all right if you're just joining us go ahead and open up your chat box i am looking forward to a wonderful session and i'm so glad you are here go ahead and say hello and where you're from in the chat box i love how many people we have right now coming into the classroom this is absolutely awesome we're going to be starting in about five minutes guys so get ready and make sure that you have the handout ready as well we're gonna fill that in as we are going through the session i will be posting the handout link as well just in case you missed it so look for it in the chat box all right everyone if you look in the chat box and click that google drive link that will take you to the table which we are going to be filling out as we master the cardiac cycle if you are viewing this on youtube i've also put this in the stream chat box all right wow we have so many amazing people in the chat box good morning mary carmen mai suman hari priya marco carmen ivy hari priya preethi amish anjal yusuf edgar uh thank you all so much for joining arvin good morning adeshwar if you are just joining right now please go ahead and type a hello or good morning into the chat box we will be getting started soon if you're just joining us and have missed the handout please scroll up in the chat box i posted the google drive link so you can follow along with me during this session we're going to get started in just a little bit foreign all right good morning everyone i am so glad you are here joining me today for this webinar this is going to be a jam-packed session and it's going to be very high yield for your usmle exam i just want you all to stay active and engage during this webinar if you can hear me and see me go ahead and type in yes into the chat box just want to do a quick audio visual check awesome wow look how many people we have today that is absolutely amazing again i did email a google drive link uh to you all in your reminder email and i've also posted it in the chat box i'm gonna go ahead and do it again this will be a very high yield table for us to go through during this session today ladies and gentlemen we are going to be going through some important cardiac physiology topics and i'm going to make it very practical because my goal is for you to think like the test maker just some ground rules for today there are going to be probably some questions that come about throughout the session i ask you if you can hold your questions until the end i promise to stay afterwards and answer all of your questions and make sure that you have understood the concepts and are optimized for your study i first off just want to thank you all for attending if you are new welcome to the hi guru family and if you've been to my webinars before i especially welcome you back and i really thank you for using these webinars and my resources for your usmle preparation as you may know my name is rahul i am a second year pediatric critical care fellow and most importantly over the past six years i have been absolutely passionate about helping students just like you kick ass on the usmle exam i absolutely love making sure that we grow this high guru family i mean look at this guys we are an absolute community and i've been humbled to teach classrooms all across the country and today we are going to be going through some important concepts in the comfort of your own home the way that i like to go about us mla preparation is focusing on three things learning the material integrating the material and applying the material and what i want to base this review on and all of my resources is active recall because that's what the evidence states is the best way to learn i want to make sure that we integrate across organ systems so that you are able to actually conceptualize many of the high-yield concepts and most importantly i want to make sure that i am relevant for the usmla exam now today we are going to have a high energy review and my goal is to modify and motivate i want to motivate you to be inspired to go through this whole process study in an effective manner and also master the cardiac cycle so that you can apply these important concepts to your nbme questions to your actual exam to those new world blocks that you're going through so let's start with a little bit of an overview as to what we're going to be going through i'm going to be focusing on three things today for our webinar number one i'm going to be focusing on the cardiac cycle we're going to be going through the wiggers diagram step by step number two i'm going to be focusing on pressure volume loops these frequently show up on exams and number three i'm going to be focusing on the cardiac action potential and in particular we are going to be comparing and contrasting the ventricular action potential with the sinoatrial action potential all right everyone let's go ahead and start with our first concept which is going to be the cardiac cycle i believe that this is the fundamental way for you to learn the both the mechanical and the electrical activity of the heart and these concepts come up both from a pathophysiology standpoint on your exam as well as a pharmacology standpoint on your exam so just a historical perspective this cardiac cycle diagram is also known as the wiggers diagram the earliest description of this diagram is dates back to 1915 by dr carl wigger who made this important diagram that helps conceptualize the electrical activity and the mechanical activity of the heart and he actually was one of the department chairs at case western university in cleveland ohio and that's where i did my pediatrics residency so nice historical tie-in and you know in honor of him we are going to be going through this diagram and spending about our first half hour of this session really capturing the essentials from this diagram breaking it down for you for the usmle now guys you've probably seen this diagram in so many different texts right brs you've probably seen it in uworld you've seen it in first aid and if you just sit there and try to rote memorize these concepts you know what's gonna happen your head is absolutely going to spin so today what we're going to do is really break down the cardiac cycle and i'm going to start by giving you some strategies on how to master the cardiac cycle number one we're going to do an active recall of the various cardiac events we're going to really ask ourselves where is the blood actually flowing we are also going to isolate each curve and understand the relationship between pressure and volume and then what we want to really understand especially as we integrate these pressure and volume loops as we integrate the ekg findings you have to really understand please please put this in your mind electrical activity of the heart slightly precedes mechanical activity what that means is that the p wave which represents atrial depolarization is going to proceed what mechanical event ah that's going to be atrial contraction or atrial systole alright so this is going to be the table that we are going to be using please fill out this table as we go along we are really going to break down the cardiac cycle into systole and diastole and so let's go ahead and first look at the major events that we have to define for the cardiac cycle so just in an active recall manner the first event which we're going to be talking about is isovolumetric ventricular contraction and in this phase as you can see guys there is no change in volume but you notice that the ventricular pressure which is that red line is slightly increasing the next phase is going to be ventricular ejection i call this the sexy phase of systole why is that because that's where the blood is leaving the left ventricle and going into the aorta so what defines this phase well guys it's going to be a decrease in ventricular volume as well as an increase in aortic pressure as blood is going to be going from left ventricle into the aorta now after this phase we are going to be going into diastole and if somebody asks you what's the first phase of diastole the answer is going to be bam you are going to be thinking of isovolumetric ventricular relaxation after isovolumetric ventricular relaxation remember this is a phase where the volume is not changing however the the pressure in the ventricle is actually going down because we're talking about relaxation you are going to have rapid inflow and rapid inflow is a diastolic event major diastolic event in which you are going to have what you are going to have blood going from the left atrium into the left ventricle followed by this rapid inflow the phase that goes after this rapid inflow um portion is going to be a reduced inflow portion which we call the diastasis not particularly high yield but is actually one of the longer portions of this cardiac cycle and finally you are going to end diastole with atrial systole now guys atrial systole has the word systole in it but remember it represents the atria giving the last about 10 percent of preload into the ventricle and what's really important for us to understand is atrial systole is actually going to be a diastolic event all right so now what we're going to do is we're going to shift this curve and we're going to talk about the major lines that this diagram is going to have the first line is going to be the aortic pressure and as you can see in ventricular ejection we have an increase in aortic pressure which makes sense as blood is going from the left ventricle into the aorta we also have the atrial pressure tracing and the atrial pressure tracing has some very important portions that the usmle likes to test for example they love for you to know that the a wave represents atrial systole they'd love for you to know that and we're going to get into it a little bit more but that's the atrial pressure curve the ventricular pressure curve is also going to be very relevant that's in this red and we saw that the ventricular pressure increased in isovolumetric ventricular contraction and it decreased in isovolumetric ventricular relaxation but you notice in those phases the ventricular volume which is the curve in blue both the in both of those phases you had no change in the volume now the ekg is going to be important for us to integrate with the mechanical activity of the heart because remember electrical activity slightly precedes your mechanical activity so for example if we have atrial systole which is a mechanical event that is going to be preceded by what electrical activity that's going to be the p wave and that's actually very important for you to understand and then finally we have what we call the phonogram and the phonocardiogram is going to be the audible sounds that we hear with our stethoscope we are going to be talking about the physiologic sounds which is going to be the first heart sound which represents the mitron tricuspid valve closure compared to the second heart sounds which is going to be the aortic and pulmonic valve closure and then we have these somewhat pathological sounds that we hear it on the phonocardiogram in various cardiac um phases and these are actually going to be very important for our us mla why because they love for you to know that the s3 represents the atria filling into a very dilated left ventricle whereas the s4 is going to be a late diastolic event and that is going to represent the atria contracting into a very stiff non-compliant ventricle and this is such an important concept for us to know the difference between s3 and s4 s3 questions on your usmle that's going to be the patient who potentially has dilated cardiomyopathy who potentially is going to have congestive heart failure whereas s4 that's going to represent patients who are going to have for example systolic hypertension or systemic essential hypertension and chronically their left ventricle undergoes hypertrophy and thus you are going to have the s4 sound heard on exam which represents again the atria contracting into a stiff non-compliant ventricle so the first phase we're going to be going through is isovolumetric ventricular contraction remember that this is the first phase of systole very important for us to understand in this phase i'm going to ask you what do you think the heart is doing well remember that the ventricles are contracting and if the ventricles are contracting what does this say about the pressure well the pressure is actually going to be increasing and subsequently what ekg event precedes this mechanical activity and that's going to be the qrs complex remember electrical activity precedes mechanical activity so the qrs complex which represents ventricular depolarization is going to precede this mechanical event of isovolumetric ventricular contraction the next question we have is what heart sound do you hear clinically at the beginning of this phase so we are contracting the ventricles what just happened prior to this hmm that's going to be bingo you are going to hear s1 remember s1 represents the mitral or tricuspid valve closure and obviously that's going to close and then you are going to have isovolumetric ventricular contraction so let's break this down on the wiggers diagram we see that we have isovolumetric ventricular contraction we see that the ventricular pressure is going up and this is going to be related to the qrs complex and most importantly it's called isovolumetric the ventricular volume is not changing so when we think about isovolumetric ventricular contraction remember that there is going to be an increase in ventricular pressure and that increase in ventricular pressure is going to be after the mitral valve closed which is going to be s1 so the mitral valve closes and bam now we have an increase in that ventricular pressure the reason why it's called isovolumetric is the pressure is increasing the volume is remaining the same and all valves are closed during this cycle just as a little aside this diagram is actually from grey's anatomy's original textbook can you believe that we're we are learning medicine from a historical perspective today but i wanted to use these images because hey they are so pretty and we're able to understand the cardiac cycle from these images all right so now we're going to move on to the sexy phase of systole and that's going to be rapid ventricular ejection so rapid ventricular ejection what is the heart doing well we are going to have now the ventricles contracting and the blood is flowing from where the left ventricle into the aorta as that blood is going into the aorta the aortic pressure is increasing and what do you think is happening to ventricular volume ventricular volume during this phase is actually going down because the blood is going from left ventricle into the aorta i know that this is some basic stuff and i know i'm repeating some stuff but guess what you need to burn it into your mind because these events are going to be essential and if you don't have the good foundation it's going to be very challenging for you to think on your feet during difficult exams and difficult questions in your url blocks as well as on nbme exams so on the ekg what wave does this correlate to well rapid ventricular ejection actually correlates to the st segment and that's why guys as a clinical correlate st segment elevations or depressions are so profoundly impactful on this phase rapid ventricular ejection so when you are thinking about rapid ventricular ejection what valve do you think is open and that's going to be the aortic valve aortic valve is going to be open during rapid ventricular ejection so let's break this down even more graphically we see that in the ejection phase the aortic pressure is going up as you can see by the dotted lines the ventricular pressure is also going up as the ventricles are contracting and the ventricular volume is going down and you see the st segment peaking in as the electrical activity related to this phase all right so rapid ventricular ejection if i look at it from a visual standpoint i know that my left ventricular pressure is going to be very high and blood is going to be going into the aorta and as the blood goes into the aorta what are you going to have well your aortic pressure is going to increase and that's important now what kind of pathologies can the u.s emily talk about during this phase well remember that if you hear a systolic murmur heard best at the right second intercostal space at the mid-clavicular line you are going to be thinking of what you are going to be thinking of aortic stenosis and aortic stenosis on your usmle there are two kind of uh questions that they love for you to know one is the older person who has aortic stenosis just due to wear and tear of that aortic valve but also they want you to know that aortic stenosis can occur prematurely in those patients who have bicuspid aortic valve so what patients have bicuspederic wealth well you might be born with it such as for example on your usmle exam them talking about turner syndrome or watch for that 50 year old male who yes was born with the aortic or bicuspid aortic valve and now prematurely has aortic stenosis take home point bicuspid aortic valve ends up causing you to have premature aortic stenosis so now let's go ahead and review some of the most important portions we talked about in systole remember we started our discussion with isovolumetric ventricular contraction and in this phase you see that the ventricles are contracting the pressure is increasing it's related to the electrical activity of the qrs complex all valves are closed that's why the volume is constant and right before this phase you heard the first heart sound what about ventricular ejection well rapid ventricular ejection the ventricles are contracting you are going to have an increase in pressure the blood is going to be flowing from the left ventricle into the aorta and your left ventricular volume is going to decrease this represents what this represents the electrical activity of the st segment that's related to this phase and we know that the aortic valve opens understand that aortic stenosis is going to be heard best during this phase aortic stenosis is going to be what aortic stenosis is a systolic murmur so if i gave you just a little bit of a test taking strategy on how to master murmurs for your usmle i will say two things number one understand that it's all about real estate location location location on the usmla they're going to have in the test question where exactly you are hearing it well are you hearing the murmur in the mitral area are you hearing it in the second intercostal space aortic area on the right hand side or on the left-hand side second intercostal space the pulmonic area figure out where the murmur is going to be heard and then number two categorize whether or not the murmur is systolic or diastolic so understand that as a important test taking concept because guess what guys the murmur questions can sometimes show up on your usmle as these multimedia questions in which you have to wear your headphones and you have to click on the diagram and actually listen to the sounds and characterize whether it's systolic diastolic and where exactly you're hearing it best now guys we are going to be moving on to diastole now when we talk about diastole we really have to understand that diastole starts with isovolumetric ventricular relaxation so in isovolumetric ventricular relaxation we have to ask ourselves what exactly is the heart doing well the heart in this phase is actually relaxing and the ventricular pressure is decreasing but what do you note about the volume well the volume in the heart is not changing so understand that right before we ended up having this event isovolumetric ventricular contraction right before what valve just closed and that's the aortic valve remember the aortic valve was open during systole now it's going to be closed now what heart sound do you hear clinically the heart sound you're going to hear is going to be the second heart sound why because that is going to represent aortic valve closure and remember the second heart sound most importantly on your exam has this aortic pulmonic split which is going to be heard best on inspiration so when we look at isovolumetric ventricular relaxation that's a diastolic phase you note that the ventricular pressure is actually going down which is that red bar we also notice that you have the ventricular volume being constant and on your phonocardiogram you just heard s2 why because s2 represents the aortic valve closing and now you're going to have this diastolic event so isovolumetric ventricular relaxation we note that the pressure is going down in the left ventricle and the aortic valve which is pictured right here the aortic valve is actually going to be closed now in diastole if the aortic valve is incompetent which means that it is slightly open and leaky you are going to have the diagnosis of aortic regurgitation so remember aortic regurgitation is going to be a diastolic murmur whereas aortic stenosis is going to be a systolic murmur very important for you to know and the way that i integrate it in my mind as i say okay what valve should be closed in diastole the aortic valve should be closed in diastole but if it's not that's pathology so if the aortic valve should be closed in diastole but it's not you're going to hear aortic regurgitation so again location location location usually this is going to be at the right second intercostal space you also are going to note aortic regurgitation in patients on your exam that have for example connective tissue disorders marfan syndrome ehlers-danlos syndrome patients who have tertiary syphilis in which you get destruction of the vasovasorum which is the blood vessels that are perfusing the aortic valve these are all vignettes that you need to integrate with aortic regurgitation all right so moving on to the sexiest phase of diastole we're going to be talking about rapid ventricular filling now in rapid ventricular filling let's ask ourselves what's the heart doing all right so rapid ventricular filling your heart is going to have blood flow from the left atrium into the left ventricle and the ventricles are passively filling with blood and we know to now that the ventricular volume is increasing because the blood is going from left atrium to left ventricle now remember that the pressure is going to be low and constant and this is actually going to be a very important concept for you to understand and that is the concept of gradient gradients really help you conceptualize cardiac questions on the usmle what that means and we'll see it in the next slide what that means is that you need to have a gradient from high to low a high pressure system which we note in this phase as the left atrium to a low pressure system which is going to be in the ventricle and how did we get that low pressure system well we got that low pressure system from isovolumetric ventricular relaxation the ventricles started relaxing in order for us to create that gradient between the left atrium and the left ventricle do you see guys how we're building on these concepts inch by inch this is very relevant for your usmle now what valve is open during this time you are going to note that the mitral valve is open during this time so do you hear a murmur during this phase hmm and likely you may not hear a murmur unless you have very severe mitral stenosis but understand that you do not have a heart sound on the phonocardiogram during this phase why is that well because usually on the phonocardiogram the various sounds are going to be represented by valves closing so yes during this phase you may have for example your mitral stenosis very severe mitral stenosis where you hear the opening snap but remember you won't hear s1 you won't hear s2 why is that because those sounds s1 and s2 are going to be not valves opening but they are vowels closing so heart sounds that you hear clinically during this phase is pathologically or sometimes physiologically in athletes and adolescents is going to be the third heart sound and i really want you to understand the third heart sound guys the third heart sound is going to represent the atria filling into a very dilated left ventricle the atria when it fills into a very dilated left ventricle you are going to be thinking about the third heart sound and that's seen in your test questions for example dilated cardiomyopathy related to trypanosoma cruise eye or you are going to have cardiomyopathy related to congestive heart failure or due to coxsackie b all of these different pathologies can cause you to have the s3 heart sound and the s3 heart sound is what we call a early diastolic heart sound an early diastolic heart sound so let's go ahead and understand this on the graph after we talk about reduced ventricular filling reduced ventricular filling again i don't think that this is going to be super high yield for you on your usmla exam but just understand that the ventricles are relaxed and the mitral valve continues to be open as blood is going from the left atrium to the left ventricle but at a reduced rate of note this is one of the longest phases of the cardiac cycle so one of the things that we have to understand are the vignettes that come with these certain phases so i wanted to give you a sample vignette that we can apply so here we have a patient who's undergoing an exercise stress test on the treadmill what effect will this have on this phase of the cardiac cycle so during an exercise stress test your heart rate is going to go up and if your heart rate goes up you are going to reduce the amount of time available for ventricular filling and i think that that is actually really really important for you to understand that if you have extremely high heart rates you can actually reduce ventricular filling you reduce diastole now fine dandy that's great if you are just seeing diastole in isolation you're like okay wow the ventricles are not filling as much well what does that do that actually reduces your cardiac output at times but what's also important for you to know guys burn this into your mind the coronaries fill during diastole so if you have decreased time because of extremely high heart rates if you have decreased time available for ventricular filling you may compromise coronary perfusion and that concept usually shows up on exams so ventricular filling remember i talked about the g word and that is gradients we have the left ventricular pressure being relatively low in order for us to have passive flow from the left atrium into the left ventricle and that passive flow is all due to gradients remember that your left atrial pressure on your usmle exam is also going to be known as your pulmonary capillary wedge pressure and your pulmonary capillary wedge pressure is what i call a surrogate for left atrial pressure so when is pulmonary capillary wedge pressure increased on your exam well most importantly they give you test questions related to congestive heart failure and in congestive heart failure you note that there is backup of blood from the left ventricle into the left atrium and subsequently you are going to have a high pulmonary capillary wedge pressure why is that because pulmonary capillary wedge pressure is a surrogate for left atrial pressure how do these questions manifest again this review is so like chock full of usmle pearls and they usually ask these questions with arrow questions right they will ask you okay what is cardiac output that's going to be low what is pulmonary capillary wedge pressure that's going to be elevated these are just some basic questions but understand that when you see pulmonary capillary wedge pressure you can kind of conceptualize it as left atrial pressure all right guys let's go ahead and just wrap up diastole understand that the av valve is going to open during the phase after your isovolumetric ventricular relaxation during diastole you are going to have a ventricular pressure that's going to remain low and constant and that allows that gradient from the left atrium into the left ventricle and that's why your left ventricular volume is going to increase so now let's go ahead and answer a sample usmle question and for those of you who know me you know my strategy for answering questions is stem paraphrase and predict stem let's start with the last line of the question which of the following physical exam findings would be less likely to be associated with this presentation now let's go line by line a middle-aged male presents with shortness of breath while lying flat he is found to have a 3 out of 6 holosystolic murmur that is heard best at the apex dilated cardiomyopathy is suspected which of the following physical exam findings would be less likely to be associated with this presentation a apical impulses shifted to the axillary line b s four gallop c by basal crackles d peripheral edema e hepatomegaly if you are still paying attention in this chat box go ahead and type in your answer into the chat box i would love for you to answer this question go ahead all right nada is saying that lucas we have a lot of awesome awesome answers and the answer is you're absolutely correct s for gallop is going to be less likely to be heard in dilated cardiomyopathy what are you going to hear well you're likely going to hear the s3 and remember the s3 if this is s1 closure of the mitral valve and this is s2 closure of the aortic valve remember that this is systole and that means that the phase between s2 all the way back to s1 that's known as diastole so an early diastolic sound in which the left atrium is going to be filling into a very dilated left ventricle that's going to be known as s3 and so we typically call that the s3 gallop and the s3 gallop sounds something like this kentucky kentucky whereas the s4 which is a late diastolic sound that sounds like tennessee tennessee let's go ahead and conceptualize s4 a little bit more and we're going to conceptualize s4 during this final phase of diastole ah it says atrial systole but it's actually a diastolic event atrial systole remember that during this phase the atria is contracting giving that last little bit of preload to the left ventricle and so on the ekg what does this correlate to so atrial systole is a mechanical event and on the ekg this correlates to the p wave because that's the electrical activity electrical activity which is atrial depolarization precedes mechanical activity which is atrial systole clinically what do you hear on exam well that's going to be the fourth heart sound so what is the fourth heart sound it is the atria contracting against a stiff non-compliant ventricle and i can't stress that enough it's a late diastolic sound in which patients on your usmle exam are going to have things like hypertension or anything that causes left ventricular hypertrophy because that makes the compliance of the left ventricle reduced and what is compliance well compliance is that ability to fill if you have a thick thick thick left ventricle you're going to have a decreased ability to fill i.e a decreased compliance so as we can see in atrial sicily which is this diastolic event you see that the atrial pressure is slightly increasing and why is that well that's known as the atrial kick the atrial kick and how does the usmle kind of modulate this answer for you or modulate this concept and that is going to be giving you a patient with mitral valve stenosis in mitral valve stenosis you are going to have a prominent a wave and why do you have a prominent a wave because if this is the atria and you have a very stenotic mitral valve the atria is going to increase its pressure so so high and you'll see a prominent atrial pressure during mitral stenosis remember in mitral stenosis that can be actually due to what rheumatic fever rheumatic fever late stages of rheumatic fever that's going to be mitral stenosis that's the association all right so let's kind of re-go through this on this diagram remember that if you have your mitral valve right here normally you are going to have the atria contracting into the left ventricle and that's going to give you that little bump up of preload i.e left ventricular and diastolic volume but test questions that they love for you to know mitral stenosis related to for example rheumatic fever they also want you to understand that patients who have atrial fibrillation if you have atrial fibrillation you are going to lose the ability for the atria to contract during diastole because atrial fibrillation is this chamber of the heart kind of quivering over the left ventricle and so what are other usmla questions that they are going to ask they are going to note that in atrial fibrillation patients get stasis and that's related to the gen path concept for a cow's triad stasis endothelial injury and hypercoagulable state that stasis obviously leads to a clot and if that clot goes up and goes into your brain you end up getting a stroke or if that clot goes into your celiac or superior mesenteric artery you are going to get intestinal ischemia what we know as acute mesenteric ischemia so do you understand how we're integrating things i first tell you atrial fibrillation it affects the atrial systole which is a diastolic event i say that that's going to cause you to have quivering of the atria stasis of blood and then watch for your vignettes if they say atrial fibrillation and then badness happening afterwards ie stroke acute mesenteric ischemia you are absolutely ready for it all right so let's go ahead and understand some of the various events we note that isovolumetric ventricular relaxation you are going to have the ventricles relaxed there is going to be a decrease in pressure all the valves are closed and you just heard the second heart sound prior to this event what does the second heart sound represent the aortic valve closing rapid ventricular filling the ventricles are still relaxed but the ventricular volume is increasing the mitral valve is going to open and if the atria are filling into a very dilated left ventricle you're going to hear the third heart sound rapid ventricular filling as you know and excuse me that's supposed to be reduced ventricular filling sorry about that reduced ventricular filling you are going to have the micro valve continuously be open and then we have atrial systole in which the atria is contracting giving that last little bit of preload to the left ventricle the electrical activity that preceded this mechanical event is the p wave which represents atrial depolarization the mitral valve is going to be open and if the atria is contracting against a stiff non-compliant ventricle you are going to hear the fourth heart sound all right so we are going to be talking a little bit about the jugular venous tracing now the jugular venous tracing is basically us looking at the pressure we're in the atria and we have a catheter with the pressure probe and that is going to be right in the atria so think about the jvp tracing as a pressure probe right kind of here okay and in a structurally normal heart we sometimes think of this jvp tracing on the right side of the heart but also on the left side of the heart it's just very hard for a catheter to reach that left side of the heart so that's where the catheter is and let's start with the various events we see that a wave represents right atrial contraction and we already had that test question related to microstenosis and how you would get a very prominent a wave remember that the c wave is going to represent the bulging of the tricuspid valve during ventricular contraction obviously after you had the a wave which is atrial contraction you had the tricuspid valve talking about the right side of the heart close and if you had that tricuspid valve close the next step is going to be what isovolumetric ventricular contraction and in isovolumetric ventricular contraction you may get a increase in right ventricular pressure but most importantly a little bit of a bulge back in to the right atrium and so that is known as the c wave the x descent is right atrial relaxation in which now as the right ventricle is contracting doing its thing in the bottom you are going to have the right atrium starting to relax why do you have the right atrium starting to relax well guys it's all about gradients you need to have a gradient between your superior and inferior vena cava and have that gradient so that blood can passively fill into the right atrium so atrial relaxation is going to be the x descent now the v wave is going to represent inflow of the venous blood so let me do that in blue you note that the venous blood is going to come from the svc from the ivc now that the atrial pressure is going to be low thanks to the x descent the v wave represents ah it is going to be filling the vena cava are going to fill the atrium and then finally you have the y descent and the y descent is going to represent all of this blood that is in this highlighter blue going down into the right ventricle because you have passive emptying of the right atrium after tricuspid valve opening so now what we need to understand is that the jvp tracing super important for you to know i think the prominent a-wave is going to be your test question but you now know the whole phase and all of the elements of the jvp tracing all right wonderful let's go ahead and go through this question we're going to say the word stem first what is the most likely vital sign change which may be present in this patient let's go line by line a 30 year old male is hit in the chest with the baseball bat he is tachycardic and has shallow respirations on palpation of his abdomen a prominent jugular vein is appreciated bedside echo shows a collapsed atria on diastole what do you think is going to happen go ahead and take some time and answer this question put your answer into the chat box this is a tough question and as this session is going on we're building on concepts we're building on concepts hmm what do you think the answer is here well whenever you see the atria being collapsed in diastole especially after a trauma you should think about an important important pathology and that is cardiac tamponade and in cardiac tamponade you are going to hear something known as pulses paradoxes so now let's go into what is pulses paradoxes well that is actually answer choice d or excuse um answer choice which is oh did i make a mistake here sorry it is going to be a decrease in systolic blood pressure by 10 during inhalation i apologize for that so the answer everybody got it uh correct because i didn't put the correct answer in there but it is a decrease in systolic blood pressure by 10 during inhalation so when you're thinking about pulses paradoxes that finding is seen in various pathologies but most importantly on your usmle it is going to be seen in cardiac tamponade now in cardiac tamponade remember that there is fluid that surrounds the heart and if there's fluid that surrounds the heart what we have to understand is that excuse me the non-muscular chambers of the heart i.e the atria those are going to collapse during diastole because there is so much fluid as the atria is going to relax remember during that x descent you are going to have the collapse of the atria now on your usmle you are going to note a triad that sneakily shows up for cardiac tamponade and that is what jvd hypotension and muffled heart tones but you need to understand that the practical way this shows up on your exam is they'll say physical exam shows a prominent jugular vein blood pressure in the vital signs is going to be low and you are going to hear heart sounds that are inaudible or muffled now what happens during cardiac tamponade that you get pulses paradoxes well remember as the left ventricle or right ventricle because it's a more non-muscular chamber as a right ventricle is going to expand expand expand expand you're going to have an impedance of actually expanding that right ventricle so if you can't expand that right ventricle well the interventricular septum is going to shift over and let me do that in red so you really conceptualize that and as that interventricular septum shifts over you are going to have a impedance in the left ventricular outflow track and if you're going to have the impedance in the left ventricular outflow track you are actually going to have this phenomena of pulses paradoxes because during inspiration you increase preload that causes you to have an exaggerated shift in your interventricular septum such that you decrease your systolic blood pressure by 10 during this time and so why were was it called pulses paradoxes what's the paradox well the paradox is is that you are still going to hear a heartbeat but during inspiration you did not have a pulse you still hear a heartbeat but you did not have a pulse that's a paradox and remember pulse's paradoxes is a decrease in systolic blood pressure by 10 during inspiration they love for you to note that and pathologies like cardiac tamponade can lead to pulses paradoxes all right we are almost rounding out the session i do want to go through pressure volume loops with you now pressure volume loops i want you to recognize the various labels number one let's go ahead and do this active recall question a patient has a rumbling diastolic murmur that's heard at the apex the snap of this murmur occurs at which of the following points so a rumbling diastolic murmur heard at the apex location location location that is mitral stenosis and you hear the opening snap of microstenosis where well when the mitral valve opens and so that's going to be answer choice d that is where the mitral valve opens so let's go ahead and go through all of these cardiac events remember that a represents the mitral valve closure and that mitral valve closure is going to be related to what heart sound guys s1 yes that's going to be related to s1 remember that your end diastolic volume is going to be very very high when the atrial or when the mitral valve closes why is that because the ventricles just got filled point b is going to represent aortic valve opening so what's this point between a and b that's isovolumetric ventricular contraction an isovolumetric ventricular contraction you are going to have an increase in your pressure which is going to be this y-axis but no change in your volume and you recognize that the qrs complex is going to be the electrical activity that precedes this mechanical activity and all valves are going to be closed during this phase and then at point b the aortic valve is going to open at point c you are going to note your aortic valve closed asd just a nice little test taking pearl and then d is going to represent the mitral valve opening which we just covered in that active recall question so what's the point between c and d well you remember the the volume is not necessarily changing but the pressure is decreasing and if the pressure is decreasing you're worried about or thinking about isovolumetric ventricular relaxation now let's understand some important physiology concepts here this right here point b represents your end diastolic volume and point c represents your end systolic volume so remember hey i'm done filling is end diastolic volume hey i'm done contracting is end systolic volume so edv minus esv that's known as your stroke volume and so what if i gave you this edv hey i'm done filling minus hey i'm done contracting which is your stroke volume and divided it by edv which is going to be the original well that's known as your ejection fraction so your ejection fraction which we commonly see in test questions come up during uh questions related to congestive heart failure ejection fraction is merely your stroke volume over your end diastolic volume the change over the original and also note that two um and also note that when you're talking about stroke volume stroke volume is actually one of the mediators for cardiac output so remember cardiac output is stroke volume times heart rate you know that and what are the mediators that affect stroke volume that's going to be contractility afterload and preload so how to optimize your stroke volume you increase contractility you increase preload and you reduce after load i.e the resistance coming out of the heart so why did i put these two stars here and i'm going to put a blue highlighter to show you this well remember that this portion right here where this first star is right before your aortic valve opens that's going to be known as your diastolic blood pressure your diastolic blood pressure is going to be right before your aortic valve opens and then this curve right here this star that's going to be your systolic blood pressure because that's going to be the peak of ventricular ejection so another way to kind of conceptualize this and now what we're going to do is we're going to look at various changes that they put on the usmle so remember that the black is going to represent the original and the red is going to represent the change and as you can see you have an end diastolic volume here but look at this end systolic volume this end systolic volume is actually a little bit less so what are test vignettes related to this well the concept here is for us to understand that this may represent increased contractility the heart is squeezing more and if you have higher contractility you are going to have a higher stroke volume and thus you're going to end at a lower end systolic volume end of sicily so that high stroke volume is going to also be related to the concept of a high ejection fraction and understand that your usmle vignettes relevant to this change are going to be worded in the following way they'll say increase beta 1 mediated activity maybe they gave dobutamine maybe they gave epinephrine that pharmacology question is going to be very important increase in intracellular calcium remember that if you phosphorylate phospholamban you are going to get an increase in intracellular calcium which is going to cause you to have an increase in contractility what about this one a patient started on a medication for heart failure and suddenly develops vision changes and increase k what do you think this is well the point that i'm going for here is going to be digoxin toxicity you're absolutely correct so remember digoxin is used as an agent to increase contractility it has a narrow therapeutic index and we note that the mechanism of action is blocking the potassium leaflet of the sodium potassium atpase so when patients have digoxin toxicity they can get hyperkalemia and what's important for us to know in the mechanism of action of digoxin is that yes it inhibits the sodium potassium atpase but as a result it makes calcium more difficult to leave the myosin and so if calcium is within the intracellular space of the myocyte you get increase in contraction another advanced concept that you can see in test questions is understanding the slope of these curves and let me highlight the first slope in green and you see that this represents your end systolic pressure volume relationship and that's actually really important for us to know end systolic pressure volume relationship and if the slope is going to be downtrended like for example in the green line that you see that's going to represent a decrease in ionotropy i.e a decrease in contractility whereas if you see a patient or a curve on your usmle with the slope that's a little bit more steep that means that you have a higher steep and that means you have a increase in ionotropine and that increase in ionotropy is the same thing as increasing contractility you note that your end systolic volume is going to be obviously on the lower end because your heart is squeezing more of that blood out and those are the vignettes that we just talked about in the last slide another element that we need to think about is going to be the end diastolic pressure volume relationship so you see here that there is not only a curve that we see at the top where the lines were but in purple watch my purple line this represents the end diastolic pressure volume relationship and that is kind of related to the compliance of the heart so for example if you have increased compliance you are going to have a shift this way whereas if you have a decrease in compliance think about a very stiff stiff stiff left ventricle you're going to have a decrease in compliance the shift of those curves may show up on your exam and so remember when you have decreased compliance that means that the left ventricle is going to be very very thick left ventricular hypertrophy all right another important curve for you to understand is going to be a curve in which you have an increase in pre-load and so you have an increase in pre-load that means that you are going to have a higher end diastole volume remember left ventricular end diastolic volume is the same thing as preload just understand basically to summarize it it is how much goes back to the heart i.e how much blood goes back to the heart that is going to be your preload which is your end diastolic volume so remember when you have an increase in venous tone all of that blood that is pooled in your venous system that is going to go up and go into your heart and you get an increase in end diastolic volume so exercise for example causes you to release a lot of catecholamines and you increase your venous tone and that shifts you to having more preload to your heart high venous tone related to exercise that's a common question that they ask on the usmle nitrates for example do the opposite nitrates are going to decrease your venous tone and it they're going to cause you to have pooling of the blood into your extremities another u.s emily vignette is going to be the following here you have a patient who recently was placed on hemodialysis for chronic kidney disease the patient is noted to have a hyperdynamic precordium so they're bouncing bouncing bouncing they have bounding pulses what is the diagnosis well remember any time on your usmle questions you see an av fistula man think about an increase in preload i cannot call i cannot stress that enough that an increase in preload is going to be due to an av fistula in which the blood is bypassing your capillaries and you're going artery to vein and bam back to the heart so av fistula is very important questions related to av fistula related to chronic kidney disease and having a dialysis catheter or even for uh fracture healing remember that during fracture healing you have an increase in blood vessels that occur in your bone remember those havershan and volkman canals exactly that histology tine is very relevant here you get more arterial venous connections passive leg raise as well as squatting those are two maneuvers that are going to increase the amount of blood coming back to your heart i.e increase your preload and remember guys you have an increase in end diastolic volume during this time all right another thing that is going to increase your preload is going to be inspiration please know this inspiration is going to increase your preload am i an inspiration to you dad joke but inspiration is going to increase your preload why well understand that during inspiration follow this graph with me you have in intercostal muscles that are going to contract and you are going to have the diaphragm contract remember that inspiration is going to be an active process and what does that do well that causes your pleural pressure here i'm going to highlight in yellow your pleural pressure ends up becoming very negative well if your pleural pressure ends up becoming very negative you have a better gradient that forms between your vena cava system here in blue and what yes you got it your right atrium which is going to be marked in purple right here so as you are going to expand the lungs with your inspiration you get a negative intrapleural pressure and that causes blood from the svc to ha plop into the right atrium and so in pathology such as constrictive pericarditis this relationship actually is not going to be there because your heart is going to be unable to take that preload that is coming from the svc and the ivc especially during inspiration why because constrictive pericarditis the heart is trying to come out but oh there's calcification surrounding that heart what are vignettes related to that ah recurrent tuberculosis for example that's gonna cause you to have constrictive pericarditis ladies and gentlemen this is the way that you have to learn right you have to learn the concept and the way that i like to teach it as i like to say hey yo how does it present on the exam how does it predict on the exam how do the test makers go for it what is the strategy to get to the correct answer that's innovative that's unique let's keep going five more slides guys five more slides stick with me respiratory muscles are going to contract during inspiration you are going to get an increase in your negative intrapreneur pressure obviously your intrapleural pressure is going to become more negative you're going to get more of your venous pool causing you to have a higher venous return and the other mediators are a little bit more advanced i.e you're decreasing right ventricular afterload or an increase in lv afterload you don't need to worry about that right now on this slide but i do want to let you know that inspiration causes a negative intrathoracic pressure and increases your preload please know that concept for your us emily all right just wrapping up here you are going to note here in this curve anytime you see the curve shifting upwards put that capital a just like first aid has it i like that mnemonic that means that you have an increase in afterload you also are going to have an increase in n-systolic volume why is that because after you contract and if you have a high afterload system you're contracting contracting contracting contracting contracting but because you are unable to actually contract all of the blood due to high resistance in the aorta your end systolic volume the volume after systole is going to be increased why because you weren't able to pump it out and so thus you have a reduced stroke volume because remember stroke volume is going to be end diastolic volume minus end systolic volume and so if you have a higher end systolic volume your stroke volume is going to go down so what are going to be us emily vignettes related to this change well afterload is largely dependent on aortic pressure high aortic pressure high afterload your left ventricle gets pissed off high blood pressure is going to cause an increase in afterload and then also this question right here a 70 year old man who presents with passing out he has chest pain non-tender to palpation walk test notes a murmur at the right second intercostal space is noted what is the likely mechanism so in this patient you note ah and this is related to aortic stenosis and remember it's an elderly person so it's age-related calcific stenosis aortic stenosis causes you to have a high afterload so you can see this curve in aortic stenosis so remember that if i gave you the same question and i changed this to like a 50 year old patient think about bicuspid aortic valve that causes you to have premature aortic stenosis very important for you to know all right guys cardiac action potentials we're going to be talking about the ventricular and we are going to be talking about the sinoatrial action potential stick with me here where is the ventricular action potential well in order to conceptualize it it's primarily going to be in the muscles of your left ventricle also in the muscles of your atria that's where you see this action potential so remember that this action potential is going to be defined by phase 0 in which sodium is going to come in very quickly phase 1 is just the abrupt closure of the sodium channel not as high yield but phase two is actually really really important in which you have this isoelectric stage calcium is coming in through the l-type calcium channels and potassium is coming out and that type of charge differential causes you to have a neutral line on the action potential phase three just like in skeletal muscle for example or just like even in the nodal action potential as we're going to talk about that is going to be potassium effluxing out and you're going to have repolarization back to phase four and remember phase four of the ventricular action potential is defined by potassium very important phase four from the ventricular action potential is defined by potassium many cell membranes actually are defined by the equilibrium potential of potassium so in ventricular muscle what ion determines phase 4 of the cardiac action potential we talked about this that's going to be your potassium permeability and recognize that phase 0 is going to be related to sodium influx and what phase of the ventricular action potential defines the difference between skeletal action potential versus ventricular action potential and that is phase two remember phase two that was what here we have zero one and ah two that's very unique to ventricular action potential remember that skeletal action potential is very simple up down ventricular action potential has that phase two that isoelectric phase other differences between cardiac and skeletal muscle remember cardiac muscle has what we call calcium induced calcium release and cardiac cardiac muscle has gap junctions and those gap junctions are really important because that's what allows the electrical activity of the heart to kind of propagate everywhere and allows the ventricles in particular to contract in a sensation did we just go through physiology a little bit of histology we went through a little bit of anatomy we are putting all of the puzzle pieces together and this is the way that questions are also asked in this integrative fashion all right wrapping up guys the nodal action potential this is typically seen see where all this red stuff is in the sa node in the av node right you see this type of action potential the other one was in the muscles this is seen in the actual electrical portions the circuitry you see that the phase four of this action potential is actually going to be defined by funny channels and those sodium funny channels are going to be these leaky leaky channels that as soon as you then hit threshold you are going to trigger phase zero and put a star right here because phase zero in the nodal action potential is calcium mediated if i asked you what was it in the ventricular action potential you would say that that was sodium sodium is phase zero in the ventricular action potential in the nodal action potential it's calcium there is no plateau phase so adios phase one and phase two and phase three is going to be potassium repolarization all right guys well if we look at this application question as we close this session let's go through it a farmer is working in the field and suddenly experiences lacrimation rhinorrhea and diarrhea he is wet wet wet leaky leaky leaky he begins to have sweating and bronchospasm so he has what high parasympathetic state his heart rate is found to be 45. you notice that he has high parasympathetic state so if you have a high parasympathetic state this is going to be your organophosphate poisoning and yes the neurotransmitter that's going to be elevated is going to be acetylcholine now what phase of the nodal action potential does his bradycardia affect well that's going to be phase 4. remember phase 4 of the nodal action potential actually defines your heart rate and that's high yield for you to understand in fact if i gave you different curves remember that bradycardia i'm going to put it in red is going to represent your phase 4 slope going like this in which it takes longer for you to actually fire that action potential and that is basically what bradycardia bradycardia is going to be a very prolonged phase 4 slope and remember phase 4 determine is going to be mediated by what it's going to be mediated by your funny channels all right well enough funny jokes today we have covered a lot i really encourage you all to put in the chat box questions before you start asking your questions i do want to let you know that i have many resources for you to check out number one i do want to let you know that when i was going through my usmle preparation it took me forever to go through my u-world blocks especially the dense explanations so i made a set of notes for you that you can use to follow along with your u world explanations have everything in one place so you don't have to make a very detailed journal on your own i did give you a sample of the cardiology um and i will provide that also at the end of the session and then i have revamped my rapid review course and the rapid review course guys is basically the top concepts that you need to know for your exam i recommend you getting this like three four five weeks before your exam or even right before you take an nvme you can watch this rapid review course now there are some free lectures there are some paid lectures but let me tell you even if you don't get my rapid review course let me tell you what i think is so important in the days leading up to the exam that's why i made this resource because i was like holy i don't know what to study in the days leading up to the exam and i think that chapters one through three of pathoma which i have made an active recall integrative just like this question based review of the concepts that's in my rapid review course the first aid rapid review section forget the anki cards i mean come on you need to go through the first aid rapid review section in an organ system based way so you'll see in those lectures you'll see bam cardiology what are the top concepts endocrine what are the top concepts and i give you these pearls test taking pros as you're going through i also wanted to make a lecture reflecting the october and november 2020 changes because i know this is anxiety provoking for a lot of us what are they going to test well i went through the newest content outline and i said all right here are the ethical concepts and the ethical scenarios they may test the patient safety concepts pbli these are all important important elements that they are starting to put now more with these november changes 100 concepts in gross anatomy i have a lecture on youtube on that that's part of my rapid review course that's a free one for you guys to check out just to see if you like the way that i'm teaching autonomic pharmacology i also think that that's important because remember those questions are going to have a lot of not only farm times but physiology times you got to know for example in my lecture i say alpha 1 causes vasoconstriction well beta 2 causes vasodilation v1 causes vasoconstriction so see i'm comparing and contrasting things and this is just a very dynamic way to learn and i've asked you so many questions throughout this session next i think it's important for us to go through metabolic pathways so i've made a active recall powerpoint that you can flip through right before your usmle exam and master things like glycolysis things like fatty acid oxidation etc and you can at least get the endocrine tie-ins that's related to biochemistry as well as the physiology and path tie-ins so this course is really really important for you to really kind of get and also make sure that you just cover these material even if you don't get the course go through patoma chapters one through three go through the rapid review these are the essential elements here is the pricing um for all of these uh resources i also have a study plan that comes with a session with me that i walk you through how to make a study plan and feel free to just email me if you are interested in any of this and also check out my website my website higru.com i just actually uh revamped this website so check it out i made a cool video and everything like that all of these purchases that you make on my website guys goes back into making these kind of webinars for you making youtube videos study diagrams integrative questions etc i really thank you all for attending and i would be more than happy to take any questions at this time thanks again for your active participation all right