulmonary aorta and then we have the aortic valve going from the left ventricle out to the body. So just remembering what where in the heart the valve is will help you in terms of symptomatology when we get to that in a bit. This graphic I like because it kind of is a nice visualization of what a normal valve should look like versus when there's either prolapse like you can see here this prolapse valve is where the the valves don't close completely so you have a little bit of a leak or a gap for blood to blood and fluid to move through versus this is a aortic valve with stenosis you can see where normally it would be nice and open this one is calcified it's stiff so it's not able to open fully and that impedes blood flow. So valvular heart disease means that the valves are diseased and they may not open or close fully so it is one or the other and as we mentioned the aortic valve is the most commonly affected valve and just think of it as this regurgitation is leaky valve where stenosis is more of a stiff valve so if you see regurgitation that means those leaflets are not closing all the way so there there's gaps in there so blood is still continued to pass through if it's stenosed or stiffened then that valve is not able to open fully which impedes that blood flow moving forward. Okay so causes as we mentioned rheumatic heart disease is common and basically what happens is it's after an infection usually strep and it causes scarring of those valves so we do see this commonly not so much in the U.S. but worldwide it is a problem. Infective endocarditis can really cause a it's an infection of the blood and it can settle into those heart valves and cause issues in those leaflets there. Congenital heart valve disease maybe maybe the tricuspid valve is missing a leaflet or something so it's it's basically a deformation of the valve and then other heart other types of heart disease can cause valve valve disorders so think hypertension, heart failure, atherosclerosis, things of that nature and then other things like autoimmune diseases, exposure to high dose radiation so maybe cancer patients that are getting high dose radiation therapy for treatment and then just the aging process can put us at risk for basic kind of wear and tear if you will. So diagnosis again clinical presentation is a little bit vague just how several cardiovascular diseases present so they they too may have fatigue, shortness of breath, dizziness. Some things you may notice are weight gain, dyspnea on exertion so similar to things you would expect with heart failure and and it's kind of hard to differentiate because the symptoms can come on quickly or they may develop over a long time so if the disease progression is slow obviously those symptoms aren't really going to present or be obvious until the disease is is pretty advanced. So the number one diagnostic tool is actually listening and hearing for a murmur so noting the location the sound and the rhythm can really give a lot of insight into what type of murmur is it is if it's a mitral valve regurg or aortic stenosis so once you identify or the provider identifies a murmur generally we'll move forward with other testing like an echo trans thoracic or transesophageal EKGs, cardiac cath, chest x-ray or CT depending on how that patient is presenting and then treatment is really based on the severity so it's really focused at symptom management. Again a lot of these patients are going to present like they're in heart failure or volume overload so you can expect those similar presentation and then there are surgical options depending on the valve that's involved and what's causing that. So let's look at a couple of these specific disorders because they're all very common and just to be familiar with them I want you to have a good understanding. So our mitral stenosis remember we said stenosis was stiff so you can see the mitral valve on that left side of the heart kind of the leaflets are thick and it's really more of a funnel shape so it's impeding the blood flow to the from the left atrium to the left ventricle. So our symptoms typically start as kind of a mild dyspnea on exertion and then as the disease or progresses patients are going to have more severe symptoms like that PND in the middle of the night, tire during the day, they may even have atrial fibrillation. So in managing these patients we're really managing those symptoms like we would with heart failure at alleviating some of those fluid volume issues and we want to make sure of course if they have AFib that we're preventing complications of any embolization. Okay mitral regurg on the other hand remember is that leaky valve so instead of the blood moving forward because the mitral valve doesn't close all the way you're going to have blood leaking back into that left atrium. So symptoms again they can be rapid it just depends on the fluid status of that patient or they can be kind of gradual. They are associated with LV failure and new onset AFib so you want to you know kind of when we have patients that are diagnosed with new LVH or LV failure or new AFib we do want to assess their valves and they can also have chest pain associated with this. So with this kind of management again symptom management but what we're trying to do is promote that blood flow forward through the heart. So symptom management including diuretics and then if they do have LV failure with an EF of less than 40 percent obviously we want to follow those guideline directed medical therapy prescriptions that we've talked about in the previous modules. Tricuspid regurgitation very similar except on the right side of the heart. So these patients are going to kind of present like they're in right-sided heart failure like we used to say so they may have swelling in the abdomen, liver congestion. They're generally kind of quick in onset once they do occur so you may not see it until again it's progressed and again management is just focused on fluid volume through diuretics to relieve that congestion and MRAs or aldosterone as an example may actually help with some of that liver congestion so it's common to see patients on those. Aortic stenosis so this is that stiff valve and does not close so this disease is actually pretty typically it's a gradual progression so we're not going to see as much symptoms until it's closer to advanced stage. This is something that again very common and on you can kind of see on this image as you will see the little calcifications that have formed on the leaflets and that is what causes those valves to be stiff. This is where we get that classic mid-systolic murmur so maybe heard that may be the first detection of it is through auscultation and our management again depends on the severity so managing any heart failure symptoms, fluid overload and then these patients would be someone depending on their severity that we may consider for valve repair or replacement. Aortic regurg again so instead of moving forward through the aorta out to the body blood is going to go backwards into the left ventricle so this one is very much presents as a heart failure patient, lots of fatigue, volume overload so management again really depends on the progression and the stage and we want to make sure that we're managing those symptoms. These patients are the ones that we're looking at to do the valve repair or replacement so we really want to be aggressive in managing their volume status and trying to get that intervention if they're not candidates or willing to get their valve repaired or replaced we would do symptom management through medications. All right and this is just a kind of a graphic that shows the risk in deciding do we do surgical or TAVR so SAVR versus TAVR and some considerations that patients have when making this decision and we we do see TAVR you know it has grown rapidly over the past decade and it's really become kind of the recommended therapy for patients with higher surgical risk profiles is how it started but we are seeing more patients that are undergoing TAVR so it's generally through the transfemoral artery and these are two of our examples of TAVRs and basically it's a kind of a minimally invasive procedure that's done in the cath lab and it can be done without stopping the heart. Patients can even be under conscious sedation and not have to use general anesthesia and the device is just determined the size is determined based on the anatomy and the hospital stay is pretty minimal so up to three days but sometimes even less than that depending on how well the patient recovers and we do see you know a lot of programs that are moving from SAVR to TAVR and it's really likely to become the standard of care in our aortic stenosis population. This is just that graphic where we take that the the implanting or the procedural physician will access through the transfemoral artery and they will go through across the septum and deploy the valve right there over the diseased valve. Something I want to highlight that's a class one recommendation in the guidelines is this heart team which is a collaborative approach so it's a multidisciplinary team specifically for TAVR patients so under structural heart programs and I'm so excited to see that this is a class one recommendation that includes this team of valuable care members around the patient to develop the best plan or therapy plan for this patient so we really are leveraging the expertise of cardiologists, cardiac surgeons, nurses, imaging, other anesthesia, other specialties to create the best plan based on the patient's medical condition and their valve disease and basically everyone will present and discuss decide on a treatment plan that everybody agrees upon to present to the patient and make the decision together. Lastly, I wanted to just go over the transcatheter mitral valve repair which is becoming more common to the mitra clip. This is for patients with chronic MR who are symptomatic so that's your NYHA class three to four despite being on optimal medical therapy so they may be considered inoperable so this is actually the only FDA approved device that is an option to treat these patients so this is something to consider. It's really interesting there are some other devices that they don't have FDA approval. These trials on the mitra clip specifically did demonstrate a reduction of symptoms in MR patients so they had improved heart failure symptoms and they actually saw reverse remodeling of the left ventricle so I think it's just kind of a fascinating time and we're going to see more and more therapies and treatment options for our patients who cannot undergo the traditional therapies and eventually we will see moving to some of these more non-invasive or minimally invasive therapies for these complex diseases. I hope you've enjoyed this module. Please feel free to reach out with any questions at academy at medaxium.com.

Atrial Fibrillation

Valvular Heart Disease

Pathophysiology

Diagnosis

Treatment

Risk Factors

Minimally Invasive