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Join us for a riveting session on hypertrophic cardiomyopathy (HCM) led by the esteemed CRNA, Shannon Pecka! As the Assistant Program Director at Bryan College of Health Sciences, Shannon Pecka brings a wealth of knowledge and experience to the table. In this informative session, Shannon will delve deep into the intricacies of HCM, equipping you with a comprehensive understanding of this most common inherited cardiac abnormality. She explains how to manage potential complications associated with HCM. Shannon also shares strategies to optimize anesthesia care for HCM patients. Don’t miss this opportunity to learn from the best! This episode is an invaluable resource for CRNAs, anesthesiologists, and healthcare professionals seeking to refine their knowledge of hypertrophic cardiomyopathy and its management.
Learn More about the Bryan College of Health Sciences DNAP Program: https://www.bryanhealthcollege.edu/bcohs/academic-programs/nurse-anesthesia/
Get access to planning tools, interview preparation opportunities, valuable CRNA Faculty guidance, and mapped-out courses that have been proven to accelerate your CRNA success! Become a member of CRNA School Prep Academy: https://cspaedu.com/join
Fast-Track Your CRNA Interview Prep with our CRNA Interview Crash Course! https://www.cspaedu.com/4wotmlds
Have you gained acceptance to CRNA school? Congratulations! Prepare with the #1 pre-anesthesia curriculum, as recommended by CRNA program faculty. Start the NAR Boot Camp today: https://www.cspaedu.com/bootcamp
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Watch the episode here
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Pathophysiology Of Hypertrophic Cardiomyopathy With Dr. Shannon Pecka, Bryan College Of Health Sciences
This episode is going to cover the pathophysiology of hypertrophic cardiomyopathy. It is my pleasure to introduce Dr. Shannon Pecka, an assistant program director in the School of Nurse Anesthesia at Bryan College. She has over a decade of experience teaching advanced principles of nurse anesthesia. She also has mentored countless students guiding them to publish their capstone projects. Her diverse clinical background includes rural anesthesia practice and moderate-sized private practice groups in a large academic setting.
Before specializing in anesthesia, she gained extensive experience as a registered nurse in various intensive care units, including the surgical ICU, neuro ICU, and the general med-surgical ICU. Dr. Pecka has made a significant contribution to the field through her numerous publications in the AANA journal and presentations at the Nebraska Association of Nurse Anesthetist Conferences.
She is also an active member of the Bryan College of Health Sciences, serving on multiple committees, including as faculty senate chair. In addition to her academic and clinical roles, she has held key positions in professional organizations such as the Nebraska Association of Nurse Anesthetists and the International Student Journal of Nurse Anesthesia.
She is also a dedicated peer reviewer for the Higher Learning Commission and several scholarly journals, including the textbook Nurse Anesthesia, fifth edition by Nagelhout and Plaus. I hope you’re as excited as I am to dive into the topic of hypertrophic cardiomyopathy with Dr. Pecka, who’s a passionate advocate for advancing nurse anesthesia and a dedicated mentor to the next generation of nurse anesthetists. Without further ado, let’s go ahead and get into the show.
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Hypertrophic Cardiomyopathy
My name is Shannon Pecka and I am a CRNA and the Assistant Program Director at Bryan College of Health Sciences in Lincoln, Nebraska. I teach advanced pathophysiology courses as well as advanced principles of nurse anesthesia practice courses. I’m going to talk about hypertrophic cardiomyopathy. Hypertrophic cardiomyopathy is the most common inherited cardiac defect. It is autosomal dominant. It’s characterized by left ventricular hypertrophy that occurs in the absence of any other cardiac disease that results in ventricular hypertrophy.
Any condition in the left ventricle where the ventricle has to pump and eject blood flow into the systemic circulation that occurs in response to an increase in afterload will result in a compensatory mechanism where the left ventricle will hypertrophy and increase its muscle mass in an attempt to try to compensate for that increase in afterload or resistance when it’s ejecting.
The definition again of hypertrophic cardiomyopathy is that there’s no other disease that causes an increase in resistance. Things like chronic systolic hypertension or aortic stenosis will produce a situation in which the ventricle has to eject more forcefully to get blood flow out. Hypertrophic cardiomyopathy is that there are no other situations where ventricular hypertrophy develops.
There are several different forms and we are going to talk about the most common form, which is characterized by asymmetric hypertrophy of the interventricular septum. That hypertrophy is disproportionate, disorganized, and located in the upper portion of the septum. Those anatomical changes then go on to cause the obstruction to left ventricular outflow. The initial event is that the left ventricle starts to remodel.
Asymmetric Hypertrophy of the interventricular septum is disproportionate. It's disorganized. It's located in the upper portion of the septum. Share on XRemember, there’s no initiating event that causes an obstruction to outflow. The initial problem is that genetically the left ventricle develops abnormally. Our myocytes, generally when we look at how our myocytes are laid down on our myocardium, they’re very much in parallel and organized in such a fashion that they can all work together to help facilitate contraction but that’s laid down in a very organized, systematic manner.
In hypertrophic cardiomyopathy, what we see is that those myocytes are laid down haphazardly and not in a nice pattern. What results is that the myocytes are abnormal. There’s also abnormal collagen that is laid down in interstitial space. Between all of our myocytes, there is the tissue that holds those myocytes together to create a ventricular mass and that is the interstitial space between cells in the myocardium. That interstitial space in hypertrophic cardiomyopathy is different because there is abnormal collagen and other proteins that are laid down in the interstitial space.
When that happens, interstitial fibrosis develops. What happens is that when the myocardium tries to stretch and relax, it cannot do that because it becomes more rigid as these interstitial spaces are filled with fibrosis and it cannot stretch normally resulting in diastolic dysfunction. The other bullet point was that hypertrophic cardiomyopathy is characterized by a disproportionate left ventricular hypertrophy. That hypertrophy is preferentially deposited in the septum.
This is the left ventricle and the septum of the left ventricle. In hypertrophic cardiomyopathy, what happens is that the septum, so up over in here situated upward on the top portion, is the aortic valve. The septum itself, those myocytes that are laid down, preferentially get abnormally laid down on the top part of the septum. What you end up with is a septum that is disproportionate and not consistent from top to bottom.
The problem with that is that the septum then obstructs some of the ejection to outflow from the left ventricle into the aortic valve causing an obstruction in the left ventricular outflow tract. That occurs during systole because as the ventricle contracts, it’s going to squeeze inward. When it squeezes inward, this places the position of this septum closer to the aortic valve making and further obstructing outflow out of the left ventricle.
Over time, this limitation or this obstruction to outflow is going to produce a generalized hypertrophy of the entire left ventricle because that’s going to be an added resistance. The longer the obstruction happens, the more ventricular hypertrophy that you get. You get a generalized left ventricular hypertrophy in response to that. The large septum can cause the obstruction.
It’s important to know that hypertrophic cardiomyopathy can be either obstructive or non-obstructive. Not every diagnosis with hypertrophic cardiomyopathy is an individual going to have an obstructive component. Sometimes the obstructive component is dynamic, meaning that depending on different conditions of the myocardium, it can increase the amount of obstruction that it has. One of those events is any increase in contractility of the left ventricle. Think about an individual where you have an epinephrine drip produced, that’s going to increase contractility.
Hypertrophic Cardiomyopathy: Sometimes, the obstructive component is dynamic depending on different conditions of the myocardium; it can increase its obstruction.
If we have this septum that is laid down incorrectly, you have increased contractility that’s going to produce increased squeeze of the left ventricle. That contractility is then going to position that septum further over and cause further obstruction. You can have an individual who doesn’t. Maybe they don’t have a lot of sympathetic activation happening at that time. They might be not obstructive but then you create an event where there’s increased sympathetic activation, or you give epinephrine, or some event happens where contractility increases. That becomes dynamic and then your obstruction can develop.
It is also dynamic in that it’s dependent on the location of the hypertrophy. It’s not always at the top portion of the septum. It is the most common for it to be there but not always. It’s dependent upon the left ventricular preload so the amount of volume and stretch that you can get into the left ventricle during diastole or filling. You can see that this interventricular septum that’s larger produces a problem because it takes up space inside our interventricular cavity.
That is going to create a situation where we’re not going to be able to fill the left ventricle as much as we could. If you think about situations where you have a lot of blood loss that’s happening or you have dehydration of an individual that’s happening, all of these situations are going to decrease the amount of preload that you can get into the left ventricle. When that happens, that positions the interventricular septum closer inward and causes greater obstruction during that time.
Obstruction can also be dynamic and be due to systolic anterior motion or something that is referred to as SAM. This is a description of restriction to the left ventricular outflow tract that can occur in a dynamic situation. One of the things that happens is that this left ventricle when it is faced with an outflow obstruction, what it’s going to have to do is it’s going to have to increase its contraction or pressure to overcome whatever it must overcome. If that is pressure in the aortic arch or an obstruction to the outflow, it’s going to increase its pressure as much as it can to force blood flow across that aortic valve and out the aortic arch.
Venturi Effect
That is going to produce pressure differences between the left ventricle and the aortic arch. What that’s going to produce is there’s a physical principle called the Venturi effect whereby if you have increased pressure, the pressure in the initiating chamber, which is, in this case, the left ventricle, has a very slow velocity. It cannot move because of that outflow obstruction. The differences between the two chambers, for which the initiating chamber and the chamber that it needs to go to, produce a situation where blood flow velocity or how fast blood is flowing across an opening, which in this case is the aortic valve, that when that pressure difference is great, the velocity or flow across that obstruction or in this case on the left ventricular outflow tract will increase dramatically in velocity.
The blood flow that’s going across the aortic is going at a very fast velocity compared to the initiating chamber. One of the problems is that the mitral valve is located within the left ventricle. As that velocity flow goes very quickly up across the aortic valve, it pulls and trains the leaflets of the mitral valve and pulls them closer toward the septum. What happens is that is one of the other additional components that contribute to the left ventricular outflow tract obstruction. It’s important to recognize things that exacerbate or make SAM worse. That is a decrease in afterload. It’s anything on the systemic side that decreases blood pressure, vasoconstrictors, for example, anything that will reduce or make the pressure in the aortic arch less.
As we have pressure in our aortic arch, if we have a great large amount of pressure that we need to generate to get blood flow out, if we decrease this amount of pressure in here, what we’re doing is increasing the velocity of flow again across that aortic valve. That’s going to exacerbate this systolic anterior emulsion that was discussed. Increases in contractility for the same reason that the septum is then pushed closer towards the left ventricular outflow tract and obstructing the outflow tract and for the same reason, the decreases in preload, which we discussed earlier as well.
Diastolic Dysfunction And Systolic Function
Any dynamic conditions will exacerbate the issue of obstruction. Diastolic dysfunction is also universal in all types of hypertrophic cardiomyopathy. When the myocytes are laying down genetically, there’s interstitial fibrosis that is laid down within the myocardium itself. What that means is when filling happens from the left atria into the left ventricle, it makes stretching of the ventricles much more difficult.
Hypertrophic Cardiomyopathy: Any dynamic conditions will exacerbate the issue of obstruction.
Diastolic dysfunction develops as the ventricle is not able to stretch to accommodate the blood flow that comes in. The left ventricle becomes stiff, its compliance goes down, and therefore ventricular preload is reduced and the ability to fill becomes reduced. Systolic function, when we look at ejection fraction, it is normal or maybe being slightly increased.
If we look at the formula for what ejection fraction is, ejection fraction equals left ventricular end-diastolic volume minus left ventricular end-systolic volume divided by left ventricular end-diastolic volume. This is just a percentage. It means that as the left ventricle stretches, it’s going to accommodate a certain amount of volume until it gets full.
When the ventricle contracts, it is going to contract and eject a certain amount of blood flow that is going to then leave the ventricle, be ejected across the aortic valve, and then the valve is going to slam shut over here. We’re going to get that certain amount of stroke volume or cardiac output that’s going to be ejected. The amount of ejected does not equal the ejection fraction. It’s important to recognize that ejection fraction does not equal stroke volume and equal cardiac output.
The reason for that is that the ejection fraction is the amount that we started with and the amount that was ejected. That means that this is the amount that is remaining in the ventricle at the end of the contraction, which means that this is the amount that was ejected. It’s the amount that you started with minus the amount that you ended with and a percentage of that is your ejection fraction.
Hypertrophic cardiomyopathy, when we think about the left ventricle and we said that its interventricular chamber was smaller because we’ve got all these anatomical changes, that means that the amount that we started with is much less. If we don’t have a lot of obstruction that happens, that means that the amount that we can eject is quite large.
The ejection fraction may be quite high because the percentage that leaves might be quite high. Ejection fraction could be normal or slightly high in individuals with hypertrophic cardiomyopathy because it does not equal cardiac output or stroke volume. The other consideration is the effect on coronary perfusion, the left ventricle and the aorta.
When we think about supply and we talked about the fact that the amount of cardiac output that’s going across the aortic valve may be decreased, that means that our diastolic blood pressure out here is likely to be decreased. When we look at the flow that comes across the left ventricle, across the aortic valve, and out the aorta, blood flow that’s going to perfuse our coronaries is going to happen on this aortic valve slams shut.
The ostia to the left coronary and the right coronary are right distal to the aortic valve. We get our supply to our coronaries during diastole when that valve slams shut. The pressure from diastole is then going to be the driving pressure for our coronaries. If we think about the impact of obstruction and the fact that we don’t have as much cardiac output stroke volume and therefore decrease blood pressure.
For supply, that means that we have decreased supply because we have decreased beginning pressure. If we look at the formula for coronary perfusion pressure or the amount of coronary perfusion that our coronaries get, it is diastolic blood pressure minus left ventricular and diastolic pressure. When you start with a decreased amount of diastolic pressure, you’re going to end up with decreases in coronary perfusion pressure.
From the start, our supply of coronary flow is reduced. It also impacts demand. The resistance to outflow is going to cause increases in muscle mass of that ventricle. The coronary vessels are on the epicardial surface. They dive down and are able to provide perfusion for the sub-endocardial portions of the ventricle itself. If we have a greater mass that we have to account for, that means that we have a greater oxygen demand that we need to account for. In addition to decreases in supply, what we end up with is increases in demand.
Ultimately, the balance between supply and demand is sacrificed and individuals are at risk for myocardial ischemia. Balances in myocardial ischemia, in myocardial oxygen in supply and demand occur in all people regardless of the presence of coronary artery disease because of that increase in muscle mass. Also, we have an increase in our systolic wall tension. If this left ventricle has to accommodate this obstruction to outflow, it’s going to increase the pressure during systole to accommodate that and contract against that obstruction. That is going to produce increases in demand for our oxygen. Decreases in cardiac output are going to result in decreases in diastolic blood pressure.
If we think about manifestations, they’re very consistent with what we see in the path of physiology. We see cardiomegaly because we see changes in that left ventricle. Those changes are all left-sided. Our right-sided structures are generally normal because it doesn’t generally affect our right side. We will say left ventricular hypertrophy for all the reasons we talked about. We will also see an enlarged dilated left atria because as pressure in the left ventricle increases, what happens is pressure is then transmitted to the left atria causing dilation over time when that mitral valve is open at certain points of the cardiac cycle.
In terms of the EKG, we also see left ventricular hypertrophy and left atrial enlargement causing a high QRS voltage. In our echocardiogram, we will also see that left ventricular hypertrophy. We will see that asymmetrical wall thickness because our septum is improperly constructed. We will see that the septal hypertrophy. When looking at the echocardiogram, one should assess what’s going on with the mitral valve leaflet.
You would want to look at the mitral valve to see what the echo is saying is happening with that mitral valve. Is it causing further obstruction or is it okay as it is? Reviewing ejection fraction and then interpreting that with the knowledge that ejection fraction does not equal cardiac output and ejection. It means the amount that we started with minus the amount that we ended with and then a percentage of how much was ejected.
For anesthesia, our treatment goals are aimed at contractility. We want to make sure that we don’t create situations that increase contractility, increases in sympathetic nervous system stimulation. Epinephrine is not always a good solution. Labetalol may be a good solution because it is not going to increase that contractility. What you want to do is aim for situations where you’re not increasing contractility but still maintaining cardiac output and forward flow.
For anesthesia, our treatment goals are basically aimed at contractility. We want to ensure that we don't create situations that increase contractility. Share on XYou want to try to make sure to maintain preload. We think about estimated blood loss in the operating room, volume, and fluids. What we want to do is optimize our ventricular filling to try to stretch that out to try to get that interventricular chamber stretched out as much as possible and try to open up this left ventricular outflow tract to optimize the amount of blood flow that can get across. Our afterload we want to look at because decreases in afterload and decreases in blood pressure cause those big dramatic changes between the chambers which then increases the velocity of flow across the aortic valve which then pulls that mitral valve leaflet over that direction.
We want to sometimes at some points tighten people up optimally enough to get diastolic pressure so that our coronaries can get slow and optimize supply and demand for our coronaries. We have a very short video of our program. Thank you for reading the hypertrophic cardiomyopathy. I invite you to listen to a short video for the College of Nurse Anesthesia.
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Bryan College of Health Sciences School of Nurse Anesthesia
I’m Dr. Sharon Hadenfeldt, a CRNA and the Program Director at Bryan College of Health Sciences School of Nurse Anesthesia. We’d like to introduce you to our program and tell you about a few of our highlights. There are many exciting opportunities in the CRNA career, and you are choosing a great time to further your education. Please let me introduce you to our graduate student coordinator, Lauren Erickson.
Thank you, Dr. Hadenfelt. My name is Lauren Erickson and I am here to help you every step of the way. Whether you’re learning about our program or applying, I’m going to be your main point of contact. I’m going to tell you a bit about our program and what makes us special. Our program is a Doctor of Nurse Anesthesia Practice program and is three years in length. We begin once a year in May.
Over the course of the three-year program, you’ll complete 86 semester credit hours. Students are full-time. You can typically expect 50 to 60 hours a week of attending class, studying, and completing clinicals. One of the items that makes our program very unique is we are primarily face-to-face. Our campus is located in Lincoln, Nebraska and the vast majority of courses are held in person here in Lincoln.
We have a few select courses that are offered in a hybrid format but for the vast majority of your learning, you’ll be here in person. Our program is divided into two unique phases. Phase one involves twelve months of classroom study and clinical practice. Phase one of the program feels very much like you are in school full-time. You’re typically on campus at least three days a week and you’re studying a lot.
Phase two is the final 24 months of the program. This is where students engage in active clinical practice and are mentored in clinical leadership. During phase two, it’s going to feel like you’re working full-time and going to school part-time. You’re typically in a clinical setting 4 to 5 days a week but you are still taking classes and you’re going to be on campus a few times a month. You’ll be reconnecting with your fellow students and participating in simulation but that portion of the program feels more like you’re in school part-time but working full-time.
We are very proud of our clinical experience while you’re in the program. You’re assigned a clinical home site and that clinical home site is where the vast majority of your clinical experience is done. Usually, 50% to 75% of your clinical experience is done at the home site. We have options in Lincoln, Nebraska, Omaha, Nebraska, Hastings, Nebraska, and Kearney, Nebraska.
In addition to those home sites, we have a variety of relationships with hospitals throughout Nebraska and even a few in Iowa. You will go on these rural rotations to gain additional experience, work with independent CRNAs, and broaden your scope. If you like that rural setting, we always have additional opportunities available if you’d like to experience different clinical sites.
We all know you are probably looking around at different programs, trying to figure out which is the best fit for you. I want to highlight a few of the items that make our program unique. First and foremost are our faculty. We feature five CRNA faculty members. They hold advanced degrees and have a wealth of knowledge in both the classroom and clinical settings.
Our CRNA faculty teach all but three courses within the program. They’re known for their close collaboration and investment in students and their open-door policy. During your very first semester, we feature a human anatomy lab where you’re working with cadavers. Last but not least, we’re going to return to that clinical piece. You are going to get a vast array of clinical experiences by coming to Bryan College.
The minimum number of clinical hours you need is 2,000. However, our May 2023 graduates averaged over 3,000 clinical hours. That means when they graduate, they’re ready to get into their profession and have the confidence to work on a variety of cases. From here, we’d love to hear from you. Our application cycle is open from April 1st through August 31st, 2024.
If you’re thinking of applying, it is a great time to get in contact with us. I’ll be your main point of contact from start to finish. If you have questions, you want to chat, or you’re ready to apply, please let us know. Thank you for considering Bryan College of Health Sciences. We hope to hear from you soon.
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FREE! CRNA School Interview Prep Guide: https://www.cspaedu.com/irptwqbx
Learn More about the Bryan College of Health Sciences DNAP Program: https://www.bryanhealthcollege.edu/bcohs/academic-programs/nurse-anesthesia/
Get access to planning tools, interview preparation opportunities, valuable CRNA Faculty guidance, and mapped-out courses that have been proven to accelerate your CRNA success! Become a member of CRNA School Prep Academy: https://cspaedu.com/join
Fast-Track Your CRNA Interview Prep with our CRNA Interview Crash Course! https://www.cspaedu.com/4wotmlds
Have you gained acceptance to CRNA school? Congratulations! Prepare with the #1 pre-anesthesia curriculum, as recommended by CRNA program faculty. Start the NAR Boot Camp today: https://www.cspaedu.com/bootcamp
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