All right. Good morning. Thanks for joining. This series is a six-part series that really focuses on acute care medicine. And so we're going to start here with chest pain evaluation and emergency department. But again, I really appreciate your engagement and look forward to sharing some of these insights with you. So let's start with chest pain. So chest pain is the second most common presenting complaint to the United States Emergency Department. It's about 7.6 million patients a year present with chest pain. And I spent a lot of time in a co-managed chest pain unit in our local hospital back in the day, and so I've seen a lot of chest pain over the years. But in kind of a breakdown, most of these patients actually do not come in with cardiac-related chest pain. 33% to 50% musculoskeletal pain. 10% to 20% ends up being GI. 10% have stable angina, so it is cardiac pain, but it's just not yet an acute coronary syndrome where it's an unstable presentation. And then a smaller percentage of them, as you can see, actually have acute myocardial ischemia, so it does fall under that category of acute coronary syndrome. So this particular presentation today is going to really just discuss how do we work up a patient with chest pain? Where do we start? So first of all, you have to think about your differential diagnosis, and I always thought about the worst-case scenario and started working from there because that's the last thing that you want to miss when working up a patient. So those life-threatening conditions, you need to think about, of course, acute coronary syndrome, non-STEMI, STEMI, unstable angina, acute aortic dissection, pulmonary embolism, very interesting because sometimes the symptoms don't always match with what you think, tension pneumothorax, which is not as common, pericardial tamponade, and then mediastinitis. So again, as we kind of work through this, these are the things you're also going to want to rule out as part of your differential. Some of the common conditions that we see, and there are some cardiac conditions that are not necessarily related to acute coronary syndrome. Patients with heart failure oftentimes describe chest tightness or chest discomfort. And then there's some valve disorders such as aortic stenosis or mitral valve prolapse that can cause some chest type symptoms. From a pulmonary perspective, there's pneumonia or infections. There's pleural disease. So pleuritis is a common one that we'll see again can be very painful. From a GI perspective, there's reflux, there's esophageal spasm and inflammation, and the tough part about this one is in that case, sometimes the nitroglycerin actually improves that discomfort. From a musculoskeletal standpoint, costochondritis, trauma, there's certainly some folks have issues related to psychological sorts of pieces like anxiety or panic attacks can cause a significant amount of chest discomfort. And then the other ones you don't want to forget about are herpes zoster, referred pain from other, especially abdominal organs or inflammatory conditions. And I'll tell you some stories about herpes zoster when we get into our workup. So when it comes to cardiac chest pain, your job is really to understand what the pathophysiology is behind what you're doing. And so when you think about ischemic cardiac chest pain, where does that come from? Well, it's an oxygen demand mismatch. So anytime there's lack of oxygen or the right amount of oxygen in the myocardium, you're going to switch your metabolism from aerobic to anaerobic. And once you hit that anaerobic, then you start to build up that lactic acid and you start to get symptoms. So this is not something that can happen in just a matter of a few seconds. It really requires a few minutes. And we'll talk a little bit more about that. Associated symptoms, shortness of breath, some people will get quite nauseous and even have some vomiting, as well as some diaphoresis. They get very sweaty, get cold and clammy. Myocardial injury can occur in as few as two hours. So we really want to make sure that we're working through this as much as, you know, quickly to come up with what the plan is or what the decision is around the differential. What chest pain is not is twinges. So sometimes patients will describe it, you know, I get this twinge, it lasts a few seconds and then it goes away, it comes and goes. That is very low likelihood to be cardiac in nature, just because of what has to happen in order for that pain to occur. Some folks come in and say they've had the same chest pain for the last two weeks. Well, if the tropons are negative, we just showed myocardial injury can happen within two hours. If the tropons are negative, it's much less likely to be cardiac in nature. It's typically not reproducible. So when the patient describes something, if you can reproduce it through palpation of the chest wall or certain positionings, then that's less likely to be cardiac. And then certainly worse with coughing is less likely to be cardiac. Those are pleuritic type symptoms. And again, I kind of mentioned these already, but shortness of breath, weakness, nausea, vomiting, palpitations, even syncope or near syncope can also be symptoms associated with that cardiac discomfort. So when you think about your chest pain history, what you need to know is that some things to ask. So what's the quality of the pain? Is it pleuritic in nature, positional? Is it sharp? Is it dull? Is it ripping, tearing? Is it reproducible? Where's the location? Is it localized in a particular spot? Is it all general and all over the chest? Is there on a particular side? Does it radiate at all? Again, hearts typically for most patients on the left and radiation tends to be in the left arm. Not that we haven't seen radiation other places and people do present with atypical, but if they're describing right-sided chest discomfort, unless they, you know, are one of the rare that have the switch, it's less likely to be cardiac. And then what are the temporal elements? What's the onset? Was it abrupt? How long did it last? Was there any provoking symptoms such as post-meal, cold, different activities? Are there certain things that brought it on or certain body positions? Some people will describe if I'm laying on my left side or I'm laying on my back or lean forward, the pain is worse. Those are the sorts of things that again can help you better understand. Does this seem more like cardiac or less? And then what makes it better? So the palliation, did they take something? Did they move a certain way? Did they stop doing a certain activity? What improved it? And then finally severity, timing, and associated symptoms. So how severe was it on a scale? We love our scales of one to ten. How long did it last? And then any of those other symptoms, the nausea, vomiting? Did they break out into a sweat? Did they feel dizzy or lightheaded? Did they have any palpitations? So again, as you ask these questions, you'll begin to put the story together and in your mind as you think through this, the question you have to ask yourself is does this sound like cardiac ischemic pain? And going back to what causes that ischemic pain and that oxygen mismatch, does this begin to make sense or does this seem extremely atypical or much less likely to be cardiac? So your first question is does that pain in and of itself sound like cardiac? The second question you have to ask yourself is just based on the patient and comorbidities, are they someone that could have coronary artery disease? A 25-year-old with no past medical history is low likelihood of having cardiac disease. And when they come in with chest pain, your differential is going to look a lot different. If they are 48 years old and have a history of hypertension, diabetes, smoker, hyperlipidemia, they're likely to have cardiac disease. Now, is this pain significant for that or representative of that? That's the question you have to ask yourself or really figure out as part of this workup. But they're much more likely to be a patient with coronary disease. And then if they have a previous history, so they've had an MI in the past or had some unstable angina or had PCI in the past, ask them about symptoms. Are these symptoms the same? Are they different? I had a patient once that described this strange headache that he would get, but what he said to me was, this is the same as it was when I had my MI three years ago. And so although the symptom didn't even fall anywhere on the list of typical things that we would see, our workup did show he was having another acute coronary syndrome episode. And so that's a really important question, that previous symptom. And I always try to get your hands on previous records, previous EKGs, understanding what has happened in the past for that patient and does this look anything like that? So where do you start as far as workup? So we start a physical exam. Again, most of these patients is going to be normal. But things to look for. So from your pulmonary exam, is there any wheezing, any rails, anything to suggest pleural disease or pulmonary disease or anything to suggest heart failure type symptoms? From a heart and vascular, you're certainly going to want to know their rhythm and listen. Is it a regular rhythm on auscultation? Do they have a gallop that could suggest volume overload or some ischemia? Any murmurs that you might find? And then do a good vascular exam because again, there's high correlation between patients that have vascular disease other places. So if they've got pulses that are diminished or breweries, renal artery breweries or carotid breweries, those are things that would give you a sign to suggest that this patient has risk for coronary disease as well. From an abdominal exam, we're looking for tenderness. Any masses? Again, that brewery question. And then in some cases looking for heme positive stools. Part of that, there's a couple reasons for that. One would be if you're worried at all about it being a GI, a peptic ulcer disease type of pain, or if you are going to be thinking that this is acute coronary syndrome and we need to intercoagulate the patient, then understanding if there's any issues there is important. From a musculoskeletal standpoint, any chest wall tenderness and from a skin standpoint rash. And this is where I'm going to tell you my story about herpes zoster. In my 10 plus years of doing hospital-based cardiovascular medicine, at least once a year, we would get called down to do a consult on a patient that came in through the emergency room and got admitted to the chest pain center. I'd be talking to the patient, start to examine the patient, pull the gown down, and there would be a classic rash for the herpes zoster with the red through the dermatome with the the beginnings of blisters. And so the question, you know, in that particular patient, it was not acute coronary syndrome. It was herpes zoster, which as you know is extremely different in management. So always look at the skin because you will feel very foolish when the attending comes by and they look at the skin and they find something that you didn't. So really important. From a diagnostic standpoint, we're doing EKG certainly upon presentation. So the goal in any program is an EKG within 10 minutes of the time the patient hits the door. That should have already been done before you even get called. But you then continue those EKGs for any changes. So if they have, if the pain was gone and now they develop pain, you get another EKG. They had pain and the pain is now gone, get another EKG because we're looking for any changes. Patients with acute coronary syndrome can have a normal EKG one to five percent of the time. So normal EKG does not for sure rule them out. And four to 23 percent of the time there's unstable angina and that EKG was normal. So certainly it's a great tool. But don't discount or rule out coronary disease just because the EKG was normal. The next piece of this is your cardiac biomarker. Some of you use troponin I's or T's. There are some high sensitivities. So many of the programs may have adopted high sensitivity, which just means it picks it up earlier and at smaller amounts. But just remember when it comes to the typical troponin, we usually see an increase at around the three hour mark when myocardial ischemia starts and peaks at about 12 hours. So most programs will do a 0, 3, and 6 troponin. And maybe even a 12 if you're keeping them longer. And especially if they're positive to kind of look to see the timing. And then from those high sensitivity because it's picking them up earlier, if the symptoms are less than two hours and it's negative, then you're going to want to do another one. In some cases programs are moving to a single high sensitive troponin if the symptoms are longer than two hours and the troponin was negative. Have the opportunity, especially in low-risk patients, to rule them out. So make sure you look to see what your protocol is at your particular center. And also understand which type of troponin that they're utilizing. Other things to think about. A D-dimer can certainly rule out if it's negative. Pulmonary embolism, CBC. It's not going to necessarily rule it in. So remember if it's positive, it's just a finding. Now you need to go find out where that clot is. But certainly if you're worried about, you have a suspicion for PE, checking that D-dimer. CBC, just to understand, they may be anemic. I've seen patients come in with chest pain and ended up with a hemoglobin of six because they had a slow GI bleed. And so yes, they have an oxygen mismatch. They may even had a bump in their troponin. But their issue was not as much of a coronary artery disease issue as it was a lack of hemoglobin issue. BNP, brain natriuretic peptide, very helpful for looking for volume overload or heart failure. And then again, if you're all worried about PE, checking in ABG, looking for any mismatch or hypoxia. There. Chest x-rays, going to be non-diagnostic for your typical acute coronary syndrome patients, but it is a common test that we order. You'll be looking for any pneumonias or any chest pulmonary type abnormality. So we have had patients that come in with chest pain and we find a mass on their chest x-ray. So certainly a good part of your diagnostic workup. So the next piece, so now you've seen the patient, you've talked to the patient, you've examined, you've ordered a bunch of labs and some other diagnostics. How do we approach this? Well, your job is now to risk stratify. So you need to decide yes, this is definitely acute coronary syndrome. No, all is negative and likelihood is low and they're safe to go home. Or the maybes, where all is negative, but likelihood is still intermediate to high and they need further workup. And this of course is assuming that you have low likelihood for other life-threatening conditions that you need to continue to work up. But that's your job. But the good news is we've got some pretty good tools to help us with that. There's the TIMI risk score and you'll kind of see this here in front of you. And then the other one that we see commonly is the heart score. And so I'll give you an example here and you'll have access to all of these slides for future reference. But this is an algorithm that we that was put together in 2018 utilizing the heart score. So if you can kind of see the heart score there on the left and see the kind of the workup on the right, but based on the heart score, it's going to either low or intermediate or high risk stratify. You either go on to discharge the patient home for follow-up with primary care and possibly a stress test if you're still concerned. Or if it's intermediate, you may admit them to observation for those serial troponins and stress testing. And then if it's certainly if it's high and or, you know, which make it high, you'd have to have some troponins. Then you know, now you've got a patient with acute coronary syndrome and they need to be admitted for management. So this is a really great tool. So one of the things, actually let me go back to this other slide, that we talk about here is stress testing. So we've got low risk stress testing as an outpatient and we've got intermediate risk stress testing. For those patients, we're going to keep an observation. So understanding our different options for stress testing is really important. And as you can see, it's mildly complex. This is really more complex than what it actually is, but wanted to give you some insights into ways to think about which test and for which patient. So the first question you have to ask yourself is can the patient exercise? So yes or no. If yes, they can exercise, then you have a couple choices. Number one, do they have a history of any PCI or CABG so that they've had coronary disease in the past? If the answer is yes, then we're going to need some imaging associated with that and you're probably going to want to choose nuclear imaging because we're actually, they're able to look for perfusion and we're looking for before and after stress perfusion changes. So if they have an abnormality on the front end that's old, it's going to show up on your rest and you're looking for changes with your stress. So patients with known coronary disease, nuclear imaging is a great choice because again, you're looking at perfusion. So let's say they do not. But they do have a left bundle branch block or their PACE or, and again, left bundle branch block, I'm going to tell you when we get into talking about STEMI, if this is a new left bundle branch block, then we have to worry about this could be a STEMI. So if this is a new left bundle, that's a completely different management option. But if they have a previous history and this EKG is unchanged or they have a PACE rhythm, then we cannot rely on EKG changes and we need to again add imaging. So we're either going to look at nuclear imaging or echo imaging. Now remember with your echo, you're looking at wall motion changes. So nuclear, you're looking at perfusion. Echo, you're looking at wall motion changes. So with those wall motion changes, we're looking from rest to stress. And so that's why it's really important that we start off with a normal because it's much easier to go from normal and pick up the abnormal than it is for someone that's already got an abnormal wall motion related to a previous event and now we're looking for additional change. So that's kind of the thinking related to nuclear versus stress imaging. And if the answer to all of that is no, they have a normal EKG, they're a low risk patient, no previous history, you may not need imaging at all. You can move straight to an exercise EKG or a graded exercise test. If the patient cannot exercise, then we have to think about pharmacologic. And the answers are, you know, the imaging portion is the same. So if we have a previous abnormality, we're probably going to want to move forward with a nuclear perfusion imaging test using vasodilator therapy such as adenosine or ragadenosine. If we are having normal and the wall motion is normal, then we may think about dibutamine stress echo. Because again, we're looking at wall motion versus perfusion. So again, lots of different options there. The other piece with the vasodilator therapies is that some of them have some issues related to patients with significant reactive airway disease. And so in that case, you would want to use dibutamine because it does not have that concern for our reactive airway patients. There's much more detail on this in the readings. And so if you still have questions, I would recommend that you go through the readings as well as talk to the physicians and the team and the program in which you're working. Because most programs have very specific lines and kind of typical protocols that they follow. So that would be another really great resource for you. So some additional considerations. So as you're thinking about taking care of these patients, any patient without a clear explanation after initial workup has acute coronary syndrome until proven otherwise. So remember I said that normal EKG does not rule out. And so you're going to need to do serial EKGs, troponins, and risk scoring. Now in the patient that I described to you with the herpes zoster, we have a clear explanation. If you're able to reproduce the chest pain through palpation of the chest wall, you probably have a clear explanation if everything else is negative. But in the cases that you don't, you really need to take the next step and really rule them out. Understanding the time of onset, when the troponins would typically elevate, and make sure that all of that is negative. Elderly, diabetics, and women may have atypical symptoms. So as much as I talked about kind of left-sided chest pain, pressure, burning, these patients may present something a little different. So again, you have to really think about all those other comorbidities, risk factors, and certainly risk stratify and do the full rule out protocol. And then never rely on a single EKG or a single set of cardiac biomarkers. Always check them again. Now I say that if we have a STEMI situation, and we're going to talk about STEMI in another talk, that's different. You see a STEMI, you have to act on it. You don't wait and repeat or look for the biomarkers. We move. But in this case where this is more of a rule-out scenario, if the EKG is normal, don't just rely on one. You need to look at all those other factors. And then the other piece is if your patient's representing after recent revascularization, your job is to rule out abrupt occlusion. So did they have instant re-stenosis or thrombosis of that previously stented segment, and you're going to need to look through that. And I will tell you, just because I did this for a lot of years, it's not uncommon for patients to present back with chest discomfort. They're nervous, they're anxious, and any twinge or anything they feel in their chest, they're going to be very sensitive about. So lots of these patients will present, and they do not have abrupt occlusion. But that is your first job, is you have to rule that out first. And so again, sometimes we have to take them back to the cath lab. Sometimes if EKGs are negative and troponins are negative. And that's another thing. Sometimes those troponins are still positive from before if it was only a few days. So you're going to want to go back and see. Maybe today they come in and it's their 1.2, but you go back and you look and the last troponin that we had from three days ago was 2.4. So in that case, it gets the second troponin and maybe it's down to 0.8. So it's, again, there's lots of things to think about there. But that is not an uncommon scenario for these patients to present back, even without abrupt occlusion, just because they're anxious about the event, the original event, and is there something more happening. So we'll also want to leave you, each one of these will have some references. These references, most of them are included in your readings. But these are really important places for you to go to get more information. So we appreciate it. If you have any questions, please feel free to reach out at academy at medaxeum.com. We'll be happy to answer any additional questions that you have and we always appreciate the feedback. So thank you for your time today and let us know if you have any questions.

chest pain evaluation

differential diagnosis

acute coronary syndrome

pulmonary embolism

diagnostic tests

stress testing