Chapters Transcript Video Common Pediatric Cardiology Referrals Part 1 (Chest pain, Syncope, and Heart Murmurs) Thank you Chris for that lovely introduction. It's truly so special to have you here again. Um And it's great to see everyone in person and not on a team screen. So, um uh this morning, I've been charged with discussing 0 85% of outpatient pediatric cardiology in 30 minutes. So I hope you all have had at least one cup of coffee. Um uh These are the three most common pediatric cardiology referrals and there's a good reason why that's the case. These are extremely common in the pediatric population. Over 80% of Children at some point in development have a murmur, over half a million Children in the United States um present with a primary complaint of chest pain each year. And by the end of adolescence, um at least 20% of Children will have had at least one syncopal episode. Um but there is some good news. Uh cardiac pathology rarely underlies. These lesions up to 75% of uh murmurs are functional or innocent, less than 1% of cardiac um of chest pain and pediatric population is cardiac in origin and close to 90% of syncope in the pediatric population is neurocardiogenic in origin. Uh So when faced with one of these common, exceedingly common complaints in your office, I would just like to encourage you to remember that it's vastly more likely to be a horse than a zebra. I recognize that's easier said than done though. Um There's a good reason why we focus on these zebras. The families are anxious, they assume that all murmurs equal serious cardiac diagnosis that their child is at risk of or is having a heart attack when they complain of chest pain and that their child with syncope will be the next case of sudden death. And you the providers, you guys are anxious and not just because the families are anxious, the cardiac diagnoses underlying these ideologies can have serious and, and even life threatening implications and I'm sorry, missing just one of them um is not an option when the stakes are as high as they are. But I would like to remind you that you have a tool which is free, readily available and highly effective. It can contribute greatly to excluding a cardiac diagnosis for this these problems or at least move the cardiac diagnosis um farther down on your differential so that you can alleviate some of the anxiety while you get more information and sort sort it out. And that is a complete and thorough history. I know you all, we all haven't seen time constraints. Unfortunately, for all of us, the thorough history is, is sometimes one of the first things that gets sacrificed. And I'm sure you remember this statistic from training um history provides 60 to 80% of information needed for an accurate clinical diagnosis. And uh this is especially true in evaluating these pediatric complaints. So I'd like to show you in the next um few minutes how a thorough history is often one of the most valuable tools in flagging the concerning murmur, chest pain or syncopal episode. So, to start with murmurs in evaluating a patient with murmur, one, often, one of the most relevant pieces of information is um the age at which the patient first developed the murmur. This is especially true in infancy. So within the 1st 24 hours of birth, if you hear a murmur, there's a good likelihood that that murmur is pathologic. This is especially true for the first six hours of birth and most often those will be valva lesions. Um You can have stenosis of your semi lunar valves or regurgitation of your uh um A V valves, your atrioventricular valve. Um but it's important to remember that this might not just be isolated valva issue that that anything that presents with these valve problems as part of the part of the broader complex congenital heart lesion can present um with these murmurs. So um that includes things like tautology of flow and A V canal defects. Once we get beyond the 1st 24 hours, um the more likely lesions that you'll be hearing are shunt lesions. And that's because um shunt lesions are influenced by your pulmonary vascular resistance. When the infants are born, their pulmonary vascular resistance is sky high and it's acting um to limit uh shunting across these lesions. Uh Within the 1st 1 to 3 days of life, the pulmonary vascular resistance falls dramatically and you're gonna start to get enough blood flow flowing across these lesions that you'll be able to hear it once we're out of um that first immediate um few, first few days of life and move into several weeks or even months of life. These become more prevalent. I include V SDS here as well because while most of the pulmonary vascular resistance falls within the first three days of life, it doesn't fall to completely normal levels until 6 to 8 weeks of life. So, depending on the size of the VSD and how rapidly the PV R is normalizing, you can get V sds presenting um up to several months of life. Uh Another very common one we hear is um PPS or peripheral pulmonic stenosis. You'll recall that's a benign murmur of infancy that um is thought to occur because of the acute angle of takeoff of the branch pas from the main pulmonary artery, which resolves by 6 to 12 months of life. There's nothing pathologic underlying it and finally, flow murmurs. Specifically, I'm in this age group, we can often hear flow murmurs related to anemia as their hemoglobins um reach their nar ok. So what about older Children? Most murmurs um that present after in, in uh infancy are usually innocent and these are some of, um, the three most common, uh, innocent murmurs we'll hear in childhood. Um, stills murmur is by far the most common. You'll remember the most notable feature of that is its vibratory musical quality that sounds like the plucking of a guitar or violin string. Um It's also louder um in the supine position. Uh Then we also have Venus hum which is caused by the normal um return of blood um through the jugular vein. Uh these murmurs tend to be continuous. So we have to be careful to distinguish them from patent ductus arteriosus. Um but these uh murmurs will be influenced by neck maneuvers. Uh whereas the pa patent ducted Saros, um that murmur will not be um influenced by these maneuvers. These two murmurs are more common in your toddlers and your younger school age Children. Whereas the pulmonary flow murmur is more common in the older school age Children and adolescent population. And there's nothing underlying these pulmonary flow murmurs. We're just hearing normal blood flow across the pulmonary valve. Um important to distinguish from a valva, pulmonary stenosis. These murmurs are soft as opposed to the kind of the harsh murmurs of the valva lesions. Um They don't radiate and there's no click again as opposed to the, the valva lesions. So school age Children, the young, the toddlers, the young school age Children, um especially with these two murmurs um uh that have completely otherwise normal um exams and no, concerning other personal or family history. It's reasonable to follow these murmurs. Um and, and see if they go away um because especially the sts murmurs um are influenced by hyperdynamic states. So if you're hearing it for the first time during a sick visit, um you know, it's not unreasonable to bring those patients back and see when their heart rates are lower or they're not febrile, not dehydrated. Um Maybe the murmur goes away. Uh After each two, it's unlikely though not impossible that a pathologic murmur will present for the first time. The exceptions are that it was previously missed uh that the patient had an intervening medical um condition uh that created a new murmur such as rheumatic fever or endocarditis, um or um one of these three entities, uh A SDS. The reason why they can present later is because the their shunt is um different is influenced for a different reason than the V SDS. The V SDS we spoke about are uh the shunt is influenced by pulmonary vascular resistance. A SDS um are influenced by the compliance of the right uh atrium. So our compliance, the compliance of the right atrium naturally um increases as we get older, it becomes more compliant and that um increased compliance will allow more flow across the atrial septum. And therefore, the murmur can present later. And there are even some adults that don't, don't get um presented and uh don't get diagnosed until later. Mitral valve prolapse is another common one that can kind of appear with age. And that's because mitral valve prolapse can actually be progressive, can um evolve throughout um growth and, and adolescence. And if it um uh if the, if the mitral regurgitation doesn't happen until later, um it might present later and then finally, um a BSD aortic valve um to you um should have a systolic ejection click depending on how, how um how influenced that valve is. Um uh you know, you could have aortic stenosis and aortic insufficiency sometimes just uh without aortic stenosis. Sometimes you just hear some flow across that, that valve that's not in the aortic stenosis territory, but some turbulence creates a flow that again with time will come out. Um So in addition, we spoke a lot about age. In addition to age, there's obviously some other elements of the history you want to pay attention to, especially in babies, you want maternal history. Um and everybody, you want family history, obviously, any symptoms suggestive of heart disease are gonna put these patients in a different category. And furthermore, there are abnormalities in osculated um uh exams um in the general exam and in diagnostics that if, if these things um are appearing you're gonna have um a higher suspicion of a pathologic murmur. Ok. So we're gonna move on to chest pain now. Um, so the differential of pediatric chest pain is broad and this list is far come from comprehensive, but it highlights some of the more important and common causes. And I just want to point out a few, first of all, um, some opinions feel that idiopathic chest pain comprises the largest bucket in this, um, uh for, for pediatric chest pain, um which can be really frustrating because you're not giving the families a pre precise diagnosis or um uh you know, explanation. Um But musculoskeletal comprises a fair number after that. Uh And I'd just like to point out here a lot of um people practitioners get concerned if they can't reproduce the pain on exam because obviously costochondritis um is marked by that reproducibility. Um But there are other forms of musco skeletal chest pain. And I actually find that I get histories more consistent with precordial Cap syndrome in the office than I do with costochondritis. And you are aware that the pardal cast syndrome has this acute onset of chest pain. It's um it's sharp, it's highly focal um and uh it's very short lived, the patients feel like um any movement. It, it's exacerbated by chest well movements. So, um uh any movement or um inspiration will exacerbate the pain until these patients describe sitting very s um still and not and taking shallow breaths during it. Um So just think about other things. Um in addition to costochondritis with the musculoskeletal pain, two other ones, I want to point out here the exercise related transient abdominal pain, uh that was known as a stitch or um uh and uh exercise induced asthma. And the reason why is because by definition, both of these occur with exertion and that we're gonna talk a lot about exertion um coming uh in the next couple of slides. Um But I just want to remind you that there are non cardiac chest pains that um can be uh exertionally associated. Ok. So here is a list of cardiac chest pain. Uh Remember that che chest pain is least likely to be cardiac uh in origin in the pediatric population. Now, your role is not to figure out which one of these cardiac chest pains. Uh It is, but rather to say, um this patient might have cardiac chest pain to kind of put them in this bucket. So, what I want to point out here um is that all of these except for pericarditis produce chest pain in the same way pericarditis um is, is caused by an inflammation of the pericardium. Um And the, and the pain is, is from that irritated pericardium. But all the rest of these produce pain by causing coronary ischemia. And so your patients are gonna describe angina and it's not gonna be subtle. Um They're gonna have substernal pain, they're gonna report crushing pain burning pain, it might radiate to the arm, the jaw, the neck, the shoulder, it has an acute onset which builds an intensity over time and it's provoked by exertion. Uh, you're not gonna have a patient at risk for cardiac chest pain that doesn't get worse with exercise. Um, and then these patients are not gonna look, well, they're gonna be diaphragm, they're gonna be pale, they're gonna be dy neck. So we've all seen this a million times in, in training. But I just want again to encourage you to fill in as many of these boxes as possible because as we're gonna see in a few minutes, it can really help us. But just to point out to again timing, um uh everyone gets this one whether or not it's with exertion. Um The thing I want to, in addition to reminding you a couple slides back that there are non exertional forms of, of, um, I mean, exertional of noncardiac chest pain. And the other important thing to um, try to tease out is, is it is pain actually happening with exertion. We get a lot of patients coming in with pain during recess and gym and in sporting events and then when you take it one step further and ask them what they were exactly doing. Well. The kid during recess was playing cards and the kid in gym hadn't started gym class yet and there was actually no exertion involved. The other important one I find is the, the positional one. we'll get patients that report pain worse when lying down. And so everyone starts thinking about pericarditis, which obviously gets worse in the, in the reclining position. Um, push it one step further and ask them, does it hurt when you lie on the couch in the afternoon watching television or when you take a nap and nine times out of 10, I get the history. No, it's just when at night, when I'm trying to fall asleep. And this is a big one in our adolescent population. That's when all their kind of issues from the day kind of come to the consciousness and where we might see psychogenic chest pain related to anxiety and pushing it one step further. If you ask them what they're doing, they're usually on their phones and looking at social media. So to drive home, this point about how important a history is. I wanted to present two cases that um we take care of um in our practice within the last year or so. They both had the same presenting complaint. They were females with exertional chest pain. They both experienced this chest pain by running time, miles and track practice. The first case reported a sharp pain which increased with aspiration. And the second one, a burning pain. Uh The first patient localized her pain to un uh bilaterally under both ribs. And the second one, it was mid sternal. There was no associated symptoms in the first case. And the second case reported palpitations and dizziness shortly after the chest pain started. The first one found that, um, if she pressed deeply on, uh, the area that relieved the pain as well as bending over, the second one was relieved at rest, but then they started running again. The first one was able to run without problems and the second one, the pain returned almost immediately. The first one had no um past medical or family history. And the second one had months of complaints of shortness of breath palpitations and a gray appearance during dance that actually caused her to quit and was being managed as long COVID by another provider. So these are some of the features on history, um which are extremely reassuring and you'll recognize that our first case had many of these was sharp, it was highly focal, it wasn't radiating it uh increased with inspiration, but benign intervention to relieve the pain and there were no associated symptoms and there's a few others in here um that can be helpful. Conversely, there are red flags that can be raised during the history and you'll recognize a few of these from our second case. So both of them presented with exertion. But the second case was the only one to complain of additional symptoms referable to the cardiovascular system. And she was really describing um uh a burning pain that was not classic for um uh a noncardiac pain. So now we do a gut check and I think you'll all agree that case one is provided us a lot of reassuring information. And again, this is just based on history. I haven't given you any other information. So we're reassured by case one, in case two, we're like, uh, I don't know, there's enough there that maybe we can't exclude a cardiac diagnosis. We need more information. So I'll tell you at this point that both of their um EKG S and exams were normal. Um this um patient, um uh I diagnosed with um uh exercise related transient abdominal pain and we discussed um stretching and breathing techniques and adequate hydration. And I will give you the rest of the history on this patient. She continued running despite the chest pain, she lost vision and then suffered an acute loss of consciousness secondary to a cardiac arrest. She received prompt CPR from her coaches and ad was placed and a shock was delivered for ventricular fibrillation. Ross was achieved in the field and she was brought to our institution where she was diagnosed with an anomalous origin of the left coronary artery from the right sinus, which I think you'll be hearing about more later, she underwent surgery and thankfully, she's doing well without any neurologic deficits. Um But the key here is that most of that information, uh the gut check was provided by the history alone. So now we're going to move on to syncope, uh copy is is defined by transient loss of consciousness resulting from a decrease in cerebral perfusion. And there should be um there is an associated loss of postural tone. I'd like to encourage here that um we really need to on history. Again, distinguish between syncopy and pre syncopy. A lot of patients use the terms blacking out or falling out. And when pushed, I find that the term blacking out means loss of vision and falling out means that they've gotten so weak that they feel like they either need to lower themselves to the ground or they kind of stumble. Um but they remember everything, there's no loss of consciousness and that's really important um for our history. So the different types of syncope, um there's reflex syncope, which um comprises these three entities, which we're gonna talk a lot about in a minute. There's cardiac syncope, which um the mechanism is that you can't get the blood out of the heart to get to the, to get to the brain. So there's inadequate cardiac output and neurologic syncope, the brains, the heart's pumping enough blood, but there's some obstruction on the cerebral level. So reflex syncope is by far the most common cause of pediatric syncope. These patients experience an event um where the sympathetic tone should increase your heart rate and blood pressure should increase. But for whatever reason in these, in these individuals, the signals get crossed and the parasympathetic system dominates um and they get bradycardia, um vasodilation or some combination of both, this results in venous pooling and ultimately decreased return of blood to the heart. And finally, um circulatory collapse. Luckily, these, these experiences are rapid, they're shortly um there's the loss of consciousness is short and they have a complete spontaneous recovery and the majority of these patients outgrow these tendencies in their twenties. So the triggers um for the neurocardiogenic syncope um is, is often a sudden emotional stress, uh either experience with pain or fear. Um And a lot of our complain our patients, it's postural. So either prolonged standing or um a positional shift can prompt. These then a second category is situational on the adolescent population itself. These first two stretcher hair grooming, these are more seen in the adult population. And then finally, there's breath holding. The, the mechanisms of of the syncopy with breath holding isn't entirely understood. But the autonomic system um is implicated, I'd like to point out one important cause of reflex syncopy, which is exercise related syncopy. These events occur during exercise um where there's um uh and can make it complicated in our history because um that is is so relevant for cardiac etiology. But basically, when you're exercising the heart rate and stroke volumes are really high and you get a dramatic increase in your cardiac output. And what's supporting that cardiac output are the muscle muscular contractions, sending that blood back up to the heart then you stop exercising. This is especially um relevant if there's, if the patient hasn't cooled down appropriately, but you get this abrupt removal of the skeletal contraction in the presence of the in of um vasodilation, which is um another um feature of of exercise. And then the blood just again, pulls in your extremities and you're not getting enough back up north to, to um uh support your cardiac output. Despite this, it's really important to evaluate these patients because some forms of cardiac syncope um do present in the recovery period most notably along QT syndrome. So I'm not telling you to disregard these um cases, but just be mindful that the majority of them are not going to be cardiac. So the cardiac causes, you can have structural or functional causes um of cardiac syncope um or r arrhythmogenic causes um either tachy or radiate arrhythmias. So, again, history, history, history, really important to get details. Um You want everything before that event, you wanna know the last time they were feeling well, exactly what they were doing, what position they were in, what time of day it was, how hot it is, all of those things because this is gonna be essential for the history. I'll just take one second here, the palpitation history, we get a lot of complaints of palpitations um associated with neuro cardio and syncopy. And if you get the nice progression of the dizziness coming first and the vision loss and the palpitations is kind of, you know, secondary and later um that is reassuring as opposed to the patient that complains first of palpitations and then they're getting the dizziness and, and vision changes. It's not perfect. But again, uh it helps sort these patients for us. You want to get as much information during the activity and after the event as well. Ok. So two more cases um again, cared for. Um I saw that both of these patients within the last year, 16 year old, competitive athletes with exertional syncopy and palpitations. Um Again, just to illustrate how important the history is. So they're both competitive um athletes, one, a soccer player, one, a basketball player, they were both in the heat, one was outside, one was in a gym, neither one had eaten well that day. Uh And both of them were standing listening to their coach. This is where the story diverged case. One practice hadn't started yet. He had just come from school. He was standing outside that did nothing athletically. The other one had just completed an aggressive session of suicide drills. The first one complained of lightheadedness with vision changes and then palpitations. Uh The second one was bending forward at the waist trying to catch his breath and he stood up and that's the last thing he remembered. Uh the first one returned to baseline within seconds. The second one, the loss of consciousness lasted at least a few minutes. Um and he was confused for up to six hours presumably because he smacked his head pretty hard. Uh The first one had no significant past medical uh or family history. The second one on further inquiry had palpitations with exertions, 1 to 2 times a week and long standing brief dizziness on standing for one time uh each day. So again, re reassuring features on uh history. Um You will recognize that our first patient had all of these reassuring features. Uh It was a rest, it was um it was briefed. Uh There were no um other um uh uh kind of concerns related to the heart there, it was during the heat, he had decreased fluid intake. All of all of these um features were, were met. And so if you have a patient like this, the history is consistent with reflex syncope, there's no exercise involved. Um the exam if you've gotten an EKG and that's normal too and there's no personal or family history, you really don't need to do anything else but counsel them about hydration. Um And what to do. Um If you, if they feel these presync symptoms, again, the conversely, we have these red flags and you'll recognize a couple of them from our second case. The most concerning was that there was no pro whatsoever such that he sustained a pretty significant head trauma. Um And then the second one of course is that it was post exercise. So again, gut check the first patient, we have all these reassuring features. Um The second one, some questions still, we need more information. So I'll tell you at this point that this exam, his um the first patient's exam and EKG were normal. I, we diagnosed him with neurocardiogenic syncopy. And as I said, we discussed hydration and if he ever feels those feelings again, that he should uh you know, at least sit down if not lie down. Um The second patient had a highly abnormal EKG. He had increased um left ventricular forces in the uh left precordial leads. And most notably, there were these T wave inversions uh in those same leads. So he with between the uh history and an abnormal EKG bought himself the million dollar cardiac work up. He had an echocardiogram which showed some mild left ventricular hypertrophy. It seemed concentric by echo. There was no love ventricular for tract obstruction or sam. Um Then he went on to have a cardiac MRI where the, the hypertrophy was a little more focal um in the um septal region, but it was only 12 millimeters which really um is in the gray zone for us. Um Most more um importantly, um I should sorry back up by saying one thing regards to that EKG those findings are quite consistent with hypertrophic cardiomyopathy, sorry for that relevant piece of information. Um So here, there was no leak, the line enhancement on cardiac MRI which um we see in hypertrophic cardiomyopathy um because of the fibrosis, um that happens uh again, no left ventricular alpha tract obstruction or S am the event monitor was negative. The stress test, there was no arrhythmia um and no clear left ventricular alpha tract obstruction, although an accurate ingredient couldn't be obtained and the genetic testing there was a V US. So basically, um the uh jury is still out on this patient. Um The, the differential is whether he had an athlete's heart with some mild LVH and suffered a neurocardiogenic syncope. You'll recall he was reporting some postural dizziness. Um So it could be those two kind of benign things and that's why he went down. Um or he could have had an uh arrhythmia, he could be an evolving, we think he's an evolving hypertroph. Um And he could have suffered an arrhythmia related to that hypertroph will faint either from a left ventricular alro tract obstruction or an arrhythmia. But generally when you have an arrhythmia in the hypertroph, you have uh fibrosis as the um substrate and we didn't have any fibrosis on the, on the MRI. So this is a perplexing case. Needless to say he's being followed quite closely. Um He is being allowed to play sports. Thankfully, I'm not thankfully for my gray hair. I am not the one following him. Now, I have uh sent him on to our sports um cardiologist, but he is being allowed to play currently and I think the jury is still out on him. Um So that's where I'm gonna end. But I think my just if I haven't emphasized it enough that really um the, the history can be so vital in these patients and can really help alleviate the anxiety while we're getting additional information. Thank you. Published Created by
