117: Pericarditis vs Myocardial Infarction

she had diffuse ST segment elevation in multiple leads. I was so expecting a perfectly normal EKG. So I reached out to my lead placement to make sure I hadn't somehow created a STEMI looking EKG by mixing the leads up. And in fact, I had done the EKG correctly. So I asked, have you ever had any problems with your heart or do heart problems running your family? She said, no. So I excused myself like a ghost in the EKG to the physician. I approached the doctor with an EKG in hand saying, am I seeing what I think I'm seeing? This is the EKG from a 20-year-old. [MUSIC PLAYING] Hey there. I'm your host, Sarah Lorenzini, a rapid response nurse and educator who loves telling stories to teach critical thinking. This podcast is for nurses who want the knowledge, skills, and confidence to respond to any emergency. With almost 20 years of experience in the ER and critical care nursing and a master's degree in nursing education, I have a lot of stories to share. And I love to nerd out and break down the path of physiology, pharmacology, and nurses' role in emergencies. Stories bring learning to life. It is way easier to learn from and remember the stories that my colleagues and mentors have told me than anything I've read in a textbook. And that is why I made this podcast. Every episode is packed full of exactly what you need to know to handle whatever crisis that could arise on your shift. It's one thing to get the right answer on the test, but knowing how to detect when your patient is declining and what to do when your patient is crashing is what will make or break your day and might just save your patient's life. Welcome back to the Rapper's sponsor and podcast. Today we're going to be talking about a not-so-common diagnosis pericarditis. We will cover how it presents the diagnostic criteria, some common, more dangerous diagnosis that you don't want to fall asleep or pericarditis, and the nurses' role in recognizing and treating pericarditis. So let's first dive into a case. I was working nights in the ER as a new-ish grad and brought a young woman in her 20s from the waiting room back to my room. She was complaining of chest pain. Now as an ER nurse, I think the most common chief complaints that we see are chest pain, abdominal pain, headache, and tornness of breath. So now this is a, we see a lot of chest pain. And the bulk of it is not from a myocardial infarction, but we pretty much assume all chest pain is from a acute coronary syndrome until proven otherwise. So I bring this from him back and I started placing the leads on to get a 12 lead EKG while I was getting this toy from her. So she'd been sick for a few weeks prior with an upper respiratory infection and had gotten better, but her chest pain had gotten progressively worse over the past few days. I asked all the typical PQRST pain assessment questions, but I usually go backwards. It just makes more sense in my mind. That way it feels more conversational and less robotic, in my opinion. In case you don't remember, the PQRST acronym for Nursing School P is what provokes or palliates the pain. Q is what is the quality of the pain like to scribe it? R is for region or radiation? Like where is the pain? S is for severity. So how bad is it? You can use the pain scale, if you'd like. And then T is for time. Like when did it start and how long does it last? So in reverse order, I asked her time, when did it start? She said a few days ago, but got really bad tonight. Severity. I asked her to rate it on a scale from zero to 10, and she said sometimes it's a 10. Sometimes it's a three or four, but it's definitely painful enough to keep her from sleeping. Region, I asked, where does it hurt the most? Can you point to it? And does the pain radiate anywhere? She responded and pointed towards the center for chest and into our shoulder neck area. And I pointed to her left center chest, and then to her trapezius and shoulder. And she confirmed, yes, that's where her's the most. Quality, so I asked her to describe the pain. Was it sharp, dull, throbbing, aching, stabbing pressure? She said, all of the above. And then I asked the most valuable question that should have clued me in, that this was paracarditis. But it didn't, because I was new, and I didn't know as much as I know now. So I asked her, like I ask every patient, does anything make the pain feel better or worse? And she said, I absolutely cannot lay down. I have to set up laying down is excruciating. So by that time, I had captured the EKG, and she had diffuse ST segment elevation in multiple leads. So I asked, have you ever had any problems with your heart, or do heart problems running your family? She said, no, so I excused myself, like I go show the EKG to the physician. I approached the doctor with the EKG in hand, saying, am I seeing what I think I'm seeing? This is the EKG from a 20 year old. She looked at it and quickly said, it's probably paracarditis. But let's go assess the patient because anything's possible. So I've turned to the room with the doctor, and I started an IV and drew blood while she osculated the patient's chest. I knew she was looking for a paracardial friction rub. I got that answer right on the test in nursing school, and I knew it was associated with paracarditis, but I never actually heard it on a real patient at that point. Unfortunately, there was no rub to hear on this patient, or not at least at the time that I or the physician listened. We juiced opponents that came back negative, chest x-ray, negative, chest CT, for good measure, negative, and did another EKG three hours later just to make sure things weren't changing. We've ruled out all of the deadly diagnoses associated with chest pain. It's not a new withdrawal act, it's not a pulmonary embolism, it's not a dissecting aortic aneurysm, it's not a acute coronary syndrome. So all signs reporting towards paracarditis, and she met the diagnostic criteria. So we gave her some ibuprofen and sent her on her way with taper instructions for taking ibuprofen and a script for colgicine. I learned so much from caring for that patient, and all of the research that I did after the fact, I swear, the only fact that I learned about paracarditis in nursing school was that I produced a paracardo friction rub, and that was the extent of my knowledge at the time. But this patient did not have a rub and scared the crap out of me when I saw her ST segments on her EKG. So let me share what I have learned since that night, starting with the basics. By definition, paracarditis is inflammation of the paracardium, which is the thin double walled sac that surrounds the heart. So not myocarditis, that's when the heart muscle itself is inflamed, just the paracardial sac surrounding the heart. The paracardium consists of two layers. The visceral layer, which is attached directly to the heart, and the parietal layer, which forms the outer sac. And between these layers, there's a small amount of fluid that's like lubricating the tube. But when you hear that there's a paracardial friction rub, it's those two layers rubbing against each other. However, you only hear the rub in about 30% of the time. And paracarditis inflammation of the paracardium leads to an influx of inflammatory cells. So it creates vascular permeability and the release of inflammatory mediators like prostaglandins and cytokines. And that process can result in the accumulation of excessive fluid in that paracardial cavity, known as a paracardial effusion. The inflammation can also cause fibrin to be deposited in there. And that leads to thickening and scarring of the paracardium, which could potentially result in constrictive paracarditis. This chronic condition restricts the heart's normal movement, which impacts its function and can lead to heart failure. But that's like worst case scenario. Point is paracarditis is not a heart attack. They are very different. They present a different. As far as the cause of paracarditis, well, that's the tough part. Paracarditis can have numerous ideologies, but they all blow down into one of two categories, infectious and non-infectious. So viral infections are the most common cause. Viruses like coxacuivirus, ecovirus, adnavirus are the most common culprits. My patient had a virus a couple weeks ago. Thought she was getting better and then her chest pain started. There's also bacterial paracarditis, though it's less common. It can occur, particularly in cases of tuberculosis or in postcardiac surgery infections. Even fungal and parasitic infections are possible. They're rare, but they're more likely in immunocompromised patients. Then there's non-infectious causes, like autoimmune conditions, lupus, rheumatoid arthritis, where the immune system mistakenly attacks the paracardium. Paracarditis can also result from trauma, like blood chest trauma, or from medical procedures, like cardiac surgery, and metabolic disorders like uremia, particularly in chronic kidney disease, can also cause paracarditis. Certain medications like procanomide and hydrozene have also been associated with drug-induced paracarditis. And then lastly, paracarditis can develop following a myocardial infarction. That's known as dressler syndrome. And this is due to an autoimmune response that's triggered by the heart disease. muscle injury. So you don't want to miss that zebra and accidentally diagnose it as just paracarditis and miss the underlying myocardial infarction that caused it. More on that in a minute. Okay, so we talked about paracarditis and what causes it, but how can we diagnose it? Well, the diagnostic criteria are pretty simple. You can diagnose paracarditis if the patient has two or more of the diagnostic criteria. So number one is that classic paracarditis chest pain history. The patient says it's sharp, it's pleuritic, it's positional, it radiates to the trapezius, all those things are like the classic chest pain. Number two, a paracardial friction rub. That's for the most part, it's pretty indicative of paracarditis. But again, so that I was there. Number three, paracardial effusions on echo. And number four, characteristic EKG findings. So my patient only had two of the four. She did have the sharp positional chest pain that felt worse laying down and better when she sat up and leaned forward. And she also had diffuse s/e segment changes. But no rub, at least when I listened, and I listened good, and no effusion. So I wanted to break down each of these a little more, but I wanted to make one very important point before I do. So if you are multitasking right now, come back to me to catch this point. All right, here it is. Paracarditis is a diagnosis of exclusion. Meaning you have to exclude all of the other big killers that cause chest pain before you can make this diagnosis. It would be easy just to say chest pain, check, diffuse s/e segment changes, check, and label it as paracarditis and miss a stemmy or a PE. Not every patient is textbook. So rule out all the big stuff first. And then, and only then, can you call it paracarditis? Okay, you can go back to multitasking now. So as far as each of those criteria, let's start with chest pain. Paracarditis chest pain tends to be pleuritic, meaning it may get worse with coughing, sneezing, debriefing, certain position changes. Not always, but the classic paracarditis chest pain is reported by the patient that a hurts worse to lay flat, and it feels better when they sit up and lean forward. The patient might say, "I can't sleep because I have to sit up." Sitting forward can reduce the pressure on the parietal paracardium, especially during inspiration. Patients may also report the chest pain radius to the trapezius ridge. Interestingly, chest pain is likely to be present with infective paracarditis that may be minimal or absent, and patients with paracarditis associated with rheumatologic disorders, and your remit paracarditis. So summary, chest pain is tricky. It's not always textbook, and every patient's experience with chest pain may be described a little differently. So you don't want to wait for them to say, "My chest pain feels pleuritic," or it feels sharp and stabbing. Everyone experiences it very differently. So that's why you need two or more criteria to diagnose paracarditis. The next diagnostic criteria of paracarditis is that classic paracardial friction rub. And the pathophys is in the title. The sound you hear is literally the friction between the sliding of the inflamed visceral paracardium against the parietal paracardium or the parietal paracardium rubbing against the pleura. It can be difficult to hear, especially in a noisy room. Hey guys, I'll get back to the episode in just a second, but I wanted to pause to let you know that if you love my podcast, but wish there were more of these awesome episodes? Well, I have great news for you. There is more. My rapid response academy is basically podcast 2.0, plus the huge added bonus of community. I love hosting this podcast, but it's just me, recording it to a microphone often by myself. And this extra word of gal who loves to both teach and mentor nurses just wanted more. So in the community I created, I could teach live every Friday and breakdown topics that I think every nurse needs to know. From deep dives to the pathophys of every emergency you can think of, to some of the hearted nursing topics as well, like how to advocate with confidence for your patient, how to de-escalate situations, how to deal with bullies on the unit, how to be an amazing preceptor and charge nurse, and some of the mindsets and boundaries that have helped me stay in nursing for the last 20 years, not burn out, and thrive at the bedside. I love the opportunity to answer your questions live, and it's such a joy to see nurses supporting each other in this community. So if you're an acute care nurse that wants to expedite your growth as a nurse and invest in yourself so that you can provide the best care to your patients, you would love my rapid response academy. So to learn more, I put a link in the shown that's for you. Hope to see you there. Friction rubs are best heard at the left sternal border around the third and a coastal space. Some of the things you can do to optimize your ability to ascultate a rub is to sit the patient up and lean a little forward and have them hold their breath, ideally at the end of forced exploration. So, and then listen, I've heard the sound described as sandpaper rubbing together, but I think that might be a little harsher than the actual sound. So when I worked in the cardiac ICU, I heard pericardial friction rubs a lot more often than when I was in the ED. A lot of inflammation kind of occur when you cut the chest open, and a pericardial friction rub was not that uncommon or alarming in that patient population. So to me, it sounds like if you take your hair and rub it between your fingers, that's a rub. Let me say I can mimic it in the mic. But here's the thing. If you hear a rub, that can be very specific for pericarditis. But if you don't hear a rub, they can still have pericarditis. And they could have a rub one minute and it go away with position change. It's very unpredictable. So another reason why you can't rely on a pericardial friction rub to make your diagnosis. So it's worth listening for yes, but it's only one of the four diagnostic criteria. And remember, two are needed to make the diagnosis of pericarditis. The next is a pericardial effusion. So that is where fluid, like more than the normal amount needed for lubrication, builds up between the layers of the pericardium. Remember, this is an inflammatory process. Hence theitis at the end of pericarditis. With inflammation, often comes increased vascular permeability. And this can result in an accumulation of excessive fluid in the pericardial cavity known as a pericardial effusion. These are usually small and don't even require intervention, but sometimes they're big enough to be drained. The presence of a pericardial effusion may or may not affect your ability to hear the pericardial friction rub. Pericardial effusions are diagnosed with an echocardiogram or even at the bedside with point of care ultrasound. And the final criteria is EKG changes. So first thing to note is that there may be diffuse ST segment changes, meaning you might see an elevated ST segment in multiple leads, like all of them. When someone's having a myocardial infarction, it would be highly unlikely and a really bad luck than to have an occlusion in all of their coronaries resulting in ST segment elevation across all the leads. Usually you'll just see ST segment changes in the leads that reflect a particular vessel or a particular portion of the heart. For example, elevation leads to three and ABF, usually reflects an inferior wall in my, but elevation leads to three and V4 is from an anterior in my. My patient had elevation in almost all the leads, and that's because the whole heart is inflamed, not because an occlusion in all the vessels, but it definitely scared me. Additionally, the shape or morphology of the ST elevation and pericarditis is a little different than the morphology of elevation and a myocardial infarction. So if you look closely at that elevated ST segment, you'll notice that it either scoops into a convex or a concave shape ending at the T wave. You might have heard ST segment elevation referred to as "toomsdones" because the ST segment looks like a big hump or a tombstone. That is a convex shape. Another way to remember that is that convex ST segment morphology looks like a frown face, like the hump of a frown, right? The two-point facing down. So, what do you remember that is you would be frowning if you were having an MI. On the flip side, ST segment is of those with pericarditis often have a more concave shape, meaning they dip down and slope up before reaching the T wave, kind of like a smiley face. So if you had chest pain and found out it was just pericarditis and not a heart attack, you would be smiling. Okay, that's how I remember it. Now, this is not 100% of the time, but according to a study done in 2001 by Brady et al, looking at the morphology frowny faces versus smiley faces, those had a 94% predictive value of myocardial infarction versus other sources of ST segment elevation. So that's pretty darn valuable, pretty darn close, right? 94%. Another thing to look at is if you have elevation and leads two and three, compare which one is worse. Because the normal repolarization of the heart will occur at lead two before lead three, S elevation at lead two should be bigger than lead three. But, in a myocardial infarction, specifically an inferior wall of my, if you have a schemia, you're probably going to see the opposite, meaning lead 3 st-cellivations will be more pronounced than lead 2. So just to review, look at the EKG, if lead 2 is better than lead 3, it's probably paracarditis, but if lead 3 is better than lead 2, it could be a myocardial infarction. That's not 100%, but it's something to note. And then there's also the thing called spotics sign, which is the down-sloping of the Tp segment. So after the end of the T, that point is higher than the start of the next P wave. So it's almost like it's sloping down, but this is only present about 30% of the time. So again, all these criteria are not 100%, but they are worth noting. There's actually a ton more, but I think I would lose you if I start listing all the multiple options for how paracarditis presents, because there are so many variations. But the only thing I did want to mention is that depending on where in the course of their disease process they present, the EKG can look very different as the inflammatory response mounts and then resolves after days, weeks, and months. So there are four stages. Stage 1 occurs over hours to days, it's characterized by diffuse ST elevations, meaning like all over the board. Then we're following it tends to be that concave shape. You may see ST depression and AVR and V1. You should not see any reciprocal ST depressions. That often is from a stemmy. You might have PR segment depression, and then there's that whole spotics sign, the down-sloping of the Tp segment. All right, they're Stage 2. So that's when the ST and the PR segment starts to normalize again. The T waves kind of flatten out and then transition to deep symmetrical T wave inversions. Then they're Stage 3, that's when things are starting to resolve. So the ST and the PR segment has resolved. And the T wave inversions may persist a little bit. Stage 4 is completely returned back to the baseline EKG morphology. So like I said, there are no 100% definitive signs of paracreditis on the EKG. You can have diffuse ST segment changes in a wrap-around LED occlusion. Patients can have spotics sign during a heart attack. And the whole smiley face versus roundy face, concave versus convex, EKG morphology isn't predictive 100% of the time. But if you put all the pieces together and you look at your patient and listen to their history, listen to their heart, review their labs, and maybe look at their heart with an ultrasound, that can help you make the best diagnostic and treatment decisions. You don't want to send a patient having a heart attack home with a script for instance. So to review, you need to have two of the four diagnostic criteria to call it paracreditis. And that's only after you've excluded all of the other really bad stuff. Those criteria are Pluritic chest pain that's worse, laying down, then sitting up, diffuse ST segment changes, paracardial effusion, and paracardial friction rub. The last thing to discuss is the treatment. And really, it's pretty simple. Non-sderrudo anti-inflammatory medications like ibuprofen or aspirin, you would usually taper it. So like, 600 milligrams, Q8 hours for 10 days, and then taper to 400 milligrams for 10 days, and then 200 milligrams for 10 days. So coltocene is recommended to reduce inflammation and prevent chronic recurrent paracarditis. That's the big thing you don't want to happen to these patients. So patients will go home on coltocene for like three months or more. And finally, a PPI or proton pump inhibitor because insides and coltocene are pretty rough on the stomach lining. So we're not giving the PPI to fix the paracarditis, we're giving it because of the medications we have to give for the paracarditis. All right, in rare cases, where the paracarditis is from bacteria, antibiotics may be needed and possibly in a mission to the hospital. Sometimes it's so severe that a paracardiocentesis is required, and maybe even a paracardial window if the patient's paracarditis is restrictive and affecting cardiac function. But the majority of the cases, patients can go home on PO meds. So there you have it. Those are all the things I have learned since my first encounter with a scary looking EKG with the fuse SD segment changes that turned out to be paracarditis. If you remember anything from this episode, may it be that paracarditis is a diagnosis of exclusion. So make sure that you have effectively ruled out all of the killer diagnoses before sending a patient with paracarditis like symptoms home.